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

Over the last 40 years effective drug treatment of hypertension has become available. Newer classes of drugs offer efficacy with simplicity of dosing regimen and good patient acceptability. However, there is increasing interest in the long-term benefits of treatment, particularly influences on total mortality and morbidity and mortality from coronary artery disease and its complications. Established treatments with diuretics and beta blockers do reduce stroke risk but have less than predicted effects on coronary heart disease. While there is experimental evidence and clinical pointers that ACE inhibitors and calcium antagonists may influence atherosclerosis in the long-term, there is as yet no objective clinical confirmation. The aim of treatment in the 1990s is to control blood pressure (and other risk factors) in the short-term with a view to improving long-term outcome. Many clinicians have modified step-care approaches to individualize drug treatment using one or two agents, selected from older and newer classes, which on clinical grounds are most appropriate in the individual patient. Factors determining choice are race, other risk factors and associated diseases.
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PMID:Drug treatment of hypertension. 836 Nov 33

While the circulating renin-angiotensin system (RAS) plays an important role in short-term maintenance of cardiovascular homeostasis, recent studies point to a role in long-term cardiovascular regulation for endogenous RAS in target tissues. This article focuses on the multiple effects of tissue angiotensin enzyme (ACE) and angiotensin II (Ang II), its active peptide product. Ang II has been shown to be a potent growth factor in vascular smooth muscle cells. Depending on the local conditions, the vascular response may be either hypertrophy or hyperplasia. The molecular mechanisms involved in the interactions of Ang II with endothelium- and smooth muscle-derived cell products may play important roles in the modulation of vascular structure in hypertension and vascular injury. Evidence also points to a role for Ang II in the development of left ventricular hypertrophy in hypertension. In addition, cardiac RAS may contribute to the pathophysiology of heart failure. Experimental and clinical studies with ACE inhibitors point to a role for tissue ACE activity in the development of atherosclerosis, as well as cardiac hypertrophy and remodeling.
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PMID:Local expression and pathophysiological role of renin-angiotensin in the blood vessels and heart. 839 69

The role of renin-angiotensin system in the development of atherosclerosis is not yet defined, even though several actions of angiotensin II have been suggested as contributing to the development of the atherosclerotic lesion. Local renin-angiotensin system may exert a variety of autocrine or paracrine influences on vascular tissue leading to important trophic and growth regulatory effects and participating to well known events in atherogenesis as control of smooth muscle cell growth and proliferation. The existence and the specific function of components of this system in blood vessels wall suggest its possible involvement in atherosclerotic process. On these bases, the antiatherogenic properties of ACE-inhibitors have been recently evaluated in animal models where a protective effect of ACE-inhibition over the development of experimental atherosclerotic lesions has been observed. This favorable effect could follow the antihypertensive action of ACE-inhibitors even whether other potential mechanisms, including prevention of angiotensin II-induced vascular proliferation and interference with sympathetic nervous system activity and insulin sensitivity, have to be considered. Despite some clear-cut experimental evidences, the clinical importance of such findings as well as the precise mechanisms by which ACE-inhibition is able to interfere with the pathogenesis of atherosclerosis is still matter of debate and need to be assessed in future investigations.
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PMID:Ace-inhibitors and experimental atherosclerosis. 851 7

Hypertension is the leading cause of death in the elderly in Western countries. The Authors remark that hypertension is not only a purely hemodynamic phenomenon, but is a multifaceted disease frequently associated with metabolic disorders in the elderly. Among the latter, hyperinsulinism could be the linking pathogenetic factor with atherosclerosis progression. Then the Authors suggest a unitary pathogenetic hypothesis of hypertension and atherosclerosis. The crucial points are the inborn alteration of cellular sodium transport systems and the modulating action of environmental factors, first of all insulin. According to this hypothesis, the goal of the management of elderly hypertensives is the prevention of the fatal or invalidant cerebro- and cardiovascular event. To follow a good "pathogenetic" treatment of elderly hypertension and atherosclerotic process evolution, the first step is a dietetic approach avoiding acute load of sodium and lipids. Furthermore, the pharmacological treatment with calcium antagonists and ACE inhibitors is respectful of associated metabolic disorder and positively modulate the cellular sodium transport systems activity.
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PMID:Hypertension and atherosclerosis in the elderly: pathogenetic common mechanism and intervention strategies. 851 16

