Cardiovascular atherothrombosis is the most common cause of death globally, with several well-known risk factors. Air pollution is a byproduct of fuel combustion by motor vehicles, power plants and industrial factories. It is composed of gases, fluids and particulate matter (PM) of different sizes, which include basic carbon, organic carbonic molecules and metals such as vanadium, nickel, zinc and iron. These particles are subdivided by their median size, a major contributing factor for their capability to enter the human body through the respiratory system. Most of the epidemiological studies have shown correlation between acute and long-term exposure to air pollution elements and cardiovascular morbidity in general, and angina pectoris and acute myocardial infarction specifically. Physiological studies have found different arrhythmias as the etiologic cause of cardiovascular morbidity and mortality following exposure to air pollution. A major finding was a decline in heart rate variability, a phenomenon known as endangering for cardiovascular morbidity and mortality, especially in patients after acute myocardial infarction. To date, several pathways have been proposed, including a hypercoagulable state following an inflammatory response, cardiac nervous autonomic disequilibrium, endothelial dysfunction with blood vessel contraction and direct toxic impact on cardiac muscle. Additional research is needed for clarifying the pathophysiological pathways by which air pollution affects the cardiovascular system. That might allow forthcoming with preventive measures and correct treatment, and hence a decrease in cardiovascular morbidity and mortality. Another important target is dose-outcome correlation curves for safety threshold calculation as a basis for air pollution regulations.