Left ventricular mechanical efficiency in man with heart disease.

Thirty-eight adults with valvular and/or myocardial disease had heart catheterization with coronary blood flow and myocardial O2 consumption (MVO2) per 100 g measured by the nitrous oxide washout technique. Quantitative biplane angiocardiography was performed to assess left ventricular volume, mass, ejection fraction and work. Left ventricular efficiency was calculated from work, MVO2/100 g and mass. Efficiency ranged from 4 to 40% and was normal in some patients with severe ventricular pressure-volume work overloads. Total left ventricular MVO2 ranged up to 461 ml/min. Neither total MVO2 nor MVO2/100 g was significantly related to ventricular work, ejection fraction, or tension-time index. These data suggest 1) a relationship between left ventricular efficiency and myocardial function in chronic valvular or myocardial disease, 2) that efficiency may be normal in hypertrophied ventricles, and 3) that chronic increases in resting ventricular metabolic requirements are met by hypertrophy rather than by increased MVO2/100 g.     

Left ventricular function in patients with and without myocardial infarction and one,two or three vessel coronary artery disease

Ninety-six patients with chest pain were studied to determine the relation between left ventricular function and severity of coronary artery disease in patients with and without a history of myocardial infarction. Coronary arteriography was performed obtaining cineangiograms (60 frames/sec) and large roll film angiograms (2 to 6 frames/sec) for precise definition of the coronary anatomy. The criteria for diagnosis of myocardial infarction were a typical history, a rise and fall in serum glutamic oxaloacetic transaminase levels and evolutionary S-T segment changes associated with Q waves of at least 0.03 second. Left ventricular function was assessed by measurement of left ventricular end-diastolic pressure and volume, and left ventricular ejection fraction, mass and compliance. Fifteen patients had normal findings; 81 were classified according to number of diseased vessels and presence or absence of myocardial infarction. There were no group differences in age or heart rate. Left ventricular end-diastolic pressure was abnormally increased in patients with three vessel disease and myocardial infarction. Left ventricular end-diastolic volume was increased and the ejection fraction was reduced in patients in each vessel disease group with myocardial infarction. Although ejection fraction was reduced in patients with three vessel disease without myocardial infarction, it was further reduced when infarction occurred. Left ventricular mass increased in patients with three vessel disease with or without myocardial infarction. Values for ventricular compliance were reduced in all patients with myocardial infarction and were lower in those with two and three vessel disease and infarction than in those with two and three vessel disease without infarction. These findings suggest that a previous history of myocardial infarction needs to be considered together with anatomic abnormalities of the coronary arteries in assessing cardiac performance in patients with ischemic heart disease. In patients with one, two or three vessel coronary artery disease, a previous myocardial infarction significantly alters left ventricular performance; the ejection fraction is a more sensitive measurement of left ventricular function than left ventricular end-diastolic pressure or volume.     

Fibrinopeptide A, platelet factor 4, and beta-thromboglobulin levels in coronary heart disease

In vivo platelet alpha-granule release and fibrin I formation were measured in 82 patients with ischemic heart disease by radioimmunoassay of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A. The presence and extent of coronary artery disease were determined by coronary arteriography, and the extent of left ventricular regional dysfunction was assessed by contrast left ventriculography. In patients with abnormal coronary arteriograms without previous myocardial infarction, mean levels of platelet factor 4, beta-thromboglobulin, and fibrinopeptide A were not elevated. In patients in whom myocardial infarction had occurred more than 6 mo previously, platelet factor 4 (8.3 ng/ml; p less than 0.01) and beta-thromboglobulin (33.2 ng/ml; p less than 0.001) levels were significantly elevated, but fibrinopeptide A levels were normal. Levels of platelet factor 4 and beta- thromboglobulin were unrelated to the extent of coronary artery disease. In the patients with prior infarction, beta-thromboglobulin correlated directly with extent of left ventricular regional dysfunction (r = 0.53; p less than 0.01) and inversely with ejection fraction (r = -056; p less than 0.05). In a small group of patients with left ventricular aneurysm, mean fibrinopeptide A levels were also elevated. We interpret these findings as indicating that platelet release in patients with ischemic heart disease results from platelet reaction with previously infarcted myocardium rather than with the atherosclerotic coronary arteries.     

