If the position of the wire appears satisfactory and yet the pacing thresholds are high, th e wire may be in a left hepatic vein. Pull the wire back into the atrium and try again, loo king speci \201 cally for the ventricular ectopics as the wire crosses the tricuspid valve . The pacing threshold commonly doubles in the \201 rst few days due to endocardial oedema. If the pacemaker suddenly fails, the most common reason is usually wire displacement. Increase the pacing output of the box. \200 Check all the connections of the wire and the battery of the box. \200 Try moving the patient to the left lateral position until arran gements can be made to reposition the wire. Perforation \200 A pericardial rub may be present in the absence of perforation (especially post-MI). Presentation : pericardial chest pain, increasing breathlessness, falling blood pressure, e nlarged cardiac silhouette on CXR, signs of cardiac tamponade, left diaphragmatic pacing at low output. Management: if there are signs of cardiac tamponade arrange for urgent echocardiography (ECHO) and reposition the wire. monitor the patient carefully over the next few days, with repeat ECHOs to detect incipient cardiac tamponade. TEMPORARY PACING: COMPLICATIONS 813 Diaphragmatic pacing \200 High-output pacing (10 V), even with a satisfactory position of the ventricular lead may cause pacing of the left hemidiaphragm. At low voltages, this suggests perforation (see above). Right hemidiaphragm pacing may be seen with atrial pacing and stimulation of the right phrenic nerve. Reposition the wire if symptomatic (painful twitching, dyspnoea). Complications of temporary pacing \200 Complications associated with central line inserti on \200 Ventricular ectopics \200 Non-sustained VT \200 Perforation \200 Pericardit is \200 Diaphragmatic pacing \200 Infection \200 Pneumothorax \200 Cardiac tamponad e 814 CHAPTER 18 Practical procedures Pericardial aspiration (1) Equipment Establish peripheral venous access and check that full facilities for resusci- tation are available. Pre-prepared pericardiocentesis sets may be available. You will need: \200 trolley as for central line insertion, with iodine or chlo rhexidine for skin, dressing pack, sterile drapes, local anesthetic (lidocaine 2 % ), syrin ges (including a 50 mL), needles (25G and 22G), No. 11 blade, and silk sutures. pericardiocentesis needle (15 cm, 18G) or similar Wallace cannula. \200 J guide wire ( (c id:2) 80 cm, 0.035 diameter). \200 dilators (up to 7 Fr). \200 pigtail catheter ( (cid: 2) 60 cm with multiple sideholes, a large Seldinger-type CVP line can be used if no pigtail is available). drainage bag and connectors. \200 facilities for \202 uoroscopy or echocardiographic sc reening. Technique (see Fig. 18.8 ) \200 Position the patient at 730 * . This allows the effusion to pool inferiorly within the pericardium. Sedate the patient lightly with midazolam (2.5 \200\2237.5 mg IV) and fentanyl 50 \200\2232 00 mcg IV) if necessary. Use with caution as this may drop the blood pressure (BP) in patie nts already compromised by the effusion. \200 Wearing a sterile gown and gloves, clean th e skin from mid-chest to mid-abdomen and put the sterile drapes on the patient. In \201 ltrate the skin and subcutaneous tissues with local anesthetic starting 1 \200\2231.5 cm below the xiphisternum and just to the left of the midline, aimin g for the left shoulder and staying as close to the inferior border of the rib cartilages a s possible. The pericardiocentesis needle is introduced into the angle between the xiphisternum and the left costal margin angled at 730 * . Advance slowly, aspirating gently, and then injecting more lidocaine every few millimeters, aiming for the left shoulder. As the parietal pericardium is pierced, you may feel a \200\230give \200\231 and \202 ui d will be aspirated. Remove the syringe and introduce the guide wire through the needle. Check the position of the guide wire by screening. It should loop within the cardiac silhou ette only and not advance into the superior vena cava (SVC) or PA. Remove the needle, leaving the wire in place. Enlarge the skin incision slightly using the blade, and dilate the track. Insert the pigtail over the wire into the pericardial space and remove the wire. Take specimens for microscopy, culture (and inoculate a sample into blood culture bottles), cytology, and haematocrit if blood stained (a full blood count (FBC) tube; ask the hematol ogists to run on the Coulter counter for rapid estimation of Hb). PERICARDIAL ASPIRATION (1) 815 Aspirate to dryness watching the patient carefully. Symptoms and haemodynamics (tachycardia) often start to improve with removal of as little as 100 mL of p ericardial \202 uid. If the \202 uid is heavily blood stained, withdraw \202 uid cautiously \200\224 if the pigtail is in the right ventricle, withdrawal of blood may cause cardiovascular collapse. Arrange for urgent Hb/haematocrit. Leave on free drainage and attached to the drainage bag. \200 Suture the pigtail to the s kin securely and cover with a sterile occlusive dressing. Fig. 18.8 Pericardial aspiration. Reproduced with permission from Ramrakha P, Moore K, and Sam M (2010). Oxford Handbook of Acute Medicine . 