Results of heart transplantation as therapy for end-stage cardiac diseases are encouraging not only because of actuarial survival curves but also because of the recovered quality of life for the heart transplant recipient. Although heart transplantation drastically improves the physical capacity of the patients, heart recipients still have a reduced maximal aerobic capacity compared to healthy people. Altered resting and exercise haemodynamics, due to cardiac denervation, are a common finding after orthotopic heart transplantation: increases in heart rate and stroke volume at exercise are first linked with the augmented venous return and later with the increased plasmatic nor-adrenaline level. Maximal heart rate and stroke volume are both reduced when compared to innervated heart. Reduced cardiac output response to exercise therefore results in early anaerobic metabolism, acidosis, hyperventilation and diminished physical capacity. In spite of an altered ventilatory adaptation to exercise, characterised by hyperpnoea in most transplant patients, ventilation is not the limiting factor for exercise in heart recipients without associated obstructive pulmonary disease. Endurance training restores lean tissue, decreases submaximal minute ventilation, increases peak work output, maximal ventilation and peak heart rate. Guidelines for prescribing exercise are not yet standardised due to the limited number of studies on a sufficient cohort of heart recipients. Nevertheless, recommendations similar to those used for persons with coronary heart disease, with modifications due to the denervated heart, seem to be used. The cardiocirculatory and pulmonary capacity of heart transplant recipients allow them to undertake endurance sports activities such as walking, jogging, cycling and swimming, and these should be encouraged.
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.
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.
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