Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aim of recent experimental and clinical studies has been to evaluate the important role of the renin-angiotensin system in the development of cardiac hypertrophy, of vascular hypertrophy and of left ventricular fibrosis and remodelling in essential hypertension and ischemic heart disease. It has been suggested that ACE-inhibitors are the class of antihypertensive drugs more effective in reducing left ventricular hypertrophy (LVH) in hypertensive patients. The possible mechanisms are, beyond the decrease in blood pressure, the possibility of interfering not only with the renin-angiotensin system activity, but also with the sympathetic nervous system activity as well as with aortic distensibility, all factors that can influence the development of LVH. Vascular changes in essential hypertension are complex and depend not only on the severity of blood pressure levels, but are related to diameter and structure of the vessels and to the presence of other atherosclerosis risk factors. ACE-inhibitors are effective in inducing the regression of structural changes in resistance arterioles and furthermore can increase arterial compliance in large arteries; new studies are undergoing in order to assess the effects of these drugs on atherosclerotic plaque progression/regression. The results of large clinical trials have shown the efficacy of ACE-inhibitors in the treatment of heart failure, in addition, after it has been demonstrated that ACE-inhibitors can influence the structural remodelling process after myocardial infarction, their use has been extended to patients with ischaemic heart disease.
 ...
PMID:[ACE-inhibitors and cardiovascular protection]. 763 57

Various antihypertensive agents may reduce blood pressure to a similar degree, yet they produce different outcomes with respect to long-term end-organ damage. Effective antihypertensive therapy can prevent or even reverse established left ventricular hypertrophy. The most rapid and extensive regression occurs with agents that block the reninangiotensin system or reduce entry of calcium into the cells. Other classes of drugs that reliably reverse left ventricular hypertrophy are centrally acting adrenergic inhibitors and beta blockers. The effect of antihypertensive agents on atherosclerosis appears to differ widely with regard to lipid metabolism, insulin sensitivity, and the biology of endothelium and vascular smooth muscle. Hypertension and chronic renal failure (diabetic and nondiabetic) are closely allied, but available antihypertensive agents are not equally potent in reducing intraglomerular pressure.
 ...
PMID:Physiologic effects of long-term hypertension control. 763 59

Antihypertensive therapy has been used for almost 40 years to reduce blood pressure and to prevent morbidity and mortality related to the hypertensive state. Cardiovascular events are related to the initial elevation of blood pressure; the benefits of treating malignant, severe or moderate hypertension are well established. Although large scale clinical trials have demonstrated a decrease in morbid events when mildly elevated blood pressures is treated, the benefits are neither universal or dramatic and treatment is certainly less cost effective than no treatment. Recently it has been emphasised that the absolute risk of cardiovascular events is determined only in part by blood pressure, and that it is also influenced by age, gender, race and the presence of other cardiovascular risk factors. For example, in older individuals where the absolute risk of vascular complications is greater than in younger individuals for any given level of blood pressure, the benefits of therapy will be greater. It has been suggested that in younger individuals with mild hypertension and a low absolute risk of developing cardiovascular morbid events it may be more appropriate to monitor the effects of drug therapy on measures of cardiac and vascular damage that are associated with the hypertensive state. Drug therapy has been shown to be extremely effective in reducing the incidence of stroke, congestive cardiac failure and renal failure associated with elevated blood pressure. Meta-analysis of randomised large scale clinical trials indicates that drug therapy may not reduce coronary events to the extent expected in patients with hypertension. One plausible explanation is that the trials have been of insufficient duration to detect the benefit of blood pressure lowering on coronary heart disease. It has also been suggested that certain adverse metabolic effects associated with the use of thiazide diuretics and beta-blockers employed in these trials may have partially offset the benefits of blood pressure reduction. However, the clinical significance of these drug-induced metabolic disturbances remains unclear. Experimental data suggesting differences in the ability of antihypertensive drugs to inhibit atherosclerosis in animal models are also of interest, but again the relation of the findings to the clinical situation is unknown. Thiazide diuretics, beta-blockers, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors and alpha-blockers can produce regression of left ventricular hypertrophy (LVH). While LVH is clearly a strong and independent predictor for coronary disease, it remains to be shown that a lower risk for coronary morbid events exists in patients whose LVH has undergone regression over and above that attributable to blood pressure reduction.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Goals of antihypertensive therapy. 772 25

