Mitral insufficiency other than rheumatic, ischemic, or infective: emphasis on mitral valve prolapse.
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Biomedical subjects
Publications and source records attributed to J L Titus.
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The tissue distribution and possible neuroendocrine nature of atrial natriuretic factor (ANF) were studied, using the avidin-biotin-peroxidase technique and antibodies to ANF, chromogranin (Ch), and neuron-specific enolase (NSE). Tissues examined included: Group 1, formalin-fixed and fresh frozen atrial tissue from adjacent areas of the hearts from two heart-lung-transplant patients; Group 2, the entire atria and sampling of other areas from formalin-fixed hearts of five gunshot wound or automobile accident victims; and Group 3, formalin-fixed right auricular tissue from 19 open-heart-surgery patients. In each case of Group 3, the ANF score, expressed as the product of the percentage of stained areas by the staining intensity, was correlated with age, weight, height, blood pressure, ejection fraction, and degree of coronary arterial stenosis. It was found that: (a) ANF was limited to atrial myocytes; the staining was significantly stronger in the right atrium, diffuse and most intense in auricles and pectinate muscles, diffuse and strong in subendocardium, focal and weak in other areas; (b) although ANF has been reported to be a peptide hormone stored in dense-core granules, it does not seem to belong to the diffuse neuroendocrine system because Ch and NSE were consistently absent in cardiac myocytes; and (c) although the limited numbers of evaluable clinical parameters do not significantly correlate with ANF scores, a change in the pattern and intensity of ANF staining was noted in some cases of Group 3.
In order to differentiate between malignant pleural mesothelioma and adenocarcinoma of the lung, the glycoconjugate profiles of 6 reactive mesothelial lesions, 23 mesotheliomas (17 epithelial, 1 desmoplastic, 2 biphasic, and 3 fibrous types), and 28 well-differentiated pulmonary adenocarcinomas were evaluated with the use of 8 lectins in addition to anti-carcinoembryonic, anti-keratin and anti-epithelial membrane antigen. Formalin-fixed, paraffin-embedded tissues were stained with the avidin-biotin peroxidase complex method. Reactions of wheat germ (WGA) and peanut (PNA) agglutinin with neuraminidase treatment lectins were positive in 5 of 6 (83%) and 3 of 6 (50%) cases, respectively, in reactive mesothelial lesions. Thirteen of 23 (57%) malignant mesotheliomas of the pleura showed a positive reaction for WGA and PNA with neuraminidase treatment; other lectins were low-positive, below 9%. In contrast, pulmonary adenocarcinomas showed positive reactions in 27 of 28 cases (96%) for PNA, 26 of 28 (93%) for Ricinus communis (RCA-I), 25 of 28 (89%) for WGA, and 22 of 28 (79%) for succinylated WGA (SucWGA). The findings suggest that malignant pleural mesothelioma and pulmonary adenocarcinoma have consistent and distinct glycoconjugate profiles, and that stains for RCA-I and SucWGA may be useful for differential diagnosis.
Morphological abnormalities related to the surgical treatment of ischemic heart disease are discussed. Catheterization, angioplasty, or intraarterial thrombolysis may lead to perforation, endothelial injury, thrombosis, or dissection of the artery; endothelial injury results in intimal thickening. Laser angioplasty produces a localized area of thermal and acoustic injury that may heal without luminal compromise. Endarterectomy may be followed by thrombosis or exuberant muscular proliferation. Changes in saphenous veins used as coronary artery bypass grafts are mainly thrombotic in the early postoperative period; years after operation failure usually is due to some combination of fibromuscular intimal thickening, atherosclerosis, thrombosis, and dissection. Surgically resected areas of myocardial dysfunction show one or more abnormalities of hypertrophy, myocytolysis, fibrosis, and endocardial thickening. Perioperative ischemic injury is manifested by contraction band necrosis or coagulation necrosis. Excised arrhythmogenic foci have mixtures of normal and abnormal myocytes. The pathological features of pacemakers and circulatory assist devices include thrombosis, embolism, infection, dissection, and mechanical failures.
In order to evaluate the staining pattern of glycoconjugate profiles in adenocarcinomas of the lung, pulmonary adenocarcinomas were classified according to their: (a) degree of differentiation; (b) cellular subtyping and mucus secretion; and (c) immunohistochemical characteristics. Studies were performed on 42 pulmonary adenocarcinomas using eight lectins. Formalin-fixed, paraffin-embedded tissues were stained with avidin-biotin peroxidase complex methods. Four lectins [wheat germ (WGA), succinylated WGA (SucWGA), peanut (PNA) with neuraminidase (N) treatment, and Ricinus communis (RCA-I)] showed strong positive staining reactions in well-differentiated adenocarcinomas. Bronchial surface epithelial type, one of the subtypes among 26 cases of well- and moderately differentiated adenocarcinomas, displayed strong positive staining for WGA, SucWGA, PNA N(+), RCA-I, and Bandeirea simplicifolia (BSA-I). Goblet cell types stained positive for all lectins except Dolichos biflorus (DBA). Bronchial gland cell types also showed a strongly positive stain for WGA, SucWGA, soybean (SBA), PNA N(+), RCA-I, and Ulex europaeus (UEA-I). The lectin positive staining reaction was related to the degree of mucus secretion within the tumor cells. These results revealed that the glycoconjugate profile of pulmonary adenocarcinomas was basically sialic acid, together with N-acetyl-glucosamine and beta-D-galactose. The observation that UEA-I showed a strong staining reaction in mucus-producing adenocarcinomas, such as goblet cell and bronchial gland cell types, indicates that localization of alpha-L-fucose may be a specific carbohydrate from non-mucus-producing pulmonary adenocarcinomas.
