Citations

Two hundred seventy-one patients with unequivocal systemic scleroderma for whom the diagnosis was first established at the Mayo Clinic between January 1, 1945, and December 31, 1952, have been studied. Follow-up information was obtained 5 to 13 years after the diagnosis at the clinic concerning 236 of these patients, 115 of whom were dead. The cases were analyzed in an effort to determine what factors had a bearing on prognosis. The following seemed to bear little relation to the ultimate prognosis: sex, mode of onset, Raynaud's phenomenon, involvement of lungs and periodontal membrane, calcinosis cutis, and trophic changes. The following were considered poor prognostic omens: cardiac or renal involvement, significant elevation of the erythrocyte sedimentation rate, and anemia. The prognosis in systemic scleroderma was found to be worse than previous reports had indicated. This study yielded no basis for the subdivision of systemic scleroderma into acrosclerosis and generalized progressive scleroderma.

The purpose of this investigation was to study the incidence and location of systemic arterial occlusion and pulmonary embolism in a consecutive series of cases of fatal acute myocardial infarction. Another consecutive series of cases in which healed myocardial infarction was demonstrated at necropsy was similarly studied. In none of the cases included in this study had anticoagulant therapy been employed. Massive pulmonary embolism was the most frequent fatal thrombo-embolic complication found among the cases of acute myocardial infarction. Cerebral infarction was the most frequent fatal thrombo-embolic complication found among the cases of healed myocardial infarction. Cerebral infarction was the most frequent fatal systemic arterial thrombo-embolic lesion in both groups. Acute splenic and renal infarcts were frequently demonstrated but with one exception appeared to play an incidental role in the clinical course of the patients. Although systemic arterial occlusion was frequently found in association with intracardiac mural thrombi, there were many other cases in which evidence of systemic arterial occlusion was found in the absence of intracardiac mural thrombi. A positive correlation existed between the presence of pulmonary and systemic arterial occlusion and the occurrence of congestive cardiac failure.

This is a study of the location and incidence of intracardiac thrombi in acute and in healed myocardial infarction. In myocardial infarction intracardiac thrombi occur predominantly in the left ventricle. Anterior myocardial infarcts are more commonly associated with mural thrombi than posterior myocardial infarcts. Large myocardial infarcts and congestive failure are factors which predispose to the formation of left ventricular mural thrombi in myocardial infarction.

Congenital insufficiency of the pulmonary valve may result if the valvular cusps develop faultily or fail to develop. It is commonly associated with ventricular septal defect, with or without pulmonary stenosis. Under these conditions a continuous precordial murmur may be present. Less commonly, congenital pulmonary valvular insufficiency may appear as an isolated cardiac malformation.

Because of reports that derivatives of Rauwolfia serpentina may cause severe mental depression when used in the treatment of hypertension, the depressive reactions and possible contributing factors were studied in a group of 387 hypertensive patients. Some of the patients received no specific antihypertensive medication; some were treated with Rauwolfia derivatives alone and some with Rauwolfia and other antihypertensive drugs. Of the patients receiving Rauwolfia, alone or with other drugs, 26 per cent experienced depressive reactions whereas only 5 per cent of the others had them.

Nicotinic acid was administered orally to 33 patients with hypercholesterolemia in doses varying from 1.5 to 6.0 Gm. per day for periods of 3 months to 1½ years. Significant, sustained, and reproducible decreases in the concentration of cholesterol and total lipids in the plasma and of serum beta-lipoprotein cholesterol were observed in a majority of patients. This form of therapy appears to be effective, practical, and probably free from serious harmful effects.

In normal subjects smoking or the injection of nicotine produces transient vascular effects on the heart and blood vessels. Apparently tobacco angina or tobacco heart is a clinical entity. Abnormal vascular responses after smoking in normal subjects may be due to hypersensitivity to nicotine, such as occurs in tobacco heart, or to the effect of nicotine on a vascular system demonstrated to be hyperreactive by the cold pressor test. Tobacco is one of the most prominent contributing factors in thromboangiitis obliterans, as thromboangiitis is rarely found in nonsmokers. The question as to whether the effects of smoking are due to sudden increased work of the heart or constriction of the coronary artery has stimulated a great amount of research. There is evidence to support both theories. The findings of abnormal ballistocardiograms before and after smoking in the offspring of hypertensive parents and after smoking in the offspring of parents with coronary heart disease are highly important. Statistically coronary artery disease seems to occur more frequently and at an earlier age in the person who smokes much than in the nonsmoker. Likewise, the mortality rate is higher among younger persons with coronary disease who are smokers than among those who are nonsmokers.

Considerable variation exists in the interplay of the factors influencing the occurrence of strokes and their final outcome. A final statement about the usefulness of anticoagulant drugs in the treatment of cerebrovascular disease must await further study. The current indications for their use include: (1) intermittent insufficiency of the basilar arterial system, (2) intermittent insufficiency of the internal carotid system, (3) thrombosis within the basilar arterial system, (4) recurrent cerebral emboli associated with a likely cardiac source and (5) possibly, recurrent cerebral thromboses.

Background —Patients with treated diabetes in the randomized-trial segment of the Bypass Angioplasty Revascularization Investigation (BARI) who were randomized to initial revascularization with PTCA had significantly worse 5-year survival than patients assigned to CABG. This treatment difference was not seen among diabetic patients eligible for BARI who opted to select their mode of revascularization. We hypothesized that differences in patient characteristics, assessed and unmeasured, together with the treatment selection in the registry, at least partially account for this discrepancy. Methods and Results —Among diabetics taking insulin or oral hypoglycemic drugs at entry, angiographic and clinical presentations were comparable between randomized and registry patients. However, more registry patients were white, and registry diabetics tended to be more educated and more physically active and to report better quality of life. Procedural characteristics and in-hospital complications were comparable. The 5-year all-cause mortality rate was 34.5% in randomized diabetic patients assigned to PTCA versus 19.4% in CABG patients ( P =0.0024; relative risk [RR]=1.87); corresponding cardiac mortality rates were 23.4% and 8.2%, respectively ( P =0.0002; RR=3.10). The CABG benefit was more apparent among patients requiring insulin. In the registry, all-cause mortality was 14.4% for PTCA versus 14.9% for CABG ( P =0.86, RR=1.10), with corresponding cardiac mortality rates of 7.5% and 6.0%, respectively ( P =0.73; RR=1.07). These RRs in the registry increased to 1.29 and 1.41, respectively, after adjustment for all known differences between treatment groups. Conclusions —BARI registry results are not inconsistent with the finding in the randomized trial that initial CABG is associated with better long-term survival than PTCA in treated diabetic patients with multivessel coronary disease suitable for either surgical or catheter-based revascularization.