Prediction and mechanism of frequent ventricular premature contractions related to haemodynamic deterioration.

UNLABELLED

Aim Frequent ventricular premature contractions (VPCs) may cause haemodynamic deterioration and reversible left ventricular (LV) dysfunction. We aimed to clarify this mechanism.

METHODS AND RESULTS

The haemodynamics, echocardiographic parameters, and plasma brain natriuretic peptide (BNP) level were assessed in 31 patients with idiopathic, frequent VPCs undergoing radiofrequency catheter ablation. The patients were classified into two groups according to the presence (n = 19) or absence (n = 12) of marked augmentation of the pulmonary capillary wedge pressure (PCWP) following VPCs (VPC-induced-PCWP augmentation; VI-PA). The VI-PA(+) group was defined as those with a peak PCWP of >15 mmHg measured after a VPC. Before the ablation, the mean PCWP, right atrial pressure (RAP), left ventricular end-diastolic pressure (LVEDP), and plasma BNP level were significantly greater in the VI-PA(+) group than in the VI-PA(-) group. In the VI-PA(+) group, the mean PCWP, RAP, LVEDP, and cardiac index all improved immediately after a successful ablation. At 7.4 ±0.9 months after the ablation, almost all the echocardiographic parameters and plasma BNP level also significantly improved in the VI-PA(+) group, and the magnitude of the improvement in those parameters measured was greater in the VI-PA(+) group than in the VI-PA(-) group. The left atrial contractions during mitral valve closure during VPCs caused a marked pulmonary venous flow regurgitation and VI-PA. VPC coupling intervals of <500 ms and the presence of a following P-wave of <300 ms predicted VI-PAs with a high accuracy.

CONCLUSIONS

The VI-PA may be the main mechanism of the haemodynamic deterioration in patients with frequent VPCs. This haemodynamically deteriorating subgroup could be identified by the surface electrocardiogram and improved dramatically with catheter ablation.