13. Thompson PD, Buchner D, Pina IL, Balady GJ, Williams MA, Marcus BH, Berra K, Blair SN, Costa F, Franklin B, Fletcher GF, Gordon NF, Pate RR, Rodriguez BL, Yancey AK, Wenger NK; American Heart Association Council on Clinical Cardiology Subcommittee on Exercise, Rehabilitation, and Prevention; American Heart Association Council on Nutrition, Physical Activity, and Metabolism Subcommittee on Physical Activity. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Pre- vention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity). Circulation. 2003;107:3109 –3116. 14. UK Department of Health. At Least Five a Week: Evidence on the Impact of Physical Activity and Its Relationship to Health: A Report From the Chief Medical Officer. London, England: Wellington House; April 29, 2004. Available at: http://www.dh.gov.uk/assetRoot/04/08/09/81/ 04080981.pdf. Accessed March 15, 2006.
Many patients with organic heart disease can be broadly categorized into those with HF, CAD, or hypertension, although other types of heart disease can also be associated with AF. For patients with HF, safety data support the selection of amiodarone or dofetilide to maintain sinus rhythm. Patients with ischemic heart disease often require beta-blocker medication. Then so- talol, a drug with both beta-blocking activity and primary antiarrhythmic efficacy, is considered first unless the patient has HF. Amiodarone and dofetilide are considered secondary agents in this situation. The clinician may consider disopyramide, procainamide, or quinidine on an individual basis. In patients with hypertension without LVH, drugs such as flecainide and propafenone, which do not prolong repolarization and the QT interval, might offer a safety advantage and are recommended first. If these agents either prove ineffective or produce side effects, then amiodarone, dofetilide, and sotalol represent appro- priate secondary choices. Disopyramide, procainamide, and quinidine are considered third-line agents in this situation. Hypertrophied myocardium is prone to proarrhythmic toxicity and development of the torsade de pointes type of ventricular tachycardia. Amiodarone is suggested as first-line therapy in patients with LVH (wall thickness greater than or equal to Figure 9. Pharmacological management of patients with newly discovered AF. AF indicates atrial fibrillation; HF, heart failure.
Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (www.americanheart.org), and the Society for Cardiovascular Angiography and Interventions (www.scai.org). Single copies of this document are available by calling 1-800-253-4636 or writing the American College of Cardiology Foundation, Resource Center, at 9111 Old Georgetown Road, Bethesda, MD 20814-1699. Ask for reprint number 71-0346. To obtain a copy of the full text published in the January 3, 2006, issue of the Journal of the American College of Cardiology, the January 3, 2006, issue of Circulation, and the January 2006, issue of Catheterization and Cardiovascular Interventions, ask for reprint number 71-0347. To purchase bulk reprints (specify version and reprint number): Up to 999 copies, call 1-800-611-6083 US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1789, fax 214-691-6342, or e-mail email@example.com.
CAD on the basis of a history and/or electrocardiographic (ECG) evidence of previous MI, coronary angiography, or an abnormal noninvasive test. The inclusion of asymptomatic patients with abnormal noninvasive tests does not constitute an endorsement of such tests for the purposes of screening but simply acknowledges the clinical reality that such patients often present for evaluation after such tests have been performed. Multiple ACC/AHAguidelines and scientific statements have discouraged the use of ambulatory monitor- ing, treadmill testing, stress echocardiography, stress myocar- dial perfusion imaging, and electron-beam computed tomog- raphy (EBCT) as routine screening tests in asymptomatic individuals.
