Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Molsidomine is a derivative of the sydnonimines and is a long-acting vasodilator that may be effective in the treatment of chronic stable angina pectoris. To evaluate the therapeutic efficacy and drug tolerance, eight men with stable angina pectoris performed a symptom-limited maximal exercise test on a computer-assisted treadmill. After ingesting either placebo or molsidomine administered in single blind fashion 90 min before the exercise test on the first day of treatment, molsidomine decreased the average systolic blood pressure response from 154 +/- 3 (SEM) to 135 +/- 4 mmHg (p less than 0.01). However it did not significantly change the average heart rate response (117 +/- 7 to 124 +/- 8 beats/min) and the rate-pressure product (18.1 +/- 1.2 X 10(3) to 16.8 +/- 1.1 X 10(3]. The average time up to the onset of ischemia at which significant ST-segment deviation (0.1 mV) first appeared was increased from 9.0 +/- 1.7 to 12.8 +/- 1.2 min (p less than 0.001) after molsidomine. At peak exercise after molsidomine, the mean value of ST-segment deviation in V5 or aVF was decreased (p less than 0.001). This result was obtained even though the average exercise duration was increased from 11.4 +/- 1.7 to 13.6 +/- 1.2 min (p less than 0.001). The treadmill score according to Hollenberg was also improved from -47 +/- 24 to 1 +/- 14 after molsidomine administration. After six weeks of continued therapy with molsidomine the favorable effect on exercise tolerance was significantly decreased in terms of exercise duration, the time up to the onset of ischemia, and the treadmill score.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of molsidomine on exercise tolerance in patients with exertional angina pectoris. 668 83

Preliminary results from multicenter double-blind placebo-controlled studies involving crossover and parallel designs were analyzed in 32 and 34 patients with stable angina pectoris entered respectively into the two protocols. The frequency of anginal attacks and the intake of nitroglycerin were decreased about 50 percent in patients receiving nifedipine, and the difference from those on placebo was statistically significant. Similarly, exercise tolerance was significantly increased with nifedipine, as evidenced by several variables, and the degree of ischemia was believed decreased, as reflected by lesser ST segment depression at peak exercise. The heart rate-blood pressure product, an approximation of myocardial oxygen consumption, was slightly but significantly decreased at equivalent workloads, but was not significantly different from placebo at the onset of angina or at maximal exercise. Adverse reactions to nifedipine, although frequent, were generally benign and usually responded to dose adjustment or improved spontaneously. These results suggest that the calcium antagonist nifedipine is effective and safe in the treatment of chronic stable angina.
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PMID:Interim report of multicenter double-blind, placebo-controlled studies of nifedipine in chronic stable angina. 679 16

The antianginal effects of two active drugs, nifedipine and propranolol, alone in combination, were compared with those of placebo in a double-blind clinical trial that included 16 patients with chronic stable angina triggered by exertion. A low dose and a high dose of the active drugs were used (nifedipine, 30 and 60 mg/day; propranolol, 240 and 280 mg/day). Precordial exercise mapping and continuous electrocardiographic recordings were used to assess objective response to therapy, and the patients were asked to keep a diary of episodes of chest pain and consumption of nitroglycerin tablets for subjective appraisal. Both frequency of chest pain and nitroglycerin consumption were significantly reduced by each of the active drugs when compared with placebo, and the combination of nifedipine and propranolol added significantly to the effectiveness. Reductions in area of ischemia and number of episodes of ST segment depression on 48-hour ambulatory electrocardiographic monitoring corroborated the efficacy of each active treatment with respect to placebo. Nearly 60 percent of all episodes of ST segment depression were painless and responded to the active treatment in the same manner as did the episodes associated with chest pain. Side effects were mild and all treatments were well tolerated. The objective methods used allowed for clear-cut differentiation of treatment effects with the various regimens. Although the two drugs alone were significantly more effective than placebo, their combination provided an even greater improvement (p less than 0.005), and therefore it appears to be a safe and effective form of treatment for chronic stable angina.
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PMID:Nifedipine and propranolol: a beneficial drug interaction. 702 25

