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Nature Reviews. Cardiology Aug 2023The past two to three decades have seen a steady increase in the prevalence of hypertension in China, largely owing to increased life expectancy and lifestyle changes... (Review)
Review
The past two to three decades have seen a steady increase in the prevalence of hypertension in China, largely owing to increased life expectancy and lifestyle changes (particularly among individuals aged 35-44 years). Data from the China hypertension survey conducted in 2012-2015 revealed a high prevalence of grade 3 hypertension (systolic blood pressure ≥180 mmHg and diastolic blood pressure ≥110 mmHg) in the general population, which increased with age to up to 5% among individuals aged ≥65 years. The risk profile of patients with hypertension in China has also been a subject of intense study in the past 30 years. Dietary sodium and potassium intake have remained largely the same in China in the past three decades, and salt substitution strategies seem to be effective in reducing blood pressure levels and the risk of cardiovascular events and death. However, the number of individuals with risk factors for hypertension and cardiovascular disease in general, such as physical inactivity and obesity, has increased dramatically in the same period. Moreover, even in patients diagnosed with hypertension, their disease is often poorly managed owing to a lack of patient education and poor treatment compliance. In this Review, we summarize the latest epidemiological data on hypertension in China, discuss the risk factors for hypertension that are specific to this population, and describe several ongoing nationwide hypertension control initiatives that target these risk factors, especially in the low-resource rural setting.
Topics: Humans; Hypertension; Blood Pressure; Cardiovascular Diseases; Risk Factors; Sodium Chloride, Dietary; Prevalence
PubMed: 36631532
DOI: 10.1038/s41569-022-00829-z -
European Heart Journal Aug 2023To examine the decongestive effect of the sodium-glucose cotransporter 2 inhibitor dapagliflozin compared to the thiazide-like diuretic metolazone in patients... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND AND AIMS
To examine the decongestive effect of the sodium-glucose cotransporter 2 inhibitor dapagliflozin compared to the thiazide-like diuretic metolazone in patients hospitalized for heart failure and resistant to treatment with intravenous furosemide.
METHODS AND RESULTS
A multi-centre, open-label, randomized, and active-comparator trial. Patients were randomized to dapagliflozin 10 mg once daily or metolazone 5-10 mg once daily for a 3-day treatment period, with follow-up for primary and secondary endpoints until day 5 (96 h). The primary endpoint was a diuretic effect, assessed by change in weight (kg). Secondary endpoints included a change in pulmonary congestion (lung ultrasound), loop diuretic efficiency (weight change per 40 mg of furosemide), and a volume assessment score. 61 patients were randomized. The mean (±standard deviation) cumulative dose of furosemide at 96 h was 977 (±492) mg in the dapagliflozin group and 704 (±428) mg in patients assigned to metolazone. The mean (±standard deviation) decrease in weight at 96 h was 3.0 (2.5) kg with dapagliflozin compared to 3.6 (2.0) kg with metolazone [mean difference 0.65, 95% confidence interval (CI) -0.12,1.41 kg; P = 0.11]. Loop diuretic efficiency was less with dapagliflozin than with metolazone [mean 0.15 (0.12) vs. 0.25 (0.19); difference -0.08, 95% CI -0.17,0.01 kg; P = 0.10]. Changes in pulmonary congestion and volume assessment score were similar between treatments. Decreases in plasma sodium and potassium and increases in urea and creatinine were smaller with dapagliflozin than with metolazone. Serious adverse events were similar between treatments.
CONCLUSION
In patients with heart failure and loop diuretic resistance, dapagliflozin was not more effective at relieving congestion than metolazone. Patients assigned to dapagliflozin received a larger cumulative dose of furosemide but experienced less biochemical upset than those assigned to metolazone.
TRIAL REGISTRATION
ClinicalTrials.gov Identifier: NCT04860011.
Topics: Humans; Metolazone; Sodium Potassium Chloride Symporter Inhibitors; Furosemide; Heart Failure; Diuretics; Sodium
PubMed: 37210742
DOI: 10.1093/eurheartj/ehad341 -
Clinical Research in Cardiology :... Aug 2023We sought to compare cardiovascular outcomes, renal function, and diuresis in patients receiving standard diuretic therapy for acute heart failure (AHF) with or without... (Comparative Study)
Comparative Study Meta-Analysis
BACKGROUND
We sought to compare cardiovascular outcomes, renal function, and diuresis in patients receiving standard diuretic therapy for acute heart failure (AHF) with or without the addition of SGLT2i.
METHODS AND RESULTS
Systematic search of three electronic databases identified nine eligible randomized controlled trials involving 2,824 patients. The addition of SGLT2i to conventional therapy for AHF reduced all-cause death (odds ratio [OR] 0.75; 95% CI 0.56-0.99; p = 0.049), readmissions for heart failure (HF) (OR 0.54; 95% CI 0.44-0.66; p < 0.001), and the composite of cardiovascular death and readmissions for HF (hazard ratio 0.71; 95% CI 0.60-0.84; p < 0.001). Furthermore, SGLT2i increased mean daily urinary output in liters (mean difference [MD] 0.45; 95% CI 0.03-0.87; p = 0.035) and decreased mean daily doses of loop diuretics in mg of furosemide equivalent (MD -34.90; 95% CI [- 52.58, - 17.21]; p < 0.001) without increasing the incidence worsening renal function (OR 0.75; 95% CI 0.43-1.29; p = 0.290).
CONCLUSION
SGLT2i addition to conventional diuretic therapy reduced all-cause death, readmissions for HF, and the composite of cardiovascular death or readmissions for HF. Moreover, SGLT2i was associated with a higher volume of diuresis with a lower dose of loop diuretics.
Topics: Humans; Diabetes Mellitus, Type 2; Diuretics; Heart Failure; Kidney; Randomized Controlled Trials as Topic; Sodium Potassium Chloride Symporter Inhibitors; Sodium-Glucose Transporter 2 Inhibitors
PubMed: 36592186
DOI: 10.1007/s00392-022-02148-2