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Fastest Basicmedical Insight Engine
GENERAL & FAMILY MEDICINE
HUMAN BIOLOGY & GENETICS
MEDICAL DICTIONARY & TERMINOLOGY
PATHOLOGY & LABORATORY MEDICINE
Sarah A. Spinler and Simon de Denus
The cause of an acute coronary syndrome (ACS) is the rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, and aggregation, and the activation of the clotting cascade. Ultimately, a clot forms composed of fibrin and platelets.
The American College of Cardiology Foundation (ACCF), American Heart Association (AHA), and Society for Cardiovascular Angiography and Interventions (SCAI) recommend strategies, or guidelines, for ACS patient care for ST-segment elevation (STE) myocardial infarction (MI) and non–ST-segment elevation (NSTE) ACS, including guidelines for patients undergoing percutaneous coronary intervention (PCI).
Patients with ischemic chest discomfort and suspected ACS are risk-stratified based on a 12-lead electrocardiogram (ECG), past medical history, and results of the troponin and creatine kinase (CK)–myocardial band (MB) tests. The diagnosis of MI is confirmed based on the results of the CK-MB and troponin biochemical marker tests.
Early reperfusion therapy with primary PCI of the infarct artery is the recommended therapy for patients presenting with STE MI within 12 hours of symptom onset.
The most recent PCI ACCF/AHA/SCAI clinical practice guidelines recommend coronary angiography with either PCI or coronary artery bypass graft (CABG) surgery revascularization as an early treatment (early invasive strategy) for patients with NSTE ACS at an elevated risk for death or MI, including those with a high risk score or patients with refractory angina, acute heart failure, other symptoms of cardiogenic shock, or arrhythmias.
In addition to reperfusion therapy, other early pharmacotherapy that all patients with STE MI and without contraindications should receive within the first day of hospitalization, and preferably in the emergency department, are intranasal oxygen (if oxygen saturation is low), sublingual (SL) nitroglycerin (NTG), aspirin (ASA), a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor depending on reperfusion strategy), and anticoagulation with bivalirudin, unfractionated heparin (UFH), enoxaparin, (agent dependent on reperfusion strategy), or fondaparinux. A glycoprotein (GP) IIb/IIIa inhibitor should be administered if UFH is selected as the anticoagulant for patients undergoing primary PCI. A statin should be administered prior to PCI. IV β-blockers and IV NTG should be given in selected patients. Oral β-blockers should be initiated within the first day in patients without contraindications.
In the absence of contraindications, all patients with NSTE ACS should be treated in the emergency department with intranasal oxygen (if oxygen saturation is low), SL NTG, ASA, and an anticoagulant (UFH, enoxaparin, fondaparinux, or bivalirudin). High-risk patients should proceed to early angiography, and may receive a GP IIb/IIIa inhibitor. A P2Y12 inhibitor (selection of agent and timing of initiation dependent on selection of an interventional approach involving PCI or CABG surgery vs. a noninterventional approach with medical management alone) should be administered to all patients. A statin should be administered prior to PCI. IV β-blockers and IV NTG should be given in selected patients. Oral β-blockers should be initiated within the first day in patients without contraindications.
Secondary prevention guidelines from the ACCF/AHA suggest that following MI from either STE MI or NSTE ACS, all patients, in the absence of contraindications, should receive indefinite treatment with ASA, a β-blocker, a statin, and an angiotensin-converting enzyme (ACE) inhibitor for secondary prevention of death, stroke, or recurrent infarction. The goal low-density lipoprotein cholesterol is less than 100 mg/dL (2.59 mmol/L) and ideally less than 70 mg/dL (1.81 mmol/L). A P2Y12 inhibitor should be continued for at least 12 months for patients undergoing PCI and for patients with NSTE ACS receiving a medical management strategy of treatment. Clopidogrel should be continued for at least 14 days in patients with STE MI in patients not undergoing PCI. An angiotensin II receptor blocker and a mineralocorticoid receptor antagonist should be given to selected patients. For all patients with ACS, treatment and control of modifiable risk factors such as hypertension (HTN), dyslipidemia, obesity, smoking, and diabetes mellitus are essential.
To determine the efficacy of nonpharmacologic treatments and pharmacotherapy, monitor patients for relief of ischemic discomfort, return of ECG changes to baseline, and absence or resolution of heart failure signs and symptoms. The most common adverse effects from pharmacotherapy of ACS are bleeding and hypotension.
Cardiovascular disease (CVD) is the leading cause of death in the United States and one of the major causes of death worldwide. Acute coronary syndromes (ACSs), including unstable angina (UA) and myocardial infarction (MI), are a form of coronary heart disease (CHD) that comprises the most common cause of CVD death.1 The cause of an ACS is primarily the rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, and aggregation, and the activation of the clotting cascade. Ultimately, a clot forms composed of fibrin and platelets. The American Heart Association (AHA) and the American College of Cardiology Foundation (ACCF) recommend strategies, or guidelines, for ACS patient care for ST-segment elevation (STE) and non–ST-segment elevation (NSTE) ACS. In collaboration with the Society for Cardiovascular Angiography and Interventions (SCAI), the ACCF and AHA issue joint guidelines for percutaneous coronary intervention (PCI), including PCI in the setting of ACS. These practice guidelines are based on a review of available clinical evidence, have graded recommendations based on evidence and expert opinion, and are updated periodically. These guidelines form the cornerstone for quality care of the ACS patient.2–7
Each year, more than 1.1 million Americans will experience an ACS, and 150,000 die of an MI.1 In the United States, more than 7 million living persons have survived an MI.1
CVDs are the leading cause of hospitalization in the United States, resulting in about 6.2 million hospital discharges per year. Each year, there are more than 1.3 million MIs, and one in six deaths is secondary to CHD.1
The proportion of patients with MI presenting with STE MI compared with those presenting with NSTE MI decreased from approximately 80% in the early 1990s to between 25% and 30% currently.1 This may be secondary to the use of the more sensitive biomarker troponin (increasing the diagnosis of MI in the NSTE ACS group), greater use of antecedent revascularization procedures, decreased reinfarction from enhanced medical therapy after an initial event, or prevention of progression of UA to MI through more effective anticoagulant and antiplatelet therapy.
According to data from the National Registry of Myocardial Infarction, in-hospital mortality has decreased by more than 20% during the last 20 years. Improvements in care that may have contributed to this mortality reduction include greater use of guideline-recommended drugs (e.g., aspirin [ASA], β-blockers, angiotensin-converting enzyme [ACE] inhibitors and angiotensin receptor blockers [ARBs], statins, clopidogrel), reductions in the door-to-needle time for administering fibrinolytics and in the corresponding first medical contact time to primary PCI, treatments for heart failure (HF), and increased use of early coronary angiography and PCI for high-risk patients with NSTE ACS.1
In patients with STE MI, in-hospital death rates are approximately 3% in patients receiving primary PCI, 7% for patients who are treated with fibrinolytics, and 16% for patients who do not receive reperfusion therapy. In patients with NSTE MI, in-hospital mortality is less than 5%. At 6 months and 1 year, mortality and reinfarction rates are similar between STE and NSTE MI.1 Other than persistent ST-segment changes and troponin, other predictors of in-hospital mortality include older age, elevated serum creatinine (SCr), tachycardia, and HF.1,2,8 One-year mortality following STE MI ranges from 7% to 18%.2
CHD is the leading cause of premature, chronic disability in the United States. The risks of CHD events, such as death, recurrent MI, and stroke, are higher for patients with established CHD and a history of MI than for patients with no known CHD. The cost of CHD is high, with estimated direct and indirect costs of more than $195 billion.1 The estimated cost of hospitalization for MI is $14,000, and the median length of hospital stay is 3.2 days.1,2 Risk-standardized hospital mortality for MI and 30-day hospital readmission rates following MI and PCI are quality performance measures and Outcome of Care Measures that are publically reportable by the Center for Medicare and Medicaid Services.6 The Patient Protection and Affordable Care Act of 2010 links quality performance measures to hospital reimbursement.
Endothelial dysfunction, inflammation, and the formation of fatty streaks contribute to the formation of atherosclerotic coronary artery plaques, the underlying cause of coronary artery disease (CAD).7 The predominant cause of ACS in more than 90% of patients is atheromatous plaque rupture, fissuring, or erosion of an unstable atherosclerotic plaque that occludes less than 50% of the coronary lumen prior to the event, rather than a more stable 70% to 90% stenosis of the coronary artery.9 Stable stenoses are characteristic of stable angina.
Spectrum of ACSs
ACSs include all clinical syndromes compatible with acute MI resulting from an imbalance between myocardial oxygen demand and supply. In contrast to stable angina, an ACS results primarily from diminished myocardial blood flow secondary to an occlusive or partially occlusive coronary artery thrombus. ACSs are classified according to electrocardiogram (ECG) changes into STE MI or NSTE ACS (NSTE MI and UA) (Fig. 7-1).10 An STE MI occurs when symptoms of myocardial ischemia occur in conjunction with new STE with subsequent release of biomarkers of myocardial necrosis, mainly troponins T or I, but also creatine kinase (CK)–myocardial band (MB).2 An STE MI, formerly known as Q-wave or transmural MI, typically results in an injury that transects the thickness of the myocardial wall. Following an STE MI, pathologic Q waves are frequently seen on the ECG, indicating transmural MI, whereas such an ECG manifestation is seen less commonly in patients with NSTE MI.3 NSTE MI, formerly known as non–Q-wave or nontransmural MI, is limited to the subendocardial myocardium. Patients in this case do not usually develop a pathologic Q wave on the ECG. Moreover, an NSTE MI is smaller and not as extensive as an STE MI. NSTE MI differs from UA in that ischemia is severe enough to produce myocardial necrosis resulting in the release of a detectable amount of biomarkers, mainly troponins T or I, but also CK MB, from the necrotic myocytes in the bloodstream. The clinical significance of serum markers will be discussed in greater detail in later sections of this chapter.
FIGURE 7-1 Evaluation of the acute coronary syndrome patient. aAs described in Table 7-1. b"Positive": Above the myocardial infarction decision limit. c"Negative": Below the myocardial infarction decision limit. (ACS, acute coronary syndrome; CABG, coronary artery bypass graft; CAD, coronary artery disease; CK-MB, creatine kinase myocardial band; ECG, electrocardiogram; PCI, percutaneous coronary intervention.) (Modified with permission from Spinler SA. Evolution of antithrombotic therapy used in acute coronary syndromes. In: Richardson MM, Chant C, Cheng JWM, et al., eds. Pharmacotherapy Self-Assessment Program. Book 1: Cardiology, 7th ed. Lenexa, KS: American College of Clinical Pharmacy, 2010.)
Plaque Rupture and Clot Formation
Following plaque rupture, a clot (a partially or completely occlusive thrombus) forms on top of the ruptured plaque. The thrombogenic contents of the plaque are exposed to blood elements. Exposure of collagen and tissue factor induces platelet adhesion and activation, which promote the release of platelet-derived vasoactive substances including adenosine diphosphate (ADP) and thromboxane A2 (TXA2).7 These produce vasoconstriction and potentiate platelet activation. Furthermore, during platelet activation, a change in the conformation in the glycoprotein (GP) IIb/IIIa surface receptors of platelets occurs that cross-links platelets to each other through fibrinogen bridges. This is considered the final common pathway of platelet aggregation. Inclusion of platelets gives the clot a white appearance. Simultaneously, the extrinsic coagulation cascade pathway is activated as a result of exposure of blood components to the thrombogenic lipid core and disrupted endothelium, which are rich in tissue factor. This leads to the production of thrombin (factor IIa), which converts fibrinogen to fibrin through enzymatic activity. Fibrin stabilizes the clot and traps red blood cells, which gives the clot a red appearance. Therefore, the clot is composed of cross-linked platelets and fibrin strands.9,11
Ventricular Remodeling Following an Acute MI
Ventricular remodeling is a process that occurs in several cardiovascular (CV) conditions including HF and following an MI. It is characterized by left ventricular dilation and reduced pumping function of the left ventricle, leading to cardiac failure.12 Because HF represents one of the principal causes of mortality and morbidity following an MI, preventing ventricular remodeling is an important therapeutic goal.
ACE inhibitors, ARBs, β-blockers, and mineralocorticoid receptor antagonists (MRAs) are all agents that slow down or reverse ventricular remodeling through inhibition of the renin–angiotensin–aldosterone system and/or through improvement in hemodynamics (decreasing preload or afterload).12 These agents also improve survival and will be discussed in more detail in subsequent sections of this chapter.
This chapter focuses on management of the uncomplicated ACS patient. However, it is important for clinicians to recognize complications of MI, because MI is associated with increased mortality. The most serious complication of MI is cardiogenic shock, occurring in approximately 5% to 6% of hospitalized patients presenting with STE MI.13 Mortality complicated by cardiogenic shock with MI is high, approaching 60%.14 Other complications that may result from MI are HF, valvular dysfunction, bradycardia, heart block, pericarditis, stroke secondary to left ventricular thrombus embolization, venous thromboembolism, left ventricular free wall or ventricular septal rupture, left ventricular aneurysm formation, and ventricular and atrial tachyarrhythmias.2 In fact, more than one quarter of MI patients die, presumably from ventricular fibrillation, prior to reaching the hospital.1
CLINICAL PRESENTATION Diagnosis of ACSs
• The patient is typically in acute distress and may develop or present with acute HF, cardiogenic shock, or cardiac arrest.
• The classic symptom of ACS is midline anterior chest discomfort. Accompanying symptoms may include arm, back, or jaw pain, nausea, vomiting, or shortness of breath.
• Patients less likely to present with classic symptoms include elderly patients, diabetic patients, and women.
• No signs are classic for ACS.
• Patients with ACS may present with signs of acute HF including jugular venous distention and an S3 sound on auscultation.
