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Tomasz J Guzik

Publications and source records attributed to Tomasz J Guzik.

2 recordsLinked to original sources

Global inequalities in cardiometabolic care and achievable cardiovascular risk reduction by wealth, region, and sex: a pooled analysis of individual participant data from 76 countries.

BACKGROUND: Wealth-related inequalities affect cardiometabolic health worldwide, but their implications for cardiometabolic care and potentially preventable cardiovascular disease remain poorly understood. We aimed to quantify wealth-related inequalities in the care cascade for hypertension, diabetes, and hypercholesterolaemia by wealth quintile, region, and sex. METHODS: In this cross-sectional, individual-level analysis, we analysed harmonised, nationally representative health examination surveys conducted in five WHO regions. Adults aged 18 years or older with data on age, sex, wealth, and at least one cardiometabolic outcome were eligible. All variables in the surveys were obtained from standardised in-person examinations. We evaluated hypertension, diabetes, and hypercholesterolaemia and applied a care cascade of disease awareness, treatment, and control for each condition uniformly across all surveys. Disease status was defined from measured biomarkers, self-reported diagnosis, or current medication; awareness and treatment were based on self-reported information, and control on measured biomarkers. Each indicator was expressed as the proportion of all individuals with the corresponding condition. Socioeconomic position was assessed using household wealth indices derived within each survey, and participants were ranked within each country and categorised into country-specific quintiles (quintile 1 to quintile 5), with quintile 1 including those with the least household wealth. Inequality was quantified by the quintile 5 minus quintile 1 difference, the slope index of inequality (SII), and relative index of inequality (RII). Predicted 10-year cardiovascular risk was estimated with the Globorisk equations, and trial-derived relative risk reductions were applied to estimate achievable absolute risk reduction. The ASANDE consortium is registered with ClinicalTrials.gov (NCT07427355). FINDINGS: We analysed data from 109 surveys conducted in 76 countries between 2002 and 2024. 315 403 (65·9%) of 478 947 survey participants with available data were included in this analysis (median age 40 years [IQR 30-52], 185 209 [58·7%] women, and 130 194 [41·3%] men). Inequalities widened progressively across the care cascade in all regions and were most pronounced for disease control. Pooled across regions, the SII for control was 4·4% (95% CI 2·4-6·4) for hypertension (RII 1·1, 1·1-1·2), 4·8% (0·6-9·0) for diabetes (RII 1·1, 1·0-1·2), and 6·5% (3·8-9·2) for hypercholesterolaemia (RII 1·1, 1·0-1·1). However, regional patterns varied substantially. In the region of the Americas, disease control consistently favoured wealthier individuals (SII 9·2% for hypertension, 4·8-13·5; RII 1·2, 1·1-1·3). In the African region, coverage was uniformly low, and the largest absolute inequality favoured individuals with the least wealth, particularly for hypercholesterolaemia treatment (SII -37·6%, -49·7 to -25·5; RII 0·6, 0·5 to 0·7). Baseline cardiovascular risk was higher in individuals with the least wealth than among the wealthiest (13·6% vs 12·2%), but achievable absolute risk reduction was correlated with baseline risk rather than with treatment coverage: achievable reduction was greatest in the European Region (3·9%) and lowest in the Africa region (2·5%). Across all regions, achievable absolute risk reduction was greater in men than in women (4·6% vs 3·5% in the European region). INTERPRETATION: The populations with the largest treatment gaps are not necessarily those that could achieve the greatest absolute reduction in cardiovascular risk through treating individuals who are currently untreated. In settings where coverage is uniformly low, expanding the supply of care matters more than redistributing access to it. Moreover, because socioeconomic inequalities widen after diagnosis, screening alone is unlikely to reduce disparities unless accompanied by sustained access to treatment. Policy should prioritise overall population health over maximise equity within the population. FUNDING: None.

Journal Article

Urate-lowering effects of losartan: a meta-analysis of randomised controlled trials and target trial emulation.

Common in hypertensive patients, hyperuricaemia is often exacerbated by guideline-recommended antihypertensive therapies such as thiazide diuretics. Losartan is known as an angiotensin II receptor type 1 antagonist with a uricosuric effect, but the magnitude of its efficacy in lowering urate has not been quantified versus a placebo-reference. We sought to quantify the urate-lowering effect of losartan versus placebo using two complementary approaches. We first conducted a meta-analysis of randomised controlled trials (RCTs) to quantify the effect of losartan on serum urate levels versus placebo. We then applied a target trial emulation framework in the UK Biobank as a secondary source of data and a replication experiment. The meta-analysis of six prospective randomised controlled trials (RCTs), including 1119 losartan-treated patients and 1093 controls, demonstrated that losartan reduced serum urate levels by approximately 0.29 mg/dL relative to placebo (95% CI: -0.46 to -0.12, p = 0.0009). In the target trial emulation, 23 losartan-treated individuals showed a reduction in serum urate of approximately 0.35 mg/dL (95% CI: -0.66 to -0.03, p = 0.03) when compared with 92 matched controls, and after accounting for 12 potential confounders including established urate-lowering therapies. Our results provide evidence for a modest yet consistent urate-lowering potential of losartan. This modest biochemical effect (~0.3 mg/dL) may be an attractive option to mitigate the diuretic-induced urate elevation. Thus, losartan can be considered as a favourable antihypertensive choice for patients managed with diuretics or those who are at risk of hyperuricaemia/gout.

Losartan