HF and Intensive Care: Editorial Comment Cardiology 2020;145:356–358 No Time to Die: Can We Fix a Broken Cardiovascular Clock? Simon Matskeplishvili Alexander Kalinkin Medical Research and Education Center, Lomonosov Moscow State University, Moscow, Russia Received: February 17, 2020 Accepted: February 24, 2020 Published online: April 29, 2020 Simon Matskeplishvili, MD, PhD Medical Research and Education Center, Lomonosov Moscow State University 27/10 Lomonosovsky prospect Moscow 119234 (Russia) simonmats @yahoo.com © 2020 S. Karger AG, Basel karger@karger.com www.karger.com/crd DOI: 10.1159/000506730 Circadian (from Latin circā diēm – around a day) rhythms (CR) – the biological oscillations based upon our built-in diurnal clock – have a profound effect on human physiology and cellular functions. A master clock in the suprachiasmatic nucleus of the hypothalamus, or SCN, coordinates and synchronizes all the biological clocks in a living organism [1]. Historically, the first research of CRs was published in 1729 by a French astronomer Jean Jacques d’Ortous de Mairan [2]. He experimented with plants and sleep cycles and observed that the daily opening and closing of the leaves of a heliotrope plant in a dark room occurred with- out any exposure to sunlight. This proved that plants had intrinsic CR working regardless of lighting conditions. For quite a long time, it was not clear whether the CR existed as a response to the external stimuli or whether there was an endogenous trigger behind physiological changes. It took many years of research until the Nobel Prize for Medicine in 2017 was awarded to Michael Young, Michael Rosbash and Jeffrey Hall for their discov- eries of molecular mechanisms controlling the CR [3]. Genome-wide transcriptome, metabolome and proteome studies have significantly improved our understanding of the circadian regulation. In addition to the central clock, many fundamental “housekeeping” mechanisms were identified in different tissues. Importantly, disorders of human biological clocks in- crease the risk of disease. These disturbances can arise from various sources and are important to identify as they can cause serious dysfunction in major internal systems or even increase the probability of many diseases includ- ing depression, stroke and cancer. CRs continuously control our cardiovascular system through gene and protein manipulation resulting in the diurnal variation of cardiovascular events [4]. In the morning, heart rate, blood pressure, platelet reactivity, vasoconstriction and intra-arterial pressures increase af- ter the night-time dip, coupled with endothelial dysfunc- tion and decreased fibrinolysis. This leads to increased vulnerability of the cardiovascular system leading to acute cardiac events, such as sudden cardiac death, acute coro- nary syndrome, stroke, and ventricular arrhythmias [5]. The first analysis of such a relationship was performed by Schneider [6] in 1859 who investigated time and cause of death in 114,183 people who died in Berlin between January 1847 and December 1857. Only 126 years later, Muller et al. [7] published the first study on circadian variation of the incidence of cardiovascular events. Au-