Response to Increased Intervisit Blood Pressure Variability and β-Blockade: Measurement Imprecision Related to Bradycardia?

We welcome the letter from Ben-Dov and Bursztyn¹ and agree that further studies are required to confirm the influence of medium-term blood pressure variability (BPV) on outcome and to elucidate the underlying pathogenetic mechanisms. However, we must take issue with the alternative explanation put forward for the association of β-blockers with intervisit BPV.

First, in support of the theory that β-blocker–induced bradycardia can decrease the precision of blood pressure measurement, ambulatory data from a cohort are presented in which subjects with the slowest heart rate had greatest BPV. This association is hardly surprising, but to postulate that it can be explained by measurement inaccuracy with validated automated devices such as those used in the Anglo-Scandinavian Cardiac Outcomes Trial is simply not sustainable.²

The authors then speculate that the theoretical measurement induced by bradycardia accounts for the negative outcome associated with medium-term variability. However, this is refuted in the analysis by Rothwell et al,³ which confirmed that the prognostic value of visit-to-visit systolic BPV was independent of mean heart rate and heart rate variability in the Anglo-Scandinavian Cardiac Outcomes Trial. Furthermore, the Ohasama group showed that both increased visit-to-visit mean heart rate and heart rate variability were complementary to the prognostic benefit of increased medium-term BPV in a community-dwelling cohort.⁴