record phasic and mean pressures. With a pigtail catheter in the LV, measure and record the LV pressures. Record simultanous pulmonary capillary wedge pressure (PCWP) and LV pressure, ensuring that the scale allows i nterpretation of the end-diastolic pressures with accuracy (to assess for mitral valve (MV) gradient). Withdraw the wedge catheter slightly and record pulmonary artery phasic and mean pressure. Obtain oxygen saturations from the main PA (also right and left pulmonary arteries (RPA and LPA) if a PDA is suspected). Withdraw the pulmonary catheter to the right ventricle (RV). Measure and record simultanous RV and LV pressures. Withdraw the catheter to the RA and measure the pressures again. RIGHT-HEART CATHETERIZATION 327 The LV catheter should be pulled back to the ascending aorta while the pressure is being mo nitored to record any pull-back gradient. Aortic saturations should be measured to allow ca lculation of cardiac output (see Fig. 6.10 ) and to compare with saturations from the right side if a shunt is suspected. For shunts, a full saturation run should be performed (superior vena cava (SVC); high, mid, and low right atrium (RA), IVC, RV; main, right, and left pulmonary artery (MPA, RPA, LPA) ; etc.). Right ventricle Right atrium Pulmonary artery Pulmonary capillary wedge x v y a 30 20 10 0 a c x v y a ) g H m m ( Left atrium Left ventricle Aorta e r u s s e r P 150 100 50 0 a x v y a c Fig. 6.10 Cardiac catheterization \200\224 normal pressure waveforms. 328 CHAPTER 6 Cardiac catheterization & intervention Cardiac output and left ventricular function Cardiac output is most often measured using th e thermodilution method with a pulmonary \202 otation catheter. Cardiac output can also be measured using the Fick principle, which assesses the difference between the pulmonary arterial and aortic O 2 saturation. ( ) mL min )) \227Hb \2271.34 oxygen consumption PA SaO Ao SaO PA SaO ( L min = ) Cardiac output ( 2 2 Where Ao = aorta; Hb = hemoglobin; PA = pulmonary artery; SaO 2 = arterial oxygen saturatio n. Systemic and pulmonary vascular resistance Pulmonary vascular resistance (PVR) is an import ant prognostic factor in patients with valvular heart disease, heart failure, and cor pulmo nale. The measurement of PVR and systemic vascular resistance (SVR) is especially important in patients being assessed for cardiac transplantation. PVR and SVR are measured in Woods units (mmHg/L/min) or dynes/cm 5 , with 80 dynes/cm 5 = 1 Woods unit. \210\222 mean aortic pressure mean right atrial pressure stemic vascular resistance = Cardiac output sy \210\222 mean PA pressure mean left atrial pressure = Cardiac output pulmona ryrr vascular resistance CARDIAC CATHETERIZATION IN VALVE DISEASE 329 Cardiac catheterization in valve disease Valve stenosis Several parameters can be assessed during cardiac catheterization. \200 Peak-to-peak gradient : aortic and LV pressures are recorded during withdrawal of the pigtail catheter across the aortic valve. The gradient is the difference between peak aortic and peak LV pressure. \200 Peak instantaneous gradient : more accurat e and measured using a double-lumen pigtail catheter. Mean gradient : the mean pressure gradient measured using planimetry of the area by aortic and LV pressure traces. This can be used to calculate the valve area using the Gorlin equation, and a similar method can be used to assess the mitral valve area . 50 40 30 g H m m LV 20 LA x y 10 0 Fig. 6.11 Simultanous LV and PCWP tracing in mitral stenosis. Reproduced with permission fr om Braunwald E (ed) (2001). Heart Disease: a textbook of cardiovascular medicine , 5th ed. Philadelphia: WB Saunders. Valve regurgitation \200 The severity of aortic regurgitation can be estimated by perform ing an aortogram. In severe aortic regurgitation, the LV is seen to opacify within one or two b eats after contrast injection. Mitral regurgitation may be assessed by left ventriculography, with contrast seen to opacify the left atrium and pulmonary veins in severe regurgitation. In ad dition, mitral regurgitation (MR) may be associated with a prominent \200\230v \200\231 wa ve in the pulmonary capillary wedge tracing. 