Left atrial function in patients with a high C-reactive protein level and paroxysmal atrial fibrillation.

OBJECTIVE

We evaluated left atrial dimensions and function in high C-reactive protein (CRP) patients with paroxysmal atrial fibrillation.

BACKGROUND

In patients with increased plasma levels of CRP left atrial dysfunction may enhance the occurrence of arrhythmias.

METHODS

Two-dimensional and pulsed Doppler echocardiography, were performed in 20 consecutive patients with high CRP levels and paroxysmal atrial fibrillation (group CRf) and in 20 patients with high CRP levels without this arrhythmia (group CR). Twenty normal subjects (group N) were also investigated. Groups were matched for age and gender.

RESULTS

CRP was increased in the CRf (median = 1.03 mg/dl), CR (median = 0.84 mg/dl) and N groups (median = 0.23 mg/dl), (p < 0.001) for all comparisons. The CRf, CR and N groups had similar systolic and diastolic blood pressure, left ventricular mass index, left ventricular ejection fraction, isovolumic relaxation time and peak early and late transmitral Doppler flow velocities. Maximal left atrial volume was greater only in the CRf group (54.4 +/- 6.3 ml) compared with the N group (50.3 +/- 4.9 ml, p < 0.05). Left atrial volume preceding atrial contraction was similar in all groups, p=NS. Left atrial minimal volume decreased from 23.0 +/- 1.8 ml in the CRf group, to 19.8 +/- 1.8 ml in the CR group, p < 0.001 and to 18.1 +/- 2.1 ml in the N group, (p < 0.02). The passive emptying fraction of the CRf and CR groups was comparable to that of normal subjects. The CRf group had a decreased left atrial active emptying fraction (0.25 +/- 0.08) compared with the CR (0.36 +/- 0.09) and N groups (0.39 +/- 0.08), p < 0.001 for both comparisons. The reservoir fraction was decreased only in the CRf group compared to normal subjects (1.37 +/- 0.25 vs. 1.82 +/- 0.43, p < 0.001).

CONCLUSIONS

These results suggest that the occurrence of paroxysmal atrial fibrillation in patients with a high CRP level is associated with enlargement of the left atrium, depression of its contractile function and is independent of left ventricular hypertrophy and function. The mechanisms linking these variables remain undefined.