Left ventricular wall motion at rest in patients with organic coronary artery disease vs coronary spasm

Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.     

Value of two-dimensional echocardiography in evaluating coronary artery disease: a randomized blinded analysis

Two-dimensional echocardiography at rest was used to analyze segmental wall motion abnormalities for detecting coronary artery disease in patients with and without a history of myocardial infarction. One hundred twenty-five echocardiograms were analyzed in a randomized, blinded fashion. They were obtained from 55 consecutive patients found to have significant coronary artery disease at angiography, 59 consecutive normal subjects and 11 patients with dilated cardiomyopathy. The overall sensitivity of two-dimensional echocardiography was relatively low at 67%. However, specificity was 99%. The sensitivity was higher in patients with past myocardial infarction than in those without myocardial infarction (81 versus 42%), as expected. Echocardiography can detect segmental wall motion abnormalities in some patients with coronary artery disease and no overt prior myocardial infarction. This was highlighted by nine such patients with coronary artery disease and no prior myocardial infarction or electrocardiographic Q waves who were found to have segmental wall motion abnormalities. A semiquantitative, two-dimensional echocardiographic segmental wall motion score was derived for 47 patients and was correlated with angiographic left ventricular ejection fraction (r = 0.71). This score differentiated patients with a normal ejection fraction (greater than 50%) from those with a depressed ejection fraction (less than 50%): 1.1 +/- 1.6 versus 6.9 +/- 3.1 (p less than 0.001). Almost all patients (92%) with an echocardiographic score of five or more had an abnormal ejection fraction of less than 50%. In patients with chronic congestive heart failure, the echocardiogram separated those with dilated cardiomyopathy from those with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired right ventricular filling in old myocardial infarction

To evaluate ventricular filling and interactions between right and left ventricles in patients with old myocardial infarction, right and left ventricular time-volume curves were analyzed from a cineangiographic study of 10 normal subjects (Group 1), 10 patients with old anterior myocardial infarction (Group 2) and 10 patients with old inferior myocardial infarction (Group 3). Volumes of both ventricles were calculated from each frame over an entire cardiac cycle using Simpson's method. From time-volume curves, peak ejection rates, peak filling rates and atrial kick rates were obtained for both ventricles and these parameters were normalized by end-diastolic volume. All patients were in sinus rhythm with heart rates less than 80 beats/min. There were no significant differences among the 3 groups in end-diastolic pressure of both ventricles and mean pulmonary artery pressure. Left ventricular ejection fractions were significantly lower in Groups 2 and 3 than in Group 1 (p less than 0.001, p less than 0.005, respectively), although there were no significant differences in end-diastolic volume indexes of either ventricle among the 3 groups. Peak left ventricular ejection rate and peak filling rates of the left and right ventricles were lower in Group 2 than in Group 1 (p less than 0.01, p less than 0.05, p less than 0.01, respectively) and peak filling rate of the right ventricle in Group 2 correlated with the peak filling rate of the left ventricle and left ventricular ejection fraction (r = 0.64, r = 0.64, respectively). Peak filling rate of the right ventricle in Group 2 correlated inversely with left ventricular peak negative dp/dt (r = -0.72), but no correlation was found between peak filling rate of the right ventricle and left ventricular end-diastolic volume index or mean pulmonary artery pressure. Peak ejection rate of the left ventricle and peak filling rates of both ventricles in Group 3 were lower than in Group 1 (p less than 0.02, p less than 0.02, p less than 0.01, respectively) and no correlation was found between peak filling rates of both ventricles. Wall motion of the right ventricular septal portion was slightly reduced in 5 patients in Group 2. In all patients in Group 3, right ventricular wall motion centering around the right ventricular diaphragmatic portion was reduced. These results suggest that in old inferior myocardial infarction, right ventricular wall motion abnormality results in impaired right ventricular filling, whereas in old anterior myocardial infarction, right ventricular filling is reduced indirectly due to impaired left ventricular filling.     

