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

In 1977 the National Heart, Lung and Blood Institute in the USA drew together a panel of experts as the first 'Joint National Committee' to provide guidelines on the detection, evaluation and management of hypertension. This was the birth of 'stepped care', which was internationally adopted, and consisted of: step 1--a diuretic; step 2--if step 1 is inadequate, add a beta-blocker; step 3--if step 2 is inadequate, add a vasodilator (e.g. hydralazine). With the evolution of a broader, multiple risk factor approach to the management of hypertension, and the development of newer agents, this simple system was modified during the 1980s. The relative importance of non-pharmacological intervention resulted in step 1 becoming drug-free, and alternative agents necessitated wider 'steps'. The interaction of hypertension with other coronary heart disease (CHD) risk factors, the disappointing effect of thiazides and beta-blockers on CHD events in intervention trials, and the increasingly large list of potential drug combinations meant that by 1989 several international consensus bodies no longer considered stepped care to be viable. Stepped care has been replaced by 'tailored therapy'. That is, based on an assessment of the patient's overall cardiovascular risk profile, the choice of first-line drug therapy has been broadened beyond diuretics and beta-blockers to include ACE inhibitors, calcium antagonists and selective alpha 1-blockers. Many hypertension experts are now of the opinion that, except in limited circumstances, diuretics and beta-blockers should only be used as second-line or third-line agents.
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PMID:From stepped care to tailored therapy. 179 14

Hypertension, a condition characterized by narrowing of the arteriolar lumen, is related in part to vasoconstriction and in part to vascular hypertrophy. Complex and interlocking mechanisms involving the autonomic nervous system and both circulating and local vasoconstrictor and vasodilator hormones contribute to this narrowing. Endothelin, 5-HT (serotonin), the kinins and ouabain may all participate by altering sodium, potassium and calcium fluxes in vascular smooth muscle cells. Recently the concept of insulin resistance as a mechanism of hypertension has emerged. Insulin may be a vascular growth factor as well as a local hormone facilitating a rise in intracellular sodium concentration. The observation that ACE inhibitors lower BP when plasma renin and angiotensin levels are low has led to an increased interest in local non-circulating renin-angiotensin systems. These systems probably influence arteriolar tone as well as vascular hypertrophy, and their inhibition leads to reduction in BP and some reversal of arteriolar thickening. Thus the ACE inhibitors represent a logical and effective method of treating hypertension and their use is likely to increase in the next few years.
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PMID:The mechanisms of hypertension and the role of ACE inhibitors. 179 16

The most common cause of death in hypertensive patients is myocardial infarction (MI), being three times more common than stroke. Lowering raised BP results in 40% fewer strokes, but only 14% fewer MIs. This may be because other coronary risk factors that often accompany hypertension (e.g. obesity, lipid and thrombotic disturbances, insulin insensitivity, increased plasma renin activity and increased sympathetic activity) are either unaffected or exacerbated by some of the traditional antihypertensive agents. Some of these risk factors show a diurnal rhythm peaking at 07.00-10.00 hours, thus this time constitutes a 'vulnerable period' for sudden death or death from MI. beta-blockers and diuretics have been effective in preventing stroke, but diuretics (at least potassium-losing diuretics) might actually increase the incidence of sudden death and MI in young to middle-aged hypertensive subjects (though elderly patients may benefit). Quality of life can be impaired by some beta-blockers, and diuretics can cause metabolic upset and male impotence. Thus, antihypertensive agents that are not only effective and well tolerated but are beneficial to the broader coronary risk profile are desirable. ACE inhibitors should prove particularly useful in terms of: good quality of life; non-exacerbation or improvement of coronary risk factors; treating patients with impaired left ventricular function; reversing left ventricular hypertrophy and vascular wall hypertrophy, thus improving coronary flow reserve; atheroma regression; renal protection, particularly in diabetes; and prevention or regression of LV dilatation (remodelling) following MI.
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PMID:What does the future hold for ACE inhibitors? 179 18

