A long-term retrospective analysis of 248 patients, 11-25 years after surgical correction of coarctation of the aorta, revealed a high incidence of premature cardiovascular disease. Twelve percent of patients with follow-up have died. It is suggested that premature death in patients with adequate surgical repair may be related to the duration of preoperative hypertension. Fifty-nine patients were evaluated on a standard hospital protocol. Seventy-eight percent had evidence of cardiovascular disease and over 40% had no change or had increased blood pressure over the preoperative value. These data emphasize the importance of early diagnosis and treatment for patients with coarctation of the aorta as well as the need for close postoperative follow-up.

Patients who survive an acute myocardiac infarction (AMI) have significant coronary disease and are at risk for angina pectoris, recurrent myocardiac infarction and sudden death. This study provides data gathered prospectively for 106 patients surviving myocardial infarction who had coronary arteriography, left ventriculography and 24-hour electrocadiographic recordings before hospital discharge and were followed 30 months. Univariate analysis showed that low ejection fraction, proximal left anterior descending coronary disease and significant disease in all three coronary arteries were associated with a high risk of sudden cardial death. The ECG location or type of infarction was not helpful in predicting mortality, reinfarction or continuing angina. Multivariate analysis of 30 clinical and laboratory variables identified previous myocardial infarction and an ejection fraction less than 40% as the best predictors of mortality; all 13 patients who died were identified by these two variables. Three-vessel coronary artery disease, proximal left coronary disease and complicated late hospital-phase ventricular arrhythmias did not provide additional information about mortality once the information provided by the first two variables was considered. Multivariate analysis identified hypertension, three-vessel coronary disease, postinfarction angina pectoris and previous AMI as significant predictors of recurrent AMI during the 30 month follow-up.

Mitral regurgitation can result from a variety of anatomical and functional abnormalities and can be the consequence of several disease processes. Clinical recognition of the etiology is most often based on the history, while the functional anatomy of the lesion can occasionally be predicted by certain auscultatory findings. This paper describes a unique anatomical type of mitral regurgitation, recognized cine-angiographically, which occurs in association with a murmur in the latter part of systole or marked accentuation of a soft holosystolic murmur in late systole. Correlations of the cine-angiograms with phonocardiograms have provided a functional anatomical basis for the late onset of the murmur as well as the systolic click which was present in 3 of the patients. SUBJECTS AND METHODSFive patients, ages 5 to 56, were studied because of the presence of a late systolic murmur (Table I). These patients were selected from a list of 79 patients on file in the Heart Sound Laboratory, who had systolic murmurs beginning after the onset of systole and extending to the second heart sound. Spectral and oscillographic phonocardiograms (McKusick, 1958), right and left heart catheterization, and selective 60-frame per second cine-angiography were performed on each patient. At the time of cine-angiography, correlations of pressures, phonocardiograms, and motion of intracardiac structures were made possible by the use of an electrocardiographic R wave marking device in the x-ray field (Ross, Criley, and Morgan, 1961 CASE REPORTS Case 1. J. M., a 39-year-old Caucasian man, had "growing pains" at the age of 9 but no clearly defined episode of rheumatic fever. At the age of 20 a murmur was heard during an induction physical examination, and he was accepted into the service only after repeated examinations indicated that the murmur was probably functional. He subsequently engaged in combat without any symptoms of heart disease. Because of slight exertional dyspncea, fatigue, chest discomfort, and the presence of a murmur, he was referred for evaluation. His symptoms had begun insidiously 3 years before, 11 years after discharge from the Army. On examination the heart was not enlarged and the heart sounds were of normal quality. A grade 3/6 systolic murmur, beginning abruptly after a quiet interval in early systole, was heard maximally at the apex, but transmitted well to the left sternal border, base, and neck vessels. The electrocardiogram showed a wandering atrial pacemaker, diphasic T waves in lead II, inverted T waves in lead III, peaked T waves in leads V3-6, and no evidence of chamber hypertrophy. Chest radiography and fluoroscopy were normal. A phonocardiogram demonstrated low amplitude vibrations in early systole with a striking accentuation 0-12 sec. after the first sound and continuing to the second sound. Right and left heart catheterizations were performed, and the pressures in all chambers were normal. Left ventricular cine-angiograms in the left anterior oblique (LAO) and right anterior oblique (RAO) projections (...

The severity of the atherosclerotic disease of the coronary arteries is demonstrated to be an important predictor of survival in a group of 224 patients followed from 5 to 12 years after coronary arteriography. The group consisted of young patients (average age 41.8 years) without hypertension or congestive heart failure, who were studied during the stable phase of their disease. The current status of 218 or 97% of this group of patients is known.

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