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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of hypertension in the elderly has so far mainly been based on clinical judgment and very few large controlled trials. During the last year several large new trials have been published, the so-called STOP-Hypertension, SHEP, and MRC trials. All have shown that drug treatment of hypertension in the elderly (65-85 years) with permanent diastolic hypertension or isolated systolic hypertension reduces stroke incidence. Most patients have needed combined drug treatment with diuretics and beta-blockers. When thiazide diuretics are used, serum potassium should be followed very closely and most likely amiloride should be added to the thiazide therapy, since this was done both in the STOP and the MRC trials. Since many elderly patients with hypertension suffer from other diseases that might represent contraindications to thiazide diuretics or beta-blockers, the choice of drug must be made after careful clinical evaluation. With the newer classes of antihypertensive agents (calcium antagonists, ACE inhibitors and alpha-blockers) side effects are probably seen less often, but long-term data on morbidity and mortality are still lacking.
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PMID:Treatment of hypertension in the elderly--what have we learned from the recent trials? 129 75

The already strong case for drug treatment of hypertensive patients aged over 60 has been reinforced by the reports on the SHEP, STOP, and, to a lesser extent, MRC trials. SHEP showed benefit in "isolated systolic" hypertension, mainly in relation to stroke, but with a strong trend towards also reducing myocardial infarction. SHEP demonstrated advantages from low-dose chlorthalidone, especially if hypokalemia was prevented. STOP in patients aged 70-84 at entry demonstrated a reduction in stroke and all-cause mortality but not in myocardial infarction; benefit was apparent in women as well as men. The MRC trial, in subjects over 65, many of whom had "isolated systolic" hypertension, found a reduction in stroke but not in coronary events or all-cause mortality. Extensive cross-contamination of allocated treatment groups restricted worthwhile evaluation of different drug regimens in MRC. Potential benefits from antihypertensive drug treatment in old people are substantial but are in danger of being discredited because of intemperate and inaccurate claims.
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PMID:The case for antihypertensive drug treatment in subjects over the age of 60. 129 77

The large multicenter trials of treatment in mild to moderate hypertension have shown unequivocally that the risk of stroke is reversed. The impact of treatment on ischemic heart disease is more debatable. Since there is no discontinuity in the risk of different levels of blood pressure, any advice about the level of pressure to treat must be arbitrary. The British Hypertension Society Guidelines recommend a sustained diastolic pressure of 100 mmHg or more over a 3- to 4-month period. This empirical advice is based upon subgroup analysis of the MRC and Australian Therapeutic Trials that suggests most of the benefit in treating the mildest degrees of hypertension occur in this group of patients. The role of newer classes of agent, such as ACE inhibitors or calcium-channel blockers, cannot be fully assessed in the absence of proper end-point trials. Whilst reasons for using these agents as first-line therapy have been put forward, these remain speculative in the absence of such trials. The much greater cost of newer agents in the context of universally cost-constrained health services also has to be borne in mind before recommending their widespread use as first-line therapy.
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PMID:The level at which blood pressure should be treated. 180 96

Theoretical and experimental data coupled with findings from several studies, showing the beneficial effect of beta-blocking therapy in reducing the risk of death and re-infarction among infarct patients (secondary cardioprotection), suggested that beta-blockers could reduce the incidence of coronary events also in hypertensive patients with no clinical evidence of coronary heart disease (CHD) (primary cardioprotection). In order to evaluate the primary cardioprotective potential of beta-blockers as compared to diuretics in the treatment of hypertension, some large-scale, randomized, prospective studies were set up in the middle and late 1970s. The results of three of these trials, the MRC, the IPPPSH and the HAPPHY studies, were negative or non-conclusive and somehow conflicting. None of them showed any difference between beta-blockers and diuretics in reducing the incidence of CHD, but the MRC and the IPPPSH studies suggested that beta-blockers were better than diuretics in male non-smokers. However, the HAPPHY study did not confirm such a hypothesis. More recently, two studies, the Clatterbridge study (retrospective, non-controlled) and the MAPHY study (prospective, controlled) gave positive results about the primary cardioprotective effect of beta-blockers. In particular, the MAPHY study demonstrated that starting antihypertensive treatment with the beta1-selective beta-blocker metoprolol instead of a thiazide diuretic led to lower total and cardiovascular mortality, mainly by reducing fatal CHD and fatal stroke. Although more evidence is needed, the primary cardioprotective effect demonstrated with metoprolol in the MAPHY study might have important implications for clinical practice and public health.
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PMID:Beta-blockers and primary cardioprotection in hypertension. 197 38

There is no doubt about the association between coronary heart disease (CHD) and smoking, high serum cholesterol and high blood pressure, but association does not mean causation. To prove causation we must mount intervention trials and show that changing a risk marker changes total mortality: a) Trials of dietary reduction of serum lipids: The US Veterans dietary study and the North Karelia project showed no significant reduction in total mortality, nor did the Multiple Risk Factor Intervention Trial (MRFIT) or the WHO "paired-factories" Collaborative Group Study, where other risk factors were also being corrected. In the latter study there was a barely significant reduction in non-fatal CHD but fatal CHD, like total mortality was unchanged. b) Trials of lipid-lowering drugs: The first large-scale study, using clofibrate, showed an increase in total mortality; the screening of 500,000 men and the comparison of cholestyramine with placebo for the top 5% of lipid levels resulted in 68 deaths on the active resin and 71 on placebo. Less expensive measures (alcohol testing; safer roads) could surely do more good to half a million men? These 3 lives "saved" were "lost" in the Helsinki gemfibrozil study where there were 45 deaths in the active group and 42 in the placebo group. c) Effect of blood-pressure reduction. The assumption that reducing a risk marker will reduce CHD was challenged by the massive MRC Mild-to-Moderate Hypertension trial which showed no significant effect of treatment on CHD, CHD death or total mortality, even though stroke mortality was modestly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:What do we gain by modifying risk factors for coronary disease? 218 41

