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)

Transmural myocardial infarction occurred in a 48-year-old woman with syndrome X -- atypical angina pectoris and angiographically normal coronary arteries. Before the infarction her electrocardiogram had been normal at rest but showed ischemia after exercise. Angiography 3 months after infarction revealed a normal coronary tree but hypokinesia of the posterior left ventricular wall.
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PMID:Syndrome X: case report. 84 23

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.
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PMID:Beta-blockers: primary and secondary prevention. 128 45

Transient ST-segment changes during continuous ECG monitoring occur not only in many clinical ischemic syndromes, but also in a proportion of the normal population. The pathophysiology of episodes of ST-segment change that represent transient periods of myocardial ischemia varies according to the underlying disease process, which may include stable coronary artery disease, unstable angina, variant angina, and syndrome X. Patients with stable coronary artery disease have episodes of ischemia as a result of an imbalance between increases in myocardial oxygen demands and changes in coronary blood flow due to physiologic changes in coronary vasomotor tone. Both these factors are subject to a circadian rhythm that results in a preponderance of ischemia in the morning hours. Vasospasm, often beyond the physiologic range, in localized segments of epicardial coronary arteries causes ischemia and ST-segment changes in variant angina, whereas luminal thrombosis with superimposed vasoconstriction is an important cause of continued ischemia in unstable angina.
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PMID:Current concepts of pathophysiology, circadian patterns, and vasoreactive factors associated with myocardial ischemia detected by ambulatory electrocardiography. 150 72

The effects of glutamate on anginal threshold, cardiac metabolism and hemodynamics were studied in 11 patients with stable angina pectoris, positive stress test results, and pacing-induced myocardial lactate release due to coronary artery disease (CAD) (n = 9) or syndrome X (n = 2). Data were obtained before, during and after 2 identical periods of coronary sinus pacing, the second being preceded by an intravenous injection of monosodium glutamate 1.2 (n = 7) or 2.5 (n = 4) mg/kg body weight. After glutamate administration, pacing time to onset of angina increased from mean +/- standard deviation 103 +/- 53 to 166 +/- 71 seconds (p less than 0.01) and ST-segment depression after pacing decreased from 2.3 +/- 1.0 to 1.6 +/- 1.1 mm (p less than 0.01). Arterial glutamate concentration increased 60% (p less than 0.01) after the low dose and 150% (p less than 0.01) after the high dose of glutamate. Regardless of dose, myocardial glutamate uptake increased by 25% (p less than 0.01). Pacing-induced cardiac release of lactate diminished 50% (p less than 0.05), whereas the releases of xanthine and hypoxanthine were unchanged by glutamate. Arterial free fatty acids decreased 20% (p less than 0.01). Circulating levels and cardiac exchanges of alanine, glucose and citrate were unchanged. Glutamate did not influence heart rate, arterial blood pressure, coronary blood flow, coronary vascular resistance or myocardial oxygen consumption. One patient complained of short-lasting burning sensations after receiving the high glutamate dose. In conclusion, augmented provision of glutamate enhances pacing tolerance in stable angina, presumably by a metabolic improvement of cardiac energy production during ischemia.
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PMID:Antiischemic and metabolic effects of glutamate during pacing in patients with stable angina pectoris secondary to either coronary artery disease or syndrome X. 185 69

Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects. At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p less than 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS). At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p less than 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during spacing and recovery, whereas normal subjects produced alanine throughout the study. Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p less than 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p less than 0.01). The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.
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PMID:Coronary hemodynamics and myocardial metabolism in patients with syndrome X: response to pacing stress. 203 78

Patients with syndrome X or microvascular angina present complains of effort angina associated with normal--appearing coronary arteries. Ischemia seems to be caused by myocardial perfusion abnormalities, related to microcirculatory disfunction, characterized by excessive vasoconstriction and/or inadequate vasodilation response. The intimal cause of this microcirculatory disfunction, located in the small pre-arteriolares arteries with 100-200 microns caliber, is still unknown. It seems that these patients present a generalized abnormality of the systemic smooth muscle, affecting territories other than the vascular. The diagnosis should be suspected whenever a patient presents effort angina, angiographically normal arteries and evidence of ischemia to exercise. As this syndrome is better understood some subsets of patients with different clinical characteristics and prognosis, are being identified. The calcium channel blockers seem to be the drug more effective in the control of ischemia and symptoms. The prognosis is, in general, better than in patients with coronary angiographic lesions.
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PMID:[X syndrome: review of concepts]. 207 60

