[Impact of chronic Chlamydia pneumoniae infection on left ventricular remodeling after myocardial infarction]

Postmyocardial infarction left ventricular remodeling is modified by inflammatory processes and structural changes in the myocardium. Chlamydia pneumoniae (Chp) causes chronic myocyte infection, affects apoptosis and TNF-alpha production, and may induce cross reactivity with alpha myosin. This is the way in which this intracellular pathogen may modulate remodeling on the cellular and organ level.

The study was conducted in 101 patients with a first myocardial infarction in whom we evaluated the serological features of Chp infection using the ELISA method and echocardiographic left ventricular volume at 10 days and 10 weeks after the infarction.

Patients with chronic Chp infection had a tendency toward higher end-diastolic volume at 10 weeks after the infarction (123 +/- 32.9 ml vs. 134 +/- 34.7 ml, p = 0.09). In order to better define this relationship we used ROC analysis and measured levels of antibodies: IgG = 117 EIU and IgA = 15.6 EIU by which we divided the patients into two subgroups. Those with IgG > or = 117 EIU and IgA > or = 15.6 EIU belong to the subgroup with chronic and active Chp infection. These patients had larger left ventricular end-diastolic volumes (155.8 vs. 123.1 ml, p = 0.0005) and end-systolic volumes (77.4 vs. 59.5 ml, p = 0.006) at 10 weeks after the infarction. Both subgroups were similar with respect to age, gender, history of arterial hypertension, systolic and diastolic blood pressure values, infarct site, reperfusion, infarct size, left ventricular ejection fraction and left ventricular contractility index. Type of reperfusion therapy and pharmacological treatment at 10 days and at 10 weeks did not differ, either.

Chronic Chlamydia pneumonie infection modifies the course of left ventricular remodeling.