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

The aim of this study was to evaluate the number, outcome, survival time, and causes of death of patients with severe arterial hypertension who were admitted to the Department of Medicine at Landspitalinn (National Hospital) in Reykjavik during the years 1957 to 1971. During this period 117 patients were found to have severe arterial hypertension (12.6% of all cases of hypertension diagnosed) according to the grading of Keith and Wagener, 20 patients with grade IV retinopathy and 97 patients with grade III. The case histories were analysed according to age and sex distribution, blood urea, electrocardiographic changes, heart size by X-ray at the time of diagnosis and final outcome. The survival calculations were done by the decrement method (life tables) and aim taken from patient age 65 years and less. Relatively fewer patients with severe arterial hypertension were admitted during the last five year period (1967-1971) than during the two previous five year periods. The main causes of death were cerebrovascular accidents (26.6%), myocardial infarctions (22.8%), and renal failure (22.8%). Approximately 50% of the men and 60% of the women survived five years. Elevated blood urea values and signs of left ventricular hypertrophy on ECG at the time of diagnosis carried a more sinister prognosis.
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PMID:Severe arterial hypertension (grade III and IV). 107 39

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

Left heart diseases, in particular mitral stenosis, are often associated with anatomic and functional alterations of the lung. According to the pulmonary structures involved they could be named chronic secondary intersticial and vascular lung diseases. Congenital heart diseases with pre- or post-tricuspid shunts are also often associated with anatomic and functional alterations of the lung. This condition also constitutes a chronic secondary vascular lung disease (atrial septal defect) or a chronic primary vascular lung disease ( ventricular septal defect, patent ductus arteriosus). Primary lung diseases (interstitial pulmonary fibrosis, pulmonary emphysema, recurrent pulmonary embolism) are often associated with right ventricular hypertrophy with or without dilation, a condition commonly named chronic cor pulmonale. On the whole the interrelationships between heart and lung diseases are as follows: a) anatomic and functional alterations of the lung due to left heart diseases are mediated through pulmonary venous hypertension; b) anatomic and functional alterations of the lung due to congenital heart diseases are mediated through the increased pulmonary blood flow with or without transmission of the systemic blood pressure to the pulmonary vasculature, and c) anatomic and functional alterations of the right ventricle due to primary or secondary lung diseases are mediated through arterial pulmonary hypertension. In summary, the interrelationships between heart and lung diseases are mainly mediated through the pulmonary venous or pulmonary arterial hypertension.
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PMID:Cardiac and pulmonary diseases. A pathophysiologic interelationship. 113 Sep 7

The prevalence of primary and secondary hypertension and of heart and kidney involvement was thoroughly studied in 689 hypertensive subjects derived from a blood pressure screening examination of a total population sample of Swedish men (n = 7,452). The prevalence of secondary hypertension was found to be only 5%, the prevalence of surgically curable hypertension being even lower. Left ventricular hypertrophy and slight heart enlargement were each found in about one-third of the hypertensive patients, while severe heart enlargement, left ventricular hypertrophy on ECG, proteinuria, abnormal serum creatinine and urinary sediment were each found in about 5%. On the basis of these findings, a minimum pre-treatment workup in uncomplicated hypertension is proposed.
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PMID:Pre-treatment workup for antihypertensive treatment. 127 68

SCH 34826, i.e., (S)-N-(N-(2,2[(2,2-dimethyl-1,3-dioxolan-4- yl)methoxy]-2-oxo-1-(phenyl-methyl)ethyl)-phenylalanyl)-beta-alanine, is a potent and selective inhibitor of neutral endopeptidase 24.11 (NEP), an enzyme that degrades the atrial natriuretic peptide (ANP). The effects of SCH 34826 on hypertension and left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) were evaluated following 1 month of treatment by measuring the blood pressure, cardiac weight, and left ventricular fibrosis. Adult SHRs were treated with SCH 34826 at 10, 30, or 100 mg/kg given orally twice daily or with vehicle. The systolic blood pressure (SBP) and heart rate (HR) were recorded weekly by the tail-cuff method. Cardiac structural damage was determined by morphometric analysis. Over the dose range examined, the drug produced no significant changes in either blood pressure or heart rate. Despite the lack of antihypertensive activity, SCH 34826 at 100 mg/kg reduced both the cardiac mass (-10%) and the amount of fibrotic tissue present in the left ventricle (-42%). These data indicate that chronic inhibition of NEP by SCH 34826 interacts with mechanisms underlying myocardial hypertrophy and cardiac remodeling.
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PMID:The neutral endopeptidase inhibitor, SCH 34826, reduces left ventricular hypertrophy in spontaneously hypertensive rats. 127 98

