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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac disease and cardiac death in AIDS patients is seldom reported. In recent years minor cardiac abnormalities have been demonstrated, especially by echocardiography. Cardiac pathology in AIDS patients is here reported from 60 consecutive autopsies where the heart was investigated either using single samples of ventricular myocardium (the first 21 cases) or by an examination of the whole heart (the last 39 cases). Myocarditis according to the Dallas criteria was seen in 25 of 60 cases (42%), and in seven of these cases a probable pathogen (Toxoplasma gondii, cytomegalovirus, fungi) was demonstrated. Diffuse myocardial fibrosis was seen in 40 of 60 cases (67%) and is considered to be partly due to repair after myocyte necrosis/myocarditis. A myocardium thus weakened might not be able to meet an increase in functional demand, and in 15 of the 39 cases (38%) where an examination of the whole heart was performed, there was dilation and/or hypertrophy of the right ventricle. This is in agreement with our knowledge that the main diseases and main causes of death in AIDS patients are pulmonary. Survival time in AIDS is increasing due to ever improving symptomatic treatment, and the results of this study indicate that the prevalence of especially right-sided heart failure will increase.
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PMID:Pathology of the heart in AIDS. A study of 60 consecutive autopsies. 156 20

Prior studies of vascular rejection in transplanted human hearts have stressed the importance of accelerated coronary arteriosclerosis (chronic vascular rejection). We, however, have had four patients with sudden onset of acute heart failure within 90 days of transplantation who have died without significant myocardial interstitial rejection or the concentric intimal thickening with dense collagen that is typical of chronic vascular rejection. In contrast, the coronary arteries in our patients had a prominent lymphocytic infiltrate, a loosely organized intimal thickening composed of smooth muscle cells, and extensive endothelial injury. We believe that these changes define acute vascular rejection of the coronary artery. In 14 transplanted hearts obtained consecutively, at autopsy or at a second transplant procedure, graft failure was caused by acute coronary vascular rejection in six cases and by chronic coronary vascular rejection in one case. The remaining seven patients showed no evidence of vascular rejection and died primarily of sepsis. Cytomegalovirus (CMV) disease was present in 6 of 7 patients with vascular rejection, of which 43% were CMV-negative recipients of hearts from CMV-positive donors. The adoption of a triple-drug protocol, in which azathioprine was added to cyclosporine and prednisone, reduced the incidence of acute vascular rejection from 27% to 8%. We conclude that acute coronary vascular rejection may be initially seen as global cardiac ischemia in the absence of significant interstitial myocardial rejection. Further, acute vascular rejection should be pathologically distinguished from chronic vascular rejection, although both are probably stages in the natural history of immune-mediated vascular injury.
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PMID:Acute vascular rejection of the coronary arteries in human heart transplantation: pathology and correlations with immunosuppression and cytomegalovirus infection. 165 3

A 78-year-old man visited our department for macroscopic hematuria in June, 1989. On the basis of the diagnosis of tumor of the bladder and right afunctional kidney, total right nephro-uretero-cystectomy and skin grafting of the left ureter were performed on August 2. The patient continued to have fever of unknown origin postoperatively. Repeat laparotomy, which was performed for rectal fistula on August 25, revealed that the abdominal wall, colon, small intestine and mesenterium adhered to one another, producing a mass and that two sites in the rectum were perforated. A part of the small intestine was excised, the perforated sites were sutured, and an artificial anus was created at the transverse colon. Since the patient had intermittent fever and continued to complain of abdominal pain after creation of the artificial anus, nosotropic therapy was continued. However, the patient died from cardiac insufficiency on October 10. Erosion and ulcer were histologically observed over a wide range in the excised small intestine. In addition there was a defect in one area of the small intestine, penetrating the tunca muscularis propria, in which many cytomegalovirus (CMV) inclusion bodies were observed. CMV inclusion bodies were also detected in the bladder with re-examination of specimens from the excised bladder. From these findings, it appears that endogenetic CMV may have been reactivated in the present case.
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PMID:[A case of cytomegalovirus infection that caused gastrointestinal perforation after surgery for cancer of the bladder]. 166 62

