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)

Thirty-one patients, mean age 54 years, had been on chronic ambulatory peritoneal dialysis (CAPD) for an average of 38 months. Mean values (mg/dl) for triglycerides (567), total-C (267), LDL-C (133), and Apo-B (154) were elevated, and HDL-C (30) were low. The low values for total-C/Apo-B and LDL-C/Apo-B suggest an increase in the number of low density lipoprotein (LDL) particles, rather than in the amount of cholesterol per LDL particle. Without knowledge of lipids, ischemic heart disease for the 31 patients was categorized into five grades in the following manner. All patients were graded based on history (angina, myocardial infarction, and bypass surgery), electrocardiogram (EKG), and echocardiography. In addition, five patients underwent coronary angiography, the results of which were considered in their grading. The five grades were assigned as follows: Grade I, no evidence (n = 15); Grade II, angina with EKG ischemia (n = 4); Grade III, myocardial infarction (MI) (n = 1); Grade IV, MI with dyskinesia-akinesia on echo (n = 4); Grade V, severe three vessel disease on angiography, or multiple infarcts, or Grade IV with heart failure (n = 7). Only Apo-B (r = 0.56) and total-C/HDL-C (r = 0.57) correlated with severity of grade, with p less than 0.001. When patients with and without detectable ischemic heart disease were compared by stepwise logistic regression, Apo-B was the only variable that independently predicted heart disease (p = 0.001). However, contribution of the lipid changes induced by CAPD has not been established.
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PMID:Ischemic heart disease, serum cholesterol, and apolipoproteins in CAPD. 175 Dec 58

To determine the importance of right atrial function with acute right ventricular dysfunction, sequential right ventricular and right atrial ischemia were induced in 15 dogs. Right ventricular ischemia resulted in right ventricular free wall dyskinesia, right ventricular dilation by ultrasound, elevated right ventricular filling pressure and paradoxic septal motion. There were decrements in right ventricular systolic pressure (28.9 +/- 5.5 to 25.5 +/- 4.6 mm Hg) (p less than 0.05 for these and all subsequent values) and stroke work (5.66 +/- 0.94 to 2.66 +/- 0.62 g.m/m2), resulting in reductions in left ventricular preload, systolic pressure (123 +/- 11 to 97 +/- 12 mm Hg) and stroke volume (24.2 +/- 4.3 to 19.1 +/- 5.2 ml). Right atrial contractility was augmented, as indicated by increases in peak A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.22 +/- 0.02 to 1.46 +/- 0.3) and right atrial stroke work (0.11 +/- 0.02 to 0.25 +/- 0.05 g.m/m2). Right atrial ischemia depressed right atrial contraction, as indicated by decreased A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.46 +/- 0.3 to 1.04 +/- 0.2) and stroke work (0.25 +/- 0.05 to 0.04 +/- 0.01 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Right atrial ischemia exacerbates hemodynamic compromise associated with experimental right ventricular dysfunction. 193 62

To determine the safety and efficacy of synchronized coronary venous retroperfusion during brief periods of ischemia, 30 patients undergoing angioplasty of the left anterior descending coronary artery were studied. Each patient underwent a minimum of two angioplasty balloon inflations. Alternate dilations were supported with retroperfusion; the unsupported inflations served as the control inflations. Synchronized retroperfusion was performed by pumping autologous femoral artery blood by means of an electrocardiogram-triggered retroperfusion pump into the great cardiac vein through a triple lumen 8.5F balloon-tipped retroperfusion catheter inserted percutaneously from the right internal jugular vein. Clinical symptoms, hemodynamics and two-dimensional echocardiographic wall motion abnormalities were analyzed. Retroperfusion was associated with a lower angina severity score (0.8 +/- 1 vs. 1.2 +/- 1) and delay in onset of angina (53 +/- 31 vs. 37 +/- 14 s; p less than 0.05) compared with the control inflations. The magnitude of ST segment change was 0.11 +/- 0.14 mV with retroperfusion and 0.16 +/- 0.17 mV without treatment (p less than 0.05). The severity of left ventricular wall motion abnormality was also significantly (p less than 0.01) reduced with retroperfusion compared with control (0.7 +/- 1.4 [hypokinesia] vs. -0.3 +/- 1.6 [dyskinesia]). There were no significant changes in hemodynamics, except in mean coronary venous pressure, which increased from 8 +/- 3 mm Hg at baseline to 13 +/- 6 mm Hg with retroperfusion. Four patients required prolonged retroperfusion for treatment of angioplasty-induced complications. The mean retroperfusion duration in these patients was 4 +/- 2 h (range 2 to 7). In the three patients who underwent emergency bypass surgery, the coronary sinus was directly visualized during surgery and found to be without significant injury. There were no major complications. Minor adverse effects were transient atrial fibrillation (n = 2), jugular venous catheter insertion site hematomas (n = 4) and atrial wall staining (n = 1), all of which subsided spontaneously. Thus, retroperfusion significantly reduced and delayed the onset of coronary angioplasty-induced myocardial ischemia and provided effective supportive therapy for failed and complicated angioplasty.
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PMID:Synchronized coronary venous retroperfusion for support and salvage of ischemic myocardium during elective and failed angioplasty. 205 Sep 31

