Mood Disorders and Cardiovascular Disease

Cardiovascular disease (CVD) accounts for 29% of global deaths, making it the leading cause of mortality worldwide. In 2004, 17.1 million people died from CVD and this number is expected to increase to 23.6 million by 2030 (World Health Organization, 2007). The most important mechanism contributing to the development and progression of CVD is atherosclerosis, the process by which fatty plaques accumulate on the inner walls of arteries, leading to their narrowing and loss of elasticity. This process is thought to generally begin with damage to the vascular endothelium, which is a layer of cells lining the vascular wall. The endothelium plays a critical role in many important functions, such as the dilation and constriction of blood vessels and arteries, thrombus (blood clot) formation, and inflammation (Quyyumi, 2003). When damage to the endothelium occurs, low-densitylipoproteins (LDL’s), commonly known as “bad” cholesterol, permeate the endothelial lining, allowing them to enter the inner layer of the arteries. An inflammatory response, the immune system’s attempt to promote self-repair, is triggered. As part of this inflammatory response, macrophages, whose function is to ingest and decompose pathogens found in the body, engulf these LDL particles and form what are called “foam cells”. The accumulation of foam cells in the arterial wall form a “fatty streak”, a yellowish slightly raised area that is the precursor to atherosclerotic plaques. If the endothelium continues to be damaged, triggering an escalation of the inflammatory response, a fibrous cap eventually covers the lesion, forming a hard plaque. The arterial wall calcifies and hardens. The formation of the plaque and the hardening of the artery cause obstruction of blood flow. If a plaque cap is unstable and becomes damaged, a thrombus can form, increasing the risk of a myocardial infarction (heart attack) or stroke (Stanner, 2005), which occur when blood flow to the heart or brain are completely obstructed. Given that endothelial damage and inflammation are so critical to the atherosclerotic process, factors that damage the endothelium or promote the inflammatory response indirectly contribute to atherosclerosis and therefore CVD.