Background: Deterioration of left ventricular function during follow-up was reported in some patients with syndrome X and concomitant left bundle branch block. The patients with syndrome X and left bundle branch block has been frequently presented with elevated Endothelin-1 (ET-1) level while brain natriuretic peptide (BNP) (a sensitive marker of left ventricular dysfunction) has not been measured in patients with syndrome X.
Methods: The purpose of the present study was to assess left ventricular diastolic function, levels of N-terminal Brain Natriuretic Peptide (NT-proBNP) precursor and biochemical parameters of endothelial function in patients with syndrome X complicated by left bundle branch block but preserved left ventricular systolic function (group A, n=8). The echocardiographic and neurohormonal measures in these patients were compared to those in patients with syndrome X without left bundle branch block (group B, n=13), and controls (group C, n=15).
Results: At rest and after exercise the serum concentration of NT-proBNP was significantly higher in group A than in the controls (at rest: 232+/-96 vs. 133+/-23 fmol/ml, P=0.03; after exercise: 313+/-96 vs. 180+/-33 fmol/ml, P=0.02). The highest concentration of endothelin-1 was also found in group A, being significantly higher than in the controls (6.81 vs. 4.52 pg/ml, P<0.05). Mitral flow abnormalities were detected in left bundle branch block patients. Accordingly, the lowest E/A ratio was in group A and it differed significantly from that in group C (0.85 vs. 1.1, P<0.05). E/A ratio inversely correlated with plasma NT-proBNP concentration in patients with left bundle branch block (r=-0.48, P=0.02).
Conclusions: Elevated NT-proBNP and endothelin-1 plasma concentrations were demonstrated in patients with syndrome X complicated by left bundle branch block even when left ventricular systolic function was still preserved. In this subgroup the magnitude of left ventricular diastolic dysfunction correlated with the increase of BNP level which reflects neurohormonal activation.