Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by left atrial pressure-dimension relation

Abstract

To analyze left atrial (LA) pump function in normal subjects, in patients with essential hypertension and in patients with a healed myocardial infarction, LA dimension (aortic-root echogram) and pressure (catheter-tip manometer) were simultaneously recorded in 25 patients (8 normal subjects, 7 with hypertension and 10 with myocardial infarction). The pressure-dimension relation of the left atrium was composed of 2 loops: the A loop (expressing the pump function of the left atrium) and the V loop. LA dimension at the beginning of active LA shortening was significantly greater in hypertensive subjects (33 ± 3 mm) and in those with myocardial infarction (32 ± 4 mm) than in normal subjects (28 ± 3 mm) (p < 0.01, p < 0.05, respectively). The area of the A loop significantly increased in subjects with hypertension (48 ± 3 mm Hg · mm, p < 0.01) and in subjects with myocardial infarction (29 ± 10 mm Hg · mm, p < 0.05), compared with normal subjects (20 ± 8 mm Hg · mm). The mean fractional shortening velocity of the left atrium significantly increased in subjects with hypertension, compared with normal subjects and those with myocardial infarction (p < 0.05 for both). LA peak wall tension during the LA active contraction period significantly increased with hypertension and with myocardial infarction, compared with normal subjects (p < 0.01, p < 0.05, respectively). The area of the A loop was directly proportional to the LA dimension at the beginning of active LA shortening (r = 0.53), p < 0.01). The mean fractional shortening velocity of the left atrium was inversely correlated with the LA peak wall tension during the LA active contraction period (r = −0.44, p < 0.05). With hypertension, the relation between the mean shortening velocity and the peak wall tension of the left atrium shifted up and rightward. It is concluded that the augmented pump function of the left atrium in patients with a healed myocardial infarction is attributed to Starling's mechanism, whereas with hypertension the increased pump function of the left atrium may be attributed not only to Starling's effect, but also to the enhanced inotropic state of the left atrium.