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)

Left ventricular hypertrophy (LVH), diagnosed by ECG and echocardiography, is commonly associated with coronary heart disease. Hypertensive patients with LVH and myocardial ischaemia may be at particular risk. The prevalence of ischaemia in hypertensive LVH was addressed in THAMES (Tenormin in Hypertension and Myocardial Ischaemia Epidemiological Survey), which comprised 205 men with hypertension. Echocardiography revealed LVH (defined as a left ventricular mass index > or = 130 g m-2) in 140 patients (68%). Of these patients with LVH, myocardial ischaemia was diagnosed on exercise ECG testing in 24%, and by thallium scintigraphy in 14%. Although not proven, a logical approach would be to improve the prognosis by reversing LVH and reducing ischaemia. A recent meta-analysis has indicated that angiotensin-converting enzyme (ACE) inhibitors are the most effective drugs in reversing LVH. But beta-blockers may still be a logical first choice of drug, because of their valuable anti-ischaemic properties.
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PMID:Ischaemia and left ventricular hypertrophy. 790 44

The effects of bopindolol (a new, nonselective beta-adrenoceptor antagonist) and its active metabolite, 18-502, on the regional myocardial pH during coronary occlusion were studied. Mongrel dogs were anesthetized with pentobarbital and the thorax was opened to expose the heart. The left anterior descending coronary artery (LAD) was incompletely (or partially) occluded so that the LAD flow could be reduced to about one third of the original flow. Regional myocardial pH of the LAD area was continuously measured by a tissue pH monitor. Drugs were injected intravenously 30 minutes after LAD partial occlusion. The myocardial pH in the LAD area decreased in response to LAD partial occlusion (from 7.3-7.4 to 6.72-6.92), and the low pH value was sustained for 60 minutes after LAD occlusion. Atenolol (1 mg/kg) decreased heart rate markedly and attenuated the regional myocardial acidosis induced by LAD partial occlusion. Bopindolol (1 mg/kg) decreased heart rate and 18-502 (0.5 mg/kg) decreased heart rate and blood pressure. Both drugs attenuated to a similar degree the decrease of regional myocardial pH induced by LAD occlusion. In the dog whose heart rate was maintained constant, however, bopindolol (1 mg/kg) did not attenuate the decrease of regional myocardial pH induced by LAD occlusion. These results suggest that both bopindolol and 18-502 attenuate the ischemia-induced regional acidosis of the myocardium as does atenolol, and, hence, have an anti-ischemic action. The beneficial action of bopindolol on ischemia-induced myocardial acidosis is possibly due to a decrease of heart rate, which corresponds to a saving of energy in the myocardial cells.
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PMID:Bopindolol and its metabolite 18-502 attenuate regional myocardial acidosis during partial occlusion of the coronary artery in dogs. 794 27

Antianginal drug treatment reduces symptoms and ischemia but may also influence the prognosis of patients with stable angina pectoris. The Atenolol Silent Ischemia Study (ASIST) compared atenolol and placebo treatment (about 140 patient-years on each) in patients with mainly silent ischemia and found less aggravation of angina and a tendency toward fewer cardiac complications with atenolol treatment. The Total Ischaemic Burden European Trial (TIBET) compared slow release nifedipine, atenolol, or the combination (about 450 patient-years on each) and found no significant differences with regard to cardiac complications, a nonsignificant trend toward better prognosis on combined treatment, and more side effects on nifedipine alone compared with the other treatments. The Angina Prognosis Study in Stockholm (APSIS) compared metoprolol and verapamil (about 1,400 patient-years on each) and found similar effects on cardiovascular endpoints, tolerability, and psychosocial variables with the 2 treatments. Hypothesis-generating subgroup analyses in APSIS suggest that treatment effects may differ in hypertensive and diabetic subgroups. Beneficial effects in primary and secondary prevention, together with data from ASIST, suggest that beta 1 blockade influences prognosis favorably. The safety of short-acting nifedipine in ischemic heart disease is questioned, but TIBET data suggest that slow release nifedipine may be safe. Verapamil has beneficial effects after myocardial infarction (Danish Verapamil Infarction Trial II) and shows similar efficacy as metoprolol in the APSIS study. The paucity of placebo data (antianginal treatment cannot be withheld during long periods of time in symptomatic patients) precludes firm conclusions regarding effects of drug treatment on prognosis. It is argued that patients with stable angina pectoris do well on medical treatment, and that beta 1 blockers, verapamil, and, possibly, slow-release nifedipine may influence their prognosis favorably.
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PMID:Prognosis of patients with stable angina pectoris on antianginal drug therapy. 867 97

Anginal symptoms alone are not a reliable guide to the extent of patients' ischaemic heart disease and silent episodes of ischaemia are associated with increased morbidity and mortality. It is becoming apparent that effective treatment of ischaemia will have to target the pattern of ischaemic events seen in patients' daily lives and treatment strategies are now being developed which aim to eliminate both silent and symptomatic episodes of ischaemia over the whole 24-h period. For example, the Circadian Anti-ischaemia Program in Europe (CAPE) trial has shown that significant improvements in objective and subjective measures of ischaemia occurred over 24 h when the once-daily third-generation dihydropyridine calcium antagonist amlodipine was added to background medical therapy. In addition, the Canadian Amlodipine/Atenolol in Silent Ischaemia Study (CASIS) has clearly shown the complementary effects of combination therapy with amlodipine and the long-acting beta-blocker atenolol. Ongoing and future outcome studies will determine the impact of such approaches on the prognosis for patients with ischaemic heart disease.
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PMID:Treatment effects on the total ischaemic burden and prognostic implications. 896 Apr 59

