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

The relative time courses of early changes in myocardial metabolism and function during anoxia, global ischemia, and regional ischemia were compared in isolated rat hearts. Transmural anoxic wave front was determined with NADH fluorescence photography, and oxygen saturation of myoglobin and dynamic systolic wall thickening were measured with spectrophotometry of light transmitted through the left ventricular free wall. In all three treatments, anoxic wave front first appeared in the subendocardium and reached the epicardial half of the myocardium in 10 s, when oxygen saturation of myoglobin decreased by 50% and tissue ATP and creatine phosphate remained at aerobic levels. During this period, systolic wall thickening decreased gradually in anoxia and global ischemia, whereas a marked decrease in systolic wall thickening and appearance of dyskinesia (wall thinning) occurred in regional ischemia. Thus the early extension of anoxic wave front and metabolic changes are similar with all three treatments, and dyskinesia, observed only in case of regional ischemia, occurs when the inner half is ischemic or anoxic.
 ...
PMID:Transmural anoxic wave front and regional dysfunction during early ischemia. 361 98

The 1st myocardial infarction requires the identification of patients who are at high risk of malignant ventricular arrhythmias. Our study group included 55 consecutive patients (age less than 70): all had non-invasive "signal averaging" recording and 24 hour dynamic electrocardiogram at the post-acute phase of their 1st myocardial infarction (MI) and 3 months later. Wall motion abnormalities were evaluated in each patient but two. 24 randomized patients (without documented sustained ventricular tachycardia) underwent right programmed ventricular stimulation at the 3rd month after MI and pathological repetitive responses were evaluated (Table III); they were hemodynamically stable and without persistent ischemia. Late potentials have been compared to spontaneous and induced ventricular arrhythmias, wall motion abnormalities (Table II) and two-year follow-up (Table VI), in order to identify predictive markers of sudden death or malignant arrhythmias. Ventricular late potentials were identified in 28 patients (51%) 4-8 days after MI: mean duration was equal to 75 +/- 33 msec; they did not show any relationship to the site (Table I) and to the extension of necrosis (Table II). Ventricular late potentials had no significant association with myocardial dyskinesia (Table II) while their association with complex ventricular arrhythmias, detected on Holter monitoring within 8 days after MI, and with the induction of repetitive ventricular responses (greater than or equal to 2 complexes) showed significant correlations (respectively p = 0.02; p = 0.01). In regard of the recognition of spontaneous ventricular tachycardia (greater than or equal to 3 complexes) in the follow-up, the detection of late potentials showed 75% sensibility with predictive value equal to 32% (Table V); the combination of late potentials and ventricular dyskinesia exhibited the highest specificity (88%) and predictive value (54%). By the end of follow-up there had been 6 cardiac deaths (2 sudden, 4 from left ventricular failure): late potentials longer than 75 msec were recorded in all patients who had cardiac death; in the post acute phase of MI repetitive ventricular arrhythmias were detected in only 1 of the 2 case of sudden cardiac death and in none of the patients who developed sustained ventricular tachycardia in the follow-up (Table VI). Myocardial dyskinesia was present in each patient who developed non sudden cardiac death (Table VI).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Late potentials, myocardial kinetics and ventricular vulnerability as markers of sudden death after myocardial infarct]. 372 Nov 3

