Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

Hypertension is the commonest cardiovascular disease in Africans occurring in more than 15% of the adult population in some studies. It occurs in the lower as much as in the higher socio-economic groups. Recent studies have confirmed earlier findings that essential hypertension in Africans is characterised by volume loading, low plasma renin activity, high salt taste threshold, high urinary sodium and low potassium excretion and high plasma aldosterone. The commonest complication of hypertension in Africans is congestive cardiac failure followed by cerebrovascular accidents. Coronary heart disease is rare. Even in the absence of overt heart failure and compounding factors like obesity, alcoholism, cigarette smoking, diabetes mellitus and myocarditis, evidence of abnormal left ventricular morphology and function is often present in newly diagnosed patients with moderate or severe hypertension. Response to monotherapy with beta-blockers or ACE inhibitors is usually poor but is good with thiazide diuretics or calcium channel blockers. The diuretics are an essential component of a two or three drug regime containing other classes of antihypertensive drugs. Cost of drugs is the most important determinant of compliance with drug treatment and consequently the likelihood of progression of the diseases to more severe forms in long term follow-up.
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PMID:Hypertension in Africa and effectiveness of its management with various classes of antihypertensive drugs and in different socio-economic and cultural environments. 826 3

Cocaine abuse is widespread in North America. It is estimated that almost one in every four Americans has used cocaine at least once in his/her lifetime. In the past two decades, cocaine related cardiovascular complications have mushroomed because cocaine has become cheaper and more readily available. The fundamental effects of cocaine on cardiovascular system are similar to those observed following an intense, sympathetic stimulation. Cocaine intake results in marked increase in blood pressure, myocardial oxygen demand and heart rate. Coronary blood flow, which increases in response to exercise (endogenous sympathetic stimulation) however, is decreased by cocaine intake. Increased demand of oxygen by the myocardium in the face of decreased supply in subjects with cocaine use, leads to myocardial ischemia, which in turn forms a substrate for most of the cardiovascular complications, namely, myocardial infarction, cardiac arrhythmias and acute pulmonary edema. Hypertension related complications, dissection and rupture of aortic aneurysm, hemorrhagic stroke, in addition to infective endocarditis, myocarditis, cardiomyopathy all occur more frequently in cocaine addicts. In this review, pertinent clinical pharmacology and cardiovascular risks associated with cocaine abuse are presented.
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PMID:Cardiovascular effects of cocaine abuse. 829 63

After decades of focus on the effects of cocaine abuse on the central nervous system (CNS), the cardiovascular toxicity of cocaine is just beginning to be appreciated. The most common cardiovascular pathologies associated with cocaine use include: cardiomyopathy, left ventricular dysfunction, myocarditis, arrhythmia, hypertension, myocardial infarction, stroke, arterial thrombosis, deep vein thrombosis, and gastrointestinal, renal, and skeletal muscle ischemia. This article reviews the above pathologies with speculations on the mechanisms by which cocaine produces cardiovascular tissue damage.
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PMID:Cardiovascular and thrombosis pathology associated with cocaine use. 829 12

Although an etiologic link between viral myocarditis and idiopathic dilated cardiomyopathy has long been recognized, the actual extent of this relation has been uncertain. In this review, we examine recent developments in the molecular analysis of endomyocardial biopsy specimens, particularly techniques for gene amplification, which have unequivocally confirmed this relation and given us some insight into its significance. In addition, we show that viral myocarditis in a murine model is associated with spasm of the coronary microvasculature, leading to myocyte necrosis, fibrosis, calcification and cardiac dilation. These findings are similar to those seen in the hearts of genetically cardiomyopathic hamsters, rats and humans with hypertension and diabetes, rats after acute brain injury and models of Chagas' disease. Treatment of microvascular spasm with verapamil, captopril or alpha 1-adrenergic blocking agents appears to interrupt this pathway and has been shown to markedly impede the evolution of dilated cardiomyopathy in the genetic hamster model and a murine model of myocarditis. There is some suggestion that digitalis, though beneficial during cardiac decompensation, may actually be detrimental when administered during the early stages of myocardial disease. These experiments have led to a new paradigm for the pathogenesis of cardiomyopathy after viral myocarditis, as well as a general hypothesis for the pathogenesis of some types of dilated cardiomyopathy. They also suggest that the selection of therapeutic agents for some forms of dilated cardiomyopathy may differ significantly between the early and late stages of the disease.
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PMID:Viral myocarditis: a paradigm for understanding the pathogenesis and treatment of dilated cardiomyopathy. 837 2

Thirteen patients with non-specific aortoarteritis and endomyocardial biopsy evidence of myocarditis were followed-up on immunosuppressive therapy comprising of prednisolone and cyclophosphamide in addition to conventional treatment for hypertension and/or congestive heart failure. Serial determinations of erythrocyte sedimentation rate, chest roentgenogram, radionuclide ventriculogram and hemodynamic study including endomyocardial biopsy were carried out at 12, 24 and 52 weeks of therapy. Arterial lesions were also assessed by digital subtraction angiography at 0 and 52 weeks of immunosuppressive therapy. At the end of a year of treatment all patients with congestive heart failure (10/13) showed symptomatic improvement by at least one New York Heart Association (NYHA) class. There was a significant fall in erythrocyte sedimentation rate (48 +/- 12 mm/1st h to 31 +/- 12 mm/1st h, P < 0.05), pulmonary artery pressure (32 +/- 14 mmHg to 20 +/- 9 mmHg, P < 0.05), left ventricular filling pressure (20 +/- 11 mmHg to 11 +/- 7 mmHg, P < 0.05) and increase in left ventricle ejection fraction (39 +/- 16% to 51 +/- 14%, P < 0.05) associated with resolution of morphological changes on endomyocardial biopsy. Arterial lesions remained static with neither progression nor appearance of new lesions. No significant complications of therapy were noticed in any patient. Our uncontrolled observations suggest that immunosuppressive therapy is safe and results in clinical, hemodynamic and myocardial morphological improvement in a subset of patients with non-specific aortoarteritis and associated myocarditis.
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PMID:Non-specific aortoarteritis: long-term follow-up on immunosuppressive therapy. 840 11

