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)

Several studies have shown evidence of the key role of the endothelium in modulating the tone of epicardial coronary vessels, in the different manifestations of coronary artery disease. Recently, the role of endothelium-dependent vasodilation has been focused, because clinical observations have suggested that myocardial ischemia might be caused or aggravated by inappropriate vasoconstriction of resistance vessels. An abnormal endothelium-dependent vasodilation, either of epicardial and of coronary microvasculature, has been documented in patients with syndrome X and in patients with history of hypertension and left ventricular hypertrophy. Vasoconstriction of the small coronary vessels is probably the mechanism underlying the impaired increase of coronary blood flow during atrial pacing and the wide variations of the ischemic threshold in some patients with chronic stable angina. In patients with variant angina, the endothelial function seems abnormal only in the conductance vessels. It is likely that the endothelial dysfunction of the small coronary arteries be present in many clinical situations in which a discrepancy between a mild atherosclerosis of epicardial coronary artery and signs of ischemia exists, as it has been observed early after successful angioplasty and after coronary artery reperfusion during acute myocardial infarction.
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PMID:[Endothelial dysfunction in ischemic syndromes]. 802 14

The use of nitrates in chronic stable angina is reviewed, with special emphasis on everyday clinical practice. The expectable benefits are referred, namely symptoms improvement and objective reduction os ischemia in the stress test and Holter monitoring. The use of nitrates in acute angina and in prophylaxis of chronic ischemia as well as their adverse effects are also discussed. Nitrates efficacy is compared against beta-blockers and calcium antagonists. In conclusion, nitrates have a moderate efficacy and should be used in association with other anti-ischemic drugs, in eccentrical therapeutical schemes with a free interval between doses.
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PMID:[Nitrates in the treatment of chronic stable angina]. 809 45

The effects of atenolol (100 mg/day) and nifedipine (60 mg/day) on angina symptoms and exercise tolerance were compared in an open, randomized study. Twelve-week treatment period was compared with two weeks of placebo treatment in 51 patients with chronic stable angina pectoris. Mean frequency of angina attacks decreased significantly from 8.3 to 1.6 attacks per week after atenolol treatment (p < or = 0.05). Both drugs increased exercise tolerance to development of signs of ischemia on electrocardiogram (p < or = 0.05) and increased maximal exercise tolerance as well (p < or = 0.05). Mean ST segment depressions at peak exercise were significantly decreased after treatment with atenolol and nifedipine (p < or = 0.05). Both drugs also increased total exercise capacity in comparison with placebo period, stated as 100%:192% after atenolol and to 191% after nifedipine. No significant changes of heart rate and blood pressure were noted during treatment period. Twelve patients did not finished study, two of them suffered myocardial infarction with death in one of them (atenolol group, other one nifedipine group). Thus, atenolol in one daily dose is as effective as nifedipine in chronic stable angina patients when administered as single therapy.
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PMID:[Comparison of the effects and safety of atenolol and nifedipine in the treatment of angina pectoris]. 835 62

There are conflicting results concerning the anti-ischemic effect of nifedipine in patients with chronic stable angina. Therefore, the purpose of this study was to assess whether the anti-ischemic effect of nifedipine may be related to coronary collateral circulation. Forty-one patients with stable angina and coronary artery disease were randomized to a parallel double-blind study with nifedipine and metoprolol, and compared for effects on transient ischemic episodes during ambulatory electrocardiographic monitoring and exercise-induced ischemia. The effects were correlated to the presence of collateral circulation. In 17 patients, angiographically poor or no collateral flow was observed (group 1), and 24 had good collateral flow (group 2). Nifedipine was administered to 20 patients (8 in group 1, and 12 in group 2). In group 1, nifedipine reduced the frequency of total and asymptomatic ischemic episodes (p < 0.05), whereas significant increases in both total (p < 0.05) and silent (p < 0.01) ischemia were observed in group 2. Exercise variables were slightly improved (p = NS) during nifedipine therapy in group 1, and slightly worsened (p = NS) in group 2. Reflex tachycardia was not observed at either the onset of transient ischemia out of the hospital or exercise-induced ischemia. This was in contrast with the effect in 21 patients treated with metoprolol (9 in group 1, and 12 in group 2) where significant reductions were observed in the frequency of both total (p < 0.01) and silent (p < 0.01) ischemia in both groups. Furthermore, a beneficial effect was observed on all exercise variables.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transient myocardial ischemia during nifedipine therapy in stable angina pectoris, and its relation to coronary collateral flow and comparison with metoprolol. 842 80

