Left Atrial Performance Research Articles

Pulmonary venous flow pattern studied by transoesophageal pulsed Doppler echocardiography in mitral stenosis in sinus rhythm: effect of atrial systole.

In 13 patients with isolated mitral stenosis in sinus rhythm the pulmonary venous flow was evaluated by transoesophageal pulsed Doppler echocardiography. The patients were divided into two groups according to their mitral valve area (MVA); Group I (MVA < 1.5 cm2, n = 7 patients); and Group II (MVA > 1.5 cm2, n = 6). The patients in group I with haemodynamically significant mitral stenosis had lower velocities of systolic (S), diastolic (D) and atrial retrograde (A) waves of pulmonary venous flow (PVF) compared to milder stenosis (P < 0.05). The peak velocity of pulmonary retrograde venous flow at atrial contraction (A) primarily depends on the relative amplitude of the atrial transmitral wave (RA), which is measured from the onset of atrial systole to its peak velocity. We found a highly positive correlation between RA of mitral valve flow (MVF) and A wave of PVF (r = 0.87, P < 0.0001). There was also a highly negative correlation (r = 0.80, P < 0.001) between A of PVF and ratio of early (PE) to late (PA) velocities of MVF. Therefore, the retrograde A wave of PVF is related to the pressure generated in the left atrium during atrial systole. Use of pulmonary vein velocities in conjunction with mitral flow velocities can increase our understanding of the haemodynamics of mitral stenosis and provide a new insight into left atrial performance.

Time-course of left atrial performance during coronary artery occlusion followed by reperfusion in anesthetized dogs by densitometric analysis of digital atrioventriculographic images.

The left atrial (LA) function during coronary artery occlusion followed by reperfusion using densitometric analysis of digital atrioventriculographic images was evaluated. Eight anesthetized dogs underwent atrioventriculography at baseline, 10 and 60 min after left circumflex coronary artery (LCX) occlusion and 5, 30, 60, and 120 min of reperfusion. Time-density curves were obtained for LA and left ventricle (LV). The ratios of passive atrial video-densitometric change (VC) to total VC (Passive Ratio), and active VC to total VC (Active Ratio) were calculated. Left ventricular ejection fraction (LVEF), peak ejection rate (PER), and peak filling rate (PFR) were derived. Active Ratio, an index of atrial contraction, increased to 144%, and Passive Ratio decreased to 75% of baseline at 60 min of LCX occlusion. Two hours after reperfusion, both Active and Passive Ratios returned to control level. While LVEF reduced to 70%, PER to 67%, LV peak positive dP/dt to 88% of baseline at 60 min after occlusion, and remained depressed at 2 h after reperfusion. However, PFR, LV peak negative dP/dt and LV isovolumic pressure decay rate showed recovery at 2 h after reperfusion. There were significant correlations between PFR and Passive Ratio (r = 0.41), and between Active and Passive Ratios (r = 0.55). Thus, time-course of recovery of LV post-ischemic systolic and diastolic function was different. Return of LA function to control level during 2 h after reperfusion may be depend on recovery of LV diastolic function.

The effect of acute hypoxia on left ventricular function with special reference to diastolic function--an analysis using ultrasonic method.

In order to evaluate the effect of acute hypoxia on left ventricular (LV) contractility and diastolic function, hemodynamics and LV wall motion were investigated in anesthetized open-chest paced dogs using M-mode or pulsed Doppler echocardiography. Animals were ventilated with 10% oxygen (Hypo 1) and 6.3% oxygen (Hypo 2). LV contractility and diastolic functions were enhanced under "Hypo 1" and at an early phase of "Hypo 2". However, LV functions, both systolic and diastolic, were simultaneously reduced in the presence of hypercapnic acidosis by "Hypo 2". Peak velocities of diastolic rapid filling flow (R) and atrial contraction flow (A) were increased under "Hypo 1", but showed a biphasic change (an increase and a subsequent decrease) under "Hypo 2". The ratio of A/R, known as an index of LV diastolic function, was not altered under hypoxia alone or even under hypercapnic acidosis. Even when hypoxia seems to enhance LV contractility, LV function has already begun to be depressed with a reduction of pH. This seems, however, to be compensated for by LV dilatation and increase in preload, or preservation of left atrial performance.

Effects of left ventricular dysfunction on left atrial performance in previous myocardial infarction and during pacing-induced myocardial ischemia in angina pectoris.

This study aimed to evaluate acute and chronic response of left atrial function to left ventricular dysfunction in patients with coronary artery disease. We studied simultaneous measurements of left atrial volume by biplane cineangiography and left ventricular pressure at rest and after pacing in 59 patients with coronary artery disease and 11 normal subjects. At rest, 35 patients with previous myocardial infarction (MI group) had low left ventricular filling rate of the first third in diastolic time, large left atrial volume before contraction (LA pre-ACV) and large left atrial ejection volume (LAEV), compared with control group. Left atrial ejection fraction (LAEF), the ratio of LAEV to LA pre-ACV, was similar between both groups. LAEF was maintained within a wide range of values in accordance with left ventricular peak A pressure, except for 3 patients who had high values of left ventricular peak A pressure and low values of LAEF. After a right atrial pacing stress test, time constant was prolonged and mean emptying rate of left atrial volume during early diastole decreased in 11 patients with angina pectoris who had an increase greater than 5 mmHg in left ventricular end-diastolic pressure after pacing. In these group, LA pre-ACV increased, LAEF decreased and LAEV was unchanged. These results suggest that left atrial performance responds differently to acute and chronic left ventricular dysfunction in patients with coronary artery disease.

Atrial function during volume loading.

Atrial function during volume loading.