330 CHAPTER 6 Cardiac catheterization & intervention Intravascular ultrasound ( Figs. 6.12 and 6.13 ) Intravascular ultrasonography (IVUS) is a technology that allows direct visualization of atherosclerotic plaque and the vessel lumen, with recent advances allowing the echogenic characteristics of an IVUS image to give insig hts into the underlying histology. Ultrasound images are produced by passing an electrical current through a piezoelectric crystal that expands and contracts to produce sound waves w hen electrically stimulated. These sound waves are re \202 ected from tissues, and return to the transducer, where they are detected and converted to an electrical impulse that can be presented graphically. A phased array of crystals (usually 64) is used, and these are se quentially activated to produce circumferential imaging. The equipment required to perform an IVUS examination involves a mini- aturized ultrasound transducer mounted on a catheter ( usually 2.6 \200\2233.5 Fr gauge), and computer interface that carries out image reconstruc tion. Examination technique \200 Intracoronary isosorbide dinitrate and IV heparin should be administered. The IVUS catheter should be carefully advanced distal to the area of interest. A motorized pullback device is then used to draw the IVUS catheter proximally at a \201 xed speed. Landmarks such as side branches can be useful, and positions may also be recorded angiographically. Advantages of ultrasound \200 The full circumference of the vessel wall is seen, not just two surfaces as in angiography, and is thus the method of choice to determine vessel luminal area. It is useful in imaging ambiguous lesions such as: \200 intermediate lesions of unknown s everity \200 ostial stenosis \200 left main stem disease \200 disease at bifurcation sites. It images the plaque, not just the lumen. \200 It allows optimal results during angioplas ty and stenting. INTRAVASCULAR ULTRASOUND 331 Fig. 6.12 Example of image obtained by IVUS. Fig. 6.13 IVUS image of a coronary stent. 332 CHAPTER 6 Cardiac catheterization & intervention Angioplasty and coronary stenting \200 Currently, coronary stents are implanted in > 85 % of revascularization procedures in the UK. National Institute for Health and Clinical Excellence (NICE) guidelines state that \200 \230stents should be used routinely for people with either stable or unstable angina or wit h acute myocardial infarction undergoing percutaneous intervention \200\231. Angioplasty Before stents became widely used in the mid to late 1990s, balloon angio- plast y alone was the commonest percutaneous treatment for coronary artery narrowings. The two ma in designs of balloon catheters now com- monly used are over-the-wire and rapid-exchange sy stems. Both types of catheter consists of three parts: \200 the shaft : there are two mai n varieties: the hypotube, the advantage of which is a better balance between pushabillity and \202 exibility the corewire design, which is superior in terms of \202 exibility \200 the lumen : coax ial design (a tube within a tube) is the most common \200 the balloon : these are constru cted from varying plastics (e.g polyethylene, nylon), the mix of which affects the balloon \200\231s compliance. The design of the tip is important, as tapered tips are less traumatic when crossing narrowings. The balloon may also have a hydrophilic coating to render it more lubricious. \200\230Plain old balloon angioplasty \200\231 (POBA) remains indicated in the treat- ment of some coronary artery narrowings, particularly small vessels, vein grafts, and bifurcati on side branches, in which the bene \201 t of stenting has not been clearly demonstrated. Coronary stenting The primary function of a stent is to act as a scaffold to maintain vesse l patency, and thus much of the success of stents is primarily due to their mechanical abil ity to produce large acute gains in lumen dimensions. Stents can be made of stainless steel , cobalt-based alloy, tantalum, nitinol, or polymer; however, the majority of stents used t oday are stainless steel and balloon mounted. Many designs have been experimented with, in an attempt to obtain an ideal balance of \202 exibility and radial strength, with \202 exibility allowing the stent to be positioned easily, and radial strength necessary for the scaffold function of the stent. ANGIOPLASTY AND CORONARY STENTING 333 Angioplasty procedure (Fig. 6.14 ) \200 Consent the patient. \200 Cannulate the artery with the chosen guiding catheter. Ideally, the guiding catheter should be coaxial with the coronary ostium (thus allowing maximum support, and minimizing trauma to the vessel). \200 A steerable 0.014" guide wire is introduced to the catheter via the haemostatic valve. Th e tip of the guide wire may be pre-shaped; however, many operators prefer to take a straigh t guide wire and shape the tip by hand. Using X-ray screening, and contrast to delineate the coronary anatomy, the guide wire is advanced along the vessel, beyond the narrowing, and placed as d istally as possible in the vessel. An appropriately sized balloon is then chosen; the guiding catheter can be used as a reference when sizing the vessel. For calci \201 c lesions and in-stent r estenosis, shorter balloons with more highly rated burst pressure may be better. The balloon is now advanced along the guide wire to the correct position. In some situations, it will prove dif \201 cult to pass the balloon to the desir ed position, and in these instances deeper insertion of the guide catheter, or a more suppo rtive guide catheter may be needed. \200 Radio-opaque markers are used to position the ba lloon accurately. In \202 ation should be undertaken under X-ray screening, to ensure that the balloon does not move. (a) (b) (c) (d) Fig. 6.14 Coronary stenting: a guide wire is introduced across the stastic segment of arter y (a) and is used to position the stent (b). The stent is deployed by in \202 ating the ba lloon (c). The balloon and guide wire are removed, leaving the stent in place (d). 