Role of previous angina pectoris and collateral flow to preserve left ventricular function in the presence or absence of myocardial infarction in isolated total occlusion of the left anterior descending coronary artery

The aim of this study was to determine whether previous angina pectoris and collateral circulation influenced myocardial function after isolated coronary occlusion. In 58 consecutive patients, coronary angiography showed a complete isolated occlusion of the left anterior descending coronary artery; 43 patients (74%) had previous myocardial infarction. Duration of previous angina pectoris was defined as the time from the first ischemic symptom to the date of myocardial infarction or of coronary angiography in the absence of myocardial infarction. Left ventricular ejection fraction was measured on the 30 degrees right anterior oblique projection of the left ventricular angiogram. Collateral circulation was graded as follows: none or filling limited to side branches (group 1) and partial or complete filling of the epicardial arterial segment (group 2). Group 2 (40 patients) had higher ejection fraction (57 vs 38%; p less than 0.0001) and longer duration of previous angina pectoris (11 vs 0.1 months; p less than 0.002) than group 1 (18 patients). A longer duration of previous angina pectoris probably allows collateral development before coronary occlusion in 1-vessel coronary artery disease, thereby limiting myocardial damage.     

Asynchronous left ventricular regional function and impaired global diastolic filling in patients with coronary artery disease: reversal after coronary angioplasty

Left ventricular diastolic filling is impaired in many patients with coronary artery disease and normal left ventricular systolic function, and is improved in many patients after coronary angioplasty (PTCA). To investigate the mechanisms for this improvement, we studied regional asynchrony by radionuclide angiography in 26 patients with single-vessel coronary artery disease before and after successful PTCA. Before PTCA, all patients had normal ejection fractions at rest and normal qualitative left ventricular regional wall motion, as determined by radionuclide and contrast angiography. Quantitative left ventricular regional function was assessed by dividing the left ventricular region of interest into 20 sectors. Phase analysis was performed on each sector's time-activity curve, and the average intersector phase difference was used as an index of left ventricular regional synchrony. Before PTCA, average intersector phase difference was increased compared with normal (6.0 +/- 2.2 vs 4.0 +/- 1.7 degrees, p less than .005), indicating asynchronous regional function. After PTCA, ejection fraction at rest was unchanged, but peak left ventricular filling rate at rest increased from 2.5 +/- 0.6 to 3.0 +/- 0.6 end-diastolic volume/sec (p less than .001) and was associated with a decrease in average intersector phase difference from 6.0 +/- 2.2 to 5.1 +/- 2.3 degrees (p less than .05). Average intersector phase difference decreased in 16 of 21 patients in whom peak filling rate increased after PTCA (p less than .005), compared with one of five patients in whom peak filling rate was unchanged or decreased. Hence, improved global left ventricular filling after PTCA was associated with more synchronous left ventricular regional behavior. To identify the cause of regional asynchrony before PTCA, we then generated time-activity curves from each of four left ventricular quadrants. These data indicated that the asynchrony was caused by regional variation in timing of diastolic rather than systolic events and that PTCA resulted in reduction in regional diastolic asynchrony. These data suggest that in many patients with coronary artery disease and normal left ventricular systolic function, impaired global diastolic filling may result from asynchronous left ventricular regional diastolic function, which is a reversible manifestation of myocardial ischemia or reduced coronary flow.     

Effect of beta blockade on silent regional left ventricular wall motion abnormalities

The effect of beta-adrenergic blockade on regional left ventricular wall motion abnormalities was studied in 11 patients with coronary artery disease and silent myocardial ischemia during exercise testing. Four patients were asymptomatic; 7 were asymptomatic after a myocardial infarction. Left ventricular wall motion abnormalities were characterized by reduced regional ejection fraction (EF) during exercise determined by gated left anterior oblique images of the cardiac blood pool. In the 11 patients, 10 anteroseptal and 8 inferoposterior regions were subserved by stenotic coronary arteries. Before beta blockade, regional EF decreased in 15 of 18 regions. After beta blockade, this occurred in only 6 of 18 regions (p less than 0.05); the other 12 regions showed no change or an actual increase in regional EF. Thus, beta-adrenergic blockade effectively improved the reduction in exercise regional EF usually seen in patients with coronary artery disease with silent myocardial ischemia. One probable mechanism of action is a reduction in myocardial oxygen requirement at peak exercise.     

