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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial imaging with 133-Xe and a gamma camera was employed to evaluate total and regional myocardial blood flow. The technique detected vasodilatation after injection of papaverine or diatrizoate. Contrast medium caused transient vasodilatation with return to baseline flow within five minutes. Myocardial tissue flow tended to decrease as coronary artery stenosis became more severe. There was overlap of flow measurements in patients with and without coronary artery disease. Coronary flow measurements made at rest are not considered to be an essential clinical tool. gpreater diagnostic benefit is obtained from the scintigram which distinguishes between akinesia caused by ischemia and akinesia due to extensive scarring.
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PMID:Regional Myocardial Blood Flow Measurement in the Evaluation of Patients with Coronary Artery Disease. 114 55

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

A case of a 60-year-old woman suffering from hypertension, who presented an episode of acute myocardial ischemia with an elevation of the ST segment in the anterior ECG lead, is reported. On examination, a transient loud systolic murmur was present; it completely disappeared soon after the cessation of acute myocardial ischemia. Doppler echocardiography was performed a few times, during and after the acute ischemia: it was able to show a sort of "hour-glass" deformation of the left ventricle due to the akinesia of the anterior and apical segments. This functional anatomic deformation hampers the outflow from the left ventricle thus creating a dynamic left intraventricular gradient, which is clearly shown by pulsed wave and continuous Doppler echocardiography.
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PMID:[Dynamic left intraventricular obstruction in acute myocardial ischemia]. 260 82

This study analyzed the pattern of regional wall motion in 58 dogs undergoing 4 to 6 hours of left anterior descending coronary artery occlusion. Regional wall motion was measured by ultrasonic crystals and ischemic muscle either remained dyskinetic (-40% of control systolic shortening, n = 26) or progressed toward akinesia (less than 20% of control systolic shortening or greater than 50% reduction in passive lengthening, n = 32). Ten dogs underwent unmodified blood reperfusion. Regional blood flow (radioactive microspheres), histochemical damage (triphenyltetrazolium chloride staining), and mitochondrial function were determined. Hearts showing persistent dyskinesia had more collateral flow (12 versus 2 ml/100 gm/min, p less than 0.05), less histochemical damage (26% versus 63% area at risk/area of nonstaining, p less than 0.05), and better retention of mitochondrial oxidative phosphorylation capacity (adenosine triphosphate, 622 versus 444 nmol/mg protein/min, p less than 0.05), and tended toward mitochondrial calcium accumulation (48 versus 64 nmol/mg protein). Unmodified blood reperfusion after 4 hours of ischemia produced prompt akinesia (-2% +/- 3% systolic shortening) and was associated with increased edema (82% water content), caused the low-reflow phenomenon (19% control subendocardial flow, 13 ml/100 gm/min), and increased histochemical damage (69% triphenyltetrazolium chloride nonstaining, p less than 0.05). These findings suggest that persistent dyskinesia during early ischemia (first 6 hours) may reflect a relatively optimistic sign, as regression to akinesia occurs in muscle with less collateral flow, more impaired mitochondrial function, worsened calcium homeostasis, and more severe histochemical and ultrastructural damage. These observations imply that careful evaluation of ischemic wall motion may provide a valuable insight into potential muscle salvage.
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PMID:Studies on prolonged acute regional ischemia. II. Implications of progression from dyskinesia to akinesia in the ischemic segment. 275 55

Balloon inflation performed during percutaneous transluminal coronary angioplasty causes transient total occlusion of the coronary artery and thus provides a model for evaluation of the regional myocardial responses to transient ischemia. Twenty patients with normal left ventricular function undergoing angioplasty of isolated stenosis of the proximal left anterior descending coronary artery were studied. In group A (14 patients) analysis of one inflation-deflation sequence per patient was performed. Group B (six patients) had multiple (greater than 5) inflations; the first and last sequences were analyzed. Assessment included continuous two-dimensional echocardiography with computerized quantitative analysis of regional left ventricular wall motion, and continuous 12 lead electrocardiographic recordings. The mean duration of inflation in group A was 62 +/- 6 seconds (mean +/- SD). The onset of regional left ventricular dysfunction was 12 +/- 5 seconds after inflation. Profound dysfunction was noted in all patients. After 60 seconds of balloon occlusion of the coronary artery, 29% of patients had severe hypokinesia of the ischemic region and 71% had akinesia or dyskinesia. With deflation there was prompt recovery of regional function, with full recovery at 43 +/- 17 seconds. Comparison of data from first and last inflations in group B revealed no significant differences in time to onset of dysfunction, magnitude of dysfunction or time to complete recovery of function. The onset of ischemic electrocardiographic changes lagged behind the onset of wall motion abnormalities, with only 64% of patients showing evidence of ischemia on 12 lead electrocardiograms at 20 seconds of inflation. After 60 seconds, 86% had ischemia detectable by electrocardiography. Thus, balloon inflation during coronary angioplasty leads to profound but reversible regional left ventricular dysfunction. Repeated occlusions of the coronary artery during angioplasty do not have a cumulative ischemic effect. It may be hazardous to apply these findings to patients who have underlying major left ventricular dysfunction and in whom the reversibility of dysfunction and lack of cumulative ischemic effect may not be assured.
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PMID:Regional myocardial dysfunction during coronary angioplasty: evaluation by two-dimensional echocardiography and 12 lead electrocardiography. 294 Feb 83