Healthcare providers should lower both systolic and dias- tolic blood pressure in accordance with the recommendations provided in published guidelines, including the most recent- ly published report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (61); target levels of blood pressure are lower in patients with associated major cardiovascular risk factors, especially those with diabetes mellitus (62, 63). When an antihypertensive regimen is devised, optimal control of blood pressure should remain as the primary goal, with the choice of drugs determined by the concomitant medical problems (e.g., coronary artery disease, diabetes, or renal disease). Diuretic-based antihypertensive therapy has repeat- edly been shown to prevent HF in a wide range of target pop- ulations (64). ACE inhibitors (ACEIs) and beta-blockers are also effective in the prevention of HF (61), whereas calcium antagonists and alpha-blockers are less effective in prevent- ing HF syndrome (65). However, ACEIs and beta-blockers, as single therapies, are not superior to other antihypertensive drug classes in the reduction of all cardiovascular outcomes. Nevertheless, among patients with diabetes or other cardio- vascular complications (66, 67), ACEIs have been most notable with respect to a reduction in the onset of HF and new-onset diabetes. Likewise, compared with placebo, the ARBs losartan (68) and irbesartan (69) significantly reduced the incidence of HF in patients with type 2 diabetes mellitus and nephropathy. Ultimately, an appropriate antihypertensive regimen frequently consists of several drugs used in combi- nation. Although prevention of HF is the focus of these guidelines, overall cardiovascular preventative strategies have also been the subject of published guidelines (70). 184.108.40.206. Treatment of Diabetes
sented to the initial receiving hospital or within 60 minutes com- pared to when fibrinolysis with a fibrin-specific agent could be initiated at the initial receiving hospital); or (3) fibrinolysis is administered and is unsuccessful (ie, “rescue PCI”). Secondary nonemergency interhospital transfer can be considered for recurrent ischemia. Patient self-transport: Patient self- transportation is discouraged. If the patient arrives at a non– PCI-capable hospital, the door-to-needle time should be within 30 minutes. If the patient arrives at a PCI-capable hospital, the door-to-balloon time should be within 90 minutes. The treatment options and time recommendations after first hospital arrival are the same. Panel B, For patients who receive fibrinolysis, nonin- vasive risk stratification is recommended to identify the need for rescue PCI (failed fibrinolysis) or ischemia-driven PCI. See Sec- tions 220.127.116.11.4.5. and 18.104.22.168.7. in the full-text guidelines. Regardless of the initial method of reperfusion treatment, all patients should receive late hospital care and secondary pre- vention of STEMI. EMS indicates Emergency Medical System; PCI, percutaneous coronary intervention; CABG, coronary artery bypass graft surgery; Hosp, hospital; Noninv., Noninvasive. * Golden hour ⫽ First 60 minutes;† The medical system goal is to facilitate rapid recognition and treatment of patients with STEMI such that door-to-needle (or medical contact–to-needle) time for initiation of fibrinolytic therapy is within 30 minutes or that door- to-balloon (or medical contact–to-balloon) time for PCI is within 90 minutes. These goals should not be understood as ideal times but rather as the longest times that should be considered acceptable for a given system. Systems that are able to achieve even more rapid times for treatment of patients with STEMI should be encouraged. Modified with permission from Armstrong et al. Circulation. 2003;107:2533–7. 25
20% by 1 year. The initial cost and length of stay were lower for angioplasty than for CABG. Patients having angioplasty returned to work sooner and were able to exercise more at 1 month. The extent of revascularization achieved by bypass surgery was generally higher than with angioplasty. Long- term survival was difficult to evaluate owing to the short period of follow-up and the small sample size of the trials. However, for the Bypass Angioplasty Revascularization In- vestigation (BARI) trial, bypass patients had a 5-year survival of 89.3% compared with 86.3% for angioplasty. Secondary analysis revealed that in treated diabetic patients in the BARI trials, CABG led to significantly superior survival compared with percutaneous transluminal coronary angioplasty (PTCA). However, this finding was not evident in other trials. In long-term follow-up, the most striking difference was the 4- to 10-fold-higher likelihood of reintervention after initial PTCA. Quality of life, physical activity, employment, and cost were similar by 3 to 5 years after both procedures. The BARI trial suggested higher mortality associated with PTCA in several high-risk groups, including those with diabetes, unstable angina, and/or non–Q wave MI, and in patients with heart failure.