To determine if alterations in regional coronary vascular resistance could occur in the type of myocardial ischemia present in severe angina pectoris, regional perfusion and function were studied in 35 conscious sedated dogs. A stenosis producing severe hypokinesia of the perfused segment was created for 2 h on the left anterior descending coronary artery and 10 episodes of 1 min of high demand ischemia (atrial pacing at a rate sufficient to induce dyskinesia in the hypoperfused segment) were superimposed before reperfusion. The dogs were randomized into three treatment groups: control (n = 13), dipyridamole (n = 10) or WEB-2086 (n = 12), an antagonist of the effects of the endogenous platelet-activating factor. During stenosis, residual endocardial blood flow in the ischemic but nonnecrotic area averaged 0.72 +/- 0.14, 0.38 +/- 0.13 and 0.68 +/- 0.17 ml/min per g in the control, WEB-2086 and dipyridamole groups, respectively. Twenty-four hours after reperfusion, endocardial blood flow in the ischemic area was significantly lower in control dogs (1.04 +/- 0.15 ml/min per g) than in dogs treated with WEB-2086 (1.44 +/- 0.28 ml/min per g; p less than 0.03) or dipyridamole (3.00 +/- 0.83 ml/min per g; p less than 0.01). Accordingly, in control dogs, endocardial coronary vascular resistance in the ischemic area was increased after reperfusion from 85 +/- 11 to 124 +/- 27 mm Hg/(ml/min per g) (p less than 0.05) after 24 h. In contrast, coronary vascular resistance in the ischemic area remained unchanged in dogs receiving WEB-2086 (77 +/- 8 to 79 +/- 9 mm Hg/(ml/min per g); p = NS) and it decreased significantly in dogs receiving dipyridamole (72 +/- 8 to 44 +/- 8 mm Hg/(ml/min per g); p less than 0.01). Regional function after 24 h remained depressed in all three groups. These data indicate that low flow, high demand ischemia induces alterations in the subendocardial microvasculature. Such alterations in regional coronary vascular resistance might play a role in several forms of ischemic heart disease such as in severe angina, but they appear susceptible to improvement by therapeutic interventions that influence granulocyte and platelet activation.
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PMID:Alterations in endocardial vascular resistance after reperfusion in a low flow, high demand model of ischemia: effects of dipyridamole and WEB-2086, a platelet-activating factor antagonist. 225 62

The reinjection of a small dose (40 MBq) of thallium-201 after stress and delayed imaging often shows new redistribution in the regions with persistent defect. To assess whether these segments may represent reversible ischemia, reinjection thallium-201 single-photon emission computed tomography (SPECT) was performed after stress and 3-hour delayed imaging in 24 patients before coronary artery bypass grafting (CABG). The left ventricular myocardium was divided into 5 myocardial segments and regional wall motion was scored on a scale from 0 (normal) to 4 (dyskinesia). Thallium-201 findings were compared with improvement in regional perfusion and wall motion 1 to 2 months after CABG. The reinjection imaging identified new redistribution in 15 of 32 persistent defects (47%) on the 3-hour delayed images. In the study of stress and delayed SPECT imaging, the improvement in perfusion was observed in 34 of 43 segments (79%) exhibiting redistribution and 15 of 32 (47%) segments without redistribution (p less than 0.01). The reinjection SPECT identified new redistribution in 12 of the 15 improved segments that were not detected on the delayed images. Similarly, the improvement in wall motion was observed in 23 of 31 segments (74%) exhibiting redistribution and 14 of 30 segments (47%) without redistribution on the delayed images (p less than 0.05). The reinjection identified new redistribution in 10 of the 14 improved segments that were undetected on the delayed images. The predictive values for improvement in perfusion and wall motion by the reinjection imaging were significantly higher (92 and 89%) than those by the delayed imaging (69 and 62%, respectively, p less than 0.05 each).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Value of thallium-201 reinjection after delayed SPECT imaging for predicting reversible ischemia after coronary artery bypass grafting. 238 13

