Two hour bivalirudin infusion after PCI for ST elevation myocardial infarction.

The standard of care for STEMI PCI for the past decade has been aspirin, clopidogrel, heparin, and a glycoprotein IIbIIIa receptor inhibitor (GPI). A bivalirudin strategy was shown to be superior to a GPI strategy in the HORIZONS AMI trial for net adverse clinical events (combined MACE and bleeding). An increased risk of acute stent thrombosis in the bivalirudin arm may have prevented broader adoption of bivalirudin for this indication. We hypothesized that acute stent thrombosis risk could be ameliorated by a 2 h infusion of bivalirudin following STEMI PCI. We implemented a multicenter, prospective registry for all STEMI patients in Vermont treated at a single PCI center. Each patient was routinely pre-loaded with dual antiplatelet therapy and 75% received an unfractionated heparin bolus prior to PCI. The utilization of bivalirudin bolus and continued 2 h infusion after PCI was routine with GPI bailout optional. 128 consecutive STEMI patients underwent primary PCI from October 1, 2008 to September 30, 2009. 92% of primary PCI patients received bivalrudin during and after the procedure with a 9% rate of bail out GPI. There was one case of probable or definite acute stent thrombosis (0.7%), and this single case occurred despite use of bailout GPI. Despite the prolonged infusion of bivalirudin, major bleeding occurred in only 1.7% of STEMI patients. In conclusion, prolonging bivalirudin for 2 h after STEMI PCI may be a promising method to alleviate acute stent thrombosis risk without losing the bleeding complication benefit of the bivalirudin strategy.

Atypical presentation of anomalous origin of the left main coronary artery from the pulmonary artery.

Anomalous origin of the left main coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly that usually presents in childhood. Ninety percent of the patients with ALCAPA die within the first year of life without surgical intervention. In adults, ALCAPA is associated with left ventricular dysfunction, mitral regurgitation, and sudden death. The present report describes the case of an adult patient who presented with an abnormal stress test and ALCAPA was diagnosed during cardiac catheterization.

Extravascular closure for patients with high-risk femoral anatomy.

BACKGROUND: Vascular closure devices (VCDs) improve patient comfort and decrease time to ambulation. However, VCD studies have excluded patients with high-risk femoral artery anatomy; we examined the safety and efficacy of clip-based extravascular closure in this high-risk group. METHODS: We performed a prospective registry enrolling 98 consecutive patients undergoing diagnostic coronary angiography. Inclusion criteria were femoral artery calcification, moderate femoral artery stenosis, or non-femoral arterial sheath insertion. All patients underwent immediate vessel closure with the Starclose device (Abbott Vascular). Patients with severe femoral arterial disease or femoral arterial diameter < or = 4.0 mm were excluded. Hospital outcomes were assessed prospectively and femoral arterial stenosis was determined by quantitative angiography. RESULTS: Inclusion was mainly related to at least one of 3 main high-risk characteristics: moderate femoral arterial stenosis (30%), femoral arterial calcification (24%) or nonfemoral sheath insertion (46%). The average femoral stenosis was 35.3 +/- 5.1% among patients included for a significant femoral disease. There was a 100% procedural and 94% device success: 1 patient required manual compression for greater than or equal to 30 minutes. The average time from sheath removal to hemostasis was 0.76 +/- 1.3 minutes. Despite the higher-risk anatomy, there were no major vascular complications and only one minor vascular complication. The average time to ambulation was 78.1 +/- 47.3 minutes. CONCLUSIONS: In this prospective registry, the Starclose VCD was safe and effective for early ambulation of patients despite the presence of high-risk femoral arterial anatomy.

Changes in patterns of coronary revascularization strategies for patients with acute coronary syndromes (from the CRUSADE Quality Improvement Initiative).

Since the introduction of drug-eluting stents (DESs), patterns of revascularization strategies for patients with non-ST-segment elevation acute coronary syndromes have not been assessed. We studied 82,924 patients from the CRUSADE Initiative who presented with non-ST-segment elevation acute coronary syndromes and underwent coronary angiography at 365 United States hospitals that had capabilities for surgical (coronary artery bypass grafting [CABG]) and percutaneous (percutaneous coronary intervention [PCI]) revascularization from January 2002 to June 2005. Temporal trends in the use of PCI, CABG, and medical management without revascularization were analyzed with respect to the introduction of DESs. In total, 73,577 patients (89%) had >50% stenosis in > or =1 coronary artery, and there was a significant increase in the use of PCI (vs CABG or medical management without revascularization) during the study period (38.3% vs 52.5%). By quarter 2 of 2005, 80% of patients who underwent PCI received a DES. In total, 18,462 of 25,068 patients (73.6%) with 3-vessel disease (3VD) underwent revascularization and use of CABG decreased for these patients (48.9% to 39.9%, p <0.001), whereas use of PCI increased (51.1% to 60.1%, p <0.001). Factors significantly associated with use of PCI for patients with 3VD who underwent any revascularization included previous PCI, previous CABG, cardiology inpatient care, care at an academic hospital, renal insufficiency, and previous congestive heart failure. In conclusion, coinciding with the introduction of DESs, there has been a significant increase in the use of PCI and, in those patients with 3VD, a decrease in the use of CABG with a shift toward increasing use of PCI. Long-term implications of this shift remain uncertain, especially in patients with 3VD.

Osteoprotegerin is not associated with angiographic coronary calcification.

