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Assesses the natural history of isolated left ventricular diastolic dysfunction. Patients and methods; Results; Cardiac catheterizations; Comment.

The so-called calcium antagonists-verapamil, nifedipine, diltiazem, and perhexiline-are pharmacologic agents that will have a dramatic impact on the medical therapy of individuals with ischemic heart disease. They have been used extensively in Europe and Japan for over 15 years, and more recent studies from this country have demonstrated their efficacy in the treatment of patients with Prinzmetals "variant" angina pectoris, stable (exertional) angina pectoris, and unstable angina pectoris. In addition, they appear effective in protecting ischemic myocardium both in patients with acute myocardial infarction as well as in those undergoing cardiopulmonary bypass. The purpose of this review is twofold: (a) to describe the mechanism of action and pharmacology of these agents and (b) to delineate their role in the treatment of individuals with ischemic heart disease. [ABSTRACT FROM AUTHOR]

Objective: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites.Design: Randomized, double-blind, controlled clinical trial.Setting: Cardiac catheterization laboratory of a large teaching hospital.Patients: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain.Measurements: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine.Results: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 +/- 1.6 mm (mean +/- SD) at baseline to 2.0 +/- 1.4 mm at 30 minutes (P less than 0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 +/- 1.6 mm) (P greater than 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 +/- 1.4 mm, P less than 0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group.Conclusion: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites. [ABSTRACT FROM AUTHOR]

Study Objective: To determine whether beta-adrenergic blockade augments cocaine-induced coronary artery vasoconstriction.Design: Randomized, double-blind, placebo-controlled trial.Setting: A cardiac catheterization laboratory in an urban teaching hospital.Patients: Thirty clinically stable patient volunteers referred for catheterization for evaluation of chest pain.Interventions: Heart rate, arterial pressure, coronary sinus blood flow (by thermodilution), and epicardial left coronary arterial dimensions were measured before and 15 minutes after intranasal saline or cocaine administration (2 mg/kg body weight) and again after intracoronary propranolol administration (2 mg in 5 minutes).Measurements and Main Results: No variables changed after saline administration. After cocaine administration, arterial pressure and rate-pressure product increased; coronary sinus blood flow fell (139 +/- 28 [mean +/- SE] to 120 +/- 20 mL/min); coronary vascular resistance (mean arterial pressure divided by coronary sinus blood flow) rose (0.87 +/- 0.10 to 1.05 +/- 0.10 mm Hg/mL.min); and coronary arterial diameters decreased by between 6% and 9% (P less than 0.05 for all variables). Subsequently, intracoronary propranolol administration caused no change in arterial pressure or rate-pressure product but further decreased coronary sinus blood flow (to 100 +/- 14 mL/min) and increased coronary vascular resistance (to 1.20 +/- 0.12 mm Hg/mL.min) (P less than 0.05 for both).Conclusions: Cocaine-induced coronary vasoconstriction is potentiated by beta-adrenergic blockade. Beta-adrenergic blocking agents probably should be avoided in patients with cocaine-associated myocardial ischemia or infarction. [ABSTRACT FROM AUTHOR]

Evaluates the potential value of nifedipine treatment for primary pulmonary hypertension, hemodynamic and scintigraphic measurements. Information on primary pulmonary hypertension; Potent systemic vasodilator agents that have been reported to reduce pulmonary vascular resistance in some patients with pulmonary hypertension; Other beneficial effects of nifedipine therapy; Clinical features of patients with primary pulmonary hypertension.

Presents a randomized and double-blind study to assess the effectiveness and safety of oral verapamil in patients with frequent episodes of paroxysmal supraventricular tachycardia. Materials and methods; Results; Discussion.

The goals of this investigation were: 1) to examine the pattern of evolution of epicardial R wave voltage during the 24 h after experimental coronary artery occlusion; and 2) to determine whether hyaluronidase, an agent shown previously to reduce myocardial ischaemic injury, alters this evolution. Coronary artery occlusion was performed in 36 dogs. In the control dogs, the average R wave voltage (R) recorded over the ischaemic myocardium increased by 7.6 ± 0.8 mV (P <0.001) from before to 15 min after coronary artery occlusion, then gradually returned to baseline over the ensuing 4 h. Subsequently, R wave voltage continued to fall, and 24 h after occlusion, R was 17.8 ± 1.8 mV (P <0.001) less than before occlusion. In the hyaluronidase-treated dogs (500 NF units·kg−1), R recorded over the ischaemic myocardium increased similarly to the controls before hyaluronidase administration. However, in contrast to the control dogs, the administration of hyaluronidase 20 min after occlusion caused R to return to baseline over the ensuing 40 min and 24 h after occlusion, the treated animals lost significantly less R wave voltage than the controls (P <0.001). [ABSTRACT FROM PUBLISHER]