Many cell types in myocardial tissue, including cardiocytes, contain receptors for angiotensin-II, but the activation of these receptors requires angiotensin concentrations in the micromolar range, which do not occur in plasma in vivo. However, angiotensins formed locally in the heart can activate these receptors in a paracrine and autocrine mode. In cardiac hypertrophy due to hemodynamic overload, the myocardial angiotensin formation is enhanced due to an augmented expression of angiotensinogen and ACE. Though the mRNA for prorenin is expressed in myocardium, the formation of active renin within the heart has not yet been demonstrated and myocardial renin activity is mainly due to contamination from circulating active renin. Intracoronary application of ACE inhibitors in hypertrophied hearts in vivo and in vitro indicates that the locally formed angiotensin-II contributes to coronary constriction, impairment of diastolic relaxation and marginally to the maintenance of systolic tension development. Angiotensin-II can exert trophic effects on cardiocytes and cardiac fibroblasts, and chronic inhibition of the cardiac RAS by ACE-inhibitors or AT receptor antagonists can induce partial regression of overload hypertrophy, even without normalizing the overload. This anti-trophic action may be partially due to the impairment of the angiotensin axis, but also due to enhancement of bradykinin availability, which results in an augmented release of endothelial anti-trophic signals such as EDRF/NO and prostacyclin. Preliminary evidence is compatible with the hypothesis that an activated local RAS in elastic arteries contributes to the localization and progression of atherosclerosis by suppressing EDRF releasability. However, the anti-atherosclerotic potential of ACE inhibitors and AT receptor antagonists in humans is still unknown.
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PMID:The cardiac renin-angiotensin system: physiological relevance and pharmacological modulation. 851 37

The pathological chain of events that stretches from the earliest atheromatous lesion to end-stage myocardial failure and death is amenable to attack in many places. It may well prove that a multifaceted intervention offers the best therapeutic option. Two important cardiovascular therapies, the calcium entry blockers and ACE inhibitors, may offer more than their effects on vascular tone and remodeling. Both have actions on the basic process of atheroma. Individually, or more challengingly in combination, they may strike at the basic pathogenesis of atherosclerosis yet still provide their more general beneficial effect on vasomotor tone. Whilst clinical data are yet scant, there is a plausible biological basis for their coprescription.
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PMID:Coadministration of calcium antagonists and ACE inhibitors--is a skeptic convinced?: a personal view. 856 69

Diabetes and hypertension have a higher than expected comorbidity. They share common etiology, pathophysiology, and organ effects. Long-term therapeutic goals are to prevent renal failure and atherosclerosis. Management should inhibit pathophysiologic mechanisms and avoid stimulating them. The most appropriate pharmacologic agents to treat hypertension in the diabetic are ACE inhibitors, selected calcium channel blockers, alpha adrenengic blockers, and certain central alpha agonists. The only diuretics that should be used are indapamide and torsemide.
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PMID:Diabetes and hypertension. 856 30

