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

Myocardial involvement was indicated by isolated findings (especially on the ECG) without corresponding functional disorders in one third of cases of dermatomyositis. Rapidly fatal heart failure occurred rarely in this disease, and was noteworthy for a QS complex in the central precordial leads, and for the presence of intracardiac thromboses which could give rise to emboli. Terminal cardiac failure was the rule in cases of periarteritis nodosa, which is a much rarer disease; this occurrence was secondary to hypertension. The most characteristic lesions were nodular coronary arteritis and disseminated myocarditis due to the arteriolar lesions.
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PMID:[The myocardiopathies of dermatomyositis and periarteritis nodosa]. 2 56

Myocardial involvement in lupus erythematosis takes the form of an interstitial myocarditis with cellular infiltration and fibrinoid necrosis. The most lesions are perivascular, and involve the arterioles. The myocardial fibres are involved secondarily to the vascular lesions, or by grossly, damaging sclerosis. The clinical features are variable:--no clinical features, but haemodynamic evidence of abnormal ventricular function, and perhaps sudden death;--arrhythmias and disorders of atrio-ventricular conduction;--cardiac failure, which may be due to a genuine cardiomyopathy (a part may be played by hypertension, pulmonary hypertension, renal failure, constrictive pericarditis or haemodynamically major valve disorders);--abnormalities of the coronary trunk in a certain number of cases. If anti-nuclear antibodies are present in a cardiomyopathy, the presence of DLE or of a drug-induced lupus syndrome must be suspected. There remain some awkward cases which defy classification, and which systematic use of echocardiography and pericardial and myocardial biopsy may be able to define more accurately.
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PMID:[The myocardiopathies of systemic lupus erythematosus]. 9 56

There are two types of compensatory hypertrophy of the heart. In valvular diseases, systemic hypertension and pulmonary arterial hypertension, the resultant hypertrophy compensates the increased load on the organ and is designated as hypertrophy due to overload. In ischemic disease, hereditary cardiomyopathies and myocarditis, the hypertrophy compensates for the functional insufficiency of the damaged myocardial tissue and is designated as hypertrophy due to damage. It is shown in this paper that increase in cardiac mass in both types of compensatory hypertrophy prevents acute cardiac insufficiency but at the same time is a non-balanced form of growth. As a result, in severe hypertrophy a disturbance of normal proportions at all levels of cardiac structural integration occurs. Disturbances of this type which gradually become causes of cardiac insufficiency are the main subject of this paper.
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PMID:Insufficiency of hypertrophied heart. 13 57

Male and female, nonarteriosclerotic (virgin) and arteriosclerotic (breeder), Sprague-Dawley rats were subjected to the hypertension-producing regimen of uninephrectomy, 1% saline drinking water, and desoxycorticosterone (Percorten) pivalate. Just before autopsy, some of the animals were given a single injection of corticotropin. The acute challenge of corticotropin caused a definite increase in free fatty acids, systolic blood pressure, creatine phosphokinase, glucose, and corticosterone. The two weeks of desoxycorticosterone and 1% saline-induced hypertension caused myocarditis and hyalinization of the coronary arteries of the nonarteriosclerotic (virgin) rats and definite exacerbation of the preexisting arteriosclerosis in breeder rats, severe myocarditis, and polyarteritis nodosa. All of the treated animals manifested lipid depletion of the zona glomerulosa indicative of reduced biosynthesis and secretion of endogenous mineralocorticoids due to the exogenous desoxycorticosterone and saline treatment.
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PMID:Corticotropin stimulation of hypertensive rats with and without arteriosclerosis. 21 53

1) A systematic search was made for cardiac abnormalities (clinical, radiological and EKG) and for haemodynamic disorders (catheterisation of the right side of the heart and pulmonary artery). It was generally found that: -- 14 patients (37.8%) had no symptoms; -- 8 patients (21.6%) had pulmonary arterial hypertension (PAHT) with the corresponding cardiac signs; -- 15 patients (40.5%) had cardiac signs with no evidence of PAHT. 2) The 8 patients with PAHT (21.6%) had precapillary type of PAHT with an arteriocapillary gradient. The symptoms were those of PAHT and of the right ventricular failure; but this desorder could be latent. PAHT can be in relation with inflammatory lesions. In these 8 patients, S. Mansoni was to blame in 6 cases and 5 S. Hematobium in 2. 3) In 9 patients (24.3%), cardiac signs were connected indirectly with bilharziasis by anemia, iatrogenic injury or hypertensive myocardial disease of renal origin. 4) In 3 patients (8.1%), cardiac signs were found because of coexistant disease. 5) In 3 patients (8.1%), cardiac signs could have been due to bilharzia myocarditis. The authors reviewed the experimental and clinical discussions for such a possibility.
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PMID:[Systematic cardiologic study in 37 schistosomiasis patients]. 21 89