This study tests the hypothesis that metabolic support of remote "nonischemic" myocardium during acute infarction will reverse the trend toward cardiogenic shock. Thirty-seven dogs underwent ligation of the left anterior descending coronary artery and 50% stenosis of the circumflex coronary artery. Irreversible ventricular fibrillation developed in 11 of them. The 26 survivors were observed for up to 6 hours; global and regional left ventricular function (cardiac index, stroke work index, ultrasonic crystals) and regional blood flow (radioactive microspheres) were measured. After 2 hours, eight dogs received an intravenous infusion of glutamate/aspartate, glucose-insulin-potassium, coenzyme Q10, and 2-mercapto-propionyl-glycine for 4 hours. Five dogs received the mannitol infusion to raise serum osmolarity 30 mOsm. Four additional dogs received the intravenous substrate infusions over 4 hours without undergoing ischemia. The substrate infusion for 4 hours caused no change in regional or global cardiac function in the four control dogs. Three of nine untreated dogs died of cardiogenic shock, and progressive left ventricular power failure occurred in the six others (40% decrease in cardiac index, 50% decrease in stroke work index, p less than 0.05) because of persistent dyskinesia in the left anterior descending region (-40% of systolic shortening, p less than 0.05) and hypocontractility in the circumflex region (48% of control systolic shortening, p less than 0.05), despite normal transmural blood flow in the posterior left ventricular wall (76 ml/100 gm/min). In contrast, in treated dogs, hypercontractility recovered in the circumflex segment (138% of systolic shortening) and stroke work index rose to control levels (91%) without a change in regional blood flow. Mannitol infusion did not improve hemodynamics or avoid the development of progressive left ventricular power failure. We conclude that cardiogenic shock after myocardial infarction is due, in large part, to impaired ability of "nonischemic" myocardium to maintain hypercontractility. This limitation can be prevented by metabolic support of viable muscle, and the data imply that intravenous substrate infusions may be helpful before definitive treatment (i.e., coronary artery bypass grafting) is undertaken.
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PMID:Studies on prolonged acute regional ischemia. V. Metabolic support of remote myocardium during left ventricular power failure. 250 26

The effects of the intravenous administration of the antianginal drug, nicorandil, 50 micrograms/kg administered over 2 minutes, were investigated during pacing-induced ischemia in 8 patients with coronary artery disease. Hemodynamic parameters were measured and single-plane left ventriculograms were obtained in control and postpacing periods both before and after pretreatment with nicorandil. Regional wall motion of the left ventricle was assessed by measuring shortening of the radial axes originating from the center of gravity of the end-diastolic silhouette. Heart rate, left ventricular (LV) systolic pressure and end-diastolic volume index did not change in the immediate postpacing period with or without medication. LV end-diastolic pressure decreased with nicorandil, from 22.0 +/- 3.4 to 17.0 +/- 2.3 mm Hg (mean +/- standard error of the mean) (p less than 0.05), and LV systolic volume index, from 39.6 +/- 8.0 to 30.4 +/- 6.8 ml/m2 (p less than 0.05). Ejection fraction increased from 55.2 +/- 5.0 to 64.3 +/- 3.8% (p less than 0.05). Stroke index and cardiac index (calculated from heart rate and stroke index) did not change significantly. Rapid right ventricular pacing increased the extent and degree of dyskinesia of the left ventricle, but premedication with nicorandil improved the wall motion. Thus, nicorandil has salutary effects on ventricular contractile and hemodynamic responses to transient ischemia induced by pacing stress.
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PMID:Effects of intravenous administration of nicorandil on cardiovascular hemodynamics and left ventricular function. 252 27

