blood pressure

Blood Pressure Targets for the Treatment of People with Hypertension and Cardiovascular Disease

Author/s: 
Saiz, Luis Carlos, Gorricho, Javier, Garjón, Javier, Celaya, Mª Concepción, Erviti, Juan, Leache, Leire

BACKGROUND:

Hypertension is a prominent preventable cause of premature morbidity and mortality. People with hypertension and established cardiovascular disease are at particularly high risk, so reducing blood pressure below standard targets may be beneficial. This strategy could reduce cardiovascular mortality and morbidity but could also increase adverse events. The optimal blood pressure target in people with hypertension and established cardiovascular disease remains unknown.

OBJECTIVES:

To determine if 'lower' blood pressure targets (≤ 135/85 mmHg) are associated with reduction in mortality and morbidity as compared with 'standard' blood pressure targets (≤ 140 to 160/ 90 to 100 mmHg) in the treatment of people with hypertension and a history of cardiovascular disease (myocardial infarction, angina, stroke, peripheral vascular occlusive disease).

SEARCH METHODS:

The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to February 2017: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched the Latin American and Caribbean Health Science Literature Database (from 1982) and contacted authors of relevant papers regarding further published and unpublished work. There were no language restrictions.

SELECTION CRITERIA:

We included randomized controlled trials (RCTs) with more than 50 participants per group and at least six months follow-up. Trial reports needed to present data for at least one primary outcome (total mortality, serious adverse events, total cardiovascular events, cardiovascular mortality). Eligible interventions were lower target for systolic/diastolic blood pressure (≤ 135/85 mmHg) compared with standard target for blood pressure (≤ 140 to 160/90 to 100 mmHg).Participants were adults with documented hypertension or who were receiving treatment for hypertension and cardiovascular history for myocardial infarction, stroke, chronic peripheral vascular occlusive disease or angina pectoris.

DATA COLLECTION AND ANALYSIS:

Two review authors independently assessed search results and extracted data using standard methodological procedures expected by The Cochrane Collaboration.

MAIN RESULTS:

We included six RCTs that involved a total of 9795 participants. Mean follow-up was 3.7 years (range 1.0 to 4.7 years). Five RCTs provided individual patient data for 6775 participants.We found no change in total mortality (RR 1.05, 95% CI 0.90 to 1.22) or cardiovascular mortality (RR 0.96, 95% CI 0.77 to 1.21; moderate-quality evidence). Similarly, no differences were found in serious adverse events (RR 1.02, 95% CI 0.95 to 1.11; low-quality evidence). There was a reduction in fatal and non fatal cardiovascular events (including myocardial infarction, stroke, sudden death, hospitalization or death from congestive heart failure) with the lower target (RR 0.87, 95% CI 0.78 to 0.98; ARR 1.6% over 3.7 years; low-quality evidence). There were more participant withdrawals due to adverse effects in the lower target arm (RR 8.16, 95% CI 2.06 to 32.28; very low-quality evidence). Blood pressures were lower in the lower' target group by 9.5/4.9 mmHg. More drugs were needed in the lower target group but blood pressure targets were achieved more frequently in the standard target group.

AUTHORS' CONCLUSIONS:

No evidence of a difference in total mortality and serious adverse events was found between treating to a lower or to a standard blood pressure target in people with hypertension and cardiovascular disease. This suggests no net health benefit from a lower systolic blood pressure target despite the small absolute reduction in total cardiovascular serious adverse events. There was very limited evidence on adverse events, which lead to high uncertainty. At present there is insufficient evidence to justify lower blood pressure targets (≤ 135/85 mmHg) in people with hypertension and established cardiovascular disease. More trials are needed to answer this question.

Omega-3 Fatty Acids and Cardiovascular Disease: Current State of the Evidence

Author/s: 
Balk, Ethan M., Adam, Gaelen P., Langberg, Valerie, Halladay, Christopher, Chung, Mei, Lin, Lin, Robertson, Sarah, Yip, Agustin, Steele, Dale, Smith, Bryant T., Lau, Joseph, Lichtenstein, Alice H., Trikalinos, Thomas A.

Focus of This Summary

This is a summary of a systematic review that evaluated the recent evidence regarding the effects of omega-3 fatty acids (FAs), primarily from marine oil supplements, on clinical and selected intermediate cardiovascular (CV) outcomes (i.e., blood pressure, lipid concentrations) and the association of omega-3 FA dietary intake and biomarkers with CV outcomes. The systematic review included 147 articles published between 2000 and June 2015. Studies that analyzed levels of fish (or other food) consumption without exact quantification of omega-3 FA intake were excluded from this review. This summary is provided to assist in informed clinical decisionmaking. However, reviews of evidence should not be construed to represent clinical recommendations or guidelines.

Background

The first observation of a link between fish consumption and cardiovascular (CV) health was made in the late 1970s in a Greenland Eskimo population. This population exhibited a comparatively low rate of CV mortality and consumed a greater than average amount of fish. Since this original observation, there have been hundreds of studies conducted to evaluate the effect of omega-3 fatty acids (FAs) on cardiovascular disease (CVD), its risk factors, and its biomarkers.

The omega-3 FAs include eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and alpha-linolenic acid (ALA). These are essential long-chain and very-long-chain polyunsaturated fatty acids that have many physiological effects, including inflammation regulation. EPA, DHA, and DPA are found in fish and other seafood (called dietary marine oils), as well as in supplements prepared from these foods (referred to here as marine oil supplements). ALA is found in walnuts, leafy green vegetables, and oils such as canola, soy, and flaxseed.

An original systematic review of omega-3 FAs was prepared by the Agency for Healthcare and Research Quality in 2004.1,2 Based on the observational studies available at that time, several expert panels suggested that regular consumption of fish and seafood is associated with lower risk of coronary heart disease (CHD) and cardiac death. The recommendations were based on assumptions of benefits from EPA and DHA and their content in fish and seafood.

The current systematic review aimed to update the evidence in light of the more recent literature published on the topic and included both randomized controlled trials (RCTs) and observational studies. Studies that analyzed levels of fish (or other food) consumption without exact quantification of omega-3 FA intake were excluded.

Conclusions

Observational studies suggest possible benefits of dietary intake of marine oils (such as through consumption of fish) for CV death and total stroke (mainly ischemic stroke).

In contrast, there is high strength of evidence (SOE) from RCTs that marine oil supplements do not affect the risk of major adverse cardiac events (MACE), all-cause death, sudden cardiac death, revascularization, or high blood pressure (BP). Marine oil supplements also have no effect on the risk of atrial fibrillation (moderate SOE). Importantly, RCTs focused primarily on marine oil supplements, not on food sources.

Marine oil supplements affect several intermediate outcomes. First, they significantly lower triglycerides (TGs)—possibly having greater effects in higher doses and in people with higher baseline TGs. Second, they cause small increases in both high-density lipoprotein cholesterol (HDL-c) and low-density lipoprotein cholesterol (LDL-c). Finally, marine oil supplements produce small changes in the ratio of total cholesterol to HDL-c (high SOE).

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