Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular hypertrophy (LVH), as assessed by ECG or echocardiography, is a powerful independent coronary risk factor. The present overview of 104 studies sets out to compare the ability of various forms of antihypertensive therapy to reverse LVH as assessed by echocardiography. Most observations involved four classes of treatment--combination therapy, ACE inhibitors, beta-blockers and calcium antagonists (mainly dihydropyridines). The former two therapies were significantly more effective than the latter two in reversing LV mass, independently of length of time on treatment and degree of fall in blood pressure. Possible reasons for these differences are discussed. The clinical significance of these results is unclear although preliminary data indicate that regressing LVH is associated with fewer cardiovascular events.
...
PMID:Reversibility of left ventricular hypertrophy by differing types of antihypertensive therapy. 153 82

The risk for cardiovascular complications is already substantially increased in persons with borderline elevation of arterial pressure (141-159/90-94 mmHg and transiently below). It increases progressively with higher grades of hypertension. The main aim of treatment is thus a significant improvement in survival for the patient. Persons with raised blood pressure (BP) have often additional cardiovascular risk factors such as deranged carbohydrate metabolism, dyslipidemia, left ventricular hypertrophy, smoking and others. Treatment of hypertensive patients should thus not only normalize BP but should at the same time reduce associated risk factors or at least not increase them. Conventional antihypertensive treatment based on thiazides in high doses or beta-blocking agents led to marked reduction of strokes and heart failure, but did not satisfactorily reduce coronary heart disease or sudden cardiac death. It has been suspected that other cardiac risk factors are insufficiently influenced or eventually even deteriorated by conventional therapy, thus counteracting partly a beneficial effect of lowered BP. Beta-blockers however have at least a secondary preventive effect after myocardial infarction. Newer antihypertensive drugs such as ACE-inhibitors, calcium antagonists and alpha 1-blockers reduce left ventricular hypertrophy and are at least neutral with regard to metabolism of lipids and carbohydrates. The non-thiazide diuretic indapamide and the serotonin (S2-) blocker ketanserin likewise are neutral with regard to glucose and lipid metabolism. The efficacy of these new drugs regarding long term survival is as yet undetermined. Persisting borderline or established hypertension should as a rule always be approached with basic non-pharmacologic measures: loss of overweight, reduction of alcohol intake, exercise, avoidance of high salt foods, abstention from smoking and withdrawal of BP-raising drugs. If antihypertensive medication is indicated, potential first line drugs are ACE-inhibitors, calcium antagonists, beta-blockers, thiazides at low dose, indapamide, ketanserin, the alpha 1-blocker prazosin and others; initially as monotherapy, if needed in combinations of 2 or 3. Older patients or those will with additional disturbances such as diabetes, hypercholesterolemia, nephropathy, heart failure, ischemic heart disease, arrhythmias, claudication, asthma and others need problem-adjusted modifications of treatment.
...
PMID:[Antihypertensive therapy in the nineties]. 153 54

In a half-year open clinical study the authors investigated the antihypertensive action of enalapril--an inhibitor of the angiotensin converting enzyme--and its action on renal functions in a group of 11 patients with nephrogenic hypertension. In seven patients monotherapy, using a mean dose of 12 mg, was sufficiently effective. In the remaining four patients treatment was combined with diuretics. It was revealed: that: 1. a significant drop of systolic and diastolic pressure occurred with a concurrent decline of the total peripheral vascular resistance, 2. a slight (statistically not significant) reduction of the glomerular filtration as well as quantitative proteinuria with a decline of glomerular hypertension. 3. In this group of patients without left ventricular hypertrophy no signs of regression of its mass were present. 4. Even in patients with nephrogenic disease no negative effect on the lipid, carbohydrate and purine metabolism was observed. The subjective tolerance of the preparation was very satisfactory.
...
PMID:[Enalapril in the treatment of nephrogenic hypertension]. 159 1

Experimental myocardial infarction is a model of cardiac overload due to amputation of part of the cardiac muscle. The development of cardiac failure depends on the size of the infarct and the time factor. This model of overload is associated with changes of the phenotype of the remaining healthy muscle and with peripheral vascular modifications partially dependent of the activation of pressor and/or deactivation of dilator systems. These changes are proportional to the size of the infarction at a given time after induction of the model. The degree of right ventricular hypertrophy and the decrease in blood pressure reflect the severity of infarction and the deterioration of the remaining myocardial function, affecting the haemodynamics both before and after the left ventricle. The increases in the 1/3 forms of isomyosins, the amount of subendocardial collagen, the biosynthesis, stocking and secretion of ANF are related to the infarct size and degree of overload. Similarly, the concentration of cyclic GMP is proportional to the infarct size. These parameters reflect ventricular overload, the increase of stress and energy deprivation of the remaining healthy muscle. The activation of peripheral pressor systems is also dependent on the infarct size reflects the effect of cardiac pump dysfunction on the kidney, liver, brain and endothelium. Large infarcts are associated with increased circulating renin and renal concentrations, with a decrease in angiotensinogen levels related to its consumption by the renin and to reduced hepatic synthesis and also with increased secretion and biosynthesis of vasopressin by the hypothalamus. In this model, Perindopril is beneficial by decreasing the cardiac load. It reduces the blood pressure, causes regression of bi-auricular and right ventricular hypertrophy. Changes in myosin isoenzyme configuration regress and subendocardial fibrosis and ANF concentrations are normalised. The effects of ACE inhibitors in this context, though very beneficial, are limited by the impossibility of normalising cardiac load and stress when the initial amputation of cardiac contractile mass exceeds 40%.
...
PMID:[Experimental myocardial infarction in the rat. Effect of perindopril]. 166 27

