Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results from SOLVD, SAVE, AIRE, GISSI-III, ISIS-IV, and the Chinese Captopril Trial suggest that therapy with ACE inhibitors, at least with enalapril, captopril, ramipril, and lisinopril, induce significant reduction in morbidity and mortality rates in patients with ischemic heart disease, myocardial infarction, and a wide range of ventricular function and myocardial infarction. SOLVD and SAVE results, in particular, demonstrate improved survival and reduced major ischemic events in patients with depressed systolic ventricular function. SOLVD points out that institution of ACE inhibitor therapy need not be done immediately post-myocardial infarction to accrue benefit. GISSI-III and ISIS-IV, on the other hand, suggest that use of ACE inhibitor drugs early post-myocardial infarction produces significant, albeit small, benefits when drugs are begun early post-event in conjunction with other routinely used therapeutic strategies. The prospective, well-designed, and well-controlled nature of these clinical trials, the consistency of their findings, and the high level of morbidity and mortality in placebo groups establish the importance of preventing ischemic events with the prescribed ACE inhibitors. Particularly important is the fact that none of these clinical trials were designed to determine optimal dose or frequency of administration of the ACE inhibitors chosen. Targeting dose principles were utilized and clinicians wishing to generate similar results in their own patient population should choose one of the ACE inhibitors studied and administer it in the manner described in hopes of achieving outcomes similar to those detailed in the summarized clinical trials. Finally, recommendations regarding post-myocardial infarction therapy with ACE inhibitors can be summarized. Patients having acute or remote infarction should have an assessment of ventricular function. All patients with depressed systolic function, whether they are or are not symptomatic, should receive a trial of an appropriate ACE inhibitor. Patients suffering an acute myocardial infarction should have an assessment of ventricular function early and, if the ejection fraction is low (probably < 50%), an appropriately chosen ACE inhibitor should be begun after 24 hours have elapsed. ACE inhibitor therapy should be begun in combination with other proven effective post-myocardial infarction treatment strategies. In patients with normal systolic function, advantages of ACE inhibitor therapy are less clear, but patients with large anterior wall myocardial infarction will likely benefit, even without objective evidence of left ventricular systolic dysfunction. Concomitant utilization of thrombolytic agents, aspirin, and beta blockers should not interdict use of ACE inhibitor therapy.
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PMID:Angiotensin-converting enzyme inhibitors post-myocardial infarction. 758 74

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.
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PMID:[ACE-inhibitors and cardiovascular protection]. 763 57

Myocardial interstitium plays an important role in the regulation of cardiac function compared with myocytes and it is actively involved in ischemia-reperfusion damage and in the acute and chronic remodelling during ischemic heart diseases. Myocardial post-ischemic oedema seems to interfere in this process. Myocardial oedema is able to induce structural alterations, to reduce myocardial function and to activate the renin-angiotensin-aldosterone system. Angiotensin II and aldosterone seem to be the cause of myocardial fibrosis that is detected during ischemic heart disease. Post-ischemic vascular permeability alterations have a similar role. In clinical conditions, ACE-inhibitors have important effects on cardioreparation and are able to improve cardiac function and reduce early and late mortality. The effects of myocardial oedema reduction (i.e. hypertonic reperfusion) on ischemia-reperfusion damage and myocardial fibrosis are still to clarify. A reduction in myocardial fibrosis may improve cardioreparation and prevent congestive heart failure, following ischemic heart disease.
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PMID:[Role of interstitial myocardium in ischemia-reperfusion injury: experimental data and clinical implications]. 763

