Biomedical subjects
Publications and source records attributed to G J Dehmer.
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BACKGROUND: Elevated interleukin-6 (IL-6) levels are present in patients with New York Heart Association (NYHA) class III and IV congestive heart failure (CHF) and are associated with a poor prognosis. We sought to determine whether elevated IL-6 levels are also present in patients with left ventricular (LV) dysfunction but without clinical symptoms. METHODS: Blood samples were obtained from the femoral artery of 58 patients who underwent cardiac catheterization for recognized clinical indications. In a subgroup of 44 patients, samples were also obtained from the femoral vein, the left main coronary artery, and the coronary sinus. Patients with prior coronary artery bypass surgery, recent acute coronary syndrome, or steroid therapy were excluded. All samples were obtained before heparin or contrast administration. IL-6 was measured by enzyme-linked immunosorbent assay and values are expressed in picograms per milliliter. RESULTS: Three groups of patients were identified: controls, no CHF, LV ejection fraction >/=0.55 (n = 32); asymptomatic LV systolic dysfunction, no CHF, LV ejection fraction <0.55 (n = 14); and CHF, pulmonary edema (n = 12). IL-6 levels were higher at all sampling sites in both the asymptomatic LV systolic dysfunction and CHF groups compared with controls with the IL-6 levels inversely related to LV ejection fraction. CONCLUSIONS: Elevated IL-6 levels are present in patients with LV dysfunction even in the absence of the clinical syndrome of CHF. These data suggest that IL-6 may be involved in the progression of subclinical LV dysfunction to clinical CHF. IL-6 may be a marker of patients at risk for progression to clinical CHF or a novel target for therapeutic intervention.
Acute coronary syndromes (ACS), including unstable angina, non-Q wave myocardial infarctions (MI) and Q-wave MIs, are usually the result of plaque rupture and subsequent thrombus formation. Commonly, patients with ACS have significant underlying coronary artery disease (CAD) demonstrable by coronary angiography and are candidates for prompt revascularization. In many cases, however, ACS are due to coronary thrombosis in the absence of obstructive CAD and therefore aggressive medical therapy may be sufficient. Coronary angiography is an invaluable resource for individualized treatment decisions. We describe a patient with thrombosis of the left main coronary artery successfully treated with aggressive and prolonged antiplatelet and anticoagulant therapy under the guidance of serial coronary angiography.
This study examines the source of elevated interleukin-6 (IL-6) levels in patients with acute coronary syndrome (ACS) and congestive heart failure (CHF). IL-6 is elevated in the peripheral blood of patients with ACS and CHF, but it is not known if this proinflammatory cytokine is from a cardiac or extracardiac source. Blood samples were obtained from the femoral artery, femoral vein, left main coronary artery, and coronary sinus in 57 patients during cardiac catheterization. IL-6 levels from 12 patients with ACS and 12 patients with CHF were compared with the IL-6 levels in 33 patients who had neither of these clinical conditions. Median IL-6 levels in the peripheral and coronary circulation were a minimum fivefold higher in patients with ACS or CHF relative to control patients. An elevated transcardiac IL-6 gradient (coronary sinus-left main level) was present in patients with ACS (median 5.2; 25th and 75th percentiles 3.9 and 29.3 pg/ml, respectively) compared with control patients (median 0, -0.7 and 0.5 pg/ml; p < 0.001), but not in patients with CHF (median 0.4, -0.7 and 3.5 pg/ml; p = NS). Elevated IL-6 levels in patients with ACS derive from a cardiac source, presumably from "inflamed" coronary plaques and areas of myocardial necrosis, whereas elevated levels in patients with CHF are most likely the result of extracardiac production.
An analysis of 183 patients in sinus rhythm who underwent coronary artery bypass grafting was conducted to determine the association of multiple preoperative factors, including an elevated left ventricular end-diastolic pressure, with early postoperative atrial fibrillation. An association with advanced age, a history of atrial fibrillation, and preoperative digoxin use was found, but not with an elevated left ventricular end-diastolic pressure, irrespective of left ventricular systolic function.
