Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An high frequency of antimitochondrial autoantibodies has been reported in subjects affected with primary cardiomyopathies and it has been hypothesized that they could be involved in the pathogenesis of these diseases. In order to find out whether such autoantibodies could on the contrary represent an epiphenomenon of myocardial cell damage, we searched for antimitochondrial (AMA), antinuclear (ANA) and antismooth-muscle (SMA) non-organ specific autoantibodies in a group of 50 subjects (47 females and 3 males), over 65 years of age, affected with ischemic cardiomyopathy (ICM) due to atherosclerosis, a condition resembling other cardiomyopathies as it concerns ultrastructural aspects of myocardial tissue. The frequency of the autoantibodies tested in our patients resulted quite similar to that occurring in our healthy elderly control subjects (AMA: 14% vs 5.7%; ANA: 28% vs 23%; SMA: 12% vs 11.4%) and in normal aged population. On the basis of our data, the myocardial cell damage "per se" does not seem to influence significatively the production of non-organ specific autoantibodies.
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PMID:Autoimmune features in atherosclerotic ischemic cardiomyopathy. 128 43

The improved longevity of heart transplant recipients demands heightened awareness of the long-term complications of the procedure. Between 1979 and 1990, 232 patients received 241 heart transplants at our institution. Accelerated coronary atherosclerosis occurred in 45 (19%) of the 232 patients, typically appearing within 2 years of transplantation, whereas peripheral vascular disease (PVD) appeared in 23 (10%) of the 232 patients, usually within 3 years of transplantation. In the patients with PVD, 13 had occlusive disease, nine had aneurysms, and one patient suffered a vertebral artery dissection. Accelerated coronary atherosclerosis afflicted 12 (52%) of the 23 patients affected by PVD (p < 0.05) and preceded the development of PVD in all 12. Logistic regression analysis revealed risk factors predictive of the development of PVD after transplantation to be a pretransplant history of ischemic cardiomyopathy and posttransplant hypertension and hypertriglyceridemia (p < 0.05), with the presence of more than one risk factor increasing the probability of development of PVD. Those patients thus identified as at risk should be closely monitored for the development of PVD. Aggressive medical management of hypertension and hyperlipidemia in this subpopulation may forestall or prevent the development of peripheral vascular disease after heart transplantation.
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PMID:Peripheral vascular disease in heart transplant recipients. 140 76

We investigated incidence, severity, and distribution of coronary atherosclerosis, acute thrombosis, and plaque fissuring in ischemic heart disease (both unstable-acute syndromes and chronic ischemia) and in nonischemic controls. We also studied the structural, immunohistochemical, and biochemical profile of plaques, with and without thrombus, including morphometry, immunophenotyping of inflammatory infiltrates, cytokine presence, and ultrastructural features. Critical coronary stenosis was almost the rule in both acute and chronic ischemic series (greater than 90%) whereas it reached 50% in control subjects. Thrombosis was principally characteristic of unstable-acute ischemic syndromes (unstable angina, 32%; acute myocardial infarction, 52%; cardiac sudden death, 26%) but was also found in chronic ischemia (stable angina, 12%; ischemic cardiomyopathy, 14%) and in control subjects (4%). Plaque fissuring without thrombus occurred in low percentages in lipid-rich, severe eccentric plaques in most series. Major differences were found between pultaceous-rich versus fibrous plaques rather than between plaques with or without thrombus. Pultaceous-rich plaques were frequent in sites of critical stenosis, thrombosis, and ulceration. Inflammatory infiltrates, i.e., T cells, macrophages, and a few beta cells, mostly occurred in lipid-rich, plaques unrelated to thrombus. In adventitia, infiltrates were a common finding unrelated to any syndrome. Necrotizing cytokines such as alpha-TNF were immunohistochemically detected in macrophages, smooth muscle, and intimal cells and detected by immunoblotting in 67% of pultaceous-rich plaques, either with or without thrombus. Immune response mediators such as IL-2 were also expressed in analogous plaques but in a minor percentage (50%-40%). Media were extensively damaged in severely diseased vessels with and without thrombus. Ultrastructural study showed that the fibrous cap was either highly cellular or densely fibrillar. Intimal injury with collagen exposure was often associated with platelet adhesion, whereas foamy cell exposure was not. In conclusion, investigated parameters were essentially similar in plaques, both with and without thrombus, whereas major differences were found between pultaceous-rich and fibrous plaques. Since platelets adhere to exposed collagen and not to foam cells, the type of exposed substrates could play a major role in thrombosis.
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PMID:Coronary atherosclerotic plaques with and without thrombus in ischemic heart syndromes: a morphologic, immunohistochemical, and biochemical study. 189 66

