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עמוד בית
Thu, 13.06.24

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April 2007
S. Alroy, M. Preis, M. Barzilai, A. Cassel, L. Lavie, D. A. Halon, O. Amir, B. S. Lewis and M. Y. Flugelman

Background: The etiology of chest pain with normal epicardial coronary arteries (cardiac syndrome X) seems to be related to endothelial cell dysfunction. Multiple factors are implicated in the pathophysiology, including evelated levels of homocysteine in the blood. Mutations in the MTHFR gene are associated with evelated levels of homocysteine.

Objectives: To test whether abnormal homocysteine metabolism is associated with syndrome X.

Methods: Forty-two women with chest pain, positive stress test and normal coronary arteries (syndrome X) and 100 asymptomatic women (controls) were studied for the C677T mutation. Vitamin B12, folic acid, and plasma levels of homocysteine were also measured. Endothelial cell function was studied in 10 patients with syndrome X and homozygosity for C677T mutation, and in 10 matched healthy controls. Folic acid (5 mg daily) was prescribed to syndrome X patients after initial measurements of ECF[1]. Following 13 weeks of treatment, ECF and blood tests were repeated and compared to baseline measurements.

Results: Homozygosity for C677T mutation was doubled in syndrome X vs. control (33%, 14/42 vs. 16%, 16/100, P < 0.02), and homocysteine levels were increased (9.16 ± 2.4 vs. 8.06 ± 2.6 μmol/L, P = 0.02). In the 10 homozygous patients, homocysteine levels decreased significantly after treatment with 5 mg/day folic acid (10 ± 3.3 vs. 5.4 ± 1.1 µmol/L, P = 0.004). Abnormal baseline ECF improved after treatment with folic acid: flow-mediated dilatation was greater (11.3 ± 7.9% vs. 0.7 ± 4.5%, P < 0.002), as was nitroglycerin-mediated dilatation (15.2 ± 9.0% vs. 5.6 ± 6.4%, P < 0.003). Frequency of chest pain episodes was significantly reduced after 13 weeks of folic acid treatment.

Conclusion: Our findings establish the association between the C677T mutation, endothelial cell dysfunction and cardiac syndrome X, and provide a novel and simple therapy for a subset of patients with syndrome X and homozygosity for the C677T mutation.

[1] ECF = endothelial cell function

December 2000
Rosalie Ber, MD, DSc, Gershon B. Grunfeld, PhD and Gideon Alroy, MD
 The Rappaport Faculty of Medicine of the Technion established an Ethics in Medicine Forum in March 1993. The main objective of the forum was to increase awareness of the philosophical principles of ethics in medicine, as defined and developed in the western world during the last three decades. The multidisciplinary forum meets once a month during the academic year. Our 7 years experience is documented. Of the 45 meetings, 30 were clinically oriented and of these more than half were based on cases. Only 15 meetings were purely theoretical. Our principal a assumption was that any and every topic could be discussed, including those covered by the law We explored a how well western philosophical principles and rules fit the Israeli picture. Many of the forum discussions related to 0 the draft of the Patient’s Bill of Rights which came into effect on 12 May 1996. The role of the ‘legal’ hospital ethics committees was compared to that of the “advisory” ethics committees whose members constituted a large share of our forum. The multicultural Israeli population and the practice of medicine therein raised many lively discussions. The principle of autonomy in the ultra-orthodox and in the family setting was a highly controversial issue. The forum served as a workshop for examining traditional medical ethical principles, which we strongly feel needs to he amended in light of the 1996 Patient’s Bill of Rights. From our 7 years experience with an Ethics in Medicine Forum we recommend that medical ethical deliberations focus on genuine medical cases.

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