334 CHAPTER 6 Cardiac catheterization & intervention Restenosis following percutaneous transluminal coronary angioplasty (PTCA) Pathophysiology The restenotic process consists of a series of complex events: \200 vessel injury leads t o platelet activation and local thrombosis . \200 an in \202 ammatory reaction is invoke d, with neutrophil, monocyte, and lymphocyte migration to the site of injury. smooth muscle proliferation is driven by activated platelets and in \202 ammatory mediators. \201 nally, negative remodeling can occur. \200 these processes occur at different rate s, and may occur to different degrees depending upon the nature of vessel injury, and indiv idual patient characteristics. The problem Large randomized trials have established that, following percutaneous intervent ion, restenosis rates in the treated vessel are between 30 % and 60 % (following angioplast y) and 15 \200\22330 % (following stent implantation), and higher still in selected high-ri sk patients (e.g. those with diabetes). This relatively high incidence of angiographic rest enosis, however, translates into revascularization in about 10 % of patients, in whom clini cal restenosis is said to have occurred. Prevention of restenosis Mechanical Stent implantation \200 Stent implantation reduces re stenosis rates by increasing the mean luminal diameter after angioplasty, and preventing el astic recoil and adventitial constriction. Optimization of stent deployment by IVUS guidance \200 Using intravascular ultrasound to establish whether a stent has been adequately deployed improves the results of percutaneous intervention. Pharmacological Studies examining pharmacological interventions for reduction of restenosis have been disappointing. Antithrombotic and antiplatelet treatment Early aggressive antithrombotic and antiplatelet therapy using heparin, aspirin, GPIIb/IIa antagonists, and clopidogrel reduce the incidence of acute stent thrombosis. This page intentionally left blank 336 CHAPTER 6 Cardiac catheterization & intervention Drug-eluting stents Implantation of stents has, to a great extent, overcome the problem of elastic recoil and negative remodeling following PTCA. It is thus evident that neointimal p roliferation, resulting in stent restenosis, remains the major limiting factor for stenting procedures. Much research has focused on the role of anti-proliferative agents in the redu ction of restenosis, and recently drug-eluting stents (DESs) have emerged as the pre-eminen t solution to this problem. Drug-eluting stents are coated stents, capable of releasing bio active components into the local tissue and bloodstream. The advent of stents as a platform for the delivery of drugs, with subsequent reduction in rates of stent restenosis, is radi cally changing the treatment of patients with coronary artery disease. The number of CABG p roce- dures performed worldwide is falling, with increasing numbers of patients, who previo usly would only have been candidates for CABG, being treated by percutaneous coronary inter vention (PCI). Increasingly the favorable results obtained with DESs mean that PCI is perfo rmed in \200\230complex \200\231 cases such as left main coronary artery (LMCA) stenosis, diffuse disease, and bifurcation anatomy. The latest randomized controlled trial evidence shows rates of target lesion revascularizat ion (TLR) at 1 year for procedures carried out with DESs were less than 5 % , compared to 1 0 \200\22325 % for procedures that used a bare metal stent (BMS). This bene \201 t appears to be maintained for up to 3 years in long-term follow-up studies. No statistically signi \201 cant differences in rates of mortality or acute myocardial inf arction (MI) have been shown between DES types, although TLR rates for the Cipher \204 si rolimus-eluting stent (SES) up to 9 months were statistically superior to the Taxus \204 paclitaxel-eluting stent (PES). In addition to development of DESs, advances in the platform itself such as design, materia l, and strut thickness also help combat restenosis rates. Reducing the quantity of metal re sults in less wall injury. The \200\230holy grail \200\231 of coronary stent technology is a \200\230bio-absorbable \200\231 stent that will be completely absorbed over time, while maintaining vessel patency by altering arterial geometry at the time of implantation. Such stents are now in developm ent, and phase two human trials have shown promising results