We describe an autopsy patient in whom a rare congenital anomaly of quadricuspid semilunar aortic valve and coronary arteries originating from a single orifice of one aortic sinus occurred. To the best of our knowledge, this combination of cardiac anomalies has not been reported.
Infants with incessant ventricular tachycardia (occurring greater than 10% of the day) have generally been described in pathologic studies. This report describes 21 patients with incessant ventricular tachycardia present greater than 90% of the day and night; the age at diagnosis ranged from birth to 30 months (mean 10.5 months). The most common clinical presentation was cardiac arrest (11 patients, in 5 after digitalis for presumed supraventricular tachycardia); another 6 patients had congestive heart failure and 4 were asymptomatic. Three patients had coexisting Wolff-Parkinson-White syndrome. The rate of incessant ventricular tachycardia ranged from 167 to 440 (mean 260 beats/min) and the QRS duration from 0.06 to 0.11 second. The most common electrocardiographic (ECG) pattern (10 of 21) was right bundle branch block with left axis deviation, but other right and left bundle branch block patterns were observed. Conventional and investigational antiarrhythmic agents (nine patients received amiodarone) failed to eliminate incessant ventricular tachycardia in all. Electrophysiologic studies localized incessant ventricular tachycardia to the left ventricle in 17 (to the apex in 2, the free wall in 9 and the septum in 6) and to the right ventricular septum in 4. No structural abnormalities were found on the echocardiogram or angiocardiogram. All 21 patients had surgery at an age of 3.5 to 31 months (mean 16). In 15 a tumor was found: 13 myocardial hamartomas (9 discrete, 4 diffuse throughout both ventricles) and 2 rhabdomyomas (1 multiple). Myocarditis was found in one patient (the oldest). In four, only myocardial fibrosis was found; results of one biopsy were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
We have observed in 11 infants, aged 2 years or less, a distinct clinicopathologic lesion responsible for tachyarrhythmias that were fatal in 96% (25/26) of previously reported cases. Nine of the 11 patients, who underwent electrophysiologic mapping and surgical excision of the lesion, have survived, with follow-up periods ranging from 1 month to 6 years. The morphologic findings in these 11 patients and in the 26 cases cited in the literature are reviewed. Pathogenic considerations have included viral-induced lesion, cardiomyopathy, neoplasm, and developmental disorder of Purkinje cells. We believe this lesion to be a myocardial hamartoma. Supportive evidence includes prevalence in infants, tumorlike growth pattern without mitotic figures, and association of other developmental abnormalities. Through electrophysiologic mapping, this myocardial hamartoma is potentially accessible to surgical excision and long-term cure.
An unusual, uniformly stenotic arteriopathy involving the aorta and its major branches, the pulmonary trunk, and the left and right pulmonary arteries was found in association with a persistent common atrioventricular canal in an otherwise normal stillborn female infant. The uniform arterial thickening was due to hyperplastic medial elastic laminae, which were in an orderly arrangement in the inner two thirds but dysplastic in the outer third of the media of the arteries.
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To determine the dependence of myocyte hypertrophy in chronic valvular heart disease on the site and type of lesion, the myocardium was studied from 11 patients with either pressure-overload hypertrophy (PO; four patients with aortic stenosis and two with mixed aortic stenosis/insufficiency) or pure volume-overload hypertrophy (VO; two patients with mitral regurgitation and three with aortic insufficiency). These patients, all without coronary artery disease, died zero to 34 days after valve replacement surgery. Diameters of 25 longitudinally oriented myocytes in the circular midwall myocardium were measured with a calibrated light microscope eyepiece reticle on each of five transmural, transverse, histologic sections from the apical, anterolateral, posterolateral, anteroseptal, and posteroseptal left ventricle. Statistical analysis by modified two-way analysis of variance (ANOVA) demonstrated that mean myocyte size (based on 125 measurements) varied widely among cases but was not statistically different among sites. The myocyte diameter for PO lesions (25.9 +/- 1.1 micron, mean +/- SEM) was significantly greater (P less than 0.05) than that for pure VO lesions (20.4 +/- 0.7 micron), despite equal relative heart weights (measured/predicted from body weight: 2.5 +/- 0.2 [mean +/- SD] versus 2.5 +/- 0.5). This study suggests that 1) cellular hypertrophy in valvular heart disease occurs uniformly throughout the left ventricular myocardium; and 2) mean myocyte diameters are greater in PO than in VO hypertrophy for equivalent cardiac enlargement.
