Clinical Outcomes of Patients Treated With the Bioresorbable Scaffold.

INTRODUCTION: Bioresorbable scaffold (BRS) is a novel device to treat coronary lesions. It may induce a revolution in percutaneous coronary intervention (PCI) and a novel treatment termed vascular restoration therapy. These devices provide short-term scaffolding of the vessel and then dissolve, which would treat the plaque and coronary lumen without inflicting a permanent foreign body in the coronary artery. AIM: This study sought to describe scaffolding in a cohort of Tunisian coronary diseased patients and assess its immediate and mid-term outcomes. METHODS: Twenty nine patients with 42 lesions were enrolled. Mean age was 51.4 years. Mean number of scaffolds per patient was 1.57. RESULTS: Our population was at high cardiovascular risk cumulating at least 3 risk factors. Most of them presented with an acute coronary syndrome (66.6%). In 76.1% there were type A/B1 lesions. Moderate calcification was present in 42.2%. Bifurcation lesions were present in 21.3% and just one chronic total occlusion was treated. Clinical device success and clinical procedural success were respectively 93.1% and 90.3%.Using Kaplan-Meier methods. At 18 months : - The major adverse cardiac events (MACE) rate was 44.8%. - The probability of survival without target lesion revascularization (TLR) was 59.5%. - Definite or Possible scaffold thrombosis rate was 6.9%. In our study, BRS implantation was associated with a high rate of adverse events in the longer term except in case of IVUS guidance with respect of Predilatation + Sizing + Postdilatation (PSP) protocol. CONCLUSION: The theoretical concept of Scaffolding is attractive. One must put into perspective that it is still significantly evolving and improving.

Association of FV G1691A Polymorphism but not A4070G With Coronary Artery Disease.

Coronary artery disease (CAD) is one of the chief causes of death in the world. Several hypotheses have been promoted as for the origin of the disease, among which are genetic predispositions and/or environmental factors. The aim of this study was to determine the effect of factor V (FV) gene polymorphisms (Leiden, G1691A [FVL] and HR2 A4070G) and to analyze their association with traditional risk factors in assessing the risk of CAD. Our study population included 200 Tunisian patients with symptomatic CAD and a control group of 300 participants matched for age and sex. All participants were genotyped for the FVL and HR2 polymorphisms. Multivariate logistic regression was applied to analyze independent factors associated with the risk of CAD. Our analysis showed that the FVL A allele frequency ( P < 10-3, odds ratio [OR] = 2.81, 95% confidence interval [CI] = 1.6-4.9) and GA genotype ( P < 10-3, OR = 4.03, 95% CI = 2.1-7.6) are significantly more prevalent among patients with CAD compared to those controls and may be predisposing to CAD. We further found that the FVL mutation is an independent risk factor whose effect is not modified by other factors (smoking, diabetes, hypertension, dyslipidemia, and a family history of CAD) in increasing the risk of the disease. However, analysis of FV HR2 variation does not show any statistically significant association with CAD. The FVL polymorphism may be an independent risk factor for CAD. However, further investigations on these polymorphisms and their possible synergisms with traditional risk factors for CAD could help to ascertain better predictability for CAD susceptibility.

The Effect of ACE I/D Polymorphisms Alone and With Concomitant Risk Factors on Coronary Artery Disease.

BACKGROUND: Coronary artery disease (CAD), also known as atherosclerotic heart disease, is a leading cause of mortality and morbidity throughout the world. The role of insertion/deletion (I/D) polymorphisms of the angiotensin-converting enzyme (ACE) gene in the etiology of CAD remains to be more completely clarified. The aim of this study was to determine the role of the ACE I/D polymorphism in patients with CAD and to study the association together with traditional risk factors in assessing the risk of CAD. METHODS: Our study population included 145 Tunisian patients with symptomatic CAD and a control group of 300 people matched for age and sex. All participants in the study were genotyped for the ACE I/D polymorphisms obtained by polymerase chain reaction amplification on genomic DNA. RESULTS: Our analysis showed that the ACE D allele frequency ( P < 10-3; odds ratio [OR] = 5.2; 95% confidence interval [CI] = 3.6-7.6) and DD genotype ( P < 10-3; OR = 6.8; 95% CI = 4.4-10) are significantly more prevalent among patients with CAD than in controls and may be predisposing to CAD. We further found that the risk of CAD is greatly potentiated by several concomitant risk factors (smoking, diabetes, hypertension, dyslipidemia, and a family history of CAD). CONCLUSION: The ACE D allele may be predictive in individuals who may be at risk of developing CAD. Further investigations of these polymorphisms and their possible synergisms with traditional risk factors for CAD could help to ascertain better predictability for CAD susceptibility.