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ing toxicity or large overdoses, but it should be remembered that its half-life is shorter than that of digoxin and so repeat administration may be required 5 Vasodilators Agents that dilate arteriolar smooth muscle and lower peripheral vascular resistance reduce LV afterload Medications that diminish venous tone and increase venous capacitance reduce the preload of both ventricles as their principal effect Because most patients with moderate to severe heart failure have both elevated preload and reduced cardiac output, the maximum benefit of vasodilator therapy can be achieved by an agent or combination of agents with both actions Many patients with heart failure have mitral or tricuspid regurgitation; agents that reduce resistance to ventricular outflow tend to redirect regurgitant flow in a forward direction Although vasodilators that are also neurohumoral antagonists specifically, the ACE inhibitors improve prognosis, such a benefit is less clear with the direct-acting vasodilators The combination of hydralazine and isosorbide dinitrate has improved survival, but to a lesser extent than ACE inhibitors The A-HeFT trial studied hydralazine (75 mg) and isosorbide dinitrate (40 mg) three times a day in 1050 African Americans with NYHA class III or IV chronic heart failure, most of whom were treated with ACE inhibitors and -blockers The primary endpoint was a clinical composite The trial was stopped early because of a significant 43% reduction in allcause mortality with hydralazine and nitrates, although the relatively small sample size limits the confidence in the results Whether the benefits of this approach are limited to African Americans, who may have a less active renin angiotensin system is not known, but it is appropriate to use this combination in addition to other effective therapies in African Americans with severe heart failure See section on Acute Myocardial Infarction earlier in this chapter for a discussion on the intravenous vasodilating drugs and their dosages a Nitrates Intravenous vasodilators (sodium nitroprusside or nitroglycerin) are used primarily for acute or severely decompensated chronic heart failure, especially when accompanied by hypertension or myocardial ischemia If neither of the latter is present, therapy is best initiated and adjusted based on hemodynamic measurements The starting dosage for nitroglycerin is generally about 10 mcg/min, which is titrated upward by 10 20 mcg/min (to a maximum of 200 mcg/min) until mean arterial pressure drops by 10% Hypotension (BP < 100 mm Hg systolic) should be avoided For sodium nitroprusside, the starting dosage is 03 05 mcg/ kg/min with upward titration to a maximum dose of 10 mcg/ kg/min Isosorbide dinitrate, 20 80 mg orally three times daily, has proved effective in several small studies Nitroglycerin ointment, 125 50 mg (1 4 inches) every 6 8 hours, appears to be equally effective although somewhat inconvenient for longterm therapy The nitrates are moderately effective in relieving shortness of breath, especially in patients with mild to moderate symptoms, but less successful probably because they have little effect on cardiac output in advanced heart failure Nitrate therapy is generally well tolerated, but headaches and hypotension may limit the dose of all agents The develop-.

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intermittent inotropic therapy has never been evaluated in controlled trials, and its use is largely based on anecdotal experience A randomized placebo-controlled trial of 950 patients evaluating intravenous milrinone in patients admitted for decompensated heart failure who had no definite indications for inotropic therapy showed no benefit in terms of survival, decreasing length of admission, or preventing readmission and significantly increased rates of sustained hypotension and atrial fibrillation Thus, the role of positive inotropic agents appears to be limited to patients with symptoms and signs of low cardiac output (primarily hypoperfusion and deteriorating renal function) and those who do not respond to intravenous diuretics In some cases, dobutamine or milrinone may help maintain patients who are awaiting cardiac transplantation 8 Calcium channel blockers First-generation calcium channel blockers may accelerate the progression of CHF However, two trials with amlodipine in patients with severe heart failure showed that this agent was safe, though not superior to placebo These agents should be avoided unless they are being utilized to treat associated angina or hypertension, and for these indications amlodipine is the drug of choice 9 Anticoagulation Patients with LV failure and reduced EFs are at somewhat increased risk for developing intracardiac thrombi and systemic arterial emboli However, this risk appears to be primarily in patients who are in atrial fibrillation or who have large recent anterior myocardial infarction, who should generally be anticoagulated with warfarin for 3 months following the MI Other patients with heart failure have embolic rates of approximately two per 100 patient-years of follow-up, which approximates the rate of major bleeding, and routine anticoagulation does not appear warranted except in patients with prior embolic events or mobile LV thrombi 10 Antiarrhythmic therapy Patients with moderate to severe heart failure have a high incidence of both symptomatic and asymptomatic arrhythmias Although less than 10% of patients have syncope or presyncope resulting from ventricular tachycardia, ambulatory monitoring reveals that up to 70% of patients have asymptomatic episodes of nonsustained ventricular tachycardia These arrhythmias indicate a poor prognosis independent of the severity of LV dysfunction, but many of the deaths are probably not arrhythmia related -Blockers, because of their marked favorable effect on prognosis in general and on the incidence of sudden death specifically, should be initiated in these as well as all other patients with heart failure Empiric antiarrhythmic therapy with amiodarone did not improve outcome in the SCD-HeFT trial, and most other agents are contraindicated because of their proarrhythmic effects in this population and their adverse effect on cardiac function.

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