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)

Isosorbit 5-mononitrate is useful in ischaemic heart disease and in cardiac failure because of its favourable pharmacokinetic properties, in particular the absence of the so-called first pass effect, the great biological availability and long elimination time. The authors demonstrated on the preparation Elentan long, Schwarz Monheim GFR, which contains 50 mg isosorbit 5-mononitrate the improved efficiency of the left ventricle after three months administration to 15 patients with confirmed ischaemic heart disease, by exerting a favourable effect on the diastolic, systolic and global left ventricular function. Nitrates are drugs of first choice in some forms of ischaemic heart disease and are also effective in cardiac failure because they exert a marked effect on some cardiac functions on which the efficiency of the left ventricle depends. Elentan long proved, while using simple dosage, a preparation with favourable characteristics as regards biological availability and nitrate tolerance.
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PMID:[Effectiveness of the delayed-action form of isosorbide 5-mononitrate in ischemic heart disease]. 203 13

Mechanocardiography has been in use to evaluate ventricular function and the cardiac effect of drugs. Twenty-five patients with ischemic heart disease (IHD) and 25 patients with IHD and mild hypertension (HTN) were enrolled in a double-blind, placebo controlled study of Abana. Half the patients in each group received Abana--a formulation based on Ayurvedic principles--and the other half received a placebo in a randomized manner. The effect of Abana was evaluated by means of LV apex cardiogram (ACG), phonocardiogram and carotid pulse tracing and ECG (mechanocardiography) before and at the end of 8 weeks of treatment. As compared to placebo, Abana significantly reduced the frequency and severity of anginal episodes, as judged by clinical improvement and nitrate consumption. Significant improvement in ventricular function was observed as reflected by a decrease in ACG A amplitude and A wave duration, along with a significant increase in LV ejection fraction and VCF. The decrease in double and triple products reflected decreased MVO2. A significant fall in diastolic blood pressure was noted in patients with mild hypertension. Abana seems to reduce preload and afterload and improve diastolic function and pump function, which may be responsible for the beneficial effects of Abana in ischemic heart disease.
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PMID:Effect of Abana on ventricular function in ischemic heart disease. 208 79

Nitrates are highly effective both in terminating acute attacks of angina pectoris and in the prophylaxis of symptomatic and asymptomatic myocardial ischemia. Preload reduction by venodilatation is the prevailing mechanism of nitrates in patients with chronic stable angina and is the unique feature distinguishing them from beta and calcium-channel blockers. Nitrates dilate coronary arteries not only in pre- and poststenotic vessels, but also in eccentric lesions. In patients with endothelial dysfunction, nitrates seem to be the physiological substitute for endothelium-derived relaxing factor. During the past decade, however, there has been substantial evidence of a clinically relevant loss of the anti-ischemic effects ("nitrate tolerance"). Many studies with oral dosing of isosorbide dinitrate or isosorbide-5-mononitrate at least three times daily have proven nitrate tolerance in patients with coronary artery disease and/or congestive heart failure. Complete loss of anti-ischemic effects after repetitive, continuous patch attachments has also been found. As we first showed in 1983, intermittent therapy with once-daily ingestion of high-dose sustained-release isosorbide dinitrate was successful in preventing the development of tolerance. Similarly, tolerance to isosorbide-5-mononitrate also does not develop when it is ingested once daily. It is now generally accepted that a daily low-nitrate interval is required to prevent tolerance development. Although the minimal patch-free interval required to prevent tolerance needs further investigation, a 12-h patch-free interval should prevent tolerance in most patients. The prolonged duration of action of once-daily high-dosage administration of sustained-release formulations, the improved patient compliance with a single daily administration, and the increased likelihood of maximal anti-ischemic effects are important reasons for recommending high single daily doses of isosorbide dinitrate or isosorbide-5-mononitrate.
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PMID:Nitrates: why and how should they be used today? Current status of the clinical usefulness of nitroglycerin, isosorbide dinitrate and isosorbide-5-mononitrate. 211 3

