Individuals exhibiting precursor symptoms of diabetes mellitus or reaching diagnostic thresholds for diabetes are at increased risk of death due to cardiovascular disease (CVD). Moreover, patients with diabetes alone, as well as those who have diabetes paired with established CVD, remain undertreated for cardiovascular risk factors. The clear correlation between these disease processes has led many to speculate that they share common pathogenetic processes. Recent research has made it increasingly evident that the core metabolic defects that mark diabetes, including impaired glucose tolerance, insulin resistance, and proinflammatory and prothrombotic states, lead to endothelial dysfunction and accelerate atherogenesis. Moreover, increases in sympathetic tone with diabetes are associated with changes in cardiac and vascular function that lead to hypertension, left ventricular dysfunction, and cardiac autonomic neuropathy; such changes set the stage for arrhythmia, silent infarction, and sudden death. Furthermore, diabetes-related changes in metabolic and autonomic functioning, as well as increases in inflammatory and thrombotic signaling, compromise the ability of myocardial and vascular tissue to remodel after injury and to recover and sustain functionality. Because potentiation of atherogenesis and cardiac dysfunction occurs in the presence of early diabetic symptoms as well as in the established disease, early implementation of strategies to reduce cardiovascular risk factors and to slow diabetes progression may help to improve long-term outcomes for at-risk individuals. Such interventions may include well-established treatments for hypertension and dyslipidemia, diet improvements, weight loss, and exercise as well as novel pharmacologic interventions aimed at newly identified therapeutic targets.