This study assesses the regional oxygen requirements of muscle segments that are beating and working, beating and empty, arrested and decompressed, and nonischemic that move dyskinetically. Regional oxygen demands were evaluated by producing a dyskinetic segment by infusing regional cardioplegic solution through a left anterior descending coronary artery catheter with and without extracorporeal circulation. The results show that the O2 demands of the perfused dyskinetic cardiac muscle segment (4 to 8 ml/100 gm/min) are approximately 55% of the contracting (beating, working) segment (7 to 12 ml/100 gm/min) and are fivefold more than when the same muscle segment is arrested and decompressed by total vented bypass (0.8 to 1.2 ml/100 gm/min). Additional studies showed that ischemia for 2 hours (left anterior descending coronary artery ligation) produced severe dyskinesia (-24% control systolic shortening), which failed to recover after reperfusion with the heart in the beating, working state. In contrast, lowering O2 demands by reperfusion during bypass restored occasional contractile function as a consequence of left ventricular decompression. Dyskinetic muscle segments have a high oxygen requirement that may affect their capacity to be salvaged if reperfusion is conducted without left ventricular decompression. These observations suggest that the value of revascularization in the working heart (i.e., streptokinase with or without angioplasty) may be limited unless the left ventricle is decompressed during reperfusion and provide an explanation for the delayed recovery of mechanical function in hearts reperfused surgically with normal blood during cardiopulmonary bypass.
 ...
PMID:High oxygen requirements of dyskinetic cardiac muscle. 374 82

This review deals with the pathogenesis of ischemia-related abnormalities of ventricular repolarization. The most common repolarization abnormality during acute myocardial ischemia is the deviation of ST segment from the baseline due to diastolic and systolic currents of injury. The patterns of primary and reciprocal ST deviations during and after myocardial infarction are discussed. A very tall upright or a deeply inverted T wave, and shortened QT interval are transient phenomena followed by postischemic T wave abnormalities associated with QT lengthening. These changes are associated with lengthening of the ventricular action potentials at the border of infarction. Persistence of ST elevation after myocardial infarction is usually associated with ventricular dyskinesia. The differential diagnosis of this pattern and its possible mechanism are discussed. Also the mechanisms of ST alternans, T alternans and negative U waves, i.e. less common manifestations of myocardial ischemia are discussed. Studies of exercise-induced T wave normalization suggest that the behavior of primary T wave abnormalities after exercise does not alter the interpretation of the ischemic changes. T wave abnormalities are frequently non-specific but the post myocardial infarction T wave changes persist after administration of isoproterenol while various functional and neurogenic T wave abnormalities are corrected by isoproterenol.
 ...
PMID:ST-segment, T-wave, and U-wave changes during myocardial ischemia and after myocardial infarction. 375 2

Limitations of the standard 12-lead electrocardiogram in sensitivity, specificity and information content on the effort induced ischemic process might be partly due to an inadequate sampling of cardiac electrical events. An extensive array of electrodes is an effective way to verify this hypothesis. Actually body surface mapping provides: a 10-15% increase in diagnostic yield mainly in patients with mild coronary artery disease and elusive signs of ischemia in standard leads a very approximate indication of the extent of coronary artery disease a substantial contribution to the identification of the site of ischemia. Regarding the last point, preliminary results of an ongoing study are reported. One hundred and three patients with recent myocardial infarction have been studied by exercise test with simultaneous recording of surface map and Thallium 201 scan. So far in the subset with inferior myocardial infarction (76 patients) three different map patterns corresponding to different ischemic regions (anterior, inferior and posterior) have been identified. In anterior myocardial infarction (27 patients) a characteristic map pattern for exercise-induced myocardial ischemia has been observed, apparently able to discriminate between ischemia and the changes of early repolarization induced by the dyskinesia of the infarcted ventricular wall. In conclusion, electrocardiographic mapping makes a practical contribution to the understanding of ischemia-induced cardiac electrical events.
 ...
PMID:Can body surface mapping improve the diagnostic power of standard electrocardiography in effort myocardial ischemia? 375 6

