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Biomedical subjects

H Hammerman

Publications and source records attributed to H Hammerman.

34 records · Page 2Linked to original sources
PubMed1984

Morphologic and functional effects of piroxicam on myocardial scar formation after coronary occlusion in dogs.

To determine whether piroxicam, a widely used, long-acting anti-inflammatory agent, causes scar thinning after acute myocardial infarction (MI), MI was produced in 16 anesthetized, open-chest dogs by ligation of the proximal left anterior descending coronary artery. The dogs were randomized into 2 groups and treated in a blinded fashion, 8 with piroxicam, 1 mg/kg i.v. at 15 minutes and at 3 hours after ligation (Group 1) and 8 with saline solution (Group 2). Two-dimensional echocardiograms were performed 7 days and 6 weeks after ligation. At 6 weeks, the dogs were killed and the hearts examined. Scar thickness was 7.1 +/- 0.3 mm in control dogs and 5.2 +/- 0.4 mm in piroxicam-treated dogs (p less than 0.01). The ratio of scar thickness to noninfarcted wall thickness was 0.87 +/- 0.03 (mean +/- standard error of the mean) in the control group, and was significantly lower (0.62 +/- 0.04) in the piroxicam-treated group (p less than 0.001). Regional function, expressed as the percent change in the area of the left ventricular cavity (% delta A) from short-axis 2-dimensional echocardiograms, was 42 +/- 3% 7 days after occlusion in the control group and was not significantly different in the treated group (34 +/- 5%). At the end of 6 weeks % delta A had improved in the piroxicam-treated group to 44 +/- 3% (p less than 0.05 compared with the value after 7 days), and was similar to % delta A of the control group at 6 weeks (43 +/- 3%). Thus, clinical doses of piroxicam administered early after MI caused moderate scar thinning, which was not associated with impairment of regional left ventricular function 6 weeks later.

Animals↗
PubMed1984

Angiography of azygos continuation of inferior vena cava in situs ambiguus with left isomerism (polysplenia syndrome).

We have in our records 11 patients with situs ambiguus and left isomerism (polysplenia). Ten had an interruption of the inferior vena cava (IVC) with azygos continuation; in eight cases the continuation was to the left superior vena cava (LSVC), in one case to the right superior vena cava (RSVC) and in one case to both the LSVC and RSVC. Two patients underwent surgical correction by a baffle procedure of the functioning single atrium. The angiographic confirmation of the azygos system anatomy is important in planning the surgical correction of patients with left isomerism. Clinically, given the same heart defects with normal pressures, the right-sided drainage is probably more favorable, producing less peripheral desaturation.

Azygos Vein↗
PubMed1984

Enhancement of salvage of reperfused myocardium by early beta-adrenergic blockade (timolol).

Although reperfusion of severely ischemic myocardium with thrombolytic agents or surgery has shown reduction in infarct size, the time after coronary occlusion during which reperfusion can salvage ischemic myocardium is limited. To determine whether beta-adrenergic blockade could enhance the salvage of ischemic myocardium by reperfusion, the left anterior descending coronary artery was occluded in 18 anesthetized dogs. An in vivo area at risk was determined by injecting technetium-99m-labeled albumin microspheres into the left atrium 5 minutes after occlusion and carrying out radioautography to define the poorly perfused tissue. Fifteen minutes after coronary occlusion, the dogs were randomized either to a control (saline-treated) group (n = 8) or to a timolol-treated group (n = 10). Timolol was administered until a decrease of 20% in heart rate or blood pressure occurred (mean total dose = 0.85 +/- 0.22 mg/kg +/- standard error of the mean). Coronary occlusion was maintained for 3 hours and was followed by 3 hours of reperfusion in both groups. At the end of 6 hours, infarct size was defined by triphenyltetrazolium chloride staining and masses of infarct and risk were calculated. Percent left ventricular mass at risk was similar for both groups (control = 20.9 +/- 2.4%, timolol-treated = 23.7 +/- 2.1%, p = not significant). Mass of necrosis/mass at risk was significantly smaller in the timolol-treated reperfusion group (27.3 +/- 2.7%) versus saline reperfusion alone (46.5 +/- 5.6%) (p less than 0.005). Thus, beta-adrenergic blockade administered early after coronary occlusion results in substantial enhancement of the salvage achieved by reperfusion alone.