• Patients may also present with arrhythmias, and therefore may have tachycardia, bradycardia, or heart block.
• Troponin I or T and CK-MB are measured at the time of first assessment and repeated at least once, 6 to 9 hours later to ascertain heart muscle damage, confirmatory for the diagnosis of infarction. For patients with NSTE ACS, an elevated troponin is diagnostic for MI, defining a NSTE MI. Patients presenting with suspected NSTE ACS who do not have an MI undergo further diagnostic testing to determine whether or not they have UA or ACS.
• Blood chemistry tests are performed with particular attention given to potassium and magnesium, which may affect heart rhythm.
• SCr is measured and CrCl is used to identify patients who may need dosing adjustments for some medications as well as those who are at high risk of morbidity and mortality.
• Baseline complete blood count (CBC) and coagulation tests (aPTT and INR) should be obtained, as most patients will receive antithrombotic therapy that increases the risk for bleeding.
• Fasting lipid panel (optional).
• The 12-lead ECG is the first step in management. Patients are risk-stratified into two groups: STE ACS and suspected NSTE ACS.
• High-risk ACS patients and those with recurrent chest discomfort will undergo coronary angiography via a left heart catheterization and injection of contrast dye into the coronary arteries to determine the presence and extent of coronary artery stenosis.
• During hospitalization, a measurement of LVF, such as an echocardiogram, is performed to identify patients with low EFs (less than 40%) who are at high risk of death following hospital discharge.
• Selected low-risk patients may undergo early stress testing.
With permission from reference 10.
Symptoms and Physical Examination Findings
The classic symptom of an ACS is midline anterior anginal chest discomfort, most often occurring when an individual is at rest, as a severe new onset, or as an increasing angina that is at least 20 minutes in duration. The chest discomfort may radiate to the shoulder, down the left arm, and to the back or to the jaw. Associated symptoms that may accompany the chest discomfort include nausea, vomiting, diaphoresis, or shortness of breath. Although similar to stable angina, the duration may be longer and the intensity greater. All healthcare professionals should review these warning symptoms with patients at high risk for CHD. On physical examination, no specific features are indicative of ACS.
Twelve-Lead ECG
There are key features of a 12-lead ECG that identify and risk-stratify a patient with an ACS. Within 10 minutes of presentation to an emergency department with symptoms of ischemic chest discomfort, a 12-lead ECG should be obtained and interpreted. When possible, a 12-lead ECG should be performed by emergency medical system providers in order to reduce the delay until myocardial reperfusion. If available, a prior 12-lead ECG should be reviewed to identify whether or not the findings on the current ECG are new or old, with new findings being more indicative of an ACS. Key findings on review of a 12-lead ECG that indicate myocardial ischemia or infarction are STE, ST-segment depression, and T-wave inversion (Fig. 7-1).10 ST-segment and/or T-wave changes in certain groupings of leads help to identify the location of the coronary artery that is the cause of the ischemia or infarction. In addition, the appearance of a new left bundle-branch block accompanied by chest discomfort is highly specific for acute MI. About one half of patients diagnosed with MI present with STE on their ECG, with the remainder having ST-segment depression, T-wave inversion, or, in some instances, no ECG changes. Some parts of the heart are more "electrically silent" than others, and myocardial ischemia may not be detected on a surface ECG. Therefore, it is important to review findings from the ECG in conjunction with biochemical markers of myocardial necrosis, such as troponin I or T, and other risk factors for CHD to determine the patient's risk for experiencing a new MI or having other complications.
Biochemical Markers/Cardiac Enzymes
Biochemical markers of myocardial cell death are important for confirming the diagnosis of MI. The diagnosis of acute MI is confirmed when the following conditions are met in a clinical setting consistent with myocardial ischemia: "Detection of a rise and/or fall of cardiac biomarkers (cardiac troponin preferred) with at least one value above the 99th percentile of the upper reference limit with at least one of the following: (a) symptoms of ischemia; (b) new or presumed new significant ST-segment–T wave changes or new left bundle-branch block; (c) development of pathologic Q waves; or (d) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality."15 Typically, a blood sample is obtained once in the emergency department, and then 6 to 9 hours later, and in patients at a high suspicion of MI but in whom previous measurements did not reveal elevations in biomarkers, 12 to 24 hours after. A single measurement of a biochemical marker is not adequate to exclude a diagnosis of MI, as up to 15% of values that were initially below the level of detection (a "negative" test) rise to the level of detection (a "positive" test) in subsequent hours. While troponins and CK-MB appear in the blood within 6 hours of infarction, troponins stay elevated for up to 10 days while CK-MB returns to normal values within 48 hours. Hence, traditionally, CK-MB was used to detect reinfarction. However, more recent data have suggested that troponins provide similar information to CK-MB in such a situation that has led to the use of troponins in this setting as well. Current guidelines suggest that, in patients in whom a recurrent MI is suspected, a cardiac biomarker should be immediately measured, followed by a second measurement 3 to 6 hours later. A recurrent MI is diagnosed when there is an increase of at least 20% in the second measurement of the biomarker, if this value exceeds the 99th percentile of the upper reference limit.15
Patient symptoms, past medical history, ECG, and biomarkers, particularly cardiac troponins, are utilized to stratify patients into low, medium, or high risk of death, MI, or likelihood of failing pharmacotherapy and needing urgent coronary angiography and PCI (Table 7-1).3,5,16 Initial treatment according to risk stratification is depicted in Figure 7-1.2–5,8,10 Patients with STE MI are at the highest risk of death. Initial treatment of STE MI should proceed without evaluation of the troponins because these patients have a greater than 97% chance of having an MI subsequently diagnosed with biochemical markers. The ACCF/AHA define a target time to initiate reperfusion treatment as within 30 minutes of hospital presentation for fibrinolytics (e.g., streptokinase, alteplase, reteplase, and tenecteplase) and within 90 minutes or less from first medical contact for primary PCI.2,5 The sooner the infarct-related coronary artery is opened for these patients, the lower their mortality and the greater the amount of myocardium that is preserved.17,18 Although all patients should be evaluated for reperfusion therapy, not all patients may be eligible. Indications and contraindications for fibrinolytic therapy are described in Treatment below. Less than 25% of hospitals in the United States are equipped to perform primary PCI. If patients are not eligible for reperfusion therapy, additional pharmacotherapy for STE patients should be initiated in the emergency department and the patient transferred to a coronary intensive care unit. The typical length of stay for a patient with uncomplicated STE MI is less than 4 days.19
TABLE 7-1 Risk Stratification for Acute Coronary Syndromes (ACS)3,4,16,23,24
Risk stratification of the patient with NSTE ACS is more complex because in-hospital outcomes for this group of patients vary with reported rates of death of 0% to 12%, reinfarction rates of 0% to 3%, and recurrent severe ischemia rates of 5% to 20%.17 Not all patients presenting with suspected NSTE ACS will even have CAD. Some will eventually be diagnosed with nonischemic chest discomfort. In general, among NSTE patients, those with ST-segment depression (Fig. 7-1) and/or elevated biomarkers are at higher risk of death or recurrent infarction.
Short-term desired outcomes in a patient with ACS are: (a) early restoration of blood flow to the infarct-related artery to prevent infarct expansion (in the case of MI) or prevent complete occlusion and MI (in UA); (b) prevention of death and other MI complications; (c) prevention of coronary artery reocclusion; and as evidence of restoration of coronary artery blood flow; (d) relief of ischemic chest discomfort; and (e) resolution of ST-segment and T-wave changes on the ECG.
Long-term desired outcomes are control of CV risk factors, prevention of additional CV events, including reinfarction, stroke, and HF, and improvement in quality of life.
General Approach to Treatment
Selecting evidence-based therapies described in the ACCF/AHA guidelines for patients without contraindications results in lower mortality.20–22 General treatment measures for all STE MI and high- and intermediate-risk NSTE ACS patients include admission to hospital, oxygen administration (if oxygen saturation is low, less than 90%), continuous multilead ST-segment monitoring for arrhythmias and ischemia, frequent measurement of vital signs, bedrest for 12 hours in hemodynamically stable patients, avoidance of the Valsalva maneuver (prescribe stool softeners routinely), and pain relief (Figs. 7-2 and 7-3).2–4,8,10,16
FIGURE 7-2 Initial pharmacotherapy for ST-segment elevation myocardial infarction. aFor at least 48 hours. bSee Table 7-2 for dosing and specific types of patients who should not receive enoxaparin.c For the duration of hospitalization, up to 8 days. dFor selected patients, see Table 7-2. eIf pretreated with UFH, stop UFH infusion for 30 minutes prior to administration of bivalirudin (bolus plus infusion). fIncreased risk of major bleeding and intracranial hemorrhage if a GP IIb/IIIa inhibitor is added to an anticoagulant for PCI following fibrinolysis, especially in the elderly; weight risk versus benefit. (ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; CABG, coronary artery bypass graft; GP, glycoprotein; NTG, nitroglycerin; PCI, percutaneous coronary intervention; Subcut, subcutaneous; SL, sublingual; UFH, unfractionated heparin.) (Modified with permission from Spinler SA. Evolution of antithrombotic therapy used in acute coronary syndromes. In: Richardson MM, Chant C, Cheng JWM, et al., eds. Pharmacotherapy Self-Assessment Program. Book 1: Cardiology, 7th ed. Lenexa, KS: American College of Clinical Pharmacy, 2010.)
FIGURE 7-3 Initial pharmacotherapy for non–ST-segment elevation ACS. aFor selected patients, see Table 7-2. bPreferred in patients at high risk for bleeding. cIf pretreated with UFH, stop UFH infusion for 30 minutes prior to administration of bivalirudin bolus plus infusion. dMay require IV supplemental dose of enoxaparin; see Table 7-2. eDo not use if prior history of stroke/transient ischemic attack (TIA), age older than 75 years, or body weight less than or equal to 60 kg. fSubcut enoxaparin or UFH can be continued at a lower dose for venous thromboembolism prophylaxis. (ACE, angiotensin-converting enzyme; ACS, acute coronary syndrome; ARB, angiotensin receptor blocker; CABG, coronary artery bypass graft; CAD, coronary artery disease; CHD, coronary heart disease; GP, glycoprotein; NTG, nitroglycerin; PCI, percutaneous coronary intervention; Subcut, subcutaneous; SL, sublingual; UFH, unfractionated heparin.) (Modified with permission from reference 16.)
Because risk varies and resources are limited, it is important to triage and treat patients according to their risk category. Initial approaches to treatment of STE MI and NSTE ACS patients are outlined in Figures 7-2 and 7-3. Patients with STE are at high risk of death, and efforts to reestablish coronary perfusion, as well as adjunctive pharmacotherapy, should be initiated immediately.
Features identifying low-, moderate-, and high-risk NSTE ACS patients are described in Table 7-1.16,23,24
Nonpharmacologic Therapy
Primary PCI for STE MIs
Early reperfusion therapy with primary PCI of the infarct artery within 90 minutes of first medical contact is the reperfusion treatment of choice for patients presenting with STE MI who present within 12 hours of symptom onset2 (Fig. 7-2). First, emergency medical services are activated for a patient complaining of ischemic symptoms. Paramedics arrive to care for the patient out of the hospital and they perform a 12-lead ECG that demonstrates STE. Sometimes, the 12-lead ECG is transmitted electronically or via telephone to an emergency department where a physician reviews the ECG and may "activate" the cardiac catheterization medical team to alert them that a patient with STE MI will be arriving at the hospital shortly. The patient is transported to the emergency department. For primary PCI, the patient is taken from the emergency department to the cardiac catheterization laboratory and undergoes coronary angiography with either balloon angioplasty or placement of a bare metal or drug-eluting intracoronary stent in the artery associated with the infarct. In order to meet the quality of care metric of less than 90 minutes from first medical contact to primary PCI, many transitions of care occur and care coordination between paramedics, emergency department staff, and cardiac catheterization is vital. Every minute delay results in additional myocardial cell damage that may be irreversible.
About 62% of patients with STE MI are treated with primary PCI; 18% are treated with fibrinolytics. Results from a meta-analysis of trials comparing fibrinolysis with primary PCI indicate a lower mortality rate with primary PCI.25 One reason for the superiority of primary PCI compared with fibrinolysis is that more than 90% of occluded infarct-related coronary arteries are opened with primary PCI compared with fewer than 60% of coronary arteries opened with currently available fibrinolytics.2 In addition, intracranial hemorrhage (ICH) and major bleeding risks from primary PCI are lower than the risks of severe bleeding events following fibrinolysis. An invasive strategy of primary PCI is generally preferred in patients presenting to institutions with skilled interventional cardiologists and a catheterization laboratory immediately available, patients in cardiogenic shock, those with contraindications to fibrinolytics, and those with continuing symptoms 12 to 24 hours after symptom onset.2
A quality performance measure (quality performance measures are measures of quality healthcare developed from practice guidelines and intended to permit the quality of patient care to be assessed, compared between institutions and over time, and, ultimately, improved) in the care of MI patients with STE MI is the time from first medical contact to the time the occluded artery is opened with PCI. This "first medical contact-to-primary PCI" time should be equal to or less than 90 minutes.2 Efforts to improve system-wide rapid triage of patients with STE MI such as participation in the Door to Balloon Time Alliance and Get with the Guidelines (GWTG) educational programs within health systems have resulted in shorter primary PCI times in the United States. In 2010, the median door-to-primary PCI time (meaning the time from hospital arrival to primary PCI) was 64 minutes, decreasing from a median of 96 minutes in 2005.26 In 2005, 44% of patients treated with primary PCI had door-to-primary PCI times of less than 90 minutes, while in 2010 this percentage had increased to 94%.26 Unfortunately, most hospitals do not have interventional cardiology services capable of performing primary PCI 24 hours a day. Patients presenting to facilities that do not have interventional cardiology services can be transferred to such facilities when a transfer protocol that minimizes transfer delays has been established between the institutions and if primary PCI can be performed within the first 120 minutes of medical contact.2
