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Biomedical subjects

E Gurfinkel

Publications and source records attributed to E Gurfinkel.

30 records · Page 2Linked to original sources
PubMed1996

Coagulation and fibrinolytic parameters in patients with pulmonary hypertension.

BACKGROUND: Vascular endothelium reacts to various pathophysiologic stimuli by releasing several autocoids and cytokines that can be used along with the coagulation and fibrinolytic markers for the diagnosis of hemostatic alterations. Several newer markers for vascular distress, such as tissue plasminogen activator (TPA), tissue plasminogen activator inhibitor-1 (PAI-1), TPA/PAI-1 complex, and the newly reported inhibitor of the coagulation process, namely, tissue factor pathway inhibitor (TFPI), have been implicated in the pathogenesis of pulmonary hypertension. METHODS: To investigate the behavior of endothelial cells at basal and time-dependent venous stasis-induced changes, various markers were measured in patients with primary and secondary pulmonary hypertension and compared with healthy human volunteers (controls) without any family history of thromboembolism or history of hypertensive disorders. The right atrial pressure (RAP) and pulmonary arterial pressure were measured and the hemostatic parameters were correlated to determine the relevance of these parameters with the alterations in the present indices. RESULTS: A fibrinolytic deficit exists in patients with pulmonary hypertension, indicated by the prolongation of the euglobulin clot lysis time at basal conditions and after the venous occlusion test. This defect was mainly due to increased production of PAI-1 by endothelium (patients 59.8 +/- 22.3 AU/ml; controls 30.3 +/- 14.5 AU/ml; p = 0.005). We also report for the first time that a decrease in tissue factor pathway inhibitor antigen was also observed in these patients when RAP was > 9 mmHg [controls 95.6 +/- 61.6 ng/ml; patients with RAP > 9 mmHg 47.2 +/- 19.2 ng/ml (p = 0.044); patients with RAP > 9 mmHg 96.6 +/- 32.4 ng/ml (p = 0.002 compared with patients with RAP > 9 mmHg)], indicating endothelial cell and hemostatic disturbances. CONCLUSIONS: We conclude that the euglobulin clot lysis time was prolonged in patients with pulmonary hypertension compared with controls. The impairment of the fibrinolytic system was due to an elevated concentration of PAI-1. In RAP > 9 mmHg, an additional prothrombotic factor is the decrease in plasma tissue factor pathway inhibitor antigen. It appears from this study that antithrombotic treatment is indicated in these patients.

Adolescent↗
PubMed1995

Time significance of acute thrombotic reactant markers in patients with and without silent myocardial ischemia and overt unstable angina pectoris.

Ischemic electrocardiographic changes were recorded within 2 hours of admission using a 12-lead electrocardiographic continuous monitor with a 20-second scanning interval and an alarm mode for asymptomatic events. Blood samples were obtained at admission and at the moment of asymptomatic events (group A). In the other patients who did not develop ischemia, a second blood sample was taken 12 hours later (group B). We determined prothrombin time, activated partial thromboplastin time, clotting factor VIII activity, tissue plasminogen activator activity, tissue plasminogen activator inhibitor-1, cross-linked fibrin degradation product, and thrombin-antithrombin III complexes. There was a statistically significant difference between group A and B patients when the basal samples were analyzed for thrombin-antithrombin III (p = 0.046) and d-Dimer (p = 0.005). Prothrombin fragment 1 + 2 were significantly reduced, and d-Dimer was elevated when basal blood samples were compared with the second sample in patients who developed silent events (p = 0.008 and 0.055, respectively). A plasma concentration of thrombin-antithrombin III complex was also significantly decreased when sample 2 was compared with the basal blood sample (p = 0.039). Five recurrent episodes of angina and 2 nonfatal infarctions occurred, and 4 urgent revascularization procedures were performed in group A. In group B, there was only 1 nonfatal infarction (p = 0.01). The results of the present study suggest that a time-dependent thrombotic process is detectable in the blood stream as a cyclic movement. Further studies are needed to determine if some other factors, such as intensive shear stress in the vessel wall, may activate plaque instability during asymptomatic episodes.

Acute Disease↗
PubMed1995

Efficacy and Safety of Low-Dose Streptokinase plus Desmopressin in Acute Myocardial Infarction: A Pilot Study.

