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Biomedical subjects

D Hasdai

Publications and source records attributed to D Hasdai.

At least 91 records · Page 5Linked to original sources
PubMed1996

Increased serum concentrations of interleukin-1 beta in patients with coronary artery disease.

OBJECTIVE: To assess serum interleukin-1 beta (IL-1 beta) concentrations in patients with ischaemic heart disease, to characterise subgroups of patients with raised IL-1 beta concentrations, and to examine whether serum IL-1 beta concentrations correlate with non-specific indices of inflammation. DESIGN: Survey study of patients with ischaemic heart disease. SETTING: Cardiac catheterisation laboratory of a tertiary medical centre. PATIENTS: Consecutive patients with angina pectoris and patients recovering from uncomplicated acute myocardial infarction and undergoing elective coronary angiography. RESULTS: Mean(SD) serum IL-1 beta concentrations were higher (P < 0.001) in patients with angina and < 50% coronary artery stenosis (n = 11; 18.8(19.9) pg/ml), patients with angina > or = 50% stenosis (n = 23; 10.2(11.4) pg/ml), and patients 8(0.8) days post-infarction (n = 13; 4.4(5.8) pg/ml) than in 15 healthy, age-matched controls (0.3(0.5) pg/ml). Serum IL-1 beta concentrations did not correlate with total blood leucocyte counts (r = -0.07, P = NS), blood lymphocyte counts (r = -0.24, P = NS), and blood monocyte counts (r = -0.29, P = NS), or with fibrinogen (r = -0.16, P = NS) and C-reactive protein concentrations (9(10.5) mg/dl v 14.1(19) mg/dl for patients with undetectable and detectable concentrations, respectively, P = NS). CONCLUSION: Serum IL-1 beta concentrations are raised in patients with ischaemic heart disease, in particular in those with minimal coronary artery disease and angina. The precise role of IL-1 beta in coronary artery disease remains to be determined.

Aged↗
PubMed1996

The effect of low molecular weight heparin (fragmin) on myocardial neutrophil accumulation and infarct size in a rat model of myocardial infarction.

BACKGROUND: Heparin molecules possess immunomodulating properties, which are thought to complement their established antithrombotic activity. The purpose of this study was to evaluate whether the antiinflammatory properties of low molecular weight heparin (LMWH) can attenuate polymorphonuclear neutrophil accumulation and infarct size in a rat model of myocardial infarction. METHODS: Myocardial infarction was induced by ligating the left main coronary artery. LMWH (fragmin 500 anti-FXa u/kg) or vehicle (saline) were administered subcutaneously thirty minutes prior to coronary artery occlusion. Significant anticoagulant activity was attained with LMWH for more than eight hours. Twenty-four hours later, neutrophil accumulation and infarct size were determined by measuring left ventricular free wall myeloperoxidase and residual creatine kinase activity, respectively. RESULTS: As compared with rats administered vehicle, myeloperoxidase activity was insignificantly decreased in rats treated with LMWH (1.24 +/- 0.28 u/g vs 1.66 +/- 0.15 u/g, P = 0.16. Infarct size was also not significantly different between the groups (62.48 +/- 3.5% and 50.67 +/- 7.2% of left ventricular free wall with vehicle and LMWH, respectively, P = 0.1). CONCLUSION: The authors conclude that LMWH does not significantly reduce myocardial neutrophil accumulation and infarct size twenty-four hours after myocardial infarction in the rat.

Animals↗
PubMed1995

ST segment reelevation after acute myocardial infarction: marked differences in the electrocardiographic pattern between early and late episodes.

This study assesses the electrocardiographic (ECG) morphologic differences between early (< 24 h) and late (> 24 h) episodes of ST segment reelevation after acute myocardial infarction. We studied the records of 101 consecutive patients with acute myocardial infarction whose admission ECG demonstrated ST segment elevation with positive T waves, without pathological Q waves in the relevant leads, and without signs of bundle branch block or left ventricular hypertrophy. Thirty-five patients had 44 episodes of early ST segment reelevation, while 22 patients experienced 26 late episodes of ST segment reelevation. Seven patients experienced both early and late episodes. Early episodes of ST segment reelevation was seen more often after thrombolytic therapy: 43% (32 of 74 patients) versus 11% (3 of 27 patients) (P < 0.006). No differences were found in the incidence of late episodes between those who underwent (23%) or did not undergo (19%) thrombolytic therapy. Two patterns of ST segment elevation were distinguished. Pattern A with positive T waves, ST segment elevation (> or = 0.1 mV), but without distortion of the terminal portion of the QRS complex. Pattern B characterized by positive T waves, ST segment elevation (> or = 0.1 mV) with distortion of the terminal portion of the QRS complex. Each ECG was categorized according to these two patterns. The admission ECG pattern was A in 75 patients, and B in 26. No significant differences were found between patients with early, late, or no episodes of ST segment reelevation in the appearance of pattern A or B on admission.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

ST segment depression in lateral limb leads in inferior wall acute myocardial infarction. Implications regarding the culprit artery and the site of obstruction.

