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Dive into the research topics where Ehud Davidson is active.

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Featured researches published by Ehud Davidson.


American Heart Journal | 1986

Unstable angina: The significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand

Samuel Sclarovsky; Ehud Davidson; Boris Strasberg; Ruben F. Lewin; Alexander Arditti; Mordechai Wurtzel; Jacob Agmon

We evaluated 46 patients with unstable angina (UA), who showed no significant changes in heart rate, blood pressure, and double product (as evidence of increased oxygen demand) during episodes of chest pain. Coronary angiography was performed in all patients during the same hospitalization. Of 26 patients with UA and ST depression (group A), 10 had left main coronary artery disease (CAD) and eight had left main equivalent CAD. Of 20 patients with UA and ST elevation (group B), only one had left main CAD and one had left main equivalent CAD. All patients in group A had ST depression in leads V4 and V5, and all patients in group B had ST elevation in leads V2 and V3. The presence of ST depression in leads V4 and V5 in UA patients without evidence of increased oxygen demand may be suggestive of significant left main or left main equivalent CAD. Therefore, coronary angiography is recommended during the same hospitalization.


American Heart Journal | 1986

Unstable angina pectoris evolving to acute myocardial infarction: significance of ECG changes during chest pain

Samuel Sclarovsky; Ehud Davidson; Ruben F. Lewin; Boris Strasberg; Alexander Arditti; Jacob Agmon

We retrospectively evaluated 32 patients with unstable angina (UA) and no evidence of increased oxygen demand during episodes of chest pain (no significant changes in heart rate and blood pressure), who developed an acute myocardial infarction (AMI) during the same hospitalization. Based on the type of ST changes during anginal pain, two groups were defined: Group A included 19 patients who developed ST elevation during AMI; 15 of these 19 patients (79%) were in Killip class I, two were in class II, and there was one patient each in classes III and IV, respectively. Only one of the 19 patients died. Group B included 13 patients who developed ST depression during AMI; nine of these 13 patients were in Killip class IV and the remaining four patients died before they could be evaluated. Ten patients died (77%) (p less than 0.01), seven in electromechanical dissociation and three in cardiogenic shock. Postmortem examination, performed in four patients, revealed total obstruction of the left main coronary artery. It is concluded that patients with UA who, during attacks of chest pain, develop ST depression and no evidence of increased oxygen demand may have a poor prognosis when they develop an AMI. This selected group of high-risk patients appears to need immediate intensive medical care and most probably early surgical treatment.


American Heart Journal | 1984

Plasma viscosity in ischemic heart disease

Jacob Fuchs; Itzhak Weinberger; Zvi Rotenberg; Alexander Erdberg; Ehud Davidson; Henry Joshua; Jacob Agmon

Plasma viscosity was measured by the capillary method in 108 patients with ischemic heart disease. The highest value of plasma viscosity was found in 11 patients with severe unstable angina (1.66 +/- 0.068), while in 18 patients with less severe unstable angina plasma viscosity was lower (1.61 +/- 0.056; p less than 0.025). In 43 patients with acute myocardial infarction plasma viscosity was 1.53 +/- 0.10, significantly lower than in the two groups with unstable angina (p less than 0.005). In 36 patients with stable angina plasma viscosity was 1.42 +/- 0.089, similar to that found in 100 normal subjects. Plasma viscosity did not increase in 30 ischemic heart disease patients during exercise-induced myocardial ischemia. It is suggested that the elevated plasma viscosity in unstable angina demonstrated in this study compromises the oxygen delivery to the myocardium and coronary blood flow and therefore may possibly be a factor in the pathophysiology of this syndrome.


Cancer | 1984

Elevation of serum lactic dehydrogenase levels as an early marker of occult malignant lymphoma.

Zvi Rotenberg; Itzhak Weinberger; Y. Fuchs; Alexander Erdberg; Ehud Davidson; Jacob Agmon

Elevated serum lactic dehydrogenase (LDH) levels, 595 to 615 μm/ml (normal < 225 μm/ml) with predominance of LDH isoenzymes 2 and 3 was the early and only sign of occult malignant lymphoma in three patients. In the first patient, overt lymphoma appeared clinically only 2 months after the finding of elevated serum LDH levels, whereas in the other two asymptomatic patients, pathologic LDH levels were the only clues to the need for further diagnostic investigation. It is concluded that LDH may have a diagnostic value in the preclinical stage of malignant lymphoma. Thus, a patient with no apparent cause for elevated serum LDH levels warrants a thorough work‐up including abdominal CT scan and even explorative laparotomy.


The Journal of Clinical Pharmacology | 1992

Big platelets in hyperlipidemic patients.

Jacob Fuchs; Yitzhak Beigel; Pnina Green; B. Zlotikamien; Ehud Davidson; Zvi Rotenberg; Itzhak Weinberger

Both “big” platelets and hyperlipidemia are associated with increased coronary risk. This study was undertaken to search for a possible effect of various hypolipidemic drugs on big platelets. The percentage of big platelets, assessed microscopically, was measured in 66 patients who had hyperlipidemia of various types. Twenty‐seven patients with hypertriglyceridemia were randomly selected to receive either fish oil or placebo in a crossover study. Another group of 39 patients with hypercholesterolemia, among them 13 with heterozygous familial hypercholesterolemia (FH), received lovastatin. The pretreatment level of big platelets was elevated, and similar in all groups: 23.3 ± 12% versus 22 ± 9%, in the fish oil versus placebo group, 19.1 ± 6.3% versus 24 ± 11% in the FH versus non‐FH primary hypercholesterolemia group (reference value, 6.8 ± 3.5%). After treatment, despite the improvement in lipoprotein profile, the percentage of big platelets did not change. The relationship between lipid reduction and big platelets is thus questionable, and necessitates further study.


International Journal of Cardiology | 1985

Amiodarone-induced sinoatrial block.

Boris Strasberg; Ehud Davidson; Michael Berand

We observed sinoatrial block due to chronic amiodarone administration in a 5-year-old boy with primary cardiomyopathy, Wolff-Parkinson-White syndrome and supraventricular tachycardia. Reduction in the dosage of amiodarone resulted in the disappearance of the sinoatrial block and the persistence of asymptomatic sinus bradycardia.


JAMA Internal Medicine | 1989

Atrial Fibrillation: Cause and Time of Onset

Ehud Davidson; Itzhak Weinberger; Zvi Rotenberg; Jacob Fuchs; Jacob Agmon


Chest | 1989

Diagnosis and Characteristics of Lone Atrial Fibrillation

Ehud Davidson; Zvi Rotenberg; Itzhak Weinberger; Jacob Fuchs; Jacob Agmon


American Journal of Cardiology | 1992

Circulating aggregated platelets, number of platelets per aggregate, and platelet size during acute myocardial infarction

Itzhak Weinberger; Jacob Fuchs; Ehud Davidson; Zvi Rotenberg


European Heart Journal | 1990

Plasma viscosity, fibrinogen and haematocrit in the course of unstable angina

Jacob Fuchs; A. Pinhas; Ehud Davidson; Zvi Rotenberg; Jacob Agmon; Itzhak Weinberger

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