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.

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 μmol/l at baseline to 51 μmol/l, p < .0001) and were unchanged in the placebo group (32 μmol/l at baseline to 34 μmol/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.

Background: The acute coronary syndromes are associated with an intense inflammatory response and sustained leukocyte activation. This inflammatory state has been correlated with an adverse prognosis, but the source of this inflammation remains controversial, with evidence that it may arise either from the coronary vasculature or from the systemic endothelium. Methods: Levels of soluble cell adhesion molecules, and of their respective monocyte cell surface ligands, were measured in the peripheral serum of 21 patients presenting with acute coronary syndromes. Soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 were measured by enzyme linked immunosorbent assay and expression of the monocyte integrins CD11b (Mac-1) and CD49d (VLA-4) was measured by direct immunofluorescence using flow cytometry. Results: High levels of the monocyte receptor CD11b (531 vs. 345 MFI, P<0.01), and its soluble intercellular adhesion molecule-1 (329 vs. 232 ng/ml, P<0.01), were noted in patients with acute coronary syndromes compared to healthy controls. Conclusions: Reciprocal activation of monocyte receptor ligands and endothelial adhesion molecules was found in the peripheral blood of patients with acute coronary syndromes. This may indicate a coordinated state of pro-inflammatory upregulation with widespread activation of both leukocytes and endothelium and suggests a systemic rather than local source for inflammation in acute coronary disease.

The aim of the study was to determine the relationship between the rate of peak early mitral inflow velocity and the peak early diastolic mitral annular tissue velocities in normal controls and to compare them with subjects with diastolic dysfunction.

0.66, p< 0.05). The normal group did not show a correlation between the acceleration of transmitral flow and mitral annular relaxation velocity (r=0.18, p < 0.22). Those with diastolic dysfunction also had a lower E/A ratio than the normal group (0.7 ± 0.2 vs. 1.9 ± 0.5, p < 0.001), a higher time-velocity integral of the atrial component (11.7 ± 3.2 cm vs. 5.5 ± 2.1 cm, p < 0.0001) and a lower rate of acceleration of blood across the mitral valve (549.2 ± 151.9 cm/sec2 vs. 871 ± 128.1cm/sec2 ,p <.001). Conclusions In diastolic dysfunction where the influence of preload is minimal, recoil and the acceleration of early diastolic blood flow are reduced compared to normals. Also the rate of flow across the mitral valve was found to be strongly related to mitral annular tissue velocity. This relationship reveals the influence of recoil on flow in diastolic dysfunction. However in normal subjects the acceleration of early diastolic blood flow and recoil are not correlated. Recoil in normal provides the potential energy for rapid early diastolic filling and occurs during isovolumic relaxation before filling. Therefore rapid early diastolic filling under the influence of preload occurs after isovolumic relaxation and no relationship exists. This supports the existence of an early diastolic mechanism in normal.

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.

Of 147 patients admitted with acute coronary syndromes, 17 were taking statins at the time of presentation. These were matched with 17 subjects not taking statins. We found that statin therapy was associated with lower levels of sP-selectin, a marker of platelet and vascular endothelial activation. This provides further insight into the extralipid effect of statins in clinical practice and may help explain the greater-than-expected benefits of statin therapy in ischemic heart disease.

We studied the relation between angiographically defined coronary artery disease and serologic evidence of Helicobacter pylori infection in 488 patients undergo ing elective coronary angiography. There was no association between Helicobacter pylori infection and coronary artery disease (odds ratio 1.3, 95% confidence interval 0.83 to 2.16).