The direct manipulation of coronary blood flow to induce regional myocardial ischemia has been almost entirely limited to experimental animal models. Thus, the detection of ischemia-induced left ventricular dysfunction in human subjects has been generally limited to observations made under conditions of diagnostic loading or during spontaneous clinical events. Percutaneous coronary angioplasty requires repeated interruptions of coronary blood flow for periods as long as 1 minute. The resulting appearance of or increase in ischemia-produced changes in myocardial function were detected by two-dimensional echocardiography in 18 patients undergoing angioplasty of 22 coronary stenoses. Accordingly, left ventricular contraction was studied during 52 episodes of regional coronary blood flow interruption and reperfusion in the process of inflating and deflating the angioplasty balloon. Before angioplasty, left ventricular wall motion was normal in 14 patients. There was mild anteroapical hypokinesia in two patients, anteroapical akinesia in one and mild inferior hypokinesia in one. Balloon inflations repeatedly produced new or increased wall motion abnormalities in the distribution of the instrumented coronary artery in 19 (86.4%) of the 22 procedures, but did not alter wall motion during angioplasty of one left circumflex artery lesion, one highly collateralized left anterior descending artery stenosis and one left anterior descending stenosis that had already caused severe anteroapical dyssynergy. Hypokinesia, usually rapidly progressing to dyskinesia, began 19 +/- 8 seconds (mean +/- SD) after coronary occlusion. Wall motion began to normalize 17 +/- 8 seconds after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sequence of mechanical, electrocardiographic and clinical effects of repeated coronary artery occlusion in human beings: echocardiographic observations during coronary angioplasty. 315 58

Increasingly longer balloon inflation times during coronary angioplasty can create significant left ventricular ischemia, amelioration of which was attempted in this study using nitroglycerin. Hemodynamic variables were assessed during inflation of an angioplasty balloon in the proximal left anterior descending coronary artery of 10 patients. Regional wall motion was assessed by left ventriculography during a separate balloon inflation. Nitroglycerin (200 micrograms) was then administered intravenously, and hemodynamic and ventriculographic assessments during balloon inflations were repeated. Balloon inflation resulted in a marked increase in left ventricular end-diastolic pressure (from 9.2 +/- 2.1 to 19.4 +/- 2.9 mm Hg) and time constant of left ventricular relaxation (from 44.2 +/- 6.2 to 62.3 +/- 11.3 ms) and a decrease in distal coronary artery perfusion pressure (from 54 +/- 9 to 33.1 +/- 4 mm Hg). Time to onset of angina was 29 +/- 3 seconds and time to ST segment depression of 1 mm or greater was 30 +/- 3 seconds. Regional wall motion analysis 30 seconds after onset of balloon inflation revealed marked hypokinesia and akinesia in the anteroapical segments with graduated depression of inferior wall motion, greatest at the apex. After the administration of nitroglycerin, balloon inflation resulted in a smaller increase in end-diastolic pressure (from 5.0 +/- 2.7 to 8.3 +/- 2.6 mm Hg) and time constant (from 47.9 +/- 4.7 to 54.4 +/- 9.2 ms; both p less than 0.01 versus standard balloon inflation). Distal coronary artery pressure remained similar to standard balloon inflation (32 +/- 3 mm Hg) despite lower mean arterial pressure (89 +/- 5 mm Hg, p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration by nitroglycerin of left ventricular ischemia induced by percutaneous transluminal coronary angioplasty: assessment by hemodynamic variables and left ventriculography. 316 Jul 55

Contractile dysfunction of reversibly injured, reperfused myocardium can be enhanced by inotropic interventions. A decrease in the Ca-sensitivity of contractile proteins with slow recovery during reperfusion has been suggested as a potential mechanism underlying this postischemic dysfunction. We therefore tested the effects of the cardiotonic agent AR-L 57 (1 mg/kg i.v.) in six anesthetized, vagotomized dogs during constant atrial pacing at 192 +/- 6 beats/min. Before ischemia, AR-L 57 increased left ventricular pressure from 131 +/- 22 to 138 +/- 21 mm Hg and maximum dP/dt from 3,022 +/- 1,427 to 4,337 +/- 2,608 mm Hg/s. Mean systolic thickening velocity of the posterior myocardium was increased from 8.9 +/- 1.1 to 11.7 +/- 1.1 mm/s. After release of a 15 min LCX-occlusion which caused complete regional akinesia, baseline function in the posterior myocardium was severely depressed and only gradually returned towards control values over 8 h of reperfusion. AR-L 57 increased systolic thickening velocity at 10 min, 4 and 8 h reperfusion to a similar extent as before ischemia. With reference to a purported Ca-sensitizing mechanism underlying the positive inotropic action of AR-L 57, our data suggest no change in the Ca-sensitivity of reperfused myocardium.
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PMID:Recruitment of inotropic reserve in "stunned" myocardium by the cardiotonic agent AR-L 57. 322 76

During Ergonovine-test a patient with Prinzmetal angina presented (in I, aVL, V3-V6) ST downsloping which, after a temporary phase of alternative normalization (AST) beat to beat in V5, progressed to ST upsloping with typical angina. The M-mode echo-study first discovered, before than ecg, septal impairment (hypokinesia which increased to akinesia in the AST phase) and also asynergy of posterior wall of left ventricle. After intravenous nitrate echo-alterations reversed more rapidly than ecg one (transitional phase of ST decrease). The authors relate the AST to temporary alternative pseudonormalization caused by a phase of electrical instability during progressive vasospastic ischemia involving first the endocardial layers and after the epicardium of a single myocardiocoronary district. Probably also other partially opposite ischaemic districts, as suggested from echo data of posterior wall asynergy took a part in these events. This rare ST-alternans type as new pseudonormalization phenomenon and the usefulness of echo-study during ischaemic attacks are stressed.
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PMID:[Clinical, electrocardiographic and echocardiographic findings in a case of vasospastic angina with alternating pseudonormalization of the ST segment]. 383 2

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.
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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


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