If LDL-C is above goal range, initiate additional therapeutic lifestyle changes consisting of dietary modifications to lower LDL-C: ⬍ 7% of calories from saturated fat, cholesterol ⬍ 200 mg/d, and, if further LDL-C lowering is required, dietary options (plant stanols/sterols not to exceed 2 g/d and/or increased viscous [soluble] fiber [10–25 g/d]), and additional emphasis on weight reduction and physical activity. If LDL-C is above goal range, rule out secondary causes (liver function test, thyroid-stimulating hormone level, urinalysis). After 12 weeks of therapeutic lifestyle change, consider LDL-lowering drug therapy if: ⱖ 2 risk factors are present, 10-y risk is ⬎ 10%, and LDL-C is ⱖ 130 mg/dL; ⱖ 2 risk factors are present, 10-y risk is ⬍ 10%, and LDL-C is ⱖ 160 mg/dL; or ⱕ 1 risk factor is present and LDL-C is ⱖ 190 mg/dL. Start drugs and advance dose to bring LDL-C to goal range, usually a statin but also consider bile acid–binding resin or niacin. If LDL-C goal not achieved, consider combination therapy (statin ⫹ resin, statin ⫹ niacin). After LDL-C goal has been reached, consider triglyceride level: If 150–199 mg/dL, treat with therapeutic lifestyle changes. If 200–499 mg/dL, treat elevated non-HDL-C with therapeutic lifestyle changes and, if necessary, consider higher doses of statin or adding niacin or fibrate. If ⬎ 500 mg/dL, treat with fibrate or niacin to reduce risk of pancreatitis. If HDL-C is ⬍ 40 mg/dL in men and ⬍ 50 mg/dL in women, initiate or intensify therapeutic lifestyle changes. For higher-risk patients, consider drugs that raise HDL-C (eg, niacin, fibrates, statins).
22.214.171.124. Distinguishing short-term and long-term treatment goals. The initial and subsequent management of sympto- matic AF may differ from one patient to another. For patients with symptomatic AF lasting many weeks, initial therapy may be anticoagulation and rate control, while the long-term goal is to restore sinus rhythm. When cardio- version is contemplated and the duration of AF is unknown or exceeds 48 h, patients who do not require long-term anticoagulation may beneﬁt from short-term anticoagula- tion. If rate control offers inadequate symptomatic relief, restoration of sinus rhythm becomes a clear long-term goal. Early cardioversion may be necessary if AF causes hypotension or worsening HF, making the establishment of sinus rhythm a combined short- and long-term therapeutic goal. In contrast, amelioration of symptoms by rate control in older patients may steer the clinician away from attempts to restore sinus rhythm. In some circumstances, when the initiating pathophysiology of AF is reversible, as for instance in the setting of thyrotoxicosis or after cardiac surgery, no long-term therapy may be necessary. 126.96.36.199. Clinical trials comparing rate control and rhythm control. Randomized trials comparing outcomes of rhythm- versus rate-control strategies in patients with AF are summarized in Tables 7 and 8. Among these, AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) found no difference in mortality or stroke rate between patients assigned to one strategy or the other. The RACE (Rate Control vs. Electrical cardioversion for persistent atrial ﬁbrillation) trial found rate control not inferior to rhythm control for prevention of death and morbidity. Clinically silent recurrences of AF in asymptomatic patients treated with antiarrhythmic drugs may be responsible for thromboembolic events after withdrawal of anticoagulation. Hence, patients at high risk for stroke may require anticoagulation regardless of whether the rate-control or rhythm-control strategy is chosen, but the AFFIRM trial was not designed to address this question. While secondary analyses support this
These guidelines are based on an update of a Medline, EMBASE, Cochrane library, and Best Evidence search of the English literature from 1995 through 2000, a review of selected journals, and the expert opinions of 12 committee members representing various disciplines of cardiovascular care, including general cardiology, interventional cardiology, noninvasive testing, vascular medicine, vascular surgery, anesthesiology, and arrhythmia management. As a result of these searches, more than 400 relevant new articles were identified. In addition, draft guidelines were submitted for critical review and amendment to the executive officers representing the American College of Cardiology (ACC) and the American Heart Association (AHA).
