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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of KoQ4 on the energetics, contractility, and electrogram of the ischemized myocardium was studied in acute experiments on dogs with induced myocardial ischemia. Intracornoary administration of KoQ4, 1.3 mg/kg, directly into the focus of ischemia for 15 min promoted a decrease in the lactate level in blood draining from the ischemic zone as compared to the control data in the absence of a difference in the dynamics of the pyruvic acid content. In distinction to the control experimental series, there was no decrease in the concentration of glucose in samples of venous blood draining from the focus of ischemia. Under the effect of KoQ4 the amplitude of left ventricular pressure and the maximum rate of its growth (dp/dt) increased moderately and the ST segment and ST/R coefficient of the epicardial electrogram from the border zone of ischemia decreased. It was shown in the rat experiments that preliminary intravenous administration of KoQ4 (14 mg/kg) increased myocardial resistance to oxygen deficiency under conditions of diacetylcholine-induced apnoe.
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PMID:[Effect of hexahydroubiquinone-4 (KoQ4) on the bioenergetics and functional activity of the myocardium in ischemia]. 59 31

It has been shown that localized myocardial ischemia is accompanied by microvascular changes which produce capillary obstruction when blood flow is restored. This so-called no-reflow phenomenon has been noted in the brain, kidney, dermis and, more recently, in the myocardium. Ultrastructural studies have pointed out the role of myocardial and endothelial cells swelling. It seems likely that such damage of the vascular bed may constitute the first irreversible change during ischemia and result in failure to obtain successful reperfusion of involved myocardium. It can be suggested on the basis of recent clinical and experimental observations, that this phenomenon may play a role in subendocardial necrosis associated with cardiac surgery, and in myocytolytic necrosis. In both of these conditions, the most salient features are the microcirculatory defect and the reperfusion injury following transient ischemia. Further investigations are needed to determine the basic alterations induced by no-reflow phenomenon and the value of various prophylactic and therapeutic measures.
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PMID:No-reflow phenomenon and acute myocardial ischemia. The need for further investigation. 60 1

In 21 patients with ischaemic heart disease, the values of the anginal threshold were investigated during cardiac pacing and an exercise test. It was found that in the pacing test, ischemia could be expected to appear at a heart rate by 30% faster than that in ischaemia induced by exercise. If ischaemia was successfully induced in both tests, the threshold values of the time-tension indexes were equal, whereas the value of the pressure-time per minute index was 20% higher in exercise-induced ischaemia. In patients with hypokinetic circulation, during pacing the pressure-time per minute index first increased and then paradoxically decreased; this reaction can help find out patients with haemodynamic signs of heart failure.
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PMID:A comparison between cardiac pacing and exercise tests in patients with angina pectoris. 61 Sep 93

To define the time course of redistribution of thallium-201 (201Tl), ischemia was induced in seven pigs by temporary occlusion of the circumflex coronary artery. After 1 1/2 min of occlusion 201Tl and labeled microspheres were injected into the left atrium. Flow was re-established 4 min after occlusion. Prior to reflow, the relative activities of 201Tl and microspheres in the ischemic area were similar, but as early as 5 min after reflow the relative 201Tl activity was considerably higher than the relative microsphere activity and from 15 to 105 min after reflow, relative 201Tl activity (averabe 69% of that in normal myocardium) continued to be higher than relative microsphere activity (average 6% of normal). Myocardial arteriovenous differences for 201Tl were followed sequentially after 201Tl injection in normal dogs and in dogs with temporary coronary occlusions. The results suggested both loss of 201Tl from normal myocardium beginning 10 min after 201Tl injection and increased extraction of 201Tl from the blood pool immediately after release of a transient occlusion. Redistribution of 201Tl therefore begins very soon after relief of myocardial ischemia and even a short delay in initiating myocardial imaging may decrease the sensitivity of the technique for detecting transient ischemia.
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PMID:Early redistribution of thallium-201 after temporary ischemia. 61 22

First heart sound (S1) energy spectra in isovolumic systole, hemodynamics, and angiographic left ventricular wall motion (LVWM) at rest and with atrial pacing were compared in 27 patients who underwent diagnostic cardiac catheterization and angiography because of chest pain. Eighteen patients were found to have coronary artery disease (CAD) and nine patients, normal coronary arteries. Eleven of the 18 CAD patients (61%) had a mean reduction in the spectral energy of S1 of 6.5 +/- 1.4 (SEM) dB below control (-52%), during interruption of ischemic stress of rapid atrial pacing, compared to only one of nine patients without CAD (P less than 0.05). Only five CAD patients (28%) had an abnormal rise (greater than or equal to 5 mm) in left ventricular end-diastolic pressure (LVEDP) either during or upon interruption of pacing, and six (33%) had ischemic ST-segment depression greater than or equal to mv in the ECG. Similarly two patients free of CAD (22%) had an abnormal increase in LVEDP, and none had ECG evidence of ischemia. Seventeen CAD patients (94%) had segmental LVWM abnormalities at rest or with interruption of pacing, while three patients with normal coronary arteries (33%) had abnormal angiographic LVWM (P less than 0.01). Thus, reduction is S1 spectral energy is a common accompaniment of myocardial ischemia. In the present study, it was more frequently observed than abnormalities in either the ECG or LVEDP, but was not was consistently seen as segmental left ventricular wall motion abnormalities.
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PMID:Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities. 62 70