We examined whether the pattern of ST segment depression in lateral leads (I, aVL, V5, V6) in the initial electrocardiogram of patients (n = 88) with inferior wall acute myocardial infarction (ST segment elevation of > or = mm in > or = 2 inferior leads) correlates with the site of obstruction, as determined angiographically during acute hospitalization. Of the 62 patients in which the culprit artery could be determined unequivocally, in 46 the culprit artery was the right coronary artery (20 proximal to the first right ventricular branch and 26 distal), and in 16 the left circumflex coronary artery (seven proximal to the first marginal branch or involving a high first marginal branch, and nine with distal obstruction). Significant ST segment depression (ST < or = 1 mm) in leads I and aVL was more common in right coronary artery obstruction (P < 0.05 and P < 0.0001, respectively). The absence of significant ST segment depression in lead aVL was most common in proximal circumflex obstruction (P < 0.0001), with a similar trend for lead I (P < 0.11). ST segment depression patterns in leads V5 and V6 were not indicative of the infarct-related artery or the site of obstruction. Thus, significant ST segment depression in leads I and aVL indicates right coronary artery-associated inferior wall acute myocardial infarction with a sensitivity of 70% and 100%, and a specificity of 63% and 38%, respectively, whereas the lack of ST segment depression in these leads indicates proximal circumflex obstruction with a sensitivity of 71% and 86%, and a specificity of 65% and 100%, respectively.

Coronary Angiography↗
PubMed1995

Exogenous insulin-like growth factor II enhances post-infarction regional myocardial function in swine.

OBJECTIVES: Insulin-like growth factor II (IGF-II) promotes cardiac myocyte growth and contractility in vitro. This study was designed to investigate the effect of exogenous IGF-II on regional myocardial function at the area of infarct in the pig. METHODS: Myocardial infarction was induced in 12 female anaesthetized pigs by affigel blue beads, embolizing microvessels of the left anterior descending coronary artery distribution. In the experimental group (n = 6), IGF-II (0.12 microgram.kg-1 in two animals and 0.6 microgram.kg-1 in four) was incorporated into the beads and delivered by them to the infarct area. Myocardial function was followed echocardiographically, and the excised heart was analysed immunohistochemically and histopathologically. RESULTS: Myocardial function in injured zones, inversely related to an echocardiographic segmental wall motion score (mean +/- SEM), was similar between the two groups at baseline, but at 4 weeks post-infarction was significantly (P = 0.008) reduced in the control group (0.58 +/- 0.38 vs 3.42 +/- 0.84), in contrast to nearly baseline values in the experimental group (0.58 +/- 0.33 vs 1.17 +/- 0.42, P = 0.41). Cardiac performance in injured segments was significantly better after myocardial injury in the experimental group (P = 0.04). Tissue samples from both groups (4 weeks post-infarction), stained with haematoxylin and eosin demonstrated peri-infarct myocyte hypertrophy, corresponding to regions selectively stained by an antibody for CD56, which highlights growing cardiac myocytes. By image analysis semi-quantification, staining for CD56 was significantly (P = 0.04) higher in the peri-infarct region of the experimental group, as compared with controls (106.5 +/- 2.8 vs 92 +/- 4.4 gray level units). Microvessels stained for von-Willebrand factor were similar in number in both groups (P = 0.8), as were mesenchymal cells stained for vimentin (P = 0.7). CONCLUSIONS: Exogenous IGF-II, delivered to the infarct area ameliorates regional cardiac function in the pig, perhaps by inducing peri-infarct myocyte growth.

Animals↗
PubMed1995

Beneficial effect of nitroglycerin on arterial rethrombosis after thrombolysis. Results from a rabbit thrombosis model.

