Otto Saphir

Acute isolated myocarditis

Abstract The clinical and pathological observations on two cases of acute isolated myocarditis of undetermined etiology are recorded, together with a tabulation of the pertinent data in thirty similar cases previously reported.

Myocarditis associated with acute nasopharyngitis and acute tonsillitis

Abstract Thirty-five instances of fatal myocarditis atributable to acute nasopharyngeal and tonsillar infections have been reported. The available evidence indicates that these are samples of a not uncommon type of cardiac disease which fortunately has a relatively good prognosis. Further investigation should be carried on to establish fully the etiological agent and the pathogenesis of the lesion. Although the pathologic observations indicated that all patients died of cardiac failure, heart disease was suspected clinically in only three, and in fifteen patients death was unexpected. Significant clinical observations which would seem to be of importance in the recognition of the process were: disproportion of the temperature and pulse rate, hypotension, thready or feeble pulse, and substernal oppression. Cyanosis, dyspnea, and orthopnea occurred frequently. Autopsy findings included significant enlargement of the heart in many cases. The microscopic changes, similar in both nasopharyngeal and tonsillar infections, have been classified in three overlapping groups. In all of these the inflammatory process was observed to be patchy, frequently showing considerable variation in intensity from one area to another and having no predilection for a particular portion of the myocardium. Significant (moderate or marked) degrees of muscle degeneration observed in the diffuse type of myocardial lesion were not present in the interstitial form. The cellular reaction, which was characteristically more intense than that observed in diphtheritic myocarditis, was predominantly mononuclear, but significant numbers of polymorphonuclear leucocytes accumulated at sites of more severe inflammation. Although the figures are too small to justify conclusions, there appears to be significant correlation between the clinical occurrence of hypotension and the estimated severity of the myocarditis, since it was a feature in every severe case in which the blood pressure was recorded. The only available electrocardiograms (four), abnormal in every case, were from patients whose hearts showed muscle degeneration of moderate or marked degree. Anginal pains were related to the presence of hypotension. Fibrosis of the heart muscle was related both to the muscle degeneration and to duration of illness. In therapy, attention is called to the danger involved in the administration of intravenous fluids.

Myocarditis associated with acute and subacute glomerulonephritis

Abstract One hundred sixty cases of anatomically proved acute and subacute glomerulonephritis, exclusive of those subsequent to scarlet fever, typhus fever, or prolonged septicemia, were reviewed to ascertain the presence and the character of any concomitant myocarditis. Such a myocarditis was found to have occurred in sixteen patients; there were clear-cut clinical manifestations of myocardial failure in twelve, and in two others the clinical records suggested it. The symptoms were those common in other forms of heart disease; namely, cyanosis, arrhythmia, temperature-pulse disproportion, and hypotension. Electrocardiographic tracings were abnormal in three of the four cases in which they were available. The increased heart weights, which were observed frequently, could be correlated better with the presence of myocarditis than with arterial hypertension, which had been noted in only four patients. The myocarditis had a distinctive character that differentiated it easily from that occurring as a result of sulfonamide hypersensitivity or after acute nasopharyngeal and tonsillar infections. Characteristically there was a widespread serous effusion into the interstitial tissues, increasing the space between the muscle fibers. The cellular elements were relatively sparse, consisting of lymphocytes, endothelial leucocytes, and Aschoff cell. The suggestion that myocardial damage is related to increased capillary permeability appears to coincide with the pathologic evidence. With regard to treatment, caution is recommended in the administration of intravenous fluids.

The tetralogy of Eisenmenger

Abstract A case of the tetralogy of Eisenmenger is presented. The literature pertaining to this complex is reviewed, and the clinical differentiation of this anomaly from the tetralogy of Fallot is discussed. To explain this anomaly, a new theory of transposition is presented. The Eisenmenger complex is produced by an abnormality in the formation of bulbar ridge 3B. Instead of this ridge, the reptilian ridge 4B develops. The subsequent absorption of this abnormally formed bulbus proceeds in an abnormal fashion, causing both the aorta and pulmonary artery to arise from the right ventricle, as in our case, or producing a riding aorta with a septal defect, or a mild form of transposition with an aneurysm of the membranous septum.

Myocarditis in senescence

Abstract Myocarditis is not rate in the aged. Among 1,629 consecutive autopsies of patients over the age of 60, there were 23 cases of myocarditis, an incidence of 1.4 per cent. Among 925 autopsies of patients 70 years and older, myocarditis was found 13 times (1.4 per cent). Most patients had cardiovascular symptoms which were diagnosed as acute myocardial infarction. All patients had characteristic clinical signs which, in retrospect, could be interpreted as having been caused by myocarditis. Comparing the degree of coronary artery disease and resulting myocardial changes with the degree and extent of the myocarditides, we believe that myocarditis was the main cause of death in 10 patients, and that it played a contributing role in the death of 7 patients. It was an incidental finding in 6 patients. Four myocarditides were typical of hypersensitivity, and 2 were due to a toxic substance, norepinephrine. These cases were discussed in more detail. Eight patients had evidence of old myocardial infarction or scattered fibrosis of the myocardium. In all hearts the anatomic changes due to coronary artery disease and infarction were distinct from the lesions of myocarditis. It was stressed that myocarditis is a specific entity of old age, as it is in younger individuals, that on critical evaluation of the patient the characteristic signs may be present, and that hypersensitivity plays an important role in the myocarditis of the aged.