The differing prognostic utility of exercise radionuclide ventriculography in coronary artery disease patients with and without prior myocardial infarction

Previous studies have documented the prognostic utility of left ventricular ejection fraction response to exercise primarily in populations without prior myocardial infarction. We undertook a study to assess the prognostic utility of exercise left ventricular ejection fraction and segmental wall motion response during exercise radionuclide ventriculography in coronary artery disease patients with and without prior myocardial infarction. Methods. We examined the comparative prognostic utility of left ventricular ejection fraction and segmental wall motion response during upright bicycle exercise radionuclide ventriculography in 419 coronary artery disease patients with (n=217) and without (n=202) prior myocardial infarction using univariate and multivariate hierarchical regression analyses. Results. During an average followup period of 61 months, 96 patients (23%) suffered cardiac events, including 55/217 (25%) of the patients with prior myocardial infarction and 41/200 (21%) of the patients without prior myocardial infarction (p=ns). Both cumulative Kaplan-Meier survival analyses and stepwise hierarchical Cox survival analyses demonstrated that peak left ventricular ejection fraction <55% was a significant predictor of cardiac events in patients without prior myocardial infarction (p=0.04), whereas an exercise wall motion worsening score 2 was a significant predictor in patients with a prior myocardial infarction (p=0.0001). Conclusions. The prognostic utility of exercise radionuclide ventriculography variables differ according to the presence or absence of prior myocardial infarction. Global function, assessed by peak left ventricular ejection fraction, adds the greatest prognostic information in patients without prior myocardial infarction, whereas regional function, assessed by exercise wall motion worsening, is the best predictor among patients with prior myocardial infarction.     

Influence of left ventricular function on signal averaged late potentials in patients with coronary artery disease with and without ventricular tachycardia

Left ventricular dysfunction has been suggested as a cause of late potentials on the signal averaged ECG of patients with coronary artery disease. We compared the averaged surface ECG with angiographic findings in 57 patients with coronary artery disease and left ventricular dysfunction. Sixteen patients had sustained ventricular tachycardia and 41 had no documented arrhythmia. These two patient groups were comparable with respect to age, mean ejection fraction, and wall motion score. Late potentials, defined as voltage less than 25 microV in the last 40 msec of the filtered QRS complex, were found in 10 of 16 patients with ventricular tachycardia and in 6 of 41 patients without arrhythmia (p less than 0.005). However, late potentials were independent of ejection fraction, wall motion score, or presence of dyskinesis in both groups. There was no correlation between the total filtered QRS duration and ejection fraction or wall motion score in either patient group. In patients with coronary artery disease, late potentials are associated with ventricular tachycardia but are independent of global or regional left ventricular function. This finding has important implications for studies of the prognostic value of late potentials following myocardial infarction.     

Noninvasive evaluation of left ventricular performance by the shortest distance between mitral leaflets coaptation and interventricular septum at end-systole.

We attempted to evaluate left ventricular performance from the shortest distance between the mitral leaflets coaptation and the interventricular septum at end-systole (MVC-IVS distance). The subjects were 37 patients with coronary artery disease (CAD) with prior myocardial infarction (MI), 8 with CAD without prior MI, 22 with atypical chest pain, and 4 with aortic regurgitation. The MVC-IVS distance was measured on a two-dimensional echocardiogram obtained from the parasternal or apical long-axis view and frozen at end-systole. Left ventricular end-systolic volume and end-diastolic volume were obtained by left ventriculography, and the left ventricular ejection fraction was calculated. A significant positive correlation was observed between the MVC-IVS distance and the end-systolic volume (r = 0.83, p less than 0.001); a close correlation was observed between the MVC-IVS distance end-systolic volume and ejection fraction by monoexponential fitting (r = -0.91, p less than 0.001). Thus, a significant negative correlation was observed between the MVC-IVS distance and the left ventricular ejection fraction (LVEF) (r = -0.83, p less than 0.001). An MVC-IVS distance of greater than or equal to 30 mm suggests diagnosis of left ventricular dysfunction (LVEF less than 50%) with high sensitivity (94.4%) and specificity (90.6%), while a value less than 30 mm suggests that the left ventricular performance is likely to be normal. Thus one can easily evaluate the left ventricular performance noninvasively using this new index.     

