Structural and Electrical Myocardial Remodeling in a Rodent Model of Depression

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

doi:10.1097/psy.0b013e318276cb0d

Cited by 44 publications

(35 citation statements)

References 25 publications

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“…Many clinical studies have suggested that depression is an independent risk of VA and sudden cardiac death [22], [23], and animal experiments have shown a link between depression and increased vulnerability to arrhythmias [24], [25]. Therefore, we hypothesized that depression would exacerbate the electrical instability and increase the onset of VA in a post-infarcted heart.…”

Section: Discussionmentioning

confidence: 97%

“…A previous meta-analysis suggested that post-MI depression is associated with a 1.6- to 2.7-fold increased risk of impaired cardiovascular outcomes within 24 months [5]. Depression is associated with abnormal cardiac electrophysiology features, such as prolonged QT duration and low heart rate variability [6], and significantly increases the risk of ventricular arrhythmia (VA) and sudden cardiac death (SCD) [7], [8].…”

Section: Introductionmentioning

confidence: 99%

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Depression Increases Sympathetic Activity and Exacerbates Myocardial Remodeling after Myocardial Infarction: Evidence from an Animal Experiment

et al. 2014

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Depression is an independent risk factor for cardiovascular events and mortality in patients with myocardial infarction (MI). Excessive sympathetic activation and serious myocardial remodeling may contribute to this association. The aim of this study was to discuss the effect of depression on sympathetic activity and myocardial remodeling after MI. Wild-type (WT) rats were divided into a sham group (Sham), a myocardial infarction group (MI), a depression group (D), and a myocardial infarction plus depression group (MI+D). Compared with controls, the MI+D animals displayed depression-like behaviors and attenuated body weight gain. The evaluation of sympathetic activity showed an increased level in plasma concentrations of epinephrine and norepinephrine and higher expression of myocardial tyrosine hydroxylase in the MI+D group than the control groups (p<0.05 for all). Cardiac function and morphologic analyses revealed a decreased fractional shortening accompanied by increased left ventricular dimensions, thinning myocardium wall, and reduced collagen repair in the MI+D group compared with the MI group (p<0.05 for all). Frequent premature ventricular contractions, prolonged QT duration and ventricular repolarization duration, shorted effective refractory period, and increased susceptibility to ventricular arrhythmia were displayed in MI+D rats. These results indicate that sympathetic hyperactivation and exacerbated myocardial remodeling may be a plausible mechanism linking depression to an adverse prognosis after MI.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Depression Increases Sympathetic Activity and Exacerbates Myocardial Remodeling after Myocardial Infarction: Evidence from an Animal Experiment

et al. 2014

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“…This stress involves placement of a rodent into the cage of an aggressive “resident” conspecific that will attack the intruder (Koolhaas et al, 1997). Repeated resident-intruder stress results in HPA dysfunction, decreased social interaction, anxiety-like behaviors, anhedonia, self-administration of drugs of abuse and decreased heart rate variability, alterations in circadian rhythm amplitudes and long lasting pro-arrhythmic effects (Carnevali et al, 2013b; Miczek et al, 2004; Rygula et al, 2005; Tornatzky and Miczek, 1994; Wood et al, 2012; Wood et al, 2010). Substantial individual variability exists in the consequences of resident-intruder stress.…”

Section: Stress Coping Strategy and Individual Differences In Stress mentioning

confidence: 99%

The brain norepinephrine system, stress and cardiovascular vulnerability

Wood

Valentino

2017

Neuroscience & Biobehavioral Reviews

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Chronic exposure to psychosocial stress has adverse effects on cardiovascular health, however the stress-sensitive neurocircuitry involved remains to be elucidated. The anatomical and physiological characteristics of the locus coeruleus (LC)-norepinephrine (NE) system position it to contribute to stress-induced cardiovascular disease. This review focuses on cardiovascular dysfunction produced by social stress and a major theme highlighted is that differences in coping strategy determine individual differences in social stress-induced cardiovascular vulnerability. The establishment of different coping strategies and cardiovascular vulnerability during repeated social stress has recently been shown to parallel a unique plasticity in LC afferent regulation, resulting in either excitatory or inhibitory input to the LC. This contrasting regulation of the LC would translate to differences in cardiovascular regulation and may serve as the basis for individual differences in the cardiopathological consequences of social stress. The advances described suggest new directions for developing treatments and/or strategies for decreasing stress-induced cardiovascular vulnerability.

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“…In the study by Verrier et al (344) discussed above, cardiac fibrillatory threshold potentials were reduced by 40% in stressed dogs. A more recent experiment in stressed rodents also reported decreased effective refractory periods, an impaired conduction of electrical activities, and ventricular fibrosis (50). Autonomic imbalance and catecholamine surges are implicated in the arrhythmogenic effects of emotional disturbance, as shown by Lampert et al (189,190) who reported that increases in catecholamine levels during human emotional turmoil are correlated with changes in heart rate, systolic blood pressure, and repolarization indexes (T-wave amplitude, T-wave area, and T-wave alternans, which is a periodic beat-to-beat variation in the amplitude or shape of the ECG and is an indicator of those at high risk of developing potentially fatal cardiac arrhythmias).…”

Section: Stress-induced Cardiac Ischemia and Arrhythmiasmentioning

confidence: 99%

“…Interestingly, the intensity of the cardiac autonomic response is related to the degree of the emotional perturbation (302). The social defeat test can also induce a proarrhythmogenic state in the myocardium, possibly through diminishing myocardial refractoriness and impaired conduction (50).…”

Section: Animal Models Of Physical Stressmentioning

confidence: 99%