Our appreciation and understanding of the interrelationships between disrupted metabolic function and depression have increased significantly over the last few decades. This review focuses still more specifically on the intersections between cardiovascular disease (CVD) and major depressive disorder (MDD). General pathophysiological mechanisms implicated in both diseases include inflammation, cytokine and hypothalamic–pituitary–adrenal axis dysregulation, oxidative stress, neurotransmitter disruptions, neuroplasticity, and the microbiome. Here, we explore these mechanistic overlaps of depression and CVD, including some discussion of related and frequently comorbid disorders, such as obesity and diabetes, and the closely related “metabolic syndrome.” Finally, we discuss integrated therapeutic strategies for treating MDD comorbid with CVD.

Background: Mood disorders have been associated with a variety of cardiovascular disease (CVD) risk factors, including inflammation and large arterial stiffness, particularly while depressed, although longitudinal studies have been limited. Materials and Methods: With measurements at baseline and 8 weeks, the researchers prospectively assessed mood, levels of inflammatory markers (high-sensitivity C-reactive protein and tumor necrosis factor-alpha [TNF-α]), serum lipids, and large arterial stiffness in a cohort of 26 participants with a diagnosis of a mood disorder, enriched for current depression. Depressive symptoms were measured using the Montgomery–Šsberg Depression Rating Scale (MADRS) at baseline and 8 weeks. Associations between depressive symptoms and other measures were assessed using linear mixed models, unadjusted and adjusted for age and body mass index. Results: The mean age of the participants (n = 26) was 41.6 (standard deviation [SD] 12.8) years, and 81% were female. During the study, there was a mean (SD) MADRS score improvement of 9.5 (9.4) from baseline to 8 weeks. Reductions in the primary outcome of tumor necrosis factor-α with improvement in depression fell short of statistical significance (P = 0.076). In secondary analyses, there was a statistically significant association between improved cholesterol ratio (P = 0.038) and triglycerides (P = 0.042) with improvement in depression. There was no statistically significant change in large arterial stiffness during the study. Conclusion: Improved depressive symptoms were associated with improved cholesterol ratios even after adjustment, suggesting a possible mechanism by which acute mood states may influence CVD risk. Future longitudinal studies with extended and intensive follow-up investigating CVD risk related to acute changes and persistence of mood symptoms are warranted.

Background: Insomnia is a prevalent sleep disorder and strong risk factor for poor quality of life, depression, and other lifestylerelated diseases. Objectives: To investigate the effect of the transcutaneous vagus nerve stimulation (taVNS) on sleep electroencephalographic (EEG) in the para-chlorophenylalanine (PCPA) insomnia rats. Methods: Rats were divided into control, model, taVNS and sham taVNS (stnVNS) (stimulate the auricular margin, as transcutaneous none VNS, stnVNS) group (n=6 in each group). A week before the experiment, the electrodes were fixed to the skull of all the rats for recording the sleep EEG. PCPA was used to establish insomnia models. The rats of taVNS and stnVNS group were treated via an electroacupuncture apparatus for seven consecutive days, and simultaneously, the sleep EEG were recorded for all groups after the treatment daily. And the power spectrum analysis was used in this experiment. Results: After modeling, the percentage of power spectrum of delta frequency band significantly decreased, while the theta, alpha, and beta frequency bands significantly increased in the model group compared to the control group. After intervention, the percentage of the delta frequency band significantly increased in the taVNS group as compared to the stnVNS group. Conclusion: These results suggest that taVNS can significantly modulate the power spectrum of the delta frequency band and may constitute a potential low-cost alternative for the treatment of insomnia.

Background: A loss of t-tubules and alterations in ultrastructure occur in cultured ventricular myocytes. A similar alteration in t-tubules and ultrastructure is well documented under certain pathological conditions such as heart failure. We examined the ultrastructural changes in cultured canine cardiac cells and determined the functional impact these changes have on excitation-contraction coupling and Ca²⁺ transients. Materials, Methods and Results: Atrial, ventricle, and Purkinje myocytes were isolated by enzymatic dispersion. Atrial and ventricular myocytes were cultured for up to 48 h. Voltage clamp recordings were made with patch electrodes. Ca²⁺ transient was recorded as a laser scanning confocal microscope in myocytes loaded with Ca²⁺ fluorescent dyes. Membrane ultrastructure was imaged in myocytes stained with the membrane selective dye, di-8-ANEPP. Freshly isolated ventricular myocytes had a well-developed t-tubule system, while Purkinje cells had no t-tubules; some atrial cells exhibited a primitive t-tubule system. In atrial and Purkinje cells, the Ca²⁺ transient had a U-shaped profile with the fluorescence highest at the edge of the cell. In contrast, ventricular myocytes showed a homogeneous rise in Ca²⁺ at the edge and center of cells. Ventricular myocytes cultured for 2 days showed a nearly complete loss of t-tubules. The Ca²⁺ transients revealed a phenotypic switch from a homogeneous profile to a “U”-shaped profile. Interestingly, atrial cells in culture maintained their primitive t-tubule system. Conclusions: Our results show that atrial and ventricular myocytes respond differently to being placed in culture. Ventricular myocytes, but not atrial myocytes, quickly lose their t-tubules accompanied by a Ca²⁺ transient profile suggestive of a phenotypic switch in Ca²⁺ handling. The differential response also suggests that the various cardiac tissue types would respond differently to pathophysiological stresses.

Takotsubo cardiomyopathy is characterized by transient systolic dysfunction of apical and central parts of the left ventricle in the absence of obstructive coronary artery disease. Usually, it is triggered by intense emotional or physical stress. The prognosis tends to be good. Rare complications include heart failure, cardiogenic shock, left ventricular free wall rupture, and cardiac arrhythmia. We present a patient with takotsubo cardiomyopathy complicated by acute heart failure and atrial fibrillation. The symptoms appeared due to emotional stress. This case highlights acute emotional stress as a potent trigger for transient myocardial dysfunction with acute heart failure and rhythm disturbance.

Cognitive impairment is a common deficit in psychological, neurological, and psychosomatic disorders. Recent studies suggest physical exercise as a new method for enhancing cognition, but not all types of physical exercises are beneficial to cognition. We propose cognition-engaging physical exercises (CEPEs) framework for purposefully and selectively enhancing cognition, which could have promising clinical implications in behavioral medicine. Here, we present results of the CEPE intervention in a patient with attention-deficit hyperactivity disorder (ADHD) in comparison with a control case who underwent treadmill exercise. Preliminary results show discernible increased accuracy and decreased response time in working memory and response inhibition task performance after CEPE but not treadmill exercise. We discuss the reason why CEPE could be more beneficial as compared to non-CEPE. Moreover, clinical implications of CEPE in behavioral medicine are discussed.