in terms of reduction in plaqu e, zero stent thrombosis, and no major cardiac events up to 2 years of follow-up in small n umbers of patients. Furthermore, studies show successful absorption of the stent and restor ation of vasomotion \200\224 the ability of the coronary artery to contract and expand wit h normal pre-stent \202 exibility. DRUG-ELUTING STENTS 337 Those patients at higher risk of restenosis who require stent insertion (small-caliber arte ries, longer atherosclerotic lesions, those with dia- betes, saphenous vein grafts, chronic total occlusions (CTOs)) should have the use of DES considered. Latest NICE guidance (2008) on the use of DESs has recommended their use if the target arte ry to be treated has less than a 3 mm caliber, or the lesion is longer than 15 mm. In real- world practice, this translates to coronary artery lesions in approximately 60 \200\22370 % of patients undergoing PCI. Drug-eluting stents \200 Similarities between tumor growth and benign neointimal proliferation introduced the concept that immunosuppressant and cytotoxic agents might be b ene \201 cial for preventing in-stent restenosis (ISR). Incorporating these agents into stent coatings, using a number of techniques, has now enabled delivery of the active agent directly to its site of action, wh ile limiting systemic side-effects. Crucially, the coatings allow sustained release of the agent, such that the therapy is present at the time that the target mechanism is physiologically active . The commonly used agents are sirolimus, which has a cytostatic action, and paclitaxel, which is cytotoxic. 338 CHAPTER 6 Cardiac catheterization & intervention Stent thrombosis Recent concerns of higher rates of acute stent thrombosis following discon tinuation of clopidogrel in DES patients prompted further inves- tigation. Delayed endothel ialization maintains a stent material substrate upon which thrombus formation can occur fol lowing the withdrawal of antiplatelet drugs. It has since been concluded that the absence of a signi \201 cant increase in associated d eath rates or MI as a result of stent thrombosis should not preclude their use within curre nt guidelines. Premature discontinuation of dual antiplatelet therapy is a very de \201 ni te risk for stent thrombosis, and an assessment of ability to comply with this must be made prior to stent implantation. Particular attention should be paid to bleeding risk and plan ned operative procedures. The debate of duration of dual antiplatelet therapy continues; currently we recommend 12 mo nths (as for non-ST-segment elevation MI) NSTEMI), but some evidence suggests that the back ground, low rate of stent thrombosis continues in a linear manner until at least 3 years po st implantation. Very late stent thrombosis rates (de \201 ned as thrombosis > 1 year from implantation) require longer-term follow-up. Current research has implied a relationship between the routine use of proton pump inhibito rs (PPIs) and clopidogrel resistance, leading to the potential for increased risk of acute stent thrombosis. While this relationship is not yet fully understood, current recommendati ons are review of the clinical need for acid-suppression therapy and use of histamine-recep tor-blocking agents as an alternative to PPIs if required. This page intentionally left blank 340 CHAPTER 6 Cardiac catheterization & intervention Physiological assessment of coronary \202 ow The shortcomings of coronary angiography in the physiological assessment of coronary stenosis are clear. Intravascular ultrasound can p rovide infor- mation on the size of the lumen and the composition of plaque, but again give s no information as to the effect that an atheromatous plaque may have on coronary \202 o w. The knowledge as to whether a narrowing seen on angiography is the \200\230culprit \200 \231 causing haemodynamic effects, and thus anginal symptoms, is valuable when guiding perc utaneous intervention. The fractional \202 ow reserve (FFR) correlates distal coronary pressure to myocardial bl ood \202 ow during maximum hyperaemia (induced by infusion of adenosine, or papaverine). FFR is de \201 ned as maximum myocardial blood \202 ow in the presence of a stenosis div ided by the theoretical maximum \202 ow in the absence of a stenosis (see Fig. 6.15 ). Thus, the information derived from FFR allows an \200\230on-the-spot \200\231 diagnosis as to what extent a given stenosis contributes to myocardial ischaemia (and angina), and can guide decisions regarding revascularization. At present, the best-established indication fo r coronary FFR estimation is as a diagnostic tool to assess \200\230severe \200\231 corona ry narrowings, and for this it is extremely sensitive when used with a cut-off point of 0.7 5. The technique has also been used to optimize the results of stent implantation. Two technologies are currently available