We studied the role of the sympathetic nervous system and the renin angiotensin system for pressure induced left ventricular hypertrophy (LVH) in 135 rats with experimental supravalvular aortic stenosis (AS). We induced this condition by a silver clip on the ascending aorta, when body weight (BW) was 90 to 100 g. Sympathectomy by 6-OH-dopamine reduced LV norepinephrine content to less than 5%. The renin-angiotensin system was blocked by quinapril, which reduced serum angiotensin converting enzyme (ACE) activity to less than 5%. Aortic stenosis (LV peak systolic pressure 212 +/- 10 mm Hg) induced significant LVH with an increase of LV weight from 198 +/- 3 (sham) to 266 +/- 6 after 6 weeks and to 303 +/- 13 mg/100 g body weight after 12 weeks. Sympathectomy did not reduce LVH 6 weeks after induction of AS (260 +/- 6 mg/100 g body weight). Angiotensin converting enzyme inhibition initiated immediately after induction of AS did not alter the increase of LV mass after 6 weeks (250 +/- 7 mg/100 g body weight). Removing the silver clip 6 weeks after induction of AS resulted in a 90% regression of LVH after 6 more weeks. When ACE-inhibition was started after 6 weeks--ie, once LVH had developed--and maintained for another 6 weeks, an 80% regression of LVH was observed despite the persistent afterload elevation. Our findings of an afterload independent regression of LVH by ACE-inhibition emphasize an important role of the renin angiotensin system for the maintenance of pressure induced LVH.
...
PMID:Role of neurohumoral systems for pressure induced left ventricular hypertrophy in experimental supravalvular aortic stenosis in rats. 167 10

The three approaches (physiopathological, epidemiological and pharmacological) to the management of hypertension should converge to provide a personalized prescription of the most appropriate treatment to prevent and/or cure the cardiovascular complications of hypertension: hypertensive left ventricular hypertrophy and the risks directly related to it (haemodynamic, arrhythmic, ischaemic) may be corrected by certain antihypertensive agents (methyldopa, ACE inhibitors, some calcium antagonists) although there is no proof as yet of the benefits of this intervention (which could suppress the adaptation to the increased wall stress of the left ventricle); malignant hypertension and its cardiovascular complications have almost disappeared with modern antihypertensive therapy. Cardiac failure can be effectively prevented and cured when exclusively related to hypertension. When diastolic pressures are lowered by 8-10 mmHg cerebrovascular risk is reduced by a half and coronary risk by a quarter. Cardiovascular mortality related to hypertension is thus reduced by 20% and total mortality is thereby significantly decreased; the large scale clinical trials which provided these data were performed in the years 1965-1985 with diuretic therapy relayed by (or compared with) betablockers from 1980 onwards. These two families remain the drugs of reference in the prevention and treatment of the cardiovascular complications of hypertension. Personalized description of antihypertensive therapy should take into account the degree of risk and previous cardiovascular complications of the hypertensive patient: betablockers eventually associated with calcium antagonists are to be preferred in cases of hypertension with coronary artery disease and/or arrhythmias, severe hypertension and hypertension complicated by cardiac failure are good indications for ACE inhibitors without prejudicing other therapeutic options necessary in certain contexts, in particular aspirin therapy in patients with previous transient ischemic cerebral attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Treatment of hypertension and cardiovascular complications]. 168 21

Several risk factors for cardiovascular disease are discussed, including blood pressure, left ventricular hypertrophy, stress and smoking. Beta-blockers have a modest effect in reversing increased left ventricular mass, compared with angiotensin converting enzyme (ACE) inhibitors, although beta-blockers are as effective as ACE inhibitors in reducing posterior wall and interventricular septal thickness. Coronary events and many risk factors show a circadian rhythm. Beta-blockers can reduce the mid-morning (0700-1000 h) risk of ischaemic events and myocardial infarction. Catecholamine levels peak at 0700-1000 h, and catecholamine-induced myocardial necrosis can be significantly reduced by beta-blockade. Beta-blockers appear to be more effective than calcium antagonists in modifying the mid-morning vulnerable period and reducing the duration of ischaemia. However, the problems of using surrogate endpoints are discussed. In young to middle-aged hypertensives, beta-blockers are more effective in primary prevention of myocardial events than diuretics, though this is not the case for the elderly. Beta-blockers are also more effective than calcium antagonists in reducing morbidity and mortality after a myocardial infarction (i.e. secondary prevention). Patients with hypertension associated with ischaemic heart disease are most likely to get maximal benefit from treatment with beta-blockers.
...
PMID:Identification of patients at risk from ischaemic complications. 168 61