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BACKGROUND: Compared with the conventional Thrombolysis In Myocardial Infarction (TIMI) flow grade system, the corrected TIMI frame count (CTFC) quantifies coronary blood flow in a more reproducible fashion. The purpose of this study was to determine if the CTFC is affected by sex, body size, hemodynamics, or other selected clinical variables. METHODS AND RESULTS: CTFC was measured in 534 coronary arteries from 200 consecutive patients referred for coronary angiography. CTFC in each artery was related to patient variables (sex, age, race, and body surface area), clinical variables (cardiac rhythm, medication use, diabetes, hypertension, hypercholesterolemia, smoking, and left ventricular hypertrophy), angiographic variables (wall motion abnormality in each coronary artery distribution, left ventricular ejection fraction, percent stenosis in the artery, and presence of collaterals), and hemodynamic variables (aortic systolic and diastolic blood pressure and left ventricular end-diastolic pressure). By multivariate analysis, CTFC in all arteries was significantly associated with aortic systolic and diastolic pressures and body surface area. In addition, there were significant associations between CTFC and age and sex in some but not all arteries. Although significant, the absolute change in CTFC associated with these variables was small. CONCLUSIONS: CTFC provides a quantitative assessment of coronary blood flow that varies only a small amount in association with body size, systemic arterial pressure, age, and sex.
This study shows an increase in von Willebrand factor antigen in blood collected from the coronary sinus shortly after coronary angiography with an ionic contrast agent (diatrizoate), but not a nonionic contrast agent (iohexol). These findings suggest that ionic contrast agents may cause more endothelial injury than nonionic contrast agents.
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The effect of chronic estrogen replacement therapy on the corrected Thrombolysis In Myocardial Infarction trial frame count of the left anterior descending coronary artery was assessed in 122 postmenopausal women. With use of multivariate analysis to account for confounding variables likely to affect the corrected Thrombolysis In Myocardial Infarction trial frame count, no chronic effect of estrogen replacement therapy on coronary blood flow was documented.
The Laboratory Survey Committee of the Society for Cardiac Angiography and Interventions was created as a resource for physicians and administrators to provide comprehensive independent outside review services for cardiac catheterization laboratories. Since 1989, when the committee began its work, surveys of 23 catheterization laboratories have been completed. Our review of this experience identified several recurring problems among the laboratories. The purpose of this paper is to summarize our experience and highlight the lessons we learned in the hope that this information will benefit many other laboratories.
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Although heparin and some radiographic contrast agents inhibit coagulation, thrombi can still form in their presence. The chemical environment in which a thrombus forms affects fibrin structure that may alter the ability of the thrombus to be lysed. Therefore, we assessed changes in fibrin structure in 13 patients referred for coronary angiography. Blood was obtained from the femoral vein, femoral artery, ascending aorta, left main coronary artery (LMCA), and coronary sinus (CS) before, during, and after coronary angiography was performed with iohexol. The number of fibrin monomers per fiber cross section was determined by turbidity measurements of fibrin gels formed from plasma samples. At baseline there was no difference in the number of fibrin monomers per fiber cross section in plasma gels generated from the different sampling sites. After iohexol administration, there was a significant decrease in the number of fibrin monomers per fiber cross section at the sampling sites ranging from - 13% to -25% compared with the respective baseline values with the largest change in the LMCA CS (51+/-16 to 38+/-15, p <0.025). Transcardiac (LM - CS value) changes in the number of fibrin monomers per fiber cross section were dependent on the timing of the sample collection in the CS. In 7 patients, the CS sample was collected approximately 2 minutes after injection of contrast material and there was no transcardiac difference. When the CS sample was obtained during contrast injection (n=6) a large transcardiac change occurred (44+/-10 to 32+/-14, p=0.01). These data show transient changes in fibrin structure during coronary angiography with iohexol. The thinner fibers formed in the presence of iohexol were more resistant to fibrinolysis.
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Three markers of platelet activation (platelet-derived microparticles, fibrinogen binding and expression of P-selectin) were assessed by flow cytometry during diagnostic coronary angiography and therapeutic coronary interventions. In 24 patients undergoing diagnostic angiography, blood was collected to determine if our sampling techniques or coronary angiography caused platelet activation. Changes during diagnostic angiography were used to establish baseline values and interpret changes during coronary interventions. In 21 patients, blood samples were obtained at 5 time points during percutaneous transluminal coronary angioplasty (PTCA) (n = 17) or directional coronary atherectomy (DCA) (n = 4). During coronary interventions, mean values for the percentage of platelets expressing P-selectin or binding fibrinogen increased, but with considerable variation among patients. Individual responses for platelet activation markers in each patient were characterized using a twofold increase to indicate elevation related to the intervention. Patients were classified as having complicated or uncomplicated procedures based on the presence of acute closure, dissection, or thrombus observed by angiography. There were no differences in the percentage of elevated markers between patients with uncomplicated (12.5%) and complicated (19%) PTCA procedures. However, patients treated with DCA had more elevated markers (38%) than those treated with PTCA (15%) (p = 0.04). Our data suggest that the extent of platelet activation in individual patients cannot be predicted by common angiographic findings or complications. More markers of platelet activation were present after DCA and may reflect a greater degree of vascular trauma associated with this procedure.