HE PREVALENCE AND PROGNOsis of unrecognized myocardial infarction (MI) in older people with and without diabetes may be higher than previously suspected in population studies. [1][2][3][4] Advances in MI detection, such as cardiac magnetic resonance (CMR) imaging with late gadolinium enhancement (LGE), are more sensitive than prior methods. 5 Ascertaining the prevalence of unrecognized MI (UMI) in these groups is relevant because age and diabetes increase the risks of coronary heart disease. 6 Pathologic studies 7 indicate that subclinical coronary plaque rupture occurs frequently, particularly in diabetic individuals, which may culminate in a high prevalence of UMI.Several population studies 1-4 have described the prevalence of UMI based on electrocardiography (ECG), but ECG Author Affiliations are listed at the end of this article.

In patients with chest pain who had MI excluded by troponin-I and non-diagnostic electrocardiograms, an adenosine CMR examination predicted with high sensitivity and specificity which patients had significant CAD during one-year follow-up. Furthermore, no patients with a normal adenosine CMR study had a subsequent diagnosis of CAD or an adverse outcome.

1. We sought to determine whether the vasodilating molecule nitric oxide (NO) contributes to the forearm hyperaemia observed during prolonged rhythmic handgripping in humans. 2. Two bouts of exercise were performed during experimental protocols conducted on separate days. During each protocol the subject performed a 10 min and a 20 min bout of rhythmic (30 min-) handgripping at 15% of maximum. Two exercise bouts were required to facilitate pharmacological interventions during the second protocol. Blood flow in the exercising forearm was measured every minute with plethysmography during brief pauses in the contractions. During both exercise bouts in the first protocol, forearm blood flow increased 2-to 3-fold above rest after 1 min of handgripping and remained constant at that level throughout the exercise. 3. During the 10 min bout of exercise in the second protocol, acetylcholine was given via a brachial artery catheter at 16 jug min-' for 3 min to evoke NO release from the vascular endothelium. This caused forearm blood flow to increase above the values observed during exercise alone. '4. During the 20 min trial of handgripping in the second protocol, the NO synthase blocker NG-monomethyl-L-arginine (L-NMMA) was infused in the exercising forearm via the brachial catheter after 5 min of handgripping. The L-NMMA was infused at 4 mg min-for 10 min.5. L-NMMA during exercise caused forearm blood flow to fall to values -20-30% lower than those observed during exercise alone. When ACh was given during exercise after L-NMMA administration the rise in blood flow was also blunted, indicating blockade of NO synthase. These data suggest NO plays a role in exercise hyperaemia in humans.