that provide haemodynamic information derived from FFR calculations; these are pressure wires (which consist of a pressure transducer mounted on a 0.014" guide wire), and Doppler \202 ow wires (which examine coronary \202 ow vel ocities using spectral analysis). Pressure wire (e.g. The PressureWire \204 (Radi Medical Systems)) \200 The pressure tra nsducer is located at the transition between the radio- opaque wire tip, and the non-radio-opaque stem. The analyzer shows simultanous aortic and intracoronary pressure, as well as instantaneous FFR. Doppler wire (e.g. FlowWire \204 (Endosonics)) \200 This obtains information on coronar y \202 ow velocity in the central area of the arterial lumen. Combining \202 ow and electrocardiographic (ECG) information, it calculates systolic and diastolic components of \202 ow velocity at baseline. Following induction of hyperaemia, the machine can calculate the coronary \202 ow velocity reserve. PHYSIOLOGICAL ASSESSMENT OF CORONARY FLOW 341 Q Pv 0 Pd 100 Pa 100 P Pd 70 Pv 0 Pa 100 Pd Pa FFRmyo = = 0.70 Fig. 6.15 During maximal arteriolar vasodilatation, the resistance of the myocardium is min imal, and so maximum myocardial blood \202 ow is proportional to hyperaemic perfusion pre ssure. This equals P d \210\222 P v . As there is no decline in pressure along a normal co ronary artery, and neglecting P v , this implies that in a normal epicardial artery, perfus ion pressure at hyperaemia equals P a . In the presence of a stenosis, hyperaemic perfusion pressure decreases to P d (after the stenosis). Thus, the maximum \202 ow in the presenc e of a stenosis as a ratio (fraction) of normal maximum \202 ow is represented by the rat io of perfusion pressures: P d /P a . This fraction of normal maximum \202 ow, which is m aintained despite the stenosis, is called the fractional \202 ow reserve (FFR). Reproduce d with permission from Pijls NH (2004). Optimum guidance of complex PCI by coronary pressur e measurement. Heart 90 : 1085 \200\22393. The FAME study This randomized, prospective, multi-center trial (FFR vs. Angiography for Mu ltivessel Evaluation) looked at 1005 patients with multivessel coronary artery disease 12 m onths after receiving a stent, and compared outcomes for patients whose treatment was guide d by FFR to those whose treat- ment was guided only by angiography. It demonstrated a statistically signi \201 cant 30 % reduction in major adverse cardiac ev ents (MACE) in the FFR arm, and also proved cost-effective with reduced need for repeat pro cedures. There was no difference in overall procedure time. Quality-of-life assessment (fre edom from chest pain) for patients whose treatment was guided by FFR) was equal to, and in some cases better than, that of patients whose treatment was based solely on angiography. 342 CHAPTER 6 Cardiac catheterization & intervention Primary angioplasty for STEMI Pathophysiology In the context of cardiac chest pain, ST-segm ent elevation on the 12-lead ECG usually signi \201 es complete occlusion of a proximal ep icardial coro- nary artery. This occurs as a result of rupture or erosion of a vulnerable a theromatous plaque, which leads to platelet activation and adhesion, for- mation of platele t-rich (white) thrombus, \201 brin deposition, and red cell entrapment (forming red throm bus). If untreated, myocardial necrosis commences within 30 minutes, affecting full myocard ial thickness within 6 hours; 40 % of patients die before reaching hospital. Treatment Urgent restoration of coronary blood \202 ow (reperfusion) prevents further LV damage and improves prognosis. The amount of myocardium that can be salvaged falls exponent ially with time, with the greatest bene \201 t within 3 hours following symptom onset, and little bene \201 t after 12 hours. Primary angioplasty is the preferred reperfusion strategy, where angiog- raphy can be perfo rmed within 90 minutes of presentation (see b STEMI: reperfusion by primary PCI, p. 268). Patients can be transferred safely (by a trained ambulance crew with an advanced life suppo rt (ALS)-trained escort) from a district hospital to a cardiac center for primary angioplas ty. Options for reperfusion \200 Primary angioplasty Immediate coronary arteriography and \200\230culprit \200\231 vessel angioplasty and stent implantation without antecedent \201 brinolysis Achieves full arterial patency (TIMI (Thrombolysis in Myocardial Infarction) grade 3 \202 ow) in 90 \200\22395 % Treats the occlusive thrombus and the culprit plaque Intravenous \201 brinolysis Immediate administration of a \201 brinolytic agent (also called thrombolysis) without pl anned coronary arteriography Achieves full arterial patency (TIMI grade 3 \202 ow) in 50 \200\22360 % \200 Contraind icated in up to 30 % of patients \200 Does not treat the culprit plaque Rescue angioplasty Urgent coronary arteriography \200\230culprit \200\231 vessel