ACC/AHA 2007 guideline update for the

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e190 Circulation August 14, 2007 in the most contemporary oral beta blocker post-MI trial, CAPRICORN (Carvedilol Post-Infarct Survival Control in LV Dysfunction) (321). In conclusion, evidence for the beneficial effects of the use of beta blockers in patients with UA is based on limited randomized trial data along with pathophysiological considerations and extrapolation from experience with CAD patients who have other types of ischemic syndromes (stable angina or compensated chronic HF). The duration of benefit with long-term oral therapy is uncertain and likely varies with the extent of revascularization. 3.1.2.4. CALCIUM CHANNEL BLOCKERS Calcium channel blockers (CCBs) reduce cell transmembrane inward calcium flux, which inhibits both myocardial and vascular smooth muscle contraction; some also slow AV conduction and depress sinus node impulse formation. Agents in this class vary in the degree to which they produce vasodilation, decreased myocardial contractility, AV block, and sinus node slowing. Nifedipine and amlodipine have the most peripheral arterial dilatory effects but few or no AV or sinus node effects, whereas verapamil and diltiazem have prominent AV and sinus node effects and some peripheral arterial dilatory effects as well. All 4 of these agents, as well as other approved agents, have coronary dilatory properties that appear to be similar. Although different CCBs are structurally and, potentially, therapeutically diverse, superiority of 1 agent over another in UA/NSTEMI has not been demonstrated, except for the increased risks posed by rapid-release, short-acting dihydropyridines such as nifedipine (Table 16). Beneficial effects in UA/NSTEMI are believed to be due to variable combinations of decreased myocardial oxygen demand (related to decreased afterload, contractility, and heart rate) and improved myocardial flow Table 16. Properties of Calcium Antagonists in Clinical Use (related to coronary arterial and arteriolar dilation) (300,325). These agents also have theoretically beneficial effects on LV relaxation and arterial compliance. Major side effects include hypotension, worsening HF, bradycardia, and AV block. Calcium channel blockers may be used to control ongoing or recurring ischemia-related symptoms in patients who already are receiving adequate doses of nitrates and beta blockers, in patients who are unable to tolerate adequate doses of 1 or both of these agents, and in patients with variant angina (see Section 6.7). In addition, these drugs have been used for the management of hypertension in patients with recurrent UA (325). Rapid-release, shortacting dihydropyridines (e.g., nifedipine) must be avoided in the absence of concomitant beta blockade because of increased adverse potential (326,327,328). Verapamil and diltiazem should be avoided in patients with pulmonary edema or evidence of severe LV dysfunction (329–331). Amlodipine and felodipine are reasonably well tolerated by patients with mild LV dysfunction (329–331,332–334), although their use in UA/NSTEMI has not been studied. The CCB evidence base in UA/NSTEMI is greatest for verapamil and diltiazem (328,331). Several randomized trials during the 1980s tested CCBs in UA/NSTEMI and found that they relieve or prevent signs and symptoms of ischemia to a degree similar to the beta blockers. The Danish Study Group on Verapamil in Myocardial Infarction (DAVIT) (332,333) studied 3,447 patients with suspected UA/NSTEMI. A benefit was not proved, but death or nonfatal MI tended to be reduced. The Diltiazem Reinfarction Study (DRS) studied 576 patients with UA/NSTEMI (329). Diltiazem reduced reinfarction and refractory angina at 14 d without an increase in Drug Dihydropyridines Usual Dose Duration of Action Side Effects Nifedipine* Immediate release: 30 to 90 mg daily orally Slow release: 30 to 180 mg orally Short Hypotension, dizziness, flushing, nausea, constipation, edema Amlodipine 5 to 10 mg once daily Long Headache, edema Felodipine 5 to 10 mg once daily Long Headache, edema Isradipine 2.5 to 10 mg twice daily Medium Headache, fatigue Nicardipine 20 to 40 mg 3 times daily Short Headache, dizziness, flushing, edema Nisoldipine 20 to 40 mg once daily Short Similar to nifedipine Nitrendipine Miscellaneous 20 mg once or twice daily Medium Similar to nifedipine Diltiazem Immediate release: 30 to 90 mg 4 times daily Short Hypotension, dizziness, flushing, bradycardia, edema Slow release: 120 to 360 mg once daily Long Verapamil Immediate release: 80 to 160 mg 3 times Short Hypotension, myocardial depression, heart failure, daily edema, bradycardia Slow release: 120 to 480 mg once daily Long *Immediate-release nifedipine not recommended for UA/NSTEMI except with concomitant beta blockade. Modified from Table 27 in Gibbons RJ, Abrams J, Chatterjee K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina. Available at: http://www.acc.org/qualityandscience (4). Downloaded from circ.ahajournals.org by on September 22, 2007