PCI during hospitalization for STE MI may also be appropriate in other patients following STE MI, such as those in whom fibrinolysis is not successful, those presenting later in cardiogenic shock, those with life-threatening ventricular arrhythmias, and those with persistent rest ischemia or signs of ischemia on stress testing following MI.2
PCI in NSTE ACSs
The most recent PCI ACCF/AHA/SCAI clinical practice guidelines recommend coronary angiography with either PCI or coronary artery bypass graft (CABG) surgery revascularization as an early treatment (early invasive strategy) for patients with NSTE ACS at an elevated risk for death or MI, including those with a high risk score (Table 7-1) or patients with refractory angina, acute HF, other symptoms of cardiogenic shock, or arrhythmias (Fig. 7-3).5,8 Several clinical trials support an "invasive" interventional strategy with early angiography and PCI or CABG versus a "conservative medical management" strategy, whereby coronary angiography with revascularization is reserved for patients with symptoms refractory to pharmacotherapy and patients with signs of ischemia on stress testing.5,27 An early invasive approach results in a lower rate of refractory angina during hospital admission and over the first year, as well as a lower frequency of MI at 5 years, but an increased frequency of minor bleeding related to the procedure.27 An early invasive strategy is also less costly than the conservative medical stabilization approach.28 Mortality is not reduced by an early invasive approach in patients with NSTE ACS.27
All patients undergoing PCI should receive low-dose ASA therapy indefinitely. A P2Y12 inhibitor antiplatelet (clopidogrel, prasugrel, or ticagrelor) should be administered concomitantly with ASA for at least 12 months following PCI for a patient with ACS (Table 7-2).2,5 Earlier discontinuation of the P2Y12 inhibitor should be considered if the risk of bleeding outweighs the anticipated benefit in reduction in risk of death, MI, or stroke as well as stent thrombosis.2,5 A longer duration of P2Y12 inhibitor therapy may be considered for patients receiving a drug-eluting stent, as the risk of stent thrombosis is greater on cessation of dual antiplatelet therapy.2,5 Drug-eluting stents reduce the rate of smooth muscle cell growth causing stent restenosis. However, there is a delay in endothelial cell regrowth at the site of the stent that places the patient at higher risk of thrombotic events following PCI. Therefore, dual antiplatelet therapy is indicated for a longer period of time following PCI with a drug-eluting stent. Trials are ongoing evaluating the need for an extended duration in patients without ACS undergoing PCI (greater than 12 months) of P2Y12 inhibitor therapy following PCI. Regardless of whether or not a patient with NSTE ACS receives a stent, the preferred duration of P2Y12 therapy is at least a year.2,5
TABLE 7-2 Evidence-Based Pharmacotherapy for ST-Segment Elevation Myocardial Infarction and Non–ST-Segment Elevation Acute Coronary Syndrome2–5,8
Additional Testing and Risk Stratification
For patients with NSTE ACS, an initial conservative strategy is recommended for patients with a low risk score, normal ECGs, and negative troponin tests who are without recurrence of chest discomfort (Fig. 7-3).3,4
Within the first 3 days of hospital admission patients with MI should have their left ventricular function (LVF) evaluated for risk stratification.2 The most common way LVF is measured is using an echocardiogram to calculate the patient's left ventricular ejection fraction (LVEF). LVF is the single best predictor of mortality following MI. Patients with LVEFs less than 40% (0.40) are at highest risk of death. Patients with ventricular fibrillation or sustained ventricular tachycardia occurring more than 2 days following MI and those with LVEF less than or equal to 30% (0.30, measured at least 40 days after MI) (and have a New York Heart Association functional class I) or who have nonsustained ventricular tachycardia secondary to a prior MI and a LVEF of less than or equal to 40% (0.40) with inducible ventricular fibrillation or ventricular tachycardia at electrophysiology study benefit from placement of an implantable cardioverter-defibrillator (ICD) for sudden cardiac death prevention.29
Predischarge from the hospital, stress testing (Fig. 7-3) is indicated in patients with NSTE ACS where an initial conservative strategy is selected and for patients with STE MI where coronary angiography was not performed and there has been no recurrent ischemia.2–4 Following the stress test, patients deemed not at low risk should undergo left heart catheterization with coronary angiography and revascularization as indicated by the results.3
Early Pharmacotherapy for STE MIs
Pharmacotherapy for early treatment of ACS is outlined in Figure 7-2 and Table 7-2.2–5,8 According to the ACCF/AHA STE MI practice guidelines, in addition to reperfusion therapy, other early pharmacotherapy that all patients with STE MI and without contraindications should receive within the first day of hospitalization, and preferably in the emergency department, are intranasal oxygen (if oxygen saturation is low), sublingual (SL) nitroglycerin (NTG), ASA, a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor depending on reperfusion strategy), and anticoagulation with bivalirudin, unfractionated heparin (UFH), enoxaparin, or fondaparinux (agent dependent on reperfusion strategy; see Table 7-2). A GP IIb/IIIa inhibitor should be administered with UFH for patients undergoing primary PCI. IV β-blockers and IV NTG should be given in selected patients. Oral β-blockers should be initiated within the first day in patients without cardiogenic shock.2–4,8 Morphine is administered to patients with refractory angina as an analgesic and a venodilator that lowers preload. These agents should be administered early while the patient is still in the emergency department. An ACE inhibitor is recommended to be administered within the first 24 hours in patients with STE MI who have either an anterior wall MI or an LVEF less than or equal to 40% (0.40) and no contraindications. Dosing and contraindications for SL and IV NTG, ASA, clopidogrel, β-blockers, ACE inhibitors, anticoagulants, and fibrinolytics are listed in Table 7-2.2–5,8
Fibrinolytic Therapy
Administration of a fibrinolytic agent is indicated in patients with STE MI who present to the hospital within 12 hours of the onset of chest discomfort, have at least a 1 mm STE in two or more contiguous ECG leads, and are not able to undergo primary PCI within 120 minutes of medical contact.2 The mortality benefit of fibrinolysis is highest with early administration and diminishes after 12 hours.30 The use of fibrinolytics between 12 and 24 hours after symptom onset should be limited to patients with ongoing ischemia. Fibrinolytic therapy is preferred over primary PCI where there is no cardiac catheterization laboratory or there would be a delay in "door-to-primary PCI" of more than 90 minutes (of first medical contact) within the institution or 120 minutes (of first medical contact) if the patient is transferred. Indications and contraindications for fibrinolysis are listed in Table 7-3.2 It is not necessary to obtain the results of biochemical markers before initiating fibrinolytic therapy. Because administration of fibrinolytics results in clot lysis, patients who are at high risk of major bleeding (including ICH) presenting with an absolute contraindication should not receive fibrinolytic therapy, as primary PCI is preferred. In patients who have a contraindication to fibrinolytics and PCI, or who do not have access to a facility that can perform PCIs, treatment with an anticoagulant (other than UFH) for up to 8 days can be administered.
TABLE 7-3 Indications and Contraindications to Fibrinolytic Therapy Per ACC/AHA Guidelines for Management of Patients with ST-Segment Elevation Myocardial Infarction2
A fibrin-specific agent, such as alteplase, reteplase, or tenecteplase, is preferred over a non–fibrin-specific agent such as streptokinase.2 Fibrin-specific fibrinolytics open a greater percentage of infarcted arteries. Two trials compared alteplase with reteplase and alteplase with tenecteplase and found similar mortality between agents.31,32 Therefore, alteplase, reteplase, and tenecteplase are acceptable as first-line agents. ICH and major bleeding are the most serious side effects of fibrinolytic agents. The risk of ICH is higher with fibrin-specific agents than with streptokinase.17 However, the risk of systemic bleeding other than ICH is higher with streptokinase than with other more fibrin-specific agents and was higher with alteplase versus tenecteplase in one study.17,30–32
As mentioned previously, less than 20% of patients with STE MI receive fibrinolysis compared with more than 60% receiving primary PCI. However, 17% of eligible patients receive neither primary PCI nor fibrinolysis despite being eligible. The primary reason for lack of reperfusion therapy is that most patients present more than 12 hours after the time of symptom onset. The percentage of eligible patients who receive reperfusion therapy is a quality performance measure of care in patients with MI.33 The "door-to-needle time," the time from hospital presentation to start of fibrinolytic therapy, is another quality performance measure.33 The ACCF/AHA guidelines recommend a "door-to-needle time" of less than 30 minutes from the time of hospital presentation until start of fibrinolytic therapy.8 The median administration time in the United States in 2006 was 29 minutes, with only 50% of patients meeting the quality performance target of less than 30 minutes.34 All hospitals should have protocols addressing fibrinolysis eligibility, dosing, and monitoring.
ASA is the preferred antiplatelet agent in the treatment of all ACSs.2–5,8 ASA administration to all patients who do not have contraindications to ASA therapy within 24 hours before or after hospital arrival is a quality performance measure for MI.33 The antiplatelet effects of ASA are mediated by inhibiting the synthesis of TXA2 through an irreversible inhibition of platelet cyclooxygenase-1. In patients undergoing PCI, ASA prevents acute thrombotic occlusion during the procedure. In patients receiving fibrinolytics, ASA reduces mortality, and its effects are additive to fibrinolysis alone.2,8,35 Additionally, in patients undergoing PCI, ASA, in addition to a P2Y12 inhibitor, reduces the risk of stent thrombosis.5
In patients experiencing an ACS, an initial dose equal to or greater than 160 mg nonenteric ASA is necessary to achieve a rapid platelet inhibition.36,37 Current guidelines for STE MI recommend an initial ASA dose of 162 to 325 mg (Table 7-2).2 This first dose can be chewed in order to achieve high blood concentrations and platelet inhibition rapidly. Preferably, patients undergoing PCI not previously taking ASA should receive 325 mg nonenteric-coated ASA.5 The notion of chewing ASA came from the use of an enteric-coated formulation of ASA in the Second International Study of Infarct Survival (ISIS-2) trial in order to break the enteric coating to ensure more rapid effect.35 Current data suggest that although an initial dose of 162 to 325 mg is required, long-term therapy with doses of 75 to 150 mg daily is as effective as higher doses, and therefore a daily maintenance dose of 75 to 162 mg is recommended in most patients to inhibit the 10% of the total platelet pool that is regenerated daily.37,38 In a large (n = 25,086) randomized trial, high-dose ASA, 300 to 325 mg daily, had similar frequency of CV death, MI, or stroke as well as major bleeding compared with low-dose ASA in the first 30 days following ACS presentation.39,40 Minor bleeding and GI bleeding were less frequent with low-dose ASA. In this trial, patients undergoing PCI during hospitalization had a lower frequency of death, MI, or stroke, but major bleeding was increased with high-dose ASA.43 Post hoc analysis from the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) trial compared outcomes in patients treated with ASA doses of less than or equal to 200 mg with doses of greater than 200 mg daily and found that higher doses were a predictor of major bleeding but demonstrated similar 3-year risk of CV events.41 In the Study of Platelet Inhibition and Patient Outcomes (PLATO), a randomized, double-blind clinical trial comparing ticagrelor with clopidogrel in patients receiving ASA, a post hoc analysis suggested that maintenance doses of ASA above 100 mg daily reduced the effectiveness of ticagrelor.42 Because of increased bleeding risk in patients receiving ASA plus a P2Y12 inhibitor compared with ASA alone, low-dose ASA (81 mg daily) is preferred following PCI.5,43 Low-dose ASA should be continued indefinitely.43
Nonsteroidal antiinflammatory agents other than ASA, as well as cyclooxygenase-2 (COX-2) selective antiinflammatory agents, should be discontinued at the time of STE MI secondary to increased risk of death, reinfarction, HF, and myocardial rupture.8
The most frequent side effects of ASA are dyspepsia and nausea. Patients should be counseled about the risk of bleeding, especially GI bleeding, with ASA.
Platelet P2Y12 Inhibitors
Clopidogrel, prasugrel, and ticagrelor block a subtype of ADP receptor, the P2Y12 receptor, on platelets, preventing the binding of ADP to the receptor and subsequent expression of platelet GP IIb/IIIa receptors, reducing platelet activation and aggregation. Both clopidogrel and prasugrel are thienopyridines and prodrugs that are converted to an active metabolite by a variety of cytochrome P450 (CYP) isoenzymes (Table 7-4).44–46
TABLE 7-4 Pharmacokinetics of Clopidogrel, Prasugrel, and Ticagrelor 44–46
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Portal Hypertension and Cirrhosis
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Looking back all the way to 2016, we had so much fun shooting this for the lovely Affordable Art Fair. We are now know all there is to know about butterflies. No. Really. We do.
As part of our stroll through the best bits of the year we bring you a rerun of October's launch film for Schön!
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As part of our look back at the best bits of 2016, we bring you our first shoot with the good people at the global art franchise: The Affordable Art Fair. This shoot was featured across the London Underground and Milan Metro networK.
London works best when you look at the sky.
Watch the funny moments unfolding behind the scenes of our latest fashion film for issue 31 of Schön! Magazine.
We're pleased to have four of our films selected to be screened at the BAFTA Qualifying Aesthetica Short Film Festival this November, in celebration of innovative short films from around the world.
What makes the perfect shoot day?
At the centre of the creative industries lies 'The Shoot Day' - this coming together of creative minds, technicians, image makers, producers, models, artists, clients, caterers, groomers, etc, is the central event in everything we do.