Myocardial reperfusion after reversible regional ischemia is known to result in delayed recovery of contractile function, but the mechanism responsible for this phenomenon remains unclear. We examined the ability of N-2-mercaptopropionylglycine, a synthetic thiol compound with oxygen free radical scavenging properties, to attenuate postischemic dysfunction in open chest dogs undergoing a 15 minute occlusion of the left anterior descending coronary artery followed by 4 hours of reperfusion. Treated animals received an infusion of N-2-mercaptopropionylglycine (50 mg/kg per h) for 4 hours starting 15 minutes before coronary occlusion. Collateral flow, as determined with radioactive microspheres after 10 minutes of ischemia, was 0.07 +/- 0.01 ml/min per g (mean +/- SE) in both control (n = 20) and treated (n = 13) groups. The occluded vascular bed, as determined by postmortem perfusion, averaged 26.1 +/- 1.2% of the weight of the left ventricle in control and 29.6 +/- 1.3% in treated animals. Systolic wall thickening (an index of regional function) was assessed with an epicardial pulsed Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions and similar degrees of dyskinesia during ischemia. Nevertheless, recovery of function (expressed as percent of baseline) was considerably greater in the treated dogs at 1 hour (44.6 versus 12.8%, p = 0.05), 2 hours (64.0 versus 31.6%, p less than 0.02), 3 hours (77.1 versus 36.7%, p less than 0.01) and 4 hours of reperfusion (75.0 versus 40.0%, p less than 0.05). Thus, N-2-mercaptopropionylglycine produced a significant and sustained improvement in recovery of contractile function after a brief episode of regional myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:N-2-mercaptopropionylglycine improves recovery of myocardial function after reversible regional ischemia. 376 Mar 90

To define the in vivo relation between abnormal wall motion and the area at risk for necrosis after acute coronary occlusion, 11 open chest dogs were studied. Five dogs underwent left anterior descending coronary artery occlusion and six underwent left circumflex artery occlusion. Area at risk was defined at five short-axis levels (mitral valve, chordal, high and low papillary muscle and apex) using myocardial contrast echocardiography. Wall motion was measured in the cycles preceding injection of contrast medium. Two observers used two different methods to measure wall motion. In method A, end-diastolic to end-systolic fractional radial change for each of 32 endocardial targets was determined. The extent of abnormal wall motion was then calculated using three definitions of wall motion abnormality: akinesia/dyskinesia, fractional inward endocardial excursion of less than 10%, and fractional inward endocardial excursion of less than 20%. In method B, the information from the entire systolic contraction sequence was analyzed and correlated with a normal contraction pattern. The best linear correlation between area at risk (AR) and abnormal wall motion (AWM) was achieved using method B and expressed by the following linear regression: AWM = 0.92 AR + 3.0 (r = 0.92, p less than 0.0001, SEE = 1.7%). Of the three definitions of abnormality used in method A, the best correlation was achieved between area at risk and less than 10% inward endocardial excursion and was expressed by the following polynomial regression: AWM = -0.01 AR2 + 1.5 AR -0.14 (r = 0.92, p less than 0.001, SEE = 1.7%). These data demonstrate that there is a definite relation between area at risk and abnormal wall motion but that this relation varies depending on the method used to analyze wall motion. However, wall motion during acute ischemia is also influenced by the loading conditions of the heart. Because these may vary in a manner that is independent of the ischemic process, measurement of both risk area and abnormal motion may provide a more comprehensive assessment of cardiac function in myocardial ischemia than is provided by the measurement of either alone.
 ...
PMID:Contrast echocardiography in acute myocardial ischemia. III. An in vivo comparison of the extent of abnormal wall motion with the area at risk for necrosis. 394 58

Reperfusion after reversible regional ischemia has been shown to result in delayed recovery of myocardial function, but the mechanism responsible for this phenomenon remains unknown. We explored the potential role of oxygen-free radicals as mediators of postischemic dysfunction in open-chest dogs undergoing a 15 min occlusion of the left anterior descending coronary artery (LAD) followed by 2 hr of reperfusion. Treated animals (n = 19) received an infusion of the oxygen free-radical scavengers superoxide dismutase (SOD; 15,000 U/kg) and catalase (CAT; 55,000 U/kg) for 1 hr starting 15 min before LAD occlusion, while control animals (n = 20) received an equal volume of saline. SOD and CAT produced no discernible effect on heart rate, aortic pressure, or left atrial pressure. Collateral flow to the ischemic zone (radioactive microspheres) was 0.07 +/- 0.01 ml/min/g in both groups. The size of the occluded bed as determined by postmortem perfusion was 26.1 +/- 1.2% of the left ventricle in the control group and 26.5 +/- 0.9% in the treated group. Systolic wall thickening (an index of regional function) was assessed with an epicardial pulsed-Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions and similar degrees of dyskinesia during ischemia. Nevertheless, recovery of function (expressed as percent of baseline) was considerably greater in the treated dogs, both at 1 hr (43.8 +/- 14.3 vs 12.8 +/- 11.6) and 2 hr of reperfusion (74.2 +/- 8.4 vs 31.6 +/- 9.8, p less than .005). This improved recovery of function obtained with SOD and CAT suggests that oxygen-free radicals play an important role in the genesis of myocardial dysfunction after a brief episode of regional ischemia.
 ...
PMID:Enhancement of recovery of myocardial function by oxygen free-radical scavengers after reversible regional ischemia. 402 84

