Impaired myocardial perfusion score and inflammatory markers in patients undergoing primary angioplasty for acute myocardial infarction.

BACKGROUND: Microcirculatory dysfunction during acute myocardial infarction is mediated by various mechanisms including inflammation, thrombus, or plaque embolization. We hypothesize that patients with acute myocardial infarction and admission Thrombolysis in Myocardial Infarction (TIMI) myocardial perfusion grade (TMP) < 2 had increased inflammatory status as measured by high sensitivity C-reactive protein (hs-CRP). METHODS: From January 2002 to December 2003, 166 patients (178 lesions) were referred for primary percutaneous coronary intervention. Patients were stratified based on pre-PCI TMP < 2 or TMP 2. Univariate and multivariate predictors of in-hospital and 30-day death were determined with logistic regression. RESULTS: Pre-PCI TMP < 2 was found in 66% vs 34% with TMP 2 (P < .001). Hs-CRP levels were high in both groups but not significantly different (37.9 +/- 6 vs 33.7 +/- 6 mg/L, P = .63). Patients with TMP < 2 had higher WBC (12.83 +/-4.55 x 10(-3) vs 10.83 +/- 3.00 x 10(-3), P = .04), lower ejection fraction (40 +/- 11% vs 46 +/- 12%, P < .001), and higher admission CK-MB levels (116 +/- 13 ng/mL vs 55 +/- 13 ng/mL, P = .006). Death occurred in 12% in the poorTMP group vs 1.8% in the good TMP group (P = .03). Advanced age, use of an intra-aortic balloon pump, and elevated admission WBC were independently associated with in-hospital and 30-day death. CONCLUSIONS: High hs-CRP levels were not associated with impaired myocardial perfusion score. Microcirculatory impairment may be related to an increased inflammatory process, independent from high hs-CRP levels.

The interaction of vascular inflammation and chronic kidney disease for the prediction of long-term death after percutaneous coronary intervention.

BACKGROUND: Patients with chronic kidney disease frequently have worse outcomes following percutaneous coronary intervention (PCI) compared to patients with normal renal function. Furthermore, they more commonly have elevated serum markers of inflammation, which may be either directly or indirectly associated with a state of accelerated atherosclerosis. We sought to assess the relationship among glomerular filtration rate (GFR), systemic inflammation, and long-term death after PCI. METHODS: In patients undergoing PCI, the intensity of vascular inflammation was measured using baseline ultrasensitive C-reactive protein (us-CRP), and GFR was calculated using the Modification of Diet in Renal Disease formula. Their association with long-term death was compared using multivariate Cox regression analysis including an interaction element for us-CRP and GFR, baseline clinical, biochemical, and angiographic variables. RESULTS: In 4522 patients (mean age 65 +/- 11 years) having undergone PCI, 332 (7.3%) deaths occurred over the median duration of follow-up of 20.1 months (interquartile range 8.5-31.3 months). The mean GFR was 77 +/- 33 mL/min per 1.73 m2 with a median us-CRP of 3.75 mg/L (interquartile range 1.5-10.1 mg/L). Both increasing levels of CRP (log rank P < .001) and decreasing levels of GFR were univariate predictors of long-term death (P < .001). In a multivariate model, both GFR and us-CRP retained independent predictive value for long-term death. CONCLUSION: Although baseline us-CRP and GFR are both independent predictors of long-term death after PCI, in concert, they impart a markedly exaggerated hazard of mortality.

Slow-flow phenomenon during carotid artery intervention with embolic protection devices: predictors and clinical outcome.

OBJECTIVES: The purpose of this research was to define the predictors of the "slow-reflow" phenomenon during carotid artery intervention with filter-type embolic protection devices (EPDs) and to determine its prognostic significance. BACKGROUND: During carotid artery intervention using filter-type EPDs, we have observed cases in which there is angiographic evidence of a significant reduction in antegrade flow in the internal carotid artery proximal to the filter device, termed "slow-flow." The predictors of this phenomenon and its prognostic significance are unknown. METHODS: Using a single-center prospective carotid intervention registry, patients with slow-flow were compared to patients with normal flow during carotid intervention with respect to clinical, procedural, and lesion characteristics, and the 30-day incidence of death and stroke. RESULTS: A total of 414 patients underwent 453 carotid artery interventions using EPDs. Slow-flow occurred in 42 patients (10.1%) undergoing 42 carotid interventions (9.3%), and most commonly occurred after post-stent balloon dilatation (71.4%). Multivariate logistic regression analysis identified the following predictors of slow-flow: recent history (<6 months) of stroke or transient ischemic attack (odds ratio [OR] 2.8, 95% confidence interval [CI] 1.4 to 5.6, p = 0.004), increased stent diameter (OR 1.4, 95% CI 1.02 to 1.94, p = 0.044), and increased patient age (OR 1.05, 95% CI 1.01 to 1.09, p = 0.025). Among patients with slow-flow, the 30-day incidence of stroke or death was 9.5% compared to 2.9% in patients with normal flow (chi-square = 4.73, p = 0.03). This difference was driven by the disparity in the 30-day incidence of stroke (9.5% vs. 1.7%). CONCLUSIONS: Slow-flow during carotid intervention with EPDs is a frequent event that is associated with an excess risk of periprocedural stroke. The association of the phenomenon with clinically symptomatic carotid lesions and use of larger stent diameters suggests that embolization of vulnerable plaque elements may play a pathogenic role.

Effect of chronic kidney disease on outcomes after carotid artery stenting.

We performed a single-center retrospective analysis evaluating the effect of chronic kidney disease among patients who underwent carotid artery stenting. The presence of chronic kidney disease is associated with higher periprocedural and 6-month death, stroke, or myocardial infarction after carotid artery stenting.