SUMMARY Left atrial function was evaluated in patients with and without remote myocardial infarction. The simultaneous left atrial pressure recording and left atrial and left ventricular cineangiograms were obtained with a catheter-tip micromanometer. The pressure-volume curve of the left atrium was composed of an A-loop and a V-loop. The ratio of active atrial emptying to left ventricular stroke volume in patients with myocardial infarction was significantly larger than that in normal subjects (42 + 12% vs 29 + 10%, p < 0.05). The left atrial work was also significantly greater in patients with myocardial infarction (1690 + 717 mm Hgml) than in normal subjects (940 426 mm Hg-ml, p < 0.05). The ratio of active atrial emptying to left ventricular stroke volume and left atrial work were significantly related in both normal subjects and patients with myocardial infarction (y = 0.72, p < 0.01). The left ventricular ejection fraction correlated inversely with left atrial work (y = -0.5, p < 0.05). Left atrial work also showed a significant linear correlation with left atrial volume before active atrial emptying (y = 0.82, p < 0.01).We conclude that the left atrial contribution to left ventricular function is increased in patients with remote myocardial infarction. This left atrial contribution to the left ventricle is attributed to the FrankStarling mechanism in the left atrium.LEFT ATRIAL function and its hemodynamic importance for overall cardiac performance have been discussed.' 1-3 The left atrium may serve as a conduit for the passage of blood from the pulmonary veins to the left ventricle during early left ventricular filling, as a reservoir for storing blood during left ventricular systole, and as a contractile chamber for augmentation of left ventricular filling. Understanding each of these functions and the contribution of the left atrium to left ventricular function in normal and diseased hearts is important.In this report, we analyze left atrial pressure-volume relationships in patients with remote myocardial infarction and discuss the importance of left atrial function. MethodsData were obtained during diagnostic cardiac catheterization in two groups of patients. The normal group consisted of eight patients who had no coronary, valvular or congenital heart disease and were hemodynamically normal. These patients were referred for diagnostic cardiac catheterization to evaluate chest pain. The myocardial infarction group consisted of 10 patients who had a documented remote transmural myocardial infarction, and no other associated heart disease. The clinical data for each patient are listed in medications were discontinued for at least 2 days before the study, except for sublingual nitroglycerin, which was allowed for anginal attack, but withheld 12 hours before the study. A Millar catheter-tip micromanometer (Model PC-484A, pigtail) was used for pressure measurement and cineangiography. The transducer was calibrated electronically against mercury at the beginning of each study. The zero shift during the proc...

In 15 open-chest, anesthetized dogs, regional systolic wall thickening (% delta WT) was measured with sonomicrometry and regional blood flow was determined with tracer microspheres (7-10 micron) before and after various degrees of coronary artery narrowing were created with a hydraulic occluder. The stenoses were categorized into four groups by the effect on % delta WT, and the corresponding myocardial blood flow (MBF) was determined in four layers across the ventricular wall (layer 1: subendocardium; layer 4: subepicardium). In group 1, % delta WT decreased 44 +/- 10% and only layer 1 MBF was significantly reduced (-28%); in group 2, % delta WT decreased 77 +/- 8% and MBF was reduced in both layers 1 and 2 (-52% and -36%, respectively); in group 3, % delta WT decreased 104 +/- 3% and MBF was reduced in the three inner layers (layer 1: -65%; layer 2: -58%; layer 3: -34%); in group 4, % delta WT decreased 145 +/- 9% (systolic wall thinning) and transmural reduction of MBF was found (layer 1: -74%; layer 2: -68%; layer 3: -55%; layer 4: -29%). We conclude that (1) up to 75% reduction in systolic wall thickening may occur when perfusion to only the inner one-half of the myocardium is decreased; (2) akinetic wall motion may be observed when perfusion remains normal in the subepicardial one-fourth of the wall; and (3) dyskinesia (wall thinning) occurs when blood flow is reduced transmurally.

