Rene A. Langou

Multiple gated cardiac blood pool imaging for left ventricular ejection fraction: Validation of the technique and assessment of variability

The intrinsic variability and accuracy of left ventricular ejection fraction determined by multiple gated cardiac blood pool imaging was evaluated in 83 patients. Ejection fraction by gated studies correlated well with data from first pass radionuclide angiocardiography (r = 0.94) and from contrast angiography (r = 0.84). Intra- and interobserver variabilities of absolute ejection fraction were minimal (mean +/- standard deviation 1.4 +/- 1.2 and 1.6 +/- 1.5 percent, respectively) and were not different for normal (ejection fraction 55 percent or greater) and abnormal patients. Ejection fraction was determined twice in 70 patients: on the same day at intervals separated by 1 to 2 hours (41 patients) and on 2 different days (29 patients). Ejection fraction ranged from 18 to 91 percent and was normal in 37 patients. There was no difference in mean serial variabilities of absolute ejection fraction for all repeat studies performed on the same and separate days (3.3 +/- 3.1 versus 4.3 +/- 3.1 percent (not significantly different). The mean variability of absolute ejection fraction for repeat studies in normal patients was significantly greater than in abnormal patients (5.4 +/- 4.4 versus 2.1 +/- 2.0 percent, P less than 0.01). The incidence rate of absolute interstudy changes of 5 percent or more was significantly higher in normal than in abnormal patients (P less than 0.01). This differential variability should be considered in interpreting sequential changes in left ventricular ejection fraction. To be attributed to nonrandom physiologic alterations, the absolute change in ejection fraction should be 10 percent or more in normal patients and 5 percent or more in abnormal patients.

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

Abstract 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 −1 to 6.53 ± 0.42 sec −1 (p 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 −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 −1 to 3.67 ± 0.39 sec −1 (p

Left Ventricular Filling in Differentiating Restrictive Amyloid Cardiomyopathy and Constrictive Pericarditis

Abstract Left ventricular filling was evaluated with use of digitized left ventriculograms in patients with (1) restrictive amyloid cardiomyopathy, (2) constrictive pericarditis, and (3) a normal heart. Restrictive cardiomyopathy (four patients) was established by right and left heart hemodynamic studies and postmortem examination; all four patients had cardiac amyloidosis. Constrictive pericarditis (seven patients) was established by characteristic right and left heart catheterizatlon data and pericardial disease at operation; four patients had calcific and three had noncalcific anatomic changes. Normal subjects (seven patients) had normal intracardiac pressures and normal findings on left ventriculography and coronary arteriography. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume and ventricular filling rate were constructed for each patient and also for each group. Patients with restrictive amyloid cardiomyopathy had no plateau in the diastollc left ventricular filling volume curve, and their left ventricular filling rate was slower than normal during the first half of diastole. Patients with constrictive pericarditis had a sudden and premature plateau in the diastolic left ventricular volume filling curve. In addition, the left ventricular filling rate was faster than normal during the first half of diastole. Statistical analysis of left ventricular filling rate in patients with restrictive amyloid cardiomyopathy, patients with constrictive pericarditis and normal patients showed significant differences during the first half of diastole; those with restrictive amyloid cardiomyopathy had 45 ± 4 percent, those with constrictive pericarditis had 85 ± 4 percent and normal subjects had 65 ± 5 percent of left ventricular filling completed at 50 percent of diastole (p Thus, this study showed a significantly different profile of diastolic left ventricular filling volume and ventricular filling rate curves during the first half of diastole in patients with restrictive cardiomyopathy and those with constrictive pericarditis. The findings suggest the importance of these determinations in differentiating restrictive amyloid cardiomyopathy and constrictive pericarditis at cardiac catheterization.

Predictive accuracy of coronary artery calcification and abnormal exercise test for coronary artery disease in asymptomatic men.

To determine the predictive accuracy of fluoroscopically detected coronary artery calcification (CAC) and a positive submaximal exercise test, 129 asymptomatic men were screened; 13 had both coronary artery calcification and positive exercise test (≥ 1.0 mm ST-segment depression). These 13 men were studied at coronary arteriography. They had a mean age of 44 years (range 41–56 years); none had history or symptoms of heart disease and all had normal resting ECGs at entry.CAC was detected in one artery in 10 men, in two arteries in two men, and in three arteries in one man. Coronary artery disease (CAD) was considered clinically significant if any major coronary branch was narrowed > 50%. Coronary arteriography revealed 12 men with clinically significant CAD (one-vessel CAD in four, two-vessel CAD in five and three-vessel CAD in three men) and one man with minor one-vessel CAD. The predictive accuracy was 100% for minor CAD and 92% for clinically significant CAD. The location of CAC and CAD correlated, but the absence of CAC did not rule out the presence of CAD at coronary arteriography. Furthermore, CAC did not indicate the location of the highest stenotic (most occlusive) lesions seen at arteriography. Follow-up for the 13 patients was 36 months; three patients developed typical angina and one patient developed a transmural myocardial infarction.This study suggests that the predictive accuracy of CAC and a positive exercise test in the middle-aged nonhyperlipidemic asymptomatic male is very high (100% for CAD and 92% for clinically significant CAD) and that CAC and a positive exercise test predict an early appearance of angina or myocardial infarction in previously asymptomatic men.

