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)

Experimental evidence suggests that ACE-inhibitors possess cardioprotective properties. Since ACE-inhibitors can prevent bradykinin breakdown and can stimulate prostaglandin production, it is thought that these cardioprotective effects are mediated by bradykinin and prostaglandins. This article summarizes the results indicating that bradykinin and prostaglandins, although not the only factors, do play an important role in cardioprotection by ACE-inhibitors. Special attention is paid to the presence of the sulphydryl moiety of certain ACE-inhibitors. Probably, these sulphydryl group-containing ACE-inhibitors have an additional protective effect through an interaction with bradykinin or through scavenging of free radicals. However, these cardioprotective effects have not yet been shown in patients with ischaemic heart disease, although some studies indicate that ACE-inhibitors are also able to cause anti-ischaemic effects in patients. Further studies are required to establish the clinical importance of cardioprotection by ACE-inhibitors in ischaemic heart disease.
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PMID:Basic pharmacology of ACE-inhibitors with respect to ischaemic heart disease: prostaglandins and bradykinin. 219 12

Myocardial salvage can be maximized by the early institution of thrombolytic therapy and aspirin. Certain patients may benefit from the administration of intravenous heparin, beta blockers, or nitroglycerin. The routine use of percutaneous transluminal coronary angioplasty (PTCA) or calcium-channel blockers does not appear to be warranted. Recurrent myocardial ischemia should be vigorously treated with medical therapy and there may be value in cardiac catheterization, followed by PTCA or bypass surgery, depending upon the extent of myocardium at risk and the underlying coronary anatomy. Long-term morbidity and mortality may be reduced by instituting aspirin and beta blockers as well as by modifying risk factors. There is no evidence for the long-term benefit from any calcium-channel blocker. Oral anticoagulation may be warranted in those patients with a mural thrombus, congestive heart failure, or atrial fibrillation. ACE inhibitors may be of value in the presence of left ventricular dysfunction and certainly in the presence of symptomatic congestive heart failure. Antiarrhythmic therapy is generally indicated only for symptomatic or life-threatening arrhythmias. Residual myocardial ischemia should be sought by exercise testing, and those patients with poor exercise tolerance generally warrant cardiac catheterization in consideration for revascularization.
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PMID:Management of the patient following coronary thrombolysis. 220 19

Apart from their established use in the treatment of hypertension and heart failure, ACE inhibitors have been suggested to exert anti-ischemic effects. This article reviews the mechanisms of systemic and intracardiac angiotensin formation, as well as its interaction with the bradykinin, the prostaglandin, and the sympathetic nervous system. While high doses of angiotensin can precipitate myocardial ischemia. experimental data on a potential beneficial effect of ACE inhibitors on ischemic myocardial blood flow and function are inconsistent and controversial. Pooling the few available clinical data, several ACE inhibitors may attenuate myocardial ischemia at rest and during exercise. However, a significant fraction of patients does not benefit or even deteriorates. Recent experimental studies suggest a beneficial role of ACE inhibitors in attenuating reperfusion arrhythmias and postinfarction left ventricular remodeling. Unless the mechanisms and determinants of potential anti-ischemic actions of ACE inhibitors can be better defined, their use for treatment of myocardial ischemia cannot be recommended at present.
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PMID:ACE inhibitors for the treatment of myocardial ischemia? 227 72

Treatment of arterial hypertension is an important part of medical care provided in industrialized countries today. When non-drug treatment turns out to be ineffective, or when hypertension levels are higher than target values, or target organ damage is ascertained, drug therapy must be started. This rationale comes from large-scale intervention trials, which have shown that the lowering of elevated blood pressure reduces cardiovascular morbidity and mortality. A logical aim in treatment of hypertension should be both to "normalize" hypertension-induced cardiovascular abnormalities and to maintain the quality of life, without undesirable influence on other cardiovascular risks. Moreover, if we could identify the major hemodynamic impairment behind increased blood pressure and correct it by an appropriate drug therapy, then we would have a satisfactory means to perform individualized treatment. Over the past years the empirical basis for the use of antihypertensive drugs has been replaced by a step-wise approach, but few attempts have been made to provide an approach that fits pathophysiological understanding. For this reason the above-mentioned step-wise approach has been found to be an uncorrected simplification of antihypertensive care. Also, the use of more recent drugs (calcium channel blockers, ACE-inhibitors and serotonin-receptor blockers) as an alternative to beta-blockers and diuretics in first step therapy, has further contributed to the abandonment of the step-wise approach. The different groups of antihypertensive agents are examined with reference to their mechanism of action, pharmacokinetics, indications, and desirable and untoward effects. At present, indirect vasodilators, such as calcium-antagonists, ACE-inhibitors and serotonin-receptor blockers, alone or combined with diuretics, represent an intrinsic part of basic antihypertensive therapy. Beta-adrenoceptor antagonists remain the agents of choice when the principal therapeutic aim is to reduce the adrenergic drive. Both these drugs and direct vasodilators or alpha-adrenoceptor antagonists can be employed in the most severe forms of hypertension. In such cases, combined therapy (vasodilator + antiadrenergic + diuretic agents) is often used. Sublingual nifedipine and intravenous diazoxide or sodium nitroprusside are the drugs of choice for the hypertensive crisis. The use of most of the central or peripheral sympatholytic agents has generally been abandoned. Finally, beta-blockers and calcium-antagonists have been shown to have a secure place in the management of ischemic heart disease complicating arterial hypertension. In this condition captopril also appears to be useful.
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PMID:[Drug therapy of arterial hypertension. Reflections and suggestions]. 252 24