Animals↗
PubMed1984

Drug-induced expansion of infarct: morphologic and functional correlations.

It has been established that glucocorticoids and several nonsteroidal antiinflammatory drugs, when administered early after coronary occlusion, interfere with myocardial scar formation. To determine whether this action is associated with expansion of myocardial infarct during the first week of coronary occlusion and whether expansion affects ventricular function, the effects of indomethacin on the left ventricle in the early phase of infarction were studied. In a blinded randomized study, experimental myocardial infarction was produced in 17 open-chest dogs by ligation of the proximal left anterior descending coronary artery; the treated group (n = 8) received 10 mg/kg iv indomethacin at 15 min and 3 hr after occlusion, and the control group (n = 9) received saline. After 7 days, regional function expressed as percent change of area (% delta A) of the left ventricular cavity was calculated from short-axis two-dimensional echocardiograms at the level of the infarct, the animals were killed, and their hearts were examined. The ratio of infarct thickness to noninfarcted wall thickness was 1.20 +/- 0.08 (mean +/- SEM) in the control group, and the ratio was lower in the indomethacin group, 0.96 +/- 0.04 (p less than .025). An expansion index of myocardial infarction was calculated as previously described and was 1.02 +/- 0.04 in the control group vs 1.29 +/- 0.06 in the indomethacin group (p less than .005). In eight dogs (six control and two treated) without expansion (expansion index less than 1.09), regional function expressed as % delta A was 46.8 +/- 2.6% (SEM), and in nine dogs (six treated and three control) with expansion, % delta A was significantly lower, 28.7 +/- 4.0% (p less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Scar thinning due to ibuprofen administration after experimental myocardial infarction.

Although much attention has been directed toward interventions which reduce myocardial infarct size, the effect of such agents on the healing phase of myocardial infarction is not well understood. The present study examines the effect of the nonsteroidal anti-inflammatory agent ibuprofen, previously demonstrated to be able to reduce infarct size, and of aspirin on the healing of experimentally produced myocardial infarcts. Thirty-nine anesthetized, open-chest dogs were subjected to proximal left anterior descending coronary artery occlusions for 6 weeks. Four groups of dogs were studied: (1) a control (untreated) group: (2) ibuprofen, 12.5 mg/kg intravenously 15 minutes and 6, 12, 18, and 24 hours after occlusion (high dose); (3) ibuprofen, 12.5 mg/kg intravenously 15 minutes and 3 hours after occlusion (low dose); (4) aspirin, 30 mg/kg intravenously 15 minutes and 3 hours after occlusion. The average thickness of the transmural scar and of the noninfarcted left ventricular wall was determined from multiple measurements of formalin-fixed left ventricular slices. The ratio of transmural scar to noninfarcted wall thickness was determined. In control animals the ratio was 0.87 with only 1 of 15 animals having a ratio less than 0.60. High-dose ibuprofen-treated animals had an average ratio of 0.59 (difference not significant [NS] compared with control values), with 6 of 9 animals having a ratio less than 0.60 (p less than 0.02 compared with control values). Low-dose ibuprofen-treated animals had an average ratio of 0.66 (p less than 0.05 compared with control values), with 4 of 8 animals having a ratio less than 0.60 (p = NS compared with control values). In the aspirin-treated animals, the ratio was 0.88 (p = NS compared with control values), with 0 of 7 animals having a ratio less than 0.60 (p = NS compared with control values). Although 1 of 22 animals had ratios less than 0.60 in the control and aspirin groups, 10 of 17 had ratios less than 0.60 in the ibuprofen-treated groups (p less than 0.001). Scars in treated animals did not differ from those in control animals histologically or by analysis of hydroxyproline content per unit weight. Thus, ibuprofen, a nonsteroidal anti-inflammatory agent which reduces infarct size, is shown to increase the incidence of scar thinning after myocardial infarction.