Pathological left ventricular hypertrophy in renovascular hypertension is associated with the accumulation of fibrillar collagen within the extracellular space and around intramyocardial coronary arteries. Even though the angiotensin converting enzyme inhibitor captopril was previously found to attenuate this interstitial and perivascular fibrosis, the relative importance of arterial and ventricular systolic pressures versus circulating angiotensin II (AII) and aldosterone (AL) in promoting hypertrophy and collagen accumulation in renovascular hypertension is uncertain. By drawing on the in-parallel arrangement of the right and left ventricles, with respect to their coronary circulation, and the in-series mechanical alignment of the ventricles, with a pressure-overloaded left and a normotensive right ventricle, this study sought to address this uncertainty. Three models of experimental hypertension, each having a different circulating AII and AL profile, were examined and compared with their controls: renovascular hypertension, where both AII and AL are increased; infrarenal aorta banding, where AII and AL are normal; and a chronic infusion of AL, where AII is suppressed or normal and AL is increased. In renovascular hypertension, as well as with AL, we found a significant rise in the interstitial collagen volume fraction and perivascular collagen area of the pressure-overloaded, hypertrophied left ventricle as well as the normotensive, nonhypertrophied right ventricle. This remodeling was not seen in either ventricle with infrarenal aorta banding despite comparable systemic hypertension and left ventricular hypertrophy. Thus, in experimental arterial hypertension in the rat, myocyte and nonmyocyte compartments of the myocardium are under separate controls: myocyte hypertrophy is most closely related to ventricular loading while circulating AII and AL, acting alone or in concert with other humoral factors, regulate the accumulation of collagen within the right and left ventricles.
...
PMID:Remodeling of the rat right and left ventricles in experimental hypertension. 170 Sep 33

Angiotensin II has previously been reported to have in vivo and in vitro cardiac hypertrophic effects. We used the salt-sensitive Dahl rat genetic strain to separate mechanical (pressure overload) vs. hormonal (renin-angiotensin system) input in cardiac hypertrophy. Blood pressure was significantly increased and left ventricular hypertrophy, as indexed by LV/BW ratios, was present at 7 and 15 days in rats receiving 4% and 8% NaCl compared to the 1% controls. There was no effect of the angiotensin converting enzyme inhibitor, enalapril maleate, on lowering the blood pressure in 8% NaCl-treated animals, however, there was a significant reduction in LV/BW ratio in 8% NaCl-treated animals that received this drug. Left ventricular angiotensinogen mRNA activity was significantly reduced in rats receiving 4% and 8% NaCl. In this model of hypertension the cardiac hypertrophy which develops is largely dependent on mechanical forces though there remains a significant contribution to this process from either circulating or localized angiotensin II production. Regulation of angiotensinogen gene expression in the hypertrophied left ventricle suggests that volume and electrolyte control of angiotensinogen gene expression in the heart and/or hereditary factors are predominant in the control of regulation of this gene in the left ventricle of Dahl rats.
...
PMID:Angiotensin converting enzyme inhibition in Dahl salt-sensitive rats. 171 20

Left ventricular hypertrophy (LVH) is both a target organ response to chronic arterial hypertension and a disorder that may be responsible for cardiovascular events. Although an increase in ventricular wall thickness may initially be compensatory and decrease wall stress, numerous studies have indicated that LVH is associated with a reduction in coronary flow reserve, diastolic and systolic ventricular dysfunction, and ventricular arrhythmias, all of which predispose to morbid cardiovascular events, including acute coronary syndromes, congestive myocardial failure, and sudden death. Reduction in LVH has been accomplished with beneficial effects on diastolic function and ventricular arrhythmias, without pressure-induced deterioration in systolic or diastolic function. Although therapy with diuretics and vasodilators effectively lowers arterial pressure, these therapies are not usually associated with significant regression of LVH. Calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, beta-adrenergic blockers, central adrenergic blocking agents, and possibly alpha-adrenergic blockers and diuretics with vasodilatory properties are associated with reductions in LV mass. However, studies are still needed to determine the relative effects of various antihypertensive therapies on LVH regression, coronary flow reserve, ventricular function, ventricular ectopy, and most importantly, on protection against major cardiac morbidity and mortality inherent to LVH.
...
PMID:Regression of increased left ventricular mass by antihypertensives. 172 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---