3rd ed. Oxford: Oxford University Press. Aftercare \200 Closely observe the patient for recurrent tamponade (obstruction of drain) and repeat ECHO. \200 Discontinue anticoagulants. \200 Remove the drain after 24 hours or when the drainage stops. \200 Consider the need for surgery (drainage, biopsy o r pericardial window) or speci \201 c therapy (chemotherapy if malignant effusion, antimic robials if bacterial, dialysis if renal failure, etc.). 816 CHAPTER 18 Practical procedures Pericardial aspiration (2) Tips and pitfalls \200 If the needle touches the heart \200 \231s epicardial surface , you may feel a \200\230ticking \200\231 sensation transmitted d own the needle: withdraw the needle a few millimeters, angulate the needle more super \201 cially, and try cautiously again, aspirating as you advance. If you do not enter the effusion , and the heart is not encountered: \200 withdraw the ne edle slightly and advance again, aiming slightly deeper, but still towards the left shoulder. if this fails, try again, aiming more medially (mid-clavicular point or even suprasternal notch). consider trying the apical approach (starting laterally at the cardiac apex and aiming for the right shoulder), if ECHO con \201 rms suf \201 cient \202 uid a t the cardiac apex. If available, intrathoracic ECG can be monitored by a lead attached to the needle as it is advanced. This is seldom clinically useful in our experience. Penetr ation of the myocardium results in ST elevation, suggesting the needle has been advanced to o far. Dif \201 culty in inserting the pigtail : this may be because of insuf \201 cient dilatation of the tract (use a larger dilator). holding the wire taught (by gentle traction) while pushing the catheter may help; take care not to pull the wire out of the pericardium. Haemorrhagic effusion vs. blood : compare the Hb of the pericardial \202 uid to the venous blood Hb \200 place some of th e \202 uid in a clean container; blood will clot, whereas haemorrhagic effusion will not, as the \200\230whipping \200\231 action of the heart tends to de \201 brinate it. con \201 rm the position of the needle by \201 rst withdrawing some \202 uid and then injecting 10 \200\22320 mL of contrast; using \202 uoroscopy; see if the contrast stays w ithin the cardiac sillhouette. alternatively, if using ECHO guidance, inject 5 \200\22310 mL saline into the needle, looki ng for \200\230microbubble contrast \200\231 in the cavity containing the needle tip. Inje cting 20 mL saline rapidly into a peripheral vein will produce \200\230contrast \200\231 i n the RA and RV, and may allow them to be distinguised from the pericardial space. connect a pressure line to the needle; a characteristic waveform will con \201 rm penetration of the RV. Complications of pericardiocentesis \200 Penetration of a cardiac chamber (usually right ventricle). \200 Laceration of an epicardial vessel. \200 Arrhythmia (atrial arrhythmia s as the wire is advanced, ventricular arrhythmias if the RV is penetrated). Pneumothorax. \200 Perforation of abdominal viscus (liver, stomach, colon). \200 Ascend ing infection. This page intentionally left blank 818 CHAPTER 18 Practical procedures DC cardioversion Relative contraindications \200 Digoxin toxicity. \200 Electrolyte dis turbance (dNa + , dK + , dCa 2 + , dMg 2 + , acidosis). \200 Inadequate anticoagulation a nd chronic atrial \201 brillation (AF). Checklist for DC cardioversion De \201 brillator: Check this is functioning with a fully equipped arrest trolley to hand in case of arrest. Informed consent: \200 12-lead ECG: Unless life-threatening emergency. AF, \202 utter, SVT, VT, signs of ischaemia or digoxin. If ventricular rate is slow have an external (transcutaneous) pacing system nearby in case of asystole. Nil by mouth: \200 Anticoagulation: For at least 4 hours. Does the patient require anticoagulants? Is the international normalized ratio (INR) > 2.0? (Has it been so for > 3 weeks?) Potassium: \200 Digoxin: Check this is > 3.5 mmol/L. Check there are no features of digoxin toxicity. If taking (cid:116) 250 mcg/day, check tha t renal function and recent digoxin level are normal. If there are frequent ventricular ect opics, give IV Mg 2 + 8 mmol. Thyroid function: \200 IV access: \200 Sedation: Treat thyrotoxicosis or myxoedema \201 rst. Peripheral venous cannula. Short general anesthesia (propofol) is preferable to sedation with benzodiazepine and fenta nyl. Bag the patient with 100 % oxygen. Select energy: \200 Synchronization: (see box