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高微血管阻力对冠状动脉波能量学的影响取决于冠状动脉微血管功能。

The impact of high microvascular resistance on coronary wave energetics depends on coronary microvascular functionality.

作者信息

Tas Ahmet, Alan Yaren, Kara Tas Ilke, Umman Sabahattin, Parker Kim H, van de Hoef Tim P, Sezer Murat, Piek Jan J

机构信息

Department of Cardiology, Amsterdam UMC, Heart Centre, Amsterdam Cardiovascular Sciences, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.

Department of Emergency Medicine, Gomec State Hospital, Ayanoglu Str. No:14, 10715 Gomec, Balikesir, Turkey.

出版信息

Eur Heart J Open. 2025 May 5;5(3):oeaf050. doi: 10.1093/ehjopen/oeaf050. eCollection 2025 May.

DOI:10.1093/ehjopen/oeaf050
PMID:40417173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12100483/
Abstract

AIMS

The pathophysiological relevance of high hyperemic microvascular resistance (hMR) in stable coronary artery disease is controversial. Using wave intensity analysis (WIA, defined as the product of the time derivatives of the coronary pressure and velocity), we aim to compare the impact of high hMR on coronary wave energetics with respect to coronary microvascular dysfunction (CMD), defined as reduced coronary flow reserve (CFR < 2.5), in unobstructed arteries.

METHODS AND RESULTS

The study population ( = 258, mean age = 68 ± 10 years, 73% male) had a high cardiovascular risk profile including dyslipidemia (88%), hypertension (70%), smoking (55%) and diabetes (28%). The mean fractional flow reserve was 0.89 ± 0.05. Vessels ( = 312) were divided into four endotypes: no CMD-low hMR (CFR ≥ 2.5, hMR < 2.5 mmHg.s.cm), Functional CMD (CFR < 2.5, hMR < 2.5 mmHg.s.cm), Structural CMD (CFR < 2.5, hMR ≥ 2.5 mmHg.s.cm), and no CMD-high hMR (CFR ≥ 2.5, hMR ≥ 2.5 mmHg.s.cm). The no CMD-high hMR endotype had the lowest mean resting velocity (bAPV = 10 ± 3 cm.s   < 0.001), highest mean basal microvascular resistance (bMR = 9 ± 2 mmHg/cm.s   < 0.001) amongst all endotypes, yet, it had reference-level CFR, microvascular resistance reserve and resistive reserve ratio ( > 0.05 for all compared to no CMD-low hMR), unlike CMD endotypes ( < 0.05 compared to CMD endotypes). The no CMD-high hMR endotype exhibited the highest hyperemic increase in the accelerating wave energy proportion (AEP) (13% ± 13%, = 0.042), indicating an intact autoregulatory response. Only in the CMD endotypes, high hMR was associated with reduced AEP ( = -0.229, < 0.001), unlike no CMD endotypes ( = 0.383).

CONCLUSION

High hMR alone is not a definitive CMD marker. In line with the adaptive high hMR hypothesis, increased hMR does not necessarily limit augmentation of AEP, and is associated with robust autoregulatory capacity in vessels with preserved CFR. Cardiologists should be alert to a potential adaptive no CMD-high hMR endotype to avoid misdiagnosis.

REGISTRATION

NCT02328820.

摘要

目的

在稳定型冠状动脉疾病中,高充血微血管阻力(hMR)的病理生理相关性存在争议。我们旨在使用波强度分析(WIA,定义为冠状动脉压力和速度的时间导数的乘积),比较高hMR对冠状动脉波能量学的影响,该影响与冠状动脉微血管功能障碍(CMD)相关,CMD定义为冠状动脉血流储备降低(CFR<2.5),且血管未阻塞。

方法和结果

研究人群(n = 258,平均年龄 = 68±10岁,73%为男性)具有较高的心血管风险特征,包括血脂异常(88%)、高血压(70%)、吸烟(55%)和糖尿病(28%)。平均血流储备分数为0.89±0.05。血管(n = 312)被分为四种内型:无CMD-低hMR(CFR≥2.5,hMR<2.5mmHg·s/cm)、功能性CMD(CFR<2.5,hMR<2.5mmHg·s/cm)、结构性CMD(CFR<2.5,hMR≥2.5mmHg·s/cm)和无CMD-高hMR(CFR≥2.5,hMR≥2.5mmHg·s/cm)。在所有内型中,无CMD-高hMR内型的平均静息速度最低(基础平均峰值速度[bAPV]=10±3cm/s,P<0.001),基础平均微血管阻力最高(基础平均阻力[bMR]=9±2mmHg/cm/s,P<0.001),然而,与CMD内型不同(与无CMD-低hMR相比P<0.05),它具有参考水平的CFR、微血管阻力储备和阻力储备比(与无CMD-低hMR相比所有P>0.05)。无CMD-高hMR内型在加速波能量比例(AEP)方面表现出最高的充血性增加(13%±13%,P = 0.042),表明存在完整的自动调节反应。仅在CMD内型中,高hMR与AEP降低相关(P=-0.229,P<0.001),与无CMD内型不同(P = 0.383)。

结论

单独的高hMR不是明确的CMD标志物。与适应性高hMR假说一致,hMR增加不一定会限制AEP的增加,并且与CFR保留的血管中强大的自动调节能力相关。心脏病专家应警惕潜在的适应性无CMD-高hMR内型,以避免误诊。

注册信息

NCT02328820

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/4c843937703d/oeaf050f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/25e0a0691eb7/oeaf050f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/e1ce5580d9aa/oeaf050f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/32ac9e8c38b0/oeaf050f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/4c843937703d/oeaf050f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/25e0a0691eb7/oeaf050f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/e1ce5580d9aa/oeaf050f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/32ac9e8c38b0/oeaf050f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4bcf/12100483/4c843937703d/oeaf050f4.jpg

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