In order to measure the protective effect of interventions following coronary artery occlusions in dogs, the creatine kinase activity of myocardial tissue was assayed after 24 h and related to the myocardial blood flow of that tissue measured with 85Sr labelled microspheres injected 15 min after occlusion. This assay showed normal levels when flow exceeded 50 cm3·min−1·100 g−1. In myocardium with flow reduced to 0 to 15 cm3·min−1·100 g−1, creatine kinase activity was 7.6 ± 0.6 IU·mg−1 protein in control dogs and 13.1 ± 1.8 IU·mg−1 protein (P<0.01) in dogs given 500 NF units·kg−1 of hyaluronidase 20 min after occlusion. Where myocardial blood flow was reduced to 16 to 50cm3·min−1·100 g−1, creatine kinase activity was increased from 14.1 ± 1.1 to 20.5 ± 1.4 IU·mg−1 protein by hyaluronidase. This method therefore assesses ischaemic damage independent of electrophysiological measurements and confirms myocardial preservation by hyaluronidase. [ABSTRACT FROM PUBLISHER]

For this article, the literature on the pathophysiology, clinical features, natural history, prognosis, and management of the Eisenmenger syndrome in adults was reviewed. English-language articles from 1966 to the present were identified through a search of the MEDLINE database by using the terms Eisenmenger, congenital heart disease, and pulmonary hypertension. Selected cross-referenced articles were also included. Articles on the pathophysiology, clinical presentation, evaluation, natural history, complications, and treatment of the Eisenmenger syndrome in adults were selected, and descriptive and analytical data relevant to the practicing physician were manually extracted. The Eisenmenger syndrome is characterized by elevated pulmonary vascular resistance and right-to-left shunting of blood through a systemic-to-pulmonary circulation connection. Most patients with the syndrome survive for 20 to 30 years. The hemostatic changes associated with the syndrome may lead to thromboembolic events, cerebrovascular complications, or the hyperviscosity syndrome. Erythrocytosis is present in most patients, but excessive phlebotomy may cause microcytosis and exacerbate the symptoms of hyperviscosity. Other complications associated with the Eisenmenger syndrome include hemoptysis, gout, cholelithiasis, hypertrophic osteoarthropathy, and decreased renal function. Pregnancy or noncardiac surgery is associated with a high mortality rate in patients with the Eisenmenger syndrome. Because most pediatric patients with the Eisenmenger syndrome survive to adulthood, primary care physicians should have a thorough understanding of the syndrome; its associated complications; and medical and surgical management, especially with regard to the appropriate timing of phlebotomy and lung or heart-lung transplantation. In addition, patients with the syndrome should undergo routine follow-up at a tertiary care center that has physicians and nurses with special expertise in congenital heart disease. In patients with the Eisenmenger syndrome who are pregnant or require noncardiac surgery, a multidisciplinary approach should be used to reduce the excessive mortality associated with these conditions. [ABSTRACT FROM AUTHOR]

Assesses the incidence of coronary artery disease in a large number of subjects with isolated aortic stenosis who did not have angina pectoris. Sensitivity of angina pectoris in identifying coronary artery disease; Evidence of hyperlipidemia in patients with angina pectoris; Importance of coronary angiography in preparation of valve replacement.

The article reports on the medical condition atrial septal defect (ASD). Many people with ASD are asymptomatic for several years but inevitably experience symptoms including fatigue or exertional dyspnoea. In order to avoid conditions including stroke, atrial tachyarrhythmias, and right ventricular dysfunction, individuals with ASD are encouraged to undergo closure. Transcatheter closure may be used as an alternative treatment in patients without ostium Drimum or sinus venosus defects. Surgical closures performed in patients under 25 years of age result in more favorable long-term outcomes.

We report the case of a 29-year-old man who developed acute congestive heart failure secondary to cardiac Chagas'' disease in the setting of Trypanosoma cruzi reactivation by acquired immune deficiency syndrome. [Copyright &y& Elsevier]

Describes patients with severe left ventricular dysfunction in association with chronic abuse of the amphetamine analog, propylhexedrine. Case reports; Background on propylhexedrine; Mechanism of these myocardial changes.

Presents a study of the cardiovascular complications of cocaine use. Pharmacology and mechanisms of action; Cocaine-related myocardial ischemia and infarction; Cocaine, cigarette-smoking and alcohol use; Cocaine-induced myocardial dysfunction and dysrythmias; Endocarditis; Aortic dissection; Conclusion that as a result of the increased use of cocaine, related visits to emergency departments, hospitalizations, cardiovascular complications, and deaths has risen dramatically.

Presents the results of a study on congenital heart disease in adults. Two of the most common causes being tetralogy of Fallot and Eisenmenger's syndrome; Definition of both; Rate of survival among patients with Eisenmenger's syndrome; Long term prognosis of infants diagnosed with tetraology of Fallot with surgical intervention.