Comment on “Time Trends in Cardiovascular Event Incidence in New-Onset Type 2 Diabetes: A Population-Based Cohort Study From Germany”

IF 3 2区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Saraswati Sah, Rachana Mehta, Ranjana Sah
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This coding limitation may partially explain the paradoxically unchanged incidence of myocardial infarction (MI) despite improvements in CHD.</p><p>Second, the use of chronic obstructive pulmonary disease (COPD) as a proxy for smoking status introduces exposure misclassification. Smoking is a potent modifiable risk factor for both MI and ischemic stroke (IS) [<span>5</span>], and its secular decline in Germany over this period likely contributed to cardiovascular risk reduction. Without direct smoking data, the differential attribution of risk to diabetes-specific interventions versus population-wide trends remains unresolved.</p><p>Third, the apparent stability in MI and IS incidence may also be an artifact of cohort composition rather than a true epidemiological plateau. Although the authors matched for age and sex, no stratification by socioeconomic status, regional healthcare access, or medication use—particularly statins and antihypertensives—was undertaken. 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引用次数: 0

Abstract

We read with great interest the study by Sarabhai et al., which provides valuable insights into the temporal evolution of cardiovascular events in newly diagnosed type 2 diabetes (T2D) patients in Germany over a 17-year period [1]. Although the reduction in the 5-year incidence of coronary heart disease (CHD) and transient ischemic attack (TIA) is encouraging, we believe several methodological and conceptual limitations deserve further discussion to contextualize the findings.

First, the study's exclusion of laboratory parameters such as glycated hemoglobin (HbA1c), lipid panels, and renal function significantly constrains the capacity to adjust for the quality of glycemic and metabolic control—central determinants of cardiovascular outcomes in T2D [2, 3]. Reliance solely on ICD-10 codes, though validated for primary diagnoses, does not differentiate between stable and unstable angina, nor does it account for silent myocardial infarctions, which are prevalent in diabetic populations [4]. This coding limitation may partially explain the paradoxically unchanged incidence of myocardial infarction (MI) despite improvements in CHD.

Second, the use of chronic obstructive pulmonary disease (COPD) as a proxy for smoking status introduces exposure misclassification. Smoking is a potent modifiable risk factor for both MI and ischemic stroke (IS) [5], and its secular decline in Germany over this period likely contributed to cardiovascular risk reduction. Without direct smoking data, the differential attribution of risk to diabetes-specific interventions versus population-wide trends remains unresolved.

Third, the apparent stability in MI and IS incidence may also be an artifact of cohort composition rather than a true epidemiological plateau. Although the authors matched for age and sex, no stratification by socioeconomic status, regional healthcare access, or medication use—particularly statins and antihypertensives—was undertaken. These variables influence the uptake and effectiveness of cardioprotective interventions [6]. Furthermore, the analysis does not disaggregate event timing within the five-year follow-up, thereby overlooking early versus late event clustering, which may offer clues about legacy effects from undiagnosed prediabetes.

Fourth, the demographic distribution masks evolving baseline risk. Although mean age and sex proportions remained unchanged, the increased prevalence of hypertension and obesity in the later cohort signals rising baseline cardiovascular risk. Paradoxically, these upward shifts might dilute the observable impact of improved care. Consequently, the unchanged IS and MI rates may reflect counterbalancing effects between therapeutic progress and population-level risk escalation.

Finally, the study's conclusion that CHD and TIA reduction reflects successful diabetes management may overstate causality. CHD includes chronic, often asymptomatic pathology amenable to long-term outpatient management and diagnostic advances [7]. In contrast, MI and IS typically reflect acute, irreversible endpoints of vascular injury accumulated over years—possibly even before overt T2D diagnosis [8]. This raises the possibility that prediabetic vascular damage, left unaddressed in this study, may be the principal driver of outcome stagnation.

In conclusion, while the study captures important temporal shifts, a more granular, biomarker-informed, and longitudinally stratified analysis is essential to disentangle the contributions of diabetes-specific interventions from broader epidemiological transitions.

Saraswati Sah: conceptualization, methodology, validation, writing – original draft, writing – review and editing. Rachana Mehta: writing – original draft, writing – review and editing. Ranjana Sah: supervision, project administration, writing – original draft, writing – review and editing.