less than 0.0001). The incidence of stroke and major bleeding was also increased in the elderly at 1 year. Abciximab administration did not confer a benefit in elderly patients but was deemed safe. In contrast, routine stent implantation in elderly patients reduced 1-year rates of ischemic target-vessel revasculariza- tion (7.0% vs 17.6%, P less than 0.0001) and subacute or late thrombosis (0% vs 2.2%, P equals 0.005) compared with bal- loon angioplasty. The authors acknowledged that additional risks/benefits of stent or IIb/IIIa inhibitor use in elderly patients with STEMI might have become evident had more patients been enrolled in this study (223). Thus, with rare exception (primary PCI for cardiogenic shock in patients greater than 75 years of age), a separate category has not been created in these guidelines for the elderly (224). However, their higher incidence of comorbidities and risk for bleeding complications should be taken into account when considering the need for PCI (218,225).
Thus, clopidogrel (in addition to aspirin and heparin or low molecular weight heparin) is recommended for patients with UA/NSTEMI in whom a noninterventional approach is planned (Class I recommendation). In patients in whom an interventional approach is planned, a GP IIb/IIIa inhibitor (in addition to aspirin and heparin or low molecular weight heparin) is recommended (Class I recommendation). No head-to-head comparison of clopidogrel, a GP IIb/IIIa inhib- itor, and their combination has been reported. The addition of a GP IIb/IIIa inhibitor to a subset of patients in the CURE trial who were receiving aspirin, clopidogrel, and heparin ap- peared to be well tolerated, and current practice frequently involves the use of this combination of drugs. However, until further information on the safety and efficacy of such quadruple therapy becomes available, a Class IIa recommen- dation is made for the addition of a GP IIb/IIIa inhibitor for patients with UA/NSTEMI who are receiving aspirin, clopi- dogrel, and unfractionated or low molecular weight heparin and who are referred for an invasive strategy. A Class I recommendation is made for a GP IIb/IIIa inhibitor at the time of PCI in patients receiving heparin and aspirin. Specific updated recommendations for the use of antiplatelet regimens in the revised guidelines are as follows:
Long-term benefits of oral flecainide in AVNRT were initially shown in an open-labeled study. At doses be- tween 200 and 300 mg/d, flecainide completely sup- pressed episodes in 65% of patients. Several double- blinded, placebo-controlled trials have confirmed the efficacy of flecainide for prevention of recurrences. Events are reduced when compared with placebo, with an increase in the median time to the first recurrence and a greater interval between attacks. Open-labeled, long-term studies suggest excellent chronic tolerance and safety. In patients without structural heart disease, 7.6% discontin- ued the drug due to a suboptimal clinical response, and 5% discontinued it because of noncardiac (usually central nervous system) side effects. Class Ic agents (ie, flecain- ide and propafenone) are contraindicated for patients with structural heart disease. Moreover, class Ic drugs are often combined with beta-blocking agents to enhance efficacy and reduce the risk of one-to-one conduction over the AV node if atrial flutter occurs.
