Search

The visualization of vegetations by M-mode echocardiography in patients with infective endocarditis has been suggested to imply a poor prognosis regarding the development of major systemic emboli, congestive heart failure and the need for early surgical intervention. The question of using the finding of vegetations by echocardiography as an indication for surgery is controversial. To answer this question, 30 patients with the clinical diagnosis of endocarditis were studied by echocardiography. In 17 of the 30 (57 per cent) vegetations were present (aortic eight, mitral four, both mitral and aortic five), whereas in 13 (43 per cent) no vegetations were visualized. Infecting organisms were similar in each group; Streptococcus viridans being the most common. The patients with echocardiographically demonstrable vegetations had a higher incidence of congestive heart failure compared to the patients without (14 of 17 versus six of 13, p

The benefits derived from inhibition of the renin-angiotensin system in chronic heart failure are mediated through multiple mechanisms that can be directly related to the pathophysiology of the syndrome of congestive heart failure. At the stage of myocardial failure, angiotensin-converting enzyme inhibition may reverse myocardial hypertrophy and lower left ventricular filling pressure, and decrease ventricular size, thereby reducing ventricular wall remodeling. At the later stages of congestive heart failure, the cardiac effects of angiotensin-converting enzyme inhibition may have added benefits in the periphery. Normalization of the vasodilatory response to exercise, increase in renal blood flow, and possibly urinary sodium excretion, as well as prevention of hypokalemia tend to improve exercise capacity, quality of life, and survival in patients with severe congestive heart failure.

Six patients with severe congestive heart failure refractory to conventional therapy, including vasodilators, were treated with oral amrinone for a mean duration of 41 weeks (range 20 to 72 weeks). At initiation of therapy, the cardiac index increased from 1.74 +/- 0.31 to 2.62 +/- 0.52 (mean +/- SD) liters/min/m2 (p less than 0.01) and pulmonary capillary wedge pressure decreased from 26.5 +/- 3.5 to 19.5 +/- 5.4 mm Hg (p less than 0.05). Symptoms were alleviated and exercise capacity increased from 5.9 +/- 2.9 to 11.5 +/- 4.5 minutes (p less than 0.05). During long-term therapy, exercise capacity remained constants in three patients whereas it decreased in three others. All patients demonstrated an increase in heart size. Withdrawal of amrinone therapy precipitated severe symptoms at rest and hemodynamic deterioration in all patients. The cardiac index decreased from 1.87 +/- 0.49 to 1.32 +/- 0.30 liter/min/m2 (p less than 0.05) and pulmonary capillary wedge pressure rose from 20.6 +/- 2.9 to 28.8 +/- 5.6 mm Hg (p less than 0.05). These changes were reversed by reinstitution of therapy. Thus, amrinone-dependent hemodynamic benefits were demonstrated during long-term therapy without tachyphylaxis. In addition, progression of the underlying cardiac disease was observed in every patient.

Both vasodilator and inotropic agents improve cardiac function in ischemic heart failure. However, since vasodilators may reduce coronary perfusion pressure and inotropic interventions may increase myocardial oxygen consumption (MVO 2 ), both may increase myocardial ischemia. Accordingly, we determined myocardial blood flow and MVO 2 in a canine model of failure induced by propranolol and volume load combined with acute coronary ligation. Both nitroprusslde and digitalis reduced ventricular diastollc pressure (LVDP) and increased myocardial blood flow in the ischemic subendocardium. Decreased systolic wall tension also caused a significant reduction in MVO 2 . The benefit of nitroprusside in falling hearts was obtained even with the addition of critical obstruction of the main left coronary artery (LCA). The role of preload reduction is emphasized by the contrasting results with nitroprusside in hearts with low LVDP: (1) decreased myocardlal blood flow in ischemic subendocardium, and (2) left ventricular decompensation in animals with critical LCA obstruction. Thus, reduction of LVDP, which decreases subendocardial ischemia, is essential for the beneficial effects of vasodilators and inotropic interventions in ischemic heart failure. Decreased MVO 2 caused by reduced heart size may also have a salutary role.