Effects of the Mueller maneuver on global and regional left ventricular function in angina pectoris with or without previous myocardial infarction

In patients with coronary artery disease, left ventricular (LV) regional wall akinesia can develop during the Mueller maneuver. The present study determines if the presence of myocardial ischemic disease with no infarction is a sufficient condition for this to occur, or if the presence of prior acute myocardial infarction (MI) is necessary. In men, first-pass radionuclide ventriculography was performed in the 30 degree left anterior oblique supine position to measure LV ejection fraction, end-diastolic and end-systolic volumes and heart rate, and to obtain an image of the LV cavitary perimeter. This procedure was performed in 4 subject groups: 13 normal volunteers, 25 patients with coronary artery disease but no prior MI, 13 patients with coronary artery disease and prior nontransmural MI, and 36 patients with coronary artery disease and prior transmural MI. All patients had angina and underwent routine contrast coronary angiography; 60 also underwent contrast coronary angiography; 60 also underwent contrast LV angiography. Ejection fraction decreased during the Mueller maneuver in each of all the coronary artery disease groups (p less than 0.01), but not in the normal subjects. Heart rate increased in groups 1, 2 and 4 (p less than 0.01), and end-diastolic volume decreased in all 4 groups (p less than 0.01), whereas end-systolic volume did not change. Only in group 4 did regional wall akinesia develop (17 patients) during the Mueller maneuver. Among patients who had akinesia during the Mueller maneuver and also underwent routine contrast ventriculography, half of the akinetic segments were not seen on routine contrast study, but were seen only on radionuclide ventriculography during the Mueller maneuver.(ABSTRACT TRUNCATED AT 250 WORDS)     

Two-dimensional echocardiographic estimation of right ventricular ejection fraction in patients with coronary artery disease

Two-dimensional echocardiographic determination of right ventricular ejection fraction was compared with right ventricular ejection fraction obtained by first pass radionuclide angiography in 39 patients with coronary artery disease. Apical four chamber and two chamber right ventricular views were obtained in 34 (87%) of the 39 patients, while a subcostal four chamber view was obtained in 31 patients (80%). Right ventricular ejection fraction by two-dimensional echocardiography was calculated by the biplane area-length and Simpson's rule methods using two paired orthogonal views and utilizing a computerized light-pen method for tracing the right ventricular endocardium. A good correlation (r = 0.74 to 0.78) was found between radionuclide angiographic and two-dimensional echocardiographic right ventricular ejection fraction for each method used. Patients with acute inferior myocardial infarction had the lowest right ventricular ejection fraction by radionuclide angiography and two-dimensional echocardiography (p less than 0.05 compared with patients with right coronary artery obstruction and no infarction). There were no differences in right ventricular ejection fraction between patients with acute and old inferior myocardial infarction by both techniques. No correlation was found between left and right ventricular ejection fraction by radionuclide angiography (r = 0.16). It is concluded that 1) right ventricular ejection fraction by two-dimensional echocardiography correlates well with radionuclide angiographic measurements and can reliably evaluate right ventricular function in coronary artery disease, 2) patients with inferior myocardial infarction have reduced right ventricular ejection fraction, and 3) changes in left ventricular ejection fraction do not directly influence right ventricular function.     

PTCA and left ventricular systolic function (evaluation by exercise two-dimensional echocardiography)]

Successful transluminal coronary angioplasty (PTCA) should improve left ventricular systolic function. To assess the effect of this procedure 25 patients with coronary heart disease were examined before and 3-to 5 days after successful PTCA with electrocardiographic treadmill exercise test, and exercise two-dimensional echocardiography (modified Bruce protocol). Echocardiographic examination was obtained prior to and immediately following exercise. Left ventricular ejection fraction and segmental wall motion at the baseline and immediately after exercise were assessed. Electrocardiographic evidence of ischemia was found in 16 of 25 patients prior to PTCA and in 9 patients after PTCA. Following angioplasty, exercise duration was increased and the exercise-induced angina rate was significantly decreased. Ejection fraction did not change significantly in patients prior and after PTCA (52 +/- 10% versus 55 +/- 16%, p = NS). Following angioplasty, ejection fraction increased from 55 +/- 10% (rest) to 64 +/- 11% (exercise) (p less than 0.001). New exercise-induced echocardiographic segmental wall motion abnormalities were found in 16 of 25 patients prior to PTCA and in only one patient following PTCA. Significant improvement of ejection fraction and segmental wall motion were also observed in 11 patients with old myocardial infarction subjected to successful angioplasty of infarct-related coronary artery. Opposite to post-exercise results, the resting mean values of these echocardiographic parameters did not differ significantly between pre and post-PTCA examinations. These data demonstrate an improvement in systolic left ventricular function and better exercise tolerance following successful PTCA. This occurs also in patients with old myocardial infarction after angioplasty of infarct-related coronary artery. Two-dimensional exercise echocardiography may be helpful in assessing the early results of successful angioplasty.     

