Citations

Eighteen patients with the combination of ventricular septal defect and aortic insufficiency were studied. Nine also had infundibular pulmonary stenosis. Seventeen were treated by open-heart operations. The physical findings were those of a typical ventricular defect murmur and thrill together with an aortic insufficiency blow and a wide pulse pressure. A systolic murmur at the upper left sternal border with thrill is strongly suggestive of the additional lesion of infundibular pulmonary stenosis, but the presence or absence of infundibular pulmonary stenosis was indicated most accurately at cardiac catheterization and on inspection at operation. It was not of sufficient severity for signs of additional right ventricular hypertrophy to appear on the electrocardiogram. Retrograde aortography serves to demonstrate the severity of the aortic regurgitation. The problem of the surgical correction of these lesions will be the subject of a separate communication.

The problem of spontaneous calcific embolization was investigated at necropsy in 165 patients with calcific aortic stenosis. Minor coronary arteries contained calcific emboli in 18 patients (11 per cent), and major coronary arteries contained calcific emboli in 10 (6 per cent). Examination of the brain, kidney, and eye also disclosed spontaneous calcific emboli. In three instances of major coronary artery embolization, there was evidence of old silent infarction but no associated clinical disorder. Calcific embolization is apparently not rare in cases of calcific aortic stenosis, but this phenomenon does not appear to lead very often to extensive infarction or to clinically obvious disorders.

Physiologic observations were made on eight patients following repair of atrial septal defect or total anomalous pulmonary venous connection. A pattern of changes in cardiac output and atrial pressures during the first 3 postoperative days was noted. Cardiac output was abnormally low in some patients with obstructive pulmonary vascular disease or low atrial pressures. Transfusion of whole blood was effective in elevating cardiac output in the operating room and after operation. Left atrial pressure was higher than right atrial pressure in the operating room. Postoperatively left and right atrial pressures tended to become equal in some patients, and the levels were slightly elevated. Heart rate did not seem to be directly related to cardiac output. Ventilation was adequate with regard to elimination of carbon dioxide. Arterial oxygen saturation was maintained at 93 per cent or more by the use of oxygen-enriched mixtures. The difference in arteriovenous oxygen content was inversely related to cardiac output. Acidemia was present 2 to 4 hours after operation, but in general the pH of arterial blood had returned to normal by day 2. Some mechanisms possibly related to the observations are discussed.

Among 13,314 necropsies following death from neoplastic and nonneoplastic diseases performed at the Mayo Clinic from 1942 through 1958, 189 cases of secondary malignant lesions of the pericardium were demonstrated, an incidence of 1.42 per cent. Carcinoma of the lung and breast, the lymphomas, and leukemia constituted the large majority of the primary malignant lesions that caused the pericardial metastasis. Fifty-five of the 189 patients were adjudged to have had some impairment of cardiac function as a consequence of the pericardial metastasis and the following conclusions concern this group. 1. In 47 patients (86 per cent), the lesions were either the immediate or a contributory cause of death. 2. The most common mechanism whereby metastatic lesions in the pericardium interfered with cardiac function was by the development of pericardial effusion. Next in frequency was effusion combined with myocardial invasion and then cardiac constriction by tumor. Combinations of these processes with malignant encroachment on the great vessels and with invasion of coronary veins were the other mechanisms noted. Involvement of coronary arteries and the cardiac nerve supply was not noted. 3. Pericardial fluid was significant in causing tamponade in 31 cases. The fluid was frankly hemorrhagic in a small minority of these cases although fibrinous pericarditis was present in 45 (82 per cent) of the group. Pleural effusion was present in 48 (92 per cent) of 52 cases and was usually bilateral. Ascites was present in 22 (50 per cent) of 44 cases; the quantity was usually rather small. 4. Only one patient had metastasis to the pericardium without metastasis to other thoracic structures; exclusive of patients with leukemia, 43 (92 per cent) of 47 patients had extrathoracic metastatic lesions. 5. Dyspnea, cough, pleural effusion, hepatomegaly, and thoracic pain were the most commonly recorded signs and symptoms that might be related to the pericardial lesions. However, more specific signs and symptoms directing attention to pericardial or cardiac involvement were not commonly recorded. 6. The diagnosis of pericardial metastatic disease was suspected or established in only 16 (29 per cent) of the 55 patients, although 34 (62 per cent) either received treatment for congestive heart failure or were given roentgen therapy to mediastinal structures. 7. Of the 27 patients whose electrocardiograms were available, 25 had T-wave abnormalities, 22 had low QRS voltage, and 15 showed sinus tachycardia. 8. Thoracic roentgenograms, made on 53 patients, supplied clues to the diagnosis of pericardial malignancy in 28.

Of 141 patients with abdominal aortic aneurysms diagnosed at the Mayo Clinic from 1950 through 1959 who were not operated on, follow-up information was obtained from 137 patients (97.1 per cent). Of those followed 1 year or more, 87.6 per cent survived 1 year or more; 52.5 per cent survived 3 years, and 36.4 per cent survived 5 years after diagnosis. These results indicate that the prognosis of abdominal aortic aneurysm in this selected group of patients was somewhat better than that previously reported. The prognosis and survival of patients who had a history of associated cardiovascular disease at the time of diagnosis of aneurysm is distinctly less good than those of patients who had no such history. Of those with such a history, 75.0 per cent survived 1 year, 33.3 per cent survived 3 years, and 20.0 per cent survived 5 years. Of those without such a history 95.7 per cent survived 1 year, 63.2 per cent survived 3 years, and 50.0 per cent survived 5 years. Patients with abdominal aortic aneurysms and associated cardiovascular diseases are more likely to die of cardiovascular complications other than ruptured aneurysms. Patients with abdominal aortic aneurysms who have no evidence of associated cardiovascular disease are more likely to die from a ruptured aneurysm than from anything else. It would appear that small asymptomatic abdominal aortic aneurysms in patients with associated cardiovascular disease may be carefully observed until signs of expansion of the aneurysm or symptoms from the aneurysm appear.

Closed-chest massage and defibrillation were used successfully in the management of six acute cardiac emergencies occurring in a cardiac catheterization laboratory. A modification of the Kouwenhoven method of closed-chest massage was used in infants and small children. It is concluded that open-chest resuscitation is usually unnecessary during cardiac catheterization.

The records of 66 necropsied cases of periarteritis nodosa in which there was no associated collagen disease were reviewed with reference specifically to the heart. Clinically, congestive heart failure and its manifestations were the most important cardiac findings. Congestive heart failure developed some time during the illness in 57 per cent of the patients, and 44 per cent died as a direct result of this cardiac condition. Myocardial infarction was diagnosed clinically in only three cases. The electrocardiogram was abnormal in 35 of 41 cases but was diagnostic of left ventricular hypertrophy in only six cases and of acute myocardial infarction in only three cases; in the other cases the changes were of a nonspecific nature. Pathologically, 41 of the 66 hearts had evidence of necrotizing arteritis of the coronary arteries; in 39 of these the arteritis had been acute, and in two it had healed. Forty-one of the 66 hearts exhibited myocardial infarcts. Evidence of acute pericarditis was found in 22 hearts; nine of these cases were attributed to uremia, one was due to transmural myocardial infarction, three could not be classified, and the remaining nine were attributed directly to the periarteritis nodosa. Forty-one of the 64 hearts that had been weighed were hypertrophied.