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

The recent increase in coronary heart disease is real and the causes must mainly be environmental. Consequently the condition should largely be preventable. The application of what is already known is likely to be a far more effective way of reducing the mortality rate than all attempts at palliative treatment, but vigorous action will be necessary. Much greater sums are being expended on coronary-care units and cardiac surgery than in preventing the need for them, although there is little evidence that they have significantly lowered the over-all mortality rate. Conventional treatment is immensely expensive. Prevention could in the long run be much cheaper. Cardiologists on their own are unlikely to succeed in a program of prevention. They need the help of many others, including community nurses, nutritionists, public health workers, sociologists, and of course general practitioners, but they have responsibility for leadership and for providing background knowledge. For the detection of certain risk factors, health examinations are necessary and should be part of general practice. Also, advice is best given on an individual basis. The chief-known risk factors (hyperlipidemia, hypertension, smoking, physical inactivity) could be controlled. CHD occurs in adults but atherosclerosis starts many years before. Prevention should begin with appropriate infant feeding, whenever possible with breast milk, and continue into childhood, when habits are formed and attitudes to life can best be influenced. It should be possible to bring up children virtually free from risk factors. It may never be possible to prove the effectiveness of such a multifactorial program by prospective controlled intervention studies, but the evidence indicates strong probability. The stakes are too high to delay action any longer. Physicians daily give advice in areas where the evidence is much less certain. Such a program for the control of coronary artery disease is urgently needed and could become one of the most rewarding activities for the medical profession.
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PMID:The cardiologist's responsibility for preventing coronary heart disease. 124 24

Asymptomatic hyperuricemia should be treated only if the plasma uric acid levels are around 10 mg/100 ml or more on several determinations. In addition, patients on a purine-free diet who excrete more than 600 mg uric acid per 24 h should be treated. In both cases, treatment is intended to be prophylactic against gouty nephropathy. At present there is no evidence that primary hyperuricemia alone is a risk factor for early atherosclerosis and especially coronary artery disease. However, more attention should be paid to the accompanying risk factors such as obesity, hyperlipoproteinemia, diabetes mellitus and hypertension.
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PMID:[Which uric acid value is in need of treatment?]. 126 67

Thirty-eight men who suffered acute transmural myocardial infarction before age 40, and after recovery were New York Heart Association functional Class I or II, were studied by noninvasive means and by coronary angiography in order to determine whether these nonivasive studies could predict the presence of significant coronary artery disease remote from that felt to be responsible for the previous myocardial infarction. Patients were divided into two groups on the basis of the absence (Group I) or presence (Group II) of obstructive disease in a major coronary artery supplying myocardium remote from the prior myocardial infarction. There were 21 patients in Group I and 17 patients in Group II. They did not differ with respect to age, abnormalities of lipid or glucose metabolism, family history, history of hypertension or cigarette use, presence of obesity, or infarct localization. Ten of 17 patients in Group II had angina pectoris; only 3/21 patients in Group I had angina pectoris (p less than 0.01). All 12 patients tested in Group II had a positive maximal exercise tolerance test; only 1/17 patients tested in Group I was similarly positive (p less than 0.001). The absence of angina pectoris and the presence of a negative maximal exercise tolerance test is strong evidence against the pressure of significant CAD remote from that responsible for the prior myocardial infarction.
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PMID:Clinical correlates of coronary cineangiography in young males with myocardial infarction. 126 11

Endothelial cells synthesize and metabolize vasoactive substances which are involved in the regulation of vascular tone. Among these factors, the endothelium-derived nitric oxide (NO) appears to be of major importance. Many studies observed an impairment of the generation, release, or the diffusion of endothelial NO across the vascular intima in laboratory animals with various experimental diseases such as hypercholesterolemia, atherosclerosis and hypertension. In human coronary arteries obtained from explanted hearts impaired endothelium-dependent relaxations were measured in atherosclerotic segments. The hypothesis of a decreased NO mediated vasodilation in patients with coronary artery disease was further underscored by in vivo studies in man using intracoronary infusions of the endothelium-dependent vasodilator acetylcholine and quantitative coronary angiographic measurements of the diameter changes. From these observations it was assumed that endothelial dysfunction, in particular a profound inability of the coronary endothelium to relax via NO dependent mechanisms may play an important role in the pathogenesis of abnormal coronary vasomotion. However, further investigations in man reveal that the ability of the coronary endothelium of patients with coronary artery disease or vasospastic angina to produce endothelial NO is less affected as judged from the effects of acetylcholine. In recent investigations a largely preserved endothelial function could be measured in these patients when the endothelium-dependent vasodilator substance P was used as a tool for the measurement of NO dependent relaxation. Thus, endothelial dysfunction does not appear to serve as a major cause of abnormal vasoconstriction in coronary artery disease or vasospastic angina in man.
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PMID:In vivo measurement of endothelium-dependent vasodilation with substance P in man. 128 20

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

Calcium antagonists are of particular importance in the treatment of hypertension because they influence the free cytoplasmic calcium concentration and thereby many pressor mechanisms in the smooth muscle cell. A fall in the peripheral resistance is the main hemodynamic effect, and this is more marked with the second-generation calcium antagonists because they are more vasoselective than the first calcium-channel blockers. Particularly important is their lack of effect on lipid and glucose metabolism, as well as the absence of serious side effects. It has not yet been possible to confirm that the antiatherogenic effect found in some animal models also occurs in humans. Calcium antagonists are effective, safe, and well-tolerated antihypertensive agents that can be combined with all other antihypertensives with the exception of the combination of verapamil and a beta-blocker. They are easy to dose for individualized "stepped" therapy. They have a particular role in hypertensive patients with cardiac effects secondary to hypertension, coronary artery disease, obstructive bronchial diseases, diabetes, renal disease, and peripheral arterial occlusive disease.
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PMID:The role of calcium antagonists in the treatment of hypertension. 128 89

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 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

A progressive rise in arterial calcium content is the most characteristic age-associated alteration in the arterial wall and the decisive factor in arteriosclerotic degeneration. Experimental studies have demonstrated that calcium antagonists can prevent or retard the development of arterial calcinosis associated with vitamin D overload, hypertension or alloxan-induced diabetes. Although similar effects are more difficult to observe in humans, they have been demonstrated in patients with coronary artery disease and in patients with end-stage renal disease, which is characterised by an acceleration of the normal arterial aging process.
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PMID:Arterial calcinosis, chronic renal failure and calcium antagonism. 128 73

The association between blood pressure and coronary artery disease may be caused by a concurrence of atherogenic biochemical abnormalities in hypertensive patients, i.e., the metabolic cardiovascular syndrome (increased total cholesterol, triglycerides, and insulin; decreased high-density lipoprotein (HDL) cholesterol; and insulin resistance, glucose intolerance, and blood platelet dysfunction). There are numerous reports of sympathetic nervous system overactivity in hypertensive subjects that could be of importance for the pathophysiology of the high blood pressure. Plasma catecholamines have metabolic hormonal effects at concentrations slightly above low normal resting levels. Even transiently and certainly chronically raised plasma catecholamine levels may cause biochemical abnormalities. Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Thus, the sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. Hypertensive subjects may respond to environmental stimuli with larger sympathoadrenal responses than normal subjects. Furthermore, emotional stress has been associated with coronary artery disease. Thus, the metabolic hormonal effects of catecholamines, by causing the metabolic cardiovascular syndrome, may be the crucial link between "stress" and cardiovascular disease.
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PMID:The sympathetic nervous system may modulate the metabolic cardiovascular syndrome in essential hypertension. 128 68


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