CONTEXT: Most guidelines for treatment of hypertension including the Joint National Committee-7 recommend a blood pressure (BP) goal of <140/90 mm Hg for hypertensive patients and a more aggressive goal of <130/80 mm Hg for patients with coronary artery disease (CAD), based largely on expert consensus.
OBJECTIVE: To evaluate the BP targets in patients with CAD DATA SOURCES: PUBMED, EMBASE and CENTRAL Study Selection: Randomised clinical trials (RCTs) of antihypertensive therapy in patients with CAD, enrolling at least 100 patients, with achieved systolic pressure of <=135 mm Hg in the 'intensive BP' group and <=140 mm Hg in the 'standard BP' group with follow-up for at least 1 year and evaluating cardiovascular outcomes.
DATA EXTRACTION: The following efficacy outcomes were extracted- all-cause mortality, cardiovascular mortality, myocardial infarction, stroke, angina pectoris, heart failure and revascularisation.
RESULTS: We identified 15 RCTs enrolling 66,504 participants with 276,328 patient-years of follow-up. Intensive BP group (= 135 mm Hg) was associated with a 15% decrease in heart failure rate and 10% decrease in stroke rate, driven largely by trials with a more intensive BP group (= 130 mm Hg), with similar outcomes for death and cardiovascular death and was associated with a 105% increase in the risk of hypotension. More intensive BP group (= 130 mm Hg) was also associated with a reduction in myocardial infarction and angina pectoris. The results were similar in a Bayesian random effects model. In addition, lower seemed to be better (based on regression analysis) for the outcomes of myocardial infarction, stroke, heart failure and perhaps angina.
CONCLUSIONS: The present body of evidence suggests that in patients with CAD, intensive systolic BP control to = 135 mm Hg and possibly to = 130 mm Hg is associated with a modest reduction in stroke and heart failure but at the expense of hypotension. Lower was better, although not consistently so for myocardial infarction, stroke, heart failure and perhaps angina. Further trials are needed to prove these findings.
This is a cardiology publication and has little that is specific to diabetes, although some diabetes studies are included. The deductions are firmly directed at a cardiology readership and it is of little interest to a diabetes readership.
The discussion states that the findings are hypothesis-generating and that RCTs evaluating specific drug regimens are needed. I agree.
Every potent medication and, in turn, intervention carries with it similarly potent potential for side effects and even harm. This meta-analysis provides more information to support the benefit of lowering systolic BP to 135mmHg and even, possibly, to <130. Not unexpectedly, hypotension as a side effect rears its ugly head. As the authors state, there are limitations to their analysis and this should be used primarily as hypothesis-generating for future studies. Nevertheless, it does provide useful and practical information to help inform clinicians' decisions in target systolic BPs that may be beneficial. So if you can get down to a systolic BP of 135 or even 130 without causing hypotension, it looks like a reasonable, useful, safe goal in practice.
Doesn`t matter whether practitioners know this or not because, as the study`s authors say, "The results are therefore best described as hypothesis generating to be further confirmed in future RCTs." Later they note, "Randomised controlled trials testing BP strategies are needed to conclusively prove the efficacy and safety of aggressive BP control in subjects with CAD." So what would be newsworthy would be the RCT`s called for by this hypothesis-generating study. I think practitioners often take hypothesis-generating data and "run with it," concluding that the evidence has shown what the truth is. I know of a NIH-sponsored trial, the SPRINT study, that mirrors the ACCORD study done in diabetes in which persons with CAD or at high risk for CAD but no history of diabetes are randomly assigned to systolic BP <120 vs <140. This should answer the question raised by this study to a great extent.
It again reinforces the fact that lowering blood pressure reduces stroke but I am unconvinced that intensive lowering blood pressure will reduce risk of cardiac events. Heterogeneity of population studied in the trials makes it difficult to deploy an average target for all patients in clinic. Nevertheless, a subgroup of patients with no significant vascular disease and who tolerate reduction of pressure well might benefit from specific drugs with lower targets.
Sounds impressive but looking at it I am less than overwhelmed. None of the studies included actually looked at BP targets (what happened to the HOT trial, for example?). The studies were mostly drug vs placebo showing that the active drug, mostly ACE inhibitors, decreased CHF and stroke outcomes. This is not terribly surprising. No significant differences seen for mortality or other cardiac endpoints.
At last data are accumulating that support the idea that lower BP targets are beneficial, an idea that many nephrologists have been promoting for many years and have been attempting to achieve for their patients.
It would have been interesting to know whether there was a difference in effects of lower target BPs in patients with CKD and coronary artery disease, although the sample size may have been limiting. In any case, the magnitude of the effect is surprisingly small and the cost (hypotension, other adverse effects, $) makes this seem close to a draw.