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Biomedical subjects

Harold L Dauerman

Publications and source records attributed to Harold L Dauerman.

At least 19 recordsLinked to original sources
PubMed2006

Detection of coronary artery stenosis using 40-channel computed tomography with multi-segment reconstruction.

Coronary angiographic studies performed with 16-channel multidetector computer tomographic scanners have demonstrated accurate detection of coronary vessel stenosis but are limited by a significant number of non-evaluable segments. To date, only single-center experience with multidetector computer tomography has been reported. We performed a prospective, blinded study at 2 institutions to determine the feasibility and diagnostic accuracy of coronary angiography using 40-channel multidetector computer tomography with multi-segment reconstruction for the detection of obstructive coronary artery disease (CAD). Multidetector computer tomographic studies were performed in 85 patients who were referred for invasive coronary angiography with clinically suspected CAD. Datasets were analyzed by blinded, independent review. Of 1,145 segments that were suitable for analysis as determined by angiography, 1,045 (91.3%) were evaluable on multidetector computer tomography. Segment-based sensitivity, specificity, and positive and negative predictive values for detecting > or =50% luminal stenoses were 86%, 97%, 75%, and 97%, respectively. The area under the receiver-operating characteristic curves for the detection of > or =50% angiographic stenosis by multidetector computer tomography was 0.94. In a patient-based analysis, the sensitivity, specificity, and positive and negative predictive values for detecting subjects with > or =1 segment with > or =50% stenosis were 98%, 93%, 94% and 93%, respectively. In conclusion, coronary angiography using 40-channel multidetector computer tomography with multi-segment reconstruction accurately detects coronary segments and patients with obstructive CAD, with a small number of non-evaluable cases.

Coronary Angiography↗
PubMed2006

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.

Aged↗
PubMed2006

Coronary venous capture of contrast during angiography.

Contrast-induced nephropathy (CIN) after angiographic procedures results in significant morbidity, mortality, and costs. Given the limitations of current prophylactic measures, we have tested the hypothesis that the majority of the contrast injected into a coronary artery can be captured from the coronary sinus before it enters the systemic circulation. The current study involves coronary venous capture after coronary angiography in dogs with determination of contrast capture using quantitative fluoroscopy. Venous contrast capture (VCC) was achieved with a balloon tipped through lumen catheter introduced into the coronary sinus via the superior vena cava. After selective injection of iohexol contrast into the left main coronary artery, the coronary sinus was balloon occluded in order to capture all contrast. The venous blood was subsequently withdrawn from the coronary sinus catheter, and then the balloon was deflated. By quantitative fluoroscopy we could demonstrate that an average 70 +/- 6% of the injected contrast could be captured without complications. Coronary sinus VCC is a novel approach to remove the majority of contrast selectively injected into coronary arteries. As an adjunct procedure in coronary angiography, VCC has the potential to significantly reduce the risk of CIN in patients at risk.

Animals↗
PubMed2005

Bleeding complications in patients with anemia and acute myocardial infarction.

Anemia has recently been associated with increased mortality in patients who undergo percutaneous coronary intervention. The mechanisms associated with increased mortality among patients who have anemia have not been defined. We sought to determine whether patients who had anemia and acute myocardial infarction (AMI) might be at higher risk for bleeding or cardiogenic shock during acute hospitalization compared with patients who did not have anemia. This population-based study included 5,378 residents of the Worcester metropolitan area who were hospitalized with a diagnosis of AMI in five 1-year periods from 1995 to 2003. Patients were analyzed according to the presence or absence of anemia (hematocrit <39% in men and <36% in women) and quintiles of baseline hematocrit levels. Differences in the frequency of death, cardiogenic shock, and major bleeding during hospitalization were analyzed in relation to the presence of anemia. Anemia was present in 31.3% of patients who were hospitalized with AMI. Mortality and bleeding complications were related to the presence of anemia on admission for all types of AMI and across a broad spectrum of anemia severities. In a multivariable model that adjusted for baseline and treatment covariates, the odds ratios for adverse events for patients who had anemia (compared with those who did not) were 1.43 (95% confidence interval 1.12 to 1.84) for hospital mortality and 3.57 (95% confidence interval 2.75 to 4.64) for major bleeding. Development of cardiogenic shock was not related to the presence of anemia (odds ratio 0.89, 95% confidence interval 0.64 to 1.23). In conclusion, these findings suggest that bleeding complications are a potential mechanism for increased mortality among patients who have anemia and present with AMI.