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

From the analysis of the epidemiological observational studies, among which one of the most famous is the Framingham study that has lasted for more than 30 years, it is evident that the risk of cardiac events and strokes is closely related to the levels of arterial systolic and diastolic blood pressure. Nevertheless, the link between hypertension and cardiovascular risk has very often been discussed, due to the results of therapeutic intervention trials, which have proved satisfactory for cardiovascular risk reduction but disappointing results for coronary disease reduction risk. Possible explanations for these poor results of antihypertensive therapy on coronary disease are different and very numerous. According to many Authors, the blood pressure was not reduced to the programmed levels in all trials and the drug used (diuretics, beta-blockers) possibly had negative effects on the lipid profile. Therefore, waiting data for new trials, will perhaps produce better results in the future taking into consideration all risks of our patient, monitoring a rigorous and steady blood pressure reduction and selecting drugs like calcium-channel blockers and ACE-inhibitors which contain characteristics similar to those ideal for the modern antihypertensive agent.
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PMID:[Arterial hypertension and cardiovascular risk. Epidemiological studies, trials and therapeutic implications]. 180 82

There are short-term and long-term modulations of cardiac function and cardiac composition by the endocrine and paracrine renin-angiotensin system. First, there is an enhancement of coronary vasoconstrictor tone in severe congestive heart failure due to stimulation of this system. Therapeutic interventions that block the RA-system are able to reduce the increased resistance to coronary flow. Second, there is a relationship between the occurrence of arrhythmias and the degree of sympathetic stimulation in congestive heart failure. The renin-angiotensin system may be involved in arrhythmogenesis because of presynaptic modulation of sympathetic neurotransmitter release. However, in the isolated perfused rat heart no class-specific antiarrhythmic properties could be found for ACE inhibitors during progressive myocardial ischaemia. Third, proliferation of the neointima following injury of a coronary artery is at least in part mediated by angiotensin II. Although ACE inhibition was an effective tool in animal experiments to prevent excessive proliferation of the neointima following ballooning, it was less effective in preventing restenosis in man following a repeat coronary angioplasty. Fourth, preferential proliferation of the cardiac interstitium in experimental hypertension has been associated with activation of the renin-angiotensin system. In patients with essential hypertension ACE inhibitors were not only capable of controlling blood pressure but also of normalizing the previously pathological pattern of diastolic left ventricular filling. In summary, by therapeutic intervention that cause a blockade of this system, cardioprotective and cardioreparative processes can be supported.
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PMID:Modulation of coronary circulation and the cardiac matrix by the renin-angiotensin system. 180 29

The impact of treatment on prognosis of patients with chronic congestive heart failure depends not only on pharmacological therapy but also on nonpharmacological aspects of patient management. Patient compliance, life style changes, salt and fluid restriction, detailed patient information and measures of self control greatly affect therapeutic efficacy. Reasons for hospitalizations and emergency room visits: In an analysis of 82 admissions of patients for decompensated chronic congestive heart failure we found poor compliance with drug treatments or dietary instructions as causally related factors in 30 patients, uncontrolled hypertension in 22 patients, acute infection in 18 and acute myocardial ischemia in 18 patients. More than half of the patients had weight gain before decompensation, that had not been adequately answered by changes in medication. Inadequate patient information: Inadequate knowledge about necessary life style changes at the time of hospital discharge is often found in patients with chronic heart failure. Less than 50% of these patients remembered correctly the instructions on key issues of necessary life style changes and diet. Drug treatment of heart failure: Recent controlled drug trials have not gained enough weight in therapeutic decisions of physicians treating heart failure patients. While ACE-inhibitors have been shown to improve longevity in congestive heart failure only 6% of patients with heart failure are treated with these drugs, while 5% are treated with calcium antagonists which have not been proven to be of symptomatic or prognostic benefit and may be harmful as well in this disease. Inadequate dosage in patients with chronic renal failure or in elderly patients as well as inadequate choice of drugs lead to side effects in a considerable percentage of patients.
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PMID:[Effects of patient information, compliance and medical control on prognosis in chronic heart failure]. 182 Feb 95