5.2.8. Prevention of Aortic Aneurysm Rupture Aside from their infrequent other complications (e.g., periph- eral or visceral embolism, aortocaval or primary aortoenteric fistula), the single most compelling reason to repair AAAs is to prevent fatal rupture. The first step in this process is to identify the presence of these aneurysms, beginning with a thorough physical examination or their recognition as an incidental finding on unrelated abdominal imaging studies. This is especially important in certain high-prevalence popu- lations, such as those with known popliteal aneurysms or a family history of aortic aneurysms. The next step is to estab- lish, on the basis of ultrasonography or computed tomogra- phy/magnetic resonance scanning, whether a particular aor- tic aneurysm already is large enough to warrant intervention or instead should be placed under periodic surveillance to determine its rate of expansion. Brown et al. have shown in a prospective but nonrandomized study that observation alone is a safe approach until an aneurysm undergoes a growth spurt or attains a threshold diameter of 5.0 cm (952). The success of watchful waiting is predicated on patient cooperation, however. In a similar study of 101 patients with aneurysms measuring less than 5.0 cm in diameter, Valentine et al. encountered no ruptures among patients who complied with their follow-up program compared with a 10% rupture rate among those who did not (1217). If continued surveil- lance is recommended, measures should be taken to control hypertension and to discourage smoking, because these risk factors are associated with accelerated rates of aneurysm growth (936,961). Ultimately, once an infrarenal aortic aneurysm reaches an appropriate size for graft replacement, a choice must be made between a traditional open operation or endovascular repair. Like all other aspects of aneurysm management, this decision requires a balanced judgment of relative risks.
Figure 2. Acute coronary syndromes. The top half of the figure illustrates the chronology of the interface between the patient and the clinician through the pro- gression of plaque formation, onset and complications of STEMI along with relevant management considerations at each stage. The longitudinal section of an artery depicts the "timeline" of atherogenesis from a normal artery (1) to (2) lesion initiation and accumulation of extracellular lipid in the intima, to (3) the evolu- tion to the fibrofatty stage, to (4) lesion progression with procoagulant expression and weakening of the fibrous cap. An acute coronary syndrome develops when the vulnerable or high risk plaque undergoes disruption of the fibrous cap (5); disruption of the plaque is the stimulus for thrombogenesis. Thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth (6). Following disruption of a vulnerable or high-risk plaque, patients experience ischemic discomfort resulting from a reduction of flow through the affected epicardial coronary artery. The flow reduction may be caused by a completely occlu- sive thrombus (bottom half, right side) or subtotally occlusive thrombus (bottom half, left side). Patients with ischemic discomfort may present with or without ST- segment elevation on the ECG. Of patients with ST-segment elevation, most (large red arrow in bottom panel) ultimately develop a Q-wave MI (QwMI), while a few (small red arrow) develop a non–Q-wave MI (NQMI). Patients who present without ST-segment elevation are suffering from either unstable angina or a non–ST- segment elevation MI (NSTEMI) (large open arrows), a distinction that is ultimately made on the presence or absence of a serum cardiac marker such as CK-MB or a cardiac troponin detected in the blood. Most patients presenting with NSTEMI ultimately develop a NQMI on the ECG; a few may develop a QwMI. The spec- trum of clinical presentations ranging from unstable angina through NSTEMI and STEMI are referred to as the acute coronary syndromes. This STEMI guideline is arranged along the chronologic interface of the clinician with the patient, as diagrammed in the upper panel, and includes sections on management prior to STEMI, at the onset of STEMI, and during the hospital phase. Secondaryprevention and plans for long-term management begin early during the hospital phase of treatment. Dx = diagnosis; NQMI, non–Q-wave myocardial infarction; QwMI = Q-wave myocardial infarction; CK-MB = MB isoenzyme of creatine kinase . Modified with permission from Libby. Circulation 2001;104:365-72 (8), Hamm, Bertrand, Braunwald. The Lancet 2001;358:1533-8 (9), and Davies. Heart 2000;83:361-6 (10) with permission from the BMJ Publishing Group.
The guidelines, incorporating the update, are available on the Web sites of both the American College of Cardiology (www.acc.org) and the American Heart Association (www.americanheart.org). In the Web site version, deleted text is indicated by strikeout, and new/revised text is present- ed as double-underlined type. Reprints of the original docu- ment with the revised sections appended are available from both organizations (see information below).