opposite). Check this is selected on the de \201 brillator for all shocks (unless the patient is in V F or haemodynamically unstable). Adjust the ECG gain so that the machine is only sensing QR S complexes and not P or T waves. DC CARDIOVERSION 819 Paddle Most centers now use \200\230hands-free \200\231 adhesive pads for DC cardioversion. Some continue with the traditional hand-held paddles. Conductive gel pads should be placed betwe en the paddles and the skin. Position one just to the right of the sternum and the other to the left of the left nipple (anterior- mid-axillary line). Alternatively, place one anteri orly just left of the sternum, and one posteriorly to the left of midline. There is some ev idence that the anteroposterior (AP) position is superior for AF. placement: Cardioversion: Check no one is in contact with the patient or with the metal bed. Ensure your own legs are clear of the bed! Apply \201 rm pressure on the paddles. Unsuccessful: Double the energy level and repeat up to 360 J. Consider changing the paddle position. If t here is prolonged sinus pause or ventricular arrhythmia during an elective procedure, stop. Successful: Repeat ECG. Place in recovery position until awake. Monitor for 2 \200\2234 h and ensure ef fects of sedation have passed. Patients should be accompanied home by a friend or relative if being discharged. Complications of DC cardioversion \200 Asystole/bradycardias \200 Ventricular \201 br illation \200 Thromboembolism \200 Transient hypotension \200 Skin burns \200 Aspir ation pneumonitis. Suggested initial energies for DC shock for elective cardioversion Sustained VT 200 J \200 Atrial \201 brillation 50 \200\223100 J \200 Atrial \202 ut ter 50 J \200 Other SVTs 50 J \200 If the initial shock is unsuccessful, increase the e nergy (50, 100, 200, 360 J) and Synchronized Synchronized Synchronized Synchronized repeat. If still unsuccessful, consider changing the paddle position and try 360 J again. It is inappropriate to persist further with elective DC cardioversion. 820 CHAPTER 18 Practical procedures Anticoagulation The risk of thromboembolism in patients with chronic AF and dilated cardiom yopathy is 0 \200\2237 % , depending on the underlying risk factors. Increased risk Low risk Prior embolic event \200 Mechanical heart valve \200 Mitral stenosis \200 Dilated lef t atrium Age <60 years \200 No underlying heart disease \200 Recent onset AF (<3 days) Anticoagulate patients at risk, with warfarin for at least 3 \200\2234 weeks. For recent on set AF (1 \200\2233 days), anticoagulate with IV heparin for at least 12 \200\22324 hours a nd, if possible, exclude intra-cardiac thrombus with a trans- oesophageal ECHO prior to DC shock. If there is thrombus, anticoagu- late with warfarin as above. For emergency cardiove rsion of AF (<24 h), heparinize prior to shock. The risk of systemic embolism with cardioversion of AF and other tachyarrhythmias is very l ow, provided there is no ventricular thrombus, since the coordinated atrial activity preven ts formation of clot. Routine anticoagulation with warfarin is not necessary but we would r ecommend heparin before DC shock, as the atria are often rendered mechanically stationary f or several hours after shock even though there is coordinated electrical depolarization. After successful cardioversion, if the patient is on warfarin, continue anticoagulation for at least 3 \200\2234 weeks. Consider inde \201 nite anticoagulation if there is intrinsic cardiac disease (e.g. mitral stenosis) or recurrent AF. DC CARDIOVERSION: SPECIAL SITUATIONS 821 DC cardioversion: special situations Pregnancy DC shock during pregnancy appears to be safe but should only be consid- ered after careful discussion with the obstetric team. Ausculta te the fetal heart before and after cardioversion and, if possible, the fetal ECG should be monitored. Pacemakers There is a danger of damage to the pacemaker generator box or the junc- tion at the tip of the pacing wire(s) and endocardium. Position the paddles in the anteroposterior position as this is theoretically safer. Facilities for back-up pacing (external or transve nous) should be available. Check the pacemaker post-cardioversion \200\224 both early and late problems have been reported. 