To determine the sequelae of transient myocardial ischemia (TMI) in term infants, we reviewed clinical and investigative data in 59 infants (37 male, 22 female) with structurally normal hearts admitted over the 2-year period of 1983-1985. Twenty-three were diagnosed prior to admission as cases of birth asphyxia (5-min Apgar score less than 6), and 36 had signs of persistent fetal circulation with electrocardiographic (ECG) changes of ischemia greater than 24 h after birth. Murmurs of atrioventricular valve regurgitation (AVVR), detected in 28 patients, were confirmed in 23 of the 24 patients investigated. The murmurs resolved over a 2-day to 6-month period (median 6 days). In three patients, AVVR, left ventricular dyskinesia, and ECG anomalies persisted for 2 months (until death), 4 months, and 48 months. Initial ECGs were abnormal in 57 patients, and (of those reviewed) 60% returned to normal over a 6-day to 7-month period (median 2 months). Residual ECG anomalies included second-degree AV block and persistent ST-T wave changes. Ten patients died from noncardiac causes. Neither the presence nor resolution of AVVR correlated significantly with the severity of birth asphyxia using the Apgar score, nor with the severity of the ischemic changes on the ECG. Although the cardiovascular sequelae of myocardial ischemia are usually transient, the data should prompt the need for careful review after the initial admission.
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PMID:Persistence of atrioventricular valve regurgitation and electrocardiographic abnormalities following transient myocardial ischemia of the newborn. 259 71

Based on experimental observations, an increase in intrinsic regional myocardial stiffness can be demonstrated during complete coronary occlusion at rest when there is dyskinesia. There is decreased chamber compliance as well during coronary occlusion, while the zero volume intercept of the ventricle in diastole is larger, changes that may relate in part to regional ultrastructural alterations at the sarcomere level. Postpacing studies suggest that decreased chamber compliance also occurs in that setting, but with an opposite shift upward of the diastolic pressure-volume relation, which may relate to reperfusion effects. The factors involved in such changes in stiffness undoubtedly are multiple, and also include delayed ventricular relaxation, which can be magnified at rapid heart rates, effects of nonuniformity, and possibly the timing of loading conditions during individual contractions. The relative influence of these multiple factors undoubtedly varies with the conditions and duration of acute ischemia.
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PMID:Is there a true increase in myocardial stiffness with acute ischemia? 264 93

Six hours of coronary occlusion has been thought to produce extensive and irreversible transmural damage and no possibility of salvage by reperfusion. This has been based on findings of adenosine triphosphate depletion and histochemical (triphenyltetrazolium chloride nonstaining) and ultrastructural changes (conventional preparatory techniques). This study tests the hypothesis that, in contrast to conventional wisdom, considerable structural and mitochondrial functional integrity remains in cardiac muscle subjected to 6 hours of regional ischemia. Twenty open-chest anesthetized dogs underwent isolation of the left anterior descending coronary artery and were observed for 6 hours. Eight of the 20 did not undergo ischemia and served as controls. Twelve underwent 6 hours of proximal ligation of the left anterior descending coronary artery (30% +/- 2% area at risk). Transmural biopsy specimens were analyzed. Coronary occlusion reduced regional blood flow (radioactive microspheres) to less than 10 ml/100 gm/min (p less than 0.05) and dyskinesia persisted in the area at risk for 6 hours. High-energy phosphates (adenosine triphosphate and creatine phosphate) declined to negligible levels and histochemical damage occurred (49% +/- 12% triphenyltetrazolium chloride non-staining). Mitochondrial ultrastructural changes (low protein denaturation embedding technique) were mild (the integrity of the inner and outer mitochondrial surface membranes and crystal membranes was maintained and myofibrillar degeneration did not occur). Mitochondrial oxidative phosphorylation rate remained at 63% of control levels, respiratory control index remained at 77%, and adenosine diphosphate/oxygen ratio was maintained at 96%. Mitochondrial Ca++ increased with lanthanum (from 26 to 46 nmol/mg protein, p less than 0.05), but irreversible calcium precipitation did not occur; calcium could be mobilized to normal levels (i.e., 13 nmol/mg protein) by ethylenediaminetetraacetic acid chelation. These data support our inference that necrosis does not occur after 6 hours of coronary occlusion and suggest that muscle salvage by reperfusion is possible after at least 6 hours of regional myocardial ischemia.
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PMID:Studies on prolonged acute regional ischemia. I. Evidence for preserved cellular viability after 6 hours of coronary occlusion. 281 16


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