Revised: January 3, 2013
Accepted: January 23, 2013
Published online: February 23, 2013
Cold is a seasonal and circadian risk factor for cardio- and cerebrovascular morbidity and mortality. Colder temperatures have been associated with higher blood pressure (BP), based on studies which show that BP levels measured during the summer months are generally lower than those measured during the winter months. Residents in geographic areas which have greater seasonal temperature differences show greater fluctuation in BP. Surprisingly, atmospheric pressure, rainfall, and humidity were not related to BP levels. The increased sympathetic nervous activity due to cold, as evidenced by elevated BP and by plasma and urinary catecholamines, has been proposed as being the underlying etiology. Patients with heart failure may experience, in cold conditions, endothelial dysfunction and produce fewer endogenous vasodilators (e.g., nitric oxide, prostaglandins) and more endogenous vasoconstrictors (e.g., endothelin), thus increasing afterload. Arterial stiffness is also related to seasonal BP changes. Increased BP, arterial stiffness and endothelial dysfunction could predispose to increased coronary and cerebrovascular events. Improved protection against lower temperatures or increased doses of existing medications or the addition of newer medications could lead to a reduction in increased cardiovascular mortality in winter. Here, we briefly review findings from existing literature and provide an update on seasonal long-term variation in BP along with the related complications.