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

The effect of lumbar epidural anesthesia on myocardial wall motion was compared in two groups of patients using precordial two-dimensional echocardiography (2DE). All patients were scheduled to undergo lower abdominal or peripheral surgery. Group 1 included five healthy ASA PS 1 subjects and group 2 included 10 patients with coronary artery disease (CAD). In all patients 12.5 ml of 2% lidocaine HCl was injected into the lumbar epidural space, and systolic and diastolic blood pressures, and heart rate were continuously monitored. 2DE evaluation was performed before and at 10, 20, 30, and 60 min (T10-T60) after epidural lidocaine injection. The left ventricular wall was divided into 16 segments for parasternal long-axis, short-axis and apical four-chamber views. The wall motion of each segment was graded on a scale from 1 (dyskinesia) to 6 (hyperkinesia), with 5 representing normal motion. A decrease in segmental wall motion greater than or equal to 2 grades was considered indicative of ischemia. Plasma lidocaine and catecholamine levels were measured before and 10, 20, and 60 min after epidural lidocaine injection. Peak plasma lidocaine levels in groups 1 and 2 were 2.79 +/- 1.06 micrograms/ml (mean +/- SD) and 2.58 +/- 1.48 micrograms/ml at 10 min, respectively (NS). Plasma epinephrine and norepinephrine levels were unchanged from baseline. Systolic pressures decreased significantly in group 2 from T10 to T60. Diastolic pressure decreased significantly in the same group from T20 to T60, and in group 1 only at T10. Mean arterial pressure decreased significantly in both groups at T30, without change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities in myocardial segmental wall motion during lumbar epidural anesthesia. 229 27

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

The early natural history of left anterior descending coronary artery occlusion was studied in 35 open-chest anesthetized dogs observed for 6 hours. Six control dogs underwent isolation of the left anterior descending without occlusion, 13 underwent isolated occlusion of the artery to simulate single-vessel disease, and 14 underwent occlusion of the left anterior descending and 50% stenosis of the circumflex coronary artery to simulate multivessel disease. Regional systolic shortening was measured by ultrasonic crystals. Control dogs had a mild fall in cardiac output (27%) and rise in aortic pressure (15 mm Hg). Ischemia produced immediate dyskinesia (-60% of control systolic shortening), and passive lengthening persisted for 6 hours. All dogs with only occlusion of the left anterior descending artery survived (0% mortality). They were less prone to ventricular fibrillation (46% versus 79%, p less than 0.05), developed compensatory hypercontractility of remote muscle (131% of control systolic shortening, p less than 0.05), mild energy and substrate depletion, and anaerobic metabolism (increased glucose-6-phosphate, p less than 0.05) despite maintenance of "normal" blood flow. In contrast, the early mortality rate was 57% (p less than 0.05) when 50% circumflex stenosis coexisted. Intractable ventricular fibrillation and/or cardiogenic shock caused the deaths. Remote muscle became progressively hypocontractile (61% of control systolic shortening, p less than 0.05), with progressive reduction in stroke work index (less than 0.5 gm-m/kg, p less than 0.05). Remote muscle showed moderate substrate and energy depletion (greater than 60% fall of adenosine triphosphate and creatine phosphate, 37% fall of glutamate) and more pronounced evidence of anaerobic metabolism (glucose-6-phosphate rose greater than 400%, p less than 0.05) despite normal blood flow. Mitochondrial ultrastructure and function remained intact in all hearts. These findings suggest that remote muscle is the principal determinant of mortality after an otherwise nonlethal ischemic event. Functional deterioration despite normal blood flow to remote muscle suggests either autoregulatory failure or substrate depletion as a cause of hypocontractility. The structural and functional integrity of mitochondria in ischemic and remote myocardium implies that salvage is possible despite hemodynamic deterioration and intractable ventricular fibrillation.
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PMID:Studies on prolonged acute regional ischemia. III. Early natural history of simulated single and multivessel disease with emphasis on remote myocardium. 277 Mar 19

Recovery of contractile function of myocardium stunned by a brief, transient period of regional ischemia is highly variable. In our experience, segment shortening (an index of regional systolic contractile function) assessed during the initial hours after a 15-minute period of coronary artery occlusion in anesthetized open-chest dogs ranged from -84 to +99% of normal preocclusion values. In this retrospective study, regression analysis was used to assess the effects of various parameters on segment shortening 2 hours after reperfusion. Parameters assessed included regional myocardial blood flow both during occlusion and after reperfusion, high-energy phosphate content of previously ischemic tissue, systemic hemodynamic parameters (heart rate, mean arterial pressure and double product), occluded bed size and segment shortening measured during coronary artery occlusion. Recovery of systolic contractile function was not influenced by the degree of ischemia during coronary artery occlusion, myocardial blood flow after reperfusion, high-energy phosphate content, hemodynamic parameters or occluded bed size (correlation coefficients, r, ranged from 0.001 to 0.37 [p = not significant]). Only the degree of dyskinesia/hypokinesia exhibited during coronary occlusion significantly and reliably predicted recovery of segment shortening measured 2 hours after reflow (r = 0.70, p less than 0.001). Thus, recovery of systolic contractile function in the anesthetized canine model of the stunned myocardium is determined primarily by the degree of dysfunction exhibited during the preceding period of ischemia.
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PMID:What factors predict recovery of contractile function in the canine model of the stunned myocardium? 278 68

