Click in the neck--unusual presentation of mitral-valve prolapse.
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Biomedical subjects
Publications and source records attributed to A Benchimol.
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With use of the Doppler ultrasonic flowmeter catheter, phasic aortocoronary bypass graft blood velocity was measured in 16 conscious subjects during ventricular arrhythmias. Ventricular extrasystoles reduced peak systolic and diastolic graft blood velocities by 20 to 80 percent, generally in relation to their respective coupling intervals. When extrasystoles appeared in closely coupled salvos diastolic bypass blood velocity virtually ceased. Nineteen episodes of ventricular tachycardia produced an average 50 percent decrease in peak graft blood velocity (control mean +/- 1 standard deviation blood velocity 28 +/- 11 cm/sec; value during ventricular tachycardia 14 +/- 8 cm/sec, P less than 0.001). An "overshoot" of peak blood velocity was observed after ventricular extrasystoles and tachycardia. All such changes in aortocoronary bypass blood velocity related to tachyarrhythmia were more prominent during the systolic fraction of flow. It is concluded that (1) ventricular arrhythmias adversely influence aortocoronary bypass graft function, and (2) this finding supports an aggressive approach to the treatment of these arrhythmias in subjects with bypass grafts.
With the use of a Doppler flowmeter catheter, phasic instantaneous aortocoronary saphenous vein bypass graft blood velocity was continuously measured during the inhalation of amyl nitrite in 20 closed-chest conscious subjects. Administration of amyl nitrite augmented peak diastolic and systolic graft blood velocity within 10 seconds and maximal blood velocities were recorded between 8 and 60 seconds after inhalation. Control mean (+/- 1 S.D.) bypass graft blood velocity was 25 +/- 10 cm. per second and after amyl nitrite 46 +/- 14 cm. per second, resulting in an average 84 per cent rise of blood velocity. It is concluded that amyl nitrite increases aortocoronary bypass graft blood velocity, suggesting a possible enhancement of blood flow to the distal native circulation in patients so operated upon.
One hundred patients, 17 to 67 years of age, had normal hearts diagnosed on the basis of complete right and left heart catheterization and coronary cineangiography. Phonocardiograms were obtained from each patient, providing an average of 17 recordings per subject for analysis; 75/100 (75%) subjects had a recordable fourth sound; 60/75 (80%) of the latter group had an audible fourth heart sound. It is concluded that recordable and audible fourth heart sounds are common findings in subjects without catheterization evidence of cardiovascular disease.
Echocardiography was performed in 28 consecutive patients who manifested accepted criteria for left ventricular hypertrophy on their electrocardiograms. Four groups of patients were identified: Group 1, nineteen (68%) who had an increase in both interventricular septal and left ventricular posterior wall thickness; Group 2, three patients (11%) with isolated enlargement of the left ventricular internal dimension; Group 3, two subjects (7%) with increased septal thickness, left ventricular posterior wall thickness and left ventricular internal dimension and Group 4, four patients (14%) with normal echocardiographic measurements. It is concluded that increases in both septal and left ventricular wall thickness are the primary echocardiographic correlates of left ventricular hypertrophy as diagnosed on the electrocardiogram.
Six highly trained marathon runners developed myocardial infarction. One of the two cases of clinically diagnosed myocardial infarction was fatal, and there were four cases of angiographically-proven infarction. Two athletes had significant arterial disease of two major coronary arteries, a third had stenosis of the anterior descending and the fourth of the right coronary artery. All these athletes had warning symptoms. Three of them completed marathon races despite symptoms, one athlete running more than 20 miles after the onset of exertional discomfort to complete the 56 mile Comrades Marathon. In spite of developing chest pain, another athlete who died had continued training for three weeks, including a 40 mile run. Two other athletes also continued to train with chest pain. We conclude that the marathon runners studied were not immune to coronary heart disease, nor to coronary atherosclerosis and that high levels of physical fitness did not guarantee the absence of significant cardiovascular disease. In addition, the relationship of exercise and myocardial infarction was complex because two athletes developed myocardial infarction during marathon running in the absence of complete coronary artery occlusion. We stress that marathon runners, like other sportsmen, should be warned of the serious significance of the development of exertional symptoms. Our conclusions do not reflect on the possible value of exercise in the prevention of coronary heart disease. Rather we refute exaggerated claims that marathon running provides complete immunity from coronary heart disease.