822 CHAPTER 18 Practical procedures Intra-aortic balloon counterpulsation (1) Indications \200 Cardiogenic shock post-MI. \200 Acute severe mitral regurgitation. \200 Acute VSD. \200 Preoperative (ostial left coronary stenosis). \200 Weaning from cardiopulmonary bypass. Rarely \200 Treatment of ventricular arrhythmias post-MI. \200 Unstable angina (as a bridge to coronary artery by pass graft (CABG)). Contraindications \200 Aortic regurgitation. \200 Bleeding diathesis. \200 Aortic dis section. \200 Severe aorto-iliac atheroma. \200 Dilated cardiomyopathy (if patient not a candidate for transplantation). Complications \200 Aortic dissection. \200 Thrombocytopenia. \200 Arterial perforatio n. \200 Peripheral embolism. \200 Limb ischaemia. \200 Balloon rupture. Principle The device consists of a catheter with a balloon (40 mL size) at its tip, which i s positioned in the descending thoracic aorta. The balloon in \202 ation/ de \202 ation i s synchronized to the ECG. The balloon should in \202 ate just after the dicrotic notch (i n diastole), thereby increasing pressure in the aortic root and increasing coronary perfusi on. The balloon de \202 ates just before ventricular systole, thereby decreasing afterload and improving LV per- formance (see Fig. 18.9 ). Counterpulsation has a number of bene \201 cial effects on the circulation: increased coronary perfusion in diastole. \200 reduced LV end-diastolic pressure. \200 reduced myocardial oxygen consumption. \200 increased cerebral and peripheral blood \202 ow. The intra-aortic balloon cannot assist the patient in asystole or VF; it requires a minimum cardiac index of 1.2 \200\2231.4 L/min/m 2 , often necessitating additional inotr opes. Balloon insertion Previous experience is essential. Formerly, a cut-down to the femoral art ery was required, but newer balloons come equipped with a sheath, which may be introduced p ercutaneously. Using \202 uoroscopy, the balloon is positioned in the descending thoracic aorta with the tip just below the origin of the left subclavian artery. Fully anticoagulat e the patient with IV heparin. Some units routinely give IV antibiotics ( \202 ucloxacilli n) to cover against Staphylococcus infection. INTRA-AORTIC BALLOON COUNTERPULSATION (1) 823 Triggering and timing The balloon pump may be triggered either from the patient \200\231s E CG (R wave) or from the arterial pressure waveform. Slide switches on the pump allow precis e timing of in \202 ation and de \202 ation during the cardiac cycle. Set the pump to 1:2 , to allow you to see the effects of augmentation on alternate beats (see Fig. 18.10 ). Balloon inflated to increase coronary perfusion during diastole Balloon deflated to allow systemic perfusion during systole Coronary perfusion (a) Cardiac diastole (b) Cardiac systole Fig. 18.9 Intraortic-balloon counterpulsation. Reproduced with permission from Ramrakha P, Moore K, and Sam M (2010). Oxford Handbook of Acute Medicine . 3rd ed. Oxford: Oxford Unive rsity Press . Diastolic augmentation \206\221 Coronary perfusion 140 Unassisted systole Assisted systole 120 g H m m 100 Balloon inflation 80 Unassisted aortic end diastolic pressure 60 Assisted aortic end diastolic pressure \206\223 MVO2 demand Fig. 18.10 Arterial waveform variations during intra-aortic balloon pump (IABP) therapy. MV O 2 = myocardial oxygen consumption. 824 CHAPTER 18 Practical procedures IABP removal \200 The patient may be progressively weaned by gradually reducing the counterpulsation ratio (1:2, 1:4, 1:8, etc.) and/or reducing the balloon volume and checkin g that the patient \200\231s BP remains stable. Stop the heparin infusion and wait for the activated clotting time (ACT) to fall <150 s (activated partial thromboplastin time (aPTT)<1.5x normal). Using a 50 mL syringe, have an assistant apply negative pressure to the balloon. Pull the balloon down until it abuts the sheath; do not attempt to pull the balloon into the sheath. Withdraw both the balloon and sheath and apply \201 rm pressure on the femoral puncture s ite for at least 30 minutes or until the bleeding is controlled. This page intentionally left blank 826 CHAPTER 18 Practical procedures Intra-aortic balloon counterpulsation (2) Trouble-shooting \200 Seek help from an expert! There is usually an on-call cardiac perfusionist or technician, senior cardiac physician, or surgeon. Counterpulsation is inef \201 cient with heart rates over 130/min. Consider anti-arrhythmics or 1:2 augmentation instead. Triggering and timing: for ECG triggering, select a lead with the most pronounced R wave; e nsure that the pump is set to trigger from the ECG not pressure; permanent pacemakers may i nterfere with triggering \200\224 select a lead with a negative and the smallest pacing ar tifact. See also Fig. 18.11. Alternatively, set the pump to be triggered from the external pacing device. A good arterial waveform is required for pressure triggering; the timing wil l vary slightly depending on the location of the arterial line (slightly earlier for radial artery line cf. femoral artery line). Be guided by the haemodynamic effects of balloon in \202 ation and de \202 ation rather than the precise value of the delay. Limb ischaemia: this is exacerbated by poor cardiac output, adrenaline, noradrenaline, and peripheral vascular disease. Wean off and remove the balloon. Thrombocytopenia: commonly seen; does not require transfusion unless there is overt bleedin g, and it returns to normal once the balloon is removed. Consider