Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man

Abstract

It has been shown in man that myocardial ischemia, whether precipitated by exercise or pacinginduced tachycardia, is associated with abnormalities of left ventricular end-diastolic pressure. There has been controversy as to whether this relationship is due to decreased myocardial compliance or to an increase in left ventricular volume as a manifestation of left ventricular failure. Simultaneous measurements of left ventricular pressure and left ventricular volume using ultrasonic techniques were carried out in five normal subjects and 21 patients with coronary artery disease. In the normal subjects a decrease in left ventricular end-diastolic pressure during pacing was associated with a decrease in left ventricular end-diastolic volume, and during interruption of pacing, pressures and volumes returned to normal. In nine patients with coronary artery disease who did not develop angina, a similar response was seen. In 12 patients with coronary artery disease who developed angina during pacing, the reduction in left ventricular end-diastolic volume during pacing was less marked than the other groups and during periods of interruption the increase in diastolic pressure to 26 mm Hg was accompanied by an increase in left ventricular end-diastolic volume to 24% above control values. The end-systolic volume showed a similar increase during myocardial ischemia.These data suggest that the changes in left ventricular filling pressure seen during myocardial ischemia are related to increase in left ventricular volume but do not exclude the possibility that there may be accompanying changes in left ventricular diastolic compliance.Additional Indexing Words: Left ventricular volume Left ventricular compliance T HE HEMODYNAMIC changes during myocardial ischemia have been examined intensively, and there is now general agreement as to the abnormalities that occur.1-9 Opinions differ however as to the pathophysiologic mechanisms involved. Some investigators interpret the elevation of left ventricular filling pressure seen during myocardial ischemia as evidence of a transient decrease in left ventricular compliance5 6, 10 while others consider that reversible left ventricular failure occurs with an associated increase in left ventricular volume.3 4 Only limited information is available in man concerning changes in left ventricular volume and compliance during myocardial ischemia.11-13 Until

Evidence for Cardiomyopathy in Familial Diabetes Mellitus

“…Whether the reduction of end-diastolic and stroke volume in Group A-1 patients is related to a nonspecific factor, such as diminished physical activity due to angina, is considered unlikely. Patients with angina attributable to coronary disease, who do not have elevated filling pressures at rest and with heart rate in the normal range, have been shown to have a normal left ventricular end-diastolic volume (50); those with end-diastolic pressure elevation usually have enhanced end-diastolic volume (51). At rest, subjects with normal filling pressures have stroke index (48), or stroke work (52) levels which are not significantly different from controls.…”

A theoretical model of regionally ischemic myocardium.

“…In man, there is contradictory data on the effect of ischemia on the passive properties of the ventricle. McCans and Parker 8 indicate that the passive pressure-volume relation of the ventricle is unchanged by ischemia. The data of Barry et al 9 indicate that, although the stiffness of the ventricle, dP/dV, remains essentially unchanged, the pressure volume curve is shifted to higher pressures.…”

Immediate effects of bumetanide on systemic haemodynamics and left ventricular volume in acute and chronic heart failure.

“…The onset of angina pectoris is accompanied by acute but reversible left ventricular failure characterised by increased left ventricular pressure and volume; in chronic heart failure there is long-standing pressure and volume overload (McCans & Parker, 1973;Sharma et al, 1976;Rerych et al, 1978;Nechwatal et al, 1980;Freeman etal., 1981;Manyari etal., 1981;Hakki et al, 1983;Mancini et al,-1983;Manyari et al, 1983;Osbakken et al, 1983;Steingart et al, 1984). It is widely believed that the immediate and long-term benefits of diuretic therapy in such patients are due to reductions in left ventricular filling pressure and volume (Nechwatal et al, 1980).…”