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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1982 to 1986, 1230 sudden death cases were autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were sudden cardiac deaths (SCD) including coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours of the appearance of the fatal symptoms, and most of them (72%) were considered instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%), or at work (8%). Thirty-four percent of them were thought by themselves or by their families to be healthy before the death. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were the major past history recorded. Microscopic observation of the hearts of 200 cases autopsied in 1986 showed various cardiac lesions: hypertrophy, atrophy, degenerations of myocytes, cellular and fatty infiltrations of the interstitium. According to their cardiac lesions and degrees of severity of coronary sclerosis, patients who died suddenly were divided into 8 groups as follows: 1. myocardial infarction (41) 2. myocarditis (6) 3. hypertrophic cardiomyopathy (19) 4. chronic ischemia with severe coronary sclerosis (65) 5. chronic ischemia with moderate coronary sclerosis (27) 6. small vessel disease (18) 7. amyloidosis (1) 8. unknown (23). These results suggest that coronary heart disease and hypertension play an important role in SCD.
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PMID:An epidemiologic and histopathological study of sudden cardiac death in Osaka Medical Examiner's Office. 263 29

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

Myocardial involvement in nonspecific aortoarteritis was evaluated in 16 patients (age 7-37 years, 2 males, 14 females) with the help of endomyocardial biopsy obtained from the right ventricle using the Cordis bioptome introduced from the right femoral vein. Morphological features of myocarditis were present in 8, endocardial thickening in 2, mild to moderate myofibre hypertrophy in 11, and a normal biopsy in 3 patients. Myocarditis was present in 8/11 cases with active disease and in none with inactive disease. Five of the 8 patients with myocarditis presented with congestive cardiac failure with 3 of them having no associated hypertension or valvar involvement to account for it. Immunosuppressive therapy was given to all patients with myocarditis. Serial studies (ongoing) showed clinical, haemodynamic and morphological improvement. Myocarditis appears to occur commonly in nonspecific aortoarteritis during the acute phase of the disease and may precipitate congestive cardiac failure in some patients. Immunosuppressive therapy shows promise and merits further evaluation.
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PMID:Myocardial involvement and its response to immunosuppressive therapy in nonspecific aortoarteritis (Takayasu's disease)--a study by endomyocardial biopsy. 290 33

During a 12-year period, when more than 106,000 women were delivered, 28 women with peripartum heart failure of obscure etiology that initially was diagnosed as peripartum cardiomyopathy were studied. None had obvious underlying cardiac disease or iatrogenic fluid overload, and in all an assiduous search for underlying cardiovascular disease was launched. In 21 of these 28 women, heart failure was attributed to chronic underlying disease (chronic hypertension in 14, forme fruste mitral stenosis in four, and morbid obesity in one) or viral myocarditis. Importantly, these women also had multiple compounding cardiovascular factors--preeclampsia, cesarean section, anemia, and infection--which, when superimposed on those of pregnancy, acted in concert to cause heart failure. In seven women, the cause for cardiomegaly and global hypokinesis was not found, and peripartum cardiomyopathy was diagnosed. Compared with women with explicable causes of peripartum heart failure, these women did poorly: six had persistent cardiomegaly and heart failure, and four of these died within four months to eight years. From these observations, the authors conclude that idiopathic peripartum cardiomyopathy is uncommon, and that in most women with peripartum heart failure of obscure etiology, underlying chronic disease will be identified. Heart failure in these women ensues when the cardiovascular demands of normal pregnancy are amplified further by common pregnancy complications superimposed upon these underlying conditions that cause compensated ventricular hypertrophy.
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PMID:Peripartum heart failure: idiopathic cardiomyopathy or compounding cardiovascular events? 293 58

We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, asymmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.
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PMID:Idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. 295 39

Chronic and acute lead poisoning cause overt, clinical symptoms of cardiac and vascular damage with potentially lethal consequences. Morphological, biochemical, and functional derangements of the heart have all been described in patients following exposure to excessive lead levels. Disturbances in cardiac electrical and mechanical activity and postmortem evidence of morphological and biochemical derangements of the myocardium have all been reported following excessive exposure to lead in humans. In addition, signs of vascular degeneration, abnormal vascular smooth muscle function, and altered vessel compliance have been described in humans chronically and acutely exposed to toxic lead levels. Similar cardiovascular complications have been detected following excessive lead exposure in experimental animals. Myocarditis, electrocardiographic disturbances, heightened catecholamine arrhythmogenicity, altered myocardial contractile responsiveness to inotropic stimulation, degenerative structural and biochemical changes affecting the musculature of the heart and vasculature, hypertension, hypercholesterolemia, atherosclerosis, and increased vascular reactivity to alpha-adrenergic agonists have been among the reported cardiovascular disturbances linked to lead poisoning. Less certain are the cardiovascular effects of subclinical lead poisoning. Although controversial, chronic low-level lead exposure has been linked to hypertension and other cardiovascular disturbances in both clinical and experimental studies. In general, it can be concluded that lead over a wide range of exposure intensities can induce significant changes in the function of the cardiovascular system. Evidence points to the involvement of multiple sites of action. Cardiac and vascular sites, as well as sites within the central nervous system, have all been implicated in the sequelae of cardiovascular effects. The exact pathogenic mechanisms that underlie the actions of lead in the cardiovascular system, however, have yet to be elucidated definitively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular actions of lead and relationship to hypertension: a review. 306 Mar 56

