Association of the interleukine-6 polymorphism with catheter-induced coronary artery spasm in Egyptians.

BACKGROUND: The role of coronary artery spasm (CAS) was extended beyond variant angina to ischemic heart disease in general, including effort angina, unstable angina, acute myocardial infarction (MI) and sudden death. It is difficult and cumbersome to examine CAS during coronary angiography. Risk factors for CAS include smoking and genetic polymorphisms. AIM: We aimed to investigate the association of the interleukin-6 (IL-6) polymorphism with catheter-induced CAS in Egyptian patients who undergo coronary angiography. METHODS: This is a case-control study. Two hundred patients with chronic coronary artery disease who underwent elective coronary angiography were included in the study. Patients were divided into two groups: the non-CAS group (100 patients) and the CAS group (100 patients). The subjects were genotyped to the -572 C>G (rs 1800796) polymorphism of the IL-6 gene by PCR-restriction fragment length polymorphism. RESULTS: We found that patients with CAS have more risk factors for atherosclerosis compared to those without CAS. Smoking, the IL-6 GG genotype, and the G allele were independent risk factors for CAS. CONCLUSION: We concluded that the GG genotype and G allele of the IL-6 gene are associated with CAS. Smoking, the GG genotype, and the G allele of the IL-6 gene are independent predictors of catheter-induced CAS.

Association of endothelial nitric oxide synthase (Glu298Asp) gene polymorphism with radial artery spasm during cardiac catheterization in Egyptians.

BACKGROUND: Nitric oxide (NO) exerts diverse effects on the cardiovascular system. Impairment of NO production plays a key role in cerebral and coronary artery spasm. We aimed to explore the predicting factors of radial artery spasm (RAS) and the association of eNOS gene polymorphism (Glu298Asp) with RAS during cardiac catheterization. METHODS AND RESULTS: 200 patients underwent elective coronary angiography through a trans-radial approach. The subjects were genotyped to the Glu298Asp polymorphism (rs1799983) on the eNOS gene by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Our results showed that the subjects with the TT genotype and T allele were significantly more likely to develop radial artery spasms (OR = 12.5, 4.6, P < 0.001 respectively). TT genotype of eNOS Glu298Asp polymorphism, number of punctures, size of the radial sheath, radial tortuosity, and right radial access are independent predictors of radial spasm. CONCLUSION: The eNOS (Glu298Asp) gene polymorphism is associated with RAS during cardiac catheterization in Egyptians. TT genotype of eNOS Glu298Asp polymorphism, number of punctures, size of the radial sheath, right radial access, and tortuosity are independent predictors of RAS during cardiac catheterization.

Effect of Presence of Ramus Intermedius Artery on Location of Culprit Lesions in Acute Left Circumflex Coronary Artery Occlusion.

BACKGROUND AND AIM: Coronary artery anatomy frequently affects location of atherosclerotic plaques and subsequent culprit lesions. We sought to clarify whether presence or absence of Ramus Intermedius coronary artery (RI) would affect location of culprit lesions in acute left circumflex (LCX) coronary artery occlusion. METHODS: The study included 180 patients, 100 with a diagnosis of non-ST elevation myocardial infarction (NSTEMI) and 80 with ST elevation myocardial infarction (STEMI). All culprit lesions were located in the LCX coronary artery. RI group included 45 patients and the No RI group included 135 patients. RESULTS: Culprit LCX lesions were similarly located at a comparable distance from LCX ostium in both groups and the presence of RI was not associated with significantly more proximally located culprit LCX lesions (34.7 ± 15.2 mm compared to 30.8 ± 17.9 mm respectively, p > 0.05). The frequency distribution of culprit lesions' distance from LCX ostium showed no significant difference between both groups in any of the segments studied (10 mm each). There was no significant difference between both groups regarding markers of myocardial necrosis size as cardiac biomarkers (peak cardiac troponin-T 1077.4 ± 361.2 pg/dl vs 926 ± 462.2 pg/dl respectively, p = 0.13), (peak creatine kinase-MB 232.2 ± 81 ng/dl vs 194.7 ± 99.2 ng/dl respectively, p = 0.07) or left ventricular ejection fraction (EF 46.3 ± 6.3% vs 48.3 ± 8.3% respectively, p = 0.76). CONCLUSION: Presence of RI coronary artery, as an additional flow divider, may not be associated with more proximal culprit lesions, compared to its absence, in cases of acute LCX coronary artery occlusion. Possible underlying pathophysiologic mechanisms remain to be clarified.

Hyperuricemia and its association with carotid intima-media thickness in hypertensive and non hypertensive patients.

Carotid intima-media thickness (C-IMT) measured noninvasively by ultrasonography is widely used as a marker for increased risk of cardiovascular disease. Also hyperuricemia (HU) is a well recognized risk factor for cardiovascular diseases. The study was designed to assess the relation between hyperuricemia and carotid intima-media thickness C-IMT in patients with and without hypertension (HTN). This study included 126 patients divided into four groups: (1) Group A, included 59 hypertensive patients with hyperuricemia. (2) Group B, included 29 hypertensive patients without hyperuricemia. (3) Group C, included 17 patients with hyperuricemia and normal blood pressure without history of hypertension. (4) Group D, included 21 control subjects. We measured carotid intima-media thickness by B-mode ultrasound in the common carotid and internal carotid artery. Routine echocardiography and uric acid level was assessed for all patients. We found that C-IMT was significantly higher in group A, B and C than group D; and it was significantly higher in group A than B. This means that C-IMT is significantly higher in all hypertensive groups than control group but it was significantly higher in hypertensive hyperuricemia (group A) than those hypertensives without hyperuricemia. We also observed a higher C-IMT in hyperuricemic non hypertensive patients than control group this means that hyperuricemia per se could be a risk factor for atherosclerosis. Uric acid levels among the whole number of patients included in the study and among the groups with hyperuricemia (group A and C) were positively correlated with the intimal-media thickness (IMT) while there were no correlations in the other two groups without hyperuricemia. We found that left ventricular hypertrophy (LVH) was significantly higher in hypertensive patients (group A&B) than normotensives (group C&D) either with or without hyperuricemia and this was evident in the hypertensive hyperuricemic patients (group A); but unexpectedly we observed the presence of LVH in the hyperuricemic non hypertensive patients (group C) which was significantly higher than the control group (group D). This means that hyperuricemia is a risk factor for development of LVH hypertrophy independently of hypertension. Therefore, higher serum uric acid levels are associated with increased C-IMT and left ventricular hypertrophy in hypertensive and even non hypertensive patients. So, early screening for hyperuricemia and lowering serum uric acid levels might be beneficial in slowing progression of atherogenesis.