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International Journal of Cardiology 2008-Jan

Alimentary lipemia enhances procoagulatory effects of inflammation in patients with a history of acute myocardial infarction complicated by ventricular fibrillation.

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Thorsten Kälsch
Elif Elmas
Xuan Duc Nguyen
Hans Leweling
Harald Klüter
Martin Borggrefe
Carl Erik Dempfle

Nøgleord

Abstrakt

BACKGROUND

Acute myocardial infarction, often occurring postprandially, can be complicated by ventricular fibrillation. The role of acute alimentary lipemia and inflammation in the occurrence of ventricular arrhythmias in acute myocardial infarction has not been described yet.

RESULTS

Before and 2 h after consumption of a defined fatty meal, blood samples of 27 patients with a history of acute myocardial infarction (AMI) were incubated with lipopolysaccharide (LPS). In 10 patients, AMI was complicated by ventricular fibrillation (VF), in 17 patients, AMI occurred without VF. CD40-ligand and CD62P expression on platelets, tissue-factor binding on monocytes and platelet-monocyte aggregates were measured with flow cytometry. Soluble CD40-ligand plasma levels were measured with an ELISA. With the meal, serum triglyceride levels increased from 211.85+/-94.60 mg/dl to 273.59+/-122.52 mg/dl (p=0.0002). LPS stimulation before the meal showed a non-significant tendency to increase platelet-monocyte aggregates and tissue factor on monocytes in both patient groups. LPS stimulation in acute alimentary lipemia significantly increased tissue-factor expression on monocytes in both patient groups and platelet-monocyte aggregates in patients with VF. Baseline plasma levels of soluble CD40L did not differ significantly between both groups. Acute alimentary lipemia significantly decreased total plasma levels of sCD40L, leading to a significantly lower level of sCD40L in patients with a history of VF.

CONCLUSIONS

Alimentary lipemia enhances procoagulatory effects of inflammatory stimulation in patients with a history of AMI complicated by ventricular fibrillation. These observations might reveal a mechanism for an increased risk of VF in acute coronary syndromes in a postprandial state.

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