UNLABELLED: Coronary artery calcification may play a significant role in the pathophysiology of plaque progression and healing. We hypothesized that osteoprotegerin, an inhibitor of osteoclastogenesis, may participate in the calcification of coronary plaques or the response to injury after coronary stenting. A prospective registry was performed in 2004. Blood samples from 100 patients undergoing percutaneous coronary intervention (PCI) were obtained before PCI and 24 h after PCI. The concentrations of osteoprotegerin (OPG), C-reactive protein, interleukin-6, and soluble CD40 ligand (sCD40L) were determined by ELISA. Quantitative coronary angiography was performed to define the presence of culprit lesion calcification (CLC). Comparisons among markers of inflammation and tertiles of OPG were stratified with respect to CLC. Patients with CLC (n = 28) compared with no CLC (n = 71) were older (P < 0.01), had lower creatinine clearance (P < 0.01), lower hemoglobin (P = 0.02), and were less likely to smoke (P = 0.04). Patients without CLC were over twice as likely to present with a marker-positive acute coronary syndrome. CLC was associated with less pre-PCI platelet-mediated inflammation as measured by sCD40L (4.65 vs. 7.15 pg/ml, P = 0.05), but not with lower levels of OPG. Inflammatory cytokines increased significantly after PCI for patients with and without CLC. For patients in the highest tertile of OPG at baseline, there was a reduction in OPG after PCI. Systemic osteoprotegerin levels are not associated with angiographic calcification of culprit plaques. For patients with elevated levels of OPG prior to PCI, there is a significant reduction after PCI consistent with a counterregulatory role for OPG. CONDENSED ABSTRACT: Both calcified and non-calcified culprit plaques exhibited a similar inflammatory response to stent-mediated injury. After PCI, osteoprotegerin decreased while proinflammatory cytokines increased, which may be consistent with a counterregulatory role for osteoprotegerin.

The evaluation and management of cardiogenic shock.

Cardiogenic shock (CS) continues to be the leading cause of death in patients who present to the hospital with acute myocardial infarction (AMI). Mortality in patients with AMI complicated by CS remains extremely high, with 1-month mortality rates ranging from 40% to 60%. Although pump failure is the dominant etiologic feature of CS after AMI, the inflammatory system has been implicated in its pathogenesis. The dominant therapy for treatment of CS is early mechanical revascularization with either percutaneous coronary intervention or coronary artery bypass graft surgery. Supportive measures such as intravenous vasopressors or intra-aortic balloon counterpulsation can complement the benefit of definitive revascularization. Newer therapies are directed at mitigating the inflammatory response or supporting cardiovascular function until either patient recovery or until other destination therapy is available. The strategies in this critical pathway outline the general approach in treating CS after AMI at our institution.

Relation of leukocytosis to C-reactive protein and interleukin-6 among patients undergoing percutaneous coronary intervention.

An elevated white blood cell (WBC) count and elevated C-reactive protein (CRP) have been associated with an increased risk of adverse cardiac events. The relation between these 2 parameters of heightened systemic inflammation was characterized in patients who underwent percutaneous coronary intervention (PCI). Femoral arterial blood samples from a prospective registry of 100 patients who underwent PCI were obtained immediately before the procedure. The concentrations of CRP and interleukin-6 were determined by an enzyme-linked immunosorbent assay. Patients were stratified according to tertiles of ascending WBC counts before PCI. Univariate analysis compared patients in the highest WBC count tertile with the lower tertiles for clinical, angiographic, and procedural characteristics, as well as pre-PCI cytokine concentrations. Multiple logistic regression analysis was performed to examine the association between the elevated WBC count and baseline elevations in either CRP or interleukin-6, accounting for the simultaneous effect of confounding characteristics. Approximately 75% of patients had stable or unstable angina pectoris versus a marker-positive acute coronary syndrome. Patients in the highest WBC count tertile were more likely to be smokers, have received unfractionated heparin, have a marker-positive acute coronary syndrome, and have a CRP >3.0 mg/L. Multivariate analysis showed that only elevated troponin-I before PCI was independently associated with the highest WBC count tertile (odds ratio 10.9, 95% confidence interval 3.7 to 32.4, p < 0.01). In patients with negative troponin I findings, CRP >3.0 mg/L was a powerful independent predictor of an elevated pre-PCI WBC count (odds ratio 3.78, 95% confidence interval 1.07 to 13.3, p = 0.04). In conclusion, in patients with troponin I negative coronary syndromes, a pre-PCI elevation in the WBC count reflected cytokine-mediated inflammation.

Systemic inflammation after drug-eluting stent placement.

BACKGROUND: Systemic inflammation after coronary intervention identifies patients at increased risk of subsequent cardiac events. Cardiac events are less frequent after use of drug eluting stents (DES) compared with bare metal stents (BMS). Thus, we sought to determine whether attenuation of the systemic inflammatory response was contributing to the improved outcomes. METHODS: A prospective registry was initiated in late 2003. Peripheral venous blood samples from 75 patients undergoing percutaneous coronary intervention (PCI) were obtained before PCI, and both 1 hour and 24 hours after stenting. The concentrations of C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL1-Ra) were determined by ELISA. Eleven patients were excluded from the analysis because they had both DES and BMS. RESULTS: Patients treated with BMS (n=29) compared with DES (n=34) had a higher incidence of marker-positive acute coronary syndromes (40% vs. 17%, p=0.06), vein graft PCI (p=0.02) and a larger final balloon diameter (p=0.04). Consistent with the lower baseline clinical risk, pre-PCI concentrations of cytokines were lower in the DES group (p=0.04 for IL-6 and p=0.08 for CRP). Comparable and significant increases in CRP, IL-6 and IL1-Ra were evident 24 hours after PCI in patients treated with either DES or BMS. After controlling for baseline levels of CRP, there remained a similar and robust (300%) relative increase in CRP for both DES and BMS patients. CONCLUSIONS: The inflammatory response to PCI appears similar in those treated with DES and BMS. Accordingly, the reduction in restenosis after DES is likely not mediated by attenuation of the systemic markers CRP, IL-1Ra, or IL-6.