In this pilot study the combined use of desmopressin, which releases tissue plasminogen activator from vascular endothelium, and a low dose of streptokinase as a new thrombolytic regimen for acute myocardial infarction is proposed. Eighteen patients with acute myocardial infarction were treated intravenously with 150,000 U (4 patients) or 250,000 U (14 patients) of streptokinase infused over 10 minutes, followed by 24 µg of desmopressin infused over 5-10 minutes. Aspirin and beta-blockers were administered at admission, and heparin and oral anticoagulants were started at the end of the thrombolytic regimen. Hemostatic parameters were studied before and 30, 60, 120, and 240 minutes after starting thrombolytic therapy. Fifteen patients (83.3%) had evidence of clinical reperfusion. Angiography was performed with a mean delay of 8.8 hours (range 1.5-22 hours) from the start of thrombolytic therapy. Fourteen patients (77.8%) had patency of the infarct-related artery: 10 patients (55.6%) achieved TIMI grade 3, and 4 patients (22%) achieved TIMI grade 2. Two patients (one TIMI grade 1 and one TIMI grade 2) underwent coronary angioplasty. No patient died during the in-hospital period. At 18 months follow-up, all patients are alive. No major or minor bleeding was detected. The significant decline in plasma fibrinogen and in the euglobulin lysis time, and the increase in fibrinogen/fibrin degradation products, indicate a plasma lytic state. Crosslinked fibrin degradation products increased from 310 +/- 120 ng/ml to 670 +/- 310 ng/ml (p = 0.009), suggesting that fibrin digestion occurred in vivo. This pilot study provides data supporting the feasibility and efficacy of a new and more economic thrombolytic treatment of acute myocardial infarction without hemorrhagic complications.

Journal Article↗
PubMed1995

Oral anticoagulant treatment with and without aspirin.

For preventing thromboembolic events, the concurrent use of oral anticoagulant and antiplatelet drugs has been proposed. In prosthetic heart valves the use of moderate intensity anticoagulants [International Normalized Ratio (INR) 2-3] plus aspirin (100 mg/day) decreases the amount and severity of embolic episodes. The possibility that the same regimen could provide benefit in the prevention of thrombotic events in other arterial diseases is also indicated by the ATACS trial in unstable angina. The ongoing studies in ischemic heart diseases will also give the answer to this possibility.

Administration, Oral↗
PubMed1994

ST-segment computerized monitoring before and after angioplasty: clinical correlation with recurrent angina during the short-term follow-up.

The purpose of this study was to determine whether computerized ST-segment monitoring previous to percutaneous transluminal coronary angioplasty (PTCA) and after performance of this procedure may be useful to discern a pattern of recurrent angina. For this purpose, we analyzed 57 patients (11 women and 46 men, mean age 60 years) before and after treatment with balloon procedure. These patients were followed up during the next 3 months. A computerized electrocardiographic (ECG) device was used which was capable of recording simultaneously all 12 leads at rest. It was programmed to store a complete ECG every 5 min and was capable of detecting any abnormal ST alteration > than 0.5 mV at 80 ms after J junction, including R-wave amplitude. Measurements were started before (mean time 7.26 h) and after (mean time 7.96 h) the procedure. The value for ST amplitude at the J junction was used as the 0 point; then the most negative depression or the most positive elevation value was considered as the most abnormal ST alteration during monitoring. The patients were followed up for 3 months for the purpose of recognizing recurrent angina or establishing the occurrence of death. Twelve patients (30%) had recurrent angina. Discriminant function analysis revealed that ST monitoring in these patients showed significant difference after PTCA in comparison with controls, both in the frontal plane [ST depression 170 +/- 52 mV vs. 231 +/- 23 (p = 0.02)] and in precordial leads [176 +/- 16 vs. 80 +/- 6.19 mV (p = 0.0001)].(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Importance of thrombosis and thrombolysis in silent ischaemia: comparison of patients with acute myocardial infarction and unstable angina.

OBJECTIVE: To investigate whether plaque rupture and thrombosis have a role in silent ischaemia as well as in unstable angina. DESIGN: Prospective analysis of the results of haemostatic diagnostic tests at the moment of developing silent ischaemia at rest. SETTING: Coronary care unit. PATIENTS: 22 patients with acute myocardial infarction, 12 patients with symptomatic angina (unstable angina), and 10 normal volunteers (control group). INTERVENTIONS: Continuous cardiac monitoring detected 15 asymptomatic episodes (silent ischaemia) in 6 patients with unstable angina. Blood samples were obtained at admission and when an asymptomatic alteration was detected and 10 minutes later. MAIN OUTCOME MEASURES: Comparisons of concentrations of tissue plasminogen activator, urokinase type plasminogen activator, tissue plasminogen activator inhibitor-1, cross-linked fibrin degradation products, von Willebrand factor, and thrombin-antithrombin III complexes in patients and controls at admission; same comparisons in patients with silent ischaemia at the start of an episode and 10 minutes later. RESULTS: Tissue plasminogen activator concentrations were raised at admission in patients with acute myocardial infarction (mean (SD) 14.2 (6) ng/ml) and in patients with unstable angina (10.1 (2.5) ng/ml) in comparison with controls (5.1 (2.7) ng/ml, p < 0.01 and < 0.05 respectively). There was no differences between the two groups of patients, however. Similar results were observed at the start of a silent ischaemic episode (9.8 (1.9) ng/ml) and 10 minutes later (10.5 (2.9) ng/ml) compared with controls (p < 0.05). Tissue plasminogen activator inhibitor-1 concentrations were raised in patients with acute myocardial infarction (45.1 (15) ng/ml) compared with volunteers (20.6 (16) ng/ml, p < 0.01). In patients with silent ischaemia tissue plasminogen activator inhibitor-1 concentrations were slightly but not significantly increased. Concentrations of cross-linked fibrin degradation products (D dimer) increased during unstable angina (2150 (350) ng/ml) and silent ischaemia (2270 (450) ng/ml) compared with the concentrations in volunteers (340 (80) ng/ml) and patients with acute myocardial infarction (310 (120) ng/ml; p < 0.01). CONCLUSIONS: The results suggest that thrombosis mediates the pathophysiological mechanisms of silent ischaemia and unstable angina.