Echocardiography was performed in 25 consecutive patients with angina pectoris and angiographically demonstrable coronary artery disease. Left ventricular echograms detected late or pansystolic mitral valve bowing suggesting of mitral valve proplapse in 6/25 (24%). Left ventricular angiography showed prolapse of the posterior mitral leaflet in 15/25 (60%), including 5 detected by echocardiography. Significant triple vessel coronary disease was present in 11 of 15 patients with prolapsed mitralvalve. In each of the latter a greater than 90 per cent obstructive lesion was noted in at least one coronary artery: right coronary artery, 9 subjects (82%); left circumflex coronary artery, 5 patients (33%); and left anterior descending coronary artery, 4 patients (27%). Of 15 subjects with angiographic evidence of mitral valve prolapse, 13 had left ventricular asynergy-inferior or inferoposterior in 8 subjects (62%) and anterior or anteroapical in 5 subjects (38%). Eleven subjects had vectorcardiographic evidence of transmural myocardial infarction-inferior or inferoposterior in 9 (82%) and anteroseptal in 2 (18%). A single subject with mitral valve prolapse had mild mitral regurgitation. It is concluded that: (1) coexisting prolapse of the posterior mitral valve leaflet and coronary artery disease is usually associated with triple vessel obstructive lesions, (2) severe right coronary disease, inferior left ventricular wall asynergy, and inferior myocardial infarction are important angiographic and vectorcardiographic correlates, and (3) echocardiography will detect such mitral valve prolapse in only one-third of affected cases.
A 54-year-old woman underwent replacement of a thrombosed Björk-Shiley aortic valve prosthesis. Post operative electrical defibrillation resulted in isolated T wave alternation which progressed to total QRS-T electrical alternans. This report represents the first description of such a phenomenon.
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Pre- and postoperative hemodynamic indices were compared in 116 patients subjected to aorto-coronary bypass after an average interval of 128 days. The patients were separated into three different groups according to graft status: Group 1 (n = 77), all grafts patent; Group 2 (n = 27), one occluded graft out of two or three implanted; Group 3 (n = 12), all grafts occluded. There were no significant major changes of values so obtained in the three groups. Those subjects with initially depressed cardiac indices or elevated left ventricular end-diastolic pressures manifested a significant trend toward improvement when at least one bypass graft was patent. A reduction of cardiac index was noted in patients with occluded left anterior descending coronary grafts only in association with closure of other grafts. Deterioration of cardiac index or left ventricular end-diastolic pressure into the abnormal range was unusual in the study group, even when all grafts were occluded. It is concluded that data relating to the influence of aorto-coronary bypass on standard indices of left ventricular function can be properly interpreted only when certain subsets of patients are studied.
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Electrocardiograms and Frank vectorcardiograms were recorded in 156 consecutive patients with total occlusion of at least one coronary artery (on arteriography) and associated left ventricular contraction abnormality (on ventriculography). The angiograms and cardiograms were independently reviewed. In the presence of single vessel occlusion, appropriate vectorcardiographic diagnosis of myocardial infarction was determined in 118 of 156 cases (76 percent) compared with a lower electrocardiographic detection rate in 77 of 156 cases (49 percent). Findings diagnostic of two coexisting infarctions were observed in 71 percent of vectorcardiograms and 37 percent of electrocardiograms in 51 patients with double vessel occlusion and two areas of left ventricular dyskinesia. The vectorcardiographic detection rate was similarly superior to the electrocardiographic rate in the presence of subtotal coronary occlusion and myocardial asynergy in single (73 percent versus 53 percent) and double (53 percent versus 28 percent) vessel disease. The incidence rate of false positive diagnoses was 3 percent for electrocardiography and 4 percent for vectorcardiography. It is concluded that the vectorcardiogram is superior to the electrocardiogram in the diagnosis of obstructive coronary artery disease and left ventricular contraction abnormality.