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)

In poorly perfused myocardium with resultant ischemic dysfunction, augmentation of contractility can, under certain conditions, be used to detect viable but ordinarily noncontracting muscle. Two methods of inotropic augmentation, pharmacologic inotropic stimulation and postextrasystolic potentiation (PESP), were studied in acutely ischemic canine myocardium with controlled coronary blood flow. A caliper length gauge to record segmental shortening and left ventricle pressure was used to construct pressure-length loops. Acute regional ischemia depressed segmental function: early segmental shortening decreased (-20 plus or minus 0.02% [SE]) and frequent dyskinesia occurred. Restoring coronary blood flow corrected segmental shortening to control levels. During acute regional ischemia, PESP consistently augmented segmental function (+49 plus or minus 0.03%) and abolished dyskinesia. Pharmacologic inotropic stimulation with isoproterenol or calcium administered into the coronary arteries did not produce a comparable improvement in segmental function (+9 plus or minus 0.05%). Although early shortening markedly increased with pharmacologic stimulation, there was no consistent change in total shortening, and the area of the pressure-length loop decreased. Due to late dyskinesia, there was a decrease in injection shortening. Systemically administered pharmacologic agents accentuated early dyskinesia but caused no consistent change in total shortening. Unlike PESP, pharmacologic agents either worsened segmental function or caused responses that were minimum and inconsistent; such responses clearly cannot be used to identify viable ischemic myocardium.
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PMID:Detection of latent function in acutely ischemic myocardium in the dog: comparison of pharmacologic inotropic stimulation and postextrasystolic potentiation. 4 92

50 patients, 20 without heart disease and 30 with coronary heart disease (CHD), were studied by kinetocardiography (KCG), before and after administration of isoproterenol (initial dose 2 microgram/min, maximum dose 6 microgram/min). In the control subjects the KCG was unaffected by the drug. In contrast, in most of the patients with CHD isoproterenol induced the appearance or the increase of paradoxical systolic bulges, which are regarded as the expression of ventricular dyskinesia resulting from isoproterenol-induced transient regional ischemia. This test is recommended as a valuable noninvasive method for the diagnosis of ischemic ventricular dyskinesia.
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PMID:The kinetocardiogram during the isoproterenol test for the assessment of coronary heart disease. 58 10

51 patients with coronary heart disease had exercise tests on a bicycle ergometer (86 +/- 32 watts). Compared to a normal control group, only 13 patients had normal contractile reserve (group 4.1). In 32 patients the increase in contractility during exercise was reduced (max dP/dt below 3200 mm Hg/s, group 4.2). Patients with reduced contractile reserve were graded according to the height of left ventricular enddiastolic pressure during exercise: In patients with grade 1, enddiastolic pressure was normal. In patients with grade 2, enddiastolic pressure increased between + 4 and + 15 mm Hg and in the patients with grade 3a a above + 15 mm Hg. Contractile and relaxation reserve decreased along with a rise in enddiastolic pressure and an increase in the complaints of the patients. Severe chest pain led to termination of exercise in patients of grade 3b. Enddiastolic pressure increased above + 15 mm Hg. During ischemia, peak-measured velocity of contractile elements (dP/dt/P) and the maximal rate of left ventricular pressure fall (min dP/dt) decreased. In conclusion, with increasing chest pain a decrease of contractile reserve was observed. Left ventricular enddiastolic pressure rose excessively. This has to be taken as a sign of myocardial failure due to ischemic dyskinesia and impeded relaxation.
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PMID:[Contractile and relaxation reserve of the left ventricle. IV. Patients with coronary heart disease (author's transl)]. 62 71

The patterns of regional contractile function were examined with ultrasonic crystals in "open-chest" anesthetized dogs. In normal myocardium, the base-line end-diastolic segment length (EDL) was 1.63 +/- 0.12 cm. and the mean systolic length (MSL) was 1.47 +/- 0.17 cm. Mean velocity of shortening over the first one third of systole (V1/3) was 15.9 +/- 2.3 mm. per second. Coronary occlusion induced regional ischemia with segmental dyskinesia (MSL = 1.84 +/- 0.12 cm). Reperfusion after 5 or 10 minutes of occlusion induced rapid recovery of contractile function that was independent of catecholamine release, as demonstrated in animals pretreated with 6-OH dopamine. After initial recovery, however, contractile function deteriorated. There were an increase in EDL (from 1.73 +/- 0.11 to 1.78 +/- 0.11; p less than 0.001) and the appearance of early systolic dyskinesia. V1/3 diminished from 5.6 +/- 4.6 to -6.6 +/- 2.5 mm. per second (p less than 0.005). Thus reperfusion damage, defined as late deterioration after recovery from brief periods of ischemia, may be partly distinct from ischemic damage per se. It is possible that the deterioration of myocardial function which accompanies reperfusion of previously ischemic myocardium may be a contributing factor in the transient myocardial dysfunction that is occasionally seen following cardiopulmonary bypass.
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PMID:Contractile damage from reperfusion after transient ischemia in the dog. 63 43