after the publication of the primary reference(s). Thus, the development of the present statement involved a process of partial adaptation of other guideline statements and reports and supplemental literature searches (2–32). (For specific search criteria, see the Appendix.) The findings from addi- tional lipid reduction trials (33–37) involving more than 50 000 patients resulted in new optional therapeutic targets, which were outlined in the 2004 update of the National Heart, Lung, and Blood Institute’s Adult Treatment Panel (ATP) III report (6). These changes defined optional lower target cholesterol levels for very high-risk coronary heart disease (CHD) patients, especially those with acute coronary syn- dromes, and expanded indications for drug treatment. Subse- quent to the 2004 update of ATP III, 2 additional trials (8,9) demonstrated cardiovascular benefit for lipid lowering signif- icantly below current cholesterol goal levels for those with chronic CHD. These new trials allow for alterations in guidelines, such that low-density lipoprotein cholesterol (LDL-C) should be ⬍ 100 mg/dL for all patients with CHD and other clinical forms of atherosclerotic disease, but in addition, it is reasonable to treat to LDL-C ⬍ 70 mg/dL in
In developing this revision of the guidelines, the Writing Committee considered evidence published since 2001 and drafted revised recommendations where appropriate to incor- porate results from major clinical trials such as those that compared rhythm-control and rate-control approaches to long-term management. The text has been reorganized to reflect the implications for patient care, beginning with recognition of AF and its pathogenesis and the general priorities of rate control, prevention of thromboembolism, and methods available for use in selected patients to correct the arrhythmia and maintain normal sinus rhythm. Advances in catheter-based ablation technologies have been incorpo- rated into expanded sections and recommendations, with the recognition that that such vital details as patient selection, optimum catheter positioning, absolute rates of treatment success, and the frequency of complications remain incom- pletely defined. Sections on drug therapy have been con- densed and confined to human studies with compounds that have been approved for clinical use in North America and/or Europe. Accumulating evidence from clinical studies on the emerging role of angiotensin inhibition to reduce the occur- rence and complications of AF and information on ap- proaches to the primary prevention of AF are addressed comprehensively in the text, as these may evolve further in the years ahead to form the basis for recommendations affecting patient care. Finally, data on specific aspects of management of patients who are prone to develop AF in special circumstances have become more robust, allowing formulation of recommendations based on a higher level of evidence than in the first edition of these guidelines. An example is the completion of a relatively large randomized trial addressing prophylactic administration of antiarrhythmic medication for patients undergoing cardiac surgery. In devel- oping the updated recommendations, every effort was made to maintain consistency with other ACC/AHA and ESC practice guidelines addressing, for example, the management of patients undergoing myocardial revascularization procedures.
The 5-y mortality for DCM has been recently estimated at 20% with SCD accounting for approximately 30% (8% to 51%) of deaths (614,615). Ventricular arrhythmias, both symptomatic and asymptomatic, are common, but syncope and SCD are infrequent initial manifestations of the disease (616,617). The incidence of SCD is highest in patients with indicators of more advanced cardiac disease who are also at highest risk of all cause mortality. Although VT and/or VF is considered the most common mechanism of SCD, bradycardia, pulmonary embolus, electromechanical disso- ciation and other causes account for up to 50% of SCDs in patients with advanced HF (107,618,619). Risk stratifica- tion is difficult in DCM. SCD occurs less frequently in patients with less advanced cardiac disease but the propor- tion of SCD to all-cause death is higher in this group (617,618,620). Predictors of overall outcome also predict SCD and generally reflect severity of disease (EF, end- diastolic volume, older age, hyponatremia, pulmonary cap- illary wedge pressure, systemic hypotension, AF) (614). Unfortunately, they do not specifically predict arrhythmic death and are not useful in the patient with less severe disease (3,621). Even a low EF (less than 20%) may not have high positive predictive value for SCD (622– 624). Syncope has been associated with a higher risk of SCD regardless of the proven etiology of the syncope (223,625) and patients with ICD implantation receive appropriate shocks comparable to a secondaryprevention cohort (223,625,626). Premature ventricular complexes and NSVT correlate with the severity of cardiac disease and occur in the majority of patients with severe LV dysfunction (619,627,628). This limits the utility of ventricular arrhyth-