Altered Diastolic Distensibility during Angina Pectoris

Abstract

Numerous studies have been done in both clinical and experimental settings to describe the acute hemodynamic and left ventricular volume changes during ischemia. Although it has been well accepted that an increase in left ventricular filling pressure relative to volume is the characteristic feature of the pacing-induced [1–4] or exercise-induced [5–7] ischemia in the ventricle with limited coronary reserve, controversy has continued on the underlying mechanisms of these changes. Some investigators accounted for an increased left ventricular end-diastolic pressure by an increase in diastolic volume with depressed myocardial contractility, whereby the ventricle moves up toward a higher and steeper portion of the pressure-volume curve [8, 9], while others have emphasized the altered diastolic distensibility of the left ventricular chamber, with the distortion of the entire pressure-volume relation resulting in higher pressures at any given volume [1, 10, 11]. Mann and coworkers [2] studied diastolic left ventricular pressure-volume curves before and immediately following rapid atrial pacing in patients with significant coronary artery stenoses and demonstrated that both impaired left ventricular systolic performance and altered left ventricular diastolic properties play a role in producing elevated left ventricular diastolic pressure during ischemia. The relative contributions of these two mechanisms were assessed by Aroesty and colleagues [12] using radionuclide angiography. Using serial pressure-volume analysis in conjunction with pressure recordings, they demonstrated that the ischemic response to pacing tachycardia involves both systolic and diastolic dysfunction but that diastolic impairment precedes systolic depression. From the latter finding, these investigators suggested that impaired diastolic performance is the first manifestation of ischemia.