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עמוד בית
Mon, 29.04.24

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December 2013
Osamah Hussein, Jamal Zidan, Michael Plich, Hana Gefen, Roberto Klein, Karina Shestatski, Kamal Abu-Jabal and Reuven Zimlichman

Background: Coronary slow flow phenomenon (CSFP) is a functional and structural disease that is diagnosed by coronary angiogram.    



Objectives: To evaluate the possible association between CSFP and small artery elasticity in an effort to understand the pathogenesis of CSFP.

Methods: The study population comprised 12 patients with normal coronary arteries and CSFP and 12 with normal coronary arteries without CSFP. We measured conjugated diene formation at 234 nm during low density lipoprotein (LDL) oxidation, as well as platelet aggregation. We estimated, non-invasively, arterial elasticity parameters. Mann-Whitney non-parametric test was used to compare differences between the groups. Data are presented as mean ± standard deviation.

Results: Waist circumference was 99.2 ± 8.8 cm and 114.9 ± 10.5 cm in the normal flow and CSFP groups, respectively (P = 0.003). Four patients in the CSFP group and 1 in the normal flow group had type 2 diabetes. Area under the curve in the oral glucose tolerance test was 22% higher in the CSFP than in the normal group (P = 0.04). There was no difference in systolic and diastolic blood pressure, plasma concentrations of total cholesterol, triglycerides, high density lipoprotein, LDL and platelet aggregation parameters between the groups. Lag time required until initiation of LDL oxidation in the presence of CuSO4 was 17% longer (P = 0.02) and homocysteine fasting plasma concentration was 81% lower (P = 0.05) in the normal flow group. Large artery elasticity was the same in both groups. Small artery elasticity was 5 ± 1.5 ml/mmHgx100 in normal flow subjects and 6.1 ± 1.9 ml/mmHgx100 in the CSFP patients (P = 0.02).

Conclusions: Patients with CSFP had more metabolic derangements. Arterial stiffness was not increased in CSFP.

December 2006
A. Nemets, I. Isakov, M. Huerta, Y. Barshai, S. Oren and G. Lugassy
 Background: Thrombosis is a major cause of morbidity and mortality in polycythemia vera. Hypercoagulability is principally due to hyperviscosity of the whole blood, an exponential function of the hematocrit. PV[1] is also associated with endothelial dysfunction that can predispose to arterial disease. Reduction of the red cell mass to a safe level by phlebotomy is the first principle of therapy in PV. This therapy may have some effect on the arterial compliance in PV patients.

Objectives: To estimate the influence of phlebotomies on large artery (C1) and small artery compliance (C2) in PV patients by using non-invasive methods.

Methods: Short-term hemodynamic effects of phlebotomy were studied by pulse wave analysis using the HDI-Pulse Wave CR2000 (Minneapolis, MN, USA) before and immediately after venesection (300–500 ml of blood). We repeated the evaluation after 1 month to measure the long-term effects.

Results: Seventeen PV patients were included in the study and 47 measurements of arterial compliance were performed: 37 for short-term effects and 10 for long-term effects. The mean large artery compliance (C1) before phlebotomy was 12.0 ml/mmHg x 10 (range 4.5–28.6), and 12.6 ml/mmHg x 10 (range 5.2–20.1) immediately after phlebotomy (NS). The mean small artery compliance (C2) before and immediately after phlebotomy were 4.4 mg/mmHg x 10 (range 1.2–14.3) and 5.5 mg/mmHg x 10 (range 1.2–15.6) respectively (delta C2–1.1, P < 0.001). No difference in these parameters could be demonstrated in the long-term arm.

Conclusions: Phlebotomy immediately improves arterial compliance in small vessels of PV patients, but this effect is short lived.


 





[1] PV = polycythemia vera


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