To assess the importance of contraction band necrosis (CBN) in reperfusion, CBN, coagulation necrosis (CN), and infarct size, expressed as CBN + CN, were quantitatively analyzed in 25 porcine hearts without collateral circulation. The left anterior descending coronary artery was ligated for 20, 30, 60, and 120 min and then reperfused for 8 hr (groups 1 to 4, respectively). Five hearts were not reperfused (group 5). The areas of CBN and CN were traced at a magnification of X 100 under an inverted microscope and quantified with use of an image analyzer. There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method. decreased to almost zero after occlusion but recovered during reperfusion. Percent of risk area infarcted in groups 1 to 4 was 0 ± 0%, 1 1 + 7%, 80 ± 9%, and 96 ± 2%, respectively, and the percent of risk area infarcted in group 4 was the same as that in hearts subjected to permanent occlusion (95 ± 3%). The percent area of CBN was 100 ± 0% in group 2 68 ± 1 1% in group 3, 2 ± 1% in group 4, and 2 ± 2% in group 5. In group 3, the inner third of the ischemic left ventricular wall showed CN and the middle and outer third CBN. These findings show that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even when reperfusion is achieved after 1 hr occlusion. Therefore, protection against CBN might reduce infarct size after reperfusion.

To study the relationship between global and regional filling of the left ventricle, we conducted resting gated radionuclide ventriculographic studies in 15 control subjects (group 1) and 22 patients with isolated disease of the left anterior descending coronary artery (group 2). None had had a previous myocardial infarction. A computer program subdivided the image of the left ventricle into four regions. The time-activity and first-derivative curves of the global and regional left ventricles were computed. In the global left ventricle, the normalized peak filling rate (PFR) was decreased (p < .01) and the ratio of the time to PFR (time interval from global end-systole to PFR) to the diastolic time, TPFR/DT, was greater (p < .02) in group 2 than in group 1. In the regional left ventricle, in the side perfused by the stenosed vessel (septal and apical), PFR was slightly decreased in the apical (p < .05), but not the septal region (p = NS); TPFR/DT was greater in the apical (p < .02) and in the septal region (p < .01) in group 2. In the normally perfused lateral side, there were no significant differences in PFR or in TPFR/DT between group 1 and group 2. Total At/DT, which was defined as the ratio of the sum of the absolute values of the time differences from global PFR to regional PFR (septal, apical, and lateral) to the diastolic time, was significantly greater in group 2 (0.09 0.05 vs 0. 16 + 0.05; p < .001). This indicates the existence of asynchronous diastolic filling in the different regions of the left ventricle in group 2. A negative correlation existed between total At/DT and global PFR (r -.64, p < .001). Thus, in patients with one-vessel disease, asynchronous diastolic filling occurs due to the filling disturbance in the affected regions, which may cause impairment of the filling of the global left ventricle. Circulation 69, No. 5, 933-942, 1984. LEFT VENTRICULAR diastolic filling has been reported to be impaired in many patients with coronary artery disease in whom there is no evidence of previous myocardial infarction. 8

Descending intervention induced greater prolongation of T than ascending intervention. Prolongation of T was closely related to an increase in AoESP in the descending intervention but a decrease in AoESP in the ascending intervention. These data suggest that not only the loading sequence but also the pressure level at the onset of isovolumic relaxation determines LV relaxation.

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Left ventriculography with simultaneous pressure micromanometry was performed in 11 normal control subjects and 17 patients with dilated cardiomyopathy (DCM). Left ventricular silhouettes in the right anterior oblique projection were divided into eight areas, and regional wall stress was computed by Janz's method in each area excluding the two most basal areas. Wall stress was higher in DCM patients than in control subjects (p<0.01). The percent area changes from end diastole to end systole in each area were lower in DCM patients than in control subjects (mean for six areas, 22+14% versus 54±9%o, respectively, p <0.01), but the coefficient of variation for the percent area changes in the six areas of the left ventricle in DCM patients was greater than that in control subjects (32±17% versus 15±4%, respectively, p<0.01), indicating regional differences in hypokinesis. There was a significant negative correlation between end-systolic regional wall stress and percent area change (r=-0.60 to -0.86, p<0.05) in each area. Thus, excessive regional afterload may play an important role in causing regional hypokinesis in DCM. (Circulation 1990;82:2075-2083 iffuse hypokinesis of the left ventricular wall D motion has been reported in patients with dilated cardiomyopathy (DCM).' However, recent studies on DCM with the use of left ventricular cineangiography2-5or radionuclide ventriculography6,7 suggest that left ventricular wall motion is not always diffusely hypokinetic and that regional differences in the degree of hypokinesis are frequently present. In clinical settings, patients with segmental wall motion abnormality may have better global left ventricular function and better prognosis than patients with diffuse wall motion abnormality.6 Thus, the importance of estimating left ventricular regional wall dynamics in patients with DCM has been emphasized.3-7

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