Microparticles in acute coronary syndrome.

BACKGROUND: Emerging evidence supports the role of cell-derived microparticles (MPs) in the pathophysiology of acute coronary syndrome (ACS). OBJECTIVES: To explore the relationship between coronary and systemic MP levels, investigate the correlation between MPs, inflammatory markers and Troponin T in patients with ACS. METHODS: Thirty seven patients with ACS scheduled for percutaneous coronary interventions (PCI) were studied. Eleven patients with stable angina (SA) were included as a control group. AnnexinV+MPs (AnV+MPs) and activated platelet-monocyte aggregates (PMA) from right atrium (RA) and culprit coronary artery (CO) distal to culprit lesion were measured using flow cytometry. High sensitivity C-reactive protein (CRP), Interleukin - 6 (IL-6), tumour necrosis factor - α (TNF-α), serum amyloid A (SAA) and Troponin T were assayed. RESULTS: Total and cell specific AnV+MP expression were higher in the ACS group in both the CO and RA, with greater levels detected in the CO. Platelet activation showed positive correlation with Troponin-T and platelet MP in both CO and RA of the ACS group (r=0.4 for both; p=0.04 & p=0.03 respectively). Inflammatory markers levels did not differ between the ACS and SA patients. CONCLUSIONS: Elevated coronary and systemic MP levels and positive correlation of platelet activation with Troponin-T and platelet MPs suggest a pathogenic role for MPs in ACS.

Superior long term outcome associated with native vessel versus graft vessel PCI following secondary PCI in patients with prior CABG.

BACKGROUND: Secondary percutaneous coronary intervention (PCI) in patients with prior coronary artery bypass graft surgery is increasingly common. Graft vessel PCI has higher rates of adverse events compared with native coronary vessel PCI. AIM: To investigate the clinical outcomes of patients with prior CABG who underwent secondary PCI of either a graft vessel (GV), a native coronary vessel (NV) or both graft and native (NG) vessels. METHODS: 220 patients (84% male) who underwent PCI in our institution to either GV (n=89), NV (n=103) or both GV and NV (NG group) (n=28) were studied. The study population underwent 378 procedures (GV group; n=126, NV group; n=164 and NG group; n=88). Median follow up was for 36months [range 2-75months]. RESULTS: Target vessel revascularisation (TVR) occurred in 12.5% of the GV group and 3.6% in the NV group [p=0.0004], and was predominantly due to in-stent restenosis. Patients who had PCI due to TVR were more likely to suffer from diabetes and peripheral vascular disease. History of chronic renal failure was associated with higher risk (HR 2.21, p=0.005) whereas preserved left ventricular ejection fraction (LVEF) with lower risk (HR 0.17, p=0.0007) of death. The median survival (interval between CABG and end of follow-up period) was lower in the GV compared with the NV group (315 vs 372months p=0.005). CONCLUSION: This registry demonstrates inferior long term outcome for patients undergoing secondary PCI of GV versus NV. Where possible, a strategy of NV rather than GV target PCI should be considered in patients with prior CABG. CONDENSED ABSTRACT: Secondary PCI in patients with prior CABG surgery is increasingly common. Graft vessel PCI has inferior outcomes with high rates of restenosis and occlusion compared with native coronary vessel PCI. We studied the clinical outcomes of 220 patients with prior CABG who underwent secondary PCI to either a graft vessel (GV), a native coronary vessel (NV) or both graft and native (NG) vessels. Target vessel revascularisation was 5 times higher in the GV compared with the NV group. History of CRF and impaired left ventricular function were associated with higher risk of death. We also found that the median survival (interval between CABG and end of follow-up period) was better in the NV group compared with GV group. This registry study demonstrates inferior long term outcome for patients undergoing secondary PCI of GV. A strategy of NV rather than GV target PCI should be considered in patients with prior CABG.

Coronary artery disease and HIV; getting to the HAART of the matter.

Premature coronary disease is an important emerging paradigm affecting contemporary HIV patients. Through immune reconstruction HIV causes multisystem pathology. Recent advances in the treatment of AIDS, mainly highly active retroviral therapy (HAART), have transformed this previously terminal illness to a chronic disease. However, an interplay between traditional risk factors in a high risk predominantly male population together with the effect of the long term use of HAART in inducing a metabolic syndrome is leading to a premature and aggressive coronary artery disease phenotype not previously recognised. An association between HAART and increased cardiovascular events appears to exist. However, currently this risk appears to be low, and HAART is vital to maintain adequate viral suppression and disease control. HAART- and viral-associated dyslipidaemia can pose a significant challenge to the clinician as drug interactions may precipitate drug toxicity. In our institution a varied phenotypic pattern of coronary disease is seen angiographically from severe atherosclerotic calcific disease through to aneurysm formation and thrombotic occlusion. This is illustrated by case studies. There is a need for aggressive primary and secondary prevention strategies in this important sub-group of patients with a multi-disciplinary approach required in the management including cardiologists, metabolic physicians and lipidologists.