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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular hypertrophy (LVH) is a common sequela of long-standing essential hypertension. LVH cannot be considered, however, an adaptive process only serving to normalize wall stress but can be considered one that significantly increases the risk of sudden death, myocardial ischemia, congestive heart failure, and other cardiovascular diseases. Patients with LVH exhibit impaired ventricular filling, ventricular arrhythmias, and myocardial ischemia even in the absence of coronary artery disease. LVH can be prevented or reversed by a variety of antihypertensive agents including calcium channel blockers and angiotensin converting enzyme inhibitors. Calcium channel blockers, more than angiotensin converting enzyme (ACE) inhibitors, suppress ectopic impulse generation, improve ventricular compliance, and alleviate myocardial ischemia while preserving or improving the contractile state. In contrast, ACE inhibitors can be particularly useful in patients with LVH and diminished ventricular contractility and in preventing chamber dilatation after myocardial infarct. These favorable cardiovascular effects of both calcium channel blockers and ACE inhibitors are a reason for optimism that carefully tailored therapy will ultimately diminish the well-documented risk of cardiovascular morbidity and mortality associated with LVH.
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PMID:Effects of antihypertensive therapy on hypertensive heart disease. 253 79

Established essential hypertension is characterised haemodynamically by a normal cardiac output and elevated total peripheral resistance. As hypertensive cardiovascular disease progresses, and the patient grows older, cardiac output falls and total peripheral resistance is further elevated. The activity of the renin-angiotensin-aldosterone (RAA) system declines throughout life and reaches its lowest levels in the elderly, unless there is congestive heart failure. In long-standing hypertension, target organ disease such as left ventricular hypertrophy, nephrosclerosis and cerebrovascular damage is commonly observed. Rational antihypertensive therapy should therefore aim to lower total peripheral resistance, spare cardiac output, and maintain or improve blood flow to target organs. ACE inhibitors lower arterial pressure by decreasing total peripheral resistance, they maintain or improve cardiac contractility, promote regression of left ventricular hypertrophy, and increase renal blood flow. Lisinopril is a novel ACE inhibitor that does not contain a sulphydryl group. It is not a prodrug and thus does not require bioactivation by the liver. Lisinopril has a long duration of action, allowing it to be used as a single daily dose in the treatment of hypertension. Preliminary studies from our laboratory indicate that lisinopril reduces cardiac output and preload to the left ventricle. Lisinopril also reduces left ventricular hypertrophy and lowers renal vascular resistance, thereby increasing renal blood flow. In patients with mild to moderate hypertension, lisinopril is more effective than hydrochlorothiazide in reducing both systolic and diastolic blood pressure, and is at least as effective as atenolol or metoprolol in reducing diastolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lisinopril in the treatment of hypertension. 255 Jun 40

A 60-year-old woman was admitted with congestive heart failure, essential hypertension and abdominal distension. Her son reported that she appeared with red spots in the body and that she was under dapsone therapy. Seven months ago there was sudden increase of the skin lesions. In the 11th day after admission she underwent a stroke that progressed to decerebration and she expired on the fourth day. Autopsy confirmed CHF due to chronic myocarditis related to Chagas' disease. Aneurysm of the apical region of the left ventricular chamber was also observed leading to thrombosis and systemic embolism with brain and spleen hemorrhagic infarct. In the encephalous there was edema, uncus herniation and hemorrhagic infarct of the brain stem. The skin lesions were due to reactional tuberculoid hanseniasis (RHT) with focal lesions in axillary lymphnodes, nasopharyngeal mucosa and in the posterior tibial nerve. The pathogenesis of RHT is discussed as well as its differentiation with the BT group of Ridley and Jopling and its probably relationship with the secondary tuberculoid hanseniasis reported by Ridley. The focal lesions are also discussed with END to the involvement of a peripheral nerve trunk what is said to be uncommon in this form of Hansen's disease.
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PMID:[Myocardial disease, heart failure and reactional tuberculoid leprosy]. 256 89