The concept of "cardioprotection" with ACE inhibitors has evolved over the last decade. In the 1980s, protective benefits of ACE inhibitors in hypertension were established, regression of left ventricular hypertrophy was demonstrated, and improved ventricular function and survival in mild-to-moderate and severe congestive heart failure was documented. A further "protective" role of ACE inhibitors in coronary artery disease is emerging as more attention is focused on the concept of local tissue renin-angiotensin systems. Recent contributions to the literature describe significant benefits of ACE-inhibitor therapy in acute myocardial infarction, including suppression of ventricular arrhythmias and reduction of both early and late ventricular dilation, preservation of left ventricular function, and improved survival. All of the above effects can be considered "cardioprotective." However, as new benefits are reported in the 1990s, a broadened view of "cardiovascular protection" emerges from investigative studies in the literature. ACE inhibitors may reduce tolerance to nitrates, reduce angina in some but not all studies, and limit smooth muscle cell proliferation (and perhaps restenosis) induced by experimental balloon angioplasty. Local vascular effects may attenuate atherosclerotic changes in the arterial wall in experimental animals and may decrease the incidence of aneurysm formation in hypertensive animals. The effectiveness of ACE inhibitors in acute myocarditis, suggested by reports that captopril may reduce lesions of murine myocarditis when administered early after infection with coxsackievirus B3, requires clinical confirmation. Despite these apparently diverse "cardiovascular protective" consequences of ACE inhibitor therapy, the mechanism(s) of action of these agents remain to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotection with angiotensin-converting enzyme inhibitors: redefined for the 1990s. 843 34

Fifty patients in stage IV of HIV infection (including 41 AIDS patients) were prospectively studied by echocardiography. Thirteen of them showed abnormalities: 4 had pericardial effusion, 1 endocarditis, 7 myocardial disorders and 1 primary pulmonary arterial hypertension. Pericardial effusion, also present in patients who had pleuropulmonary Kaposi's sarcoma, was not specific. Myocardial disorders concerned the diastolic function in 1 case, the segmental kinetics in 2 cases and the whole systolic function in 4 cases (3 had congestive myocardiopathy and 1 had transient systole alteration without left ventricular dilatation). The mechanism of global left ventricular disorders was multifactorial, and several hypotheses were discussed: infectious myocarditis, adrenergic or nutritional deficiency myocarditis, cardiotoxicity of antiviral drugs, common pathology with HIV encephalopathy. The prognosis of congestive myocardiopathy was poor in AIDS patients and undetermined in stage IV non-AIDS patients. Echocardiography is capable of detecting these lesions, and its use may contribute to a better care of these patients.
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PMID:[Echocardiographic abnormalities in the stage IV of HIV infection]. 851 Nov 25

Misdiagnosis of primary hypothyroidism may be due to its running under the mask of myocardiodystrophy, coronary heart disease, bacterial and allergic myocarditis, arterial hypertension. It may underlie edema or accompany malignancy (thyroid cancer, in particular). Accurate diagnosis is complicated by primary damage to one organ or system.
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PMID:[Therapeutic "masks" of primary hypothyroidism]. 864 32

Major cardio-circulatory events, defined as circulatory death, myocardial infarction, unstable angina, or stroke, sometimes occur unexpectedly in patients who apparently have no evident increase in risk (absence of overt heart failure, hypertrophy, uncontrolled or severe hypertension, previous or present myocardial infarction, angina, myocarditis, infectious or any other pericardial, valvular or great vessel disease, heart malformation, significant arrhythmia or conduction disturbances). To investigate whether 2D-guided M-mode echocardiographic variables have predictive value in such patients, a retrospective analysis of 1,965 cases was performed. Twenty-one patients were found who on the day of echocardiographic examination fulfilled the above criteria, but suffered major cardio-circulatory events during the first following year (1 yr group), 12 during the second year (2 yr group), and 16 during the third year (3 yr group). Twenty-eight patients who fulfilled the same criteria, but were followed-up free of major cardio-circulatory events for 935 +/- 144 days constituted the control group. Multivariate analysis of variance (MANOVA) of echocardiographic data was used to select the final set of 11 variables from 30 measurements and calculations which enabled satisfactory discrimination between the four groups (Hotelling T2 = 3.979, Fisher F = 7.596 > Ftab = 1.585). Extension of MANOVA with the leave-one-out method revealed that none of 28 control patients was predicted to be at risk of major cardio-circulatory events in the next year, and only one of 21 patients from the 1 yr group was misdiagnosed as not being at risk. Patients at risk were older, had slightly greater body size (particularly weight), and slightly increased diastolic diameter and volume of the left ventricle. The left ventricular mass, mean wall thickness, and estimated cross-sectional area indexes were also slightly increased. The peak systolic stress was slightly increased and contractility index (BPS/ESVI) was slightly decreased. Our preliminary results suggest that easily obtained echocardiographic measurements and calculations contain clinically useful predictive information.
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PMID:Prediction of lethal or life-threatening cardio-circulatory events in patients who apparently are not at risk : a preliminary retrospective echocardiographic study. 884 Feb 15

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99


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