Aneurysm of the thoracic aorta is a serious form of disease because it may be extensive or associated with a more distant aneurysm. This manifestation occurs in about one-third of the cases. The actuarial 5-year survival of nontreated patients is only 13% with many patients dying from aortic rupture. The 5-year survival of our patients with aneurysm of the descending thoracic aorta treated by graft replacement is 58% with the two most common causes of late death being myocardial infarction and rupture of another aortic aneurysm. Effective treatment consists of initial total aortic examination, continued follow-up examination, and total replacement of disease. Aneurysmal disease that involves the entire aortic arch is especially prone to extensive involvement because it is due to diffuse aortic dissection or medial degenerative disease in most cases. The latter is most common, being present in 63 of our 81 patients requiring total arch replacement. The disease was extensive in all cases with degenerative medial disease and required extensive graft replacement. In fact, the entire thoracic aorta was involved in ten, the entire thoracic aorta and substantial segments of abdominal aorta in ten, and the entire aorta in 12 patients. Most of these patients were women (84%) over 65 years of age (63%) or older, ten (37%) were over 70 years. Associated pulmonary disease was frequent, aortic valvular insufficiency was present in 12 (38%), and symptoms were present in most. Treatment consisted of removing the disease when possible in stages, the arch in one and the remaining disease in another with the sequence and interval depending upon indications and condition of the patient. A total of 53 operations were performed in these 32 patients, the arch replaced in 29, the descending thoracic aorta in eight, and the thoracoabdominal aortic segment in 16 patients. All of the disease was replaced in 21, including the entire aorta in eight and incompletely replaced in 11 patients. Sixteen (76%) of the former are still alive 4 months to 6 1/3 years. Six (55%) of those in whom operation was limited to replacement of the symptomatic aortic segment because of limited risk are still alive. Of the ten deaths occurring during the study period, four (40%) and perhaps five (50%) were due to natural rupture of unresected disease which indicates its progressive nature and suggests the need for aggressive surgical treatment.
We reviewed records of 378 patients who died after cardiac valve replacement and underwent autopsy at The Methodist Hospital, Houston, from 1962 through 1979. Patients were divided according to postoperative interval at death: within 30 days (early) or 30 days to ten years (late). Early deaths (279 patients) were due almost exclusively to cardiovascular abnormalities or operative complications (94%). Only 6% of early deaths were caused by prosthesis-associated complications. In contrast, late deaths (99 patients) were valve related in 47% of cases, including complete thrombotic occlusion or systemic thromboembolism (21%), prosthetic valve endocarditis (14%), valve dehiscence (6%), anticoagulation-related hemorrhage (3%), and mechanical degeneration (2%). Nine percent of late deaths were unrelated to cardiovascular disease. Thus, while early deaths primarily reflected the severity of preexisting or associated cardiovascular disease, prosthesis-associated complications were an important cause of late death after cardiac valve replacement.
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To assess abrasive wear of mechanical valve prostheses containing pyrolytic carbon components, we recovered at necropsy or surgery and analyzed by scanning electron microscopy and surface profilometry eight prostheses. Seven were implanted for 30-85 (mean 50 months. Valves included DeBakey aortic (2), DeBakey mitral (1), Beall mitral (2), Bjork-Shiley aortic (1), Cooley-Cutter mitral (1), and Lillehei-Kaster (L-K) tricuspid (1). All carbon occluders had undetectable wear. Carbon cage struts had a superficial burnish. Metallic struts had insignificant wear marks. In contrast, a Teflon Beall Model 104 valve implanted for 34 days and similarly analyzed had considerable material loss from the cage struts. This study suggests that clinically important abrasive wear will not be a late complication of cardiac valve replacement with pyrolytic carbon prostheses.
Biomedical engineering inputs have been important in the design, development and testing of substitute heart valves as well as in the pre- and post-operative management of patients with cardiac valve disease. This paper is a review of heart valve replacement whose goal is the enhancement of future bioengineering contributions. We review the approach to the patient with valvular heart disease, and the sources of early and late postoperative pathology with emphasis on complications of the prostheses used. Major significant problem areas relate to the noninvasive evaluation of cardiovascular function (both before and after surgery), device design, hemodynamics, and the need for thromboresistant and durable materials.
A previously healthy 19-year-old woman died two hours after the sudden onset of severe chest pain. The only gross abnormality seen at the time of autopsy was thrombosis of the left main coronary artery. Microscopic examination of the artery showed eccentric necrotizing arteritis with giant cells, associated with the thrombus. The aorta was infiltrated with lymphocytes, histiocytes, and an occasional giant cell. Sudden cardiac death as the initial manifestation of a giant cell arteritis that involves only the coronary artery and aorta is rare.
The coronary sinus of a healthy 18-year-old man who died of a skull fracture was found to communicate with both the right and left atria. The anomaly can function as an atrial septal defect; thus, it needs recognition in the treatment of a patient with an interatrial shunt with an apparently normal right atrium.