Aged↗
PubMed2005

Increased expression of platelet P-selectin and formation of platelet-leukocyte aggregates in blood from patients treated with unfractionated heparin plus eptifibatide compared with bivalirudin.

INTRODUCTION: Platelet-leukocyte aggregates have been implicated in atherogenesis. This study was designed to determine the influence in vivo of a direct thrombin inhibitor, bivalirudin, compared with unfractionated heparin (UFH) plus the GP IIb-IIIa inhibitor eptifibatide (E) on platelet reactivity, the formation of platelet-leukocyte aggregates, and leukocyte activation. MATERIALS AND METHODS: Blood was taken before and after percutaneous coronary intervention (PCI) from 60 patients randomized to UFH+E (n=26) or bivalirudin (n=34). Platelet function and the formation in vivo of platelet-monocyte aggregates (PMA) and platelet-neutrophil aggregates (PNA) were assessed with the use of flow cytometry. Myeloperoxidase (MPO) elaborated during leukocyte activation was measured by ELISA. RESULTS: Compared with those treated with bivalirudin, patients treated with UFH+E exhibited a 45% decrease in the capacity of platelets to bind fibrinogen (p=0.006) but a 2-fold increase in platelet surface expression of P-selectin (p=0.04) in samples taken from the coronary ostium before PCI. Platelet-leukocyte aggregation in vivo was greater (PMA=2-fold, p=0.04; PNA=3-fold, p=0.006) with UFH+E as was the concentration in blood of MPO (1.5-fold, p=0.007). CONCLUSIONS: Increased platelet surface expression of P-selectin, augmented platelet-leukocyte aggregation in vivo, and consequent activation of leukocytes was seen before PCI in blood from patients treated with UFH+E compared with bivalirudin. Benefits associated with decreased platelet aggregation when PCI is performed with UFH plus GP IIb-IIIa inhibition may be partially offset by increased platelet-leukocyte aggregation.

Anticoagulants↗
PubMed2005

Comparing long-term survival of patients with multivessel coronary disease after CABG or PCI: analysis of BARI-like patients in northern New England.

BACKGROUND: Randomized trials comparing coronary artery bypass graft surgery (CABG) with percutaneous coronary interventions (PCIs) for patients with multivessel coronary disease (MVD) report similar long-term survival for CABG and PCI. These studies used a highly selected population of patients and providers, and their results may not be generalizable to actual care. Our goal in this study was to compare long-term survival of MVD patients treated with CABG vs PCI in contemporary practice. METHODS AND RESULTS: From our northern New England registries of consecutive coronary revascularizations, we identified 10,198 CABG and 4,295 PCI patients with MVD who may have been eligible for either procedure between 1994 and 2001. Vital status was obtained by linkage to the National Death Index. Proportional-hazards regression was used to calculate hazard ratios (HRs) for survival in CABG vs PCI patients after adjustment for comorbidities and disease characteristics. CABG patients were older; had more comorbidities, more 3-vessel disease, and lower ejection fractions; and were more completely revascularized. Adjusted long-term survival for patients with 3-vessel disease was better after CABG than PCI (HR, 0.60; P<0.01) but not for patients with 2-vessel disease (HR, 0.98; P=0.77). The survival advantage of CABG for 3-vessel disease patients was present in all patient populations, including women, diabetics, and the elderly and in the era of high stent utilization. CONCLUSIONS: In contemporary practice, survival for patients with 3-vessel coronary disease is better after CABG than PCI, an observation that patients and physicians should carefully consider when deciding on a revascularization strategy.

Aged↗
PubMed2005

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.

Acute Disease↗
PubMed2005

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.

Aged↗
PubMed2005

The effects of bivalirudin compared with those of unfractionated heparin plus eptifibatide on inflammation and thrombin generation and activity during coronary intervention.

