Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 +/- 12 [mean +/- standard error of the mean] percent), reduction of systolic blood pressure (9 +/- 3%), decrease in left ventricular end-diastolic and end-systolic volumes (32 +/- 5% and 34 +/- 5%), increase in coronary sinus flow (64 +/- 24%) and decrease in left ventricular stroke work (29 +/- 8%). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severly depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 +/- 8% during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.
 ...
PMID:Regional and global myocardial effects of intravenous and sublingual nitroglycerin treatment after experimental acute coronary occlusion. 81 89

Pairs of ultrasonic dimension gauges and a micromanometer implanted in the subendocardium of the left ventricles of unanesthetized dogs were used to analyze serial changes in hemodynamic status and segmental function for up to 4 weeks after permanent circumflex coronary artery occlusion. Regional function was studied in control segments and in segments identified as marginal (hypokinetic) and ischemic. In three dogs, after transient regional dysfunction, no myocardial infarction developed, whereas in five dogs regional dysfunction at 3 hours after occlusion was followed by the development of persistent dysfunction and infarction. Left ventricular end-diastolic segment length (EDL) changes over time; EDL of the control segments increased progressively, but in marginal segments EDL was 12% below control and in the ischemic segments 30% below control by 4 weeks. Progressive increases in percent active shortening occurred in control segments; but holosystolic bulging was replaced by akinesia in ischemic segments, and persistent reduction in shortening was present in marginal segments at 4 weeks. Correlations were found between percent scar and reductions in percent shortening, EDL, and the ratio of change in diastolic length to change in diastolic pressure. These methods have detected hyperfunction in normal regions and variable segmental loss of contractile function, together with reduction of subendocardial dimensions and changes that may reflect decreased diastolic compliance in ischemic regions. We conclude that this model for the conscious animals may be useful for studying the influence of therapy on the extent of myocardial damage after experimental coronary occlusion.
 ...
PMID:Regional myocardial function and dimensions early and late after myocardial infarction in the unanesthetized dog. 84 42

The purpose of this study was twofold: 1) to verify a report that a suspension of 8-phenyltheophylline (8-PT) completely abolished hypoxia-induced coronary vasodilation [H. M. Wei, Y. H. Kang, and G. F. Merrill. Am. J. Physiol. 257 (Heart Circ. Physiol. 26): H1043-H1048, 1989] and 2) to determine the effect of dissolved 8-PT on hypoxic hyperemia. The left anterior descending coronary artery of anesthetized dogs was cannulated and perfused at either constant flow or constant pressure. An 8-PT suspension (40 micrograms.kg-1.min-1) produced a twofold elevation of coronary perfusion pressure at constant flow, a 97% decrease in coronary flow at constant pressure, and regional akinesia in both conditions. The coronary vasculature was unresponsive to 60-s coronary occlusion, exogenous adenosine, and hypoxia after infusion of the 8-PT suspension. These findings are consistent with obstruction of the coronary microvasculature by the 8-PT suspension. An 8-PT solution (40 micrograms.kg-1.min-1) produced 95 +/- 3% (P less than 0.001, n = 6) attenuation of exogenous adenosine-induced vasodilation at constant pressure, a 28 +/- 5% (P less than 0.01, n = 6) attenuation of reactive hyperemia, and a 24 +/- 6% (P less than 0.05, n = 6) decrease in hypoxia-induced vasodilation. An 8-PT solution had no effect on systolic segment length shortening and myocardial oxygen consumption. We conclude that 8-PT, when in solution, attenuates but does not abolish the coronary vasodilatory response to hypoxia. Hence, adenosine appears to contribute to hypoxia-induced vasodilation but is not uniquely responsible for the hyperemic response.
 ...
PMID:Canine coronary vasodepressor responses to hypoxia are attenuated but not abolished by 8-phenyltheophylline. 156 15

The purpose of this clinical study was to (1) evaluate mortality rates after surgical interventions for patients in cardiogenic shock (CS) secondary to acute coronary occlusion, acute ventricular septal defect (VSD) or acute valvular heart disease, (2) determine the pre-operative regional wall motion, and (3) ascertain the recovery of preoperative regional wall motion abnormalities after surgical intervention. The hospital records of twenty-five consecutive patients in CS were reviewed retrospectively. Regional wall motion was assessed preoperatively by ventriculography and postoperatively by 2D echocardiography (Sonotron Kardio VUE 60) after 1 and 3 days and at the day of discharge from the surgical ward (7-10 days). The left ventricle was divided in three segments according to the blood supply: LAD artery (antero-lateral wall), circumflex artery (lateral wall), and right coronary artery (inferior and basal wall). Regional wall motion was analyzed with the use of a scoring system in which grading was from 0 to 4 according to the following criteria: 0 = hyperkinesia, 1 = normokinesia, 2 = hypokinesia, 3 = dyskinesia, 4 = akinesia. Postmortem examination was performed in 8/9 patients. Data are presented as mean +/- SD. Significant differences were defined as probabilities for each test of p less than 0.05. The hospital mortality was higher for patients with acute coronary occlusion as compared to those with acute valvular disease or VSD (54.5%, 27.3%, 0%, resp.). The cause of death was cardiac in 7/9 patients. However, postmortem examination revealed loss by infarction of only moderate quantities of myocardium which could not explain the severe postoperative heart failure in those patients. Previous myocardial infarctions and preoperative cardiac arrest were significant risk factors for hospital mortality. In all patients with acute coronary occlusion (11/11) at least one region of the left ventricle was either a- or dyskinetic in the region supplied by the acute occluded vessel. In addition five patients had akinetic regions due to previous infarctions. The remaining remote myocardium was hypocontractile due to significant stenosis in coronary arteries supplying remote areas. Of 10 dyskinetic segments before surgical intervention, 5 were akinetic postoperatively, and only 5 developed slight hypokinetic contractions. The overall hypokinetic regions were not different as compared to the preoperative data (36.4% vs 39.4%). The normokinetic segments increased from 9.1% to 33.% (p less than 0.05).
 ...
PMID:Prolonged abnormalities of LV regional wall motion after normal reperfusion in patients with preoperative cardiogenic shock. 237 33

