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Biomedical subjects

J Brendan Foley

Publications and source records attributed to J Brendan Foley.

5 recordsLinked to original sources
PubMed2005

Inflammatory markers are not associated with outcomes following elective external cardioversion.

BACKGROUND: Electrical cardioversion is a common modality of therapy for persistent atrial fibrillation. Unfortunately even if the cardioversion is initially successful many patients revert to atrial fibrillation. It has been proposed that there may be an inflammatory component to this arrhythmia. It is interesting to speculate that this may have a role in determining the outcome following elective cardioversion. METHODS: The study group consisted of 81 patients with persistent atrial fibrillation undergoing elective external cardioversion. Blood samples were taken immediately prior to the procedure. Soluble E-Selectin, P-Selectin, intra-cellular adhesion molecule and vascular cell adhesion molecule were assayed using a commercially available enzyme linked immunosorbent assay technique (R&D systems) and high sensitivity C reactive protein was measured by rate nephelometry. Patients were reviewed at 8 weeks and bloods were taken at this time. RESULTS: At baseline patients who had an unsuccessful cardioversion (n=15) were compared to those who had a successful cardioversion (n=66). Thirty-two patients of the 66 initially successful patients reverted to atrial fibrillation during the follow-up period. There was no difference in the levels of baseline serum inflammatory markers measured between those with an unsuccessful cardioversion and those who were successful. When the group who reverted to atrial fibrillation were compared to those who remained in sinus rhythm again there was no difference in the levels of serum markers measured at baseline. CONCLUSION: There was no association between maintenance of sinus rhythm following cardioversion and serum inflammatory markers.

Atrial Fibrillation↗
PubMed2004

Vitamin E modulation of C-reactive protein in smokers with acute coronary syndromes.

Acute coronary syndromes are characterized by the expression of proinflammatory cytokines such as C-reactive protein (CRP). Sustained upregulation of inflammatory markers is associated with an adverse prognosis. Vitamin E is known to have significant anti-inflammatory properties and has been associated with a reduction in cardiovascular events in some studies of high-risk patients. The mechanism of benefit remains controversial. We conducted a randomized, double-blind placebo controlled trial of vitamin E 400 IU daily for 6 months in 110 patients with acute coronary syndromes. Serum samples were collected at enrollment and at 2, 4, and 6 months. CRP, interleukin-6 and the soluble cell adhesion molecules were measured. Vitamin E levels increased significantly in the treatment group (from 31 micromol/l at baseline to 51 micromol/l, p <.0001) and were unchanged in the placebo group (32 micromol/l at baseline to 34 micromol/l, p = NS). CRP levels fell in both the vitamin E group and the placebo group over the treatment period (from 17.2 +/- 2.9 to 6.1 +/- 0.8 mg/l and from 21.5 +/- 4.9 to 5.9 +/- 0.9 mg/l, p = NS for the difference between active and placebo groups). However, vitamin E treatment was associated with significantly lower 6 month CRP levels in smokers versus smokers on placebo (4.7 +/- 0.71 mg/l vs. 8.26 +/- 1.5 mg/l, p =.02). Vitamin E reduces CRP levels in smokers with acute coronary syndromes for up to 6 months after hospitalization.

Adult↗
PubMed2003

Anti-inflammatory effects of statins in patients with aortic stenosis.

BACKGROUND: Aortic stenosis is an inflammatory process, as evidenced by increased tissue expression and serum levels of various endothelial cellular adhesion molecules. Aortic stenosis and atherosclerosis have many risk factors in common, including hypercholesterolemia. In atherosclerosis, statins lower cholesterol and display some anti-inflammatory activity. We hypothesized that statins might also have anti-inflammatory effects in patients with aortic stenosis. METHODS: This observational cross-sectional study measured levels of cellular adhesion molecules in 129 patients (88 male, mean age 68) with aortic stenosis (mean echo gradient 49 mm Hg, range 22 to 112) and compared levels in patients already on statin therapy for primary or secondary prevention of coronary artery disease, to those not on treatment. Concomitant conditions included hypertension (47%), diabetes (10%), and ischemic heart disease (54%). A comparison group consisted of 45 patients with stable ischemic heart disease. RESULTS: Patients on statins (35) were more likely to have hypertension (62% vs 42%, P =.05), but no significant differences existed in sex, age, concomitant ischemic heart disease, or diabetes. Statin-treated patients had a 20% lower vascular cellular adhesion molecule level than those without (484 +/- 143 ng/L vs 604 +/- 245 ng/L, P =.006). The reduction in cellular adhesion molecule levels was consistent in patients with aortic stenosis alone, aortic stenosis and ischemic heart disease, or ischemic heart disease alone. There were no differences in the levels of the other adhesion molecules between the three groups, or related to statin therapy. CONCLUSION: Statin therapy is associated with reduced serum levels of vascular cellular adhesion molecules in patients with aortic stenosis. Vascular cellular adhesion molecule levels are similar in patients who have aortic stenosis, ischemic heart disease, or both. A prospective study is required to confirm this finding and to determine whether this suppression of endothelial inflammation translates into a slowing of the progression of aortic stenosis.

Adult↗
PubMed2002

Endothelial inflammation and thrombolysis resistance in acute myocardial infarction.

BACKGROUND: Despite recent refinements to thrombolysis for acute myocardial infarction, a significant minority of patients still fail to reperfuse. There is no reliable predictor of this state of "thrombolysis resistance", but platelet and endothelial factors are believed to be important. Cell adhesion molecules are expressed by the endothelium when activated and their shed or soluble portion can be quantified in the peripheral serum, where they may be taken as a measure of endothelial activation. We sought to find a link between markers of endothelial inflammation at time of infarction and failure to reperfuse as measured by vessel occlusion at angiography. METHODS: Patients presenting with their first acute myocardial infarction had levels of soluble adhesion molecules, C-reactive protein and monocyte chemotactic protein-1 measured prior to thrombolysis. An angiogram on day five after admission was performed to establish patency of the index vessel. RESULTS: Levels of soluble vascular adhesion molecule-1 (sVCAM-1) taken prethrombolysis were significantly elevated compared to those with a patent vessel (620+/-90 vs. 418+/-28 ng/ml, P<0.03. The positive predictive value of sVCAM-1 for vessel patency was 88%. CONCLUSIONS: We found elevated serum levels of the adhesion molecule soluble vascular adhesion molecule-1 (sVCAM-1) at presentation in patients with acute myocardial infarction who did not respond to thrombolysis. Endothelial activation may be important in thrombolysis resistance.

Acute Disease↗