A double-blind, placebo-controlled, crossover study was carried out to evaluate the short-term effects of captopril on exercise tolerance in 18 normotensive patients with chronic stable angina pectoris and normal left ventricular function. Captopril 25 mg (or placebo) was given twice, i.e. in the evening (10 p.m.) and the following morning (8 a.m.), prior to a maximal symptom-limited bicycle exercise test (11 a.m.). Captopril reduced the systolic and diastolic blood pressures at rest (p < 0.01) without causing any reflex tachycardia. The time to onset of S-T depression was prolonged (p < 0.05), and the maximal S-T depression was reduced (p < 0.02). No differences were found between captopril and placebo in total exercise duration or time to onset of angina. The effects of captopril on exercise-induced ischemia were demonstrated most clearly in patients who responded with a greater than 10 mm Hg fall in the resting systolic blood pressure. In conclusion, this study suggests that captopril has anti-ischemic properties, which may be of importance in the treatment of patients with chronic stable angina and normal left ventricular function. These beneficial effects probably relate to a reduction in afterload and myocardial wall stress and therefore a reduction in myocardial oxygen demand.
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PMID:Short-term effects of captopril on exercise tolerance in patients with chronic stable angina pectoris and normal left ventricular function. 758 53

Ischemia refers to inadequate supply of oxygen and metabolic substrate to an organ. The term myocardial ischemia covers a heterogeneous group of clinical syndromes, globally called ischemic heart disease, which includes chronic stable angina at one end of the spectrum and acute myocardial infarction at the other end. Between these two extremes, there is a broad myriad of intermediate syndromes, all having in common a mismatch between oxygen demand and supply. Ischemic heart disease is the leading cause of all morbidity and mortality in the United States. It is reasonable to assume that proper intervention and follow-up care based on knowledge of pathophysiology is imperative to the professional nursing care of patients with this disease. In this article, the author presents a brief survey of the current state of the discussion from a pathophysiologic viewpoint that highlights the dynamic nature of the disease and its related clinical implications.
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PMID:Pathophysiology of ischemic heart disease: an overview. 762 81

Cholesterol lowering has been shown to decrease the dimensions of atherosclerotic plaques in some patients with coronary artery disease. Because of this observation, there is growing discussion about whether or not cholesterol lowering might be used in place of revascularization. The available data suggest that cholesterol lowering in place of revascularization may be appropriate for patients with chronic stable angina, for patients who are asymptomatic but have provocable ischemia after myocardial infarction, and for patients at moderate risk for cardiac events as judged by exercise test or clinical variables. The available data do not justify changing current practices; further study is necessary.
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PMID:Is cholesterol lowering an alternative to revascularization in some patients with coronary artery disease? 769 54

A significant proportion of myocardial ischemia is 'silent' in nature. Furthermore, this asymptomatic ischemia portends an adverse prognosis for patients with known coronary artery disease. Silent myocardial ischemia can be objectively assessed and quantified by a number of noninvasive means; however, ambulatory electrocardiographic monitoring has emerged as a preferred method for both detection and analysis in hospital and during daily life conditions. Silent myocardial ischemia exhibits a circadian pattern. It represents an imbalance between myocardial oxygen supply and myocardial oxygen demand, and can be triggered by both physical and mental stress. The important role of endothelial dysfunction and autonomic nervous system influences has been recently elucidated. Up to 75% of ischemic episodes in patients are silent. Patients with asymptomatic coronary artery disease, chronic stable angina and unstable angina, and those postmyocardial infarction or postrevascularization who exhibit ST segment shift all show adverse short and long term prognosis compared with controls. Treatment modalities have included nitrates, beta-blockers, calcium antagonists, phosphodiesterase inhibitors, anxiolytics, anti-platelet agents and revascularization procedures. While the majority of these studies have demonstrated significant reduction in the frequency of silent myocardial ischemia, limited data on influencing prognosis are available; thus recommendations regarding treatment of these patients await the results of ongoing clinical trials.
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PMID:Current status of silent myocardial ischemia. 772 40