prostacyclin infusion if the platelet counts fall below 100 x 10 9 /L. INTRA-AORTIC BALLOON COUNTERPULSATION (2) 827 (a) Inflation of the IAB prior to aortic valve closure Diastolic augmentation Unassisted systole Waveform characteristics: Inflation of IAB prior to dicrotic notch \200 Diastolic augmentation encroaches onto syst ole (may be unable to distinguish) Assisted systole Physiologic effects: Potential premature closure of aortic valve \200 Potential increase in LVEDV and LVEDP or PCWP \200 Increased left ventricular wall stress or afterload \200 Aortic regurgitatio n \200 Increased MVO2 demand Assisted aortic end-diastolic pressure Diastolic augmentation (b) Inflation of the IAB markedly after closure of the aortic valve Assisted systole Unassisted systole Waveform characteristics: Inflation of the IAB after the dicrotic notch \200 Absence of sharp V \200 Suboptimal d iastolic augmentation Physiologic effects: Dicrotic notch Suboptimal coronary artery perfusion Assisted aortic end-diastolic pressure (c) Premature deflation of the IAB during the diastolic phase Diastolic augmentation Waveform characteristics: Assisted systole Deflation of IAB is seen as a sharp drop following diastolic augmentation \200 Suboptimal diastolic augmentation \200 Assisted aortic end-diastolic pressure may be equal to or le ss than the unassisted aortic end-diastolic pressure \200 Assisted systolic pressure may rise Physiologic effects: Suboptimal coronary perfusion \200 Potential for retrograde coronary and carotid blood fl ow \200 Angina may occur as a result of retrograde coronary blood flow \200 Suboptimal afterload reduction \200 Increased MVO2 demand Assisted aortic end-diastolic pressure Unassisted aortic end-diastolic pressure Diastolic augmentation (d) Deflation of the IAB as the aortic valve is beginning to open Unassisted systole Waveform characteristics: Prolonged rate of rise assisted systole Assisted aortic end-diastolic pressure may be equal to the unassisted aortic end-diastolic pressure \200 Rate of rise of assisted systole is prolonged \200 Diastolic augmentation may appear widened Widened appearance Physiologic effects: Afterload reduction is essentially absent \200 Increased MVO2 consumption due to the left ventricle ejecting against a greater resistance and a prolonged isovolumetric contraction phase \200 IAB may impede left ventricular ejection and increase the afterload Assisted aortic end-diastolic pressure Fig. 18.11 Timing errors. (a) Early in \202 ation; (b) late in \202 ation; (c) early de \202 ation; (d) late de \202 ation. IAB = intra-aortic balloon; LVEDV = left ventricular e nd-diatolic volume; LVEDP = left ventricular end-diastolic pressure; MVO 2 = myocardial oxy gen consumption. 828 CHAPTER 18 Practical procedures Needlestick injuries Occupational exposures to bloodborne viruses (BBVs) in healthcare work ers can be divided into two groups: percutaneous (needlestick) and mucocutaneous (through b roken skin or via splashes into the eyes). High- risk body \202 uids include: blood, pleu ral \202 uid, peritoneal \202 uid, pericardial \202 uid, synovial \202 uid, amnioti c \202 uid, human breast milk, cerebrospinal \202 uid, saliva (in dentistry), semen, va ginal secretions, and un \201 xed tissues and organs, as well as vomit, feces, and urine w hen contaminated with blood. The major pathogens associated with needlestick injuries and m ucocu- taneous exposures are: \200 hepatitis B virus (HBV). \200 hepatitis C virus (HCV ). \200 human immunode \201 ciency virus (HIV). Occupational exposures to BBVs can be ca used by: \200 not properly disposing of used needles. \200 recapping needles. \200 no t using protective equipment, e.g. eye protection. Prevention Assume that every patient is potentially infected with a blood-borne infection. The same precautions should be taken for every patient and every procedure. \200 Cover sk in cuts and abrasions with waterproof dressings. \200 Never recap needles or pass sharps hand to hand. \200 Always dispose of used needles promptly in sharps disposal. \200 Nev er leave sharps to be cleared up by others. \200 Use eye protection. Ordinary spectacles offer inadequate protection. Use safety glasses that \201 t over spectacles. Double gloving: in case of needlestick, 80 % of the visible blood can be removed by latex i n a surgical glove. With double gloving, the inner glove will remove a further 80 % of the remaining blood on the needle. Management of exposure incidents \200 If the mouth or eyes are involved, wash thoroughly with water. \200 If skin is punctured, let the wound bleed and wash it with soap or chlor hexidine and running water. Avoid scrubbing or sucking. Report to the occupational health department to arrange immediate assessment or, if out of hours, attend the emergency department in accordance with the local policy. Assessment of the risk