Animals↗
PubMed1983

Short-term exercise has a prolonged effect on scar formation after experimental acute myocardial infarction.

The effect of early short-term exercise on late scar formation of myocardial infarction is unknown. Therefore, rats anesthetized with ether underwent proximal left coronary artery occlusion. Infarct extent was assessed 24 hours later by electrocardiographic criteria (QRS morphology). Immediately after electrocardiography, the rats were divided into two groups. Group 1 rats (n = 8) were subjected to daily graded swimming (up to 45 minutes a day) starting 24 hours after coronary occlusion for a total of 7 days followed by 2 weeks of nonswimming. Group 2 rats (n = 7) served as a control group and were not subjected to swimming. Twenty-one days after coronary occlusion, the rats were anesthetized, their heart excised and wall thickness determined histologically. Noninfarcted septal wall thickness was similar in both Groups 1 and 2. A ratio for transmural infarcts was obtained from multiple measurements by dividing scar thickness by noninfarcted septal wall thickness. Ratio of scar thickness divided by noninfarcted wall thickness for the control (nonswimming) group was 0.48 +/- 0.05 (mean +/- standard error of the mean); however, in the exercise (swimming) group, there was marked scar thinning with a ratio of 0.25 +/- 0.02 (mean +/- standard error of the mean, p less than 0.001). Infarct extent assessed by planimetry as percent of left ventricular slices was similar in both groups. Thus, early short-term swimming exercise during the first week after experimental myocardial infarction even when followed by 2 weeks without swimming, has long-lasting effects on scar formation.

Animals↗
PubMed1983

Indomethacin-induced scar thinning after experimental myocardial infarction.

We investigated the effect of indomethacin, a widely used nonsteroidal antiinflammatory drug, on the healing of myocardial infarction (MI). Experimental MI was produced in anesthetized, open-chest dogs by occluding the left anterior descending coronary artery. Ten dogs received indomethacin, 10 mg/kg i.v., and 11 received saline, 15 minutes and 3 hours after occlusion. After 6 weeks, the dogs were killed and their hearts were subjected to morphologic and biochemical analysis. The average thickness of the transmural scar and the noninfarcted left ventricular wall was measured at multiple sites in formalin-fixed left ventricular slices and the ratio of the thickness of the transmural scar to the noninfarcted wall determined. The average thickness of the noninfarcted wall was 8.80 +/- 0.19 mm (mean +/- SEM) in the control group and 8.44 +/- 0.26 mm in the indomethacin group (NS). The scar thickness was 7.24 +/- 0.64 mm in the control group and 3.56 +/- 0.40 mm in the indomethacin group (p less than 0.001). The ratio of scar to noninfarcted wall thickness was 0.83 +/- 0.07 in the control group and 0.43 +/- 0.04 in the indomethacin group (p less than 0.001). Scars in treated dogs did not differ from controls either by light microscopic histologic analysis or by analysis of hydroxyproline content per unit weight. We conclude that indomethacin results in marked scar thinning when given early after experimental MI.

Animals↗
PubMed1982

Congenital prolongation of Q-T interval: a family study of three generations.

Three generations of a family with the Romano-Ward syndrome are described. Of all the affected members, only 1 was symptomatic, experiencing episodes of syncope proven to be due to polymorphous ventricular tachycardia (PMVT) induced by chlorimipramine treatment for depression. During treatment of an episode of PMVT with lidocaine, the patient developed the 'torsade de pointes' variant of ventricular tachycardia, which progressed to ventricular fibrillation and was successfully treated with electroversion. The hazards of treating these patients with commonly used drugs, the possible etiologies for the Romano-Ward syndrome and its mode of inheritance are discussed.