Cardiovascular manifestations of tricyclic antidepressant overdose

Abstract The cardiotoxicity of tricyclic antidepressants (TCA) was studied in 35 patients admitted to Yale-New Haven Hospital for an acute overdose; 23 patients had amitriptyline overdose and 12 patients had imipramine overdose. Twenty-seven patients were female and eight were male. Their ages ranged from 13 to 73 years. Twenty patients were receiving TCA chronically, and none had prior cardiovascular disorders. Amitriptyline blood levels ranged from 180 to 1,560 ng./ml. and imipramine blood levels ranged from 150 to 1,732 ng./ml. Tachycardia occurred in 71% and systemic hypotension occurred in 51% of patients. The observed tachycardias were not corrected upon normalization of fluid and blood pressure derangements. Systemic hypotension was related to relative intravascular fluid depletion and peripheral vascular dilatation. Myocardial failure was not seen clinically or hemodynamically in studied patients. Electrophysiologic manifestations were those of conduction and repolarization abnormalities: prolonged PR interval in 11%, prolonged QRS complex in 29%, and prolonged QT c interval in 86% of the patients. No malignant ventricular arrhythmias were documented, and only 13 patients had ventricular premature beats, which were successfully suppressed with lidocaine infusions. All cardiovascular manifestations of TCA overdose disappeared when blood levels of TCA reached therapeutic range. Only supportive therapy was utilized in these 35 patients, and all patients recovered without complications.

Late cardiac tamponade after open heart surgery: incidence, role of anticoagulants in its pathogenesis and its relationship to the postpericardiotomy syndrome.

Cardiac tamponade that occurs late after cardiac surgery (7 days) is relatively uncommon but potentially fatal. We analyzed its incidence, clinical course and relationship to the postpericardiotomy syndrome in 1290 consecutive adult patients who survived surgery. Criteria for diagnosis of cardiac tamponade were (1) elevated jugular venous pressure, (2) hypotension or decreased cardiac index, (3) characteristic hemodynamics at cardiac catheterization, and (4) echocardiographic evidence of pericardial effusion.Ten of the 1290 patients (0.8%) developed cardiac tamponade. Surgery was for congenital heart disease in five patients, valvular heart disease in two patients, and coronary artery disease in three patients. The onset of hemodynamic compromise ranged from 15–180 days postoperatively (mean 49 days). All patients had echocardiographic evidence of pericardial fluid, eight had a pericardial friction rub at the time of cardiac tamponade, nine had pericardial pain, and all were considered to have a postpericardiotomy syndrome. One patient was receiving coumadin and two patients were receiving aspirin before the diagnosis of cardiac tamponade. Nine patients underwent pericardiocentesis (0.5–1 1 of fluid). There were no deaths in the group. The syndrome resolved in nine patients with conservative medical therapy and one patient required pericardial stripping for recurrent cardiac tamponade.In this study, cardiac tamponade occurred in 0.8% of patients who survived cardiac surgery; cardiac tamponade occurred in patients without prior anticoagulation, in marked contrast to previously reported cases; pericardiocentesis and conservative medical therapy were successful in treating the majority of patients; clear symptoms and signs of pericardial involvement were present before cardiac tamponade occurred.

Genesis of pericardial knock in constrictive pericarditis

A pericardial knock is a common finding in constrictive pericarditis. However, its origin has been uncertain. One hypothesis suggests that it is due to sudden deceleration of ventricular filling. To validate this hypothesis, left ventriculograms, phonocardiograms and external pulse recordings were obtained in seven patients with hemodynamic and pathologic findings of constrictive pericarditis and in seven normal subjects. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume versus diastolic filling time were constructed for each patient. Pericardial knock was recognized as an early high frequency sound recorded between 90 to 120 ms after the aortic closing sound and occurring at the trough of the Y descent of the jugular venous pressure tracing. The timing of the pericardial knock in five patients with constrictive pericarditis corresponded to a sudden and premature plateau of the diastolic left ventricular volume curve representing 85 +/- 4 percent (mean +/- standard deviation) of ventricular filling. The diastolic plateau was missing in two patients with constrictive pericarditis who had no pericardial knock. In these cases, the rate of ventricular filling was faster than normal in the first 20 percent of diastole. Thus, this study related pericardial knock to an abrupt plateau inthe diastolic left ventricular volume curve, supporting the view that sudden cessatin of ventricular filling generates the pericardial knock of constrictive pericarditis. Two mechanisms are proposed by which the filling plateau may produce the knock, and it is postulated that both ventricles may participate in the knock phenomenon.