of BBVs transmission Estimated seroconversion risks are: \200 hepa titis B : 30 % for percutaneous exposure of a non-immune individual to HBsAg- and HBeAg-positive source. hepatitis C : 1.9 % for percutaneous exposure to HCV-infected blood with detectable HCV RNA. HIV : 0.3 % for percutaneous exposure to HIV-infected blood. NEEDLESTICK INJURIES 829 Factors increasing the risk following injury include: \200 percutaneous injury is higher risk than mucous membrane or broken skin exposure. injury with a device directly from a source patient \200\231s artery/vein. \200 injury fr om a hollow-bore and wide-gauge needle. \200 deep injury. \200 visible blood on the dev ice. \200 high HIV viral load, or HBeAg in the source patient. \200 staff member inadeq uately immunized against hepatitis B. Approaching source patients for BBV testing \200 Due to the sensitivity of the issue, the source patient should not be approached by the exposed member of staff. Occupational health (or the emergency department if out of hours) will arrange this test in accordance with local policies. Post-exposure prophylaxis for HIV Risk assessment and follow-up is carried out by occupatio nal health (emergency department out of hours). If the risk of infection is consid- ered to be signi \201 cant, post exposure prophylaxis (PEP) should be started, ideally within an hour and certainly within 72h. Most hospitals recommend three agents: \200 zidovudine and lamivudine (co-administered as Combivir , 1 tablet bd) or tenofovir/emtricitabine. a protease inhibitor (e.g. ritonavir-boosted lopinavir). PEP therapy is associated with sig ni \201 cant side-effects. The initial discussion and subsequent follow-up should be with a clinician experienced in the use of these agents. If the \200\230donor \200\231 is known to be HIV positive, ask about their antiretroviral therapy history, as this may alter the choice of drugs. Where possible, the \200\230donor \200\231 in such an injury should be en couraged to test for HIV to allow PEP therapy to be stopped. Post-exposure prophylaxis for HBV If the patient has been vaccinated at least twice with HB vaccine, and is known to be a responder (anti-HBS > 10 iu/mL), they should be given a boos ter injection, with a second dose one month later. For patients who have not been vaccinate d or are known to be non-responders, they should be given an immediate injection of hepatit is B immunoglobulin (HBIG) and commence an accelerated course of HB vaccination, or have a booster dose if previously immunized. Post-exposure prophylaxis for HCV Although there is no vaccine or effective PEP against hep atitis C, evidence suggests that early treatment with high-dose interferon can result in vi ral clearance in > 90 % of recently infected individuals. This emphasizes the importance of close and timely follow-up of exposed workers. Therefore, all individuals exposed to HCV s hould be tested for HCV antibodies at the time of exposure and at 6 \200\22312 weeks and 26 weeks. This page intentionally left blank 831 Appendix Clinical trials Listed in alphabetical order 832 832 APPENDIX Clinical trials ABSORB A BioabSORBable everolimus-eluting coronary stent system for patients with single de -novo coronary artery lesions trial Purpose: to assess the ef \201 cacy and safety of a bi oabsorbable everolimus- eluting stent in 30 patients with single de novo coronary artery le sions. Follow-up: 12 months Results: procedural success was 100 % and the device success 94 % . At 12 months the rate o f major adverse clinic events was 3.3 % , with only one patient having a non-ST elevation i nfarct and no target lesion revascularization required. No late-stent thrombosis was record ed. These results suggest that bioabsorbable drug-eluting stents are safe. Reference: Ormiston JA et al . ( 2008 ). Lancet 371 : 873 \200\223 4 . ACUITY Acute Catheterization and Urgent Intervention Triage Strategy trial Purpose: a large multicentre prospective trial designed to establish the optimal antithromb otic treatment regimens in patients with unstable angina or non-ST elevation myocardial inf arction undergoing early percutaneous coronary intervention. Follow-up: 30 days Results: bivalirudin monotherapy provided superior outcomes compared with any heparin plus glycoprotein (GP) IIb/IIIa inhibitor regime at 30 days. There was also a signi \201 cant r eduction in major bleeding with bivalirudin monotherapy. Reference: Stone GW et al . ( 2006 ). N Engl J Med 355 : 2203 \200\223 16 . CARE-HF Cardiac Resynchronization \200\224 Heart Failure trial Purpose: to assess the impact of cardiac resynchronization with biventricular pacing in pat ients with New York Heart Association (NYHA) class III or IV heart failure receiving optima l medical therapy on mortality and morbidity. Follow-up: mean 29.4 months Results: cardiac resynchronization therapy improved mortality