Five patients with hypertension died as a result of myocarditis. Three were treated with methyldopa and hydrochlorothiazide, two with methyldopa alone. Their ages ranged from 30 to 71 years. In all instances death occurred suddenly, and myocarditis was not suspected clinically. The inflammatory changes in the hearts of these patients were most consistent with a hypersensitivity reaction. Additionally, there was hepatitis consistent with hypersensitivity in four of the cases.
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PMID:Myocarditis associated with methyldopa therapy. 57 72

A working classification of noncoronarogenic damage to the cardiac muscle is suggested in which 4 general-pathology groups are considered: myocardial dystrophies, myocarditis, cardiomyopathy, and neoplasms. The main principles are presented for grouping diseases of the myocardium not associated with ischemic heart disease, hypertension or rheumatic fever. Certain problems of the clinical picture and differential diagnosis of dystrophic, inflammatory, and idiopathic damages to the heart muscle are discussed.
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PMID:[Classification of non-coronarogenic myocardial damage]. 67 84

The review is based on three studies previously reported and involving the clinical, epidemiological and hemodynamic aspects of this problem. Schistosomasis may give frequently (21.6 p. 100) an arterial pulmonary hyperpressure related to the development of granulomas and arteriolitis. A myocarditis may be suspected but is rarely proved. Anemia and specific treatment are also responsible for myocardial deficiency. The parasitic changes of the urinary tract may give a systemic hypertension. Some very rare cases of acute pulmonary heart insufficiency have been reported and the responsibility of schistosomiasis in constrictive fibrous endomyocarditis is still questionned.
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PMID:[Heart and schistosomiasis (author's transl)]. 72 48

Twenty-two cases of Coxsackie virus heart disease diagnosed from November, 1969, to December, 1971, were re-examined after a period of 42 to 68 months from the acute illness. The patients with hypertension, diabetes, chronic alcohol intake, or aged over 35 were eliminated from the trial. With the purpose of assessing myocardial function, the systolic time intervals were recorded by a noninvasive standard technique. The differences in systolic time intervals between the group of patients with previous viral myocarditis and a group of normal control subjects were not statistically significant. However, the pre-ejection period was clearly prolonged in three patients out of 10, a modification consistent with a depressed myocardial function, as in patients with cardiomyopathy.
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PMID:Coxsackie virus heart disease and cardiomyopathy. 84 36

The natural history of the cardiovascular manifestations of systemic lupus erythematosus (SLE) have been altered by corticosteroids which exert their own cardiovascular effects. This study describes clinical and necropsy observations in 36 corticosteroid-treated patients with SLE and compares them to necropsy observations in patients with SLE reported before the use of corticosteroid therapy. The 36 patients averaged 32 years of age, and 33 were women. Systemic hypertension was present in 25 (69 per cent) and left ventricular hypertrophy in 23 (64 per cent) patients. Hypertension was twice as common in the 19 patients who received this drug for more than 12 months (average 38 months) than in the 17 patients who received this drug for less than 12 months (average 6 months), and was almost five times more common among our patients than in patients with SLE in the presteroid era. Congestive cardiac failure occurred in 15 patients (43 per cent), eight times more frequent than that reported in noncorticosteroid-treated patients with SLE. Subepicardial and myocardial fat was increased in all 36 patients. Lupus carditis was similar in frequency but differed morphologically in our patients compared to those not treated with corticosteroids. Libman-Sacks-type endocardial lesions, present in 18 (50 per cent) of our patients, were smaller, fewer in number, univalvular rather than multivalvular, and mainly left-sided. Most verrucae were either partly or completely healed, and some were calcified. Pericarditis, present in 19 (53 per cent) patients, was predominantly of the fibrous type. Myocarditis was present in three patients, each of whom also had endocarditis and pericarditis. The lumen of at least one of the three major coronary arteries was narrowed more than 50 per cent by atherosclerotic plaques in 42 per cent of the 18 patients who received corticosteroids for more than 1 year, but in none of the 17 patients who received corticosteroids for less than 1 year. Four of the eight patients with narrowed coronary arteries had myocardial infarcts. Although vital to the management of SLE, corticosteroids have an over-all deleterious effect on the heart. Systemic hypertension and left ventricular hypertrophy appear or, when present, worsen; congestive cardiac failure increases; epicardial apartment of Me
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PMID:The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapy. A study of 36 necropsy patients. 111 70


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