Over 30 per cent of coronary patients die of cardiac failure excluding the acute phase of myocardial infarction. With the exception of preexisting hypertension, there is no compensatory hypertrophy in ischemic heart disease. However, hypertrophy is a costly adaptation in terms of myocardial oxygen demand and, therefore, coronary flow. Fibrous zones are unresponsive to inotropic drugs and so the treatment of cardiac failure due to ischemic heart disease consists in limiting or preventing episodes of ischemia. Each mechanism of ischemia has an appropriate treatment: the preload is reduced by trinitrin and its derivatives and by molsidomine; the after-load by calcium antagonists and angiotensin converting enzyme inhibitors; tachycardia and hypercontractile states by betablockers. The risk of arrhythmia, aggravated by many inotropic therapies, constitutes the major danger to ischemic heart failure; amiodarone, betablockers and preventive nitrate therapy are the most effective and least dangerous antiarrhythmics. Revascularisation is effective for permanently ischemic segments or for ischemia on effort but does not improve large plaques of fibrosis which sometimes require surgical ablation or plastic procedures. But these measures are incomplete if all aspects of the disease are not taken in consideration: loss of excessive body weight, exercise rehabilitation by modern techniques, limitation of bed rest at the ultimate stage of the disease allowing patients with ischemic cardiac failure a better quality of life without aggravating the prognosis.
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PMID:[Treatment of cardiac insufficiency in ischemic heart disease]. 212 13

Nitro derivates are effective agents for the treatment of myocardial ischemia. The effectiveness of these compounds in anginal disease is due to their ability to induce dilatation of veins which results in decreased left and right ventricular and diastolic pressure. Furthermore nitro derivates also bring about coronary vasodilatation which is present also in conditions of stenosis of epicardial arteries. In these conditions either coronary flow increases or its redistribution is more favorable. As the vasodilatory effect of nitro derivates does not involve sound arterioles, no "theft" of blood occurs. The dilatation of veins induced by nitrates explains also their effectiveness in patients suffering from heart failure with high left ventricular pressure. Mononitrates seem more effective than dinitrates since variability problems due to hepatic metabolism disappear. Nitrate plasters do not appear favourable since they produce constant blood levels and therefore could favour the development of tolerance.
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PMID:[Current status of pharmacology and therapeutic use of nitro derivatives]. 215 28

A 64-year-old woman with a history of hypertension for ten years and of syncope 18 month previously visited our Division of Cardiology on 12 June, 1989. The S4 and mitral regurgitation were audible at the apex, and her electrocardiogram showed ST-depression in leads II, aVF, V5-6 and prominent U-wave (PU) in V1-3 when first seen. Then, she was thought to have a posterior myocardial ischemia. PU in V1-3 diminished whereas T-wave increased after nitrate and Ca++ blocker. Ergometer exercise ECG showed ST-depression in II, III, aVF, V4-6 and PU with decreased T-wave in V2-3 with no apparent symptoms. Simultaneously, Tl-201 myocardial imaging demonstrated a transient posterior defect. A silent posterior myocardial ischemia was, therefore, confirmed. Coronary arteriograms demonstrated subtotal obstruction of the proximal left circumflex artery, and the peripheral site was filled by collaterals from the right coronary artery. Angina-induced PU in the right precordial leads proved to be useful in detection of posterior myocardial ischemia, and this marker may also improve the possibility of detection of silent posterior ischemia.
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PMID:[A case of silent posterior myocardial ischemia/left circumflex artery obstruction detected by prominent U-wave in right precordial leads]. 228 23

Silent ischemia is a common finding in coronary artery disease and occurs more frequently than painful episodes in the total ischemic burden. Since painless ischemia places limits on the history, it can encourage physicians to spend more time studying and treating the electrocardiogram and less time with patients, potentially leading to a deterioration in doctor-patient relationship and care. Silent ischemia should be considered only in patients 35 years of age or older who: (a) have a strong family history of early coronary artery disease, or (b) have two major coronary risk factors. Verification is made by performing an electrocardiographic exercise stress test and followed by a thallium-201 electrocardiographic stress test when the electrocardiograms are equivocal. In females it is best to proceed directly to a thallium-201 electrocardiographic stress test because of the frequency of false positives on the exercise electrocardiograms. The results will help determine the indications for further studies and subsequently the need for drug or interventional management. Frequently a history in which symptoms of lower esophageal disorders, hiatal hernia, gastric disease and arthritic pains mimic angina or in fact coexist with ischemic heart disease makes the clinical diagnosis of angina more elusive and difficult. However, a careful unhurried history and an exercise stress test can often differentiate the etiology of the chest pains. A 24-hour ambulatory electrocardiographic recording aids in measuring the total ischemic burden. When the diagnosis and severity of the ischemic syndrome is established, a course of medical therapy tailored to the symptoms and with defined end points is initiated. Since silent ischemia and angina frequently coexist, suppression of the frequency and severity of the anginal episodes will also reduce the episodes of silent ischemia. Symptomatic improvement is thus a guide in the treatment of the total ischemic syndrome. Drug management will usually consist of two or more of the following drugs: a nitrate, beta blocker, calcium channel blocker, and aspirin. A 24-hour ambulatory electrocardiographic recording is helpful in assessing the efficacy of medical management of silent ischemia. Failures in drug management should proceed with coronary angiography, and when indicated, followed by percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery.
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PMID:Silent ischemia: a clinical update. 229 36