BACKGROUND: Although nitroglycerin (NTG) is commonly administered to patients with acute myocardial infarction, its effect on concomitant thrombolytic therapy has not been fully elucidated. We examined whether NTG administration further optimizes thrombolysis with rt-PA, combined with aspirin and heparin. METHODS AND RESULTS: Blood clots were produced in a rabbit femoral artery with endothelial damage and distal stenosis. rt-PA was administered in repeated bolus i.v. injections of 0.3 mg.kg-1 every 10 min for 50 min. Femoral artery flow was measured continuously for 2 h. Fourteen rabbits were randomized into two groups (group A and B), both receiving aspirin (i.v. 17 mg.kg-1) and heparin (i.v. 200 units.kg-1) prior to the first rt-PA bolus injection. NTG was administered in group B only, 10 min prior to the first rt-PA bolus, at 10 micrograms.kg-1.min-1 for 130 min. Reperfusion at the end of the 120 min observation period occurred in 5/7 group A and 6/7 group B rabbits (P = ns). In 3/7 group A rabbits, re-flow was achieved but persistent re-occlusion subsequently developed in 1/3 and oscillatory re-flow and re-occlusion cycles (cyclic re-flow) with subsequent patency developed in the remaining two rabbits. These flow patterns were not observed in any of group B rabbits. Overall patency duration was significantly prolonged with NTG (group B; 578/840 min) compared to controls (group A; 258/840 min) (P < 0.001). The mean recanalization time (group A; 30.8 +/- 9.3 vs group B; 22.5 +/- 4.7 min, P = 0.16) as well as mean rt-PA boluses needed to achieve complete recanalization (group A; 4.3 +/- 0.7 vs group B; 3.3 +/- 0.6 boluses/rabbit, P = 0.3) did not differ between groups. However, NTG infusion was associated with increased restored femoral flow following recanalization (expressed as % of stenotic flow value over observation time) compared to control group (P = 0.025 by repeated measures ANOVA). CONCLUSION: Adding NTG to a thrombolytic regimen with rt-PA, aspirin and heparin increases the magnitude of restored flow and total patency duration following recanalization in a rabbit model of arterial thrombosis.

Animals↗
PubMed1995

Inferior wall acute myocardial infarction with one-lead ST-segment elevation: electrocardiographic distinction between a benign and a malignant clinical course.

BACKGROUND: In most clinical trials, ST-segment elevation in two contiguous leads is required for diagnosis of acute myocardial infarction (AMI). This study describes the clinical course of patients with inferior wall AMI with one-lead ST-segment elevation in lead L3 in the initial ECG. METHODS: Of 394 consecutive patients with inferior wall AMI, 31 (7.8%) had an initial ECG showing ST-segment elevation (+/- 1 mm) only in lead L3 (ST < 1 mm in leads L2 and aVF) and upright T waves in inferior leads. Patients were categorized into three groups: (I) no precordial ST-segment depression (n = 6), (II) maximal precordial ST-segment depression in leads V1-V3 (n = 4), and (III) maximal precordial ST-segment depression in leads V4-V6 (n = 21). RESULTS: Patients in group III developed severe heart failure (pulmonary edema or cardiogenic shock) six times more frequently than those in groups I-II (62 versus 10%). Among patients who underwent coronary angiography, three-vessel coronary artery disease (> 50% stenosis) was more common in group III. Five of six patients in group III who underwent emergency angioplasty of the right coronary artery because of cardiogenic shock survived. CONCLUSION: Patients with inferior wall AMI and an initial ECG with ST-segment elevation only in lead L3, and maximal precordial ST-segment depression in leads V4-V6, are at risk of severe complications, especially heart failure, but their clinical course may be ameliorated by employing an aggressive interventional strategy.

Adult↗
PubMed1994

Prognostic significance of maximal precordial ST-segment depression in right (V1 to V3) versus left (V4 to V6) leads in patients with inferior wall acute myocardial infarction.

This study examines whether patients with inferior wall acute myocardial infarction (AMI) and maximal ST-segment depression in left precordial leads are at higher risk for in-hospital mortality. The charts of patients (n = 213) with inferior wall AMI and an initial electrocardiogram that displayed peaked, tall T waves or ST-segment elevation with upright T waves in inferior leads were reviewed, after excluding patients with inverted T waves in inferior leads (n = 75). ST-segment deviation from baseline was measured for all leads. Patients were classified into 3 types: I = no precordial ST-segment depression; II = sum of ST-segment depression in leads V1 to V3 equal to or more than the sum of ST-segment depression in leads V4 to V6; and III = maximal precordial ST-segment depression in leads V4 to V6. Thirty-six patients (17%) died in the hospital. In-hospital mortality rates for patients with types I and II were 12% and 10%, respectively, compared with 41% for those with type III (p < 0.0001). Mortality rates in surviving patients were similar for all types up to 1 year after infarction. Multivariate logistic regression models for in-hospital mortality by ST-segment depression type adjusted for age, previous AMI, diabetes mellitus, and thrombolytic therapy revealed that type III pattern was a strong predictive factor for in-hospital mortality (odds ratio = 4.9, p = 0.0008, 95% confidence interval 1.93 to 12.26). Thus, patients with inferior wall AMI and maximal precordial ST-segment depression in leads V4 to V6 are at high risk for in-hospital mortality.

