An asymptomatic, 54-year-old man was referred by his primary care physician for a treadmill stress echocardiogram. He had been asymptomatic from a cardiovascular standpoint. He denied chest pain, dizziness, syncope, shortness of breath, or palpitations. He occasionally has a “pulling sensation” in his chest related to positional changes but not exertion. He had a 30-year history of type I diabetes mellitus treated with subcutaneous insulin. He was recently started on simvastatin, and his only other medication was aspirin. He has a strong family history of diabetes mellitus and coronary artery disease (CAD) but no family history of sudden cardiac death (SCD). The patient remains active, is normotensive, and is not overweight. The treadmill stress echocardiogram was ordered for routine screening of CAD. Baseline ECG showed normal sinus rhythm, Q waves in leads V1 and V2, and nonspecific T wave changes in the lateral leads. Several episodes of nonsustained ventricular tachycardia (NSVT) developed; the longest run was 25 beats (50 beats/min) during the terminal portion of the stress test. The tachycardia had a left bundle-branch block morphology with a monophasic R wave in II, III, and aVF. The R wave transition point was in lead V3 on the precordial leads. The rhythm was asymptomatic, resolved spontaneously, and did not occur at rest. Also, the patient showed good exercise tolerance (achieving a workload of 13 metabolic equivalents), experienced no symptoms, had a normal BP response, and showed no change in baseline ST segments. The resting echocardiogram showed a congenital bicuspid aortic valve, normal left ventricular function without segmental wall motion abnormalities, increased septal thickness (1.9 cm) without dynamic outflow obstruction, and a trace of mitral regurgitation. The stress echocardiogram showed no stress-inducible wall motion abnormalities and no ventricular dilatation.