Autonomic dysfunction brings with it an adverse cardiovascular outlook, with increased mortality, left ventricular dysfunction, and risk of sudden death in diabetic patients with or without myocardial ischemia.78- 83 There may be several reasons for this finding. First, diabetic patients with autonomic dysfunction have a higher resting heart rate than nondiabetic patients,84 which might logically increase myocardial oxygen requirements, reduce coronary blood flow (shortened diastole), and exacerbate myocardial ischemia. Second, sensory autonomic dysfunction may result in impaired or altered perception of ischemic cardiac chest pain, leading to "silent" infarctions or atypical presentations, potentially delaying access to emergency treatment and increasing the risk of sudden death and complications of MI. This point, although generally accepted,85 remains to be conclusively demonstrated.86 Also, autonomic neuropathy manifests initially as parasympathetic dysfunction, which leads to an autonomic imbalance with a predominance of (particularly nocturnal) sympathetic activity. Increased sympathetic activity is known to be associated with activation of the RAAS, elevated arterial pressure, heart failure, and arrhythmogenesis (and, hence, sudden cardiac death). Findings from experimental studies54 also suggest direct cardiotrophic effects, promoting myocardial hypertrophy. Although this may be a direct effect of catecholamines, concomitant activation of the RAAS, and, hence, the release of Ang II, is likely to play a part.