Recent intervention trials failed to show a significant decrease in mortality of ischemic heart disease in hypertensive patients given pharmacological treatment. These results led to a reassessment of cardiovascular risks of antihypertensive drugs per se and particularly diuretics. Captopril and Enalapril, antihypertensive drugs acting as converting enzyme inhibitors, might have some theoretical advantage over other antihypertensive drugs. The chronic ACE inhibitors therapy does not compromise glucose, lipid and urate and it seems not to be persistent in long-term administration.
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PMID:[Effect of angiotensin converting enzyme inhibitors on lipid, purine and glucose metabolism]. 254 May 15

Control of hypertension in the elderly has been shown to reduce cardiovascular morbidity. Although it is not known if this is also true for isolated systolic hypertension, drug treatment should be considered for systolic pressures over 170 mm Hg that cannot be controlled with nondrug therapy. The diuretics, calcium channel blockers, and the ACE inhibitors are very effective and generally well-tolerated therapy for the elderly. It may be necessary to combine two of these agents for some patients. Beta blockers are particularly useful for patients with ischemic heart disease or prior myocardial infarction. Beta blockers are the only agents which have been shown to be cardioprotective. For all antihypertensive agents, the elderly should be started on low doses. The drugs should then be titrated slowly if necessary. It is common for the elderly to respond to lower dosages than younger patients, and they should be monitored carefully for adverse reactions to medications. Antihypertensives should be administered once or twice daily whenever possible. If these principles are considered, most patients can be effectively controlled with a minimum of side effects.
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PMID:Antihypertensive therapy in the elderly. 266 39

The protective effect of angiotensin-converting enzyme inhibitors (ACEI) on myocardial ischemia and reperfusion damage was estimated in rat hearts, both in vivo and in vitro. Enalapril 2.5 mg/kg ip pretreatment at 24 and 5 h before coronary occlusion, significantly blunted the rise of CPK (445 +/- 151 vs 649 +/- 244 mu/ml, P less than 0.05) and improved electrocardiogram (ECG) 8 h after coronary occlusion. In global ischemia and reperfusion ex vivo, enalapril improved contractility (0.9 +/- 0.2 vs 0.3 +/- 0.3 g, P less than 0.05) and coronary flow (15.6 +/- 3.3 vs 11.9 +/- 3.1 ml/min/g, P less than 0.05), shortened significantly the duration of reperfusion arrhythmia (3.1 +/- 2.7 vs 9.7 +/- 8.1 min, P less than 0.05). In Langendorffs heart, captopril remarkably preserved force of contraction (2.1 +/- 0.4 vs 1.4 +/- 0.4 g, P less than 0.01) and coronary flow (2.7 +/- 0.5 vs 3.6 +/- 0.9 ml/min/g, P less than 0.05) in segmental infarction deteriorated by angiotensin I. Captopril 10(-5) M infusion reduced the release of CPK (435 +/- 112 vs 640 +/- 123 mu/min coronary flow, P less than 0.05). This action was almost completely abolished by pretreating and infusing with indomethacin. As a positive control, prostacyclin 5 X 10(-7) M infusion further reduced the release of CPK to 330 +/- 77 mu/min. It is concluded that angiotensin-converting enzyme inhibitor can protect both myocardial ischemia and reperfusion damage in rat hearts. The mechanism of protection was ascribed to reduced production of angiotensin II by ACE inhibition and increased prostacyclin release in the myocardium.
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PMID:Protective effects of captopril and enalapril on myocardial ischemia and reperfusion damage of rat. 282 45