angioplasty and stent implan tation performed when \201 brinolysis has failed to achieve reperfusion (Persistent ST se gment elevation 9 pain at 60 \200\22390 min) Facilitated angioplasty Fibrinolysis prior to immediate coronary arteriography and \200\230culprit \200\231 vessel angioplasty and stent implantation PRIMARY ANGIOPLASTY FOR STEMI 343 The Thrombus Aspiration during Percutaneous Coronary Intervention in Acute Myocardial Infar ction (TAPAS) study is a single-center randomized trial involving > 1000 patients, which co mpared stenting for acute STEMI with or without prior application of the Export \204 Aspi ration Catheter (Medtronic, USA). This is designed to suck out and capture thrombus from wi thin an infarct-related artery, prior to bare-metal stenting. Thrombus aspiration was associated with signi \201 cantly improved myo- cardial reperfusio n, as gauged by blush grade, compared with stenting with predilatation. The better reperfus ion with aspiration was accompanied by signi \201 cantly better resolution of ST-segment c hanges. MACE rates were similar between the groups at 30 days, but both end-points correlat ed signi \201 cantly with blush grade and resolution of the ST-segment changes, independen tly of baseline clinical and angiographic features. The \201 nding strengthens the case for myocardial \200\230blush \200\231 grade as a pre dictor of clinical outcomes after PCI-treated acute MI, and advocates thrombus aspiration i n the setting of acute STEMI. In the context of primary percutaneous intervention for STEMI, the use of BMSs is currently recommended by NICE; however, there is emerging data that the use of DESs is safe in prima ry PCI, without increases in rates of ST, but with a reduction in the need for repeat revas cularization. 344 CHAPTER 6 Cardiac catheterization & intervention Primary angioplasty: procedure Indications \200 Cardiac chest pain <12 hours \200 ST el evation \211 1 mm in 2 contiguous leads \200 Cardiogenic shock \200 Able to consent \200 NB: left bundle branch block (LBBB) and \200\230true posterior \200\231 MI are not clear indications for primary angioplasty, though in practice some centers do include t hese patients. Discuss immediately with the cardiology registrar. Contraindications \200 Suspected aortic dissection Relative contraindications \200 Active bleeding (antiplatelet therapy may have to be avoi ded, but may compromise outcome; these cases should be discussed directly with the operator ). Pre-procedure (work quickly \200\224 minutes matter) \200 Consent \200 The risk is hig her than that of elective PCI. A procedural event rate of 5 % (death, MI, stroke) should be quoted Full blood count (FBC), clotting, group and save, urea and electrolytes (U&E), creatine kinase (CK), troponin Analgesia + anti-emetic (diamorphine 5 mg; metoclopramide 10 mg) \200 Oxygen if saturatio ns <94 % \200 Aspirin 300 mg (chewed) \200 Clopidogrel 600 mg \200 Platelet glycoprot ein GPIIb/IIIa receptor antagonist (abciximab) if no contraindication. Procedure \200 Access \200\224 femoral or radial. The femoral region should always be pr epared in case of a need for transvenous pacing or intra-aortic balloon pump (IABP) inserti on. A stent should be implanted where possible. Direct stenting without pre-dilatation may reduce the risk of distal embolization. The role of DESs in STEMI is undetermined. \200 Platelet GPIIb/IIIa receptor antagonist i f not already given. \200 See also Fig. 6.16. Additional considerations \200 Culprit vessel PCI is prognostic. Other vessels may be tre ated to provide complete revascularization. However, complex non-culprit PCI should be avoided in m ost cases. Procedural success is de \201 ned by TIMI grade 2 or 3 \202 ow with residual stenosis <20 % . PRIMARY ANGIOPLASTY: PROCEDURE 345 (a) (b) Fig. 6.16 Angiographic images from a 54-year-old male presenting with chest pain and anteri or ST elevation. (a) The left anterior descending (LAD) artery is occluded mid vessel (arro w). (b) The same artery is now widely patent following primary angioplasty; A 3.5 x 24 mm b are metal stent has been implanted (arrow). The patient sustained minimal LV damage, and wa s discharged 48 hours later. Further reading Keeley EC , Boura JA , Grines CL ( 2003 ). Primary angioplasty vs. intraven ous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomized trials . Lancet 361 : 13 \200\223 20 . Andersen HR , Nielsen TT , Rasmussen K , et al . ( 2003 ). A compariso n of coronary angioplasty with \201 brinolytic therapy in acute myocardial infarction . N Engl J Med 349 : 733 \200\223 42 . Widimsky P , Budesinsky T , Vorac D , et al . ( 2003 ). Long distance transportation for pr imary angioplasty vs immediate thrombolysis in acute myocardial infarction. Final results of the randomized n ational multicentre trial-PRAGUE-2 . Eur Heart J 24 : 94 \200\223 104 . 