It has been proposed that insulin-mediated changes in muscle perfusion modulate insulin-mediated glucose uptake. However, the putative effects of insulin on the microcirculation that permit such modulation have not been studied in humans. We examined the effects of systemic hyperinsulinemia on skin microvascular function in eight healthy nondiabetic subjects. In addition, the effects of locally administered insulin on skin blood flow were assessed in 10 healthy subjects. During a hyperinsulinemic clamp, we measured leg blood flow with venous occlusion plethysmography, skin capillary density with capillaroscopy, endothelium-(in)dependent vasodilatation of skin microcirculation with iontophoresis of acetylcholine and sodium nitroprusside combined with laser Doppler fluxmetry, and skin vasomotion by Fourier analysis of microcirculatory blood flow. To exclude nonspecific changes in the hemodynamic variables, a time-volume control study was performed. Insulin iontophoresis was used to study the local effects of insulin on skin blood flow. Compared to the control study, systemic hyperinsulinemia caused an increase in leg blood flow (؊0.54 ؎ 0.93 vs. 1.97 ؎ 1.1 ml ⅐ min ؊1 ⅐ dl ؊1 ; P < 0.01), an increase in the number of perfused capillaries in the resting state (؊3.7 ؎ 3.0 vs. 3.4 ؎ 1.4 per mm 2 ; P < 0.001) and during postocclusive reactive hyperemia (؊0.8 ؎ 2.2 vs. 5.1 ؎ 3.7 per mm 2 ; P < 0.001), an augmentation of the vasodilatation caused by acetylcholine (722 ؎ 206 vs. 989 ؎ 495%; P < 0.05) and sodium nitroprusside (618 ؎ 159 vs. 788 ؎ 276%; P < 0.05), and a change in vasomotion by increasing the relative contribution of the 0.01-to 0.02-Hz and 0.4-to 1.6-Hz spectral components (P < 0.05). Compared to the control substance, locally administered insulin caused a rapid increase (ϳ13.5 min) in skin microcirculatory blood flow (34.4 ؎ 42.5 vs. 82.8 ؎ 85.7%; P < 0.05). In conclusion, systemic hyperinsulinemia in skin 1) induces recruitment of capillaries, 2) augments nitric oxide؊mediated vasodilatation, and 3) influences vasomotion. In addition, locally administered insulin 4) induces a rapid increase in total skin blood flow, independent of systemic effects. Diabetes 51: 1515-1522, 2002

Additional CTO PCI within 1 week after primary PCI for STEMI was feasible and safe. In patients with STEMI and concurrent CTO, we did not find an overall benefit for CTO PCI in terms of LVEF or LVEDV. The finding that early CTO PCI in the left anterior descending coronary artery subgroup was beneficial warrants further investigation. (Evaluating Xience and Left Ventricular Function in Percutaneous Coronary Intervention on Occlusions After ST-Segment Elevation Myocardial Infarction; NTR1108).

Journal of Cardiovascular Magnetic Resonance Open AccessMeeting abstract 123 Functional recovery after acute myocardial infarction: a comparison between angiography, electrocardiography and cardiovascular magnetic resonance measures of microvascular injury

Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.

The contrast-devoid core of revascularized STEMI contains extensive erythrocyte extravasation with microvascular damage. Attenuating the reperfusion-induced haemorrhage may be a novel target in future adjunctive STEMI treatment.