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Objectives: External counter pulsation therapy (ECPT) offers symptomatic relief and improves ischemia in patients with refractory angina pectoris. We aimed to determine the effects of ECPT on circulating endothelial progenitor cells (EPCs)., Methods: We prospectively studied 25 patients with angina pectoris treated with ECPT (n = 15) or receiving standard care (n = 10). The number of EPCs positive for CD34 and kinase insert domain receptor (KDR) was determined by flow cytometry and the number of colony-forming units (CFUs) was assessed in a 7-day culture, before ECPT and after 9 weeks., Results: ECPT improved anginal score from a median of 3.0 to 2.0 (p < 0.001). Concomitantly, ECPT increased EPC number from a median of 10.2 to 17.8/10(5) mononuclear cells (p < 0.05), and CFUs from 3.5 to 11.0 (p = 0.01). Flow-mediated dilatation was improved by ECPT from 7.4 to 12.2% (p < 0.001) and correlated with EPC-CFUs (r = 0.461, p = 0.027). The levels of asymmetric dimethylarginine were reduced by ECPT from 0.70 to 0.60 micromol/l (p < 0.01). In contrast, the same parameters did not change in the control group, before and after follow-up., Conclusions: The present pilot study shows, for the first time, that ECPT is associated with increased number and colony-forming capacity of circulating EPCs., ((c) 2007 S. Karger AG, Basel.)

We have prospectively evaluated the risk of incident coronary events in association with serum total homocysteine in patients with preexisting chronic coronary heart disease. A nested case-control design was used. Total homocysteine concentration was measured in baseline fasting serum samples from patients with chronic coronary heart disease enrolled in the Bezafibrate Infarction Prevention Study (n = 3,090) who developed coronary events during 6.2 years of follow-up (n = 69). They were matched for age and gender with controls without subsequent cardiovascular events. Elevated homocysteine levels were associated with 2.5 times higher risk of subsequent coronary events and each 5 mumol/l increment was associated with a 25% higher risk.

Since hyperhomocysteinemia confers a prothrombotic effect and promotes proliferation of smooth muscle cells in response to vascular injury, it might be implicated in the pathogenesis of restenosis after percutaneous coronary intervention (PCI). Our study comprised 55 patients who underwent successful PCI in the acute myocardial infarction (AMI) course. Homocysteine levels were determined within 24 h of admission. During a 1-year follow-up, 16 patients (31%) underwent repeated coronary angiography for recurrent angina or re-infarction, which demonstrated re-narrowing of > or =50% at the qualifying PCI site (clinical restenosis). Irrespective of stent deployment, clinical restenosis was not associated with higher homocysteine levels (12 +/- 7 vs. 14 +/- 11 micromol/l, p = 0.77). There was no correlation between homocysteine levels and time to restenosis (r(2) = 0.06, p = 0.35). In conclusion, elevated homocysteine levels do not predict a higher incidence of restenosis after PCI., (Copyright 2002 S. Karger AG, Basel)