New South African guidelines are proposed by the Hypertension Society of Southern Africa for the management of hypertension by primary health care services in South Africa. Specific South African guidelines are appropriate for hypertension, which is now recognised as one of the five major diseases that must be given priority by the new Government. Furthermore, patient participation and empowerment in blood pressure (BP) control become feasible through the new concept of lifestyle modification. This article gives the rationale underpinning these guidelines. The correct methods to measure blood pressure (BP), with patients sitting for 5 minutes, correct cuff-size and repeated readings, are emphasised to eliminate the 'white coat' effect and ensure accurate BP readings. The rationale for the overall management of all atherosclerosis-related risk factors is given, as are the principles of non-drug hypertension treatment and patient education. We emphasise that patients must understand hypertension to be a risk factor and not a disease. Patients should also be empowered to contribute to effective BP control. The justification for the chosen BP levels at which specific action is required by the primary health care team is given. The BP levels span the range from mild hypertension, requiring conservative treatment schedules, to possible malignant hypertension, which requires urgent management and referral to the appropriate level of care. The motivation for cost-effective antihypertensive drug therapy is provided. The recommended initiation of drug therapy is with effective, safe low-cost drugs. Suggested first-line therapy comprises lifestyle management and low-dose diuretics. The second-line drugs, in order of increasing price, are low-dose reserpine, or a beta-blocker, or a calcium blocker, or an ACE inhibitor. For third-line therapy hydralazine is chosen, or other second-line drugs could be added. Where possible, the examples of specific drugs given are those for which a generic is available, to ensure cost-containment. The motivation for drug choices for hypertension in special cases such as pregnancy, the elderly, blacks and patients with diabetes and renal disease is given. The management of malignant hypertension receives special attention.
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PMID:Rationale for the hypertension guidelines for primary care in South Africa. 860 Jun 5

Acute myocardial infarction occurs with increasing frequency with advancing age, and older patients with acute MI are at increased risk of a variety of complications including congestive heart failure, arrhythmias and conduction disturbances, myocardial rupture, cardiogenic shock, and death. Older patients thus comprise a high-risk subgroup of the MI population who consequently may derive substantial benefit from appropriately selected therapeutic interventions. At the same time, many interventions are associated with increased risks in the elderly, so that individualization of treatment is essential in all patients. Optimal therapy is thus based on a careful risk-benefit assessment of the available treatment options in conjunction with information on patient preferences and other relevant factors. Though many therapeutic trials of patients with acute MI have either excluded elderly patients or enrolled too few older subjects to permit definitive conclusions, sufficient data are available to make specific recommendations in several areas. As shown in Table 6, therapies of proven value in the acute-phase treatment of elderly patients with MI include aspirin and thrombolysis. Intravenous beta blockers are likely to be of benefit as well, and long-term oral beta blockade after MI is clearly beneficial. ACE inhibitors are of proven value in the long-term management of patients with left ventricular dysfunction (ejection fraction less than 40%), but initiation of an ACE inhibitor should probably be delayed for 48 to 72 hours in most cases. The role of other agents including nitrates, magnesium, diltiazem, and verapamil requires further clarification, but anti-arrhythmic drugs and dihydropyridine calcium antagonists should generally be avoided in the absence of specific indications for their use. Finally, though the role of catheterization and revascularization in elderly patients with acute MI requires additional study, current data indicate that age alone should not be considered a contraindication to these procedures. As the age of the population continues to rise, the number of older patients at risk of acute MI also increases. Though progressively more sophisticated interventions may ultimately result in sizable reductions in post-MI morbidity and mortality, given the high risk of adverse outcomes in this population the best treatment is prevention. Thus, the greatest potential for the future, as well as the greatest challenge, is to develop more effective strategies for preventing atherosclerosis and for conquering the epidemic of coronary heart disease.
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PMID:Therapy for acute myocardial infarction. 865 55

Angiotensin formed in the renin-angiotensin system is involved in the genesis and development of atherosclerosis and coronary heart disease. It has a negative impact on the process of ischaemization/reperfusion. The renin-angiotensin system is activated during a new myocardial infarction and has an impact on the process of remodelling of the left ventricle after myocardial infarction which causes its dysfunction and heart failure. ACE inhibitors are one of the important means which influence the formation of angiotensin II and thus prevent its action on heart and vessels. They prevent the development of atherosclerosis, reduce the extent of necroses during myocardial infarction and reduce the extent of left ventricular dysfunction. They diminish also stunning of the heart muscle during ischaemia/reperfusion and significantly prolong the patients life after infarction. They do not influence the development of restenosis after percutaneous transluminal angioplasty. ACE inhibitors have a positive effect on heart failure, they reduce the rate of reinfarctions and the mortality rate.
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PMID:[Angiotensin converting enzyme inhibitors in ischemic heart disease]. 901 29


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