Myocardial ischemia at rest occurs only late in the course of coronary artery disease, but transient ischemia can often be induced by increasing myocardial oxygen demand with exercise or atrial pacing. Myocardial ischemia causes a series of physiologic abnormalities that can be detected by assessment of myocardial perfusion, regional mechanical function, electrophysiology, and metabolism. Methods of assessment vary widely in sensitivity, specificity, cost, and ease of application. Although the appropriate choice of diagnostic test may be difficult, the morbidity and mortality that result from myocardial ischemia and infarction and the demonstrated potential of coronary artery bypass surgery to reverse myocardial ischemia before the development of permanent sequellae make the detection of ischemia an important clinical problem. Present methods for quantitating myocardial ischemia are imprecise and difficult to apply but have been used successfully to evaluate the efficacy of therapies designed to reduce the size of myocardial infarction.
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PMID:Myocardial ischemia: detection and quantitation. 62 55

Twelve different approaches to laboratory diagnosis of angina pectoris are reviewed here. They employ no fewer than seven different means of intentionally provoking a disparity between myocardial requirement and supply: dynamic exercise, hypoxia, prandial stress, raised systemic vascular resistance, paced tachycardia, mental stress, and exposure to normal environment. Of these, only dynamic exercise and the diverse combinations of stresses in the normal environment are capable of altering the heart's oxygen requirement-supply ratio threefold or more, accounting for the successful results from tests using these means of stress. The reviewed tests use three different means of detecting myocardial ischemia provoked by stress: electrocardiography to indicate impaired ventricular repolarization, indirect graphic records sensitive to impairment of mechanical ventricular function, and detection of insufficient myocardial perfusion patterns by radioactive tracer. The latter approach is particularly appealing because it directly reflects the pathophysiologic anomaly of interest. It should be remembered, however, that the basic differences in these methods of detecting ischemia make them complementary to each other and encourage their use in combination for improved diagnostic sensitivity.
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PMID:Interesting approaches to the diagnosis of angina pectoris. 63 19

Although many patients with coronary artery disease (CAD) have a positive exercise test without pain, the frequency and significance of this "silent" ischemia is unclear. Therefore, we studied 122 consecutive clinically stable patients with angiographically defined CAD (greater than 75 per cent luminal stenosis) and a positive exercise test. Seventy-eight patients had pain or anginal equivalent during or after a positive exercise test; 44 did not, including 32 (26 per cent) with no symptoms at all. Patients were evaluated as to age, sex, prior myocardial infarction, congestive failure, hypertension, diabetes mellitus, and digoxin or propranolol therapy--in addition to anginal symptoms before, during, or after the exercise itself. Extent of CAD, presence of collaterals, and left ventricular ejection fraction were also determined. All exercise tests were evaluated for evidence of ST-T abnormalities or prior infarction on the control ECG as well as peak heart rate during exercise and post-exercise degree of ST segment depression. There were no significant differences between patients with and without exercise-induced pain in regard to any of the clinical and angiographic features noted above, demonstrating that "silent" myocardial ischemia during or after exercise testing is not uncommon and is not readily attributable to any obvious clinical or catheterization findings. Further studies are necessary to determine if patients with evidence of "silent" myocardial ischemia are especially prone to sudden death.
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PMID:"Silent" myocardial ischemia during and after exercise testing in patients with coronary artery disease. 63 80

The article discusses the results of experiments on 16 dogs in which acute myocardial ischemia was reproduced with intravenous infusion of baksacor and without the infusion of the drug; control experiments were also performed on an intact heart with baksacor infusion. Hemodynamics and myocardial contractility were studied throughout the entire experiment. It was found that baksacor had practically no effect on an intact heart. In acute ischemia the maximum effect of the drug was manifested on the 5th-25th minutes. An increase of the stroke volume and normalization of the rate of shortening of the contraction component were observed. An anti-arrhythmic effect of baksacor was noted.
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PMID:[Effect of baxacor on the hemodynamics and contractile function of the myocardium in acute ischemia (an experimental study)]. 64 42

The extent to which an increase in preload increases left ventricular (LV) end-diastolic (ED) diameter (D) was studied in seven conscious dogs instrumented with ultrasonic D transducers and miniature LV pressure (P) gauges. Preload was elevated by three techniques: 1) volume loading with saline infusion, 2) induction of global myocardial ischemia by constricting the left main coronary artery, and 3) infusion of methoxamine. These three interventions increased LVEDP to over 30 mmHg from a control of 10 +/- 1 mmHg. With volume loading, LVEDD rose by only 1.55 +/- 0.39 mm from a control of 44.08 +/- 1.08 mm; with ischemia LVEDD rose by only .96 +/- .29 mm from a control of 42.55 +/- 2.18 mm, while with methoxamine LVEDD rose by only 1.34 +/- 0.38 mm from a control of 43.89 +/- 2.07 mm. In contrast, in the open-chest, anesthetized dog, LVEDD was greatly reduced and volume expansion resulted in a profound increase in LVEDD. Thus, the Frank-Starling mechanism is not an important controlling mechanism in the normal, reclining, conscious animal, since LVEDD appears to be near maximal at rest and does not increase substantially despite striking increases in LVEDP.
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PMID:Extent of utilization of the Frank-Starling mechanism in conscious dogs. 64 72


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