Abstract:Background: Many psychiatric disorders including schizophrenia, bipolar disorder and major depression convey an excess burden of cardiovascular morbidity and mortality. The medications used to treat these conditions may further adversely affect cardiovascular risk and exacerbate health disparities for vulnerable populations. There is a clinical need to appreciate the cardiometabolic adverse effects of psychotropic medications. Methods: This paper reviews the most relevant cardiometabolic effects of psychotropic medications, organized around the components of metabolic syndrome. When known, the molecular and physiological mechanisms underlying any adverse cardiometabolic effects are detailed. Results: Many commonly used psychotropic medications, particularly antipsychotics, mood stabilizers and some antidepressants, have been independently associated with cardiometabolic risk factors such as insulin resistance, obesity and dyslipidemia. Stimulants, antidepressants that inhibit reuptake of norepinephrine, some antipsychotics and valproic acid derivatives may also increase blood pressure. Conclusion: Understanding, assessing and subsequently managing cardiometabolic complications of psychotropic medications are important to mitigate the excess cardiovascular morbidity and mortality in the clinical populations prescribed psychotropic medications. There is considerable variability in risk between medications and individuals. Timely management of iatrogenic cardiometabolic effects is critical.

Many single effects of glucocorticoids are known but complex metabolic reactions in pigs in response to a glucocorticoid challenge were not reported. Seven pigs (mean weight 69 kg) with indwelling catheters were kept in metabolic crates. After a 7-day control period they were fed for 9 days with 0.4 mg dexamethasone (dex) per kg body weight daily, followed by another 9-day post-treatment period. Hormones and metabolic parameters were continuously determined in urine or blood plasma. Treatment significantly changed all parameters except non-esterified fatty acids. Cortisol decreased from 84.5 to 4.9 nmol/l, insulin-like growth factor I (IGF-I) from 17.5 to 10.8 nmol/l and aldosterone from 0.36 to 0.13 nmol/l. The N-retention decreased from 1.07 to 0.53 g/kg(0.75) and hydroxyproline from 2.97 to 1.05 mmol/day. An increase was found for urine volume (5.2 versus 13.6 l/day), urea-N (0.90 versus 1.43 g/kg(0.75)), allantoin (6.40 versus 8.75 mmol/day), glucose (3.9 versus 4.34 mmol/l) and insulin (6.21 versus 11.16 mU/l). In the post-treatment period IGF-I revealed a compensatory pattern (control period versus post-treatment period: 17.5 versus 22.9 nmol/l) whereas the other parameters were not significantly elevated. Data suggest that dex increased N-excretion both by inhibiting mitosis and resynthesis of proteins partly via a reduced collagen synthesis. Increased allantoin concentrations additionally pointed to increased apoptosis.

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