Coronary artery disease is a common and particularly severe complication of cardiac transplantation because it may cause progressive destruction of the graft by acute or chronic ischemia. The ischemia is usually silent because of cardiac denervation. Cardiac failure related to graft dysfunction, asymptomatic infarction on the ECG, or sudden death, are sometimes the only signs of severe coronary disease. The prevalence of coronary lesions has been evaluated by coronary angiography at nearly 25% at 2 years and 50% at 5 years. The distribution and morphology of the lesions are characteristic: diffuse concentric, irregular and occlusive, predominantly distal stenoses, without a distal and usually without a collateral circulation. The histological features are variable: the association of medial necrosis, severe endothelial lesions and intense parietal inflammation are suggestive of acute arteriolitis, often present during acute rejection, may be related to a common pathological process. Diffuse obliterative arteriolar lesions with concentric proliferation of medial smooth muscle are the usual appearances in transplant patients who have died or been retransplanted. There is no non-invasive diagnostic method sufficiently sensitive of specific which justifies the practice of many groups of systematic annual coronary angiography in transplanted patients. The pathogenesis is poorly understood and probably multifactorial: disorders of lipid metabolism, immunological factors, the atherogenic role of Cytomegalovirus infection. The absence of an identifiable risk factor makes preventive measures difficult. The evolutive risk justifies retransplantation in selected patients, the results of which are less satisfactory but which reduces the risk of acute coronary events and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary disease in patient following heart transplantation]. 185 May 86

Cardiac transplantation is now a well recognised form of treatment for several forms of end stage cardiac failure, particularly ischaemic heart disease and cardiomyopathies. By the end of 1988, seven patients from Northern Ireland had received cardiac transplants in Papworth and Harefield Hospitals. Of these, four have died, three as a result of rejection and the fourth from widespread cytomegalovirus infection. The autopsy findings in these four cases are presented in this paper.
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PMID:Heart transplantation--an autopsy review. 208 66

Eight children with human immunodeficiency virus (HIV) infection had symptomatic cardiac dysfunction. The median age was 1.4 years (range 0.2 to 7.9 years). All had hepatosplenomegaly, fever, pneumonia with tachypnea, and tachycardia ascribed to infection and anemia. An S3 gallop was present in six of eight. All had normal creatine phosphokinase values. Chest x-rays did not aid in the diagnosis of cardiac dysfunction. ECG showed flattened T waves in five of eight with left ventricular hypertrophy, right ventricular hypertrophy, or both in seven of eight. Results of echocardiography showed decreased left ventricular function in all eight, despite anemia, with dilated left ventricular myopathy in six, concentric left ventricular wall thickening in two of eight, an enlarged right ventricle in two, and pericardial fluid in three. Medical therapy improved cardiac function in all. All patients subsequently died of noncardiac causes. Results of autopsies on four of eight patients showed focal myocarditis in two (with cytomegalovirus inclusions in one) and dilated cardiomyopathy in two others. We conclude: (1) Preexistent hepatosplenomegaly, fever, infection, and anemia result in physical findings that mimic findings of heart failure, thereby masking the occurrence of cardiac dysfunction; (2) an S3 gallop may indicate the presence of impaired heart function when other clinical signs are masked; (3) confirmation of cardiac compromise may be accomplished by noninvasive evaluation with echocardiography and (4) medical therapy can improve cardiac dysfunction in HIV-infected children.
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PMID:Symptomatic cardiac dysfunction in children with human immunodeficiency virus infection. 252 16

Ten children between the ages of five and fifteen years old with leukemia (two with acute nonlymphocytic leukemia in first remission, four with acute lymphocytic leukemia in first or second remission, one with acute lymphocytic leukemia in relapse, and one with chronic myelocytic leukemia in chronic phase), malignant lymphoma (one) or severe aplastic anemia (one) were given transplants from HLA-matched or mismatched family members between March, 1982 and April, 1984. Two patients died of leukemia relapses on days 107 and 257 following transplantation. One patient died of cardiac failure on day 157. One patient who received HLA-mismatched marrow from his father died of pulmonary edema and acute graft versus host disease on day 32. Six are alive 268-843 days post transplantation. None of the ten patients developed interstitial pneumonia due to cytomegalovirus which is one of the major causes of death reported in other published studies.
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PMID:Allogeneic bone marrow transplantation in children: Tokai experience 1982 to 1984. 301 May 9

