blood pressure

Objectives The Salt Substitute and Stroke Study (SSaSS) recently reported blood pressure-mediated benefits of a potassium-enriched salt substitute on cardiovascular outcomes and death. This study assessed the effects of salt substitutes on a breadth of outcomes to quantify the consistency of the findings and understand the likely generalisability of the SSaSS results.

Methods We searched PubMed, Embase and the Cochrane Library up to 31 August 2021. Parallel group, step-wedge or cluster randomised controlled trials reporting the effect of salt substitute on blood pressure or clinical outcomes were included. Meta-analyses and metaregressions were used to define the consistency of findings across trials, geographies and patient groups.

Results There were 21 trials and 31 949 participants included, with 19 reporting effects on blood pressure and 5 reporting effects on clinical outcomes. Overall reduction of systolic blood pressure (SBP) was −4.61 mm Hg (95% CI −6.07 to −3.14) and of diastolic blood pressure (DBP) was −1.61 mm Hg (95% CI −2.42 to −0.79). Reductions in blood pressure appeared to be consistent across geographical regions and population subgroups defined by age, sex, history of hypertension, body mass index, baseline blood pressure, baseline 24-hour urinary sodium and baseline 24-hour urinary potassium (all p homogeneity >0.05). Metaregression showed that each 10% lower proportion of sodium choloride in the salt substitute was associated with a −1.53 mm Hg (95% CI −3.02 to −0.03, p=0.045) greater reduction in SBP and a −0.95 mm Hg (95% CI −1.78 to −0.12, p=0.025) greater reduction in DBP. There were clear protective effects of salt substitute on total mortality (risk ratio (RR) 0.89, 95% CI 0.85 to 0.94), cardiovascular mortality (RR 0.87, 95% CI 0. 81 to 0.94) and cardiovascular events (RR 0.89, 95% CI 0.85 to 0.94).

Conclusions The beneficial effects of salt substitutes on blood pressure across geographies and populations were consistent. Blood pressure-mediated protective effects on clinical outcomes are likely to be generalisable across population subgroups and to countries worldwide.

Heart failure is a clinically complex syndrome that results due to the failure of the ventricles to function as pump and oxygenate end organs. The repercussions of inadequate perfusion are seen in the form of sympathetic overactivation and third spacing, leading to clinical signs of increased blood pressure, dyspnea, fatigue, palpitations, etc. This article provided a brief overview of the clinical syndrome of heart failure; its epidemiology, risk factors, symptoms, and staging; and the mechanisms involved in disease progression. This article also described several landmark trials in heart failure that tested the efficacy of first-line drugs such as beta-blockers, angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and the latest drugs in the field of heart failure: angiotensin receptor neprilysin inhibitors. Most studies described in this article were guideline-setting trials that revolutionized the practice of medicine and cardiology.

Importance: Stroke is the fifth leading cause of death and a leading cause of disability in the United States, affecting nearly 800 000 individuals annually.

Observations: Sudden neurologic dysfunction caused by focal brain ischemia with imaging evidence of acute infarction defines acute ischemic stroke (AIS), while an ischemic episode with neurologic deficits but without acute infarction defines transient ischemic attack (TIA). An estimated 7.5% to 17.4% of patients with TIA will have a stroke in the next 3 months. Patients presenting with nondisabling AIS or high-risk TIA (defined as a score ≥4 on the age, blood pressure, clinical symptoms, duration, diabetes [ABCD2] instrument; range, 0-7 [7 indicating worst stroke risk]), who do not have severe carotid stenosis or atrial fibrillation, should receive dual antiplatelet therapy with aspirin and clopidigrel within 24 hours of presentation. Subsequently, combined aspirin and clopidigrel for 3 weeks followed by single antiplatelet therapy reduces stroke risk from 7.8% to 5.2% (hazard ratio, 0.66 [95% CI, 0.56-0.77]). Patients with symptomatic carotid stenosis should receive carotid revascularization and single antiplatelet therapy, and those with atrial fibrillation should receive anticoagulation. In patients presenting with AIS and disabling deficits interfering with activities of daily living, intravenous alteplase improves the likelihood of minimal or no disability by 39% with intravenous recombinant tissue plasminogen activator (IV rtPA) vs 26% with placebo (odds ratio [OR], 1.6 [95% CI, 1.1-2.6]) when administered within 3 hours of presentation and by 35.3% with IV rtPA vs 30.1% with placebo (OR, 1.3 [95% CI, 1.1-1.5]) when administered within 3 to 4.5 hours of presentation. Patients with disabling AIS due to anterior circulation large-vessel occlusions are more likely to be functionally independent when treated with mechanical thrombectomy within 6 hours of presentation vs medical therapy alone (46.0% vs 26.5%; OR, 2.49 [95% CI, 1.76-3.53]) or when treated within 6 to 24 hours after symptom onset if they have a large ratio of ischemic to infarcted tissue on brain magnetic resonance diffusion or computed tomography perfusion imaging (modified Rankin Scale score 0-2: 53% vs 18%; OR, 4.92 [95% CI, 2.87-8.44]).

Conclusions and relevance: Dual antiplatelet therapy initiated within 24 hours of symptom onset and continued for 3 weeks reduces stroke risk in select patients with high-risk TIA and minor stroke. For select patients with disabling AIS, thrombolysis within 4.5 hours and mechanical thrombectomy within 24 hours after symptom onset improves functional outcomes.

BACKGROUND:

The long-term cardiovascular risk of isolated elevated office blood pressure (BP) is unclear.

PURPOSE:

To summarize the risk for cardiovascular events and all-cause mortality associated with untreated white coat hypertension (WCH) and treated white coat effect (WCE).

DATA SOURCES:

PubMed and EMBASE, without language restriction, from inception to December 2018.

STUDY SELECTION:

Observational studies with at least 3 years of follow-up evaluating the cardiovascular risk of WCH or WCE compared with normotension.

DATA EXTRACTION:

2 investigators independently extracted study data and assessed study quality.

DATA SYNTHESIS:

27 studies were included, comprising 25 786 participants with untreated WCH or treated WCE and 38 487 with normal BP followed for a mean of 3 to 19 years. Compared with normotension, untreated WCH was associated with an increased risk for cardiovascular events (hazard ratio [HR], 1.36 [95% CI, 1.03 to 2.00]), all-cause mortality (HR, 1.33 [CI, 1.07 to 1.67]), and cardiovascularmortality (HR, 2.09 [CI, 1.23 to 4.48]); the risk of WCH was attenuated in studies that included stroke in the definition of cardiovascular events(HR, 1.26 [CI, 1.00 to 1.54]). No significant association was found between treated WCE and cardiovascular events (HR, 1.12 [CI, 0.91 to 1.39]), all-cause mortality (HR, 1.11 [CI, 0.89 to 1.46]), or cardiovascular mortality (HR, 1.04 [CI, 0.65 to 1.66]). The findings persisted across several sensitivity analyses.

LIMITATION:

Paucity of studies evaluating isolated cardiac outcomes or reporting participant race/ethnicity.

CONCLUSION:

Untreated WCH, but not treated WCE, is associated with an increased risk for cardiovascular events and all-cause mortality. Out-of-office BP monitoring is critical in the diagnosis and management of hypertension.

PRIMARY FUNDING SOURCE:

National Institutes of Health.