Effective treatment of hypertension with permanent achievement of normal blood pressure readings is the most effective prevention of organ manifestations of hypertension. Treatment must, however, affect also other risk factors, in particular hyperlipoproteinaemia, smoking and diabetes. Treatment of hypertension is individually adjusted and depends on: a) age, b) the presence of complications of hypertension and c) the presence of associated diseases. In elderly hypertensive patients small doses of diuretics and beta-blockers are the drugs of choice. The most frequent complication of hypertension is hypertrophy of the heart and IHD. The drug of choice in patients with IHD, and in particular in patients after myocardial infarction, are beta-blockers, in patients with cardiac hypertrophy which substantially influences the prognosis in an adverse way ACE inhibitors are recommended. In patients with cardiac failure as well as in patients with asymptomatic dysfunction of the left ventricle the drugs of choice are ACE inhibitors. The author indicates therapeutic approaches used in the most frequent associated diseases--diabetes and hyperlipoproteinaemia.
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PMID:[Manifestations in cardiovascular organs of essential hypertension-- possibilities of directed therapy and prevention]. 767 62

Worsening or precipitation of asthma by beta-adrenoceptor antagonists is well recognized. Severe bronchoconstriction may be induced even in 'mild' asthmatics, and the dose of beta blocker required may be low, as in the case of eye drops of timolol, a nonselective beta blocker used to treat glaucoma. The severity of bronchoconstrictor response is not predictable. Nonselective beta blockers are more likely to precipitate bronchospasms in patients with asthma. The mechanism of beta-blocker-induced asthma is still not certain. Normal subjects develop neither a deterioration in lung function nor an increased bronchial hyperreactivity; therefore, beta blocker drugs should in general be avoided by asthma patients. Safe alternative therapies exist for both hypertension (calcium antagonists, ACE inhibitors, diuretics) and ischemic heart disease (calcium antagonists, nitrates).
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PMID:[Beta blockers and bronchial asthma]. 772 48

To delineate the cardioprotective actions of bradykinin (BK) and the contribution of endogenous kinins to the cardiac effects of the ACE inhibitor ramipril, we used the specific B2 kinin receptor antagonist icatibant (HOE 140) during myocardial ischemia and left ventricular hypertrophy (LVH). In isolated working rat hearts, perfusion with ramiprilat (10 nM to 10 microM) reduced the incidence and duration of ventricular fibrillation, and improved cardiodynamics and myocardial metabolism. BK perfusion (0.1 nM to 10 nM) induced comparable cardioprotective effects. In addition, perfusion with ramiprilat (0.1 microM) markedly increased kinin outflow measured by RIA. The beneficial effects of ramiprilat and BK were abolished by the addition of the specific NO synthase inhibitor NG-nitro-L-arginine (L-NNA 1 microM) or icatibant (1 nM). Similar results were obtained in dogs, rabbits and rats with myocardial infarction induced by ligation of the left descending coronary artery. The influence of the icatibant on the antihypertrophic effect of ramipril and BK in the LVH was investigated in rats made hypertensive by aortic banding. Ramipril at the antihypertensive dose of 1 mg kg-1 day-1 for 6 weeks prevented the increase in blood pressure and the development of LVH. The lower non-antihypertensive dose of ramipril (10 micrograms kg-1 day-1 for 6 weeks) had no effect on the increase in blood pressure or on plasma ACE activity but also prevented LVH after aortic banding. The antihypertrophic effect of the higher and the lower dose of ramipril as well as the antihypertensive action of the higher dose of ramipril were abolished by coadministration of the icatibant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioprotective actions of bradykinin in myocardial ischemia and left ventricular hypertrophy. 774 86