Mild-to-moderate essential hypertension is the most common medical problem seen by physicians in Western populations, and pharmacologic antihypertensive therapy is now usually undertaken. Clinical trials have shown that lowering of elevated blood pressure using diuretics and beta-blockers reduces cardiovascular morbidity and mortality. Despite these benefits, the trials have provided no convincing evidence that the incidence of coronary artery disease or its complications is reduced: Treated hypertensive patients remain at increased cardiovascular risk compared with untreated normotensive subjects. Possible explanations for this disappointing outcome are that the drugs used may themselves have negative effects on serum lipids, glucose, and insulin resistance, thereby outweighing their antihypertensive benefits. An equally important role in this respect may be played by the diseases and therapies most commonly found in association with mild-to-moderate hypertension: hyperlipidemia, type II diabetes, coronary artery disease, left ventricular hypertrophy, cardiac arrhythmias, peripheral arterial disease, and nephropathy. Such conditions may be potent determinants of what constitutes the optimal first-line choice of antihypertensive therapy. Furthermore, the negative effects that antihypertensive drugs can have on quality-of-life factors may result in noncompliance and ineffective long-term treatment. Therefore, in a new therapeutic approach to the treatment of high blood pressure, it would be logical to base antihypertensive therapy on strategies that not only lower the blood pressure but that have beneficial impacts on hemodynamics, vascular and cardiac structure, metabolism, and quality-of-life issues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antihypertensive therapy: new strategies beyond blood pressure control. 128 82

One of the earliest structural changes in the heart adapting to hypertension is left ventricular hypertrophy, which can now be exactly measured by echocardiography. Left ventricular hypertrophy increases the incidence of coronary artery disease, heart failure, and sudden death severalfold, independent of the blood pressure levels. Left ventricular hypertrophy requires specific antihypertensive therapy that controls both high blood pressure and increased left ventricular mass. Preliminary data from clinical studies indicate that regression of left ventricular hypertrophy leads to a better cardiovascular prognosis. Sympatholytic substances, angiotensin-converting enzyme (ACE) inhibitors, and calcium antagonists are antihypertensive agents that effected adequate reductions in blood pressure as well as regression of left ventricular hypertrophy.
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PMID:Hypertensive heart disease--significance of left ventricular hypertrophy. 128 90

The major target organs that suffer from sustained hypertension are the heart, kidneys, and brain. Cardiac adaptation to arterial hypertension consists of left ventricular hypertrophy (LVH) of the concentric type, that is, an increase in wall thickness at the expense of chamber volume. However, LVH can no longer be considered a simple adaptive myocardial process serving to compensate for the increase in afterload and bring left ventricular wall stress back to normal. Data from the Framingham cohort have shown that the occurrence of LVH drastically increases the risk of sudden death and other cardiovascular morbidity and mortality irrespective of the levels of arterial pressure. Renal adaptation to arterial hypertension consists of a decrease in renal blood flow with elevations in filtration fraction and renal vascular resistance. With progressive hypertensive cardiovascular disease, glomerular filtration rate will fall as well. Recent data in patients with mild-to-moderate hypertension demonstrate that despite "efficacious" antihypertensive therapy, one-third to one-half of hypertensive patients may experience a significant decline in renal function. Cerebrovascular adaptation to hypertension consists of micro- and macrovascular disease leading to vascular dementia, or ischemic or hemorrhagic stroke. Cerebrovascular autoregulation, the mechanism by which cerebral blood flow is maintained, despite changes in arterial pressure, may be altered in hypertension.
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PMID:End-organ disease in hypertension: what have we learned? 128 25

The goal of antihypertensive therapy is the reduction in morbidity and mortality associated with high blood pressure. Despite our ability to reduce blood pressure, "standard" antihypertensive therapy has not produced a general decrease in coronary heart disease. This failure might be related to the adverse metabolic consequences of diuretics and beta-adrenergic receptor-blocking agents used in most clinical trials. In the hypertensive patient population, however, the principal physiologic abnormality is increased systemic vascular resistance. This increase in vascular tone leads to compensatory changes in cardiac function that result in left ventricular hypertrophy and diastolic filling abnormalities. Diastolic ventricular dysfunction is present in approximately 50% of asymptomatic hypertensive patients and might be a precursor of the syndrome of congestive heart failure with normal systolic ventricular function. In view of the prevalence of diastolic filling abnormalities in the hypertensive patient population, one should consider the effect of an antihypertensive drug on left ventricular function. In a comparison of the angiotensin-converting enzyme (ACE) inhibitors, captopril, lisinopril, and fosinopril, only fosinopril increased stroke volume, peak ejection rate, and peak filling rate, and decreased time to peak ejection rate. These favorable inotropic and lusitropic responses to fosinopril may reflect an effect on the myocardial renin-angiotensin cascade which is dependent upon the unique chemical structure of the fosinopril molecule.
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PMID:Left ventricular hypertrophy and performance: therapeutic options among the angiotensin-converting enzyme inhibitors. 128 27

The past decade has seen a shift in the strategy for hypertension treatment from stepped therapy--a highly structured monolithic series of steps--to recommendations for a more individualized selection of treatment. Severe hypertension is a clear indicator to bypass traditional steps. Demographic factors, such as age, gender, and race, are often cited, but have proved to be less helpful. Concomitant medical conditions and problems are very common and are more often the crucial determinants in the selection of antihypertensive therapy. Coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, and chronic obstructive pulmonary artery disease, anxiety, and depression are all common, and each has implications for the selection of antihypertensive therapy. Blood pressure reduction is a surrogate for reduction of cardiovascular risk, and therefore, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, mild hyperlipidemia, and insulin resistance, as additional risk factors in hypertension. Consideration of all these factors makes it possible to individualize antihypertensive therapy in most patients today.
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PMID:Treatment of hypertension: the place of angiotensin-converting enzyme inhibitors in the nineties. 128 28


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