Does isosorbide-5-mononitrate influence left ventricular relaxation?

In 25 patients, 21 of whom had coronary heart disease, left ventricular high-fidelity pressure measurements, M-mode-echocardiograms, phono- and electrocardiograms were carried out before and 20 min after peroral administration of 50 mg isosorbide-5-mononitrate. Left ventricular relaxation was assessed by the isovolumic relaxation time, left ventricular max negative dP/dt, the time constant, T, of left ventricular pressure decay during the isovolumic relaxation period, and peak fall of meridional wall stress (max negative dS/dt). Following isosorbide-5-mononitrate the heart rate was not altered; left ventricular systolic pressure, however, decreased from 129 to 117 mmHg (P less than 0.001) as did the end-diastolic pressure from 15 to 8 mmHg (P less than 0.001). The left ventricular end-diastolic diameter decreased from 53 to 50 mm (P less than 0.001) and left ventricular peak stress from 182 to 142 X 10(3) dynes/cm2 (P less than 0.001). Max dP/dt and left ventricular systolic shortening remained essentially unchanged, indicating that contractility during the isovolumic-contraction phase as well as during ejection was not influenced. Max negative dP/dt, max negative dS/dt, and the isovolumic relaxation time also remained unchanged. T, however, decreased from 54 to 45 ms (P less than 0.001). We conclude that peroral administration of isosorbide-5-mononitrate is followed by a decrease in pre- and afterload, but also by an increase in the speed of left ventricular relaxation as evidenced by the diminished T. Since T has been reported as being load-independent, its decrease either reflects a genuine effect of isosorbide-5-mononitrate on left ventricular relaxation or results from a diminution of residual ischemia.