In the past 3 years at our institution 130 patients have undergone cardiac transplantation for ischemic cardiomyopathy in 49 (38%), idiopathic cardiomyopathy in 42 (32%), viral cardiomyopathy in 9 (6.9%), pulmonary hypertension in 8 (6%), and graft atherosclerosis in 2 (1.5%). Routine preoperative abdominal ultrasonography was performed on 98 (75%) of these patients with specific visualization of the abdominal aorta in 93 (95%). Abdominal aortic aneurysms (all infrarenal) were found before operation in four patients and only in the subgroup undergoing transplantation for ischemic heart disease (10.5%). They measured 3.4, 4.5, 3.6, and 3.8 cm before transplantation. Periodic evaluation by ultrasonography was carried out after transplantation during the 3-year period of this study. One aneurysm that was initially 3.6 cm increased to 4.0 cm and ruptured 2 months after transplantation. The patient died despite emergent surgery. Aneurysms in three patients who demonstrated rapid aneurysm expansion after transplantation were successfully repaired at 5, 20, and 33 months after transplantation when the lesions reached 5.5, 5.9, and 4.8 cm. A fifth patient with an initially normal (1.5 cm) aorta developed a symptomatic aneurysm of 4.1 cm, which was repaired uneventfully. The average expansion rate of these aneurysms after transplantation was 0.74 +/- 0.15 cm/year. This experience suggests that aneurysms are limited to patients undergoing transplantation for ischemic heart disease. Ultrasound examination may be appropriate for preoperative screening. Careful aortic surveillance after transplantation is important in patients having transplantation for ischemic cardiomyopathy because of the apparent rapid expansion rate compared to aneurysms in the population not receiving transplants.
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PMID:Abdominal aortic aneurysm in the patient undergoing cardiac transplantation. 192 Jun 43

Accelerated coronary atherosclerosis (ACA) has been documented at autopsy and was noted at coronary angiography in seven patients, 11 to 48 months after cardiac transplantation. To delineate the importance of this problem, the risk factors and the therapeutic approaches in 7 patients who had ACA after heart transplantation were compared with those in 28 patients free of ACA at annual coronary angiography. Ischemic cardiomyopathy was the preoperative diagnosis in all but one patient in the ACA group. The age of the transplant recipients, total myocardial ischemic times and arterial blood pressures at follow-up were similar in both groups. Donor age averaged 31 +/- 3 years in the ACA group and 22 +/- 1 years in patients free of ACA. Preoperative cholesterol, triglyceride and high-density lipoprotein levels were lower in ACA-free patients and the low-density lipoprotein level was higher. At the last follow-up visit, serum lipid levels were similar in both groups. The incidence of acute rejection and of infection was slightly, but not significantly, higher in patients with ACA. The actuarial survival of ACA patients 4 years after transplantation was 30% +/- 20% compared with 100% for patients free of ACA (p less than 0.01). Actuarial rates of freedom from ACA and from death due to ACA were 73% +/- 11% and 81% +/- 11% respectively. Stepwise discriminant analysis showed that older donors and higher pretransplant triglyceride levels were independently related to the development of ACA after cardiac transplantation. In conclusion ACA remains an important cause of late death after heart transplantation. Although therapeutic measures are limited, prevention should focus on strict control of serum lipid levels after transplantation.
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PMID:Accelerated coronary atherosclerosis after cardiac transplantation: major threat to long-term survival. 202 2

Although transthoracic ultrasonic visualization of the coronary arteries is technically demanding, many groups of investigators have demonstrated the feasibility of recording the proximal coronary arteries. Technical advances such as the introduction of anular array transducers and digital recording techniques have improved the prospect of obtaining this examination in a reasonable number of patients. It is now possible to detect atherosclerotic disease in the left main and the proximal left anterior descending coronary artery in 70% to 80% of all patients. This echocardiographic technique appears to be a sensitive means of detecting coronary atherosclerosis. Preliminary data suggest that this examination may be helpful in making the differential diagnosis of ischemic cardiomyopathy and idiopathic dilated cardiomyopathy.
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PMID:Transthoracic ultrasonic visualization of coronary atherosclerosis. 262 36