Global and regional left ventricular response to bicycle exercise in coronary artery disease. Assessment by quantitative radionuclide angiocardiography.

The left ventricular response to bicycle exercise was evaluated in 60 patients with coronary artery disease and in 13 normal control subjects. Left ventricular ejection fraction, mean normalized ejection rate and regional wall motion were determined using first-pass radionuclide angiocardiograms obtained at rest and again during peak graded bicycle exercise. All normal subjects demonstrated improved left ventricular function with exercise. Left ventricular ejection fraction increased significantly from 67 ± 3 per cent (mean ± SE) at rest to 82 ± 4 per cent with exercise (p < 0.001). Similarly, the left ventricular ejection rate increased significantly from 3.47 ± 0.31 sec^?1 to 6.53 ± 0.42 sec^?1(p < 0.001). In contrast, in 44 of 60 patients with coronary artery disease, the ejection fraction or ejection rate either decreased or remained the same with exercise. New or exaggerated regional wall motion abnormalities were detected in 28 of 60 patients with coronary artery disease. Over-all, global or regional evidence of compromised left ventricular reserve was found in 48 of 60 patients with coronary artery disease.The major determinant of an abnormal left ventricular response to exercise was the presence or absence of electrocardiographic evidence of myocardial ischemia. Left ventricular ejection fraction decreased or remained the same with exercise in all patients with coronary artery disease and electrocardiographic ischemia. New regional wall motion abnormalities were detected in 20 of these patients. In this group, the left ventricular ejection fraction decreased from 66 ± 2 per cent at rest to 58 ± 2 per cent with exercise (p < 0.001), whereas the ejection rate was unchanged by exercise (rest 3.33 ± 0.21 sec^?1; exercise 3.34 ± 0.22 sec^?1, p > 0.05). Of the 30 patients with coronary artery disease who exercised to symptom-limiting fatigue without electrocardiographic ischemia, 18 demonstrated compromised left ventricular reserve with exercise. Twelve of the remaining patients with coronary artery disease had normal left ventricular reserve, in eight of whom ventricular function was completely normal both at rest and during exercise. In this group exercised to fatigue, the left ventricular ejection fraction increased from 53 ± 4 per cent at rest to 58 ± 2 per cent with exercise (p < 0.001). The ejection rate also increased from 2.48 ± 0.24 sec^?1 to 3.67 ± 0.39 sec^?1 (p < 0.001). The direction and magnitude of the left ventricular responses to exercise were not affected by long-term oral propranolol administration in 22 patients. Based upon either abnormal exercise left ventricular reserve or abnormal global and regional left ventricular function at rest, the over-all sensitivity of this radionuclide technic for the detection of coronary artery disease was 87 per cent (52 of 60 patients). These data demonstrate that exercise ventricular performance studies provide important physiologic insights into left ventricular functional reserve as well as a sensitive noninvasive approach for the detection of coronary artery disease.     

Intracoronary infusion of streptokinase in patients with acute myocardial infarction: Effects of reperfusion on left ventricular performance

Cardiac catheterization and coronary angiography were performed on hospital admission in 32 consecutive patients with acute myocardial infarction. Twenty-six patients had total occlusion of an infarct-related coronary artery and six had severe proximal stenosis with poor distal flow. In 18 of the 26 patients with total occlusion, intracoronary infusion of Streptokinase resulted in reperfusion of the distal coronary artery. Seventeen of these 18 patients had severe coronary arterial stenosis at the site of the previous total occlusion. Hemodynamic indexes of left ventricular performance and ejection fraction determined by gated cardiac blood pool imaging did not change immediately after reperfusion (p [probability]= not significant [NS]). The mean (± standard deviation) left ventricular ejection fraction increased significantly (p = 0.007) from admission (44 ± 15 percent) to hospital discharge (55 ± 7 percent) in patients evidencing reperfusion of the occluded coronary artery. It did not change (p = NS) in this time span in the patients with severe stenosis alone, in those with total occlusion not demonstrating reperfusion after administration of streptokinase or in an additional 10 control patients with acute myocardial infarction not evaluated with coronary angiography. These data suggest that (1) coronary arterial thrombus is frequent in acute myocardial infarction and can be lysed by intracoronary streptokinase; (2) reperfusion with intracoronary streptokinase in acute myocardial infarction results in improved left ventricular performance between admission and hospital discharge.     

