Workplace factors can impact upon many pathways leading to CVD, promoting underlying pathological processes, as well as triggering acute cardiac events. Neuroendocrine and autonomic mechanisms are the main mediators. Elevated catecholamines and cortisol have been demonstrated in relation to occupational stressors. Exposure to job strain has been directly linked to increased workplace ambulatory blood pressure (AmBP) and hypertension. The connection among chronic exposure to job strain, high workplace AmBP and increased left ventricular mass has also been empirically confirmed. Experimental data implicate stress mechanisms at several steps in the early and late stages of atherogenesis, with corroborative occupational epidemiologic evidence for some of these processes. Patterns consistent with the Cardiovascular Metabolic Syndrome have been reported in association with Effort-Reward Imbalance. In coronary patients laboratory mental stress can provoke myocardial ischemia, the biological determinants of which are frequently work-related. However, work-place field studies of myocardial ischemia are lacking. Stress mechanisms can also compromise cardiac electrical stability; several indicators of which can now be monitored during work. Circadian and septadian data suggest that workplace factors could precipitate myocardial infarction and sudden cardiac death at vulnerable time intervals in at-risk individuals.