Balloon occlusion of a stenotic coronary artery during percutaneous coronary artery angioplasty provides a unique opportunity to study the effect of acute myocardial ischemia on left ventricular (LV) function. Simultaneous M-mode and 2-dimensional (2-D) echocardiograms and a 6-lead electrocardiogram were recorded during 20 episodes of coronary artery occlusion and release in 12 patients. No patient had previous myocardial infarction and all had normal LV function by angiography. All patients had isolated single coronary artery disease, with left anterior descending stenosis in 8 and right coronary stenosis in 4. In 18 of 20 episodes (90%), M-mode echocardiography during balloon occlusion revealed a significant (p less than 0.001) decrease in LV systolic, diastolic and percent systolic wall thickness; systolic excursion; systolic and diastolic endocardial velocities; and fractional shortening. These changes were observed in the area of the ventricular septum in patients with left anterior descending occlusion and posteroinferior wall in those with right coronary artery occlusion. Two-dimensional echocardiography revealed varying degrees of hypokinesia, akinesia and dyskinesia during balloon occlusion in 18 instances. The echocardiographic changes were observed within 15 to 20 seconds of balloon occlusion and resolved 10 to 20 seconds after balloon deflation. All patients who had echocardiographic changes during balloon occlusion also had concomitant electrocardiographic (ECG) ST-segment elevation, whereas 2 patients with normal LV function had no ECG changes. Both of these patients had profuse collateral blood supply to the stenotic coronary artery. The echocardiographic and ECG abnormalities increased proportionately to the length of balloon occlusion. This study confirms previous animal and recent human studies of transient LV dysfunction during coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Echocardiographic evaluation of left ventricular function during coronary artery angioplasty. 293 68

A 65-year-old man with unstable angina had a critical left anterior descending coronary artery stenosis which progressed to total occlusion, without evidence of acute myocardial infarction. Thallium imaging revealed defects in the distribution of the left anterior descending coronary artery on exercise and redistribution, 4 h later. 99mTc radionuclide angiography showed a fall in left ventricular ejection fraction on exercise, and contrast cineangiography showed an extensive area of akinesia. Percutaneous transluminal coronary angioplasty was successful without any complications. Repeat radionuclide studies demonstrated improvement of both myocardial perfusion and function. Angiography at 1 year showed normal left ventricular contraction and no evidence of recurrent stenosis. The patient is free of angina, on no medication 2 years after angioplasty. This case illustrates the feasibility of myocardial salvage by elective coronary angioplasty in patients with unstable angina total coronary occlusion.
 ...
PMID:Myocardial salvage following elective angioplasty for total coronary occlusion. 296 94

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)
 ...
PMID:Sequence of mechanical, electrocardiographic and clinical effects of repeated coronary artery occlusion in human beings: echocardiographic observations during coronary angioplasty. 315 58

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

Experimental animal investigations have shown that already after a few seconds of occlusion of a coronary artery a reduction in the systolic myocardial shortening and wall thickening takes place in the corresponding supply area. Following 1-2 minutes of ischemia systolic expansion occurs. Wall-thickness increase and myocardial shortening then take place during the isovolumetric relaxation phase. When at least 25% of the myocardium of the left ventricle becomes acutely ischemic the end-diastolic pressure and end-diastolic volume increase. As a rule an augmentation of myocardial contraction appears in the non-ischemic section of myocardium, which in part takes place through the Frank-Starling mechanism. With a gradual reduction of the coronary inflow, and a decline in the wall thickening of c. 50% of the control value, a significant reduction in blood flow took place only in the innermost quarter of the ventricular wall. With akinesia of the ischemic area, no reduction of the blood flow could be determined in the subepicardial region. Only with the occurrence of dyskinetic wall motion was a transmural reduction of blood flow effected. The ischemic contraction disturbances are fully reversible if coronary occlusion last only a few minutes. With a 15 minute occlusion the recovery time of the myocardial function can require several days (postischemic "stunned myocardium"). The first myocardial necroses occur after 20 minutes of ischemia, and after 3-6 hours of ischemia the infarction is complete.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Hemodynamics in ischemia. Systolic phase]. 633 23

We evaluated the effects of antecedent anginal episodes and coronary artery stenosis on left ventricular function during coronary occlusion and the role of collateral filling in 33 patients with angina pectoris who underwent angioplasty. Wall motion abnormalities were investigated by echocardiography and classified into hypokinesia and akinesia. Collateral filling during angioplasty was evaluated by using a second artery catheter. Akinesia was observed as follows: 24% of the patients had > 30 anginal episodes, 38% had 5 to 30, and 87% of the patients had < 5 (p < 0.01); 12% of patients had a lesion of 99%, 47% had a lesion of 90%, and 83% had a lesion of 75% (p < 0.05). Akinesia was observed in none of the patients with grade 3 collaterals, 57% with grade 2, and 67% with grade 1 or 0 (p < 0.01). These observations suggest that the patients with antecedent frequent anginal episodes and severe coronary stenosis have less left ventricular dysfunction during coronary occlusion. This finding may be the result of more extensive collateral development.
 ...
PMID:Effects of antecedent anginal episodes and coronary artery stenosis on left ventricular function during coronary occlusion. 763 2


1 2 Next >>