Endothelial function of epicardial arteries and coronary resistance vessels, as well as endothelial dysfunction and clinical symptoms of coronary artery disease and their therapeutic implications are reviewed including the presentation of the author's own results. Coronary endothelial vasodilator dysfunction represents a fundamental functional disturbance in vascular biology with the development of atherosclerosis. This functional alteration in coronary vascular reactivity appears to play an important integral part in the clinical presentation of coronary artery disease. Humoral and neuronal factors in favour of vasoconstrictor influences affect the balance between myocardial oxygen supply and demand, thus, facilitating the manifestation of myocardial ischemia. In order to identify more selective therapies the potential mechanisms underlying an impaired release or activity of EDRF/NO must be considered. Dysfunction of the endothelial L-arginine/NO pathway may involve decreased activity of NO synthase, increased inactivation of NO formed from its precursor L-arginine, impaired signal transduction mechanisms and reduced intracellular availability of L-arginine. Currently, initial therapeutic strategies include the supplementation of L-arginine, the use of antioxidants, as well as ACE-inhibitors. ACE-inhibitors have been shown not only to reduce vascular tone (and hypertrophy) by inhibition of angiotensin II formation, but also by increasing the endothelial production of NO and prostacyclin most likely due to the local accumulation of endothelium-derived bradykinin. Thus, ACE-inhibition appears to provide the potential to improve endothelial NO synthesis. Indeed, study results demonstrate that chronic ACE-inhibition is associated with an increased coronary blood flow response to acetylcholine suggesting an improvement in endothelial vasodilator functioning of coronary resistance vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary endothelial vasodilator dysfunction: clinical relevance and therapeutic implications. 785 84

The treatment of microvascular angina (anginal pain resulting from myocardial ischemia due to dysfunction of small coronary arteries) is empiric and often ineffective at present. The poor knowledge of the pathophysiologic mechanisms responsible for the microvascular dysfunction and the possible heterogeneous nature of the disease limit the possibility of a rational therapeutic approach to these patients. The failure of traditional antiischemic therapy is confirmed by the frequent unresponsiveness of angina and by the reduced exercise tolerance with administration of sublingual nitrates. Despite that, beta-blockers and calcium-antagonists, when given either alone or in combination, are beneficial in the control of symptoms in some patients. Alternative forms of treatment, based on some pathophysiological hypotheses and clinical observations, include xanthine derivatives, ACE-inhibitors, alpha-blocking agents, imipramine and, in women, oestrogens. The actual clinical usefulness of these drugs, however, is questionable at present, as their efficacy should be evaluated with more adequate studies in the future.
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PMID:[Therapy of microvascular angina]. 791 50

The prevalence of congestive heart failure was studied in the medical departments of eight Norwegian hospitals for two days. A mean of 179 patients with heart failure was identified, representing 20% of the total number of in-patients in the participating hospital departments. About 60% of the patients studied were over 70 years of age. There were equal numbers of men and women, but men dominated below 70 years. Ischemic heart disease (59%), valvular heart disease (15%) and hypertension (14%) were the most common primary heart diseases. The drugs used most frequently were diuretics (91%), digitalis (60%), nitrates (40%), and ACE-inhibitors (38%); the last were used more often among patients with severe heart failure (56%).
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PMID:[Heart failure in Norwegian hospital departments. Prevalence, diagnostic and therapeutic aspects]. 794 Apr 46

With rapidly progressing therapeutic methods in the cardiovascular medicine, scientific evaluations for newly developed cardiovascular drugs and therapies have become mandatory. We have launched five large scale multicenter cooperative studies, namely, Japan Multicenter Investigation for Cardiovascular Drugs/Therapies, J-MIC (I), (B), (M), (S), and (K). The aims of studies include to investigate: the best therapeutic approach in patients with acute myocardial infarction who underwent thrombolytic therapy with or without any adjunctive treatment (I), the long-term comparative study (3 years) of nifedipine (extended release tablet) with ACE inhibitor in patients with essential hypertension and ischemic heart disease (B), the long-term effect (3 years) of trapidil and/or ethyl icosapentate in patients with ischemic heart disease with or without arteriosclerotic obstructive disease in terms of progression or regression of atherosclerotic changes in coronary as well as peripheral arteries (M), the efficacy and safety of pravastatin to prevent post-PTCA restenosis (S), and regression of atherosclerotic lesion of coronary arteries in patients with familial hypercholesterolemia by LDL apheresis (K).
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PMID:[Large scale multicenter cooperative study for cardiovascular therapy (Japan Multicenter Investigation for Cardiovascular Drugs/Therapies, J-MIC)--results and perspectives]. 807 6


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