Dr. Michael Fulks discusses new evidence that could reshape how life insurers assess blood pressure risk.
Back in 2015, researchers at CRL published an article looking at insurance applicants’ blood pressure (BP) and later mortality. We found that increasing all-cause mortality correlated with increasing systolic BP (SBP) beginning around 120 mm Hg but not with increasing diastolic BP (DBP). Multiple authors before and since have noted this disparity, but our study was one of the largest and was the only recent one that used a cohort of insurance applicants. Despite all this evidence and resultant changes in guidance on DBP from the ACC and AHA, I suspect some life underwriting manuals still show debits based on it.
A recent article in the European Heart Journal provides additional evidence strongly suggesting debits for higher DBP are not justified. Rather than being an observational study as ours and most others were correlating BP with mortality or cardiovascular events were, this meta-analysis looked at 51 randomized trials where hypertension was treated by an active drug against placebo or against less effective BP therapy. It looked for any reduction in major adverse cardiovascular events (MACE) both for those with increased SBP and for those with only isolated diastolic hypertension (IDH) defined as SBP <130 and DBP ≥80 mm Hg.
The authors found that the reduction in MACE was identical for each 5 mm Hg reduction in SPB in those treated with elevated SBP and in those treated who only had IDH. They also found that the degree of reduction in DBP did not correlate with the reduction of MACE. These results reinforce those from multiple prior observational studies, including ours, showing that the DBP level has no impact on mortality or MACE.
The only exception to this finding in our study was not for elevated DBP but for low DBP with a widened pulse pressure which is associated with increased mortality likely because the widened pulse pressure was caused by (potentially undiagnosed) aortic regurgitation.
So, check that manual and make sure it acknowledges that increasing mortality risk is dependent on increasing SBP, not on DBP, and that mortality begins to increase at SBP levels well below 140 mm Hg.
About the Author
Michael Fulks, MD, Consulting Medical Director, is board-certified in internal and insurance medicine. After leaving practice, he served as a medical director, creating or editing several underwriting manuals and preferred programs. More recently, Mike has consulted for CRL participating in its mortality research on laboratory test results, BP and build, and in the development of risk-scoring tools for laboratory and non-laboratory data.