By Michael Crawford, MD
Professor of Medicine, Chief of Clinical Cardiology, University of California, San Francisco
Dr. Crawford reports no financial relationships relevant to this field of study.
SYNOPSIS: An analysis of the community-based ARIC study showed that low diastolic blood pressures were associated with higher baseline and subsequent troponin T levels and adverse cardiac events, but not stroke.
SOURCES: McEvoy JW, Chen Y, Rawlings A, et al. Diastolic blood pressure, subclinical myocardial damage, and cardiac events: Implications for blood pressure control. J Am Coll Cardiol 2016;68:1713-1722.
Bhatt DL. Troponin and the J-curve of diastolic blood pressure: When lower is not better. J Am Coll Cardiol 2016;68:1723-1726.
Aggressively lowering systolic blood pressure (SBP) also will lower diastolic blood pressure (DBP). The level at which DBP is too low for adequate coronary artery blood flow is unclear. Thus, investigators from the Atherosclerosis Risk in Communities (ARIC) study, after excluding those with known cardiovascular (CV) disease, studied 11,565 community living subjects, including a subgroup of 1,403 who met the entry criteria for the Systolic Blood Pressure Intervention Trial (SPRINT). High-sensitivity cardiac troponin T (hsT) was measured at visits two, four, and five over a span of 21 years (1990-2003). A hsT value ≥ 14 ng/L was chosen as the cutoff for subclinical myocardial damage (99th percentile in healthy adults). BP was measured after five minutes of rest sitting, and the mean of the last two to three measures over five minutes was the BP used for this analysis. Risk factors for CV disease were recorded and clinical endpoints, such as coronary events, stroke, and mortality, were noted. The study evaluated the relationship between DBP and hsT values and clinical events. The study population mean baseline age was 57 years, 57% were female, and 25% were black. Compared to those with a baseline DBP between 80-89 mmHg, the adjusted odds ratio (OR) of having a hsT ≥ 14 ng/L at baseline was 2.2 (95% confidence interval [CI], 1.2-4.1) for a DBP < 60 mmHg and 1.5 (95% CI, 1.0-2.3) for a DBP of 60-69 mmHg. Similar results were observed in the SPRINT eligible subgroup (OR = 1.7 for DBP < 60 mmHg, and OR = 1.2 for DBP 60-69 mmHg), but these results were not statistically significant. Also, a low DBP at baseline was associated with increased hsT release over follow-up compared to the baseline DBP 80-89 mmHg group (+1.5 ng/L/year in the < 60 DBP group, and +1.0 ng/L/year in the 60-69 mmHg group). In addition, a DBP < 60 mmHg as compared to 80-89 mmHg was associated with more coronary heart disease events and mortality, but not stroke. These associations were strongest in those with elevated hsT (≥ 14 ng/L) at baseline and those with a baseline SBP ≥ 120 mmHg. The authors concluded that low DBP, particularly in those with an SBP ≥ 120, was associated with subclinical myocardial damage and coronary heart disease events.
COMMENTARY
Concern over the potential downside to pushing BP targets lower, a la SPRINT, continues. This study looked at the large ARIC database, which collected hsT data and clinical outcomes over 21 years in community living subjects. Their analysis showed an association between low DBP and subclinical myocardial injury at baseline and during follow-up. Also, low DBP was associated with coronary heart disease events and all-cause mortality. In addition, the association of low DBP and adverse outcomes was strongest in those with evidence of myocardial injury at baseline (hsT ≥ 14ng/L). These findings are consistent with other studies that have suggested a J-shaped curve for DBP and coronary events. Furthermore, since coronary blood flow largely is in diastole, this makes sense physiologically. Notably, low DBP was not associated with increased strokes, which serves as a negative control in this study, because an increase in strokes would not be biologically plausible. Finally, the findings were independent of whether the lower DBP was naturally occurring or potentially caused by anti-hypertensive medications, which lends more strength to the conclusions.
McEvoy et al examined DBP in isolation, but of course it is related to SBP. The association between DBP and outcome was strongest at SBPs > 120 mmHg, which suggests that the adverse effects of low DBP are more important when myocardial energy requirements (systolic load) are higher. Other studies have emphasized the predictive ability of pulse pressure (difference between systolic and diastolic pressure) and mean BP. In this study, it appears that pulse pressures > 60 are potentially detrimental, but more work needs to be done on this area. Also, elevated SBP was associated with elevated hsT and worse outcomes, which would be expected based on other studies. All these observations make determining BP targets challenging.
The authors suggested that when treating hypertension, try to keep the DBP > 70 mmHg but certainly keep it above 60 mmHg. Of course, if you try to drive the SBP < 120 mmHg, as suggested by SPRINT, it may be difficult to keep the DBP in a safe range. This would be especially important in patients with known coronary heart disease. Unfortunately, the SPRINT eligible subgroup in this study was underpowered, but the trend was similar to the overall study results. This suggests that there may be a cost to driving the SBP < 120 mmHg, even in the relatively healthy SPRINT group. Patients with left ventricular hypertrophy also may suffer with lower DBP. They clearly need higher DBPs as they can have myocardial ischemia without coronary artery disease when BP is low. The editorial by Dr. Bhatt emphasizes that picking BP targets for individual patients requires careful thought, considering all the factors discussed above and others. One goal for all may not be wise.