text:
Joachim Duckart (* 12. Juni 1898 in Leipzig; † 14. November 1952 in Königswinter) war ein deutscher Agrarwissenschaftler, SS-Führer und Beteiligter an der "Umsiedlung" in Litauen während des Zweiten Weltkrieges.

Leben
Duckart, dessen Vater Rudolf Duckart  Reichsmilitärgerichtsrat war, beendete seine Schulzeit am Wilhelms-Gymnasium in Berlin-Tiergarten mit dem Abitur. Am Ersten Weltkrieg nahm er als Kriegsfreiwilliger teil. Danach absolvierte er ein agrarwissenschaftliches Studium an der Landwirtschaftlichen Hochschule in Berlin, das er als Diplom-Landwirt abschloss. Duckart promovierte 1923 mit der Dissertation "Faktoren-Analyse einer Weizenkreuzung" zum Dr. agr. Danach war Duckart als Experte für Saatzucht in Landwirtschaftsbetrieben tätig.

Zur Zeit der Weimarer Republik gehörte er der Deutschsozialen Partei und der paramilitärischen Organisation Stahlhelm an. Zum 1. Dezember 1931 trat Duckart der NSDAP (Mitgliedsnummer 848.887) und Anfang Januar 1933 der SS bei (SS-Nummer 137.297). Bei der SS erreichte Duckart im Juni 1944 den Rang eines SS-Obersturmbannführers. Ab 1937 war Duckart Mitglied des NS-Lehrerbundes.

