Elevated systolic blood pressure (SBP) variability is associated with higher risks of all-cause mortality, coronary heart disease (CHD), stroke, and end-stage renal disease, according to research published in the Journal of the American College of Cardiology.

Investigators, including Csaba P. Kovesdy, MD, the University of Tennessee Health Science Center and the Memphis VA Medical Center in Memphis, used data from a historic cohort study of nearly 3.6 million patients treated at Department of Veterans Affairs (VA) facility between 2004 and 2006 to examine the link between long-term, visit-to-visit SBP variability and all-cause mortality, cardiovascular events, and renal outcomes.

The researchers collected BP values for each participant from the date of study entry through the end of follow-up, measured either as death, last VA contact, or July 26, 2013. Pharmacy data were also collected to determine each patient’s baseline exposure to both antihypertensive and statin type of cholesterol lowering medications.


Continue Reading

Outcomes of interest included all-cause mortality, CHD, ischemic stroke, and end-stage renal disease. Deaths were identified using VA Vital Status Files.

The mean cohort age was 60±13 years, with the majority of patients being male (94%) and white (78%) as well as 18% being African American. All patients had a median of 24 SBP (25th to 75th percentile: 15-42). Mean baseline SBP was 133±18 mm Hg overall. Patients with higher SBP variability were older, more likely to be male, African American, and unmarried; have a higher prevalence of comorbid conditions; have lower income; and more frequently used antihypertensive medications.

The researchers measured 484,887 deaths during a median study follow-up of 8 years (16.9%; mortality rate: 22.87 [95% confidence interval (CI): 22.80-22.94] per 1000 patient-years). More than 67,000 CHD events were observed during the same follow-up period (2.7%; incident rate: 3.63 [95% CI: 3.60-3.66] per 1000 patient-years), and higher SBP variability was linked to significantly higher risk of incident CHD in unadjusted and adjusted models. The cohort also experienced 62,523 incident stroke events (median follow-up: 8 years; 2.3%; incident rate: 3.16 [95% CI: 3.14-3.19] per 1000 patient-years) and 6710 new cases of end-stage renal disease (median follow-up: 4.9 years; 0.23%; incident rate: 0.39 [95% CI: 0.38-0.40] per 1000 patient-years).

Fully adjusted subgroup analyses showed that higher SBP variability remained predictive of both worse survival rate and increased risk of incident CHD, stroke, and end-stage renal disease.

“Increased SBP variability…assessed over 8 years, was associated with a graded increase in the risks of all-cause mortality, incident CHD, stroke, and ESRD independent from baseline sociodemographic characteristics and comorbidities, including hypertension, BP, and antihypertensive medication use,” the researchers wrote. “These findings confirm and strengthen the importance of long-term variability in SBP for health-related outcomes.”

“Future studies are needed to examine the effects of interventions that lower SBVP on clinical outcomes,” they concluded.

Strengths and Limitations

  • This study benefitted from the large sample size of more than 3 million individuals, allowing the researchers access to a large number of BP measurements to calculate SBP variability.
  • This study was limited by its observational nature; the researchers could only report associations, not make inferences regarding the causality of SBP variability.
  • Although adjusted analyses were used to account for multiple baseline characteristics found in patients, the researchers could exclude the effect that potential unmeasured cofounders may have had on the study results.

Disclosures: Drs Gozmanova, Kalantar-zadeh, and Kovesdy are employees of the US Department of Veterans Affairs.

Reference

Gosmanova EO, Mikkelsen MK, Molnar MZ, et al. Association of systolic blood pressure variability with mortality, coronary heart disease, stroke, and renal disease. J Am Coll Cardiol. 2016;68(13):1375-1386. doi:10.1016/j.jacc.2016.06.054.