Frontiers in Cardiovascular Medicine
Admission platelet-to-hemoglobin ratio and 1-year outcomes after percutaneous coronary intervention: a multicenter registry cohort study
By Jeong Tae Byoun, Donghyeon Joo, Sungho Jo and 2 others.
Abstract
Background The platelet-to-hemoglobin ratio (PHR) is a proposed prognostic marker in cardiovascular disease, but it has not been evaluated against a broad major adverse cardiovascular events (MACE) endpoint in a dedicated percutaneous coronary intervention (PCI) cohort, and whether it adequately summarizes its two components remains untested. Methods We analyzed 1,551 patients pooled from two prospective Korean drug-eluting stent registries (2016–2022). The PHR was calculated as platelet count (×10⁹/L) divided by hemoglobin (g/L). The primary endpoint was 1-year MACE, with follow-up censored at 365 days, a composite of all-cause death, myocardial infarction, stroke, repeat revascularization, or heart failure hospitalization. Multivariable Cox models included eight prespecified clinical covariates; the functional form was examined with restricted cubic splines, and the PHR was decomposed using nested models and a log-scale ratio-constraint test. Results MACE occurred in 107 patients (6.9%) within 1 year. A higher PHR was independently associated with MACE (adjusted hazard ratio [HR] per 1-standard deviation, 1.21; 95% confidence interval [CI], 1.05–1.40; P = 0.008), with no evidence of nonlinearity ( P = 0.700). Adding the PHR improved the clinical model (likelihood-ratio P = 0.013); the ratio constraint was not rejected ( P = 0.765), and a single log-PHR term retained 98.7% of the two-component likelihood-ratio χ 2 increment over the clinical model in this cohort (bootstrap 95% CI, 21.8%–100%). The PHR was associated with all-cause and cardiovascular death (both HR, 1.28), paralleling hemoglobin. Repeat revascularization was associated with platelet count (HR, 1.39; P = 0.014), but not significantly with PHR (HR, 1.24; P = 0.081). Risk was concentrated in patients with both anemia and a platelet count at or above the median (adjusted HR, 1.82; 95% CI, 1.05–3.15). The gain in discrimination was negligible ( Δ AUC, +0.003; 95% CI, −0.003 to +0.012), and net benefit was virtually unchanged. Conclusions The admission PHR was independently associated with 1-year MACE after PCI, with no evidence of nonlinearity, and its log-scale component effects were compatible with the ratio constraint in this cohort. Given the negligible gain in discrimination and net benefit, the PHR is an independent prognostic marker rather than a tool for risk reclassification. Registry registration: Clinical Research Information Service KCT0003392 and KCT0005008.