Retrograde left ventricular catheterization in patients with an aortic valve prosthesis.

Twenty-seven consecutive patients with an aortic valve prosthesis were evaluated with retrograde left ventricular catheterization. The prosthesis was successfully crossed, permitting hemodynamic and angiographic evaluation of function of the prosthetic valve, left ventricle and mitral valve in all 27 cases. No complications were encountered. In patients with active endocarditis or recent embolization, the retrograde technique was avoided when possible, and attempts were made to utilize other techniques for study. However, three such patients were evaluated with the retrograde technique without complication. Examination of pressure tracings and cineangiographic films suggested only minor interference with valve poppet movement induced by the catheter transversing the valve. In three cases, hemodynamic data were recorded with the catheter crossing the prosthesis at one time and a paraprosthetic valve defect at another time. Identical gradients were recorded. This series documents the safety and efficacy of the retrograde approach, which is proposed as an alternative to the transseptal technique and left ventricular puncture.

Surgical approach for patients with unstable angina pectoris: role of the response to initial medical therapy and intraaortic balloon pumping in perioperative complications after aortocoronary bypass grafting.

Abstract The role of the response to initial medical therapy and intraaortic balloon pumping in perioperative complications was evaluated in 194 consecutive patients with unstable angina pectoris who underwent cardiac catheterization and coronary surgery from July 1975 through December 1977. Sixty-four patients (33 percent) responded to medical therapy within 48 hours after the initiation of full medical therapy in the coronary care unit and underwent elective cardiac catheterization and coronary surgery; 130 patients (67 percent) did not respond to medical therapy. Of these 130 patients, 75 (58 percent) received the preoperative assistance of an intraaortic balloon pump and underwent emergency cardiac catheterization and surgery. Fifty-five patients (42 percent) of the medical non-responders were not treated with an intraaortic pump and underwent emergency cardiac catheterization and surgery. Chi square analysis revealed that the clinical characteristics of the patients in all three groups were similar. The overall rate of operative mortality was 6.1 percent. Medical responders had no operative mortality, medical nonresponders with intraaortic balloon pumping had an operative mortality rate of 5.3 percent and medical nonresponders without balloon pumping a rate of 14.5 percent. The overall incidence rate of perioperative myocardial infarction was 13 percent; it was 6 percent in medical responders, 6.6 percent in nonresponders with intraaortic balloon pumping and 29 percent in non-responders without intraaortic balloon pumping. Thus, this study suggests that perioperative complications can be minimized by initial aggressive medical therapy. If this therapy fails, intraaortic balloon counterpulsation can produce a reduction in perioperative complications similar to that produced by medical therapy.

Prolonged benefit of nitroglycerin ointment on exercise tolerance in patients with angina pectoris

Abstract The effect on exercise tolerance of 2 per cent nitroglycerin ointment and placebo was studied on the bicycle ergometer in 10 patients with angina pectoris, a positive exercise test, and documented coronary artery disease. After a control stress test sufficient to produce angina pectoris and > 1 mm. horizontal or downsloping ST segment depression, nitroglycerin ointment or placebo was administered in a random, double-blinded manner and stress tests were repeated at 1 hour and 3 hours. End points for the exercise stress test were angina and 1 mm. ST segment depression. Forty-eight hours later, stress tests were again performed at 1 hour and 3 hours after administration of the alternate preparation. Work load (watts) plus duration of exercise (minutes) were calculated for each stage of the bicycle ergometer protocol and exercise tolerance was expressed as the sum of this product for all stages completed. Nitroglycerin ointment produced a significant increase in exercise tolerance from a control value of 877 ± 129 watt-minutes to 1165 ± 173 watt-minutes at 1 hour and 1040 ± 137 watt-minutes at 3 hours. Duration of exercise also increased significantly after nitroglycerin ointment from 13.7 ± 1.4 minutes in the control stress test to 16.8 ± 1.4 minutes at 1 hour and 16.3 ± 1.2 minutes at 3 hours. Exercise induced ST segment depression decreased significantly at 1 hour and 3 hours after nitroglycerin ointment but not after the placebo. The placebo produced a small, but statistically significant, increase in exercise tolerance and duration of exercise at 1 hour after its application. However, these increases were significantly smaller than the one observed after nitroglycerin ointment. No changes were observed 3 hours after application of the placebo. Double product at peak exercise was unchanged after nitroglycerin or placebo ointments at 1 hour and 3 hours. These data indicate that nitroglycerin ointment is capable of producing an improvement in exercise tolerance and a reduction in the magnitude of exercise-induced ST segment depression up to 3 hours in patients with coronary artery disease and angina pectoris.