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Biomedical subjects

J M Hagar

Publications and source records attributed to J M Hagar.

9 recordsLinked to original sources
PubMed1998

Detecting exercise-induced ischemia in left bundle branch block using the electrocardiogram.

We compared 12-lead electrocardiographic changes during exercise in 41 patients with left bundle branch block; 7 were nonischemic and 34 had coronary artery obstruction > or =70% as detected by angiogram. ST depression of > or =0.5 mm from baseline when measured at the J point in leads II and AVF (p=0.004) and an increase of R-wave amplitude in lead II (p=0.05) significantly identified ischemia.

Bundle-Branch Block↗
PubMed1996

Incidence of perioperative myocardial ischemia in TURP patients.

STUDY OBJECTIVE: To determine the incidence of new episodes of myocardial ischemia in patients undergoing transurethral resection of the prostate (TURP). DESIGN: Prospective, nonrandomized study. SETTING: Veterans Administration medical center. PATIENTS: 39 patients undergoing elective TURP. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Myocardial ischemia was detected with a 3-channel ambulatory ECG recorded. The ambulatory ECG recorder was applied preoperatively and removed when the patient left the recovery room. New myocardial ischemia was defined as a 1 mm or greater ST depression or a 2 mm or greater ST elevation from baseline, lasting for 1 minute or longer in at least one lead at the J point plus 60 msec unless this point fell within the T wave, in which case the J point 40 msec or greater was used. ST changes consistent with myocardial ischemia were confirmed by a cardiologist blinded to the patient's clinical course. Seven of 39 TURP patients (18%) had ST segment changes indicative of new myocardial ischemia. These seven patients had more prostate tissue resected and more blood loss than the 32 patients who did not have any myocardial ischemia (p < 0.05). CONCLUSIONS: Patients undergoing TURP have an 18% incidence of myocardial ischemia. Patients undergoing TURP with more prostate tissue resected and greater blood loss are at increased risk for perioperative myocardial ischemia.

Aged↗
PubMed1994

Endogenous endothelin-1 impairs endothelium-dependent relaxation after myocardial ischemia and reperfusion.

Endothelin (ET)-1 is produced in response to myocardial ischemia and reperfusion. It is a potent constrictor of coronary resistance vessels and may therefore contribute to myocardial injury and postischemic microvascular dysfunction. Isolated buffer-perfused rabbit hearts, under conditions of constant flow and isovolumic contraction, underwent 60 min of global ischemia and 60 min of reperfusion after pretreatment with selective ETA receptor antagonist BQ-123 (10(-7) M) in perfusate, exogenous ET-1 (10(-11) M), or control. Release of ET increased significantly at 20 and 60 min of reperfusion. BQ-123 did not enhance the recovery of left ventricular developed pressure or coronary perfusion pressure, whereas exogenous ET tended to worsen them. Cumulative creatine kinase release over 20 min of reperfusion did not differ significantly between groups. Maximum endothelium-dependent dilation to acetylcholine (ACh) was initially 62 +/- 6, 71 +/- 6, and 63 +/- 8% (SE) of U-46619-induced preconstriction in control, BQ-123-, and ET-treated hearts. At 20 min of reperfusion it was 37 +/- 5, 73 +/- 9, and 22 +/- 5%, and at 60 min of reperfusion it was 35 +/- 7, 79 +/- 6, and 22 +/- 3% (P < 0.001 for BQ-123 vs. control at 20 min and P < 0.0001 at 60 min). Endothelium-independent dilation to nitroglycerin was unaltered by ischemia and reperfusion. Neither BQ-123 alone nor a 1-h infusion of ET (10(-10) M) altered the response to ACh in nonischemic hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of amlodipine on myocardial infarction, infarct expansion, and ventricular geometry in the rat.

