Inhaled particulate matter leads to myocardial dysfunction

Abstract

Epidemiological studies have shown that the exposure to environmental particulate matter (PM) is associated with increased cardiopulmonary mortality rates. Daily changes in PM concentration have also been positively correlated with increased hospitalizations due to lower respiratory diseases, ischemic cardiovascular events, arrhythmias, and heart failure. Human and animal models have also shown a pulmonary and systemic inflammatory response and oxidative stress associated with the exposure to environmental particles which could, in turn, alter heart oxygen metabolism and cardiovascular function. Given that mitochondria play an essential role in cellular O2 and energetic metabolism, it has been suggested that mitochondrial dysfunction is a key feature in the development of cardiac alterations during the exposure to PM. This chapter is focused in the discussion of the different mechanisms triggered by PM exposure that may lead to myocardial dysfunction, emphasizing the role of the systemic proinflammatory mediators released after PM inhalation.