Higher pulse pressure associated with higher risk of CV morbidity and mortality

Diastolic Blood Pressure, Subclinical Myocardial Damage, and Cardiac Events: Implications for Blood Pressure Control

Literature - McEvoy JW, et al, JACC, 2016

McEvoy JW, Chen Y, Rawlings A, et al.
J Am Coll Cardiol 2016;68(16):1713


The optimal systolic blood pressure (SBP) targets for the prevention of adverse cardiac outcomes are debated [1]. Intensive SBP reduction lead to simultaneous diastolic BP (DBP) reduction, which are associated with CAD events in a J-curve manner, due to the lower coronary perfusion pressure that leads to ischemia and myocardial damage [2]. High-sensitivity cardiac troponin-T (hs-cTnT) can be used to detect asymptomatic myocardial damage and to predict CHD events [3]. As such, hs-cTnT may be of value in understanding whether a lower achieved blood pressure, and particularly a low DBP level, is associated with myocardial damage.

In this analysis of 11,565 participants in the ARIC (Atherosclerosis Risk In Communities) study, the association between low DBP and subclinical myocardial damage was evaluated, by measuring hs-cTnT levels at baseline and during follow-up. Moreover, the relationship between low DBP and the risk for future adverse outcomes, including CHD, stroke, and all-cause death was assessed with a median follow-up of 21-years. Characteristics were compared across 6 categories of DBP (<60, 60-69, 70-79, 80-89, 90-99, and ≥100 mmHg).

Main results

  • Compared with having a DBP of 80-89 mmHg, the adjusted OR of having hs-cTnT ≥14 ng/L at baseline was 2.24 (95% CI: 1.2 - 4.1, P=0.01) for DBP <60 mmHg and 1.52 (95% CI: 1.0 - 2.3, P=0.05) for DBP 60-69 mmHg.
  • There was a linear inverse relationship between DBP and hs-cTnT for DBP <65 mmHg.  
  • Compared with having a DBP of 80-89 mmHg, the estimated annual hs-cTnT change based on a period of 6 years was in the DBP <60 mmHg, 60-69 mmHg and 70-79 mmHg group, +1.46 ng/L (95% CI: 0.51-2.40, P=0.002), +0.95 ng/L (95% CI: 0.28-1.61, P=0.005) and +0.85 (95% CI: 0.27-1.44, P=0.004). Change was not significantly different for the 90-99 and ≥100 mmHg groups.

  • Compared with having a DBP 80-89 mmHg, HRs for CHD were 1.49 (95% CI: 1.20 - 1.85, P<0.001), 1.23 (95% CI: 1.05 - 1.44, P=0.01) and 1.20 (95% CI: 1.05 - 1.37, P=0.01) for respectively DBP <60 mmHg, 60-69 mmHg and 70-79 mmHg, over a median follow-up of 21 years. HR for all-cause mortality was 1.32 (95% CI: 1.13 - 1.55, P<0.001) when DBP <60 mmHg. All other groups were not significantly different.
  • There was no association between DBP and stroke after accounting for SBP and clinical confounders.
  • When stratified by baseline hs-cTnT (<14 or ≥14 ng/L), the risk for subsequent CHD was highest among those with both low DBP and baseline myocardial damage: hs-cTnT ≥14 ng/L, HR 2.6 (95% CI: 1.3 - 5.0) compared with hs-cTnT <14 ng/L, HR 1.3 (95% CI: 1.1-1.7), P interaction <0.001.  
  • When stratified by SBP categories, low DBP is a risk factor for elevated hs-cTnT and incident CHD (particularly after adjusting for SBP) and high SBP is a risk factor for elevated hs-cTnT and incident CHD.
  • Pulse pressure >60 mmHg is an important driver of these results.


In an analysis of the ARIC study, low DBP, particularly when <60 mmHg, were associated with higher levels of hs-cTnT, more frequent CHD events and mortality. This was particularly present when SBP exceeded 120 mmHg, resulting in higher pulse pressure. These data show that both SBP, as well as DBP are important in the management of individuals with hypertension.

Editorial Comment [4]

In his editorial article, Bhatt DL emphasises the importance of pulse pressure and the need for further investigations on this topic: ‘Analyses of pulse pressure tend to be complex, because teasing out the effects of SBP, DBP, mean arterial BP, and pulse pressure is not easy, as these parameters are inter-related. A DBP <60mmHg coupled with an SBP 120 mmHgthat is, a pulse pressure >60 mmHgseemed to be particularly deleterious in the present study. Therefore, an elevated pulse pressure might be a double whammyand should be a topic of further investigation.’

Some interesting aspects and implications of the study are also commented, for example:
  • The use of high-sensitivity troponin levels to predict future CV events in the stable setting, and the possibility to combine high-sensitivity troponin levels with hemodynamic stress and/or inflammation markers to personalise antihypertensive treatment in the future.
  • The possible application of the study results on other subgroups, for example, for patients with known CAD, HF, DM, renal dysfunction, and prior stroke.
  • The reassuring observation of the lack of an adverse association between lower DBP and stroke.

And he concludes: ‘The well done study by McEvoy et al. shows that lower may not always be better with respect to BP control and, along with other accumulating evidence, strongly suggests careful thought before pushing BP control below current guideline targets, especially if the DBP falls below 60 mmHg while the pulse pressure is >60 mmHg.’

Find this article online at JACC


1. Lonn EM, Bosch J, Lopez-Jaramillo P, et al. Blood-Pressure Lowering in Intermediate-Risk Persons without Cardiovascular Disease. N Engl J Med 2016;374:2009–20.
2. Messerli FH, Panjrath GS. The J-curve between blood pressure and coronary artery disease or essential hypertension: exactly how essential? J Am Coll Cardiol 2009;54:1827–34.
3. Eggers KM, Al-Shakarchi J, Berglund L, et al. High-sensitive cardiac troponin T and its relations to cardiovascular risk factors, morbidity, and mortality in elderly men. Am Heart J 2013;166:541–8.
4. Bhatt DL. Troponin and the J-Curve of Diastolic Blood Pressure: When Lower Is Not Better. J Am Coll Cardiol. 2016;68(16):1723

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