346 CHAPTER 6 Cardiac catheterization & intervention Invasive assessment of vulnerable plaque It has become apparent from intravascular ultrasou nd studies that non- obstructive and haemodynamically insigni \201 cant atherosclerotic pl aques can be responsible for sudden death due to MI. These high-risk, or \200\230vul- nera ble \200\231 plaques are left untreated, as it is unclear which will progress to rupture. A ngiography does not help differentiate between benign and hazardous plaques, and thus new t echnologies have been developed to assist in the identi \201 cation of these plaques. Histopathological correlates of vulnerable plaque \200 Lipid-rich core \200 Thin \201 brous cap \200 Necrotic core \200 High degree of macrophage in \201 ltration. Intravascular ultrasound \200 Able to discriminate plaques with low (lipid) and high ( \201 brous) echodensity Able to identify the capsule \200 Able to identify areas of rupture within the plaque \200 In combination with image analysis, information regarding the tissue types imaged can be derived, to provide a histological \200\230map \200\231 of the plaque. Thermography catheters \200 These catheters are able to detect the subtle temperature dif ferences caused by in \202 ammation that are present between stable and potentially unstable plaque s. Optical coherence tomography (OCT) \200 This is similar in principle to intravascular ult rasound, but uses light instead of sound waves. The system has high axial resolution, down to 20 m. \200 At present, useful anatomical information can be obtained by this technique, but this is yet to be correlated with funct ional data. Intravascular elastography \200 This technology uses sound waves in a similar way to IVUS . \200 Images are based on radial strain, and the system is therefore able to help differentiate soft from hard material. It is known that plaque rupture is often seen to occur in areas of increased strain, such as at the edge of plaques. This page intentionally left blank 348 CHAPTER 6 Cardiac catheterization & intervention Complex coronary angioplasty Chronic total occlusion A chronic total occlusion (CTO) is de \201 ned as a total coronary arterial occlusion known to be greater than 3 months old. Rec ent data suggest that nearly half of patients with signi \201 cant coronary artery disease on a coronary angiogram have at least one CTO. Despite this high incidence, only about 10 % of percutaneous interventions are performed for CTO, with the majority of patients being referred for coronary artery bypass graft surgery (CABG), which remains the \200\230gold s tandard \200\231 in CTO revascu- larization. The main reason that percutaneous intervention s to CTOs fail is that a wire cannot be passed through the point of occlusion. Why should w e treat CTO? \200 Relief of anginal symptoms \200 Improved LV function \200 Reduced n eed for CABG \200 Successful intervention confers a survival advantage. Who should treat CTO? \200 Procedural success improves with operator experience. Lower- volume centers may wish to participate in CTO clubs and invite guest operators, and dedicat ed CTO days can be implemented at institutions committed to learning advanced CTO-PCI techn iques. The following factors have been shown to improve procedural success : \200 experienced op erator(s) \200 specialist equipment such as \200\230CTO wires \200\231 hydrophilic wires, can slip through the occlusion \200 tapered-tip guide wires: Cross-IT, Conquest, Miracle \200 \200\230heavy duty \200\231 wires with stiff tips, e.g. Con \201 anza \200 procedural planning using non-invasive imaging such as multislice computed tomography (MSCT) the use of micro-catheters to allow support of the wire and improve manipulation. Predictors of procedural failure include: \200 longer length of occlusion \200 longer d uration of occlusion \200 presence of calci \201 cation \200 presence of bridging coll aterals \200 \200\230blunt \200\231 (as opposed to tapered) stump at point of occlusion \200 presence of a side branch at the point of occlusion \200 vessel tortuosity. What m akes angioplasty complex? \200 Increased risk of procedural failure \200 Suboptimal res ult likely \200 Complication rate higher \200 Worse long-term outcome (death, MI, repea t procedure) COMPLEX CORONARY ANGIOPLASTY 349 Patient characteristics: clinical presentation \200\224 acute vs. stable \200 diabetes \200 body habitus \200 signi \201 cant co-morbidity \200 access problems \200\224 peripheral vascular disease Lesion characteristics: e.g. long, calci \201 ed, bifurcation, left main stem, chronic total occlusions Dif \201 cult anatomy. Potential complications of CTO intervention These procedures may be long, involve signi \201 cant X-ray exposure, and considerable contrast load; thus, compl ications are not infrequent, and this must be considered when taking consent. Complications may include: \200 impairment