Nach der Machtübernahme durch die Nationalsozialisten war er zunächst als Schulungsleiter bzw. ab 1934 Hauptschulungsleiter des Rasse- und Siedlungshauptamts (RusHA) im SS-Abschnitt XIV sowie beim Reichsnährstand in Berlin tätig. Ab 1937 nahm Duckart an der Grenzlandhochschule für Lehrerinnenbildung in Schneidemühl eine Lehrtätigkeit für das Fach "Vererbungslehre und Rassenkunde" auf, leitete das "Vererbungswissenschaftliche Seminar" und stand dem dortigen Presseamt des NS-Dozentenbundes vor. In Schneidemühl leitete er zudem das Kreisamt der NSDAP und arbeitete beim Rassenpolitischen Amt der NSDAP (RPA) mit. Duckart war 1939 Autor einer vom RPA und dem Reichsbund der Kinderreichen herausgegebenen antisemitischen Veröffentlichung mit dem Titel: Die Juden von Betsche: Ein Beitrag zum "Wirken" der Juden im deutschen Osten.

Nach Beginn des Zweiten Weltkrieges war Duckardt zunächst bei Höheren SS- und Polizeiführer Danzig-Westpreußen Richard Hildebrandt tätig, wo er als Beauftragter des Reichskommissars für die Festigung deutschen Volkstums und Angehöriger der Abteilung "Planung und Umsiedlung" beim SS-Oberabschnitt Weichsel für die Ansiedlung von Baltendeutschen infolge der Vereinbarungen des Hitler-Stalin-Paktes zuständig war. Nach Ausbruch des Deutsch-Sowjetischen Krieges wurde Duckardt Führer im Stab SS-Oberabschnitt Ostland sowie ab Anfang März 1942 Leiter des Ansiedlungsstabes Ost und war für die Rückführung jener Personen nach Litauen zuständig, deren Ansiedlung er zuvor organisiert hatte. Duckart forcierte Siedlungsschwerpunkte der Volksdeutschen in Litauen, wodurch es zu Vertreibungen der einheimischen Bevölkerung kam. Ab 1943 war Duckart beim Reichssicherheitshauptamt (RSHA) im Referat III B (Staatsangehörigkeit) tätig. Ab 1944 war Duckart infolge des Kriegsverlaufes wieder für die Rückführung der Baltendeutschen aus Litauen ins Deutsche Reich beauftragt und wurde für seine diesbezüglichen "besonderen Leistungen" im gleichen Jahr mit dem Kriegsverdienstkreuz ausgezeichnet.

Nach Kriegsende befand sich Duckart für einige Jahre in amerikanischer Internierung. Nach der Entlassung aus alliierter Internierung fand Duckart 1949 eine leitende Anstellung in einem landwirtschaftlichen Betrieb und war beratend für die Landwirtschaftskammern Bonn und Köln tätig. Zudem war er Bundesvizepräsident des Bundesausgleichsamts.

Literatur
 Hans-Christian Harten, Uwe Neirich, Matthias Schwerendt: Rassenhygiene als Erziehungsideologie des Dritten Reichs. Bio-bibliographisches Handbuch, Akademie Verlag, Edition Bildung und Wissenschaft Band 10, Berlin 2006, ISBN 978-3-05-004094-3 ISBN 3-05-004094-7.

Einzelnachweise

Agrarwissenschaftler (20. Jahrhundert)
Person (deutsche Besetzung Litauens 1941–1945)
Person (deutsche Besetzung Polens 1939–1945)
Person (Reichssicherheitshauptamt)
SS-Mitglied
NSDAP-Mitglied
NSDDB-Funktionär
Mitglied im Stahlhelm
Mitglied der Deutschsozialen Partei (Weimarer Republik)
Person im Ersten Weltkrieg (Deutsches Reich)
Deutscher
Geboren 1898
Gestorben 1952
Mann

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text:
Now streaming: Amy Adams in 'Hillbilly Elegy,' a new 'Black Beauty,' holiday shows and more
November 25, 2020 [email protected]_84 Adams, Amy, beauty, Black, Elegy, Hillbilly, Holiday, shows, streaming
Here's what's new on Video on Demand, Netflix, Amazon Prime, Hulu and other services.
Top streams of the week
"Hillbilly Elegy" (2020, R), based on the bestselling memoir by J.D. Vance, stars Gabriel Basso as a Yale law student drawn back to Northern Kentucky to deal with his meth-addict mother (Amy Adams) and confront the dead-end life he escaped. Haley Bennett, Freida Pinto and Glenn Close co-star and Ron Howard directs. (Netflix)
Paul Bettany is "Uncle Frank" (2020, R) in Alan Ball's road movie about a closeted gay literature professor in 1969 New York who reluctantly returns to his South Carolina home with his niece (Sophia Lillis) for a family funeral. (Amazon Prime)
Charlize Theron plays Megyn Kelly and Nicole Kidman is Gretchen Carlson in "Bombshell" (2019, R), based on the true story of a scandal at Fox News. Margot Robbie and John Lithgow co-star in the film that won an Oscar for makeup and hairstyling. (Amazon Video and Hulu)
Also based on a true story, contemporary war thriller "Mosul" (2019, not rated, with subtitles) follows an Iraqi SWAT team that breaks all the rules to drive ISIS out of their city. (Netflix)
Mackenzie Foy is the spirited teenage girl who bonds with a wild horse (voiced by Kate Winslet) in the new adaptation of "Black Beauty" (2020, TV-PG). (Disney+)
Kaley Cuoco is "The Flight Attendant" (TV-MA) in the eight-episode comic murder mystery. Three episodes are available; new episodes arrive each Thursday. (HBO Max)
"Saved by the Bell: Season 1" (TV-14) updates the 1990s high school sitcom with original stars Elizabeth Berkley, Mario Lopez and Mark-Paul Gosselaar as adults with their own kids. Three episodes are available; new episodes each Tuesday. (Peacock)
Holiday trimmings
"Dolly Parton's Christmas on the Square" (2020, not rated) is a holiday musical with Christine Baranski as a Scrooge-like cynic and Parton (who also produced and wrote 14 original songs) as an angel named Angel. (Netflix)
"The Christmas Chronicles: Part Two" (2020, TV-PG), a sequel to the 2018 adventure directed by Chris Columbus, features Kurt Russell and Goldie Hawn as Mr. and Mrs. Santa Claus joining a pair of kids to (what else?) save Christmas. (Netflix)
The romantic comedy "Happiest Season" (2020, PG-13) stars Kristen Stewart as a woman at her girlfriend's (Mackenzie Davis) family Christmas dinner who discovers she hasn't come out to her parents. (Hulu)
Pay-Per-View / Video on Demand
Diane Lane and Kevin Costner play grandparents who, after the death of their son, go on a mission to rescue their grandson from a criminal family in "Let Him Go" (2020, R).
"Stardust" (2020, not rated) stars Johnny Flynn as young David Bowie at the beginning of his career.
True stories: "Shawn Mendes: In Wonder" (2020, not rated) profiles the top-selling singer-songwriter on his world tour and "Dance Dreams: Hot Chocolate Nutcracker" (2020) goes behind the scenes of Debbie Allen's annual "Hot Chocolate Nutcracker" production.
Stand-up comedy: "Larry the Cable Guy: Remain Seated" (not rated).
The three-part limited series "Black Narcissus" (TV-MA) is a hothouse melodrama starring Gemma Arterton as a British nun in a Himalayan convent in 1914.
"Superintelligence" (2020, PG) stars Melissa McCarthy as an ordinary human chosen by an artificial intelligence to prove that humanity is worth saving.
Showtime Anytime
The documentary "Belushi" (2020, TV-MA) delves into the life and legacy of comedy legend John Belushi.
Sean Axmaker
is a Seattle film critic and writer. His reviews of streaming movies and TV can be found at streamondemandathome.com.
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There are many new varieties of cat litter to choose from. If you are looking for something that is Eco-friendly, try and find a litter that is not clay based. Clay litters must be made and processed in mines which pollute the environment. Clay litter is not biodegradable and cannot be absorbed or broken down by the Earth, therefore, it will forever sit in the landfills.
Swheat scoop® has also designed a cat litter that is made from wheat. Their product is also all natural and 100% biodegradable. This pellet style litter feels similar in texture to traditional clay litters, which makes it easier to convert your cat.
Learn about Flushable Cat Litter.
If you commonly feed your cat or dog canned food, purchase a plastic, reusable lid to cover partially used cans instead of using aluminum foil or plastic wrap which gets thrown away after each use. These lids can usually be found for less than a dollar and can be used for years.
Instead of taking a regular plastic bag with you when you take your dog for a walk, look for degradable bags which are made from recycled plastic and can be recycled again, or biodegradable bags which are often made from corn. Some companies that make biodegradable doggie bags, also make litter pan liners and other environmentally friendly pet products as well.
To completely eliminate the use of bags when cleaning up after your puppy, use products like the Waste Manager. You can make a mini septic tank right in your own backyard to dispose of all of your pet waste. Simply dig a two to three-foot hole in your back yard to scoop waste into. Rain water will help to naturally breakdown the waste, which will absorb back into the soil, saving you from using dozens of bags each month to keep your lawn clean.


Kent State University in Ohio has hired John Croop, CAFM, as its new fleet services superintendent. Croop previously served as assistant fleet manager and mechanic for Geauga County Sheriff's Office in Chardon, Ohio. He started his new job in March.
The move gives Croop responsibility over a larger and more varied fleet of about 400 units including mowers, construction equipment, police vehicles, and medium-duty trucks versus the Sheriff's Office's 160 units.
In addition to vehicle maintenance, the Kent State fleet division also maintains 39 generators on campus, the largest of which is 1 megawatt. Croop oversees a division of eight employees.
"My goal for this fleet operation is to cross-train certain essential staff members to eliminate any operational gaps in the event of any staff member absence," Croop said. "I intended to update technician training. This is a big task in itself with the variety of vehicles and equipment we provide support for."
Croop was previously a patrol officer who was also responsible for fleet management, which he began in 1994. At his most previous position in Geauga County, he developed a preventive maintenance schedule, updated parts room inventory and operations, and instituted a partnership with Ford and GM for fleet parts and service.
His position at Geauga County has not yet been filled.


