Research suggests psychological distress could result in arterial endothelial injury and coronary heart disease (CHD). Studies also show Posttraumatic Stress Disorder (PTSD) victims have higher circulating catecholamines and other sympathoadrenal-neuroendocrine bioactive agents implicated in arterial damage. Here we analyzed resting 12-lead electrocardiographic (ECG) results among a national sample of 4,462 nonhospitalized male veterans (mean age = 38) about 20 years after military service by current posttraumatic stress (n = 54), general anxiety (n = 186), and depression (n = 157) disorders. ECGs were interpreted by board-certified cardiologists and summarized using the Minnesota Code Manual of Electrocardiographic Findings. Psychiatric disorders were diagnosed based on the Diagnostic Interview Schedule, Version III. Controlling for age, place of service, illicit drug use, medication use, race, body mass index, alcohol use, cigarette smoking, and education, PTSD (odds ratio [OR] = 2.23, 95% confidence interval [CI] = 1.17-4.26, p < 0.05), anxiety (OR = 1.51, 95% CI = 1.03-2.22, p < 0.05), and depression (OR = 1.71, 95% CI = 1.13-2.58, p < 0.01) were associated with having a positive ECG finding. Specific results indicate PTSD was associated with atrioventricular (AV) conduction defects (OR = 2.81, 95% CI = 1.03-7.66, p < 0.05) and infarctions (OR = 4.44, 95% CI = 1.20-16.43, p < 0.05), while depression was associated with arrhythmias (OR = 1.98, 95% CI = 1.22-3.23, p < 0.01). The PTSD associations for AV conduction defects and infarctions held, even after controlling for current anxiety and depression. These findings suggest psychological distress may result in CHD, because we controlled for obvious biases and confounders, the men studied had current PTSD due to combat exposures 20 years ago, combat exposure was associated with anxiety and depression among these men, and the men were disease free a military induction. These findings suggest the need for clinical surveillance among combat veterans, better psychobiologic models of CHD pathogenesis, and additional research.