Thromboangiitis obliterans of the coronary arteries and its relation to arteriosclerosis

Abstract The literature dealing with changes in the coronary arteries as shown by post-mortem examinations of instances of Buergers disease is reviewed, and thirty such eases are recorded. The lesions in the coronary arteries vary from simple intimal thickenings to severe arteriosclerosis and coronary thrombosis. In four instances the belief was expressed that the coronary lesions were characteristic of thromboangiitis obliterans. In none of these, however, was there given a clear-cut description of the coronary lesions or illustrations showing the characteristic lesions. An instance of sudden death is reported. The patient had shown clinical evidence of Buergers disease but no evidence of cardiac lesions. The autopsy revealed severe thromboangiitis obliterans of the coronary vessels, coronary arteriosclerosis, multiple small infarcts and fibrosis of the myocardium. Sections of the coronary arteries showed, in addition to uncomplicated lesions of thromboangiitis obliterans, a combination of thromboangiitis obliterans and arteriosclerosis. Because of these findings and because of the fact that, according to the pertinent literature, coronary arteriosclerosis was found rather frequently in relatively young patients afflicted with Buergers disease as proved by autopsy, the question of the relation between these two diseases is discussed, and the possibility is considered that a primary inflammatory lesion of the artery may be at least one factor in the causation of arteriosclerosis. Syphilitic arteritis, rheumatic arteritis, and also thromboangiitis obliterans may each constitute the primary inflammatory factor.

Endophlebohypertrophy and phlebosclerosis. III. The left innominate vein and superior vena cava.

veins it occurs not only in these areas but also adjacent to contiguous bones and muscles. Histologically, the plaques consisted of a proliferation in the direction of blood flow of elastic, muscle, and collagenous tissue of the intima and intimal aspect of the media and an increased amount of intercellular substance. With increasing age these plaques become deeper, broader, firmer and more geographic. The concomitant histologic alterations are called endophlebosclerosis. The latter alteration consists of 1) basophilic staining, vacuolization, and lacunar formation of the ground substance, 2) disruption and loss of elastic fibers, 3) loss of muscle cells, 4) fragmentation of the internal elastic lamella, 5) increased and decreased staining of the glycoprotein and reticular components of the basement membranes around muscle and elastic fibers of the intima, and 6) replacement by fibrous connective tissue. Where there is increased venous pressure, the processes of endophlebohypertrophy and sclerosis are more widespread and severe. The differences between endophlebosclerosis and senile sclerosis have been discussed (1, 2). The present report deals with similar changes in the left innominate vein and superior vena cava. The historical aspect of this subject has been presented previously. The methods used in the study of these veins were identical with those

Complications of myocarditis in children

Summary This study was undertaken to ascertain what, if any, complications may arise in instances of myocarditis. Infants and children were selected because larger relevant material was available. Since it was important to ascertain that possible complications were actually caused by the myocarditis per se and not by a primary infectious disease which originally may have caused the myocarditis, only cases of isolated (Fiedlers) myocarditis were used for the study. Of forty cases of myocarditis observed during the last eight years, fifteen fulfilled the criteria of isolated myocarditis. Outstanding were the findings of minute emboli in the coronary arteries and cerebral vessels. The sources of these emboli apparently were small mural thrombi in the heart, although these were found only in three cases. These thrombi were discovered by chance in the available section of the myocardium and adjacent endocardium. It is possible that more thrombi would have been demonstrated if more tissues had been available at the time of this study. The fact that often multiple emboli were present in several organs, speaks for the heart as the source of the emboli. The cause of these emboli is obviously the inflammatory changes close to the endocardium producing subendocardial edema or even localized foci of mural endocarditis predisposing to the formation of thrombi. From an analysis of the relevant case histories it seems quite clear that multiple emboli constitute a serious complication contributing to the death of the patients.

The venous valve in the aged

Abstract With increasing age changes occur in the vein valve. The loose connective tissue gradually changes into collagen. There is a new formation of minute elastic fibers within the parietalis. The elastica of the luminalis becomes thicker and new elastic lamellae are laid down parallel to the elastica. Endophlebohypertrophy present just distal to the valve extends from the intima of the vein into the luminalis of the valve. Increased endophlebohypertrophy is commonly encountered in this region and may be explained on the basis of abnormal eddies occurring in this area because of the thickening of the cusps of the valve.

The electrocardiogram in brown atrophy of the heart

Abstract The electrocardiograms in three instances of brown atrophy of the heart are described. Emphasis is placed on the occurrence of left axis deviation in each of these records. Left axis deviation, even of advanced degree, cannot threfore be taken by itself as evidence of cardiac hypertrophy since it can occur in an atrophied heart.