in patients with heart failur e. Reference: Cleland J et al . ( 2005 ). N Engl J Med 352 : 1539 \200\223 49 . LEADERS 833 COURAGE Clinical Outcomes Utilizing Revascularisation and Aggressive drug Evaluation trial Purpose: to evaluate the impact of percutaneous coronary intervention (PCI) on prognosis in patients with stable coronary artery disease, compared with medical therapy. Follow-up: mean 4.6 years Results: in patients on optimal medical therapy, an initial strategy of routine PCI does no t reduce the risk of death, myocardial infarction (MI), or other cardiovascular (CV) events when compared with a strategy of selective PCI for angina. Reference: Boden W et al . ( 2007 ). N Engl J Med 356 : 1503 \200\223 16 . HORIZONS-AMI Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Inf arction trial Purpose: to compare the ef \201 cacy of primary percutaneous coronary intervention (PCI) w ith paclitaxel-eluting (TAXUS) stent versus bare metal stent in patients presenting with ST elevation myocardial infarction. Follow-up: 1 year Results: a signi \201 cantly reduced rate of revascularization with no increase in the rat e of stent thrombosis in patients treated with paclitaxel-eluting stents. There was no diff erence in mortality between treatment arms, demonstrating safety of drug-eluting stenting f or primary PCI. Reference: Stone GW et al . ( 2009 ). N Engl J Med 360 : 1946 \200\223 59 . LEADERS Biolimus-eluting stent with biodegradable polymer versus sirolimus-eluting stent wi th durable polymer for coronary revascularization trial Purpose: to assess the safety and ef \201 cacy of a biodegradable biolimus- eluting polyme r stent compared with a sirolimus-eluting durable polymer stent. The primary end-point was a composite of cardiac death, MI, and target vessel revascularization. Follow-up: 9 months Results: the biodegradable biolimus-eluting stent was non-inferior to sirolimus-eluting ste nts for the primary end-point at 9 months, suggesting it represents a safe and effective al ternative to a durable stent in patients with de novo coronary artery lesions. 834 APPENDIX Clinical trials MIST Migraine Intervention with Star \202 ex Technology trial Purpose: a multicentre double-blind sham-controlled trial to evaluate the effectiveness of percutaneous patent foramen ovale (PFO) closure to resolve refractory migraine. Follow-up: 180 days Results: there was no difference in resolution of migraine with PFO closure. However, those with PFO closed did report a reduction in the number of headache days experienced. Reference: Dowson AJ et al . ( 2008 ). Circulation 117 : 1397 \200\223 404 . OASIS 5 Fifth Organization to Assess Strategies in Ischemic Syndromes Purpose: to compare fondaparinux 2.5 mg daily vs. enoxaparin 1 mg/kg of body weight twice d aily in patients presenting with acute coronary syndromes. The primary end-point was death, MI, or refractory ischaemia at 9 days. Additionally, major bleeding and longer-term mortal ity and morbidity at 180 days were evaluated. Follow-up: 6 months Results: fondaparinux is non-inferior to enoxaparin in reducing the short-term risk of isch aemic events but it substantially reduced the risk of major bleeding (2.2 % vs. 4.1 % , P < 0.001) and improves long-term mortality and morbidity. Reference: Yusuf S et al . ( 2006 ) N Engl J Med 354 : 1464 \200\223 76 . PARTNER Placement of Aortic Transcatheter Valve trial Purpose: multicentre randomized clinical trial to evaluate the impact of transcatheter aort ic valve implantation (TAVI) in patients with severe aortic stenosis considered not to be s uitable candidates for conventional surgery. The primary end-point was all-cause mortality. Follow-up: mean 1.6 years Results: signi \201 cant reduction in all-cause mortality after 1 year. There was, however , an increase in the rate of major stroke and vascular complications at 30 days. Reference: Leon MB et al . ( 2010 ). Transcatheter aortic-valve implantation for aortic ste nosis in patients who cannot undergo surgery. N Engl J Med 363 : 1597 \200\223 607 . SPIRIT IV 835 PLATO Platelet inhibition and Patient Outcomes trial Purpose: to compare outcomes in patients presenting with acute coronary syndrome with or wi thout ST-segment elevation treated with ticagrelor 180 mg loading followed by 90 mg daily d ose, vs. clopidogrel 300 mg and 75 mg daily dose. Primary end-points included cardiovascula r death, MI, and stroke. Follow-up: 1 year Results: patients treated with ticagrelor had lower cardiovascular mortality compared with clopidogrel (9.8 % vs. 11.7 % , P <0.001) but a small, albeit non-signi \201 cant, increas e in major bleeding. Reference: Wallentin L et al . ( 2009 ). N Engl J Med 361 : 1045 \200\223 57 . SCD-HeFT Sudden Cardiac Death in Heart Failure Trial Purpose: to evaluate whether amiodarone or a single-lead implantable cardiac de \201 brill ator could reduce