The authors have nothing to report.

The authors have nothing to report.

The authors declare no conflicts of interest.

《新发2型糖尿病心血管事件发生率的时间趋势:一项来自德国的基于人群的队列研究》
我们非常感兴趣地阅读了Sarabhai等人的研究,该研究为德国新诊断的2型糖尿病(T2D)患者心血管事件的时间演变提供了宝贵的见解,为期17年[10]。尽管5年冠心病(CHD)和短暂性脑缺血发作(TIA)发病率的降低令人鼓舞,但我们认为,一些方法学和概念上的局限性值得进一步讨论,以便将研究结果与背景联系起来。首先,该研究排除了实验室参数,如糖化血红蛋白(HbA1c)、脂质面板和肾功能,这明显限制了对血糖和代谢控制质量的调整能力,而血糖和代谢控制是糖尿病心血管结局的核心决定因素[2,3]。仅依赖ICD-10编码,虽然在初级诊断中得到了验证,但不能区分稳定型和不稳定型心绞痛,也不能解释在糖尿病人群中普遍存在的无症状心肌梗死[10]。这种编码限制可能部分解释了尽管冠心病有所改善,但心肌梗死(MI)发生率却矛盾地没有变化。其次,使用慢性阻塞性肺疾病(COPD)作为吸烟状况的代表会导致暴露错误分类。吸烟是心肌梗死和缺血性卒中(is)的一个有效的可改变的危险因素,在这一时期,吸烟在德国的长期下降可能有助于心血管风险的降低。在没有直接吸烟数据的情况下,糖尿病特定干预措施的风险归因与人群整体趋势的差异仍未得到解决。第三,心肌梗死和IS发病率的明显稳定性也可能是队列组成的人为因素,而不是真正的流行病学平台期。虽然作者的年龄和性别相匹配,但没有按社会经济地位、地区医疗保健获取或药物使用(特别是他汀类药物和抗高血压药物)进行分层。这些变量影响心脏保护干预措施的吸收和有效性。此外,该分析没有分解5年随访期间的事件时间,从而忽略了早期和晚期事件聚类,这可能为未确诊的前驱糖尿病的遗留影响提供线索。第四,人口分布掩盖了不断变化的基线风险。虽然平均年龄和性别比例保持不变,但后期队列中高血压和肥胖患病率的增加表明基线心血管风险上升。矛盾的是,这些向上的转变可能会淡化改善护理的可观察到的影响。因此,不变的IS和MI率可能反映了治疗进展和人群水平风险升级之间的平衡效应。最后,该研究的结论是冠心病和TIA的减少反映了成功的糖尿病管理,这可能夸大了因果关系。冠心病包括慢性的,通常是无症状的病理,需要长期的门诊治疗和诊断的进步。相比之下,心肌梗死和IS通常反映了急性的、不可逆的血管损伤终末累积,甚至可能在明显的T2D诊断之前。这提出了一种可能性,即本研究未解决的糖尿病前期血管损伤可能是结果停滞的主要驱动因素。总之,虽然该研究捕捉到了重要的时间变化,但对于从更广泛的流行病学转变中解开糖尿病特异性干预的贡献,更细粒度、生物标志物信息和纵向分层分析是必不可少的。Saraswati Sah:概念化,方法论,验证,写作-原稿,写作-审查和编辑。Rachana Mehta:写作-原稿,写作-审查和编辑。Ranjana Sah:监督,项目管理,写作-原稿,写作-审查和编辑。作者没有什么可报告的。作者没有什么可报告的。作者声明无利益冲突。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Diabetes
Journal of Diabetes ENDOCRINOLOGY & METABOLISM-
CiteScore
6.50
自引率
2.20%
发文量
94
审稿时长
>12 weeks
期刊介绍: Journal of Diabetes (JDB) devotes itself to diabetes research, therapeutics, and education. It aims to involve researchers and practitioners in a dialogue between East and West via all aspects of epidemiology, etiology, pathogenesis, management, complications and prevention of diabetes, including the molecular, biochemical, and physiological aspects of diabetes. The Editorial team is international with a unique mix of Asian and Western participation. The Editors welcome submissions in form of original research articles, images, novel case reports and correspondence, and will solicit reviews, point-counterpoint, commentaries, editorials, news highlights, and educational content.
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