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Greetings fellow Sisters and Brothers in Christ. As your new California Pacific Annual Conference Director of Lay Servant Ministries, I want to ask for your prayers as we together move forward in the ministry of the baptized.
Even as we consider our way forward, we pause as we enter the Advent Season with our hearts saddened by the tragic loss of life in Thousand Oaks. We pray for the victims, their families and friends but also for the lost soul who thought that this act of violence was an answer to something in his own life.
We also pray for the victims of the wild fires in Northern and Southern California. We pray for those who have lost their lives and those who have lost their homes and their communities. May God give them hope for the future as they rebuild. As followers of Jesus, let us be the hands and feet and the expression of God's love and grace for all, even in these most trying times.
In my new position as director, I have been blessed to be copied on the Lay Servant and Certified Lay Ministries reports that you all have been completing. Your commitment and desire to serve is impressive and heartwarming. I have also had the opportunity to read your comments about what would help you in your call as Lay Servants.
While many of you expressed your thanks for what the District Directors and the conference have done and are doing, a couple of constant themes found their way in many, if not most, of the comments.
More Educational and Training Opportunities: Many expressed the desire that there be more classes – both locally and on the district level. And, if possible that they be more convenient to get to.
Better Communication: "What classes are being offered and where they are being offered?" was a much repeated question. Many of you are willing to travel to other districts for classes, but you would like to know what is available. Can we better use the CAL PAC Lay Servant web page to communicate with Lay Servants? Can we use other social media forms of communication?
These top two themes are not new. They have been, and will continue to be, the primary challenge for your Lay Servant Ministry Directors. We would ask for your help as well. Who among you is willing to teach a class? Who among you is willing to organize a class session? Perhaps our Certified Lay Ministers will be a resource for new education and training opportunities as well.
Other themes that came out were the desire for Lay Servants to meet with other Lay Servants both to get to know one another and to share information about Lay Servant Ministry.
Several of you gave thanks for David Johnson's service as a Lay Servant Ministry director and wondered how we can fill the loss in the West District and the Conference. We give thanks for David's faithful service.
Several of you also gave thanks to Doug and Judy Lewis who played a huge role in giving life to the Lay Ministry Academy. Those of us who participated in the Lay Ministry Academy will always remember their dedication and grace in leading us forward.
We are humbled by the service of those who have gone before us, but with your help and prayers we will, together, pursue as we are able, the path of Lay Ministry.
Offer a class in train the trainer. Watch for "Called to Teach" Mark your calendars – There will be a train the trainer class – "CALLED TO TEACH" lead by Melody Ashley, Cal-Pac 2018 Lay Woman of the Year, February 23, 2019, at Wilshire UMC.
Improve the web page and the ability to communicate more directly with Lay Servants and Certified Lay Ministers.
Develop a uniform class registration form.
Improve the annual report form.
Certified Lay Ministry Training – Cycle D – March 29 and 30 – Anaheim UMC.
The link above is to the currently enrolling classes. The BeADisciple Course Catalog is available here.
Facilitate the ability of Lay Servants to communicate between and among themselves.
Several also expressed the desire to have more opportunities for service, such as being able to preach more often or serve as lay readers in service. I cannot stress enough how important and helpful it is to work with your pastor for these opportunities and to discuss engaging and involving the laity through Lay Servant Ministries. Whether as a Certified Lay Servant, a Certified Lay Speaker of a Certified Lay Minister, the laity has much to offer in our Wesleyan tradition.
Much falls to us as the laity to develop our own roles as the ministry of the baptized. We are called to go into the world to offer the unimaginable love of God as we know it through Christ's example. Filled with the Spirit, we will go forward together. We are called to serve the "least of these", to offer the "cool drink of water", the kind word of hope, the confidence of God being with us always.


text:
Why we Invested in SportVot
SportVot Founders : Siddhant Agarwal, Shubhangi Gupta, and Yash Bhagwatkar
India has over 10 million aspiring athletes under the age of 19 playing across 100K semi-professional tournaments annually. But, most of these athletes do not have access to the right networks and audience to showcase their talent. For example, athletes outside of major cities have little scope in getting noticed by scouts for professional leagues. There is little long-term growth opportunity. As a result, they leave the sports industry behind.
The Indian sports market is valued at merely $1.2 billion versus $71 billion in the United States. The rate of athletes dropout is choking the industry's full market potential. While there are multiple challenges facing the sports industry, we believe one of the key solutions is to shine the spotlight on aspiring athletes.
So far, a few sports have garnered attention from India's young population. Pro Kabaddi launched a couple of years ago and has since garnered over 350 million viewers per season — trailing the Indian Premier League for cricket. The Brahmaputra Volleyball League, Pro-basketball and Ultimate Kho-kho have also seen similar trajectories on a smaller scale. There is still much to be done to broaden the scope.
That's why we invested in Sportvot.
Sportvot is a multi-sports streaming platform for local talent and emerging leagues in India. It is a cost-effective, easy-to-use, online streaming platform that caters to the needs of franchises, teams and fans. In addition to its streaming services, Spotvot has a rich layer of tools to edit, analyse and share videos across various channels. They are enabling multiple stakeholders to engage with rich data and add value to the community.
Within a short period of time, Sportvot has streamed 18,000 sports matches amassing 75 million views, ultimately featuring over 90,000 up-and-coming athletes across different sports. The increased visibility has been instrumental in placing over 30 aspiring athletes in professional leagues including Pro-Kabbadi and city-level football divisions. Many of these athletes were from tier 3 and 4 cities.
Looking ahead, Sportvot has the potential to become India's largest multi-sport talent scouting platform. Led by second time entrepreneurs Sidhhant, Shubangi and Yash, SportVot has the right mix of technologists and sports enthusiasts to create a disruptive sportstech company.
To receive more updates about our latest investments, subscribe here.
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My Take on Major League Lacrosse Potentially Moving the Rochester Rattlers


MIAMI - May 14, 2014 – On Friday, May 9, Lennar Commercial Investors (LCI), LLC partnered with Sterling Organization to acquire North DeKalb Mall, a 622,297-square-foot center located just inside I-285 in northeastern Atlanta. LCI is a commercial real estate development and investment company and subsidiary of Lennar Corporation (NYSE: LEN and LEN.B). Sterling Organization, whose headquarters is in Palm Beach, FL, is a vertically integrated private equity real estate firm that specializes in retail focused assets.
The development team, which also includes Atlanta-based development, brokerage and management company Hendon Properties, plans to convert the enclosed portion of the property to an open-air concept. Lennar and Sterling acquired ownership interest in the property and Sterling will manage the center. Timing on the redevelopment has not been finalized.
North DeKalb Mall, which opened in 1965, is one of the last remaining large-scale infill opportunities in the Decatur/Emory area for retail or mixed-use redevelopment. Currently, the anchor tenants include AMC Theatres, Burlington Coat Factory, Macy's, Marshalls and Ross Dress for Less.
Lennar Commercial Investors, LLC is the commercial division of Lennar Corporation, specializing in the development, investment and management of retail, mixed-use and commercial office projects. The Lennar brand exemplifies creativity, innovation and teamwork, and is currently represented in 19 states nationwide. Lennar Corporation, founded in 1954, trades on the New York Stock Exchange under the symbol LEN and LEN.B. For more information, visit www.lennarcommercial.com.
Sterling Organization is a vertically integrated private equity real estate firm that has an established track record of providing exceptional risk-adjusted returns to its partners, in both relative and absolute terms. The company is focused on investing in anchored retail real estate assets in select major U.S. markets on behalf of Sterling's principals in partnership with the highest quality institutional and high net worth investors. Sterling Organization is headquartered in Palm Beach, FL.


A couple years ago I got a tattoo of a desk fan just above my knee. I got it because I was about to move to Boston and didn't know anyone out there; I wanted to remember that no matter where I lived, I was meant to cheer people on and be their biggest fan.
Cheesy, maybe. But I like it.
Now I live and write in California and want to do the same. I believe that I love because Jesus first loved us, and I write because God first wrote.
Come and hang out a bit! I'm excited to share my journey and relate a bit with you and yours.
Sign up with your name and email to get emails with random lists and thoughts and updates!
I don't sport. I don't spam.


Created a slice and then created slivers at all !OpenFlow aggregates. This confirmation test creates a sliver at each of the following aggregates using the RSpec specified. RSpecs can be found [http://groups.geni.net/geni/browser/trunk/GENIRacks/InstaGENI/Spiral5/RSpecs/ConfirmationTests/CWRU here].
Then created a sliver at each of the compute resource aggregates, RSpecs used can be found RSpecs can be found [http://groups.geni.net/geni/browser/trunk/GENIRacks/InstaGENI/Spiral5/RSpecs/ConfirmationTests/CWRU here].


Broncos President/CEO Joe Ellis announces that Owner Pat Bowlen is grappling with Alzheimer's disease and will no longer handle team operations, July 23, 2014.
The Broncos announce that Owner Pat Bowlen has been privately battling Alzheimer's disease and is no longer able to be part of the team's daily operations.
It is disclosed that the franchise is being held in a trust — the Pat Bowlen Trust — overseen by non-family trustees with President & CEO Joe Ellis continuing to operate the team with full authority on all matters.


during summer. in grant park. listening to music. this was one of those moments that made me wonder how i'd ever leave chicago. and then i remembered january. and february. march, april and well, november and december too. right - that's why i will someday leave chicago.
when i was at syndy's on saturday, we listened to fox confessor. i don't know what it is about that album but i hear it once and i can listen to nothing but that for the next week. to say i don't know what it is isn't entirely true. there are so many things about it that i love that its hard to point to one thing. it reminds me of how i felt the first time i read in watermelon sugar. that teenage feeling makes my toes tingle. maybe sparrow is one of my most favorite songs to sing in the car. other songs are a kick to the gut. regardless, its all i've listened to this week.
and its making me really happy that shawn pre-ordered the new new pornagraphers.
...even if i'm not writing about it as often as i used to. two years ago, shawn and i had decided that we were moving to new orleans someday. it was a part of our short/long term plan. we talked about it alot. i think we don't talk about it very much now because its hard. there's nowhere we'd rather be. we have obligations in chicago though, responsibilities. but i also feel a sense of obligation to new orleans. maybe its on my mind more now because august 29 is looming. i miss new orleans every single day. i feel it in my pores. and when i think about hurricane season, our friends, and our beloved city, i can't breathe.
so, this is probably the first post of many on this topic this month. and here's two articles that prompted this post.
tried to figure out exactly what it is you're supposed to do when tornado sirens go off while driving, baked a tres leches cake, key lime pie and the best chocolate chips ever.
i also experienced some big time shop love the past couple weeks. thank you thank you thank you. i do so appreciate it.


