经皮冠状动脉介入治疗（PCI）后冠心病单核细胞与高密度脂蛋白比值和血红蛋白与红细胞分布宽度比值的比较

摘要(中文译文)

冠状动脉疾病（CAD）是全球发病和死亡的主要原因，尤其是在印度等发展中国家。尽管经皮冠状动脉介入治疗（PCI）改善了冠心病（CHD）的管理，但PCI术后的结局仍受炎症和血液学参数的影响。包括血红蛋白与红细胞分布宽度比值（HRR）及单核细胞与高密度脂蛋白比值（MHR）在内的新型指标，已成为炎症、氧化应激和心血管结局的潜在标志物。本研究旨在评估接受PCI的CHD患者中HRR和MHR的短期预后关联。主要目标是评估其与PCI术后6个月临床结局的关系，次要目标包括评估死亡率、轻微症状、复合不良结局以及探索性受试者工作特征（ROC）曲线衍生的截断值。本前瞻性队列研究纳入138例在Era's Lucknow医学院及医院接受PCI的CHD患者。采用自动化技术分析血液学和血脂参数，并计算HRR和MHR。患者随访6个月以评估PCI术后结局，包括轻微症状和死亡率。统计分析采用独立样本t检验、方差分析、卡方检验和ROC曲线分析。由于队列规模有限且死亡事件数量较少，基于ROC的死亡率分析被视为探索性分析，未进行多变量回归模型分析。患者平均年龄为56.64 ± 10.05岁。138例患者中，男性103例（74.6%），女性35例（25.4%）。HRR异常（≤1.0）见于82/138例患者（59.4%），MHR异常（≥0.14）见于21/138例患者（15.2%）。PCI术后，117/138例患者（84.8%）保持无症状，17/138例（12.3%）出现轻微症状，4/138例（2.9%）在随访期间死亡。男性患者HRR值显著高于女性，而MHR无显著性别差异。MHR升高与PCI术后不良结局显著相关（p < 0.001）。ROC分析显示对死亡率具有探索性判别能力，HRR的AUC为0.838，MHR的AUC为0.863。这些AUC值系基于少量死亡事件在内部得出，因此应谨慎解读。HRR和MHR在PCI术后CHD患者中均表现出短期未校正的预后关联，其中MHR对不良结局的探索性判别性能在数值上更高。需要更大规模、更长随访的研究来验证这些发现。在HRR和MHR可被视为独立预测因子或临床可推广的阈值之前，尚需外部验证和具有足够把握度的多变量分析。鉴于队列规模小、死亡事件数少、随访时间短且缺乏多变量校正，这些发现应被解读为初步的和产生假设的证据，而非用于临床风险分层的确定性证据。

Abstract

Coronary artery disease (CAD) is a major cause of morbidity and mortality worldwide, particularly in developing countries such as India. Although percutaneous coronary intervention (PCI) has improved the management of coronary heart disease (CHD), post-PCI outcomes continue to be influenced by inflammatory and hematological parameters. Novel indices, including the hemoglobin-to-red cell distribution width ratio (HRR) and the monocyte-to-high-density lipoprotein ratio (MHR), have emerged as potential markers of inflammation, oxidative stress, and cardiovascular outcomes. This study aimed to evaluate the short-term prognostic association of HRR and MHR in patients with CHD undergoing PCI. The primary objective was to assess their relationship with six-month post-PCI clinical outcomes, while secondary objectives included evaluation of mortality, mild symptoms, composite poor outcome, and exploratory receiver operating characteristic (ROC)-derived cutoff values. This prospective cohort study included 138 patients with CHD who underwent PCI at Era's Lucknow Medical College and Hospital. Hematological and lipid parameters were analyzed using automated techniques, and HRR and MHR were calculated. Patients were followed for six months to assess post-PCI outcomes, including mild symptoms and mortality. Statistical analyses were performed using the independent-samples t-test, analysis of variance, chi-square test, and ROC curve analysis. Because of the limited cohort size and low number of mortality events, ROC-based mortality analysis was considered exploratory, and no multivariable regression model was performed. The mean age of the patients was 56.64 ± 10.05 years. Of the 138 patients, 103 (74.6%) were male and 35 (25.4%) were female patients. HRR abnormality (≤1.0) was observed in 82/138 patients (59.4%), while MHR abnormality (≥0.14) was observed in 21/138 patients (15.2%). After PCI, 117/138 patients (84.8%) remained asymptomatic, 17/138 (12.3%) developed mild symptoms, and 4/138 (2.9%) died during follow-up. HRR values were significantly higher in male than female patients, whereas MHR did not differ significantly by sex. Elevated MHR was significantly associated with adverse post-PCI outcomes (p < 0.001). ROC analysis showed exploratory discriminative ability for mortality, with AUCs of 0.838 for HRR and 0.863 for MHR. These AUC values were derived internally from a small number of mortality events and should therefore be interpreted with caution. Both HRR and MHR demonstrated short-term unadjusted prognostic associations in post-PCI CHD patients, with MHR showing numerically higher exploratory discriminatory performance for adverse outcomes. Larger studies with longer follow-up are needed to validate these findings. External validation and adequately powered multivariable analyses are required before HRR and MHR can be considered independent predictors or clinically generalizable thresholds. Given the small cohort, low mortality-event count, short follow-up, and absence of multivariable adjustment, these findings should be interpreted as preliminary and hypothesis-generating rather than definitive evidence for clinical risk stratification.

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