The authors have compared the short-term effect of two captopril (ACE inhibitor) preparations namely the Lopirin (SQUIBB) and Tensiomin (EGIS) and dihydralazine as well as placebo in 15 patients with severe heart failure (NYHA III-IV, class). In case of 8 patients with NYHA IV, functional class the short-term effect of the combined therapy of dihydralazine and Lopirin and dihydralazine and Tensiomin as well dihydralazine and placebo have been compared. The underlying disease was dilated cardiomyopathy (DCM) and ischaemic heart disease (IHD). At the end of the treatment with different drugs and placebo the clinical signs of heart failure (complaints and physical status) and the echo and mechanocardiographic parameters of left ventricular function were assessed. The parameters, apart from the clinical signs, have been evaluated in double blind fashion. Compared to placebo all the three drugs i.e. dihydralazine, Lopirin as well as Tensiomin have decreased significantly the NYHA classes, influenced favorably the non-invasive parameters of left ventricular function and decreased blood pressure. As to the dihydralazine, it improved the left ventricular ejection function and the clinical state of the patients with DCM in a higher degree than the two ACE inhibitors did. The effect of Tensiomin and Lopirin was the same in every respect. Both have influenced more favourable the complaints and physical state of patients with IHD than dihydralazine has. The left ventricular filling pressure, the double product (heart rate x wall tension) indicating the myocardial oxygen demand were more reduced in their effect than in that of dihydralazine. Unlike dihydralazine both decreased the heart rate. Administering one of the two ACE inhibitors to the dihydralazine beneficial additive effects have been experienced; the NYHA classes, the heart rate, the left ventricular wall tension and the double product diminished. The authors, on the bases of the results, consider Tensiomin and Lopirin as equivalent in their effect. In their opinion the administration of these drugs mean a new, efficient way of therapy, first of all in cases of heart failure caused by IHD. In the most severe cases they suggest a trial with the combined dihydralazine-ACE inhibitor therapy.
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PMID:Comparative study on the short-term effects of angiotensin converting enzyme inhibitors (Lopirin, SQUIBB and Tensiomin), and dihydralazine in chronic cardiac failure. 307 6

Vasodilator therapy of heart failure has through the last 5-10 years become a well established treatment. Traditionally these drugs have been classified after their primary site of action on the vascular beds. Thus drugs primarily acting on the arteriolar bed are called afterload-reducing agents and are exemplified by hydralazine. Drugs primarily acting on the venous bed have been called preload-reducing reducing agents and the typical example is nitroglycerin. Other drugs, like prazosin, act on both the arteriolar and venous vascular beds. The classification is, however, not as sharp as originally believed since preload- and afterload-reducing activities mix with each other. Treatment with vasodilators for chronic heart failure has mainly been advocated in patients with valvular regurgitation, ischemic heart disease and various types of dilated cardiomyopathies. It seems appropriate today to put some questions concerning vasodilator therapy for heart failure. Among such questions are: When in the natural history of congestive heart failure should vasodilator therapy be commenced? How effective is long-term administration of vasodilating drugs? May vasodilator therapy decrease mortality in congestive heart failure? What about the efficacy of new vasodilating drugs compared to more traditional ones? In the review of vasodilating drugs besides ACE inhibitors, these questions will be addressed.
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PMID:Aspects on "traditional" vasodilators in the treatment of chronic heart failure. 352 22

The myocardial scar, left behind by an infarct, makes up a potential substrate for complex ventricular arrhythmias due to the presence in such tissue of electrical inhomogeneity, altered refractoriness, and abnormal conduction properties, which facilitate the induction of reentrant arrhythmias and the release of abnormal automatic responses of the partially repolarised cells. The mechanism(s) by which complex ventricular arrhythmias is/are transformed into malignant arrhythmias has/have not yet been definitely proven. The observation that coronary revascularization - in patients with ischaemic heart disease surviving out of hospital cardiac arrest - improves the prognosis, indicates that transient ischaemic attacks might be the trigger of malignant ventricular arrhythmias in patients with prior myocardial infarction. Patients with large infarct scars (heart failure) have an increased incidence of complex ventricular arrhythmias, death, and ischaemic events. Antiarrhythmic medical intervention does not improve the prognosis in these patients. Intervention with ACE-inhibitors reduces the prevalence of complex ventricular arrhythmias, the incidence of death, and reinfarction, but not arrhythmic death, indicating that residual ischaemia might be the major risk variable in patients with heart failure. Ischaemia is one of several risk markers for transient supraventricular arrhythmias in patients recovering from an acute myocardial infarction (AMI). In addition, anti-ischaemic intervention in patients recovering from AMI suppresses residual myocardial ischaemia and thereby reduces major events.
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PMID:[Post-infarction, myocardial ischemia: clinical importance and risk factor]. 750 21


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