No abstract

Our findings provide evidence to support the hypothesis that endothelial dysfunction may be an important factor in the pathogenesis of SCF.

Adiponectin has multiple protective effects on vascular endothelium through anti-inflammatory and anti-atherogenic properties. Recent data suggested that endothelial activation and inflammation may contribute to the pathogenesis of slow coronary flow (SCF). Therefore, we investigated whether adiponectin plasma concentrations were decreased in patients with SCF compared to subjects with normal coronary flow. The study population consisted of 35 patients with angiographically documented SCF in all three coronary arteries and 35 sex- and age-matched cases with normal coronary flow. Coronary flow rates of all participants were determined by Thrombolysis in Myocardial Infarction (TIMI) frame count. Plasma adiponectin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available adiponectin kits. There were no statistically significant differences between the patients with SCF and the subjects with normal coronary flow in terms of demographic characteristics and cardiovascular risk factors (P>0.05). Plasma adiponectin concentrations of patients with SCF were found to be significantly lower than those with normal coronary flow (4.77+/-3.86 mg/ml vs 10.8+/-6.60 mg/ml, P=0.001, respectively). Plasma adiponectin levels were correlated significantly and inversely with mean TIMI frame count in patients with SCF (r= -0.441, P=0.008). Furthermore, the Receiver Operator Characteristics curve of adiponectin concentrations showed that an adiponectin <4.6 mg/ml is associated with SCF with a sensitivity of 68.6%, specificity of 82.9%, positive predictive value of 80.0%, and negative predictive value of 72.5%. Our findings suggest that endothelial inflammation may play a role in the pathogenesis of SCF phenomenon.

Lead perforation is a rare complication of pacemaker implantation and associated with the risk of disastrous results like cardiac tamponade or pneumo-hemothorax. We report a patient in whom a ventricular lead perforated the right ventricle and left lung parenchyma without the development of cardiac tamponade, pneumothorax, or hemothorax. No objective evidence for perforation was found on echocardiographic evaluation and thorax computed tomography has made the definite diagnosis. In the literature available to us, it is the first reported case of an uncomplicated right ventricular and lung parenchymal perforation associated with pacemaker implantation.