We investigated whether the postischemic acceleration of adenosine triphosphate (ATP) synthesis by means of precursor infusion is beneficial for the contractile function of reperfused myocardium. A coronary artery was occluded for 45 min in 21 dogs to produce a marked but reversible ischemia. During the following 3 hours of reperfusion either adenosine (n = 6) or AICAR (5-amino-imidazole-4-carboxamide-riboside) (n = 6) was infused intracoronarily by a small transfemoral catheter positioned in the LAD. ATP repletion by adenosine was nearly 50% of the deficit caused by the previous ischemia, the effect of AICAR on steady-state tissue ATP concentration was insignificant. Regional systolic function of these both groups was compared to that of a control group (n = 9) receiving only a saline infusion. We measured the regional function by subendocardially implanted ultrasound transducers using the transit time method. All three groups showed a reduction to about 25% of the initial segment shortening at the end of ischemia, followed by a quick recovery to half of the preocclusion segment shortening after reopening of the vessel. No further changes were observed in the control series during the 3 hours of reperfusion (50 +/- 10% SE segment shortening at the end). With adenosine infusion - in spite of the resulting considerable ATP elevation - no significant change of segmental contractile function occurred (44 +/- 5% SE segment shortening). Only the AICAR treated group differed from control. It produced a continuous deterioration during reflow resulting in a holosystolic bulging of -20% +/- 10% SE at the end of 3 hours of reperfusion. Our results show that there is no correlation between different ATP tissue levels achieved by adenosine infusion and systolic function in reperfused myocardium after regional reversible ischemia. We hypothesize that reperfusion dyskinesia is caused by a failure of energy utilisation rather than of energy supply.
 ...
PMID:Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium. 405 46

The purpose of this study was to investigate the relation between abnormalities of left ventricular (LV) wall thickening during systole in ischemic regions and the interaction of LV pressure and regional intramyocardial pressure. Wall thickness was measured in 10 open-chest dogs with ultrasonic dimension gauges. LV pressure, aortic pressure, and intramyocardial pressure in the subendocardium were measured with catheter-tip micromanometers. Regional ischemia was produced by occlusion of the left anterior descending coronary artery. During the control period, peak subendocardial pressure exceeded LV pressure by 44 +/- 6 mm Hg. With hypokinesia, defined as a 50% to 89% reduction of systolic wall thickening, peak subendocardial pressure exceeded peak LV pressure but to a lesser extent (15 +/- 1 mm Hg). During akinesia, defined as a 90% to 100% reduction of systolic wall thickening, there was less than 1 mm Hg difference between peak subendocardial pressure and peak LV pressure. During dyskinesia, defined as systolic thinning of the ischemic wall, peak LV pressure exceeded peak subendocardial pressure by 29 +/- 6 mm Hg. These observations indicate that regional changes of LV wall thickness characterized by hypokinesia, akinesia, and dyskinesia are associated with pressure gradients between the LV cavity and the LV wall that are compatible with the abnormalities of wall motion.
 ...
PMID:Relation of intramyocardial and intracavitary pressure to regional myocardial asynergy in the canine left ventricle. 621 65


<< Previous 1 2 3 4 5 6 7 Next >>