In parallel to increasing numbers of orthotopic heart transplantations performed during recent years, the proportion of patients with preexisting ischemic cardiomyopathy (ICM) enlarged. The present study examined peri- and postoperative risk factors and the prognosis of patients with coronary artery disease after orthotopic heart transplantation in comparison to a group with dilatated cardiomyopathy (DCM). This comparison revealed a higher risk of severe rejection episodes in patients with coronary artery disease, whereas infections were not more frequent. Graft atherosclerosis was found in a higher incidence in patients with preexisting ICM than in the DCM group. The overall incidence of graft atherosclerosis was less than 10% at one and at two years after orthotopic heart transplantation. Postoperative renal function was more impaired in the group of ICM patients, although blood levels of cyclosporine A were lower in this group. In the ICM group one and two year survival rates were 75% and 74%, respectively. Although survival rates are lower in this patient group, if compared to DCM patients (84% and 83%), orthotopic heart transplantation seems to be acceptable therapeutic alternative for endstage coronary artery disease.
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PMID:[Indications and results of orthotopic heart transplantation in coronary heart disease]. 265 97

Congestive heart failure (CHF) evolves either from an excessive workload or in response to loss of myocardium, both of which cause cardiac hypertrophy, increased cardiac pressure, and loss of functional reserve. Nearly 60% of patients in heart failure present with ischemic cardiomyopathy, which in its chronic form exhibits biventricular dilatation, elevated left ventricular mass, and extensive large-vessel atherosclerosis. The hypertrophy is proportional to the loss of myocardium, although animal studies suggest this varies with the infarct size. However, recent studies indicate that early afterload reduction may relieve the hypertrophic stimulus and prevent degeneration. Some 30% to 40% of patients in heart failure present with an idiopathic dilated cardiomyopathy, with a patchy but diffuse loss of tissue on microscopy, reactive hypertrophy in the surviving cells, and interstitial fibrosis and replacement scarring. The ultrastructural changes still await clarification. The role of pharmacologic intervention still remains unclear. However, any reduction in mortality will necessitate the identification of those cellular changes that inevitably lead to secondary degeneration of the remaining viable myocardium.
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PMID:The pathophysiologic profile of congestive heart failure. 315 47

Coronary atherosclerosis is the major health problem of the twentieth century. Although there has been a recent decrease in mortality from this condition in many Western countries, the incidence has remained the same, and coronary atherosclerosis continues to be the leading cause of death. Our understanding of the disease process has been steadily increasing; however, much still needs to be clarified. The clinical presentations of coronary artery disease are diverse and not clearly linked to the severity or extent of the disease. Patients with similar coronary lesions present variously with stable and unstable angina or myocardial infarction, and all too many have sudden death as the initial clinical presentation. Recently, much attention has focused on the initial events leading to the development of atherosclerotic plaques. Current concepts unite formerly opposed views on the roles of intimal injury, platelets, lipids, and monoclonal smooth muscle cell proliferation in initiating atherogenesis. Progress has been made in understanding the early structural and functional alterations caused by myocardial ischemia. This understanding is leading to the development of interventions such as intracoronary thrombolysis to prevent or limit permanent myocardial injury. Measures to prevent serious complications of ischemic heart disease such as infarct rupture, aneurysm formation, and ischemic cardiomyopathy are still needed.
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PMID:Pathophysiology of atherosclerotic heart disease. 654 47

The cholesterol embolization is a rare complication of atherosclerosis. A direct implication of the treatment with anticoagulants in the etiology of the disease has been questioned, and now such therapy is considered more as an adjuvant factor with angiographic procedures than as a cause. A 60-year-old patient with an ischemic cardiomyopathy presented cholesterol embolization syndrome, confirmed by cutaneous biopsy histologic examination during treatment with heparin. Spontaneous evolution was favourable and only limited amputation of the lower limbs were required. The authors think that cholesterol emboli have a direct relationship to the treatment with heparin in this case, there being no other causes to justify its appearance.
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PMID:[A cholesterol embolism during heparin treatment]. 829 Jul 79


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