Pulmonary interstitial infiltrates developed in a 22-year-old female after bone marrow transplantation (BMT) for acute lymphoblastic leukemia (ALL) in second remission. She was receiving prednisone for graft versus host disease (GvH). There was some evidence of cardiac failure, but the primary diagnosis was that of cytomegalovirus (CMV) pneumonia, which resolved. Recurrent infiltrates were associated with the appearance of fat emboli in the pulmonary capillaries. There was little histological evidence of CMV pneumonitis, although other tests confirmed persistent infection. The patient recovered after further treatment directed at CMV infection and cardiac failure with a modest reduction in steroid dose. Most previous descriptions of pulmonary fat embolization (PFE) in immunocompromised patients have been derived from autopsy studies, and the majority of patients have received steroid therapy. The present case illustrates that PFE may complicate or contribute to the picture of interstitial pneumonitis (IPN) in the BMT recipient and that this syndrome may be reversible.
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PMID:Fat embolization and pulmonary infiltrates after bone marrow transplantation. 303 37

Immunofluorescent and electron-microscopic studies were performed to determine the distribution of viral antigens and particles and to clarify the relationship to myocardial lesions in two autopsy cases with generalized infection of Coxsackie virus B3 (CVB3) or cytomegalovirus (CMV). Case 1 was a full-term newborn female infant, without any congenital anomalies, who died of cardiac failure 10 days after birth. CVB3 was isolated from the blood before death. Necrosis of the muscle fibers was observed, frequently accompanying calcification. Numerous histiocytes and a few lymphocytes and neutrophils had infiltrated in and around the necrotic areas. Immunofluorescent study (IF) revealed CVB3 antigen in the muscle fibers and vascular endothelial cells. Case 2 was a female infant, born at 28 weeks of gestation, who died of fatal arrhythmia 50 days after birth. The infant had hemocephalus and a history of idiopathic respiratory distress and underwent an operation for patent ductus arteriosus. Cytomegalic cells were frequently found in the vascular endothelial cells in the myocardium and occasionally in muscle fibers. IF showed the presence of CMV antigen in both endothelial cells and muscle fibers. CVB3 and CMV antigens were detected predominantly in vascular endothelial cells rather than in the muscle fibers. Blood flow disturbance due to endothelial damage is a cause of the myocardial lesion in addition to the direct invasion of the muscle fibers by the virus.
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PMID:Myocardial lesions by Coxsackie virus B3 and cytomegalovirus infection in infants. 303 31

The clinical status and quality of life of 40 patients who lived or are still alive more than 10 years after transplantation at our institution were reviewed with the use of our transplant database, prospective patient examinations, cardiac catheterization, and exercise testing. Patient-perceived health status was determined with use of the Nottingham Health Profile and General Well Being examinations. Factors associated with longevity were determined by a Cox proportional hazards model. Twenty-six patients are alive and 14 have died. The mean age at transplant was 32.4 +/- 12 years and the current age (or age at death) is 46.1 +/- 12.8 years. Actuarial freedom from rejection was similar to that of patients surviving less than 10 years (p = 0.8), but freedom from all types of infection was less (p = 0.005). Immunosuppressive drugs include cyclosporine (11/26 patients), azathioprine (24/26), and prednisone (26/26, mean dose 12.7 mg/day). Catheterization hemodynamic data show well-preserved graft function at a mean follow-up of 11.7 +/- 3.3 years. Graft coronary artery disease prevalence is 51.0% +/- 8%. Exercise test results are as follows: duration 8.7 +/- 3.5 minutes (range 2 to 16 minutes), maximum heart rate/expected rate 77.3% +/- 11% (50% to 92%), maximum systolic blood pressure 171 +/- 23 mm Hg (140 to 208 mm Hg), and metabolic equivalents 9.2 +/- 2.3 units (5.5 to 12.9 units), or about 84% of predicted. Mean score on the General Well Being examination was 75.3 +/- 21.6 (normal). Nottingham Health Profile scores were nearly normal, except for in the 50- to 64-year-old age group in categories of mobility, pain, sleep quality, and energy level. Causes of death were coronary artery disease in 7 of 14, infection in 4 of 14, lymphoma in 1 of 14, and nonlymphoid cancer in 2 of 14. In the Cox regression, variables most associated with survival (t > 2.0, multivariate p = 0.0005) were age at transplantation (t = 3.26), preoperative duration of illness (t = 3.57), postoperative cytomegalovirus infection (t = 2.16), and ejection fraction at 12 months after operation (t = -2.62). We conclude that cardiac transplantation can provide patients with end-stage cardiac failure an acceptable general medical condition, functional status, and perceived quality of life well into the second decade after operation.
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PMID:Characteristics of patients surviving more than ten years after cardiac transplantation. 777 75


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