Plasma levels of melatonin in dilated cardiomyopathy

Abstract

Background Melatonin is a multifunctional indolamine and has a cardioprotective role in a variety of cardiovascular processes via antioxidant, anti‐inflammatory, antihypertensive, antithrombotic, and antilipemic effects. It has been reported that lower levels of circulating melatonin are significantly associated with a higher risk of acute myocardial infarction (AMI) and later cardiac remodeling. However, levels of melatonin in patients with dilated cardiomyopathy (DCM) and associations between melatonin levels and cardiac function remain unclear. Methods and Results We measured and compared plasma levels of melatonin in 61 control subjects, 81 AMI patients, and 77 DCM patients. Plasma levels of melatonin were progressively decreased from 71.9 pg/mL in the control group to 52.6 pg/mL in the DCM group and 21.9 pg/mL in the AMI group. Next, we examined associations of melatonin levels with parameters of laboratory data, echocardiography, and right‐heart catheterization. In the DCM patients, circulating melatonin showed significant correlations with both high‐sensitivity troponin T ( R = −0.422, P < 0.001) and cardiac output ( R = 0.431, P = 0.003), but not with B‐type natriuretic peptide (BNP), left ventricular ejection fraction (LVEF), pulmonary artery wedge pressure, or pulmonary artery pressure. Conclusion Patients with not only AMI but also DCM had lower circulating melatonin levels. Circulating melatonin levels appear to correlate with myocardial injury and cardiac output in DCM patients.

High plasma levels of pro-inflammatory factors interleukin-17 and interleukin-23 are associated with poor outcome of cardiac-arrest patients: a single center experience

“…Bro-Jeppesen et al reported baseline plasma IL-6 and IL-10 levels were significantly higher in non-survivors compared with survivors [11,12]. Melatonin, an anti-oxidant and anti-inflammatory agent, improves neurological outcomes and preserves hippocampal mitochondrial function in cardiac arrest [36], which may be associated with its protection against inflammation [22,[37][38][39], myocardial ischemia-reperfusion injury [40][41][42][43], ventricular fibrillation [44], cardiac hypertrophy [45], dilated cardiomyopathy [46], and mitochondria-related disorders [47,48]. As neutralization of IL-17 rescues neuroinflammation [49], melatonin may contribute to the complex role of IL-17 signaling in ROSC [50].…”

Melatonin’s Impact on Antioxidative and Anti-Inflammatory Reprogramming in Homeostasis and Disease

“…In the field of cardiovascular effects, melatonin protects against ischemia/reperfusion injury (IRI) [ 62 , 117 , 118 , 119 , 120 , 121 ] and hypertension [ 122 , 123 , 124 ], as an endogenous effect, nutritional supplement, or acute parenteral administration [ 125 , 126 ]. In addition, it appears that other promising effects such as anti-apoptotic, anti-inflammatory [ 127 ], preconditioning [ 118 , 128 ], myocardial infarction [ 129 , 130 , 131 ], and even an implication in heart failure [ 132 , 133 , 134 , 135 ] have been documented. However, it seems than in some conditions, melatonin can have deleterious effects, as exaggerated collagen and glycosaminoglycans deposition and increased size in post-myocardial infarction scar have also been reported [ 136 , 137 ].…”

“…In addition, melatonin improves reverse remodeling after cardiac resynchronization therapy [ 132 ]. Melatonin has lower levels not only in patients with myocardial infarction, but also in dilated cardiomyopathy, and is correlated with cardiac output [ 133 ].…”

ALDH2 contributes to melatonin-induced protection against APP/PS1 mutation-prompted cardiac anomalies through cGAS-STING-TBK1-mediated regulation of mitophagy

“… 35 Although exactly how AD pathology leads to low-circulating melatonin levels is beyond the scope of our present study, but interrupted circadian cycle (defects in the retina-suprachiasmatic nucleus-pineal pathway), 48 depletion of the melatonin precursor (serotonin), 49 and pineal gland calcification and shrinkage 50 are all known to contribute to AD-induced loss of melatonin. A reduction in circulating melatonin levels was also reported in many other myopathies, including hypertensive cardiomyopathy, 51 dilated cardiomyopathy, 52 and LV remodeling following myocardial infarction. 53 Perhaps, the most intriguing finding from our present study is the involvement of ALDH2-cGAS-STING-TBK1 in the regulation of mitophagy in melatonin-mediated cardioprotection in AD (Fig.…”