Aged↗
PubMed1994

Endothelin and myocardial ischemia.

Endothelin is a potent vasoconstrictor with a wide range of effects on the heart. Changes in myocardial and circulating levels of endothelin have been described in various experimental models of myocardial ischemia, and in humans with acute myocardial infarction and different forms of angina pectoris. The role played by endothelin in the different states of myocardial ischemia is unclear. However, myocardial damage has been shown to be reduced in several experimental models of myocardial infarction by administering agents that block the action of endothelin. The aim of this review article is to present the current literature concerning the interaction between endothelin and the various forms of myocardial ischemia, and to explore the significance of such interactions.

Angina Pectoris↗
PubMed1994

Low molecular weight heparin (Fragmin) prevents early reocclusion following femoral artery thrombolysis with rt-PA in rabbits.

The purpose of this study was to evaluate the effect of low molecular weight heparin Fragmin on thrombolysis with tissue-type plasminogen activator (rt-PA) and to compare its effect to that of standard heparin. A rabbit thrombosis model was used, consisting of a blood clot produced in an isolated femoral artery segment with superimposed endothelial damage and distal stenosis. Thirty rabbits were randomized to three treatment groups with rt-PA (30 micrograms.kg-1.min-1 for 60 min and no additional therapy), rt-PA with i.v. standard heparin (200 IU.kg-1 bolus and then 70 IU.kg-1 hourly) and rt-PA with s.c. Fragmin (a single dose of 500 IU.kg-1) prior to rt-PA administration. In six of 10 rabbits given rt-PA only, recanalization was observed which was persistent in three. In eight of 10 rabbits given rt-PA with intravenous heparin, reflow was achieved, which was persistent in three. Fragmin resulted in recanalization in eight of 10 rabbits, with persistent patency in each recanalized rabbit. Reflow time was not shortened with either standard heparin or Fragmin compared with rt-PA alone (64 +/- 41, 56 +/- 18, 50 +/- 23 min respectively), (P = 0.7). Persistent reocclusion after reflow was not observed with Fragmin (0/8) but was present with both standard heparin (5/8, P = 0.03 vs Fragmin) and rt-PA alone (3/6, P = 0.05 vs Fragmin). Thus, in the femoral artery of the rabbit, Fragmin, unlike standard heparin, was found to prevent reocclusion following rt-PA thrombolysis.

Animals↗
PubMed1994

The applicability of color-labeled microspheres in a rabbit model of ischemia-reperfusion.

This study was designed to examine the ability of color-labeled microspheres to depict different states of myocardial perfusion in a rabbit model of ischemia-reperfusion. A thread was passed under the left anterior descending artery (LAD) and the first left marginal artery of anesthetized New Zealand White rabbits. Blue-labeled microspheres (500/g body wt) were injected into the left atrium. The thread was tightened in rabbits belonging to the experimental group (n = 8), and red-labeled microspheres (500/g body wt) were injected. The snare was loosened, and yellow-labeled microspheres (500/g body wt) were injected before (n = 5) or after (n = 3) methylene blue injection. In animals belonging to the "sham" group (n = 4 and n = 2, respectively), the sequence of injections was similar, but the snare was not tightened. The animals were euthanized, and 0.3-1 g sections were cut from ischemic and nonischemic regions, as determined by methylene blue in the experimental subgroups and from the corresponding regions in the "sham" subgroups. The tissue samples were digested with 4 M KOH, ethanol 70%, and ultrasonication, and the microspheres were recovered by vacuum filtration. The dye was chemically removed from the microspheres, and the photometric absorption of each sample was determined. There was no significant difference between the experimental and "sham" groups in baseline uptake of blue-labeled microspheres. Rabbits belonging to the experimental subgroups had significantly lower mean uptake of red microspheres during ischemia relative to "sham" (0.51 +/- 0.08 vs 1.06 +/- 0.24 and 0.36 +/- 0.19 vs 0.91 +/- 0.12, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Failure of captopril to attenuate myocardial damage, neutrophil accumulation, and mortality following coronary artery occlusion and reperfusion in rat.