Infarct expansion remains an important sequela of myocardial infarction. Both angiotensin converting enzyme inhibitors and intravenous nitrates reduce early infarct expansion in humans. This is believed to be caused by the reduction in left ventricular systolic wall stress that results from the arteriolar vasodilatation they produce. Patients are frequently already receiving calcium channel blockers at the time of infarction or these drugs are sometimes administered in the perimyocardial infarction period. The calcium blockers of the dihydropyridine class might be expected to modify infarct expansion. However, their effect on this process has not been studied. We therefore evaluated the effect of early treatment with the calcium blocker amlodipine, a potent arteriolar vasodilator with minimal negative inotropic properties, on chronic myocardial infarction in the rat. Permanent left coronary occlusion was created after pretreatment with amlodipine, 0.25 mg/kg (low dose) or 1.0 mg/kg (high dose), or placebo, intravenously twice a day, and continued for 7 days after infarction. Hearts (n = 50) were perfusion fixed 21 days after infarction and analyzed for infarct extent, scar thickness, left ventricular shape and size, and expansion index. Both doses decreased mean blood pressure (119 +/- 3 to 99 +/- 5 mm Hg low dose, p = 0.004; 110 +/- 5 to 84 +/- 4 mm Hg high dose, p = 0.0003), with reflex tachycardia only after the high dose (heart rate 395 +/- 9 to 434 +/- 11, p = 0.001). Infarct extent was equal in the three groups (39 +/- 2%, 41 +/- 2%, and 41 +/- 3% of left ventricular circumference for control, low, and high doses, respectively). The three groups did not differ significantly with regard to left ventricular cavity cross-sectional area (80 +/- 4, 77 +/- 3, and 87 +/- 3 mm2, control, low, and high doses, respectively; p = 0.07 high dose vs control), mean scar thickness (0.74 +/- 0.06, 0.73 +/- 0.05, and 0.65 +/- 0.06 mm, control, low, and high doses, respectively; p = NS), and expansion index (1.52 +/- 0.10, 1.58 +/- 0.12, and 1.95 +/- 0.19, control, low, and high doses, respectively; p = 0.08 high dose vs control). In the subgroup with larger infarcts (infarct extent greater than 0.39 of left ventricle), the expansion index was higher in the high-dose group (2.37 +/- 0.23 vs 1.64 +/- 0.17 control; p = 0.04). In this model, treatment with amlodipine does not limit infarct extent or reduce early infarct expansion and left ventricular dilatation, even when initiated before infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Amlodipine↗
PubMed1991

Chagas' heart disease in the United States.

BACKGROUND AND METHODS: Chagas' heart disease is believed to be rare in the United States, although many persons from countries where the disease is endemic reside here. We performed a retrospective case review and prospective follow-up of 25 patients with Chagas' heart disease and no obstructive coronary artery disease on angiography. RESULTS: The patients mainly presented with symptomatic atrioventricular block, congestive heart failure, anginal chest pain, sudden death averted by resuscitation, or sustained ventricular tachycardia. Of the 25 patients, 18 had been treated for coronary artery disease or idiopathic dilated cardiomyopathy for up to 108 months before the diagnosis of Chagas' disease was considered. The electrocardiograms frequently suggested coronary artery disease. Six of the seven patients who had exercise thallium-perfusion scans had abnormalities suggesting ischemia or infarction. A left ventricular aneurysm was found in 14 of the 25 patients, segmental akinesia or hypokinesia in 5, and diffuse hypokinesia in 3. Programmed ventricular stimulation performed in 13 patients induced sustained ventricular tachycardia in 9 and nonsustained ventricular tachycardia in 2. Actuarial survival (mean +/- SE) after four years for the entire group was 56 +/- 12 percent; it was 32 +/- 16 percent among those with global left ventricular dysfunction, and 78 +/- 14 percent among those without such dysfunction (P = 0.03). Only patients with left ventricular dysfunction or an aneurysm died (four-year survival, 45 +/- 14 percent, as compared with 100 percent for the remaining patients; P = 0.0002). Heart failure and left ventricular aneurysm or dysfunction were the only independent predictors of death. Nine patients required permanent pacemakers. CONCLUSIONS: In the United States, Chagas' heart disease commonly mimics coronary artery disease or idiopathic dilated cardiomyopathy. The prognosis is poor for patients with heart failure or left ventricular aneurysm or dysfunction. The disease may be underdiagnosed in the United States.

Chagas Cardiomyopathy↗
PubMed1991

Effect of preconditioning ischemia on reperfusion arrhythmias after coronary artery occlusion and reperfusion in the rat.

Severe arrhythmias occur predictably on reperfusion after 5 minutes of coronary occlusion in the rat. There is little data available on whether ischemic preconditioning (PC) of hearts can reduce the incidence of such arrhythmias. The effect of PC (three cycles of 2 minutes of coronary occlusion and 5 minutes of reperfusion) on development of arrhythmias after a subsequent 5-minute coronary artery occlusion and reperfusion was studied. Rats (n = 16 each group) underwent 5-minute occlusion and reperfusion alone or preceded by PC; arrhythmias were monitored during ischemia and for 10 minutes of reperfusion, and biopsies were taken for creatine phosphate and adenosine triphosphate in ischemic and nonischemic zones of the left ventricle. PC reduced the incidence of ventricular tachycardia (VT) during occlusion (81% control versus 13% PC, p less than 0.001). On subsequent reperfusion, ventricular fibrillation (VF) developed in zero PC animals versus 13 (81%) of controls (p less than 0.001), and irreversible VF in zero of PC versus seven (44%) of controls (p = 0.007). VT occurred in four (25%) of PC versus all (100%) of controls (p less than 0.001). PC reduced mean duration of VT plus VF from 320 +/- 54 to 5 +/- 1 seconds (p less than 0.001) and delayed arrhythmia onset from 8 +/- 2 to 85 +/- 35 seconds after reperfusion. There was no difference in creatine phosphate levels in the ischemic zone at the end of reperfusion in PC animals compared with controls without irreversible VF (16.2 +/- 4.1 versus 15.5 +/- 3.9 nmol/mg protein, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

Lack of significant effects of superoxide dismutase and catalase on development of reperfusion arrhythmias.