The prognosis during 1 year of follow-up in 715 patients admitted to one single hospital due to suspected acute myocardial infarction (AMI) with a history of unstable angina pectoris immediately preceding hospitalization is described. AMI developed in 192 patients (27%) during the first three days and in 255 patients (38%) during the first year. The mortality during hospitalization was 7% (50 patients) and during 1 year 19% (130 patients). Of the nonsurvivors, 54% died of AMI, 28% of congestive heart failure, and 20% of cardiogenic shock. Based on simple clinical parameters on admission to the emergency room, risk indicators for death during the following year could be identified as follows, in the order of significance: high age (p < 0.001), ST-segment depression on admission (p < 0.001), and a history of diabetes mellitus (p < 0.05). At admission to the emergency room, risk indicators for development of AMI during the following year were as follows: initial degree of suspicion of AMI (p < 0.001), electrocardiographic signs of acute ischemia on admission (p < 0.001), ST-segment elevation on admission (p < 0.01), age (p < 0.05), and lack of a previous history of chronic stable angina pectoris (p < 0.05). We conclude that, among patients admitted to hospital due to suspected AMI with a history of unstable angina pectoris immediately preceding hospitalization, 38% developed a confirmed infarction and 19% died during the following year.
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PMID:One-year prognosis in patients hospitalized with a history of unstable angina pectoris. 850 73

We recently showed that Isradipine, a calcium antagonist from the dihydropyridine group, reduces ischemia and improves ventricular function at rest and during exercise, 2 hours after a single oral dose, in patients with chronic stable angina. In the present study, we evaluated the effects of long acting slow release oral (SRO) Isradipine (5 mg) compared to a placebo in 30 coronary patients with stable chronic angina, randomized in a double blind-fashion. The following parameters were obtained at rest and during submaximal exercise: left and right ventricular (LV, RV) ejection fractions (EF; %) and peak filling rate (PFR; EDV/s), assessed by gated radionuclide angiography, clinical symptoms, electrocardiograms (ECG, ST segment depression; mm), systolic and diastolic blood pressure (SBP and DBP; mm Hg). Patients were then given two oral doses of either Isradipine or placebo (one a day). The same parameters were reassessed, at rest and during n equivalent exercise, 48 hours later (24 hours after the last administration of the drug). The results after Isradipine (n = 14) showed, at rest, a significant increase in LVEF and Pfr (51 +/- 9 to 54 +/- 8 and 1.97 +/- 0.44 to 2.36 +/- 0.71, respectively) and a decrease in DBP (93 +/- 11 to 87 +/- 13); and during exercise, a significant increase in LVEF (51 +/- 11 tot 55 +/- 13) and a decrease in ST segment depression (2.3 +/- 1.9 tot 1.9 +/- 1.6). No significant change was observed after placebo in the other 16 patients. We conclude that even 24 hours after an oral administration, Isradipine SRO maintains its beneficial effects both, at rest on LV systolic and diastolic function and pressure, and during exercise on ECG signs of ischemia with improvement in LV ejection fraction.
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PMID:Cardiac function improvement 24 hours after isradipine SRO in patients with chronic stable angina: a double-blind randomized study. 874 12

The purpose of this study was to determine the response of plasma levels of endothelin-1 (ET-1) to dynamic exercise in patients with coronary artery disease and chronic stable angina pectoris and positive exercise tolerance test, before and after treatment with the calcium antagonist nisoldipine (20 mg/day buccally for 7 days). Plasma ET-1 levels and hemodynamic parameters (blood pressure and heart rate) were determined at rest, at peak exercise and recovery. All patients had a positive electrically and clinically stress test and all of the eight patients did not developed ECG signs of myocardial ischemia after nisoldipine administration. Before nisoldipine treatment the plasma ET-1 levels did not increase significantly during exercise. After nisoldipine treatment the plasma ET-1 levels were significantly lower at rest and during exercise compared with those revealed before calcium antagonist treatment. In conclusion our results suggest that in patients with chronic stable angina pectoris the treatment with calcium antagonist nisoldipine reduced ischemia and plasma ET-1 levels.
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PMID:Plasma endothelin-1 concentrations in patients with coronary artery disease during stress test before and after nisoldipine administration. 874 13