Aged↗
PubMed1980

The heart in acromegaly: correlation of echocardiographic and clinical findings.

Echocardiography was performed in 14 patients with acromegaly in order to characterize cardiac involvement in this disease. The left ventricle was enlarged or hypertrophic in 10 patients (71%): the fraction of myocardial shortening, an index of left ventricular contractility, was normal in all but one; and 10 patients had a reduced mitral EF slope, suggesting that their left ventricular compliance was reduced. Cardiac disease was not suspected clinically as most patients had normal clinical, ECG and X-ray examinations of the heart. Left ventricular hypertrophy occurred in the absence of hypertension, diabetes or evidence of coronary artery disease. There was a positive correlation between left ventricular wall thickness and duration of acromegaly but not between the former and growth hormone levels after fasting, suggesting that ther must be prolonged hypersecretion of growth hormone, and not simply high levels, before cardiac hypertrophy develops.

Acromegaly↗
PubMed1978

Contribuiton of M-mode echocardiography to cardiac diagnosis. An assessment in 1,000 successive patients.

The contribution of M-mode echocardiography to cardiac diagnosis was evaluated in a series of 1,000 successive patients. Among subjects in whom a presumptive clinical diagnosis had been made, echocardiography demonstrated totally unexpected findings in 10 per cent, supported the clinical diagnosis in 50 per cent and was entirely within normal limits in 19 per cent. Among patients with evidence of heart disease but no firm clinical diagnosis, echocardiography established the diagnosis in 23 per cent, including 20 per cent of all patients referred for evaluation of chest pain or arrhythmia of unclear etiology. "Missed" clinical diagnosis frequently involved patients with mitral valve prolapse, congestive cardiomyopathy, pericardial disease or asymmetrical septal hypertrophy of the heart. This study quantifies the amount of independent information contributed by echocardiography to cardiac diagnosis and demonstrates that this technic provides data of important clinical relevance in a surprisingly large number of cardiac patients.

Adult↗
PubMedDate not supplied

Effect of two perfluorocarbon emulsions on reperfusion injury after coronary artery occlusion in rabbits.

Because of their high oxygen-carrying capability and small particle size, it has been suggested that perfluorochemical emulsions may be useful to reduce reperfusion injury after coronary artery occlusion and reperfusion. We tested the ability of Fluosol and a more concentrated perfluorochemical emulsion (perflubron) to decrease infarct size in anesthetized rabbits undergoing 30 min of coronary occlusion and 4 h of reperfusion. All rabbits were ventilated with 100% oxygen. Treatment was begun at 25 min of coronary occlusion, 5 min before reperfusion. Rabbits were randomized to receive saline (10 ml/kg, n = 15), Fluosol (30 ml/kg, n = 15), or a perflubron emulsion (10 ml/kg, n = 16), or the perflubron emulsion vehicle (10 ml/kg, n = 15). Collateral blood flow during occlusion was measured with radioactive microspheres. The size of the ischemic region at risk was determined by in vivo injection of blue dye and infarct size by in vitro tetrazolium staining. We found that all groups were equally ischemic during occlusion, and that risk zone sizes were comparable. Heart rate and systemic arterial pressure were also similar among groups. Infarct size expressed as a percentage of the risk zone was 30 +/- 4% in saline-treated rabbits, 27 +/- 4% in Fluosol-treated rabbits, and 21 +/- 4% and 21 +/- 3% in perflubron emulsion and perflubron emulsion vehicle treated rabbits, respectively. There was a trend for both perflubron emulsion and perflubron emulsion vehicle groups to have smaller infarcts; however, neither perfluorocarbon emulsion nor the emulsion vehicle significantly reduced infarct size compared with saline treatment. Thus, at the doses used in this study neither Fluosol nor perflubron emulsion, when given just before reperfusion, significantly reduced infarct size in this rabbit model.

Animals↗