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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

Cardiac transplantation for the treatment of end-stage congestive heart failure has been shown to be of benefit regardless of the etiology. With few exceptions, the evaluation of patients with end-stage heart failure is the same, regardless of the etiology. In those with cardiomyopathy not as a result of CAD, special attention must be given to exclude secondary causes of cardiomyopathy such as amyloidosis, hemochromatosis, and sarcoidosis, as well as generalized systemic illnesses that may also involve the heart, either secondary or hereditary, because special consideration must be given to these patients on a case-by-case basis to determine that there is no general systemic involvement of the illness that would preclude satisfactory rehabilitation after transplantation. Before cardiac transplantation becomes widely available, there must be a greater number of donor hearts, the lack of which now severely limits the number of transplants performed in comparison with the estimated need.66 Additionally, more effective and specific immunosuppressive agents must be identified in order to reduce the incidence of rejection, infection, and accelerated atherosclerosis that now limits the longevity of transplant recipients. Furthermore, the ideal immunosuppressive agent should be associated with fewer side effects than those currently available. The emotional and economic burdens placed on the patient, the family, and society must be balanced against the benefits generated by the procedure. Despite these limitations, cardiac transplantation continues to offer hope for the terminally ill patient, which must be tempered by an understanding of the real limitations of transplantation.
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PMID:Patient selection and results of cardiac transplantation in patients with cardiomyopathy. 304 84

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.
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PMID:Causes of sudden death in competitive athletes. 351 Feb 33

Inflammation is frequently associated with changes in the surrounding connective tissue. Inflammatory mononuclear cells (MNC) produce biologically active molecules, cytokines (CK), which may regulate the growth and function of connective tissue fibroblasts. In this article, we review the characteristics of lymphocyte and monocyte CK which appear to be involved in regulating fibroblast recruitment, proliferation, and matrix synthesis. Whereas these MNC products are important in normal physiologic wound healing, an imbalance of these CK may lead to pathophysiologic fibrosis and/or destruction of connective tissue components. Clinical states associated with MNC-mediated connective tissue pathology include scleroderma, rheumatoid arthritis, diffuse pulmonary idiopathic fibrosis, sarcoidosis and atherosclerosis. Characterization of the molecular pathways linking inflammatory mononuclear cells and fibrosis may provide avenues for therapeutic intervention.
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PMID:Cytokines and fibrosis. 353 33

The causes of sudden, unexpected death in highly-conditioned competitive athletes are summarized. In the vast majority of young athletes (less than 35 years of age) sudden death is due to underlying structural cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths and may account for about one-half of the sudden deaths in a youthful athletic population. Cardiovascular abnormalities that appear to be less frequent important causes of sudden death include anomalous origin of the left coronary artery from the anterior sinus of Valsalva, ruptured aorta (due to cystic medial necrosis), idiopathic concentric left ventricular hypertrophy and coronary artery atherosclerosis. Other diseases which are probably particularly uncommon causes of sudden death in the young athlete include mitral valve prolapse, aortic valvular stenosis, acute myocarditis, QT interval prolongation syndromes, hypoplasia of the coronary arteries or sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life. In only about 25% of those competitive athletes who die suddenly is underlying disease identified prior to participation and rarely is the correct clinical diagnosis made. In contrast, when sudden death occurs in older competitive or recreational athletes (over 35 years of age) it is usually due to coronary artery disease.
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PMID:Hypertrophic cardiomyopathy: a common cause of sudden death in the young competitive athlete. 668 29

A rare case of tuberculous myocarditis, miliary type, in hematogenic-disseminated tuberculosis of lungs and liver is reported. Some morphological characteristics of tubercules in myocardium require a broad differential diagnosis with idiopathic granulomatous myocarditis, sarcoidosis, lues and brucellosis. Tuberculosis was in combination with isolated heart defect-- insufficiancy of aortic valve, hypertonic disease, atherosclerosis, dissecting aneurysm of ascending aorta and left coronary artery of the heart, complicated by a rupture during the cardiac operation.
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PMID:[A case of tuberculous myocarditis and rupture of a dissecting aortic aneurysm and of the left coronary artery of the heart during surgery for an aortic heart defect]. 674 Nov 9

