Author + information
- Received June 14, 2016
- Revision received July 18, 2016
- Accepted July 20, 2016
- Published online October 18, 2016.
- John W. McEvoy, MB, BCh, BAO, MHSa,b,∗ (, )
- Yuan Chen, MSa,
- Andreea Rawlings, PhDa,
- Ron C. Hoogeveen, PhDc,
- Christie M. Ballantyne, MDc,
- Roger S. Blumenthal, MDb,
- Josef Coresh, MD, PhDa and
- Elizabeth Selvin, MPH, PhDa
- aDepartment of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
- bCiccarone Center for the Prevention of Heart Disease, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland
- cDepartment of Medicine, Section of Cardiovascular Research, Baylor College of Medicine and Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas
- ↵∗Reprint requests and correspondence:
Dr. John W. McEvoy, Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Division of Cardiology, Johns Hopkins University School of Medicine and the Welch Center for Prevention, Epidemiology and Clinical Research at the Johns Hopkins Bloomberg School of Public Health, 600 North Wolfe Street, Blalock 524C, Baltimore, Maryland 21287.
Background The optimal systolic blood pressure (SBP) treatment goal is in question, with SPRINT (Systolic Blood Pressure Intervention Trial) suggesting benefit for 120 mm Hg. However, achieving an SBP this low may reduce diastolic blood pressure (DBP) to levels that could compromise myocardial perfusion.
Objectives This study sought to examine the independent association of DBP with myocardial damage (using high-sensitivity cardiac troponin-T [hs-cTnT]) and with coronary heart disease (CHD), stroke, or death over 21 years.
Methods The authors studied 11,565 adults from the ARIC (Atherosclerosis Risk In Communities) cohort, analyzing DBP and hs-cTnT associations as well as prospective associations between DBP and events.
Results Mean baseline age was 57 years, 57% of patients were female, and 25% were black. Compared with persons who had DBP between 80 to 89 mm Hg at baseline (ARIC visit 2), the adjusted odds ratio of having hs-cTnT ≥14 ng/l at that visit was 2.2 and 1.5 in those with DBP <60 mm Hg and 60 to 69 mm Hg, respectively. Low DBP at baseline was also independently associated with progressive myocardial damage on the basis of estimated annual change in hs-cTnT over the 6 years between ARIC visits 2 and 4. In addition, compared with a DBP of 80 to 89 mm Hg, a DBP <60 mm Hg was associated with incident CHD and mortality, but not with stroke. The DBP and incident CHD association was strongest with baseline hs-cTnT ≥14 ng/l (p value for interaction <0.001). Associations of low DBP with prevalent hs-cTnT and incident CHD were most pronounced among patients with baseline SBP ≥120 mm Hg.
Conclusions Particularly among adults with an SBP ≥120 mm Hg, and thus elevated pulse pressure, low DBP was associated with subclinical myocardial damage and CHD events. When titrating treatment to SBP <140 mm Hg, it may be prudent to ensure that DBP levels do not fall below 70 mm Hg, and particularly not below 60 mm Hg.
This research was supported by National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases grants R01DK089174 and K24DK106414 to Dr. Selvin. The ARIC study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C). Reagents for the cardiac troponin assays were donated by Roche Diagnostics. Dr. Ballantyne has received support from Roche Diagnostics, Abbott Diagnostics, Amarin, Amgen, Eli Lilly, Esperion, Novartis, Pfizer, Otsuka, Regeneron, Sanofi-Synthelabo, and Takeda. Drs. Ballantyne and Hoogeveen are co-investigators on a provisional patent filed by Roche for use of biomarkers in heart failure prediction. Drs. Ballantyne and Selvin have served on an advisory board for Roche Diagnostics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received June 14, 2016.
- Revision received July 18, 2016.
- Accepted July 20, 2016.
- American College of Cardiology Foundation