Of 21 dogs undergoing ligation of the left anterior descending coronary artery and 50% stenosis of the left circumflex coronary artery, 15 developed intractable ventricular fibrillation and underwent 1 added hour of femoro-femoral bypass. Three hearts were removed after 1 hour on bypass without myocardial reperfusion for biochemical and mitochondrial analysis. After the 1 hour, five underwent unmodified blood reperfusion on bypass; seven underwent 1 hour of aortic clamping on vented bypass to simulate coronary artery bypass grafting with multidose blood cardioplegic reperfusion. Regional systolic shortening was measured with ultrasonic crystals and cardiac output was measured by thermodilution techniques. All six hearts with no ventricular fibrillation or with reversible ventricular fibrillation and hearts that were not reperfused developed cardiogenic shock (40% decrease in stroke work index, p less than 0.05) because of persistent left ventricular dyskinesia (-40% of systolic shortening, p less than 0.05) and progressive circumflex hypocontractility (48% systolic shortening, p less than 0.05) and showed extensive (68%) triphenyltetrazolium chloride nonstaining. Two dogs died of left ventricular power failure (33% mortality rate). In contrast, 11 of 12 dogs that were reperfused could be weaned from bypass (8% mortality rate). The four dogs surviving after unmodified blood reperfusion (20% mortality rate) showed severe residual left ventricular dysfunction (39% of control stroke work index, p less than 0.05), had equivocal recovery of anterior contractility (10% +/- 7% of systolic shortening), had marginal recovery of contractility in the remote myocardium (60% +/- 11% of systolic shortening), and had extensive triphenyltetrazolium chloride nonstaining (58%). Conversely, all seven dogs with intractable ventricular fibrillation undergoing controlled reperfusion after 4 hours of ischemia recovered normal stroke work index (91%), regained 23% of systolic shortening in the region supplied by the left anterior descending coronary artery (p less than 0.05), 125% of systolic shortening in the circumflex region (p less than 0.05), and showed only 25% triphenyltetrazolium chloride nonstaining (p less than 0.05). These results suggest aggressive treatment of intractable ventricular fibrillation after acute myocardial infarction by providing reperfusion on bypass can salvage hearts thought previously to be damaged irreversibly.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies on prolonged acute regional ischemia. IV. Aggressive surgical treatment for intractable ventricular fibrillation after acute myocardial infarction. 279 63

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

Patients with coronary artery disease (CAD) frequently have left ventricular (LV) wall motion abnormalities in the absence of symptoms. Thirty-one patients with such LV wall motion abnormalities in the absence of symptoms participated in a study of the response of these abnormalities to ascending doses of intravenous nitroglycerin (NTG). In a subgroup of 20 patients the relation between the location of LV wall motion abnormalities and the presence or absence of significant CAD (greater than or equal to 50% diameter reduction), in the vessel supplying the LV region, was assessed. Wall motion improved after intravenous NTG; the ejection fraction increased by 3.7% (mean p less than 0.05) and by 9.4% in the 19 patients who responded. There was no significant increase in heart rate; both LV systolic and end-diastolic pressures decreased minimally (12.5 and 3.5 mm Hg, respectively, p less than 0.05). The ejection fraction response was observed with NTG doses less than or equal to 200 micrograms and no dose-response relation was apparent. In the subgroup subjected to regional wall motion analysis, the presence of dyskinesia was significantly (p = 0.007) associated with the presence of important CAD in a vessel supplying that region. Further, the fact that wall motion improvement after NTG was significantly (p = 0.002) associated supports the concept that silent ischemia results in LV regional wall motion abnormalities, which can be reversed with low dose intravenous NTG.
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PMID:Left ventricular dyskinesia reversed by intravenous nitroglycerin: a manifestation of silent myocardial ischemia. 309 12

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

A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.
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PMID:Acute myocardial ischemia with prolonged left ventricular dyskinesia and mural thrombus formation in asymmetric septal hypertrophy. 334 53

Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last drug-induced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.
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PMID:Effect of repeated episodes of drug-induced ventricular dyskinesia on subsequent regional function in the dog: comparison with myocardial stunning produced by repeated coronary occlusions. 358 22


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