It has been reported that agents having the ability to scavenge oxygen-derived free radicals reduce the severity of ventricular arrhythmias that occur after brief coronary occlusion and reperfusion. Superoxide dismutase plus catalase (SOD + CAT) or placebo was administered in a blinded randomized fashion prior to coronary occlusion in rats (n = 25 each group) undergoing a 5-min left coronary occlusion followed by 15 min of reperfusion. During reperfusion, ventricular tachycardia (VT) developed in 96% of animals in both groups. Reperfusion ventricular fibrillation (VF) developed in 60% of the placebo group vs 56% in the SOD + CAT group (p = 1.0). Irreversible VF occurred in 40% of the placebo group vs 20% in the SOD + CAT group (p = 0.22). Atrioventricular block occurred in 12% of placebo and 4% of SOD + CAT animals (p = 0.61). There were no significant difference between groups in duration of VT (85 +/- 15 s (mean +/- SEM) placebo vs 81 +/- 14 s SOD + CAT, p = 0.81), total duration of VT plus VF (391 +/- 76 s placebo vs 256 +/- 64 SOD + CAT, p = 0.45) or numbers of single ventricular ectopic beats (65 +/- 15 placebo vs 97 +/- 18 SOD + CAT, p = 0.18). Heart rate at reperfusion was slightly higher in control than SOD + CAT animals (340 +/- 33 vs 319 +/- 32, p = 0.02). Risk zone size, determined by Monastral blue injection, was equal in both groups (34 +/- 2% of ventricular mass). The occurrence of reperfusion VF in this model could not be predicted by heart rate at reperfusion (331 +/- 33 VF animlas vs 328 +/- 36 no VF, p = 0.77), or by risk zone size (34 +/- 2%, VF and no VF groups).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Quantitative two-dimensional echocardiographic assessment of regional wall motion during transient ischemia and reperfusion in the rat.

Nonlethal myocardial ischemia produces profound and long-lasting effects on regional ventricular function and metabolism (myocardial stunning) and protects against myocardial infarction from subsequent prolonged ischemia (ischemic preconditioning). Two-dimensional echocardiography (2DE) is an essential tool for quantitative analysis of regional and global left ventricular (LV) function during myocardial ischemia and reperfusion and the study of these phenomena. However, the inability to perform 2DE in the open-chest rat heart has seriously limited the use of this model. To investigate the effect of transient coronary occlusion on segmental wall motion and LV geometry, we employed a 20 MHz intravascular ultrasound catheter placed on the epicardial surface of the rat heart (n = 15) to yield 2DE images suitable for quantitative analysis. Three 2-minute left coronary occlusions were made, separated by 5 minutes of reperfusion, with imaging during occlusion and at 5 and 60 minutes of reperfusion. Ischemic and nonischemic wall thicknesses, LV cross-sectional area, estimated LV volume, and the fractional changes of these parameters were measured. In eight animals these values were also compared with necropsy measurements of wall thickness, LV cross-sectional area, and volume. LV and right ventricular structures were well visualized in short-axis cross-sectional images in all animals, and images suitable for quantitative analysis were obtained in 92% of the periods. Coronary occlusion caused immediate, marked LV cavitary expansion, which rapidly returned to normal by 5 minutes of reperfusion. Active systolic thickening of the anterior wall at baseline (47% +/- 3%) became passive thinning during occlusion (-6% +/- 2%) and recovered partially, to 30% +/- 3% at 5 minutes of reperfusion and 42% +/- 4% at 60 minutes (p < 0.0005 at 5 minutes of reperfusion vs baseline; p not significant at 60 minutes). Recovery of thickening after 5 minutes of reperfusion was not different after the first versus third occlusion (23% +/- 4% vs 30% +/- 3%; p = 0.19). Measurements made by 2DE correlated well with those made by necropsy, although wall thickness was slightly thicker by 2DE. We conclude that epicardial echocardiography with an intravascular ultrasound catheter provides quantifiable 2DE images in this model and yields accurate information on segmental wall thickening and ventricular geometry not available by other techniques. Left coronary occlusion in the rat is associated with marked global and segmental LV expansion, which rapidly reverses with reperfusion. Postischemic regional wall motion abnormalities are present after coronary occlusion as brief as 2 minutes and can be measured accurately. The effect of multiple brief occlusions is not cumulative.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