Electrocardiographic Left Ventricular Hypertrophy and Arterial Stiffness: The Ohasama Study

Background Whether arterial stiffness per se contributes to left ventricular hypertrophy (LVH) independently of blood pressure (BP) remains unknown. We examined the relationship between pulse wave velocity (PWV) and LVH in a large population. Methods The PWV was measured between the brachial and ankle regions (baPWV) of 798 individuals. We diagnosed LVH using electrocardiographic criteria: Cornell voltage-duration product >2440 mm × msec or Sokolow-Lyon voltage >38 mm. The participants were initially separated into those with and without LVH [LVH(+) and LVH(−) groups, respectively]. To determine theoretical baPWV, we first constructed a nomogram for the LVH(−) group, calculated the PWV index (measured baPWV − theoretical baPWV) for each individual and then compared the two groups. We also examined the factors associated with LVH(+) using multivariate analyses. Results Linear regression analysis revealed that the theoretical baPWV (m/sec) = 0.20 × age (years) + 0.13 × Mean arterial pressure (MAP) (mm Hg) + 0.05 × Heart rate (beats/min) − 11.74 (R2 = 0.56). The PWV index was greater in the LVH(+) than in the LVH(−) group (P = .025). The baPWV was independently related to LVH(+) along with MAP, medication for hypertension, and for diabetes; a 1 SD (4.3 m/sec) increase in baPWV was associated with a 26% increase in the risk of LVH(+) (P = .022). When LVH(+) risk factors were defined as hypertension, diabetes, and high baPWV (≥14.6 m/sec), the prevalence of LVH(+) linearly increased with the number of concomitant LVH(+) risk factors (P< .001). Conclusions Arterial stiffness is independently related to electrocardiographically determined LVH in the general population.