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Structural and Electrical Myocardial Remodeling in a Rodent Model of Depression

2012; Lippincott Williams & Wilkins; Volume: 75; Issue: 1 Linguagem: Inglês

10.1097/psy.0b013e318276cb0d

1534-7796

Luca Carnevali, Mimosa Trombini, Stefano Rossi, Gallia Graiani, Massimo Manghi, Jaap M. Koolhaas, Federico Quaini, Emilio Macchi, Eugene Nalivaiko, Andrea Sgoifo,

Cardiac electrophysiology and arrhythmias

Objective Despite a well-documented association between stress and depression with cardiac morbidity and mortality, there is no satisfactory explanation for the mechanisms linking affective and cardiac disorders. This study investigated cardiac electrophysiological properties in an animal model of depression. Methods Depression-relevant physiological and behavioral parameters were measured in adult male wild-type rats during and after a period of intermittent social defeat stress (n = 12) or empty cage exposure (control, n = 11). Nine days after the last defeat/empty cage exposure, high-definition epicardial mapping was performed under anesthesia. Results Stressed animals versus controls displayed a larger reduction in the circadian amplitude of heart rate (−32% [3%] versus −13 [2%]; p = .001) and body temperature (−33% [4%] versus −5% [2%]; p = .001) rhythms, had smaller body weight gain (+11% [1%] versus +17% [1%]; p < .001), and showed a larger reduction in sucrose solution intake (−19% [6%] versus −7% [4%]; p = .006). Epicardial mapping analysis revealed a decrease in the transversal conduction velocity of the wavefront (0.23 [0.0] versus 0.27 [0.1] m/s; p = .02) and a shortening of the effective refractory period (86.8 [2.1] versus 95.9 [3.0] milliseconds; p = .01) in stressed animals. Upon killing, moderate left ventricular fibrosis was observed in the stressed group. Conclusions Intermittent social stress procedure is associated with depression-like symptoms and altered myocardial electrical stability in a potentially proarrhythmic manner. In particular, reduced myocardial refractoriness and impaired conduction, which are considered major determinants of arrhythmogenesis, represent possible mechanisms underlying cardiac vulnerability.