A 45-year-old man with unstable angina developed persistent ECG changes of myocardial ischemia during coronary angiography. Occlusion of the left anterior descending branch (LAD) was documented 20 minutes after these changes. Intracoronary nitrate, Ca antagonist, urokinase, removal by percutaneous transluminal coronary angioplasty (PTCA) of atherosclerotic obstructions, and emergency bypass surgery failed to restore myocardial perfusion. Only short periods of reflow were obtained by urokinase and PTCA. The repeated coronary injections demonstrated a progressive disappearance of the left anterior descending artery (LAD) starting from the distal portion and progressing retrogradely up to the origin of the vessel. The patient developed a transmural anterolateral myocardial infarction and 12 months later underwent cardiac transplantation for untractable failure. His heart was examined and the infarct confirmed. Analysis of this case suggests that coronary occlusion in acute myocardial infarction can be an event secondary to increased intramyocardial resistance rather than the cause of reduced coronary blood flow in subepicardial coronary arteries.
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PMID:Coronary occlusion: cause or consequence of acute myocardial infarction? 229 57

Fifteen patients with stable angina participated in a 12-week crossover study to evaluate the efficacy of nifedipine and nitroglycerin patches. There was an initial 2-week drug washout period followed by a 2-week control period when patients received no other antianginal treatment other than sublingual nitroglycerin for relief of angina episodes. At the end of the 2-week control period, exercise performance was assessed with treadmill exercise testing and measurement of oxygen consumption during the final third of the dosing interval. Myocardial perfusion was assessed using thallium scintigraphy with the injection of thallium at 85% of the maximum oxygen consumption. Patients were then randomized to nifedipine or nitroglycerin patches, and the dosage was titrated at weekly intervals according to symptomatic response. The final dose was received for at least 2 weeks. After 4 weeks, patients received the alternate medication. Maximal exercise testing and thallium scintigraphy were repeated after each drug period. Both nifedipine (mean dose, 70 mg/day) and nitroglycerin patches (mean dose, 16 cm/day) significantly reduced the frequency of angina and the consumption of sublingual nitroglycerin. Nifedipine decreased the reversible thallium defect score (49 +/- 29 vs. 28 +/- 26 U, p less than 0.01). Both drugs reduced electrocardiographic evidence of myocardial ischemia at submaximal exercise. Maximal oxygen consumption was not significantly increased by either drug when the test was done during the latter part of the dosing interval. The clinical implications of this study are that the dosage of nifedipine and nitrate patches, based on symptomatic criteria of angina frequency reduction, may not result in objective improvement in exercise performance.
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PMID:Comparison of nitroglycerin patches and nifedipine. 244 80

Nitrates are the most frequent agents used in the treatment of ischemic heart disease. In recent years nitrates have aroused a great interest; new pharmacological and clinical studies concern the mechanism by which nitroglycerin acts on the cell, forms of drugs prepared for intravenous, transdermal or oral (spray) routes of administration as well as sustained release preparations. The complexity of mechanisms of nitroglycerin action makes that nitrates are safe drugs and their action does not depend on the functional state of the myocardium. End-effects i.e. prevention of angina or relief of pain result from nitroglycerin action on the smooth muscles of the peripheral vessels and coronary arteries, on the coronary blood flow and left ventricle as well as on general hemodynamic indices. The role of specific sites of action of nitroglycerin changes depending on various factors and angina--inducing hemodynamic disorders. The phenomenon of nitrate tolerance investigated in recent years requires further studies but the results of the available trials are of considerable practical value.
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PMID:[Effect of nitroglycerin on the cardiovascular system]. 251 64


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