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Inadvertent implantation of a pacemaker lead in the left ventricle is an uncommon complication. We report a case of a permanent pacemaker lead inadvertently placed through the left subclavian artery, across the aortic valve into the left ventricle. A chest X-ray one month after the procedure showed an unusual course of the lead and a 12-lead ECG and a transthoracic echocardiogram confirmed the diagnosis. The patient refused surgical removal and remained on full anticoagulation. No clinical events were recorded during a 3-year follow-up. In such cases we propose life-long full anticoagulation as an alternative to surgical lead extraction.

Nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance and the metabolic syndrome and might be an important cardiovascular (CV) risk factor. Epicardial adipose tissue (EAT) has been implicated in the pathogenesis of obesityrelated CV disease. In an NAFLD population, we investigated EAT thickness and its possible relations to NAFLD and cardiac structure and function. This was an observational study of 57 patients with NAFLD and 48 age-matched controls. Patients with NAFLD had significantly higher body mass index (P < .0001), waist circumference (P < .0001), and high-sensitivity C-reactive protein (P ¼ .005), whereas high-density lipoprotein cholesterol (P ¼ .01) and adiponectin (P ¼ .005) levels were significantly lower. The EAT was not thicker in NAFLD but was positively related to indices of impaired glucose tolerance and inflammation, with diabetes being an independent predictor of EAT thickness (b* ¼ 0.29, P ¼ .04). No relations were found between EAT and cardiac structure and function. In conclusion, this study confirms a pathologic phenotype of NAFLD. Epicardial fat was not significantly related to NAFLD per se, but diabetes, glucose metabolism, and inflammation were closely related to its thickness.

Objectives:Atrial fibrillation has been associated with obesity in epidemiological studies. Epicardial adipose tissue is an ectopic fat depot in the proximity of atria, with endocrine and inflammatory properties that is implicated in the pathophysiology of atrial fibrillation. Inflammation also has a role in atrial arrhythmogenesis. The aim of this study was to investigate the potential relations of epicardial adipose tissue to left atrial size and to adiponectin and the pro-inflammatory mediators, high-sensitivity C-reactive protein, and interleukin-6 in paroxysmal and permanent atrial fibrillation.Methods:This was a cross-sectional study of 103 atrial fibrillation patients, divided into two subgroups of paroxysmal and permanent atrial fibrillation, and 81 controls, in sinus rhythm. Echocardiography was used for estimation of epicardial adipose tissue and left atrial size and high-sensitivity C-reactive protein, interleukin-6 and adiponectin were measured in all subjects.Results:Atrial fibrillation patients had significantly larger epicardial adipose tissue compared with controls (0.43 ± 0.17 vs 0.34 ± 0.17 cm, p = 0.002). Atrial fibrillation presence was independently related to epicardial adipose tissue thickness (b = 0.09, p = 0.002). Opposite associations of epicardial adipose tissue with left atrial volume existed in atrial fibrillation subgroups; in the paroxysmal subgroup, epicardial adipose tissue was directly related to left atrial volume (R = 0.3, p = 0.03), but in the permanent one the relation was inverse (R = −0.7, p < 0.0001). Adiponectin, high-sensitivity C-reactive protein and interleukin-6 were elevated in both atrial fibrillation groups. Only interleukin-6 was related to epicardial adipose tissue size.Conclusion:Opposite associations of epicardial adipose tissue with left atrial size in paroxysmal and permanent Atrial fibrillation and elevated inflammatory markers, suggest a role of epicardial adipose tissue and inflammation in the fibrotic and remodeling process.

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