Since the earlier review in Drugs substantial additional data have accumulated regarding the antihypertensive efficacy of isradipine in various clinical situations, as well as data on its clinical effects in atherosclerosis. Recent therapeutic trials confirm that the efficacy of isradipine in the treatment of patients with mainly mild to moderate hypertension, when administered orally as a conventional or modified release preparation, is similar to that of titrated dosages of amlodipine, felodipine, nifedipine, diltiazem, captopril, methyldopa, metoprolol, prazosin and hydrochlorothiazide. A further decrease in blood pressure can be expected when isradipine is combined with another antihypertensive drug in patients who have not responded adequately to monotherapy. Initial studies have shown that intravenous isradipine is effective in controlling hypertension following coronary artery bypass graft surgery and that it appears useful in the treatment of intraoperative hypertension and hypertensive crisis, and in hypertensive disorders in pregnancy, when administered orally or intravenously. A large study, the Multicentre Isradipine Diuretic Atherosclerosis Study (MIDAS), was designed to compare the efficacy of isradipine and hydrochlorothiazide in reducing the rate of progression of carotid artery wall thickness, measured by B-mode ultrasound, as a surrogate for early atherosclerosis. Results indicated that wall thickness increased significantly less with isradipine than hydrochlorothiazide after 6 months of therapy. Thereafter the rate of progression remained parallel for the remainder of the 3-year trial. The confirmation of its antihypertensive efficacy, along with its favourable haemodynamic profile and reversal of left ventricular hypertrophy, minimal effect on glucose and lipid metabolism, preservation of quality of life and good tolerability, makes isradipine a suitable drug for the treatment of most patients with mild to moderate hypertension.
 ...
PMID:Isradipine. An update of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy in the treatment of mild to moderate hypertension. 778 92

We describe the cardiovascular abnormalities found at autopsy in patients with AIDS and a description of the opportunistic infections in these cases studied between January 1988 and August 1993. There were 51 cases with such diagnosis. Pericardial effusion appeared in 9, pleural effusion in 7, myocarditis in 5, 7 with pericarditis, endocarditis in 6, left ventricular hypertrophy in 20, right ventricular hypertrophy in 21 and evidence of atherosclerosis in 15. Thus, data of cardiovascular damage was present in 42.7% of our patients. The cardiovascular abnormalities in this group are common, in contrast to the paucity of clinical findings. Diagnosis of cardiac pathology was made in only 12% of them. So in every case with diagnosis of AIDS, a careful clinical examination and cardiac diagnostic oriented tests must be done for detection of these abnormalities.
 ...
PMID:[The autopsy findings in 51 cases of AIDS with cardiovascular damage]. 784 Jul 32

Hypertension is accompanied by a series of structural adaptations and pathological alterations in the heart and vessels. These include hypertrophy of the left ventricle and walls of resistance vessels, degeneration of elastic components in the walls of large arteries, atherosclerosis and glomerulosclerosis. In order to improve prognosis it is important that the antihypertensive drugs used can prevent or regress these processes, and this review focuses on the experience with the vascular selective calcium antagonist felodipine. Clinical studies show that antihypertensive treatment with felodipine promotes regression of left ventricular hypertrophy, increases compliance of large arteries, and has favourable effects on renal function. In addition, experimental data have shown that felodipine inhibits atherosclerotic plaque development. As structural cardiovascular changes appear early in hypertension, intervention with antihypertensive therapy is better initiated sooner than later. Vascular selective calcium antagonists, such as felodipine, appear effective in reducing blood pressure and in ameliorating hypertension-induced structural changes.
 ...
PMID:Structural changes in hypertension, the potential for their prevention, arrest and reversal: a focus on felodipine. 784 95

The Joint National Committee Reports IV (1988) and V (1992) have emphasized individualization of drug therapy for patients with hypertension-a departure from the "stepped" care approach of initiating therapy with diuretics as advocated by the JNC I-III in the 1970's and 1980's. This review highlights individualization or "patient profiling" using calcium channel blockers as first-line treatment strategy for patients with primary hypertension--especially in the patient who has attendant risk factors and sequelae. The calcium channel antagonists, especially effective in elderly and Black patients, have proven efficacy in reducing left ventricular hypertrophy and improving diastolic function in patients with hypertensive heart disease. The heart rate limiting calcium antagonist, verapamil, has been found effective in outcome trials of reducing death and reinfarction rates post myocardial infarction and is an alternative therapy for the beta blocker intolerant hypertensive post myocardial infarction. More vascular specific dihydropyridines (felodipine, isradipine, and amlodipine) may be preferable to rate limiting agents in hypertensives with sinus node or AV conduction disorders and in those with impaired left ventricular systolic function. Verapamil and diltiazem have been effective in preliminary trials in reducing proteinuria and preserving renal function in both diabetic and non diabetic hypertensives. Calcium channel antagonists appear to prevent the progress of atherosclerosis independent of their antihypertensive properties. Further, they have theoretic value in improving endothelial mediated vasodilation.
 ...
PMID:Individualization of therapy for hypertension in the 1990's: the role of calcium antagonists. 785 64

