L-arginine ameliorates the abnormal sympathetic response of the dysfunctional human coronary microvasculature.

A nitric oxide (NO)-related defect may contribute to abnormal coronary sympathetic responses that can cause ischemia in patients with endothelial dysfunction. Because L-arginine, the NO synthase (NOS) precursor, augments NO bioactivity, we hypothesized that L-arginine would improve dysfunctional coronary sympathetic responses. Eleven patients with atherosclerosis or its risk factors were challenged with the cold pressor test, a specific provocative test of cardiac sympathetic activity, after 3 separate and sequential intracoronary infusions, as follows: 1) Normal saline; 2) L-NMMA, a competitive inhibitor of NOS; and 3) L-arginine. Study patients exhibited abnormal microvascular responses with coronary vascular resistance (CVR) increasing by 22.3 +/- 9.7% (mean +/- 1 SEM), p < 0.01. In addition, the change in coronary blood flow (CBF) did not correlate with the change in rate pressure product (RPP), r = -0.29, p = NS, suggesting an uncoupling of CBF from cardiac work. In the presence of L-NMMA, the CVR response, 10.3 +/- 9.8%, did not differ from the baseline response, and there was no relationship between the changes in CBF and RPP, r = 0.13, p = NS. In contrast, L-arginine ameliorated the CVR response, -3.2 +/- 3.1%, p < 0.05 vs baseline response, and restored the normal correlation between the changes in CBF and RPP, r = 0.74, p < 0.01. L-arginine not only improved abnormal microvascular responses to sympathetic activation, but it also restored the coupling that normally exists between coronary blood flow and cardiac work. L-arginine warrants further investigation as a therapy for coronary artery disease.

Assessment of contemporary stent deployment using intravascular ultrasound.

Four second- and third-generation coronary stents were evaluated using QCA and intravascular ultrasound for adequacy of stent expansion, the influence of disease burden on adequacy of deployment, and postdeployment structural effects on the artery. Despite satisfactory stent deployment rates on angiography of 92 %, adequate stent deployment by IVUS ranged from 38% to 55%. There was no significant difference in deployment success across the four stent types. Lesions with significant plaque burden were associated with a lower rate of deployment success (P = 0.04). Twenty-one edge dissections were demonstrated by IVUS; only six were detected by angiography. Observations made on first-generation stents regarding adequacy of deployment still hold true for newer-generation stents. Significant plaque burden is an independent negative predictor of stent deployment success. The presence of IVUS-detected edge dissections indicates that the extent of injury during PCI extends beyond the physical length of the stent.