OBJECTIVE: To characterize effects of bivalirudin compared with unfractionated heparin plus eptifibatide on inflammation, and thrombin generation and activity after percutaneous coronary intervention. METHODS: We measured the concentration in blood of fibrinopeptide A, prothrombin fragment 1+2, soluble CD40 ligand, interleukin 1 receptor antagonist, interleukin 6, and high sensitivity C-reactive protein in 63 patients treated with aspirin and clopidogrel and undergoing elective percutaneous coronary intervention, who were randomized to treatment with either bivalirudin (n=34) or unfractionated heparin plus eptifibatide (n=29). RESULTS: Neither generation nor activity of thrombin increased 10 min after percutaneous coronary intervention in patients randomized to bivalirudin or unfractionated heparin plus eptifibatide. However, prothrombin fragment 1+2 increased modestly and comparably in both groups after 1 day. Inflammation, reflected by concentrations of interleukin 6 and high sensitivity C-reactive protein in blood, increased similarly 1 day after percutaneous coronary intervention in patients treated with either regimen. In a subset of patients (n=12 in each group) from whom blood was obtained 30 days after percutaneous coronary intervention, the concentration of high sensitivity C-reactive protein was lower in those who had been treated with bivalirudin (by 3.5 mg/l, P=0.002). CONCLUSION: The early effects on inflammation and thrombin generation and activity are similar after treatment with bivalirudin alone compared with unfractionated heparin plus eptifibatide in patients treated with aspirin and clopidogrel who are undergoing percutaneous coronary intervention for symptoms of stable angina. The decreased concentration of high sensitivity C-reactive protein seen 30 days after percutaneous coronary intervention in those treated with bivalirudin is consistent with greater attenuation of inflammation that may have contributed to the trend toward reduced mortality 1 year later in those treated with bivalirudin in REPLACE-2.

Aged↗
PubMed2004

Endothelial dysfunction and inflammation after percutaneous coronary intervention.

We studied 30 consecutive patients who underwent coronary stenting with respect to postprocedure endothelial dysfunction and levels of pre- and postprocedure cytokines. Patients with severe impairment of flow-mediated dependent dilation, but not flow- mediated independent dilation, had higher concentrations of C-reactive protein before percutaneous coronary intervention (12.9 +/- 20.2 vs 5.6 +/- 13.0 microg/ml, p = 0.04) and 24 hours after stenting (18.8 +/- 20.8 vs 11.8 +/- 20.0 microg/ml, p = 0.05) than patients without severe abnormities of systemic endothelial function. Thus, endothelium-dependent dilation abnormalities were related to the systemic inflammatory state, whereas endothelium-independent dilation abnormalities were not related to the inflammatory status of the patient.

Aged↗
PubMed2004

Increased coronary arterial release of interleukin-1 receptor antagonist and soluble CD40 ligand indicative of inflammation associated with culprit coronary plaques.

Blood taken from the coronary artery ostium reflects biochemical changes indicative of thrombosis in the culprit vessel. We sought to determine whether inflammation is manifested by increased concentrations of selected markers in ostial blood sampled from a culprit coronary artery proximal to an atherosclerotic plaque. The concentrations of C-reactive protein (CRP), interleukin (IL)-6, IL-1 receptor antagonist, and soluble CD40 ligand (sCD40L) were measured in blood drawn from 75 patients before percutaneous coronary intervention from the femoral artery and from a guide catheter after engagement of the culprit coronary artery. Results were compared using Student's t tests. An acute coronary syndrome was present in 88% of patients. The concentrations of CRP and IL-6 were similar in coronary ostial and peripheral blood. Concentrations of IL-1 receptor antagonist were consistently greater in coronary arterial compared with peripheral arterial blood (peripheral 545 +/- 378 vs coronary 595 +/- 388 pg/ml, p = 0.003). Concentrations of sCD40L were also greater in the coronary compared with peripheral blood (peripheral 0.80 +/- 0.46 vs coronary 2.12 +/- 2.77 ng/ml, p <0.0001). The increased concentration of IL-1 receptor antagonist and sCD40L in blood drawn from the culprit coronary artery compared with that taken from the peripheral artery suggests that these cytokines contribute directly to inflammation in response to coronary intervention and may potentiate a systemic inflammatory state.

Adult↗
PubMed2004

Bleeding complications after contemporary pharmacoinvasive therapy for ST elevation myocardial infarction.

