[Syncopes: evaluation and management]. / Les syncopes: évaluation et prise en charge.

The optimal management of patients presenting with syncope depends on the aetiology of symptoms. The first step is to differentiate patients without heart disease from others. The clinical history and the examination are the most useful, and in almost half the cases, suggest a presumptive diagnostic. In patients without heart disease, tilt test and autonomic nervous system testing are the investigations with the greatest yield. In patients with heart disease, hemodynamic and electrophysiologic studies are frequently needed. Neurologic investigation are rarely useful and only needed if syncope is associated with focal neurologic manifestations. In some cases implantable ECG loop recorder has proved to be useful. In most of the patients, correlation of symptoms and results of investigations results in appropriate therapeutic strategy.

[Sudden cardiac death]. / La mort subite cardiaque.

Sudden cardiac death describes the unexpected natural death from cardiac cause within a short time period from the onset of symptoms (usually one hour) in a person without any prior condition that would appear fatal. The mechanism is generally a malignant ventricular arrhythmia (ventricular tachycardia or fibrillation). Sudden death is a major public health problem as it accounts for 3 to 400,000 deaths annually in the United States. Risk factors, physiopathological mechanisms, disease states associated with sudden death, and primary and secondary prevention treatments are reviewed.

Hemodynamic effects of SIN-1 in acute left heart failure.

To assess the hemodynamic effects of SIN-1, the active metabolite of the venodilator molsidomine, after acute as well as chronic intravenous administration, ten patients with exacerbation of chronic heart failure were studied. After a mean bolus dose of 2 mg of SIN-1, mean right atrial pressure (MRAP), mean pulmonary artery pressure (MPAP), and pulmonary capillary wedge pressure (PCAP) decreased significantly up to the 60th minute; pulmonary vascular resistance (PVR) decreased significantly up to the 30th minute, while cardiac index (CI) and systemic vascular resistance (SVR) remained unchanged. During a 24-hour continuous infusion of SIN-1, MRAP, MPAP, and PCAP decreased significantly, while CI, PVR, and SVR remained largely unaltered. No dose adjustment was required to maintain the hemodynamic effects over 24 hours. The absence of noteworthy side effects and tolerance during this prolonged administration indicate that SIN-1 is a potentially useful drug in the management of patients admitted with exacerbation of heart failure.

Secondary prevention after myocardial infarction: effects of beta blocking agents and calcium antagonists.

Therapeutic interventions in patients with myocardial infarction, whether during the first hours after coronary occlusion or several days later, aim to reduce mortality and morbidity by several mechanisms: Prevention of fatal ventricular fibrillation, limitation of infarct size, and inhibition of platelet aggregation are some examples of such mechanisms. Results from early intervention trials with beta blocking agents, particularly from ISIS-I, suggest that 1-year mortality is significantly lower in selected patients randomized to active treatment. Late intervention studies also suggest a significant reduction in coronary mortality and morbidity with beta blockade, particularly when data are pooled. Studies with the calcium channel blockers nifedipine and verapamil were unable to demonstrate any beneficial effects of these drugs on mortality or reinfarction. In this review article, attention will be directed to the most recent information about the preventive value of beta adrenergic blocking drugs and slow calcium channel inhibitors.

Exercise-induced angina alleviated by intracoronary SIN-1.

To investigate the mechanism of action of nitrovasodilators in exercise-induced angina, 15 patients with chronic stable angina underwent a symptom-limited supine exercise test (exercise 1). After recovery, in 10 patients (group I) a coronary vasodilator, SIN-1 (the active metabolite of molsidomine) was injected into the most diseased coronary artery (80 micrograms in 4 min). In the remaining 5, a placebo was injected (group II). Immediately thereafter, the same exercise (exercise 2, identical workloads and exercise duration) was repeated. In group I, after intracoronary injection of SIN-1, the control values at rest (including pulmonary wedge pressure) did not significantly change. Heart rate, blood pressure and cardiac index rose in a similar way during exercises 1 and 2 (61, 20, 26 and 62, 21, 35%, respectively). However, 3 patients were angina-free without ST-changes during exercise 2. In the remaining 7, the ST/heart rate slope was reduced (60%; p less than 0.02), the increase in pulmonary wedge pressure was less pronounced (p less than 0.01) and ST-depression at end-exercise 2 was smaller: 1.3 +/- 0.3 versus 2.1 +/- 0.3 mm (p less than 0.01) for identical work loads and double products. In group II, exercise 2 was identical to exercise 1 and the ST/heart rate slopes were quite reproducible. Therefore, these results argue for an improvement in coronary blood supply after intracoronary SIN-1 and suggest that the beneficial action of nitrovasodilators could be related to direct effects on the coronary circulation. However, the magnitude of this mechanism seems variable from one patient to another.