From the Journals

Study links low diastolic blood pressure to myocardial damage, coronary heart disease

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Lower is not always better

The average age in the study by McEvoy et al. was 57 years. One might anticipate that in an older population, the side effects from lower BPs [blood pressures] due to drug therapy such as hypotension or syncope would be greater, and the potential for adverse cardiovascular events due to a J-curve would be substantially increased compared with what was seen in the present study. Similarly, an exacerbated potential for lower DBP to be harmful might be expected in patients with established coronary artery disease.

The well done study ... shows that lower may not always be better with respect to blood pressure control and, along with other accumulating evidence, strongly suggests careful thought before pushing blood pressure control below current guideline targets, especially if the diastolic blood pressure falls below 60 mm Hg while the pulse pressure is[greater than] 60 mm Hg.

Deepak L. Bhatt, MD, MPH, is at Brigham and Women’s Hospital Heart & Vascular Center, Boston. He disclosed ties to Amarin, Amgen, AstraZeneca, Bristol-Myers Squibb, Eisai, and a number of other pharmaceutical and medical education companies. His comments are from an accompanying editorial (J Am Coll Cardiol. 2016 Oct 18;68[16]:1723-1726).


 

From the Journal of the American College of Cardiology

Low diastolic blood pressure (DBP) was significantly associated with myocardial injury and incident coronary heart disease, especially when the systolic blood pressure was 120 mm or higher, investigators reported.

Compared with a DBP of 80 to 89 mm Hg, DBP below 60 mm Hg more than doubled the odds of high-sensitivity cardiac troponin-T levels equaling or exceeding 14 ng per mL, and increased the risk of incident coronary heart disease (CHD) by about 50%, in a large observational study. Associations were strongest when baseline systolic blood pressure was at least 120 mm Hg, signifying elevated pulse pressure, reported Dr. John McEvoy of the Ciccarone Center for the Prevention of Heart Disease, Hopkins University, Baltimore, and associates (J Am Coll Cardiol 2016;68[16]:1713–22).

Blood pressue illustration ©Vishnu Kumar/Thinkstock
“Our results have a number of potential implications, particularly in the post-SPRINT era where the threshold for diagnosing and treating hypertension could be redefined,” the investigators emphasized, referring to the Systolic Blood Pressure Intervention Trial (SPRINT), which found a reduced rate of major cardiovascular events and all-cause mortality associated with a targeted systolic blood pressure below 120 mm Hg, vs. less than 140 mm Hg in a high risk population (N Engl J Med 2015; 373:2103-2116). “Despite the undeniable clinical benefits reported in SPRINT, one of many concerns related to aggressive SBP reduction with pharmacotherapy is the possibility of myocardial ischemia by lowering DBP,” they noted.

Their study included 11,565 individuals tracked for 21 years through the Atherosclerosis Risk in Communities Cohort, an observational population-based study of adults from in North Carolina, Mississippi, Minnesota, and Maryland. The researchers excluded participants with known baseline cardiovascular disease or heart failure. High-sensitivity cardiac troponin-T levels were measured at three time points between 1990 and 1992, 1996 and 1998, and 2011 and 2013. Participants averaged 57 years old at enrollment, 57% were female, and 25% were black (J Am Coll Cardiol. 2016 Oct 18. doi: 10.1016/j.jacc.2016.07.754).

Compared with baseline DBP of 80 to 89 mm Hg, DBP under 60 mm Hg was associated with a 2.2-fold greater odds (P = .01) of high-sensitivity cardiac troponin-T levels equal to or exceeding 14 ng per mL during the same visit – indicating prevalent myocardial damage – even after controlling for race, sex, body mass index, smoking and alcohol use, triglyceride and cholesterol levels, diabetes, glomerular filtration rate, and use of antihypertensives and lipid-lowering drugs, said the researchers. The odds of myocardial damage remained increased even when DBP was 60 to 69 mm Hg (odds ratio, 1.5; P = .05). Low DBP also was associated with myocardial damage at any given systolic blood pressure.

Furthermore, low DBP significantly increased the risk of progressively worsening myocardial damage, as indicated by a rising annual change in high-sensitivity cardiac troponin-T levels over 6 years. The association was significant as long as DBP was under 80 mm Hg, but was strongest when DBP was less than 60 mm Hg. Diastolic blood pressure under 60 mm Hg also significantly increased the chances of incident CHD and death, but not stroke.

Low DBP was most strongly linked to subclinical myocardial damage and incident CHD when systolic blood pressure was at least 120 mm Hg, indicating elevated pulse pressure, the researchers reported. Systolic pressure is “the main determinant of cardiac afterload and, thus, a primary driver of myocardial energy requirements,” while low DBP reduces myocardial energy supply, they noted. Therefore, high pulse pressure would lead to the greatest mismatch between myocardial energy demand and supply.

“Among patients being treated to SBP goals of 140 mm Hg or lower, attention may need to be paid not only to SBP, but also, importantly, to achieved DBP. Diastolic and systolic BP are inextricably linked, and our results highlighted the importance of not ignoring the former and focusing only on the latter, instead emphasizing the need to consider both in the optimal treatment of adults with hypertension.,”

The study was supported by the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases and by the National Heart, Lung, and Blood Institute. Roche Diagnostics provided reagents for the cardiac troponin assays. Dr. McEvoy had no disclosures. One author disclosed ties to Roche; one author disclosed ties to Roche, Abbott Diagnostics, and several other relevant companies; and two authors are coinvestigators on a provisional patent filed by Roche for use of biomarkers in predicting heart failure. The other four authors had no disclosures.

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