Some hip cats may tell you that Steve Reid made his recording debut playing on Martha and the Vandellas' Motown classic – 'Dancing in the Street' or that he's played with the likes of James Brown, Miles Davies and Sun Ra but there's something poignantly satisfying to know that he's still out there doing his thing, making creative, life affirming music on display in the energy and innovation on the new album – Daxaar .
Bringing together the playful electronic textures of Kieran Hebden aka Four Tet and the local talents of Senegal's best jazz musicians; the Steve Reid Ensemble has created what Giles Peterson calls "a rhythmic feast for those who like their jazz out there".
The ensemble will premiere this new material with a special live show at the Barbican in London on Tuesday 20th November as part of the London Jazz Festival in association with BBC Radio 3 and Serious.
In the meantime, have a look at this short film showing the endearing charm of the ensemble recording, performing and relaxing amongst the lovely people and landscape of Senegal.
Daxaar is released on 19th November but you can pre-order from our Mart now.


Chardons Corner Hotel is located in Annerley just 20 minutes from Brisbane CBD. The meandering Brisbane River is a local feature in the area. Local sites of interest include Mount Coot-Tha Forest lookout which offers a great view of the Brisbane and surrounding suburbs. The University of Queensland lies just across the river and Griffith University Mount Gravatt Campus is just 10 minutes drive from the hotel. Toohey Forest Conservation Park, Griffith University, Queen Elizabeth II Jubilee Hospital and the Brisbane Markets are all within local distance. It's easy to see why locals and tourists alike can enjoy the convenience of making Chardons Corner Hotel a great meeting point for refreshments after a day out.


Macy's Charitable "Shop for a Cause" at Westfield Sunrise on Saturday, August 29 from 7:00 a.m. – 6:30 p.m.
WHAT: All are invited to participate in Macy's "Shop for a Cause," the department store's biggest one-day charity shopping event, at Westfield Sunrise shopping center. The initiative has raised tens of millions of dollars for charitable organizations nationwide. For the first time, Macy's will offer up to 30% off all day on select merchandise to those customers with a "Shop for a Cause" savings pass. For specific details, please visit http://bit.ly/1NF7txO .
The sale of every $5 "Shop for a Cause" ticket sold in Macy's South Shore and Macy's Sunrise will benefit March of Dimes.


text:
Q: No primary SDN label exists .. (i.e one starting with _) Spring data neo4j version: 3.3.0.RELEASE
Neo4j version: 2.2.2
I ran into the following exception when I tried to query default methods exposed on a spring-data repository i.e.
personRepository.findAll(getDefaultPageable());

public static Pageable getDefaultPageable() {
    BiFunction<Integer, Integer, Pageable> biFunction = PageRequest::new; // Method reference syntax in action
    return biFunction.apply(DEFAULT_PAGE_NUMBER, DEFAULT_PAGE_SIZE);
}

Caused by: java.lang.IllegalStateException: No primary SDN label exists .. (i.e one starting with _)
      at org.springframework.data.neo4j.support.typerepresentation.LabelBasedNodeTypeRepresentationStrategy.readAliasFrom(LabelBasedNodeTypeRepresentationStrategy.java:136)
      at org.springframework.data.neo4j.support.typerepresentation.LabelBasedNodeTypeRepresentationStrategy.readAliasFrom(LabelBasedNodeTypeRepresentationStrategy.java:40)
      at org.springframework.data.neo4j.support.mapping.TRSTypeAliasAccessor.readAliasFrom(TRSTypeAliasAccessor.java:36)
      at org.springframework.data.neo4j.support.mapping.TRSTypeAliasAccessor.readAliasFrom(TRSTypeAliasAccessor.java:26)
      at org.springframework.data.convert.DefaultTypeMapper.readType(DefaultTypeMapper.java:102)
      at org.springframework.data.convert.DefaultTypeMapper.getDefaultedTypeToBeUsed(DefaultTypeMapper.java:165)
      at org.springframework.data.convert.DefaultTypeMapper.readType(DefaultTypeMapper.java:142)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityConverterImpl.read(Neo4jEntityConverterImpl.java:77)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityPersister$CachedConverter.read(Neo4jEntityPersister.java:170)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityPersister.createEntityFromState(Neo4jEntityPersister.java:189)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityPersister.projectTo(Neo4jEntityPersister.java:216)
      at org.springframework.data.neo4j.support.Neo4jTemplate.projectTo(Neo4jTemplate.java:241)
      at org.springframework.data.neo4j.support.conversion.EntityResultConverter.doConvert(EntityResultConverter.java:73)
      at org.springframework.data.neo4j.conversion.DefaultConverter.convert(DefaultConverter.java:44)
      at org.springframework.data.neo4j.support.conversion.EntityResultConverter.convert(EntityResultConverter.java:165)
      at org.springframework.data.neo4j.conversion.QueryResultBuilder$1.underlyingObjectToObject(QueryResultBuilder.java:86)
      at org.neo4j.helpers.collection.IterableWrapper$MyIteratorWrapper.underlyingObjectToObject(IterableWrapper.java:57)
      at org.neo4j.helpers.collection.IteratorWrapper.next(IteratorWrapper.java:47)
      at org.springframework.data.neo4j.repository.AbstractGraphRepository.subList(AbstractGraphRepository.java:371)
      at org.springframework.data.neo4j.repository.AbstractGraphRepository.extractPage(AbstractGraphRepository.java:355)
      at org.springframework.data.neo4j.repository.AbstractGraphRepository.findAll(AbstractGraphRepository.java:321)
      at sun.reflect.NativeMethodAccessorImpl.invoke0(Native Method)
      at sun.reflect.NativeMethodAccessorImpl.invoke(NativeMethodAccessorImpl.java:62)
      at sun.reflect.DelegatingMethodAccessorImpl.invoke(DelegatingMethodAccessorImpl.java:43)
      at java.lang.reflect.Method.invoke(Method.java:497)
      at org.springframework.data.repository.core.support.RepositoryFactorySupport$QueryExecutorMethodInterceptor.executeMethodOn(RepositoryFactorySupport.java:414)
      at org.springframework.data.repository.core.support.RepositoryFactorySupport$QueryExecutorMethodInterceptor.doInvoke(RepositoryFactorySupport.java:399)
      at org.springframework.data.repository.core.support.RepositoryFactorySupport$QueryExecutorMethodInterceptor.invoke(RepositoryFactorySupport.java:371)
      at org.springframework.aop.framework.ReflectiveMethodInvocation.proceed(ReflectiveMethodInvocation.java:179)
      at org.springframework.data.projection.DefaultMethodInvokingMethodInterceptor.invoke(DefaultMethodInvokingMethodInterceptor.java:61)
      at org.springframework.aop.framework.ReflectiveMethodInvocation.proceed(ReflectiveMethodInvocation.java:179)
      at org.springframework.transaction.interceptor.TransactionInterceptor$1.proceedWithInvocation(TransactionInterceptor.java:99)
      at org.springframework.transaction.interceptor.TransactionAspectSupport.invokeWithinTransaction(TransactionAspectSupport.java:281)
      at org.springframework.transaction.interceptor.TransactionInterceptor.invoke(TransactionInterceptor.java:96)
      at org.springframework.aop.framework.ReflectiveMethodInvocation.proceed(ReflectiveMethodInvocation.java:179)
      at org.springframework.dao.support.PersistenceExceptionTranslationInterceptor.invoke(PersistenceExceptionTranslationInterceptor.java:136)
      at org.springframework.aop.framework.ReflectiveMethodInvocation.proceed(ReflectiveMethodInvocation.java:179)
      at org.springframework.aop.framework.JdkDynamicAopProxy.invoke(JdkDynamicAopProxy.java:207)
      at com.sun.proxy.$Proxy60.findAll(Unknown Source)
      at sun.reflect.NativeMethodAccessorImpl.invoke0(Native Method)
      at sun.reflect.NativeMethodAccessorImpl.invoke(NativeMethodAccessorImpl.java:62)
      at sun.reflect.DelegatingMethodAccessorImpl.invoke(DelegatingMethodAccessorImpl.java:43)
      at java.lang.reflect.Method.invoke(Method.java:497)
      at org.springframework.aop.support.AopUtils.invokeJoinpointUsingReflection(AopUtils.java:317)
      at org.springframework.aop.framework.JdkDynamicAopProxy.invoke(JdkDynamicAopProxy.java:201)
      at com.sun.proxy.$Proxy61.findAll(Unknown Source)

I am really not trying to do anything complicated here so I'm struggling to understand if I should really introduce a custom query with underscore prefixed labels and use the annotation @Query for it? Don't the default methods from Spring data just work on SDN?

