Jack L. Titus

Clinical and pathologic features of postinfarction cardiac rupture

Abstract In a 15 year period 106 instances of myocardial rupture after myocardial infarction were observed at autopsy, an incidence of 8.6 per cent of fatal acute myocardial infarcts. This complication occurred most frequently in the seventh and eighth decades and was slightly more common in women. Clinically, rupture occurred most frequently during the first week after infarction. Historical evidence of previous coronary artery disease was uncommon. Hypertension had been present in 70 percent of the patients, but it persisted after the infarct in less than a third. Pathogenetic factors were sought in the clinical aspects of the patients. No definite role could be ascribed to anticoagulant or sympathomimetic drugs or digitalis. Physical activity after infarction may be a predisposing factor in some instances. Sudden death without antecedent change in symptoms most often occurred. Cardiac tamponade or vascular collapse was documented in a few instances prior to death. In most instances no physical findings, laboratory tests, or electrocardiographic features that indicated cardiac rupture could be ascertained. Based on histologie data, 90 per cent of the ruptures occurred during the first two weeks after infarction, at an average time of five days; 22 per cent were in the first 24 hours, and 69 per cent were in the first week. All of the infarcts were transmural and involved large areas of the left ventricle. Ruptures presented as distinct tears (79 per cent) or large areas of hemorrhagic dissection (9 per cent), or both (12 per cent). The most common site of rupture was through the anterior wall of the left ventricle; commonly, ruptures were near the septum or near the base of papillary muscle. The areas of rupture were more common in the basal two thirds of the ventricle than in the apical portion. The ruptures varied greatly in size. Most were situated within the area of infarction rather than at the junction between the infarcted and the normal myocardium. Unusual accumulations of polymorphonuclear leukocytes were not found in most specimens. Most hearts had severe coronary artery disease, but myocardial scarring was present in only a fourth. Cardiac hypertrophy was usually present. The amount of hemopericardium varied widely and was the apparent mechanism responsible for death in some patients. Mural hemorrhage, hypertension, degree of polymorphonuclear infiltration, degree of myocardial fibrosis and location of the infarct may all be of pathogenetic significance in post-infarction rupture in different situations, but these considerations did not have universal applicability. The only common morphologic features among the infarcts that ruptured were their large size and transmural extent. The major pathogenetic considerations probably are loss of tensile strength of the infarcted segment, increased tension in this area, and, in some cases, divergent vector forces.

Pathologic changes in aortocoronary saphenous vein grafts

Abstract Aortocoronary saphenous vein grafts from 40 patients (total 62 grafts) were studied at autopsy. The earliest change seen was the insudation of blood constituents into the vein intima. Occluding thrombi were seen in six grafts from short-term survivors, and one organized thrombus was seen in a graft from a long-term survivor (28 months). Various degrees of intimai thickening were seen in grafts from all patients surviving for more than a month; this had progressed to diffuse occlusion in three cases. Gross and microscopic findings correlated well with postmortem angiographic findings in the long-term survivors. Electron microscopic examination showed smooth muscle cells, collagen fibers and ground substance in the thickened intima. Fibroblasts were not a feature of this thickening. Increased permeability of the graft endothelium, due to injury or hemodynamic factors, may result in exposure of medial smooth muscle cells to certain plasma factors and thus promote smooth muscle cell hyperplasia as has been produced in certain experimental models.

Etiology of sudden death in the community: Results of anatomical, metabolic, and genetic evaluation

BACKGROUND Identifying persons at risk for sudden cardiac death (SCD) is challenging. A comprehensive evaluation may reveal clues about the clinical, anatomical, genetic, and metabolic risk factors for SCD. METHODS Seventy-one patients who had SCD (25-60 years old) without an initially apparent cause of death were evaluated at the Hennepin County Medical Examiners office (Minneapolis, MN) from August 2001 to July 2004. We reviewed their clinic records conducted next-of-kin interviews and performed autopsy, laboratory testing, and genetic analysis for mutations in genes associated with the long QT syndrome. RESULTS Mean age was 49.5 +/- 7 years, 86% were male, and 2 subjects had history of coronary heart disease (CHD). Coronary risk factors were highly prevalent in comparison to individuals of the same age group in this community (eg, smoking 61%, hypertension 27%, hyperlipidemia 25%) but inadequately treated. On autopsy, 80% of the subjects had high-grade coronary stenoses. Acute coronary lesions and previous silent myocardial infarction (MI) were found in 27% and 34%, respectively. Furthermore, 32% of the subjects had recently smoked cigarettes, and 50% had ingested analgesics. Possible deleterious mutations of the ion channel genes were detected in 5 subjects (7%). Of these, 4 were in the sodium channel gene SCN5A. CONCLUSIONS Most of the persons who had SCD in the community had severe subclinical CHD, including undetected previous MI. Traditional coronary risk factors were prevalent and undertreated. Mutations in the long QT syndrome genes were detected in a few subjects. These findings imply that improvements in the detection and treatment of subclinical CHD in the community are needed to prevent SCD.

