Acute hemodynamic and neurohumoral effects of pindolol: a beta-adrenoceptor antagonist with high intrinsic sympathomimetic activity in patients with dilated cardiomyopathy.

It has been claimed that beta-adrenoceptor antagonists produce clinical improvement and increase longevity in patients with idiopathic dilated cardiomyopathy. Dilated heart is critically dependent upon adrenergic support to maintain forward output. Acute withdrawal of such support, even with small doses of beta-blockers, may worsen myocardial function sufficiently to limit their widespread use. Pindolol (P), a potent beta-adrenoceptor antagonist, possesses high intrinsic sympathomimetic activity. Administration of P to patients with dilated cardiomyopathy may protect against the effects of high circulating catecholamines and at the same time partially maintain intrinsic left ventricular function. We examined the acute hemodynamic effects of P (2.5 mg orally) in seven patients with dilated cardiomyopathy (average ejection fraction, 23%) and resting tachycardia (average, 111 beats/min). As compared to baseline values, P produced a highly significant fall in heart rate (rest, 19%, p less than 0.001; exercise, 24%, p less than 0.01), cardiac output (rest, 20%, p less than 0.01; exercise, 25%, p less than 0.001), and systemic arterial pressure (exercise only, 13%, p less than 0.05). Calculated systemic vascular resistance increased significantly at rest (17%, p less than 0.05). Pulmonary artery pressures did not change. Compared to normal subjects, baseline norepinephrine levels were markedly elevated in patients with dilated cardiomyopathy at rest and during exercise. Pindolol produced a further significant increase in norepinephrine levels. Two of seven patients became appreciably short of breath after P. Despite its substantial intrinsic sympathomimetic activity, pindolol, like other beta-adrenoreceptor antagonists, produces significant hemodynamic impairment in patients with congestive cardiomyopathy. An exaggerated norepinephrine response after the drug may, by increasing peripheral vascular resistance, lead to further deterioration in left ventricular performance.

Favorable effects of pindolol in dilated cardiomyopathy.

We describe the clinical course of a patient with tachycardia at rest, biopsy proven dilated cardiomyopathy, and moderately severe left ventricular systolic dysfunction. Short-term use of pindolol produced a significant fall in heart rate and cardiac output at rest and during exercise. However, after addition of pindolol to the patient's previous regimen of digoxin and furosemide, he made a rapid clinical recovery and has maintained clinical improvement during the last four years of follow-up. The pattern of clinical response suggests that pindolol may have contributed substantially to this patient's recovery.

Hemodynamic effects of nifedipine in acute myocardial infarction with observations on infarct size.

To assess the safety of the slow calcium-channel blocker nifedipine in patients with acutely evolving myocardial infarction, hemodynamic effects of the drug were studied in 12 patients and infarct size was determined by enzymatic method in 14 patients presenting within 12 h of onset of pain. Nifedipine (3 doses of 20 mg given sublingually at 8-h intervals) produced a significant increase in heart rate and cardiac output accompanied by a fall in systemic arterial pressure and vascular resistance. These effects were sustained for a 24-h period of study. Despite an increase in heart rate and cardiac output, there was no worsening of symptoms or electrocardiographic evidence of myocardial ischemia. Assessment of infarct size did not reveal any differences between the control group and the patients who received nifedipine. We conclude that nifedipine may be safely given to patients with acute myocardial infarction. The drug may be usefully employed in patients with acute myocardial infarction accompanied by angina or hypertension.