clinicaltrials.gov Identifier: NCT00091637.

The purpose of this study was to assess the safety and feasibility of percutaneous interventional closure of patent foramen ovale (PFO) with or without atrial septal aneurysm (ASA) in symptomatic patients. Between June 1999 and June 2002, we performed transcatheter closure of PFO in 256 consecutive symptomatic patients (female/male = 1.45; mean age 48 +/- 16 years; range 14-75): ischemic stroke (n = 101), transient ischemic attack (n = 144), peripheral and coronary arterial embolism (n = 17); multiple events (n = 23); platypnea-orthodeoxia syndrome (n = 2); refractory hypoxemia (n = 1); and migraine aura (n = 27). The implanted devices were an Amplatzer PFO Occluder (n = 248), a Gore-HELEX Septal Occluder (n = 4), and PFO STAR (n = 4). Most procedures (n = 176.69%) were done under two-dimensional intracardiac echocardiography (ICE) guidance alone; in the last 30 patients, 3D/4D ICE reconstruction (TomTec Imaging Systems) 6mbH was obtained. In 30 cases, ICE and contrast enhanced-TCD have been used simultaneously in the catheterization laboratory. The devices were placed correctly in all patients. Mean fluoroscopy time was 9.45 +/- 5 minutes (range = 2.5-35 minutes); mean procedural time was 57 +/- 21 minutes (range = 15-135 minutes). Total occlusion rate at follow-up (mean 19 months, range 1-33) was 98.1%. No significant recurrent neurological events were observed. Transcatheter closure of PFO with or without ASA is a safe and effective, minimally invasive procedure that ensures high closure rate and avoids life-long anticoagulation. Mid-term follow-up results appear favorable with respect to recurrent thromboembolic events.

No abstract

The ICE evaluation of ASDs allows quantitative and qualitative information for both proper ASO selection and optimal device placement, thus eliminating the cumbersome balloon-sizing maneuver and the need for general anesthesia during TEE monitoring.

Objective-The purpose of this study was to investigate the relationship of plasma homocysteine (tHcy) levels with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) in high-risk patients undergoing coronary angiography for suspected CAD. Methods and Results-In 936 consecutive patients, we measured LVEF, tHcy, folate levels, and quantified CAD with a modified Duke Index score. We also genotyped patients at the methylen-tetrahydrofolate-reductase 677C3 T polymorphism. Hyperhomocysteinemia (HHcy) was defined as tHcy levels Ն15.46 mol/L; total and cardiovascular mortality was assessed at follow-up that lasted 43 months (median). CAD was confirmed in 75% of patients and ruled out in the rest (non-CAD group). No relationship of HHcy with either arterial hypertension or the CAD score was found. In contrast, there was a significant inverse relationship of tHcy with LVEF in arterial hypertensive but not in normotensive patients, regardless of previous myocardial infarction. At logistic regression, HHcy was the strongest predictor (Pϭ0.001) of a low (Ͻ40%) LVEF, followed by type 2 diabetes mellitus and cigarette smoking. At follow-up, HHcy significantly predicted cardiovascular mortality but only in the arterial hypertension subgroup. Key Words: homocysteine Ⅲ arterial hypertension Ⅲ coronary artery disease Ⅲ survival Ⅲ MTHFR 677C3 T polymorphism Ⅲ left ventricular ejection fraction H yperhomocysteinemia (HHcy) might play a causative role in the development of coronary artery disease (CAD) and cardiovascular (CV) disease 1 and originates from an interplay of environmental factors, such as folate and B 12 vitamin deficiency, and genetic factors, including the thermolabile variant (677C3 T) of methylen-tetrahydrofolatereductase (MTHFR) gene. 2,3 On the basis of plasma homocysteine (tHcy) concentrations, HHcy has been classified as mild/moderate (15 to 30 mol/L), intermediate (30 to 100 mol/L), and severe (Ͼ100 mol/L). 4 Mild/moderate HHcy is common (5% to 7%) in the population and might increase the risk of CV disease, 3,5,6 but its association with such phenotype is weaker than that of severe HHcy. Prospective studies in high-risk subjects suggested that HHcy can be a risk factor for overall mortality, 7 recurrent CV events, and hospitalization, 8 but studies of healthy subjects did not confirm this contention. 8 -10 Thus, it would appear that mild/ moderate HHcy plays a minor role for CV disease and might attain a greater importance only in high-risk patients. Conclusions-InTheoretically, HHcy could increase blood pressure by decreasing the endothelial production of NO, inducing accumulation of the endogenous NO synthase inhibitor asymmetrical dimethylarginine, 11 or lowering NO bioactivity through induction of oxidative stress. 12,13 Nonetheless, only a weak association between HHcy and arterial hypertension was found, 14 -18 and there are no data in high-risk patients.HHcy can exert nefarious effects on the heart by inducing coronary arteriolar remodeling, left ventricular (LV) hypertrophy,...