The present study was undertaken to clarify whether celiprolol and atenolol, beta1-selective beta blockers with and without intrinsic sympathomimetic activity (ISA), respectively, might improve ischemic damage in the isolated perfused hearts of spontaneously hypertensive rats (SHR), and whether long-term treatment with celiprolol may reduce left ventricular hypertrophy (LVH) in patients with essential hypertension. Atenolol (50 mg/kg/day) or celiprolol (300 mg/kg/day) for 7 weeks significantly reduced the blood pressure in SHR to the same degree, and both drugs decreased the heart rate, but the magnitude of the fall in heart rate was significantly higher with atenolol treatment than with celiprolol treatment. Both treatments significantly reduced the ratio of LV weight to body weight in SHR and significantly improved the coronary reserve in SHR to the same extent. Both treatments significantly improved the extent of recovery of the pressure-rate product and the extent of percent recovery of the coronary flow after reperfusion following 30 min of ischemia in SHR. Celiprolol treatment in patients with essential hypertension for 12 months significantly decreased interventricular septal thickness (IVST)+LV posterior wall thickness (PWT) and LV mass index (LVMI), but there was no significant correlation between IVST+PWT or LVMI and blood pressure before and after treatment. IVST+PWT and LVMI were significantly decreased after 3 months of treatment and these LVH indices were significantly smaller after 6 and 12 months of treatment than after 3 months of treatment. In conclusion, both celiprolol and atenolol treatment reduced LVH and improved the ischemic damage in SHR. In essential hypertensive patients with LVH, celiprolol treatment effectively reduced blood pressure and achieved LVH regression.
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PMID:Effect of celiprolol on cardiac hypertrophy in hypertension. 1101 1

We investigated 150 unselected patients with proven coronary artery disease. All patients were off all routine antianginal treatments and there were 598 ischemic episodes, of which 75% were silent. It was found that episodes of ischemia, both silent and painful, occurred predominantly during the daytime hours from 0730 to 1930 h. This pattern is similar to that described by others. There was a significant excess of episodes of ischemia in the morning hours (0730-1330 h), with a secondary peak occurring in the evening hours. We further investigated a subgroup of 41 patients who were monitored for 1,581 h while being treated with atenolol. These patients were investigated in a double-blind fashion, and during the off treatment phase the circadian pattern of ischemic episodes was similar to that described for the group as a whole. However, on treatment with atenolol, there was a significant reduction in the frequency and total duration of ischemic episodes throughout the day. Atenolol significantly altered the circadian distribution of ischemic episodes with elimination of the morning peak; there was some preservation of the evening peak although this was smaller than that described when the patients were off therapy. The circadian distribution of ischemic episodes and the observed changes with beta-blocking treatment resemble the reported circadian variation of acute myocardial infarction and sudden death. Although these studies do not in any way prove that myocardial ischemic episodes and their alteration by treatment are related to the development of acute myocardial infarction and death, the relationship between ischemic episodes and the end points of coronary disease require further investigation.
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PMID:Circadian variation of the total ischemic burden and influence by beta-blocking agents. 1152 11

Catecholamines bind to alpha- and beta-adrenoreceptors and are capable of preconditioning ischemic myocardium. Our purpose was to investigate the effect of acute either short or prolonged i.v. administration of beta-adrenoreceptor antagonists on ischemic preconditioning in vivo. Fifty-five anesthetized rabbits were divided into 10 groups (n=5-7 per group) and were subjected to 30-min regional ischemia of the heart after ligation of a prominent left coronary artery and 3-h reperfusion after releasing the snare. Ischemic preconditioning was obtained by three cycles of 5-min ischemia separated by 10-min reperfusion. beta-Adrenoreceptor blockade was obtained by the long acting beta-adrenoreceptor antagonist atenolol or by the short acting esmolol, which were given as a short 5-min infusion or as a prolonged 45-min infusion, starting respectively 20 min before and ending 15 min before the beginning of sustained ischemia, or starting 45 min before and ending immediately before the beginning of sustained ischemia. Atenolol was given at a rate of 0.2 mg min(-1) during 5 min or at a rate of 0.088 mg min(-1) as a 45-min infusion. Esmolol was given as an initial dose of 500 microg kg(-1) within 1 min, followed by a 4-min infusion at a rate of 50 microg kg(-1) min(-1) or as an initial dose of 3.4 mg within 1 min, followed by a 44-min infusion at a rate of 0.15 mg min(-1). Blood pressure and heart rate were continuously monitored. The infarcted and risk areas were delineated with the aid of tetrazolium chloride staining and fluorescent Zn-Cd particles. Infarct size was expressed in percent of the area at risk. All the animals without preconditioning developed an infarct size ranging between 36.3+/-2.4% and 49.6+/-7.6% (P=NS) and all the preconditioning groups developed an infarct size ranging between 14.9+/-1.2% and 21.0+/-2.2% (P=NS). All the preconditioning groups, independently of the use of beta-adrenoreceptor antagonists, had a smaller infarct size than the control group, which developed an infarct size of 47.3+/-2.5% (P<0.01). Intravenous atenolol and esmolol, independent of timing and mode of administration, does not seem to interfere with protection afforded by ischemic preconditioning in vivo.
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PMID:Intravenous atenolol and esmolol maintain the protective effect of ischemic preconditioning in vivo. 1536 63


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