Increased blood pressure can be observed in about 15-20% of the Swiss population. Hypertension causes few or no symptoms, but is an important risk factor for myocardial infarction, stroke, renal failure and peripheral vascular disease. All these clinical complications of hypertension are preceded by functional changes of blood vessels and the myocardium (left ventricular hypertrophy). In conduit arteries, hypertension is associated with atherosclerotic changes, while in resistance arteries only increased medial thickness can be observed. In atherosclerosis, functional changes of the endothelium, vascular smooth muscle, platelets and monocytes occur. These changes lead to hypercontractility, increased interaction of circulating blood cells with the blood vessel wall, and to proliferation and migration of vascular smooth muscle cells. These events impair local blood flow and eventually may cause vascular occlusion. The endothelium plays a particularly important role as a regulator of these mechanisms. Accordingly, it is likely that an endothelial dysfunction occurs at the very beginning of the atherosclerotic process. In resistance arteries, remodeling of vascular smooth muscle cells leads to thickening of the media with encroachment on the lumen due to an increased media lumen ratio. These hypertension-induced vascular changes are in part reversible by antihypertensive drugs. Hypertension-induced vascular disease is preceded by numerous alterations in the expression, secretion and action of mediators and receptors of endothelial cells, vascular smooth muscle, platelets and monocytes. It is hoped that increased understanding of the cellular/molecular mechanisms of hypertensive vascular disease will allow more effective therapy (and in the future also gene therapy) as well as better prevention of coronary artery disease in hypertensive patients.
 ...
PMID:[Hypertension and vascular diseases: molecular and cellular mechanisms]. 787 5

Several studies have shown evidence of the key role of the endothelium in modulating the tone of epicardial coronary vessels, in the different manifestations of coronary artery disease. Recently, the role of endothelium-dependent vasodilation has been focused, because clinical observations have suggested that myocardial ischemia might be caused or aggravated by inappropriate vasoconstriction of resistance vessels. An abnormal endothelium-dependent vasodilation, either of epicardial and of coronary microvasculature, has been documented in patients with syndrome X and in patients with history of hypertension and left ventricular hypertrophy. Vasoconstriction of the small coronary vessels is probably the mechanism underlying the impaired increase of coronary blood flow during atrial pacing and the wide variations of the ischemic threshold in some patients with chronic stable angina. In patients with variant angina, the endothelial function seems abnormal only in the conductance vessels. It is likely that the endothelial dysfunction of the small coronary arteries be present in many clinical situations in which a discrepancy between a mild atherosclerosis of epicardial coronary artery and signs of ischemia exists, as it has been observed early after successful angioplasty and after coronary artery reperfusion during acute myocardial infarction.
 ...
PMID:[Endothelial dysfunction in ischemic syndromes]. 802 14

Diabetic cardiomyopathy as a distinct entity was first recognized by Rubler et al. in diabetics with congestive heart failure (CHF), who had no evidence of coronary atherosclerosis. The Framingham study showed a 2.4-fold increased incidence of CHF in diabetic men and a 5.1-fold increase in diabetic women over 18 years. Pathological studies show left ventricular hypertrophy and fibrosis with varying degrees of small vessel disease, the functional significance of which is uncertain. Hypertension was recognized as an important cofactor in the development of fatal congestive heart failure in diabetics. On cardiac catheterization, in patients symptomatic of heart failure, either congestive or restrictive patterns have been observed. In contrast, asymptomatic diabetics had decreased left ventricular compliance but normal systolic function on hemodynamic study. Noninvasive studies show alterations in systolic and especially diastolic function, particularly in diabetics with microvascular complications and/or coexistent hypertension. Using load-independent measures of contractility, however, systolic function was generally found to be normal in asymptomatic normotensive diabetics. Experimental studies have focused on the mildly diabetic dog and the severely diabetic rat. Decreased left ventricular compliance and increased interstitial connective tissue were observed in chronically diabetic dogs. In contrast, ventricular myocardium from diabetic rats exhibits a reversible decrease in the speed of contraction, prolongation of contraction, and a delay in relaxation. These mechanical changes are associated with a decreased myosin ATPase, a shift in myosin isoenzyme distribution, alterations in a variety of Ca2+ fluxes, and changes in responses to alpha- and beta-adrenergic and cholinergic stimulation. These biochemical changes may be secondary to alterations in carbohydrate, lipid, and adenine nucleotide metabolism in the diabetic heart.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Diabetic cardiomyopathy. 808 30


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