In man a close interrelationship exists between hyperadrenergic states, myocardial ischemia, necrosis, infarction and sudden cardiac death. Persistent high catecholamine levels may also be associated with increased vascular endothelial turnover and permeability to calcium and lipoproteins, increased blood velocity, abnormal blood flow patterns and atheroma formation. There are thus good reasons to predict a cardiovascular protective effect of beta-blockers. Animal data indicate that in spite of apparently adverse plasma lipoprotein changes beta-blockers retard atheromatous plaque formation under conditions of high cholesterol diet with or without stress. A slow heart rate, as well as a reduction in calcium influx and inhibition of both esterification of arterial wall cholesterol (by ACAT) and endothelial permeability to lipoproteins, may be central to this process. Beta-blockers benefit a spectrum of conditions related to the atheromatous process and myocardial necrosis. These are silent ischemia; stable (including mixed), unstable and preinfarction angina; periinfarction events (including myocardial rupture and dissection of the ascending aorta); and myocardial necrosis associated with stress conditions such as head injuries and subarachnoid hemorrhage. In one study coronary deaths in hypertensive men, particularly in smokers, were significantly reduced by metoprolol (a beta 1-selective blocker) compared to a diuretic. In contrast in the MRC study of mild hypertension only nonsmoking men with mild to moderate hypertension who received a nonselective beta-blocker appeared to experience fewer myocardial infarctions. Recent clinical data showed that moderate-severe hypertensives who were optimally controlled by atenolol-based treatment over a 10-year period were less likely to die from myocardial infarction than those suboptimally controlled, irrespective of a rise in serum triglyceride levels. Thus the net effect of acute beta-blockade in hyperadrenergic states, including myocardial infarction, is to limit cardiovascular damage. Chronic beta-blockade inhibits atheroma formation (in animals) and beneficially modifies the incidence of stroke and myocardial infarction, which in man are the long-term consequences of hypertension.
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PMID:The beta-receptor, atheroma and cardiovascular damage. 257 Apr 26

In this review approaches to the treatment of hypertension were appraised by considering data from recent trials. Two main questions were asked: at what level of blood pressure is treatment justified, and which drugs should be used? It is now well established that increases in both systolic and diastolic blood pressure are correlated with an increased risk of cardiovascular disease, heart attack or stroke. However, since patients are often asymptomatic, treatment must be justifiable in terms of reversing the risk of cardiovascular disease. The Australian Therapeutic Trial demonstrated that therapy was beneficial in patients whose diastolic pressure was at or above 95 mm Hg before treatment. Three recent large studies (EWPHE, IPPPSH and MRC) have provided interesting data on the level of blood pressure at which to start treatment and the most appropriate drugs to use. In one, treatment in the elderly, which raises particular concern, has been investigated. The MRC trial compared bendrofluazide with propranolol and showed a reduction in the incidence of stroke; however, to prevent 1 stroke, 850 patients would have to be treated for 1 year. Nevertheless, the benefits of therapy were clearly greater when diastolic blood pressure was at the upper end of the range 90-110 mmHg. Myocardial infarctions, which account for more deaths than stroke in mild to moderate hypertensives, do not appear to be reduced by treatment, whether or not this includes a beta-blocker. This is difficult to reconcile with the established 'cardioprotective' action of beta-blockers post-myocardial infarction. Other important factors affecting cardiovascular disease are governed by the patient's life-style, especially whether or not the patient smokes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Future approaches to the treatment of hypertension in the light of results from recent trials. 328 69

Clinical practice must be based on the results of clinical trials, not on theories derived from epidemiology observations. The major trials of blood pressure reduction are described, and some of their shortcomings are discussed. Whenever drug treatment is necessary there will inevitably be a balance between benefits of treatment and unwanted effects of medication. The MRC trial of treatment in mild hypertension demonstrated that a small reduction in the risk of stroke is obtained at the cost of a variety of side effects which themselves depend on the medication used. Treatment of a diastolic pressure of 100 mm Hg or below will confer very little benefit on an individual patient.
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PMID:Mild hypertension: to treat or not to treat? 332 Jul 89

The justification for drug treatment of mild hypertension rests upon epidemiological data demonstrating an increased risk of heart attack and stroke and a very small number of controlled clinical trials. These data provide a slender basis for mass treatment and leave many vital questions unanswered. The incidence of stroke (and heart attack in some countries) appears to be falling irrespective of antihypertensive therapy. Are historic epidemiological findings still relevant? The level of diastolic blood pressure where risk begins to increase appears to be about 95 mmHg. Ought this also to be the target value for blood pressure reduction? Do thiazide diuretics have added risks and beta-adrenergic blocking drugs added benefits over and above their effect upon blood pressure? If the MRC Hypertension trial turns out to be the last of the big placebo controlled trials in hypertension how shall we assess the effects of new types of drugs upon outcome?
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PMID:Management of hypertension: risk-benefit ratio. 615 31

In severe and accelerated hypertension the benefits of treatment are clearcut. In patients < 60 years of age with mild hypertension the main benefit is reduction of stroke by about 40%. The death rate from stroke is declining in many affluent countries for reasons which can only be partly explained by mass treatment of hypertension. In the MRC trial in patients < 60 years old it took 2500 patient/years of treatment to save one stroke. If the number of strokes is declining for other reasons the number of patient/years to save one stroke may be increasing. In older patients the absolute benefit is greater because they suffer more stroke events and because treatment also reduces coronary events.
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PMID:Hypertension trial results: consensus and conflicts. 747 18


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