Decreased and heterogeneously distributed Cx43 protein in right ventricular biopsies was significantly associated with the development of sustained ventricular tachycardia in DCM patients (P=0.03).
Observational (n=36)
Does heterogeneous loss of connexin43 protein correlate with the development of sustained ventricular tachycardia in patients with nonischemic dilated cardiomyopathy?
Heterogeneous reduction and altered distribution of connexin43 gap junction proteins in the right ventricle are associated with the development of malignant ventricular arrhythmias in nonischemic dilated cardiomyopathy.
p-value: p=0.03
INTRODUCTION: Gap junction alterations recently have been implicated in chronic heart failure, but direct evidence between gap junction manifestation in nonischemic dilated cardiomyopathy (DCM) is lacking. The current study examines whether qualitative changes or altered distribution of gap junctional connexin43 (Cx43) are related to global ventricular function and ventricular arrhythmia in DCM. METHODS AND RESULTS: We investigated 31 DCM patients (52 +/- 15 years) and 5 control subjects (55 +/- 10 years). Expression of Cx43 proteins was qualitatively and quantitatively determined using immunoconfocal microscopy in right ventricular biopsy specimens from each patient. The expression level of Cx43 protein was defined as the proportion of tissue area occupied by Cx43 (percent tissue area) in each test area. Cx43 immunoreactive signal expressed as percent tissue area was not correlated with the change in left ventricular ejection fraction (P = 0.17). Of 31 DCM patients, 23% subsequently developed sustained ventricular tachycardia (VT), which allowed retrospective division of the samples into two groups: non-VT and VT. Left ventricular ejection fraction was comparable in both groups, but the percent tissue area in the VT groups was significantly decreased compared with that of the non-VT groups (P = 0.03). Furthermore, Cx43 protein was distributed heterogeneously in the VT groups (P < 0.0001). CONCLUSION: Heterogeneous reduction of Cx43 protein may result in development of malignant ventricular arrhythmia in DCM.
Kitamura et al. (Sun,) conducted a observational in Nonischemic dilated cardiomyopathy (n=36). Connexin43 (Cx43) protein expression and distribution vs. Non-VT group was evaluated on Development of sustained ventricular tachycardia (VT) (p=0.03). Decreased and heterogeneously distributed Cx43 protein in right ventricular biopsies was significantly associated with the development of sustained ventricular tachycardia in DCM patients (P=0.03).