Analysis of Left Ventricular Pressure During Isovolumic Relaxation in Coronary Artery Disease

When a decrease in left ventricular isovolumic pressure is considered as an exponential, the rate of relaxation can be defined by a time constant (T). Previously, T has been calculated from the slope of In (pressure) against time, but this method is valid only when the asymptote of the exponential is zero. In this study two estimates of T were made: Tin from the slope of In (pressure) against time, and TEXP by a method of exponential analysis that also estimated the asymptote. These techniques were applied to measurements of left ventricular pressure made at increasing pacing rates in three groups of patients catheterized for chest pain: group 1 (n = 9) - normal coronary arteriograms; group 2 (n = 9) - coronary artery disease (CAD) but no angina or lactate production during pacing; and group 3 (n = 9) - CAD and angina during pacing. Tjn was always shorter than TEXP, and in groups 1 and 2 TEXP was dependent on heart rate, whereas Tin was not. The asymptote was negative, and increased toward zero during pacing in groups 1 and 2. The difference between TEXP and Tin could be related to the value of the asymptote. In 18 of 20 beats tested, pressures calculated from TEXP and the asymptote were in closer agreement with measured pressures than were the pressures predicted by Tin. Despite their different values, TEXP and Tin each distinguished between the three groups. Although the choice of an exponential model is arbitrary, isovolumic pressure decrease approximates to a single expontial; but this study suggests that both T and the asymptote are variable.

[1]  R. Swanton,et al.  Long sheath technique for introduction of catheter tip manometer or endomyocardial bioptome into left or right heart. , 1974, British heart journal.

[2]  J. Weiss,et al.  Time constant of isovolumic pressure fall: determinants in the working left ventricle. , 1978, The American journal of physiology.

[3]  R. O'rourke,et al.  Pharmacologic and hemodynamic influences on the rate of isovolumic left ventricular relaxation in the normal conscious dog. , 1977, The Journal of clinical investigation.

[4]  J. Weiss,et al.  Evidence of incomplete left ventricular relaxation in the dog: prediction from the time constant for isovolumic pressure fall. , 1978, The Journal of clinical investigation.

[5]  M. Webb-Peploe,et al.  Haemodynamic and metabolic effects of atenolol in patients with angina pectoris. , 1980, British heart journal.

[6]  M. Weisfeldt,et al.  Hemodynamic determinants of maximum negative dP-dt and periods of diastole. , 1974, The American journal of physiology.

[7]  D. Gibson,et al.  Echocardiographic assessment of abnormal left ventricular relaxation in man. , 1976, British heart journal.

[8]  E. Sonnenblick,et al.  Maximal rate of pressure fall (peak negative dP-dt) during ventricular relaxation. , 1972, Cardiovascular research.

[9]  W. Grossman,et al.  Impaired left ventricular relaxation during pacing-induced ischemia. , 1973, The American journal of cardiology.

[10]  D G Gibson,et al.  Analysis of left ventricular wall movement during isovolumic relaxation and its relation to coronary artery disease. , 1976, British heart journal.

[11]  J. Weiss,et al.  Hemodynamic determinants of the time-course of fall in canine left ventricular pressure. , 1976, The Journal of clinical investigation.

[12]  H. Levine,et al.  Tension prolongation during recovery from myocardial hypoxia. , 1971, The Journal of clinical investigation.