Sinus node dysfunction during coronary vasospastic angina.
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Biomedical subjects
Publications and source records attributed to T O Cheng.
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Marked pulsus alternans was observed in a patient with primary congestive cardiomyopathy. Afterload reduction with amyl nitrite caused the disappearance of the pulsus alternans. Investigation by phonocardiography, echocardiography, systolic time interval measurement and cardiac catheterization disclosed that during pulsus alternans the weak beat originated following a short diastolic filling period and generated much lower contractile force. This report may be relevant to the currently accepted concepts of afterload reduction in the treatment of chronic congestive heart failure.
Sixty-six patients with pulmonic valvular stenosis were evaluated by cardiac catheterization and cine-angiography over the past four years in a recently established cardiovascular center in Syria. Patients were divided according to severity of pressure gradient across the pulmonic valve into three groups: Group I (25 patients) had gradients below 50 mm. Hg, Group II (14 patients) had gradients between 50 and 100 mm. Hg, and Group III (27 patients) had gradients exceeding 100 mm. Hg. Clinical symptoms and signs including dyspnea on exertion, palpitation, cyanosis, and characteristics of the murmur and the pulmonic second sound were correlated with severity and grouping along with electrocardiographic and radiographic findings. Valvulotomy was carried out in 23 patients (35%). Short term clinical results were excellent in 19 patients, but long term course of the non-operated and post-operative cases is yet to be established.
Twenty-eight cases of double-outlet right ventricle (DORV) were found from 1975 to 1980 in the Shanghai Chest Hospital. On plain films, four types of abnormal heart configuration were found: mitral, boot-shaped, atypical, and bizarre. The main angiocardiographic findings were: (1) simultaneous visualization of aorta and pulmonary artery on right ventriculography, both arising from the right ventricle; (2) D- or L-type of aortic transposition in most; (3) the two semilunar valves at approximately the same horizontal level; (4) an infundibulum present below the semilunar valve; (5) ventricular septal defect; and (6) associated pulmonary stenosis and/or other anomalies. An anatomic-radiologic classification was suggested and based chiefly on symbolic representation of segmental combinations including visceral trial situs, type of cardiac loop, relation between the semilunar valves, presence or absence of pulmonary stenosis and whether the ventricular septal defect was subpulmonary or not. The findings substantiated the viewpoint that in DORV there exists on embryologic and pathologic ground transitional changes ranging from those closely resembling tetralogy of Fallot to complete transposition of the great vessels.
Coronary artery spasm was virtually unknown not long ago, but the intense, ongoing interest it has generated in the past decade has produced a number of specific diagnostic techniques and therapeutic approaches, as well as considerable insight into mechanisms of coronary vascular tone and various coronary syndromes. There is growing evidence that coronary artery spasm is involved in unstable angina, stable angina, myocardial infarction, and sudden death. It is by no means a benign process and is associated with significant morbidity or mortality if misdiagnosed or untreated. It seems clear that what started as a mere clinical curiosity involving a minority of patients with the so-called Prinzmetal's variant angina is snowballing into a major arena for research, diagnosis, and treatment in the field of ischemic coronary artery disease.
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A 19-year-old male was found to have combined supravalvular aortic stenosis and hypertrophic subaortic stenosis. Two possible hypotheses with supportive evidence in the literature may explain this association: (1) long-standing fixed supravalvular aortic stenosis may result in secondary hypertrophic subaortic stenosis, and (2) infantile hypercalcemia, a condition closely related to supravalvular aortic stenosis, may also be involved by continuous inotropic stimulation in the pathogenesis of muscular hypertrophy and subaortic stenosis of the left ventricle. We tend to favor the second theory in light of recent evidence in the literature.
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