of collateral \202 ow \200 retrograde dissection \200 perforation \200 guide-wire entrapment \200 subacute vessel reocclusion \200 extensi ve contrast use, resulting in contrast-induced nephropathy \200 increased radiation expos ure. The use of stents in CTO intervention The implantation of a stent improves the outcome of CTO intervention when compared to balloon angioplasty alone. However, the long-term out come of CTO intervention is hindered by a relatively high rate of restenosis. This has been somewhat ameliorated by the use of DESs, with improved ef \201 cacy of DESs demonstrated in several randomized controlled trials (RCTs). Approaches to CTO percutaneous intervention \200 A normal approach to CTO PCI involves a planned, progressive escalation in the equi pment chosen to tackle the occlusion. A femoral approach, using 8 Fr guiding catheters is often chosen \200\224 such that guide catheter support can be optimized. Most operators will begin with softer wires, such that the occlusion may be \200\230probed \200\231 \200\224 before moving on to more stiff wires that may all ow the cap of the occlusion to be penetrated. Over-the-wire balloons, and micro-catheters m ay increase the chances of successful wire penetration. If the occlusion is crossed, the oc clusion can be dilated, and treated with stent implantation in a conventional manner. Several new wiring techniques and devices have evolved to treat CTO, further details on the se can be found in the reference at the end of this section. These include: \200 side-bra nch technique Fig 6.17 \200 parallel wire technique Fig 6.18 \200 subintimal re-entry t echnique \200 IVUS-guided recanalization technique Fig. 6.19 \200 retrograde approach \200 an approach that relies on access via collateral branches from the contralateral artery to gain access to the point of occlusion \200\230see-saw \200\231 wiring technique. 350 CHAPTER 6 Cardiac catheterization & intervention (a) (b) (c) (d) (e) (f) Fig. 6.17 Side-branch technique. Reproduced with permission from Y www.summitmd.com . COMPLEX CORONARY ANGIOPLASTY 351 Fig. 6.18 Parallel wire technique. Reproduced with permission from Y www.summitmd.com . False lumen Guide wire True lumen Fig. 6.19 IVUS-guided technique. Reproduced with permission from Y www.summitmd.com . 352 CHAPTER 6 Cardiac catheterization & intervention Adjunctive tools \200 FrontRunner \204 catheter controlled blunt micro-dissection Optical coherence re \202 ectometry (OCR) SafeSteer \204 system Forward-looking guidance system using OCR to determine tissue types (plaque vs. arterial wa ll) navigates through total occlusion Flow Cardia Crosser \204 system \200 High-frequency ultrasound recanalization \200 Bi ological approach \200 Prolonged pharmacological lysis infusion \200 Collagenase plaque digestion. Further reading Further information on CTO treatment can be found in: Di Mario C et al . ( 2007 ). European perspective in the recanalisation of Chronic Total Occlusions (CTO): consensus document from the EuroCTO Club . EuroInterv 3 : 30 \200\223 43 . Bifurcation lesions \200 The prescence of atheromatous narrowings involving a coronary bifurcation present unique problems to the interventional cardiologist. As a subset of coro nary artery narrowings, bifurcations are associated with higher rates of restenosis when co mpared to non-bifurcation lesions. A simple de \201 nition of bifurcation lesions can be the involvement of a side branch wit h a reference diameter greater than 2 mm in the stenosis. IVUS studies show that plaque in the main vessel almost invariably extends some distance into side branches that arise withi n the plaque. Furthermore, angioplasty to a plaque will often cause plaque-shift (the so-ca lled \200\230snowplow \200\231 effect) into the daughter vessel. The Medina classi \201 cation of bifurcation lesions, based on the presence or abscence of atheroma in the proximal main branch, distal main branch and side branch, is shown in Fig. 6.20 . Several strategies exist for the treatment of bifurcation lesions. These are broadly classi \201 ed into single-stent (or provisional) techniques, and double-stent techniques. The m ajority of operators adopt a \200\230simple \200\231 provisional strategy, in which the ma in branch stent is implanted, and the side branch only treated in the event of its occlusio n or dissection. The two-stent techniques have names such as \200\230T \200\231 stent, \200\230cullotte \200\231, \200\230crush \200\231, mini-crush \200\231, and \200\230shotg un \200\231, and are described in more detail in the reference at the end of this section. 1 Unless \202 ow in the side branch was severely impaired, or the ostium severely narrowed, during the treatment of the main vessel, a single- stent technique is preferable to the us e of two stents. This is the so-called \200\230provisional T-stenting \200\231 technique.