Postextrasystolic aortic pressure pulse response in coronary artery disease

Abstract

The response of the aortic systolic pressure after an extrasystole was evaluated in 100 consecutive patients with coronary artery disease. The patients were divided into four groups depending on the response of the first postextrasystolic beat. Group IA (45 patients), had lower systolic pressure, whereas group IB (40 patients), had a similar systolic pressure in the postextrasystolic beat, as compared to beats preceding the extrasystole. Group IIA (12 patients) and group IIB (3 patients), demonstrated an increased systolic pressure in the first postextrasystolic beat with subsequent beats in group IIB, also demonstrating pulsus alternans. Congestive heart failure and cardiomegaly were significantly more frequent in group II, as compared to group I patients. In group IIA and IIB, triple vessel disease was present in 83 and 100 per cent, respectively, as compared to 44 per cent in group I patients. Left ventricular end-diastolic pressure (mm. Hg) was 14 ± 6 and 12 ± 7 in group IA and IB respectively, as compared to 19 ± 9 (p < 0.025) in group IIA and 31 in group IIB. Comparing groups IA and IB with each other for cardiac output, stroke volume, end-diastolic volume and ejection fraction, revealed no significant difference. The cardiac output (L./min./M. 2) was 2.2 ± 0.6 for group IIA, as compared (p < 0.01) to 2.8 ± 0.5 and 2.9 ± 0.5 in groups IA and IB. Stroke volume (ml./M. 2) and ejection fraction were 30 ± 10 and 0.30 ± 0.08, respectively, for group IIA, which is signficantly less, as compared to group I patients. The end-diastolic volume (ml./M. 2) in group IIA was 102 ± 28, which is significantly (p < 0.001) higher, as compared to group IA and IB. All patients in group IIB had an abnormal cardiac output, end-diastolic volume and ejection fraction. Thus, the differences in response between group I and group II patients to an extrasystole clearly define two distinct hemodynamic groups. The responses observed to an extrasystole are best explained by variable response of each group to postextrasystolic potentiation and aortic impedance.