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79

Patients scheduled for vascular surgery are considered at risk for perioperative cardiac complications. Choice of anesthetic in such patients is guided by a desire not to adversely affect myocardial function. On the basis of data from laboratory studies, thoracic epidural anesthesia (TEA) has been advocated to prevent myocardial ischemia. The aim of this study was to assess whether TEA combined with general anesthesia has any effect on segmental wall motion (SWM) monitored by transesophageal echocardiography in these patients. Patients received alfentanil, midazolam, vecuronium, and 50% N2O in oxygen, and ventilation was controlled after orotracheal intubation; 12.5 mL of 2% lidocaine HCl was injected through an epidural catheter placed at T6-7 or T7-8. Hemodynamic measurements and transesophageal echocardiographic recordings were obtained before and 10, 20, 30, 40, and 60 min after lidocaine injection. Segmental wall motion was graded a posteriori by two independent experts on a predetermined scale (from 1 = normal to 5 = dyskinesia). A decrease greater than or equal to 2 grades was considered an SWM abnormality indicative of ischemia. Thoracic epidural anesthesia induced a decrease in systemic arterial blood pressure, heart rate, and cardiac index. The SWM score decreased slightly from 1.34 +/- 0.68 to 1.27 +/- 0.64 (mean +/- SD) (at 10 and 20 min, respectively) (P less than 0.05). Patients were a posteriori analyzed according to whether they had documented coronary artery disease or not. The SWM score before TEA was significantly higher in patients with documented coronary artery disease (1.51 +/- 0.88 vs 1.17 +/- 0.51, respectively; P less than 0.05) and did not change significantly after TEA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of thoracic epidural anesthesia combined with general anesthesia on segmental wall motion assessed by transesophageal echocardiography. 151 Feb 52

In patients with coronary artery disease and left ventricular impairment, the distinction between ventricular dysfunction due to myocardial fibrosis and postischemic, viable, although dys-synergic, myocardium has important clinical implications. Experimental studies have shown that dipyridamole can increase myocardial function in stunned segments, outlining a potential role of dipyridamole-induced functional recovery as an ultrasonic marker of myocardial viability. The aim of this study was to assess whether the increase of regional left ventricular function early during dipyridamole infusion in basally asynergic segments could identify viable myocardium recognized by rest injected, delayed (greater than 14 hours from tracer injection) thallium and (in a subset of patients) late functional recovery evaluated by a follow-up echocardiogram at rest. Twenty-two patients with angiographically documented coronary artery disease and regional dysfunction in resting conditions (average left ventricular ejection fraction 43 +/- 8%) were studied by echocardiography. All patients underwent a dipyridamole-echocardiographic test (up to 0.84 mg/kg over 10 minutes) and a delayed planar thallium study. A 13-segment model was used for both techniques. A score index ranging from 1 (normokinesia) to 4 (dyskinesia) was used for echocardiography. Thallium-201 activity was expressed in each segment as the percentage of maximal activity in the corresponding view. After dipyridamole, the wall motion score was assigned to each segment in resting conditions and at peak hyperkinesia before possible mechanical signs of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of viable myocardium by dipyridamole-induced improvement in regional left ventricular function assessed by echocardiography in myocardial infarction and comparison with thallium scintigraphy at rest. 151 18

