The severity of LV dyssynchrony by phase analysis in patients with LV dysfunction, and ICD is associated with increased risk of death and appropriate ICD shock; a phase SD < 50 degrees was associated with no events at 1 year.

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Most ventricular septal defects (VSDs) are congenital. Acquired VSDs are generally due to myocardial infarction. An unusual case of VSD from penetrating trauma is described. In this case, the lack of a hemopericardium at presentation led the treatment team not to pursue cardiac pathology. Once the patient developed heart failure, the diagnosis of a VSD was made. Patients with penetrating chest wounds should undergo echocardiography, as such lesions may not be detected by physical examination or chest exploration.

Sustained sympathetic activation not only leads to vasoconstriction but also might induce paradox vasodilation. This study was performed to explore whether and how alpha(2)-receptor stimulation mediates this vasodilation. We investigated 11 healthy subjects in 33 dermal microdialysis (MD) sessions. After nerve trunk blockade, MD fibers were inserted and perfused with physiological saline until skin trauma-related vasodilation subsided. Thereafter, fibers were perfused with either clonidine solutions (10(-3), 5 x 10(-4), 10(-4) mol/l), N(G)-monomethyl-l-arginine (L-NMMA; nitric oxide synthase blocker), acetylsalicylic acid (ASA; cyclooxygenase blocker), or combinations of these. Laser-Doppler scanning of the investigated skin revealed that clonidine not only induces vasoconstriction but subsequently also vasodilation with higher concentrations (P < 0.001). In contrast, both L-NMMA and ASA induced vasoconstriction (P < 0.001). By coapplication of 10(-3) mol/l clonidine with L-NMMA or ASA, vasodilation was partially prevented (P < 0.001). Our results demonstrate that sustained alpha(2)-receptor stimulation induces vasodilation in a dose-dependent way, which is mediated by nitric oxide and prostaglandin mechanisms in human skin.

Atrial fibrillation (AF) is the most common adverse event following cardiac surgery. A recent genome wide association study identified SNPs associated with AF on chromosome 4q25 adjacent to PITX2, a cardiac transcription factor. However, the role of these genetic variants in post-CABG AF remains unknown. We used clinical and genomic data from 3 major cardiovascular surgical programs to determine the role of 4q25 variants in new-onset postoperative AF. We conducted a prospective observational study of 1,551 consecutive patients undergoing CABG surgery within 3 US centers. Haplotype tagging SNPs encompassing ~300kbp of PITX2 genic region were genotyped. In a discovery cohort of 566 patients, the previously identified SNPs associated with clinical and genomic multivariate predictors of postoperative AF were identified and then assessed in a validation cohort of 985 patients. In the discovery and replication cohorts, 31.4% and 30.0% of patients developed postoperative AF, respectively. A multivariable logistic model of the occurrence of postoperative AF confirmed older age and prior AF to be risk factors for the development of AF. 4q25 SNPs previously associated with ambulatory AF, and other SNPs in linkage disequilibrium described a haplotype that was significantly associated with new-onset postoperative AF. Odds ratio for the associated SNPs ranged between 1.50 and 1.87 (P<10 – 6) in the validation cohort, after accounting for clinical covariates. No SNP within 90kbp of the PITX2 coding region was associated with AF. We have shown in discovery and validation cohorts that non-coding 4q25 SNPs associated with ambulatory AF are also strongly associated with postoperative AF.

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