## UPDATE ##
I adapted the cypher query and still ended up with the same error.

used by: java.lang.IllegalStateException: No primary SDN label exists .. (i.e one starting with _)
      at org.springframework.data.neo4j.support.typerepresentation.LabelBasedNodeTypeRepresentationStrategy.readAliasFrom(LabelBasedNodeTypeRepresentationStrategy.java:136)
      at org.springframework.data.neo4j.support.typerepresentation.LabelBasedNodeTypeRepresentationStrategy.readAliasFrom(LabelBasedNodeTypeRepresentationStrategy.java:40)
      at org.springframework.data.neo4j.support.mapping.TRSTypeAliasAccessor.readAliasFrom(TRSTypeAliasAccessor.java:36)
      at org.springframework.data.neo4j.support.mapping.TRSTypeAliasAccessor.readAliasFrom(TRSTypeAliasAccessor.java:26)
      at org.springframework.data.convert.DefaultTypeMapper.readType(DefaultTypeMapper.java:102)
      at org.springframework.data.convert.DefaultTypeMapper.getDefaultedTypeToBeUsed(DefaultTypeMapper.java:165)
      at org.springframework.data.convert.DefaultTypeMapper.readType(DefaultTypeMapper.java:142)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityConverterImpl.read(Neo4jEntityConverterImpl.java:77)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityPersister$CachedConverter.read(Neo4jEntityPersister.java:170)
      at org.springframework.data.neo4j.support.mapping.Neo4jEntityPersister.createEntityFromState(Neo4jEntityPersister.java:189)
      at org.springframework.data.neo4j.support.Neo4jTemplate.createEntityFromState(Neo4jTemplate.java:224)

Can you please take a look at the classes and let me know where and what I'm doing incorrectly?
Here's the repository class
public interface PersonRepository extends GraphRepository<Person>, CypherDslRepository<Person> {
String PERSONS_WITH_SEVERAL_ACME_IDENTITY = "MATCH (p:Person)-[r:HAS_LOGIN]->(a:AcmeIdp) " +
        "SET p:_Person, a:_AcmeIdp "+
        "WITH p, count(p) AS numoutgoing " +
        "WHERE numoutgoing > 1 " +
        "MATCH (p:Person)-[r:HAS_LOGIN]->(a:AcmeIdp) " +
        "SET p:_Person, a:_AcmeIdp "+
        "RETURN p";

Iterable<Person> findByFirstNameAndLastName(@NonNull final String firstName,@NonNull final String lastName);

Page<Person> findByFirstNameLike(@NonNull final String firstName,@NonNull final Pageable pageable);

@Query(PERSONS_WITH_SEVERAL_ACME_IDENTITY)
Page<Person> findOnesWithSeveralAcmeIdentities(@NonNull final Pageable pageable); }

The person entity class
import com.example.analytics.model.AbstractEntity;
import com.example.analytics.model.relationship.Login;
import org.checkerframework.checker.nullness.qual.NonNull;
import org.neo4j.graphdb.Direction;
import org.springframework.data.neo4j.annotation.*;

import java.time.LocalDateTime;
import java.util.Set;

@NodeEntity(useShortNames = true)
public class Person extends AbstractEntity {

    @GraphProperty(propertyName = "title", defaultValue = "")
    private String title;

    @GraphProperty(propertyName = "firstName", defaultValue = "")
    private String firstName;

    @GraphProperty(propertyName = "lastName", defaultValue = "")
    private String lastName;

    @GraphProperty(propertyName = "dateOfBirth", propertyType = String.class)
    private LocalDateTime dateOfBirth;

    @RelatedTo(type = "HAS_LOGIN", direction = Direction.OUTGOING, elementClass = AcmeIdentity.class)
    private Set<Login> logins;

    public String getTitle() {
        return title;
    }

    public void setTitle(final String title) {
        this.title = title;
    }

    public String getFirstName() {
        return firstName;
    }

    public void setFirstName(final String firstName) {
        this.firstName = firstName;
    }

    public String getLastName() {
        return lastName;
    }

    public void setLastName(final String lastName) {
        this.lastName = lastName;
    }

    public LocalDateTime getDateOfBirth() {
        return dateOfBirth;
    }

    public void setDateOfBirth(final LocalDateTime dateOfBirth) {
        this.dateOfBirth = dateOfBirth;
    }

    public Set<Login> getLogins() {
        return logins;
    }

    public void setLogins(@NonNull final Set<Login> logins) {
        this.logins = logins;
    }
}

The converter
import org.checkerframework.checker.nullness.qual.NonNull;
import org.slf4j.Logger;
import org.slf4j.LoggerFactory;
import org.springframework.beans.factory.annotation.Value;
import org.springframework.core.convert.converter.Converter;
import org.springframework.stereotype.Component;

import java.time.LocalDateTime;
import java.time.format.DateTimeFormatter;

@Component
public class LocalDateTimeToStringConverter implements Converter<LocalDateTime, String> {

    private static final Logger LOG = LoggerFactory.getLogger(LocalDateTimeToStringConverter.class);

    @Value("${neo4j.dateTime.format:yyyy-MM-dd HH:mm:ss}")
    private String dateTimeFormat;

    @Override
    public String convert(@NonNull final LocalDateTime source) {
        LOG.debug("Converting LocalDateTime into String using the format: {}", dateTimeFormat);
        return String.valueOf(source.format(DateTimeFormatter.ofPattern(dateTimeFormat)));
    }

}

The reverse converter
import org.checkerframework.checker.nullness.qual.NonNull;
import org.slf4j.Logger;
import org.slf4j.LoggerFactory;
import org.springframework.beans.factory.annotation.Value;
import org.springframework.core.convert.converter.Converter;
import org.springframework.stereotype.Component;

import javax.annotation.PostConstruct;
import java.time.LocalDateTime;
import java.time.format.DateTimeFormatter;

@Component
public class StringToLocalDateTimeConverter implements Converter<String, LocalDateTime> {

    private static final Logger LOG = LoggerFactory.getLogger(StringToLocalDateTimeConverter.class);

    @Value("${neo4j.dateTime.format:yyyy-MM-dd HH:mm:ss}")
    private String dateTimeFormat;

    /**
     * Convert the source of type S to target type T.
     *
     * @param source the source object to convert, which must be an instance of S (never {@code null})
     * @return the converted object, which must be an instance of T (potentially {@code null})
     * @throws IllegalArgumentException if the source could not be converted to the desired target type
     */
    @Override
    public LocalDateTime convert(@NonNull final String source) {
        LOG.debug("Converting String {} into LocalDateTime using the format: {}",source, dateTimeFormat);
        return LocalDateTime.parse(source, DateTimeFormatter.ofPattern(dateTimeFormat));
    }

}

The Main configuration class
import com.example.analytics.converter.LocalDateTimeToStringConverter;
import com.example.analytics.converter.StringToLocalDateTimeConverter;
import org.slf4j.Logger;
import org.slf4j.LoggerFactory;
import org.springframework.beans.factory.annotation.Autowired;
import org.springframework.boot.autoconfigure.EnableAutoConfiguration;
import org.springframework.context.annotation.*;
import org.springframework.context.support.PropertySourcesPlaceholderConfigurer;
import org.springframework.core.convert.ConversionService;
import org.springframework.core.convert.converter.ConverterRegistry;
import org.springframework.data.neo4j.config.Neo4jConfiguration;
import org.springframework.transaction.annotation.EnableTransactionManagement;

@Configuration
@EnableAutoConfiguration
@EnableTransactionManagement(mode = AdviceMode.PROXY)
@ComponentScan(basePackages = {"com.example.analytics"})
@PropertySource(value = "classpath:application.yml", ignoreResourceNotFound = false)
@Import({DatabaseConnectionConfiguration.class})
public class MainConfiguration extends Neo4jConfiguration {

    @Autowired
    private StringToLocalDateTimeConverter stringToLocalDateTimeConverter;

    @Autowired
    private LocalDateTimeToStringConverter localDateTimeToStringConverter;

    private static final Logger LOG = LoggerFactory.getLogger(MainConfiguration.class);

    public MainConfiguration() {
        setBasePackage("com.example.analytics.model");
    }

    @Bean
    public static PropertySourcesPlaceholderConfigurer propertyConfigIn() {
        return new PropertySourcesPlaceholderConfigurer();
    }

    @Bean
    @DependsOn({ "stringToLocalDateTimeConverter", "localDateTimeToStringConverter" })
    protected ConversionService neo4jConversionService() throws Exception {
        LOG.debug("Adding custom converters to conversion service ...");
        ConversionService conversionService = super.neo4jConversionService();
        ConverterRegistry registry = (ConverterRegistry) conversionService;
        registry.addConverter(stringToLocalDateTimeConverter);
        registry.addConverter(localDateTimeToStringConverter);
        LOG.debug("Addition of Converter from LocalDateTime to String and vice-versa has been completed!");
        return conversionService;
    }
}

Snippet of the service using the repository
public Page<Person> findPersonsWithSeveralAcmeIdentitites(final Pageable pageable) {
    LOG.debug("Fetching persons with several ACME identities");

    if(pageable != null)
        return personRepository.findOnesWithSeveralAcmeIdentities(pageable);
   else
        return personRepository.findOnesWithSeveralAcmeIdentities(getDefaultPageable());

}

A: You then have to go over your nodes and on each of them call:
neo4jTemplate.postEntityCreation(node, MyEntity.class);

Alternatively this should work too:
MATCH (n:User) set n:_User;

etc.
I think you're overdoing Java8 method references !!! Just use plain old new. Otherwise your code will be unmaintainable going forward.
public static Pageable getDefaultPageable() {
    return new PageRequest(DEFAULT_PAGE_NUMBER, DEFAULT_PAGE_SIZE);
}

redpajama_set_name: RedPajamaStackExchange


The remains of Cuthand, a town with one of the most unusual names in East Texas, are scattered around the intersection of Farm Roads 1487 and 916 seven miles east of Bogata in Red River County.
Originally known as Enterprise as it was being settled by cotton planters around 1850, the town began to grow in the l860s when E.A. Mauldin established a grist mill and cotton gin and Samuel T. Arnold opened a general store.
By 1867, the community had enough people to justify a post office, and its first postmaster, Cornelius Crenshaw, named the post office for Cuthand Creek.
The creek supposedly got its name from a Deleware Indian chief who accompanied Frank Hopkins, a soldier in the battle of Tippecanoe, from Indiana to Texas in 1823.
The chief had lost three fingers from a sabor�s slash in his younger days and because of his difigurement, he was forever known as Cuthand.
The creek bearing his name was named by General Thomas J. Rusk of Nacogdoches, a close friend of the old chief.
An old legend says that immediately after the war, a well-groomed man known as Professor Dobbs came to Cuthand and applied for a job as the teacher that fall. Dobbs was hired and, taught during the year. After the school�s closing in the spring, he left the community. It was later learned that he was William Clarke Quantrill, leader of perhaps the most savage fighting unit in the Civil War.
Quantrill, indeed, was a schoolteacher in Ohio and Kansas and brought his guereillas to a camp on the Red River near Sherman during the winters of 1862, 1863 and 1864.
The climax of Quantrill's guerilla career came on August 21, 1863, when he led a force of 450 raiders into Lawrence, Kansas, a stronghold of pro-Union support, and set the torch to much of the city. Quantrill was eventually killed on a raid into Kentucky in 1865.
As Cuthand thrived from a cotton economy, people began to settle aound the community. Six doctors practiced in the town, an indication that it was growing.
By 1880, Cuthand had a population of 130 people, two cotton gins, a church and a school. The town�s population reached 150 in 1890 but begun to decline by 1896. In 1914, ninety-one residents lived in the community and it had ninety-six from 1920 through 1956.
The town lost its post office in the 1950s and in 1986 the community reported only thirty-one residents and no businesses.
You can learn more about William Clarke Quantrill in East Texas from �A Civil War Tragedy� by John Wilkins of Tyler, which can be puchased from the East Texas Historical Association in Nacogdoches.
All Things Historical September 22, 2008 Column.