To determine whether patients with syndrome X suffer from myocardial ischemia, coronary sinus oxygen saturation was continuously measured during pacing loading in 31 patients. Subjects were categorized by groups as syndrome X (11 patients), effort angina (14), and old myocardial infarction and valvular heart disease (6). Pacing loading induced evidence of ischemia in all syndrome X patients and in eight of the 11 patients with effort angina, while there was no such evidence in those with old myocardial infarction and valvular heart disease. Coronary sinus oxygen saturation in syndrome X decreased significantly from 44.2 +/- 5.8% to 33.5 +/- 4.4% (p less than 0.01), and it decreased from 47.0 +/- 4.9% to 31.2 +/- 4.0% (p less than 0.01) in effort angina with induced ischemic evidence, indicating that a significant reduction in coronary sinus oxygen saturation reflects the presence of myocardial ischemia. In the group with old myocardial infarction and valvular heart disease, coronary sinus oxygen saturation remained nearly unchanged during pacing. The pattern of depression of coronary sinus oxygen saturation during pacing was steeper in effort angina than in syndrome X. Therefore, we conclude that, although syndrome-X may not be a homogeneous group of patients, most of them may develop myocardial ischemia due to reduced vasodilator reserves of the small coronary artery.
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PMID:[Continuous monitoring of coronary sinus oxygen saturation during pacing loading in patients with syndrome X]. 209 60

Patients with angina-like chest pain without evidence of epicardial coronary artery disease or coronary arterial vasospasm are becoming increasingly recognized. These are often related to noncardiac causes including esophageal, musculoskeletal, and hyperventilatory or panic states. However, recently a subgroup of such patients are being recognized as having true myocardial ischemia and chest pain on the basis of diminished coronary microvascular vasodilatory reserve (microvascular ischemia or Syndrome X). The authors describe such a patient who was found to have replication of anginal pain associated with a reversible ischemic defect on thallium 201 imaging during atrial pacing, suggesting ischemia in this myocardial segment. Resolution of angina and ST segment electrocardiographic changes of ischemia occurred with cessation of pacing. We believe this is the first report of a patient with this form of myocardial ischemia diagnosed by this method and should be considered in patients with anginal chest pain after significant coronary artery disease and coronary vasospasm have been excluded.
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PMID:Syndrome of diminished vasodilator reserve of the coronary microcirculation (microvascular angina or syndrome X): diagnosis by combined atrial pacing and thallium 201 imaging--a case report. 211 63

The effects of oral verapamil, 320 mg daily, propranolol, 120 to 160 mg daily, and placebo were compared in 16 patients presenting with transient myocardial ischemia without evidence of coronary atherosclerosis or vasospasm on angiography (syndrome X). Testing was done according to a randomized double-blind crossover placebo-controlled trial consisting of 3 consecutive 7-day treatment periods with verapamil or propranolol or placebo. Patients underwent continuous 48-hour electrocardiographic monitoring before therapy (run-in phase) and during the last 2 days of each treatment period. A total of 391 episodes of diagnostic (greater than or equal to 0.15 mV) ST depression was recorded during the trial. Of these, 23 were symptomatic. None of the episodes occurred while the patients were asleep, 25% during exercise, 35% during minimal physical activity and 40% at rest. Rest included activities demanding mental arousal (conversation, reading or watching television). Heart rate at the onset of ST depression was higher (greater than or equal to 10 beats/min) than that observed in the 5 minutes preceding ischemia in 95% of the episodes. In the group as a whole, the average number of ischemic episodes per 24 hours was significantly reduced during propranolol therapy compared with placebo (0.7 +/- 0.6 vs 3.9 +/- 1.8; p less than 0.0005). No significant differences were seen during verapamil treatment (3.4 +/- 1.7 vs 3.9 +/- 1.8). It is concluded that transient myocardial ischemia in syndrome X is mostly precipitated by an increase in oxygen consumption, presumably due to a heightened sympathetic activity. Accordingly, beta blockers may represent the first line of treatment.
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PMID:Comparison of verapamil versus propranolol therapy in syndrome X. 264 45

Myocardial flow maldistribution and transmural steal phenomena, due to excessive arteriolar dilation elicited by elevated adenosine release during exercise, might be the mechanism of myocardial ischemia in patients with syndrome X. The effect of the adenosine receptor blocker aminophylline (AM) on effort ischemia in patients with syndrome X was tested: following double blind, randomized intravenous infusion of aminophylline (6 mg/kg over 15 minutes) or placebo, 8 patients with syndrome X underwent exercise stress test. After AM administration there was an increase in work tolerance (AM = 7.7 +/- 1.2 minutes of exercise vs placebo = 5.6 +/- 0.9, p less than 0.01) paralleled by an increase of the ischemic threshold, evaluated through the rate pressure product (mmHg x beats/min x 1/100) at 0.1 mV of ST-segment depression or at peak exercise (AM = 278 +/- 55 vs placebo = 230 +/- 24, p less than 0.05). AM prevented the occurrence of ischemic ECG signs in all 8 patients. Thus, at a dosage which effectively inhibits adenosine receptors, aminophylline infusion exerts beneficial effect on exercise induced ischemia in syndrome X, possibly through the prevention of transmural steal phenomena, elicited by inappropriate adenosine release during effort.
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PMID:[Increase in tolerance to physical effort in patients with X syndrome after acute administration of aminophylline]. 268 20


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