The Circadian Anti-Ischemic Program in Europe (CAPE) trial was a large, multinational trial, taking place in ten countries and involving over 100 investigators. It was a double-blind, parallel, randomized, placebo-controlled trial comparing once-daily amlodipine with placebo in chronic stable angina pectoris. It consisted of two phases, the first being a 2-week, single-blind, placebo run-in phase during which stable doses of anti-anginal drugs were maintained (65% of patients were receiving beta-blockers), and the second an 8-week active treatment phase in which patients received either amlodipine or placebo, 5 mg once daily, for the first 4 weeks, increasing to 10 mg once daily for the second 4 weeks. Patients were randomized in a ratio of 2 patients receiving amlodipine to each patient receiving placebo. Out of an initial 1,160 patients screened, 315 entered the study, with 250 having complete efficacy-evaluable data. Patients were included if they experienced > or = 4 ambulatory ECG ischemic episodes (> or = 1 mm ST-segment depression for > or = 1 min) and/or > or = 20 min total ischemia time over 48 h. Data were obtained on the total frequency of ST-segment depression events, the ischemia area (ST-segment depression integral), the ischemic time and peak ST-segment depression. Patient diary information on angina attack rate and nitroglycerin tablet consumption was also collected. Patients in both groups were compared for age, blood pressure, heart rate, duration of angina and baseline ischemia at entry. Amlodipine and placebo had similar safety profiles, with 17.3% of amlodipine patients recording adverse events, compared with 13.3% of placebo patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amlodipine and the total ischemic burden: circadian anti-ischemia program in Europe (CAPE) trial-methodology, safety and toleration. The Steering Committee members and all of the investigators. 773 84

Acadesine, the first of a class of adenosine-regulating agents, has been shown to possess antiischemic properties in animal models. The aim of the study was to assess the effect of acadesine on exercise-induced myocardial ischemia in patients with chronic stable angina pectoris. Twelve patients with stable angina entered a five-way, randomized double-blind study comparing the effects of four doses of acadesine with placebo on time to 1 mm ST-segment depression and other parameters of exercise tolerance. At each study period patients underwent baseline exercise testing, followed by drug or placebo infusion after a 60 minute rest period. The exercise test was repeated after 30 minutes infusion, which continued throughout recovery. Time to angina, time to 1 mm ST depression, and total exercise time during the placebo infusion were 301.1 +/- 45.3, 314.8 +/- 50.9, and 399.4 +/- 47.6 seconds. The placebo-adjusted percentage change in time to 1-mm ST segment with acadesine 6, 12, 24, and 48 mg/kg was -0.1 +/- 6.2%, 11.1 +/- 13.8%, 12.9 +/- 8.6%, and -3.2 +/- 6.8%, respectively (p = NS vs. baseline). Time to angina, total exercise time, and recovery time of the ST segment were not consistently altered by acadesine. The lack of effect across all acadesine doses is consistent with animal data from ischemia-reperfusion injury studies, where a clear dose dependency was present with a loss of effect at higher doses. Alternatively, the extent of ischemia induced by treadmill exercise may have been insufficient for the antiischemic activity of acadesine to be evident.
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PMID:Effect of acadesine, a new metabolic agent, on exercise-induced myocardial ischemia in chronic stable angina. 791 31

This multicenter, open-label, single crossover study examined 195 patients taking an immediate-release diltiazem tablet as chronic stable angina therapy to determine if apparently logical methods of converting them to an extended-release, once-daily formulation were effective. Patients were converted from the immediate-release (Phase I) to an extended-release (Phase II) formulation of diltiazem on a mg-for-mg basis or, when a similar dose was not available, to the next higher 120 mg dose. Weekly angina occurrences and nitroglycerin use, exercise testing at the end of each phase, and ambulatory electrocardiographic monitoring (AEM) during the week prior to the exercise study were evaluated. There was a statistically significant decrease in angina frequency and nitroglycerin consumption during Phase II. In the exercise studies, there was an insignificant increase in time to 1 mm ST-segment depression and total exercise time associated with a statistically significantly lower end-exercise blood pressure and heart rate in Phase II. In those patients who had ischemia during either phase on AEM, total ischemic duration and ischemic episodes were insignificantly lower in Phase II. All observations were similar in the subgroup of patients who were converted mg-for-mg. Adverse reactions were equal. Thus, in converting patients from an immediate- to an extended-release diltiazem formulation for the treatment of symptomatic coronary artery disease, it is reasonable to convert directly to the same or, if not available, the next higher available dose of the extended-release preparation.
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PMID:Conversion from immediate-release to extended-release diltiazem in angina pectoris. 800 12


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