Echocardiographic and biomarker characteristics in diabetes, coronary artery disease or both: insights from HOMAGE trial.

IF 8.5 1区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Cardiovascular Diabetology Pub Date : 2025-03-08 DOI:10.1186/s12933-025-02609-8

Luca Monzo, Masatake Kobayashi, João Pedro Ferreira, Zohra Lamiral, Christian Delles, Andrew L Clark, Frank Edelmann, Arantxa González, Stephane Heymans, Pierpaolo Pellicori, Johannes Petutschnigg, Job A J Verdonschot, Patrick Rossignol, John G F Cleland, Faiez Zannad, Nicolas Girerd

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引用次数: 0

Abstract

Background: Coronary artery disease (CAD) and diabetes mellitus (DM) can induce changes in myocardial structure and function, thereby increasing the risk of heart failure (HF). We aimed to identify the alterations in echocardiographic variables and circulating biomarkers associated with DM, CAD, or both and to assess the effect of spironolactone on them.

Methods: The "Heart OMics in AGEing" (HOMAGE) trial evaluated the effect of spironolactone on circulating markers of fibrosis over 9 months of follow-up in people at risk for HF. From the initial population (N = 527) of the HOMAGE trial, a total of 495 participants (mean age 74 years, 25% women) were categorized according to clinical phenotype (DM-/CAD + vs. DM+/CAD- vs. DM+/CAD+), while the DM-/CAD- group was excluded due to the low sample size (N = 32). Multivariable linear regression analysis was used to assess the relations between variables and DM/CAD status.

Results: At baseline, participants with DM, whether or not they had CAD, showed lower markers of type I collagen synthesis (procollagen type I C-terminal propeptide; β [95% CI]: DM+/CAD-: -6.973 [-13.778; -0.167]; DM+/CAD+: -9.039 [-15.174; -2.903]), reduced left ventricular volumes (β [95% CI]: end-diastolic, DM+/CAD-: -6.323 [-9.696; -2.951]; DM+/CAD+: -2.503 [-5.531; 0.526]; end-systolic, DM+/CAD-: -2.905 [-4.817; -0.992]; DM+/CAD+: -1.400 [-3.120; 0.320]) and higher levels of galectin-3 (Exponential β [95% CI]: DM+/CAD-: 1.127 [1.050; 1.209]; DM+/CAD+: 1.118 [1.048; 1.192]), and growth differentiation factor-15 (Exponential β [95% CI]: DM+/CAD-: 1.542 [1.360; 1.747]; DM+/CAD+: 1.535 [1.370; 1.720]), along with an elevated E/e' ratio (β [95% CI]: DM+/CAD-: 1.355 [0.462; 2.248]; DM+/CAD+: 0.879 [0.067; 1.690]), compared with DM-/CAD + individuals (all p < 0.05). At follow-up, the effect of spironolactone on echocardiographic variables and circulating biomarkers was not significantly different across DM/CAD phenotypes (all p-interaction > 0.05), except for a more pronounced reduction in GDF-15 in the DM+/CAD + group at the 1-month visit (p-interaction = 0.03).

Conclusions: Among HOMAGE trial participants, diabetes was a powerful driver of biomarker and echocardiographic alterations irrespectively of CAD. These alterations were mainly related to the domains of inflammation and diastolic function.

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背景：冠状动脉疾病（CAD）和糖尿病（DM）会引起心肌结构和功能的改变，从而增加心力衰竭（HF）的风险。我们旨在确定与 DM、CAD 或两者相关的超声心动图变量和循环生物标志物的变化，并评估螺内酯对它们的影响：HOMAGE "试验评估了螺内酯在9个月随访期间对高危人群循环纤维化标志物的影响。在HOMAGE试验的初始人群（N = 527）中，共有495名参与者（平均年龄74岁，25%为女性）根据临床表型进行了分类（DM-/CAD + vs. DM+/CAD- vs. DM+/CAD+），DM-/CAD-组由于样本量较少（N = 32）而被排除在外。多变量线性回归分析用于评估变量与DM/CAD状态之间的关系：结果：在基线时，无论是否患有 CAD，患有 DM 的参与者的 I 型胶原蛋白合成指标（I 型胶原蛋白 C 端肽原；β [95% CI]：DM+/CAD-：-6.973[-13.778；-0.167]；DM+/CAD+：-9.039[-15.174；-2.903]），左心室容积减少（β [95%CI]：舒张末期，DM+/CAD-：-6.323 [-9.039]）：舒张末期，DM+/CAD-：-6.323 [-9.696; -2.951]；DM+/CAD+：-2.503 [-5.531; 0.526]；收缩末期，DM+/CAD-：-2.905 [-4.531; 0.526]：-2.905[-4.817；-0.992]；DM+/CAD+：-1.400[-3.120；0.320]）和更高水平的 galectin-3（指数β[95% CI]：DM+/CAD-：1.127 [1.050; 1.209]; DM+/CAD+: 1.118 [1.048; 1.192]）和生长分化因子-15（指数β [95% CI]：DM+/CAD-：1.542[1.360；1.747]；DM+/CAD+：1.535[1.370；1.720]），E/e'比值升高（β [95% CI]：DM+/CAD-：1.355 [0.462；2.248]；DM+/CAD+：0.879 [0.067；1.690]），与DM+/CAD+组相比（均为P 0.05），除了DM+/CAD+组的GDF-15在1个月访视时有更明显的下降（P-交互作用=0.03）：结论：在HOMAGE试验参与者中，糖尿病是导致生物标志物和超声心动图改变的重要因素，与CAD无关。这些改变主要与炎症和舒张功能相关。

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来源期刊

Cardiovascular Diabetology 医学-内分泌学与代谢

CiteScore

12.30

自引率

15.10%

发文量

240

审稿时长

1 months

期刊介绍： Cardiovascular Diabetology is a journal that welcomes manuscripts exploring various aspects of the relationship between diabetes, cardiovascular health, and the metabolic syndrome. We invite submissions related to clinical studies, genetic investigations, experimental research, pharmacological studies, epidemiological analyses, and molecular biology research in this field.