death in patients with NYHA class II or III heart failure. Follow-up: median 45.5 months Results: a single-lead implantable de \201 brillator reduced mortality by 23 % in patients with NYHA class II or III and left ventricular ejection fraction <35 % , whereas amiodaron e did not in \202 uence survival. Reference: Bardy G et al . ( 2005 ). N Engl J Med 352 : 225 \200\223 37 . SPIRIT IV Clinical evaluation of the XIENCE V everolimus eluting coronary stent system i n the treatment of subjects with de novo native coronary artery lesions Purpose: to compare the ef \201 cacy of everolimus-eluting (XIENCE) vs. paclitaxel-eluting (TAXUS) stents in patients undergoing PCI for de novo coronary artery lesions. Follow-up: 1 year Results: in patients without diabetes, everolimus-eluting stents reduced the primary end-po int of target lesion failure by 54 % ( P <0.0001) and major adverse cardiovascular events b y 52 % ( P <0.0001). However, in patients with diabetes, there were no statistically signi \201 cant differences at 1 year. Reference: Stone GW et al . ( 2010 ). N Engl J Med 362 : 1663 \200\223 74 . 836 APPENDIX Clinical trials TRITON-TIMI 38 Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet I nhibition with Prasugrel \200\224 Thrombolysis In Myocardial Infarction Purpose: to compare outcomes in patients with moderate \200\223high-risk acute coronary syn dromes scheduled to receive PCI, treated with prasugrel 60 mg loading followed by 10 mg dai ly dose vs. clopidogrel 300 mg loading and 75 mg daily dose. Follow-up: 15 months Results: prasugrel was associated with a signi \201 cantly lower incidence of ischaemic ev ents than clopidogrel. It was particularly effective in speci \201 c patient subgroups suc h as those with diabetes mellitus (30 % relative risk reduction). However, it was associate d with signi \201 cantly higher bleeding complications, resulting in no difference in all- cause mortality. Reference: Antman EM et al . ( 2008 ). J Am Coll Cardiol 51 : 2028 \200\223 33 . 837 Index AICDs see automatic angiography, aortic 768 angiography, coronary catheter types 318 complications 324 congenit al heart disease A Aase syndrome 698 abciximab 96 ABC in life support 710 ablation therapy implantable cardiac de \201 brillators albumin albuminuria 646 hypoproteinaemia 733 alcohol consumption 225 alcoholic cardiomyopathy 595 3D mapping 556 , 582 accessory pathways CT angiography 6 , 8 Fabry disease 438 grafts 322 interpretation 320 methods 318 \200\22319 574 , 579 446 alcohol septal ablation for LVOT obstruction 430 alcohol septal ablation 430 aldosterone antagonists 106 dilated cardiomyopathy arrhythmogenic RV angiography, pulmonary cardiomyopathy 442 422 \200\2233 745 \200\2236 atrial \201 brillation 562 , heart failure 388 , 398 renal disease and 108 , AngioGuard device 360 angioplasty see 568 , 570 atrial tachycardia 566 AV re-entrant 399 , 650 percutaneous coronary intervention (PCI) Angio-Seal device 316 \200\22317 angiotensin co nverting enzyme inhibitors (ACE-Is) 98 , 229 Al \201 di \200\231s syndrome 698 Allen test 784 ALL-HAT trial 228 ambulatory ECG monitori ng tachycardias 574 complications 560 , 563 , 570 energy sources 558 robotics 556 trans-septal puncture techniq ue 562 ventricular tachycardia 441 , 513 \200\22314 amiodarone 430 , 722 \200\2233 amlodipine 115 , 772 amoebic pericarditis 474 amyloidosis 71 , 434 , 436 anemia dilated cardiomyopathy 422 heart failure 98 , 390 myocardial infarction 98 , 582 abscesses 36 , 188 ABSORB trial 832 ACC/AHA classi \201 cation of 263 , 299 angiotensin receptor heart failure 412 , 416 pulmonary oedema 732 blockers (ARBs) 102 , 229 heart failure 375 accessory pathways 552 analgesia heart failure 102 \200\2233 , 392 NSTEMI/UA 298 pericarditis 776 pulmonary embolism 748 STEMI 262 ablation therapy 574 , 579 AVRT 498 , 528 , 572 , anion-exchange resins 127 \200\2238 , 237 anistreplase 266 ankle oedema 115 , 370 ankylosing spondylitis 634 anth racyclines 456 antiarrhythmic drugs 721 accessory pathways 574 , 721 localization 578 Mahaim pathways 579 pharmacological anatomical position 13 ANCA-positive vasculitis 632 treatments 579 , 721 WPW syndrome 576 , 708 Andersen syndrome 698 Anderson \200\223Fabry disease ACE-Is see angiotensin converting enzyme inhibitors 579 , 721 atrial \201 brillation 423 , 504 69 , 438 , 698 aneurysms aortic 662 atrial septum 34 in HIV-positive patients 658 see also pseudoaneurysms acne 606 action potentials 478 \200\2239 cardiomyopathies 423 , 430 in long QT syndrome 518 de \201 brillation and 588 interactions 113 , 116 in pregnancy 694 supraventricular ACUITY trial 832 acute coronary syndrome Anger gamma cameras 52 angina pectoris (ACS) 254 diagnosis 250 \200\2231 investigations 4 , 252 management 110 , 114 , 132 , 136 , 138 , 140 , 252 \200\2233 post-MI 276 Prinzmetal \200\231s angina 706 syphilitic 662 unstable see un stable