This was a double-blind, within-patient, crossover study to evaluate the effects of a new formulation of metoprolol on blood pressure (BP) and myocardial ischemia. Twenty outpatients with mild to moderate essential arterial hypertension, chronic stable angina pectoris and positive exercise test, after a 2-week baseline placebo period, were randomized to receive long-acting metoprolol (OROS) 14/190 mg o.d., nifedipine SR 20 mg b.i.d. or their combination in a sequence of a 3 x 3 Latin square design. Two patients withdrew from the study (1 for adverse event during metoprolol and 1 for rise of BP during nifedipine). Nifedipine, metoprolol and their combination significantly reduced the weekly number of angina attacks and nitroglycerin consumption with respect to baseline. The total number of ischemic events (at 24-hour ECG monitoring) significantly decreased after each treatment with respect to baseline. Twenty-four hours mean systolic and diastolic BP were reduced by both nifedipine alone and metoprolol alone; the combination of the two drugs led to a further decrease in both systolic and diastolic BP. The duration of silent ischemic episodes was significantly reduced by nifedipine and combination but not by metoprolol. On the other hand 24 hours symptomatic attacks/patient were significantly reduced by beta-blocker and combination, but not by nifedipine. Metoprolol alone and administered with nifedipine caused a decrease, with respect to placebo baseline, in 24-hour mean heart rate (HR) and reduced the increase of HR and systolic BP at the onset of ST depression during symptomatic ischemic episodes. The effort time and time to ST = -1 mm at treadmill were significantly increased by treatment with nifedipine alone, with metoprolol alone and with their combination, but the combination was more effective than the individual therapies. ST depression at peak exercise was significantly reduced by each treatment. The slopes of correlations between the ST-segment variation and systolic BP, HR and rate-pressure product during exercise, significantly decreased after all treatments with respect to placebo baseline, more with the combination therapy than with nifedipine alone and metoprolol alone. In conclusion, based on our results the favourable interaction of metoprolol OROS and nifedipine given concomitantly, is likely to be due to a better control, respect to each individual therapy, of the pathogenetic mechanism of myocardia ischemia: BP and HR increases during exercise and during symptomatic ischemic episodes are controlled by the beta-blocker and coronary vasoconstriction during silent ischemia is prevented by the calcium-antagonist.
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PMID:Treatment of hypertension associated with stable angina pectoris: favourable interaction between new metoprolol formulation (OROS) and nifedipine. 883 Nov 81

The purpose of this study was to elucidate the effect of repeated brief coronary occlusions on reactive hyperemia during percutaneous transluminal coronary angioplasty (PTCA) in patients with or without ischemic tolerance. Seventeen patients undergoing PTCA for chronic stable angina were studied. Patients with well developed collateral vessels were excluded. After successful predilatation, coronary flow velocity was recorded with the use of a Doppler flow guide wire, and reactive hyperemia was assessed immediately after each of two 2-min coronary occlusions followed by 2 mins of reperfusion. The intracoronary electrocardiogram (icECG) was recorded via the flow guide wire placed in the center of the ischemic zone. Patients were divided into two groups: those who showed a reduction of ST elevation in the icECG recorded at the time of the second coronary occlusion (group I), and those who showed no difference in ST elevation between the two occlusions (group II). There were no significant differences in blood pressure, heart rate, or baseline coronary flow velocity between the two groups before the first occlusion, but the ST elevation at the time of the first coronary occlusion was greater in group I than in group II (8.9 +/- 6.2 versus 1.1 +/- 2.0 mm, P < 0.01). Reactive hyperemia was significantly greater after the second coronary occlusion than after the first in group I (22.1 +/- 15.8 versus 30.4 +/- 21.0 cm/s, P < 0.05), but it did not change in group II (25.6 +/- 13.0 versus 23.5 +/- 11.2 cm/s NS). Reactive hyperemia was enhanced in patients with ischemic tolerance who showed a reduction in St elevation in the icECG. These results suggest that observed reactive hyperemia does not necessarily reflect the severity of ischemia.
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PMID:Enhancement of coronary reactive hyperemia in patients with ischemic myocardial tolerance during angioplasty. 912 44

Myocardial ischemia occurs frequently during daily life and has a circadian pattern similar to that reported for myocardial infarction and sudden death. Because of the increased risk of myocardial ischemia in the morning hours, it has been suggested that the administration of anti-ischemic medication before bedtime may be more effective than the traditional morning dosing. This randomized, double-blind, placebo-controlled, crossover study evaluated the effects of 480-mg/day diltiazem (given either in the A.M. or the P.M.) on myocardial ischemia using ambulatory electrocardiographic monitoring in 68 patients with chronic stable angina and > or = 2 minutes of ischemia per 48 hours. During treatment with diltiazem, the duration and number of myocardial ischemic episodes were reduced by 45% (94 to 52 minutes, p <0.004) and by 40% (4.5 to 2.7 episodes, p <0.003), respectively. The duration and number of myocardial ischemic episodes during daytime (6 A.M. to 6 P.M.) hours were also reduced by 52% (74 to 36 minutes, p <0.002) and by 48% (3.1 to 1.6 episodes, p <0.001), respectively. There was no significant difference between A.M. and P.M. dosing. Morning ischemia (6 A.M. to noon), considered separately from daytime ischemia, was also significantly reduced by both A.M. and P.M. dosing regimens, with no difference between the regimens. The results of this study showed that both A.M. and P.M. dosing of long-acting diltiazem were equally effective in suppressing episodes of ambulatory myocardial ischemia at all times.
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PMID:Effect of morning versus evening dosing of diltiazem on myocardial ischemia detected by ambulatory electrocardiographic monitoring in chronic stable angina pectoris. Dilacor XR Ambulatory Ischemia Study Group. 928 52


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