mortality rates. Retrospective analysis of the non–Q-wave MI subset of patients in the Multicenter Diltiazem Postinfarction Trial (MDPIT) suggested similar findings (334). The Holland Interuniversity Nifedipine/metoprolol Trial (HINT), tested nifedipine and metoprolol in a 2 2 factorial design in 515 patients (327). The study was stopped early because of concern for harm with the use of nifedipine alone. In contrast, patients already taking a beta blocker appeared to benefit from the addition of nifedipine (risk ratio [RR] 0.68) (335). Meta-analyses combining UA/NSTEMI studies of all CCBs have suggested no overall benefit (322,336), whereas those excluding nifedipine (e.g., for verapamil alone) have reported favorable effects on outcomes (332). Retrospective analyses of DAVIT and MDPIT suggested that verapamil and diltiazem can have a detrimental effect on mortality rates in patients with LV dysfunction (329,330). In contrast, verapamil reduced diuretic use in DAVIT-2, (333). Furthermore, subsequent prospective trials with verapamil administered to MI patients with HF who were receiving an ACE inhibitor suggested a benefit (330,337). The Diltiazem as Adjunctive Therapy to Activase (DATA) trial also suggested that intravenous diltiazem in MI patients can be safe; death, MI, and recurrent ischemia were decreased at 35 d and 6 months (338). In summary, definitive evidence for a benefit of CCBs in UA/NSTEMI is predominantly limited to symptom control. For immediate-release nifedipine, an increase in serious events is suggested when administered early without a beta blocker. The heart rate–slowing CCB drugs (verapamil and diltiazem) can be administered early to patients with UA/ NSTEMI without HF without overall harm and with trends toward a benefit. Therefore, when beta blockers cannot be used, and in the absence of clinically significant LV dysfunction, heart rate–slowing CCBs are preferred. Greater caution is indicated when combining a beta blocker and CCB for refractory ischemic symptoms, because they may act in synergy to depress LV function and sinus and AV node conduction. The risks and benefits in UA/NSTEMI of newer CCBs, such as the dihydropyridines amlodipine and felodipine, relative to the older agents in this class that have been reviewed here, remain undefined, which suggests a cautious approach, especially in the absence of beta blockade. 3.1.2.5. INHIBITORS OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM Angiotensin-converting enzyme inhibitors have been shown to reduce mortality rates in patients with MI or who recently had an MI and have LV systolic dysfunction (339–341), in patients with diabetes mellitus with LV dysfunction (342), and in a broad spectrum of patients with high-risk chronic CAD, including patients with normal LV function (343). Follow-up of patients with LV dysfunction after MI in the TRACE (TRAndolapril Cardiac Evaluation) trial showed that the beneficial effect of trandolapril on mortality and hospitalization rate was maintained for at Anderson et al ACC/AHA UA/NSTEMI Guideline Revision e191 Downloaded from circ.ahajournals.org by on September 22, 2007 least 10 to 12 years (344). A systematic review assessing potential ASA–ACE inhibitor interactions showed clinically important benefits with ACE inhibitor therapy, irrespective of whether concomitant ASA was used, and only weak evidence of a reduction in the benefit of ACE inhibitor therapy added to ASA (345); these data did not solely involve patients with MI. Accordingly, ACE inhibitors should be used in patients receiving ASA and in those with hypertension that is not controlled with beta blockers. Recent data on ACE inhibitor patients with stable CAD are summarized in the section on long-term medical therapy (see Section 5.2.3). In patients with MI complicated by LV systolic dysfunction, HF, or both, the angiotensin receptor blocker valsartan was as effective as captopril in patients at high risk for cardiovascular events after MI. The combination of valsartan and captopril increased adverse events and did not improve survival (346). Although not in the acute care setting, treatment of patients with chronic HF with candesartan (at least half of whom had an MI) in the CHARM (Candesartan in Heart failure Assessment in Reduction of Mortality)-Overall program showed a reduction in cardiovascular deaths and hospital admissions for HF, independent of ejection fraction or baseline treatment (347). The selective aldosterone receptor blocker eplerenone, used in patients with MI complicated by LV dysfunction and either HF or diabetes mellitus, reduced morbidity and mortality in the Eplerenone Post-acute myocardial infarction Heart failure Efficacy and SUrvival Study (EPHESUS) (348). This complements data from the earlier Randomized ALdactone Evaluation Study (RALES), in which aldosterone receptor blockade with spironolactone decreased morbidity and death in patients with severe HF, half of whom had an ischemic origin (349). Indications for long-term use of aldosterone receptor blockers are given in Section 5.2.3. 