Left atrial transport function in myocardial infarction: Importance of its booster pump function

Abstract

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significance of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean ± SD): LV vol (ml/m 2) LVSV LVDP (mm Hg) Pre‘a’ EDV Pre‘a’ EDP Control patients 76 ±16 86 ±13 56 ± 10 8 ±2 10 ±2 Patients with Ml 91 ±36 107 ±38 46 ±19 13 ±6 21 ±11 NOTE: EDV = end-diastolic volume; SV = stroke volume. Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m 2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m 2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index ≦2.0 liters/min/m 2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m 2 (p < 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume. Atrial contraction contributed 19 per cent to end-diastolic volume in patients with normal end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p < 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The “booster pump” function of the atrium cannot be ignored in assessing left ventricular performance.