Essential hypertension is a major health care problem in the elderly and requires effective treatment to reduce morbidity and mortality. The traditional stepped-care approach to therapy consisted of diuretics; sympatholytic agents, or beta-blockers for all age groups. Indeed, initial therapy with these agents is effective in 50 to 60 percent of elderly patients but may produce adverse effects. A high incidence of adverse responses, including sexual dysfunction and central nervous system impairment, has been reported with diuretic or beta-blocker therapy, and a reduction in several measures of quality of life has been noted during therapy with methyldopa or propranolol. Administration of an angiotensin-converting enzyme (ACE) inhibitor is as effective as the traditional stepped-care approach without producing the ill effects associated with diuretics, sympatholytics, or beta-blockers. The combination of an ACE inhibitor with a diuretic produces additive antihypertensive effects while minimizing diuretic-induced metabolic alterations. Orthostatic hypotension with the first dose can be minimized by making sure that patients are not hypovolemic from previous diuretic therapy. Nevertheless, in controlled trials, the combination of ACE inhibitor and diuretic has been effective in up to 85 percent of patients. In addition, the use of ACE inhibitors may be beneficial in the hypertensive patient with concomitant congestive heart failure. Most important, the patient's quality of life is maintained during therapy with an ACE inhibitor alone or in combination with a diuretic. Thus, an ACE inhibitor plus a diuretic is a valuable alternative to traditional antihypertensive therapy in elderly patients.
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PMID:Drug therapy for hypertension in the elderly. 256 74

The drug treatment of mild hypertension has been shown to afford protection against fatal and nonfatal strokes, congestive heart failure, progression to more severe levels of hypertension, and all-cause mortality, but not against the complications of coronary artery disease. The lack of benefit against coronary artery disease may result from failure to reduce other risk factors or because the drugs employed increased coronary risk. It can be taken as axiomatic that effective preventive antihypertensive therapy is more likely with drugs with mechanisms and sites of action that are focused on the underlying pathophysiology than with drugs that lower blood pressure by means unrelated to the hypertensive process. Adrenergic predominance plays a major role in the initiation and maintenance of essential hypertension and, consequently, the alpha-adrenergic receptor inhibitors were among the first substances to receive serious consideration as antihypertensive agents. However, since these drugs are nonselective, feedback control of transmitter norepinephrine was lost and, consequently, the clinical expectations of the early alpha-adrenergic receptor inhibitors in the treatment of high blood pressure were not fulfilled. The discovery of selective postjunctional alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, which preserve feedback control of transmitter norepinephrine release, was the crucially important step in the development of specific drugs to combat the hyperactivity of adrenergic vasoconstrictor nerves in hypertension. These drugs have been shown to normalize hemodynamics in hypertensive patients. They lower blood pressure through a reduction in peripheral resistance at rest and during exercise, independent of changes in heart rate and blood pressure, with minimal reflex activation or tolerance development. Alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, represent an attractive choice for initial therapy in all grades of hypertension and are especially appropriate in hypertensive patients with congestive heart failure, asthma and chronic obstructive airways disease, renal impairment, diabetes mellitus, hyperlipidemia, benign prostatic hyperplasia, or gout, and in those involved in vigorous work, sports, or exercise. There are no known contraindications to these drugs, except in patients who are sensitive to quinazolines.
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PMID:Pharmacologic basis for the use of doxazosin in the treatment of essential hypertension. 256 23

In recent years, there has been increased recognition of the relative importance of abnormalities of diastolic function in patients with essential hypertension. Indeed, diastolic dysfunction may be the earliest indicator of hypertensive heart disease. In this article, the mechanisms governing normal ventricular relaxation and the factors that may cause diastolic dysfunction are reviewed. Noninvasive clinical methods, particularly Doppler echocardiography and radionuclide angiography, for determination of diastolic function are outlined, and the limited experience in the management of hypertensive patients with abnormalities of diastolic function is discussed. When congestive heart failure develops in a patient with hypertension, it is especially important to determine whether it is due primarily to systolic or to diastolic left ventricular dysfunction.
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PMID:Hypertension and left ventricular diastolic function. 257 61

The pharmacologic therapy of mild primary hypertension (diastolic blood pressure less than 105 mm Hg) has effectively reduced hypertensive arteriolar end organ disease such as cerebrovascular accidents, congestive heart failure, and nephropathy, but there has been no convincing evidence that coronary heart disease (CHD) or its complications, acute myocardial infarction or angina, have been reduced. The risks of therapy with certain antihypertensive drugs may outweigh their treatment benefits as it relates to CHD. The optimal treatment strategy should be to reduce all CHD risk factors, reverse the hemodynamic abnormalities present by lowering the systemic vascular resistance (SVR), preserving cardiac output (CO) and perfusion, and to select the best antihypertensive drug for concomitant medical diseases or problems while maintaining a good quality of life. Antihypertensive drugs that have favorable or neutral effects on CHD risk factors include alpha blockers, calcium channel blockers, central alpha agonists, and angiotensin-converting enzyme inhibitors. On the other hand, diuretics and beta blockers without intrinsic sympathomimetic activity have unfavorable effects on many CHD risk factors. Baseline and serial evaluation of the effects of these drugs on serum lipids, lipid subfractions, glucose, uric acid, electrolytes, exercise tolerance, left ventricular hypertrophy, blood pressure, SVR, CO, perfusion, concomitant diseases, and side effects is necessary to evaluate overall cardiovascular risk.
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PMID:New insights and new approaches for the treatment of essential hypertension: selection of therapy based on coronary heart disease risk factor analysis, hemodynamic profiles, quality of life, and subsets of hypertension. 238 95