In a population sample in whom violent accident was the cause of death, the following prevalence of coronary intimal necrosis, occurring as an independent lesion and as an early step of atherosclerotic involvement, was revealed: 2% of children 6--10 years old, 6% of children and juveniles 11--15 years old, 14% of adolescents 16--20 years old, 32% of young adults 21--25 years old, 56% of young adults 26--30 years old, 72% of mature adults 31--35 years old and 84% of mature adults 36--40 years old. In each age subgroup, the percentage of subjects with coronary intimal necrosis was greater than the percentage of subjects with coronary atherosclerotic plaques. A centrifugal extension with age of intimal necrosis, along the coronary tree in the direction of blood flow, was observed. Histologically, the coronary intimal necrosis exhibited a mucoid form, a swelling form and a dissecting form. Indirect evidence was offered that some areas of coronary intimal necrosis formed an adequate nidus for lipid and fibrin accumulation and also induced the development of a peculiar type of subendothelial connective tissue. These successive changes led to the onset of atheroma-like lesions with a prevalence of lipid deposits, or of intramural thrombi or of a fibro-hyaline cap. The onset, extent and evolution of coronary intimal necrosis was accelerated by the male sex, by some minor deviations from the basal branching anatomical pattern of the coronary arteries, by the main risk factors for coronary heart disease, as well as by some terminal diseases, such as the generalized form of sarcoidosis and the renal complications of systemic lupus erythematosus.
Atherosclerosis 1981 Jul
PMID:Coronary intimal necrosis occurring as an early stage of atherosclerotic involvement. 725 28

One hundred and fifty-four (5.7%) of 2690 patients who had been admitted to a hospital for sarcoidosis of intrathoracic lymph nodes (ITLN) were diagnosed as having various cardiovascular diseases (hypertensive disease, congestive lung, congenital and acquired cardiac diseases, atherosclerosis, aortic aneurysms and myocarditis). Misinterpretation of the X-ray film of the lung root, no lateral X-ray films, inadequate scope of objective studies of the cardiovascular system are the most common errors at prehospital examination. The obligatory making of lateral X-ray films, tomograms, the use of computed tomography, ECG and phonocardiography, and thorough account of objective data are valuable additional methods in the differential diagnosis of ITLN sarcoidosis and cardiovascular diseases accompanied by the appearance of wide truncal large vessels of the root due to pulmonary hypertension.
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PMID:[The differential diagnostic characteristics of sarcoidosis of the intrathoracic lymph nodes and of cardiovascular diseases]. 902 96

The goal of the present review consists on the relationship between inflammatory disorders, such as that represented by systemic granulomatous diseases like sarcoidosis, and the cholesterol metabolism and its implication in the atherosclerosis process. Serum amyloid A is an acute phase reactant that transiently binds to the high density lipoproteins during an inflammatory response. Serum amyloid A may act either displacing apo A-I, which in turn result in increased catabolism of high density lipoproteins, or inhibiting lecithin-cholesterol acyltransferase activity which leads to low levels of esterified serum cholesterol. This lipoprotein alteration together with a direct effect of the serum amyloid A on the endothelium of the atheromatous plaque suggest a potential pathophysiological link between the inflammatory responses expressed by the serum concentrations of amyloid A and the development of the atherosclerotic process.
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PMID:[Inflammatory response, cholesterol metabolism, and arteriosclerosis]. 1132 88

Diagnosis depends on the clinical manifestations, blood or cerebrospinal fluid study and MRI findings. Acute and subacute intraparenchymal spinal cord disorders are due to vascular disorders or myelitis. Spinal cord infarction is associated with dissecting aortic aneurysm, surgical clipping of aortic aneurysms, aortic atherosclerosis or hypotension from any cause. Hematomyelia results from trauma, vascular malformations, vasculitis, or a coagulation disorder. Acute infectious myelopathies result from direct invasion of the spinal cord by bacteria, parasite, or virus. The cause of acute or subacute inflammatory disease include multiple sclerosis, Devic disease, acute disseminated encephalomyelitis, SLE, or sarciodosis. Sarcoidosis sometimes requires differential diagnosis with cord tumor. Chronic intraparenchymal spinal cord disorders are due to syringomyelia, familial spastic paraplegia, HTLV-1 associated myelopathy, adrenomyeloneuropathy, and vascular malformations. HTLV-1 associated myelopathy present with progressive spastic paraplegia with bladder disturbance and has antibodies to HTLV-1 in the cerebrospinal fluid and serum. Diagnosis of adrenomyeloneuropathy is made by demonstration of elevated levels of very long chain fatty acids in plasma. Vascular malformations are important lesions because they present a treatable cause of progressive myelopathy.
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PMID:[Medical approach to intraparenchymal spinal cord disorders]. 1278 77


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