To determine whether modulation of systolic ventricular interaction influences right ventricular performance during right heart ischemia, the effects of septal ischemia and inotropic stimulation were studied in 15 dogs in an open chest preparation. Right coronary branch occlusions led to right ventricular dilation and free wall dyskinesia, reversed septal curvature and reduced left ventricular diastolic volume. In systole, the septum thickened but bulged paradoxically into the right ventricle generating an active but depressed right ventricular systolic pressure (28.9 +/- 5.5 to 22.1 +/- 4.5 mm Hg), with associated decreases in right ventricular stroke work (5.66 +/- 0.94 to 1.92 +/- 0.53 g.m/m2) and left ventricular systolic pressure (123 +/- 11 to 80 +/- 10 mm Hg). Septal ischemia induced systolic septal thinning, left ventricular dilation and decreased left ventricular systolic pressure (80 +/- 10 to 55 +/- 10 mm Hg) and stroke work. Although the extent of paradoxic septal displacement increased, there were further decrements in right ventricular systolic pressure (22.1 +/- 4.5 to 18.7 +/- 4.3 mm Hg) and stroke work (1.92 +/- 0.53 to 0.7 +/- 0.2 g.m/m2). Dopamine infusion augmented left ventricular free wall contraction and increased left ventricular systolic pressure (55 +/- 10 to 172 +/- 17 mm Hg) and stroke work. Although systolic septal thinning persisted, the extent of paradoxic septal displacement increased strikingly and, despite continued right ventricular free wall dyskinesia, right ventricular systolic pressure increased (18.7 +/- 4.3 to 39.6 +/- 6.2 mm Hg) as did right ventricular stroke work (0.7 +/- 0.2 to 7 +/- 1.6 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of left ventricular function and systolic ventricular interaction to right ventricular performance during acute right heart ischemia. 153 32

The influence of intravenous thrombolysis on both prevalence of ventricular late potentials and incidence of late arrhythmic events was evaluated in 174 consecutive patients surviving a first acute myocardial infarction; 106 patients (61%) received thrombolysis (group A) and 68 (34%) had conventional therapy (group B). In group A, 18 patients (17%) had late potentials compared with 23 (34%) in group B (p less than 0.05); mean left ventricular ejection fraction was not different (0.50 +/- 0.09 vs 0.50 +/- 0.10; p = not significant [NS]). Of 63 patients who underwent coronary arteriography because of postinfarction ischemia, 28 (44%) had a closed infarct-related artery; of these, 11 (39%) had late potentials compared with 3 of 35 (9%) with a patent artery (p less than 0.01). Mean left ventricular ejection fraction was not significantly different between the 2 groups (0.49 +/- 0.09 vs 0.53 +/- 0.09; p = NS). At a mean follow-up of 14 +/- 8 months, 8 of 161 patients (5%) had a late arrhythmic event; 6 of 8 (75%) with and 28 of 153 (18%) without events had late potentials (p less than 0.001). In group A, 4 of 99 patients (4%) had events compared with 4 of 62 (6%) in group B (p = NS, relative risk 1.6). Of 24 patients with anterior wall AMI and left ventricular dyskinesia, 6 events occurred. In this group of patients, a higher rate of events was observed (25%); 3 of 16 (19%) treated with thrombolysis had an event compared with 3 of 8 (37%) treated conventionally (p = NS, relative risk 2.6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of thrombolysis on signal-averaged electrocardiogram and late arrhythmic events after acute myocardial infarction. 155 14

The mechanism and temporal manifestation of functional mitral regurgitation after acute myocardial ischemia were examined in eight dogs. Regional ischemia was produced by selective microembolization of the left circumflex coronary artery. Mitral regurgitation and regional left ventricular wall motion abnormalities were evaluated with use of Doppler color flow mapping and two-dimensional echocardiography, respectively. Measurements were made at baseline (before embolization) and were repeated at 30 min and 3 weeks after embolization. Mitral regurgitation developed in all dogs 30 min after embolization and completely subsided 3 weeks later. There was no evidence of mitral valve prolapse, mitral anulus dilation or left ventricular segmental dyskinesia at any time during the study. Regional wall motion analysis showed only hypokinesia of the left ventricular segment overlying the papillary muscle at 30 min with subsequent normalization of the segment at 3 weeks. Mitral regurgitation was accompanied by an increase of the end-systolic distance between the mitral anulus plane and the point of coaptation of the mitral leaflets. This distance was 0.5 +/- 0.1 cm at baseline, increased to 0.9 +/- 0.1 cm 30 min after the embolization (p less than 0.001) and returned to near baseline (0.6 +/- 0.1 cm) 3 weeks after the embolization. These data indicate that mitral valve prolapse, mitral anulus dilation and regional left ventricular dyskinesia are not necessary conditions for the development of functional mitral regurgitation after acute myocardial ischemia. Instead, hypokinesia of the ventricular segment overlying the papillary muscle and leading to retraction of the mitral leaflets toward the apex appears to be a sufficient condition for incomplete leaflet coaptation.
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PMID:Mechanism of functional mitral regurgitation during acute myocardial ischemia. 155 1


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