Clinical Research in Cardiology

, Volume 107, Issue 4, pp 312–318 | Cite as

Association between low diastolic blood pressure and subclinical myocardial injury

  • George S. Waits
  • Wesley T. O’Neal
  • Pratik B. Sandesara
  • Yabing Li
  • Amit J. Shah
  • Elsayed Z. Soliman
Original Paper

Abstract

Background

Coronary arteries perfuse cardiac myocytes during diastole. We hypothesized that marked lowering of diastolic blood pressure (DBP) is associated with increased risk of subclinical myocardial injury (SC-MI).

Methods

This analysis included 6107 participants without history of cardiovascular disease (CVD) from the third National Health and Nutrition Examination Survey. SC-MI was determined by a validated electrocardiogram-based scoring system. Logistic regression was used to examine the cross-sectional association between DBP (< 70, 70–80 mmHg (reference group), and > 80 mmHg; and per each 10 mmHg decrease, separately) with SC-MI across levels of systolic blood pressure (SBP) (< 120, 120–139, or > 140 mmHg).

Results

In a multivariable model, DBP < 70 mmHg was associated with a higher risk of SC-MI [OR (95% CI) 1.40 (1.02, 1.94)] in participants with SBP > 140 mmHg. This association was consistent in subgroups stratified by age, race, diabetes, hypertension, obesity and smoking, but was stronger in women than in men [OR (95% CI) 1.58 (1.06, 2.37) vs. 1.10 (0.62, 1.94), respectively; interaction p value = 0.006]. Also, among participants with SBP > 140 mmHg, every 10 mmHg decrease in DBP was associated with a 12% increased odds of SC-MI [OR (95% CI) 1.12 (1.01, 1.23)]. No significant associations between DBP and SC-MI were observed in those with SBP < 120 mmHg or 120–139 mmHg, or between DBP > 80 mmHg and SC-MI in any of SBP levels.

Conclusions

Low DBP < 70 mmHg in those with SBP > 140 mmHg carries higher risk of SC-MI, especially in women. Further research is needed to understand the therapeutic implications of these findings.

Keywords

Diastolic blood pressure Subclinical myocardial injury 

Notes

Acknowledgements

The authors thank Ms. Julie Hu, EPICARE Center, for her help with the art work of the manuscript.

Compliance with ethical standards

Funding

WTO is supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under award F32HL134290 and AJS is supported by K23 HL 127251.

Conflict of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2017

Authors and Affiliations

  • George S. Waits
    • 1
  • Wesley T. O’Neal
    • 2
  • Pratik B. Sandesara
    • 2
  • Yabing Li
    • 3
  • Amit J. Shah
    • 2
    • 4
  • Elsayed Z. Soliman
    • 3
    • 5
  1. 1.Department of Internal MedicineWake Forest School of MedicineWinston SalemUSA
  2. 2.Division of Cardiology, Department of MedicineEmory University School of MedicineAtlantaUSA
  3. 3.Department of Epidemiology and Prevention, Epidemiological Cardiology Research Center (EPICARE)Wake Forest School of MedicineWinston SalemUSA
  4. 4.Department of Epidemiology, Rollins School of Public HealthEmory UniversityAtlantaUSA
  5. 5.Department of Internal Medicine, Section on CardiologyWake Forest School of MedicineWinston SalemUSA

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