A comparison of hemodynamic and angiographic indices of left ventricular performance in patients with coronary artery disease

We compared ejection fraction, left ventricular end-diastolic pressure, cardiac index and the relation of left ventricular stroke work index to left ventricular end-diastolic pressure during rest and exercise in 60 patients with coronary artery disease. Left ventricular end-diastolic pressure was usually normal at rest (48/60) and abnormal during exercise (46/60) and did not correlate with ejection fraction. Cardiac index was insensitive, usually remaining normal until ejection fraction was less than 0.40. Patients with a normal left ventricular stroke work index response to exercise had higher ejection fractions than those with an abnormal response (p is less than 0.05). However, 9 patients with normal ejection fractions had an abnormal exercise response. This may reflect loss of left ventricular reserve, abnormal compliance or clinically silent ischemia during exercise. Different indices of left ventricular performance may be widely disparate in coronary artery disease, and abnormalities are frequently apparent only during exercise.     

Response of the left ventricle in coronary artery disease to postextrasystolic potentiation.

Left ventricular volumes and contractile patterns were evaluated during the first sinus beat after a compensatory pause resulting from ventricular arrhythmia and were compared to the second sinus beat (control beat) in order to evaluate the effect of postextrasystolic potentiation. Twelve patients had no evidence of heart disease (group I). Fifty patients had coronary artery disease and included 14 patients (group IIa) with no prior myocardial infarction and a normal left ventricular contractile pattern and 19 pateints (group IIb) with an abnormal contractile pattern. Seventeen pateints (group IIc) had a documented transmural myocardial infarction as well as an abnormal left ventricular contractile pattern. In all patients the first postextrasystolic sinus beat, when compared to the second sinus beat, demonstrated increases in stroke volume and ejection fraction and decrease in end-systolic volume. There were no qualitative changes in the contractile pattern in the immediate postextrasystolic beat in the patients with normal left ventricular function. In both group IIb and group IIc the changes in end-systolic volume, stroke volume and ejection fraction were significantly greater than observed in groups I and IIa. Abnormal wall segments present in the control beat in groups IIb and IIc demonstrated after postextrasystolic potentiation a normal contractile pattern, improved pattern or no change when compared to the control beat. Abnormal wall segments were more likely to revert to normal as a result of postextrasystolic potentiation in group IIb than group IIc. Akinesia was less likely to revert completely to normal than hyposinesia. In 20 of 24 patients the changes in contractile pattern after aortocoronary bypass surgery corresponded to those observed as a result of postextrasystolic potentiation.     

Right ventricular systolic and diastolic function at rest in patients with coronary artery disease. Assessment with equilibrium radionuclide ventriculography

Right ventricular systolic and diastolic function was studied in patients with ischemic heart disease using equilibrium radionuclide ventriculography. In patients with inferior myocardial infarction and proximal right coronary lesions, the right ventricular ejection fraction (0.43 +/- 0.06, n = 10, mean +/- SD) and peak filling rate (1.7 +/- 0.4 EDV/sec) were lower than normals (0.57 +/- 0.07 and 2.7 +/- 0.4 EDV/sec, n = 10, p less than 0.001, respectively). In these patients, the right ventricular time to peak filling rate was longer than in normals (225 +/- 36 msec vs 136 +/- 45 msec, p less than 0.001), while the left ventricular ejection fraction remained normal. In patients with inferior myocardial infarction and distal right coronary lesions, the right ventricular ejection fraction, peak filling rate and time to peak filling rate were not different from those in normals. Even in patients with proximal right coronary lesions, the right ventricular ejection fraction was normal unless they had an inferior myocardial infarction. A decreased left ventricular ejection fraction and abnormal motion of the ventricular septum did not affect the right ventricular ejection fraction. The present results suggest that patients with an inferior myocardial infarction and proximal right coronary lesion often develop right ventricular systolic and diastolic dysfunction.