C-reactive protein elevation independently influences the procedural success of percutaneous balloon mitral valve commissurotomy.

BACKGROUND: Markers of systemic inflammation including C-reactive protein (CRP) appear to predict morbidity and mortality in various clinical conditions. The presence of systemic inflammation and its impact on the procedural success of percutaneous balloon mitral valve commissurotomy (PBMC) in patients with rheumatic mitral stenosis has not been previously demonstrated. METHODS: Measurements of CRP with a high-sensitivity assay were performed at the time of PBMC or during post-procedural follow-up in 119 patients with mitral stenosis of rheumatic morphology. Patients were questioned to exclude confounders of CRP elevation and categorized into undetectable (< or =0.10 mg/L) and detectable (>0.10 mg/L) CRP levels. Detectable levels were further classified into assay range (>0.10 and < or =6.0 mg/L) and elevated (>6.0 mg/L). RESULTS: CRP was detectable in 76% of patients and elevated (>6.0 mg/L) in 36% of patients studied. Procedural success occurred in 89% of patients with undetectable CRP, as compared with only 67% in patients with detectable CRP (P =.028). This effect remained after controlling for age and valve score (previously described predictors of PBMC success). CONCLUSIONS: Systemic inflammation is common in patients with rheumatic mitral valve stenosis, and the relationship between procedural success and CRP suggests persistent inflammation may affect the results of PBMC.

The complementary use of glycoprotein IIb/IIIa inhibitors and drug-eluting stents in contemporary percutaneous coronary intervention.

The percutaneous treatment of symptomatic, obstructive coronary artery disease continues to undergo evolutionary changes that have led to an increase in the number of procedures performed each year. Studies on the adjunctive use of thienopyridines and glycoprotein (GP) IIb/IIIa inhibitors during and following percutaneous coronary intervention (PCI) have demonstrated a reduction in the ischemic complications following PCI. One of the GP IIb/IIIa inhibitors, abciximab, has been shown to reduce mortality one year after successful PCI compared with placebo. Despite the reduction in ischemic complications and a potential reduction in mortality at one year, the antiplatelet agents have not consistently been shown to affect the rates of restenosis following PCI. Recent, exciting data on the use of drug-eluting stents (DES) in diseased coronary vessels has generated immense enthusiasm within the interventional community about the future ability to dramatically reduce the rates of restenosis following PCI with the use of this novel stent technology. With the introduction and assumed widespread use of these new stents, it appears that the contemporary interventional cardiologist will now have two complementary therapies available for use during percutaneous revascularization: GP IIb/IIIa inhibitors for the reduction of ischemic complications during and immediately following PCI, and DES for the prevention of long-term restenosis within the treated vessel segment. Caution should be taken not to view these valuable therapies as mutually exclusive but rather to recognize that each addresses critical aspects of percutaneous revascularization that have been improved upon after being studied in thousands of patients in controlled, randomized clinical trials.