Coronary heart disease in situs inversus totalis

Abstract In patients with dextrocardia as a part of situs inversus totalis, coronary heart disease may occur with similar frequency and manifestations as in the general population. Diagnostic problems arise from the altered cardiovisceral relation; when these are recognized, coronary heart disease can be defined by the usual criteria. The use of electrocardiographic and vectorcardiographic tracings with right-left reversal of all leads in patients with dextrocardia allows the recognition of abnormalities on the basis of standard criteria. Seven cases are reported, 1 followed up clinically and 6 studied at autopsy.

The Atrioventricular Conduction System in Persistent Common Atrioventricular Canal Defect Correlations with Electrocardiogram

Serial histologic sections of the atrioventricular (A-V) conduction system were studied in four hearts with persistent common A-V canal, and the anatomic findings were related to the abnormal ECG patterns. Two hearts were examples of the partial form and two of the complete form of A-V canal. The major anatomic abnormalities were: (1) postero-inferior displacement of the A-V node; (2) relatively short distances between the A-V node and the origin of the left bundle branching; (3) marked posteroinferior displacement of the left bundle branching system; and (4) relative hypoplasia of the anterior (superior) left bundle branches. The anatomic configuration of the A-V conduction system in A-V canal could result in relatively early impulse propagation to the posterior aspect of the ventricular septum as suggested by reported electrophysiologica studies. The anatomic findings are considered to be related closely to the known ECG patterns of A-V canal.

Anomalous ventricular myocardial patterns in a child with complex congenital heart disease

Abstract Unusual ventricular myocardial patterns in a child are described. These patterns, demonstrated by angiocardiography, were associated with complex, congenital heart disease. Autopsy confirmed the bizarre, spongy myocardial patterns present in both ventricles. One explanation for the abnormal myocardial pattern observed in this case is failure of the normal differentiation of the primitive ventricular wall into compact myocardium. Thus, this case may have represented persistence of an embryonal pattern.

Bilateral Renal-vein Thrombosis and the Nephrotic Syndrome in Adults

Excerpt The nephrotic syndrome may be defined as a clinical state resulting from a renal disorder and characterized by edema, hyperlipemia, hypoproteinemia, and massive proteinuria. The underlying ...

Apparent interruption of atrial conduction pathways after surgical repair of transposition of great arteries

Abstract Apparent interruption of the atrial conduction (internodal) pathways after the Senning operation, the Mustard procedure or the creation of an atrial septal defect was sought in the hearts of 49 patients with transposition of the great arteries, and the findings were correlated with postoperative dysrhythmias. The results indicate that (1) extensive disturbance of the atrial septal connections between the sinus and atrioventricular nodes frequently is associated with serious dysrhythmia, and (2) disruption of the region of the middle atrial conduction pathway, especially when coupled with damage to another pathway, is frequently associated with dysrhythmia, most commonly nodal rhythm.

Cytodynamics in the respiratory tract of the rat.

The knowledge of cytodynamics in the respiratory tract is still in its infancy. Since Bertalanffy and Leblond (1953) described their findings in a study of the alveolar macrophage cells in the lung of the albino rat, few investigations have been reported in the literature (Koburg, 1962; Spencer and Shorter, 1962; Meyer zum Gottesberge and Koburg, 1963; and Shorter, Titus, and Divertie, 1964b), and these have indicated that the findings may vary greatly in the epithelia in the various parts of the respiratory tract, even between areas in close relationship to one another. The purpose of this paper is to report the findings obtained in

Anatomy of the Atrioventricular Conduction System in Ventricular Septal Defect

The major parts of the atrioventricular conduction system of the human heart were traced in 21 instances of ventricular septal defect: 19 were examples of variously located uncomplicated ventricular septal defects and two of the tetralogy of Fallot.In the presence of a ventricular septal defect, the conduction system was found to have a normal course, except when the ventricular septal defect lay in a position normally occupied by the conduction system. In each specimen with a defect posterior and inferior to the crista supraventricularis, the conduction system occupied a position posterior and inferior to the defect. In no instance did theconduction system occupy a position superior to a defect of this type. Defects located in the posterobasal portion of the muscular part of the ventricular septum sometimes were posterior to the main parts of the conduction system, so that the conduction tissue was related to the anterior edge of the defect. No example of a defect lying superior to the crista supraventricularis was studied. In our two examples of tetralogy of Fallot, the position of the conduction system was essentially similar to that occurring in the usual variety of ventricular septal defect, that is, posterior and inferior to the crista supraventricularis.