3.1.2.6. OTHER ANTI-ISCHEMIC THERAPIES Other less extensively studied therapies for the relief of ischemia, such as spinal cord stimulation (350) and prolonged external counterpulsation (351,352), are under evaluation. Most experience has been gathered with spinal cord stimulation in “intractable angina” (353), in which anginal relief has been described. They have not been applied in the acute setting for UA/NSTEMI. The K ATP channel openers have hemodynamic and cardioprotective effects that could be useful in UA/ NSTEMI. Nicorandil is such an agent that has been approved in a number of countries but not in the United States. In a pilot double-blind, placebo-controlled study of 245 patients with UA, the addition of this drug to conventional treatment significantly reduced the number of episodes of transient myocardial ischemia (mostly silent) and of ventricular and supraventricular tachycardia (354). Further evaluation of this class of agents is underway.
Page 1 and 2: ACC/AHA 2007 Guidelines for the Man
Page 3 and 4: Preamble ..........................
Page 5 and 6: outcomes where data exist. Patient-
Page 7 and 8: 1.2. Purpose of These Guidelines Th
Page 9 and 10: and angioscopic studies suggest tha
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Page 15 and 16: ment for the level of care needed b
Page 17 and 18: of use of these medications and the
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Page 27 and 28: When a cardiac troponin is availabl
Page 29 and 30: Troponin elevation has important th
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Page 33 and 34: embolus, dissecting aortic aneurysm
Page 35 and 36: typically done in the same sitting.
Page 37 and 38: CLASS IIa 1. It is reasonable to ad
Page 39 and 40: Table 13. Continued Patient Receive
Page 41 and 42: and even death (303). Similar conce
Page 43: acute setting. Beta blockers withou
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Page 53 and 54: maximal effect in the absence of a
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mounting evidence that statin thera
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c. The initial goal of weight loss
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the time of a cardiovascular event
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cardiac deaths but that it was stil
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(727). These include such caveats a
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similar early and late results as m
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group was similar to that of men (1
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did not significantly reduce in-hos
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define the area of ischemia in post
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from intervention, but given the ab
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CLASS IIb Administration of combine
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nature of periodic angina. The spas
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chest pain that simulates UA second
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Late thrombosis of DES (400,402,403
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APPENDIX 1. Continued Committee Mem
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APPENDIX 1. Continued Committee Mem
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APPENDIX 2. RELATIONSHIPS WITH INDU
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APPENDIX 2. Continued Peer Reviewer
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APPENDIX 2. Continued Peer Reviewer
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APPENDIX 3. Continued Anderson et a
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eases. American Heart Association S
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103. Braunwald E, Antman EM, Beasle
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phy, mitral annular calcium, and ao
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256. Sallach SM, Nowak R, Hudson MP
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337. Hansen JF, Tingsted L, Rasmuss
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damage after elective stent implant
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484. Petersen JL, Mahaffey KW, Hass
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555. Eagle KA, Guyton RA, Davidoff
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630. The Veterans Administration Co
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ADverse outcomes with Early impleme
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the Spanish Multicentre Trial of tr
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868. Togna G, Tempesta E, Togna AR,
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