Hypertension is a common problem encountered after renal transplantation. Many different mechanisms may be responsible for hypertension in this setting, and therapy will depend upon the mechanism(s) affecting the individual patient. Factors that may cause or aggravate post-transplantation hypertension include renal dysfunction secondary to rejection or other diseases of the transplanted kidney, renin production from the diseased native kidneys if these kidneys have not been surgically removed, extracellular fluid volume expansion, toxic effects of medications used after transplantation, especially cyclosporine and intravenous prednisolone, or primary hypertension in the donor or recipient. Renal artery stenosis may predispose to acute renal failure in the presence of treatment with angiotensin-converting enzyme inhibitors. Severe renal artery stenosis may also lead to refractory salt and water retention and fluid overload with congestive heart failure and hypertension, mediated primarily due to extracellular fluid volume excess. Therapy with percutaneous transluminal renal angioplasty or, as a last resort, surgery, can be successful in controlling these problems.
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PMID:Refractory hypertension after renal transplantation. 266 26

In hypertensive patients as well as in normal subjects urapidil has a hypotensive action. This is mainly mediated by a peripheral alpha 1-adrenoceptor blockade with a decrease in systemic vascular resistance; in addition, during acute animal experiments a centrally mediated hypotensive action was demonstrated, possibly by 5-hydroxytryptamine1A (5-HT1A)-receptor stimulation. Studies in humans showed an increase in cardiac output, which was not always significant; it did result either from an increased heart rate or an increased stroke volume. Acute changes in pulmonary hemodynamics after administration of urapidil were most pronounced in patients with pulmonary hypertension: pulmonary artery pressure and pulmonary vascular resistance decreased significantly and pulmonary capillary wedge pressure decreased nonsignificantly. A small reduction in pulmonary artery pressure and capillary wedge pressure were seen in patients with congestive heart failure and in patients in whom acute blood pressure elevation developed after coronary bypass surgery. In patients with essential hypertension forearm, renal and splanchnic flow were shown to increase and vascular resistance to decrease significantly after acute intravenous doses of urapidil. The hemodynamic changes during chronic therapy are largely unknown, except for systemic vascular resistance which remains decreased.
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PMID:Urapidil-induced hemodynamic changes in humans. 266 9

Lisinopril is a new, nonsulfhydryl angiotensin-converting enzyme inhibitor approved for the treatment of hypertension. After oral administration, 25-29 percent of the dose is absorbed intact; biotransformation is not required for pharmacological activity. Onset of action occurs one to two hours after administration, with effects still present 24 hours later. The major route of elimination is through renal excretion and an elimination half-life of 12.6 hours has been reported in normotensive individuals. In patients with impaired renal function (creatinine clearance less than or equal to 30 ml/min) a longer half-life and accumulation have been observed. Lisinopril 20-80 mg/d has been shown to be as effective as hydrochlorothiazide, nifedipine, and beta-blocking agents in the treatment of essential hypertension. Its efficacy in renovascular hypertension has also been demonstrated. In congestive heart failure (CHF) doses of 2.5-20 mg/d appear to provide hemodynamic effects comparable to those of captopril. Dizziness and cough have been the most frequently reported side effects; rash and proteinuria have also been reported in a small number of patients. Interactions with diuretics, potassium supplements, and possibly with nonsteroidal antiinflammatory agents may occur. Lisinopril appears to be similar in efficacy to other antihypertensive agents in the treatment of essential hypertension and to captopril in the treatment of CHF. Whether lisinopril is safer or more effective than captopril or enalapril in the treatment of hypertension or CHF requires further investigation. Prolonged duration of action of lisinopril allows once daily dosing, unlike captopril for which dosing is required every 8-12 hours or enalapril which may necessitate twice daily dosing.
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PMID:Lisinopril: a new angiotensin-converting enzyme inhibitor. 283 26


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