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started with caution Hypotension is most prominent in patients with already low BPs (systolic pressure < 100 mm Hg), hypovolemia, prerenal azotemia (especially if it is diuretic induced), and hyponatremia (an indicator of activation of the renin angiotensin system) These patients should generally be started at low dosages (captopril 625 mg three times daily, enalapril 25 mg daily, or the equivalent), but other patients may be started at twice these dosages Within several days (for those with the markers of higher risk) or at most 2 weeks, patients should be questioned about symptoms of hypotension, and both renal function and K+ levels should be monitored ACE inhibitors should be titrated to the dosages proved effective in clinical trials (captopril 50 mg three times daily, enalapril 10 mg twice daily, lisinopril 20 mg daily, or the equivalent) over a period of 1 3 months Most patients will tolerate these doses Asymptomatic hypotension is not a contraindication to up-titrating or continuing ACE inhibitors Some patients exhibit increases in serum creatinine or K+, but they do not require discontinuation if the levels stabilize even at values as high as 3 mg/dL and 55 mEq/ L, respectively Renal dysfunction is more frequent in diabetics, older patients, and those with low systolic pressures, and these groups should be monitored more closely The most common side effects of ACE inhibitors in heart failure patients are dizziness (often not related to the level of BP) and cough, though the latter is often due as much to heart failure or intercurrent pulmonary conditions as to the ACE inhibitor b Angiotensin II receptor blockers Another approach to inhibiting the renin angiotensin aldosterone system is the use of specific ARBs (see Table 11 8), which will block or decrease most of the effects of the system In addition, because there are alternative pathways of angiotensin II production in many tissues, the receptor blockers may provide more complete system blockade However, these agents do not share the effects of ACE inhibitors on other potentially important pathways that produce increases in bradykinin, prostaglandins, and nitric oxide in the heart, blood vessels, and other tissues The Valsartan in Heart Failure Trial (Val-HeFT) examined the efficacy of adding valsartan (titrated to a dose of 160 mg twice a day) to ACE inhibitor therapy While valsartan did not reduce mortality, the composite of death or hospitalization for heart failure was significantly reduced The CHARM trial randomized 7601 patients with chronic heart failure with or without LV systolic dysfunction and with or without background ACE inhibitor therapy to candesartan (titrated to 32 mg a day) or placebo Among patients with an LV EF of < 40%, there was an 18% reduction in cardiovascular death or heart failure hospitalization and a statistically significant 12% reduction in all-cause mortality The benefits were similar among patients on ACE inhibitors, including among patients on full-dose ACE inhibitors Thus, ARBs, specifically candesartan or valsartan, provide important benefits as an alternative, and in addition, to ACE inhibitors in chronic heart failure c Spironolactone There is growing evidence that aldosterone may mediate some of the major effects of renin angiotensin aldosterone system activation, such as myocar-.

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NICUS trial, carvedilol was both well tolerated and highly effective in reducing both mortality and heart failure hospitalizations in a group of patients with severe (NYHA class III or IV) symptoms, but care was taken to ensure that they were free of fluid retention at the time of initiation In this study, one death was prevented for every 13 patients treated for 1 year as dramatic an effect as has been seen with a pharmacologic therapy in the history of cardiovascular medicine One trial comparing carvedilol and (short-acting) metoprolol tartrate (COMET) found significant reductions in all-cause mortality and cardiovascular mortality with carvedilol Thus, patients with chronic heart failure should be treated with extended-release metoprolol, bisoprolol, or carvedilol, but not short-acting metoprolol Because even apparently stable patients may deteriorate when -blockers are initiated, initiation must be done gradually and with great care Carvedilol is initiated at a dosage of 3125 mg twice daily and may be increased to 625, 125, and 25 mg twice daily at intervals of approximately 2 weeks The protocols for sustained-release metoprolol use were started at 125 or 25 mg daily and doubled at intervals of 2 weeks to a target dose of 200 mg daily (using the Toprol XL sustained-release preparation) Bisoprolol was administered at a dosage of 125, 25, 375, 5, 75, and 10 mg daily, with increments at 1- to 4-week intervals More gradual up-titration is often more convenient and may be better tolerated Patients should be instructed to monitor their weights at home as an indicator of fluid retention and to report any increase or change in symptoms immediately Before each dose increase, the patient should be seen and examined to ensure that there has not been fluid retention or worsening of symptoms If heart failure worsens, this can usually be managed by increasing diuretic doses and delaying further increases in -blocker doses, though downward adjustments or discontinuation is sometimes required Carvedilol, because of its -blocking activity, may cause dizziness or hypotension This can usually be managed by reducing the doses of other vasodilators and by slowing the pace of dose increases 4 Digitalis glycosides The digitalis glycosides (primarily digoxin) are the only orally active positive inotropic agents currently available They also have electrophysiologic effects that may be beneficial or deleterious in individual patients The primary therapeutic effect is an enhancement of cardiac parasympathetic tone, which delays AV conduction and reduces sinus node automaticity, thereby decreasing the ventricular response in patients with atrial fibrillation and slightly slowing the rate of patients in sinus rhythm However, digoxin may increase the excitability of ventricular myocytes and induce ventricular arrhythmias, especially when hypokalemia or myocardial ischemia is present Although the digitalis glycosides were once the mainstay of treatment of CHF, their use in patients who are in sinus rhythm has declined because they lack the benefits of the neurohormonal antagonists on prognosis and because safety concerns persist However, their efficacy in reducing the symptoms of heart failure has been established in at.

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