Captopril, a sulfhydryl-containing angiotensin-converting enzyme inhibitor, has been suggested as possessing antiischemic and antiinflammatory properties. To test the hypothesis that captopril may prevent neutrophil-induced myocardial injury during acute myocardial infarction (AMI), the authors subjected rats to coronary occlusion for thirty minutes and reperfusion for twenty-four hours (MI) or to sham operation (sham MI). Oral captopril (100 mg/kg) or vehicle was administered thirty minutes before coronary occlusion. The effect of captopril on mean arterial blood pressure was assessed in separate group of animals (n = 8). Infarct size and neutrophil accumulation in myocardium were determined by measuring creatine phosphokinase depletion and myeloperoxidase (MPO) activity, respectively, in the left ventricular free wall (LVFW). Animals treated with 100 mg/kg of captopril exhibited significant reduction in mean arterial blood pressure compared with vehicle-treated animals (P < 0.01). Compared with vehicle-treated animals, administration of 100 mg/kg of captopril to MI animals attenuated neither twenty-four-hour mortality (56% vs 52%, respectively), nor infarct size (36 +/- 7% vs 34% +/- 7% respectively), nor MPO activity (1.0 +/- 0.17 vs 1.26 +/- 0.19). Thus, in the present experiment captopril did not reduce neutrophil-induced myocardial damage following coronary occlusion and reperfusion. These findings may be partly explained by the negative effect of captopril on arterial blood pressure during AMI.

Animals↗
PubMed1993

Intracoronary injection of basic fibroblast growth factor enhances angiogenesis in infarcted swine myocardium.

OBJECTIVES: This study was performed to examine the effect of intracoronary exogenous basic fibroblast growth factor (bFGF) on angiogenesis in infarcted myocardial regions. BACKGROUND: Exogenous bFGF is a potent promoter of angiogenesis. Little information is available on its effect on myocardial angiogenesis. METHODS: Myocardial infarction was induced in 10 pigs by intracoronary injection of microscopic beads. Four pigs served as a control group; in six pigs slow-release bFGF was delivered by the beads. Cardiac performance was evaluated by repeated echocardiographic measurement and angiogenesis was evaluated by immunohistochemical studies 14 days later. RESULTS: As compared with control pigs, pigs treated with bFGF had higher microvessel counts (mean +/- SEM) in both viable tissue (141 +/- 27 per field vs. 39 +/- 4, p = 0.01) and nonviable tissue (329 +/- 26 per field vs. 95 +/- 7, p < 0.001) within the infarct area. No significant differences in total regional left ventricular wall motion were noted between the two groups throughout the 14-day study period. CONCLUSIONS: In the swine, direct intracoronary application of bFGF to infarcted myocardium enhances myocardial neovascularization within 2 weeks.

Animals↗
PubMed1988

Effect of hyperglycemia on pain perception and on efficacy of morphine analgesia in rats.

The effect exerted by different hyperglycemic states on the pain threshold and on the analgesic potential of morphine was studied in male Sabra rats with the hot plate device. Hyperglycemia induced by an intraperitoneal injection of 0.014 mol/kg glucose or an acute or chronic diabetic state induced by streptozocin injection did not significantly alter the pain threshold. However, states of acute and chronic diabetes markedly blunted the analgesic effect of morphine (5 mg/kg). Sabra rats maintained on a cocktail of glucose-saccharin, thought to activate the release of endogenous opioids, demonstrated an increased pain threshold and rapidly developed resistance to the analgesic effect of morphine. Previous studies have shown that glucose in high concentration may interfere with the interaction of morphine on the opiate receptor. The influence of the diabetic state on beta-endorphin synthesis and concentration in the central nervous system is another factor that might change pain perception in diabetes. We propose that in diabetes, generally, the pain threshold is adequately maintained, despite the antagonistic effect of glucose, partly due to a compensatory increased secretion of endogenous opioid peptides. We hypothesize that in patients with chronic painful diabetic neuropathy, these normal analgesic response mechanisms may be overwhelmed either by an excess of nociceptive impulses from diseased peripheral nerves or conceivably by a failure of endogenous opioid secretory response to the hyperglycemia.

Action Potentials↗