Increased QT dispersion and other repolarization abnormalities as a possible cause of electrical instability in isolated aortic stenosis

Abstract

The aim of our study was to analyze the ventricular repolarization phase in patients with isolated aortic stenosis (AS) in order to search for possible abnormalities that might contribute to an explanation of the electrical instability peculiar to this valve disease. We selected a population of 39 patients with isolated AS (25 M and 14 F, mean age 60±16 yrs). As controls we considered a group of 31 age-matched healthy subjects 20 M and 11 F, mean age 55±14 yrs, P=NS. Disease severity was assessed by echocardiography, calculating the maximum and mean pressure gradients max and mean PG) and the functional valve orifice area. Various electrocardiographic intervals (QT, QT'c, JT, JTc) and indices (QT and QTc dispersion were adopted for a detailed non-invasive evaluation of the ventricular repolarization. In patients with AS, M-QT (391±45 ms vs 362±25 ms, P=0.002), M=QTc (431±29 ms vs 412±19 ms, P=0.003), M-JT (290±41 ms vs 265±26 ms, P=0.003, M-JTc 331±29 ms vs 302±19 ms, P<0.001, QTD (67±34 ms vs 40±15 ms, P<0.001), QTcD (77±36 ms vs 52±23 ms, P<0.001) all resulted significantly greater than in controls. QTD and QTcD both resulted linearly related either to max PCi ( r=0.388, P=0.018 and r=0.357, P=0.03) or to mean PG ( r=0.513, P=O.004 and r=0.438, P=O.015), while M-JT and M-JTc turned out to be directly related only to mean PG ( r=0.436, P=O.016 and r=0.483, P=O.007). Our findings suggest a prolonged duration of ventricular recovery and a greater dispersion of ventricular repolarization in patients with AS and might account for the electrical instability proper to this valve dysfunction. Besides, the existence of a linear direct relation between the severity of AS and the degree of inhomogeneity of left ventricular recovery, together with the correlation found among mean PCr and the total duration of the repolarization phase, expressed by the intervals JT and JTc, strongly suggest the hypothesis that in AS arrhythmogenic substrates development parallels the worsening of the valve defect.