What mechanisms contribute to altered left ventricular diastolic properties during angina pectoris induced by rapid atrial pacing in patients with coronary artery disease?
Impaired ventricular relaxation is a key factor contributing to altered left ventricular diastolic properties during angina pectoris.
Mechanisms involved in the altered left ventricular (LV) diastolic properties during angina were studied in 26 patients with coronary artery disease. Angina was induced by rapid atrial pacing and measurements were made at rest and during angina in the immediate post-pacing period. No changes occurred in heart rate (71 +/- 3 to 73 +/- 3 beats/min, NS) or right ventricular (RV) end-diastolic pressure (10 +/- 1 to 11 +/- 1 mm Hg, NS), while significant increases occurred in LV end-diastolic pressure (17 +/- 1 to 30 +/- 1 mm Hg, p less than 0.01), aortic diastolic pressure (74 +/- 3 to 80 +/- 3 mm Hg, p less than 0.01), coronary sinus blood flow (133 +/- 15 to 212 +/- 32 ml/min, p less than 0.01), and the time constant (T) of LV pressure fall in early diastole (43 +/- 2 to 58 +/- 4 msec, p less than 0.01). Despite the rise in arterial pressure, a significant fall was observed in peak negative dP/dt (1961 +/- 106 to 1751 +/- 80 mm Hg/sec, p less than 0.01). Changes in RV end-diastolic pressure do not explain the increased LV end-diastolic pressure during angina. Increased aortic pressure and coronary blood flow may contribute, but the simultaneous fall in peak negative dP/dt and rise in T suggest that impaired ventricular relaxation is an important factor contributing to the previously demonstrated alteration in LV diastolic properties during angina pectoris.
Mann et al. (1979) studied this question.