The most common curable cause of high blood pressure is renovascular hypertension. Although hypertension is common in the United States, only a minority, approximately 1%, of patients have a renovascular cause. Using clinical criteria, a subgroup of these patients can be selected in which the prevalence of renovascular hypertension will be approximately 15%. In these selected patients, it is appropriate to proceed to a radiographic screening modality to look for a significant renal artery stenosis. The choice of modality should reflect the strengths and expertise of each specific institution. Hypertensive urography is no longer recommended for screening. Excellent results have been reported with intravenous DSRA in institutions where a strong interest in this procedure exists. Furthermore, intravenous DSRA is easily coupled with the collection of renal vein samples for renin assay. Intravenous DSRA, however, has not maintained widespread use. Although the radionuclide renogram is no longer adequate as a radiographic screening tool, stimulation with an ACE inhibitor, such as captopril or enalaprilat, may produce excellent results. In many institutions, this is the most appropriate examination. Furthermore, it is relatively noninvasive. Merely detecting a significant renal artery stenosis does not, however, mean the patient has renovascular hypertension. Both hypertension and a renal artery stenosis may be present and not be causally related. Because renovascular hypertension is, at least initially, renin mediated, the demonstration of increased renin production by the ipsilateral kidney should confirm renovascular hypertension. Prospective application of these results to patients undergoing revascularization techniques, however, has been disappointing. This may be related to problems in patient preparation, sample collection, renin assay, or even the physiology of chronic hypertension, which is incompletely renin mediated. Thus, offering revascularization only to those patients with lateralizing renal vein renins is not appropriate. If radiographic screening is limited to those patient at greatest likelihood for a renovascular etiology, intra-arterial DSRA or conventional arteriography may be used. These techniques most reliably detect renal artery stenosis. Their main disadvantage lies in their relatively invasive nature, as an arterial puncture is required. The poor predictive value of selective RVRRs implies that revascularization may be attempted without awaiting those results. If percutaneous transluminal renal angioplasty can be performed with a satisfactorily low complication rate, both the diagnostic and the interventional procedure may be undertaken at the same setting. It is expected that further refinements in these diagnostic procedures, particularly with the use of stimulating drugs such as ACE inhibitors, will lead to further improvement in the diagnostic results.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Screening for renovascular hypertension. 182 6

The aim in treatment of hypertension is normalization of blood pressure. The impact of treatment of hypertension on the development of IHD depends not only on the treatment of hypertension but also on influencing other basic risk factors, i.e. hyperlipoproteinaemia and smoking. Treatment of hypertension can be and should be individual and depends on a) age, b) the level of hypertension, c) complications of hypertension and d) the presence of other diseases, in particular hyperlipoproteinaemia and diabetes mellitus. The treatment of choice in hyperlipoproteinaemia are calcium antagonists, prazosin, ACE inhibitors and beta-blockers with ISA. There is experimental evidence suggesting that calcium antagonists (in particular isradipine) but also beta-blockers suppress the progression of atherosclerosis and AGE inhibitors prevent the development of cardiac and vascular hypertrophy. Effective treatment leads to a decline in the mortality from cerebrovascular attacks--in the USA in the course of 20 years a decline by 60%--in Czechoslovakia so far the mortality from cerebrovascular disease did not change which indicates unfortunately a very poor control of hypertension in the population.
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PMID:[Treatment of hypertension and cardiovascular complications]. 182 87

Epidemiologic studies have revealed that in arterial hypertension left ventricular hypertrophy is an important risk factor for cardiac failure. Accordingly antihypertensive therapy should aim at preventing or regressing left ventricular hypertrophy. Reduction of blood pressure does not necessarily induce reversal of left ventricular hypertrophy. Vasodilators like hydralazine and minoxidil, which lead to augmented plasma levels of norepinephrine, were not able to diminish left ventricular hypertrophy. In contrast, a sympatholytic therapy with methyldopa caused a reversal of left ventricular muscle mass. These experimental findings in spontaneously hypertensive rats led to the hypothesis that catecholamines control the onset and progression of myocardial hypertrophy mostly independent of blood pressure. This hypothesis was supported by the experimental findings, that subhypertensive dosages of norepinephrine induce left ventricular hypertrophy and that this hormone promotes alpha-receptor mediated growth of isolated myocytes. Recent studies have revealed that also the renin-angiotension-system has trophic effect on the myocardium. Clinical investigations have documented regression of cardiac hypertrophy due to antihypertensive therapy with sympatholytic drugs, ACE-inhibitors, calcium-channel blockers and beta-receptor blockers. Diuretics failed to decrease left ventricular muscle mass along with blood pressure normalization.
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PMID:[ACE inhibition: mechanisms of cardioprotection in heart hypertrophy]. 183 Sep 11


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