Angina, Unstable↗
PubMed1993

Abnormal QT intervals associated with negative T waves induced by antiarrhythmic drugs are rapidly reduced using magnesium sulfate as an antidote.

This study was undertaken to determine whether prolonged QTc interval as a consequence of abnormal repolarization induced by coronary disease or antiarrhythmic drugs could be shortened by intravenous administration of magnesium sulfate. A total of 21 patients with basal prolonged QTc intervals (QTc > 500 ms) were divided in two groups: 7 with ischemic coronary disease and negative T waves (Group A), and 14 treated with antiarrhythmic drugs (Group B). Nine of the latter had negative T waves (Subgroup B-1) and five had positive T waves (Subgroup B-2) recorded in precordial leads. Nine patients were taking amiodarone and six quinidine. Magnesium sulfate was given intravenously in a bolus of 3.75 g (25% solution) over 3 min. Patients had normal electrolyte serum levels. The prolonged QTc and JTc intervals were shortened after magnesium sulfate in patients of Subgroup B-1 from the basal values [QTc 20.7% and JTc 25.4%, (p = < 0.0001 and 0.02, respectively)]. None of the patients in Group A or Subgroup B-2 experienced altered QTc or JTc intervals. While some antiarrhythmic drugs are capable of altering the refractoriness of ventricular cells, probably by causing changes in the intracellular metabolic pathways, in patients with coronary disease gaps in the membrane induced by ischemic injury let calcium enter the cells parallel with dispersion of ventricular repolarization. When secondary negative T waves are present, magnesium sulfate as an antidote probably acts as a blocking agent at the sarcoplasmic reticulum, thus reducing both QTc and JTc intervals.

Amiodarone↗
PubMed1991

Comparison of two levels of anticoagulant therapy in patients with substitute heart valves.

After cardiac valve replacement patients were blindly randomized into two groups, both receiving aspirin (330 mg) and dipyridamole (75 mg) twice daily and the oral anticoagulant acenocoumarol (Sintrom). An international normalized ratio of 2.0 to 2.99 was assigned to group A and 3.0 to 4.5 to group B; both groups were subsequently analyzed for thromboembolic and hemorrhagic complications. Final evaluation included 51 and 48 patients, respectively. The follow-up was 626 months for group A (12.3 months/patient) and 486 months for group B (10.1 months/patient). The frequency of thromboembolism was equal in both groups: one transient ischemic attack in group A (a rate of 1.92/100 patient-years) and two transient ischemic attacks in group B (a rate of 4.94/100 patient-years). There was, however, a statistical difference in bleeding complications between the two groups (p less than 0.02). Two patients bled in group A, a rate of 3.9% (3.8/100 patient-years), which represents an incidence of one episode each 25.6 years of treatment; 10 patients bled in group B, a rate of 20.8% (24.7/100 patient-years) representing an incidence of one episode each 4 years of treatment. We conclude that an international normalized ratio of 2 to 3 is safer than a ratio of 3 to 4.5 and confers good protection from thromboembolism when oral anticoagulant therapy is used conjointly with platelet function-inhibiting drugs in patients with mechanical substitute heart valves.

Acenocoumarol↗
PubMed1990

Incidental detection of renal tumours by abdominal ultrasonography.

One hundred and twenty-six patients with renal cell carcinoma were treated by nephrectomy between 1985 and 1988. They were classified into three groups: group A: 47 patients in whom ultrasonography revealed the renal cancer in the absence of any suggestive clinical signs of tumour; group B: 63 patients who presented with clinical urological signs suggestive of the tumour; group C: 16 patients who presented with general signs leading to the diagnosis. In group A, 50% of the tumours measured between 5 and 10 cm, 51% were located at the lower pole of the kidney and 83% were stage T2. Sixty-six percent of cancers in this group were situated on the right side, indicating that left renal cancers are missed in 16% of cases. In group B, 60% of the tumours measured between 5 and 10 cm, 44% were located at the lower pole and 56% were stage T2. In group C, 60% of the tumours measured between 5 and 10 cm, 50% were located at the upper pole of the kidney and only 38% of the tumours were still stage T2. We can conclude that incidental detection reveals renal tumours at a relatively limited stage (83% of T2), with dimensions smaller than those of the other groups. It is therefore essential for radiologists, ultrasonographists and urologists to investigate the left lumbar fossa and the upper pole of both kidneys very carefully during abdominal or vesico-prostatic ultrasound examinations.

Abdomen↗