Two young women (aged 32 and 25 years) with systemic lupus erythematosus and heart valve lesions in association with antiphospholipid antibodies are presented. In addition to the presence of the 'lupus anticoagulant' and false positive Venereal Disease Research Laboratory (VDRL) tests, both patients had high levels of IgG anticardiolipin antibodies. The first patient additionally had contraceptive induced chorea, chorea gravidarum, seven miscarriages, livedo reticularis, pulmonary embolism, and thrombocytopenia and developed culture negative endocarditis as well as hypertension. The second patient, who had presented with hypertension, developed aortic and mitral regurgitation, suspected myocarditis, manifested transient ischaemic attacks, and responded well to anticoagulation and steroid treatment.
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PMID:Diagnostic and therapeutic problems in two patients with antiphospholipid antibodies, heart valve lesions, and transient ischaemic attacks. 314 42

SLE is an inflammatory disease of unknown etiology with the potential of affecting virtually all organ systems. Cardiovascular involvement occurs frequently, although it is often mild enough not to cause clinical concern. Pericarditis is most commonly subclinical, noted only on echocardiogram. Pericardial fluid, which can accumulate rapidly enough to cause tamponade, is inflammatory in nature and can totally mimic infection. The occurrence of Libman-Sacks endocarditis, usually a pathological diagnosis of little clinical significance, has little if any correlation with the presence of audible murmurs. However, valve replacement is occasionally necessary secondary to sterile destruction. These valvular lesions can also embolize or become infected. The incidence of ischemic coronary disease is increased, both secondary to premature atherosclerosis and, rarely, coronary arteritis. Conduction disease and arrhythmias are infrequently reported in adult patients, but congenital CHB has been noted in children born to mothers who have circulating anti-Ro antibody. Evidence is accumulating that suggests there is a mild cardiomyopathy associated with SLE that may be due to thrombotic or inflammatory microvascular coronary disease. Acute clinical myocarditis also rarely occurs. Therapeutically, at present, a reasonable course would seem to be to limit all known possible contributing factors to premature coronary artery and myocardial disease (hypertension, hypercholesterolemia, smoking, steroid therapy, etc), to be vigilant about recognizing the rarer complications associated with SLE (infectious pericarditis and endocarditis, coronary arteritis, pericardial tamponade, clinical myocarditis), and to remember that these uncommon complications are indeed uncommon. The importance of vigorously treating systemic hypertension cannot be overstressed.
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PMID:Cardiovascular involvement in systemic lupus erythematosus. 333 84

To investigate the pathogenesis and pathophysiology of dilated cardiomyopathy (DCM), we studied 28 patients with DCM by echocardiography and endomyocardial biopsy, and compared their findings with those of 34 patients including eight with myocarditis, seven with alcoholics, 12 with hypertensives and seven patients with hypertrophic cardiomyopathy. All 12 patients in the hypertensive group had congestive heart failure without accompanying high blood pressure, and prominent dilatation and uniform wall motion abnormality of the left ventricle observed echocardiographically on admission. After medical management, both heart failure and the echocardiographic abnormalities gradually resolved. Those in the alcoholic group had larger left ventricles and uniform wall motion abnormality compared to those in the other groups. The myocarditis and hypertrophic cardiomyopathy groups had smaller left ventricles, non-uniform wall motion and larger % myocardial fibrosis. Both ventricles in the hypertrophic cardiomyopathy group were thicker than those of the other three groups. Each patient with DCM had individual echocardiographic abnormalities, which could be categorized as two subsets depending on the degree of left ventricular dilatation and uniformity of the wall motion. The one was characterized by a prominently dilated left ventricle and uniform wall motion abnormality similar to the alcoholic group, and the other had less marked left ventricular dilatation and heterogeneous wall motion abnormality similar to the myocarditis group. From these findings, it was suggested that there are common factors to specific myocardial disease in the pathogenesis and pathophysiology of DCM, and thus, DCM might include many subsets of different etiologies.
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PMID:[Pathogenesis of dilated cardiomyopathy: a study based on comparison of the clinical features with other related conditions]. 342 22

Between March 1981 and March 1986, 200 orthotopic heart transplantations were performed at the University of Pittsburgh. Fourteen of those procedures were carried out in children 2 to 16 years of age. Two children received combined liver and heart transplants; one because of familial hypercholesterolemia with associated ischemic heart disease, and the other because of dilated cardiomyopathy associated with intrahepatic biliary atresia. Eight patients had dilated cardiomyopathy, and two had myocarditis. Two had heart transplantations for congenital heart disease: one had multiple muscular ventricular septal defects repaired in infancy and had an associated cardiomyopathy, and the other developed a cardiomyopathic ventricle from a congenital right coronary artery to right atrial fistula. Chronic immune suppression consisted 0.2 to 0.5 mg/kg/d of prednisone and 5 to 50 mg/kg/d cyclosporine, with the addition of antithymocyte globulin for unresolved moderate or severe acute rejection. There were three early postoperative deaths: one from intracranial bleeding, one from Pseudomonas mediastinitis, and one from ischemic injury to transplanted organs. Early postoperative complications included reversible renal failure, hypertension, and seizures. Late problems were related to allograft rejection and side effects of cyclosporine and corticosteroids. Significant rejection episodes occurred in all patients surviving longer than 2 weeks, with seven requiring antithymocyte globulin. Two patients died 8 months following transplantation of severe acute and chronic rejection; another patient required retransplantation for ischemic cardiomyopathy resulting from chronic rejection but subsequently died of recurring rejection 3 months after the second transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experience with heart transplantation in children. 354 Aug 34


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