BACKGROUND: Pharmacoinvasive therapy for the treatment of ST elevation myocardial infarction (STEMI) is a strategy that combines early restoration of coronary flow via pharmacologically induced thrombolysis with subsequent, prompt percutaneous coronary intervention (PCI). Prior studies suggesting a heightened bleeding risk of PCI performed early after fibrinolysis predated contemporary pharmacoinvasive practice including use of femoral closure devices (CD), fibrin specific thrombolytics, lower doses of heparin and stents. METHODS: Consecutive patients were included in this retrospective registry study if they underwent emergent PCI for ST elevation myocardial infarction (STEMI) followed by immediate use of a groin closure device. Between Oct 1, 2002 and Jan 1, 2003, 27 patients were treated with immediate use of CD after post-thrombolytic PCI, performed within 12 hours of thrombolysis (pharmacoinvasive group). 58 patients were treated with immediate use of CD after primary PCI for STEMI. The two groups were compared with respect to the incidence of successful groin closure, bleeding complications, and clinical outcomes. Bleeding events were categorized according to the TIMI criteria. All baseline clinical and treatment variables were compared between the two groups to determine and the association of these variables (including use of thromblytic therapy) with TIMI major and TIMI minor bleeding was determined. RESULTS: Pharmacoinvasive recanalization with PCI occurred 348 +/- 183 minutes after initiation of fibrinolytic therapy. Glycoprotein IIb/IIIa inhibitors were used less frequently in the patients treated with a thrombolytic agent (59% vs. 90%, p < 0.01). Successful immediate hemostasis was obtained with CD in greater than 85% of patients in both groups (89% for pharmacoinvasive group vs. 86% for primary PCI group, p = 0.89). No patient required vascular surgical intervention. TIMI major bleeding and transfusion requirements were less than 5% in both groups. Antecedent thrombolytic therapy was not a predictor of bleeding complications after PCI. CONCLUSIONS: Use of CD as part of a contemporary pharmacoinvasive strategy is associated with a low rate of major bleeding complications.

Adult↗
PubMed2004

Triple antiplatelet therapy does not increase femoral access bleeding with vascular closure devices.

BACKGROUND: The use of arteriotomy closure devices (CDs) to achieve hemostasis after femoral artery access in percutaneous coronary intervention is steadily increasing. However, the safety information with these devices in the era of triple antiplatelet therapy is limited. METHODS: We reviewed prospectively collected data from the Do Tirofiban and ReoPro Give Similar Efficacy Outcomes Trial (TARGET), where all patients received aspirin, clopidogrel, and glycoprotein IIb/IIIa inhibitor therapy. At the treating physician's discretion, manual compression (MC) or a vascular hemostasis device was selected following femoral angiography. Patients receiving MC were to have sheaths removed 2 to 6 hours postprocedure when the activated clotting time was < or = 175 seconds. RESULTS: Of 4809 patients, 4736 had femoral access, and 985 of these had a CD (Perclose 47%, Angio-Seal 43%, VasoSeal 5%, and other 5%). The MC and CD groups were similar regarding most demographic characteristics, including age, systolic blood pressure, and weight, but those with MC were more often female, diabetic, and had history of peripheral vascular disease. Patients with a CD had a lower ischemic event rate suggesting they were a lower risk cohort overall. There were no differences in major bleeding at the access site (0.4% vs 0.5%, P =.588), minor bleeding at the access site (1.9% vs. 3.1%, P =.142) or transfusions (0.8% vs 1.0%, P =.513) between the MC and CD groups, respectively. CONCLUSIONS: In contemporary percutaneous coronary intervention practice, with appropriate patient selection, a CD can be safely utilized despite aggressive polypharmacy for procedural anticoagulation.

Angioplasty, Balloon, Coronary↗
PubMed2004

Soluble CD40 ligand is an early initiator of inflammation after coronary intervention.

BACKGROUND: This prospective study evaluated the early increase in markers of inflammation after coronary stenting, and the predictors of early rise. Elevation of markers of inflammation after percutaneous coronary intervention correlates with an increased risk of adverse events. The role of soluble CD40 ligand (sCD40L) as a potential initiator of inflammation after stenting has not been described. METHODS: Seventy-five patients were treated with heparin alone (n=25), or randomized to adjuvant treatment with eptifibatide (n=26) or abciximab (n=24) during stenting. Systemic blood was obtained before coronary stenting and at 10 min after stenting. C-reactive protein (CRP), interleukin (IL)-6, IL-1 receptor antagonist and sCD40L were determined by enzyme liberated immunosorbent assay. RESULTS: sCD40L exhibited the greatest relative rise (35%, P=0.01 compared to concentrations before intervention) in the first 10 min after stenting. In a logistic regression model, an early increase in the concentration of sCD40L was predicted by baseline laboratory values (white blood count and sCD40L level before stenting) and procedural characteristics (number of stents and glycoprotein IIb-IIIa inhibitor assignment). CONCLUSIONS: In conclusion, a systemic inflammatory response is detectable 10 min after coronary stent placement. The early increase in sCD40L suggests a possible role for this marker in the initiation of inflammation after coronary stenting.

Abciximab↗