Ahmet Tas, Yaren Alan, Ilke Kara Tas, Omer E. Aydin, Zeynep Atay, Sule Yilmaz, Alp Ozcan, Tim P. van de Hoef, Sabahattin Umman, Jan J. Piek MD, Murat Sezer
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Univariable and multivariable models evaluated the relationships between the dU/dt amplitudes, epicardial disease as well as CMD, defined by a blunted coronary flow reserve (CFR) adjusted for the concomitant epicardial disease severity (fractional flow reserve, FFR) yielding the microvascular resistance reserve (MRR). Functional CMD was defined by a blunted MRR (≤ 3.0) but normal hyperemic microvascular resistance (hMR < 2.5) whereas structural CMD was defined by a blunted MRR (≤ 3.0) combined with increased hMR (≥ 2.5). Six major acceleration or deceleration peaks were identified in each cardiac cycle; these were a (amplitude of peak diastolic acceleration), b (amplitude of early diastolic deceleration nadir), c (amplitude of peak diastolic re-acceleration), j (amplitude of end-diastolic deceleration nadir), x (amplitude of peak systolic acceleration), and z (amplitude of end-systolic deceleration nadir) waves.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Functional CMD was associated with amplification of a (<i>β</i> = 55.944, 95% CI [21.112, 90.777], <i>p</i> = 0.002) and × (<i>β</i> = 44.069, 95% CI [20.182, 67.955], <i>p</i> < 0.001), b (<i>β</i> = −34.019, 95% CI [−50.865, −17.173], <i>p</i> < 0.001), j (<i>β</i> = −48.723, 95% CI [−71.272, −26.174], <i>p</i> < 0.001), and z (<i>β</i> = −31.047, 95% CI [−53.596, −8.498], <i>p</i> = 0.007) waves. Structural CMD was associated with blunted a (<i>β</i> = −76.938, 95% CI [−113.125, −40.751], <i>p</i> < 0.001) and j (<i>β</i> = 24.787, 95% CI [1.361, 48.213], <i>p</i> = 0.039).</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Epicardial disease severity is minimally associated with alterations in the resting dU/dt pattern, whereas CMD endotypes are associated with distinctively altered intrabeat pulsatility characteristics. Stronger acceleration magnitudes at rest do not indicate a healthier microcirculation or absence of CMD.</p>\n </section>\n \n <section>\n \n <h3> Trial Registration</h3>\n \n <p>ClinicalTrials.gov (NCT02328820)</p>\n </section>\n </div>","PeriodicalId":18459,"journal":{"name":"Microcirculation","volume":"32 6","pages":""},"PeriodicalIF":2.0000,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/micc.70021","citationCount":"0","resultStr":"{\"title\":\"Coronary Microvascular Dysfunction Alters the Pulsatile Behavior of the Resting Coronary Blood Flow\",\"authors\":\"Ahmet Tas, Yaren Alan, Ilke Kara Tas, Omer E. Aydin, Zeynep Atay, Sule Yilmaz, Alp Ozcan, Tim P. van de Hoef, Sabahattin Umman, Jan J. 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Functional CMD was defined by a blunted MRR (≤ 3.0) but normal hyperemic microvascular resistance (hMR < 2.5) whereas structural CMD was defined by a blunted MRR (≤ 3.0) combined with increased hMR (≥ 2.5). Six major acceleration or deceleration peaks were identified in each cardiac cycle; these were a (amplitude of peak diastolic acceleration), b (amplitude of early diastolic deceleration nadir), c (amplitude of peak diastolic re-acceleration), j (amplitude of end-diastolic deceleration nadir), x (amplitude of peak systolic acceleration), and z (amplitude of end-systolic deceleration nadir) waves.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>Functional CMD was associated with amplification of a (<i>β</i> = 55.944, 95% CI [21.112, 90.777], <i>p</i> = 0.002) and × (<i>β</i> = 44.069, 95% CI [20.182, 67.955], <i>p</i> < 0.001), b (<i>β</i> = −34.019, 95% CI [−50.865, −17.173], <i>p</i> < 0.001), j (<i>β</i> = −48.723, 95% CI [−71.272, −26.174], <i>p</i> < 0.001), and z (<i>β</i> = −31.047, 95% CI [−53.596, −8.498], <i>p</i> = 0.007) waves. 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引用次数: 0
摘要
静息脉状血流速度加速/减速特征（dU/dt）与心外膜病变和冠状动脉微血管功能障碍（CMD）的关系尚不完全清楚。方法利用冠状动脉内多普勒速度信号的一阶导数提取冠状动脉dU/dt模式。单变量和多变量模型评估dU/dt振幅、心外膜疾病和CMD之间的关系，由钝化的冠状动脉血流储备（CFR）定义，该CFR根据伴随的心外膜疾病严重程度（分数血流储备，FFR）调整，产生微血管阻力储备（MRR）。功能性CMD由钝化的MRR（≤3.0）和正常的充血微血管阻力（hMR < 2.5）定义，而结构性CMD由钝化的MRR（≤3.0）和增加的hMR（≥2.5）定义。每个心动周期有6个主要的加速或减速峰；这些波分别是a（舒张加速峰值振幅）、b（舒张早期减速最低点振幅）、c（舒张再加速峰值振幅）、j（舒张末期减速最低点振幅）、x（收缩加速峰值振幅）和z（收缩末期减速最低点振幅）。结果功能性CMD与a波（β = 55.944, 95% CI [21.112, 90.777], p = 0.002）、x波（β = 44.069, 95% CI [20.182, 67.955], p < 0.001）、b波（β = - 34.019, 95% CI [- 50.865, - 17.173], p < 0.001）、j波（β = - 48.723, 95% CI [- 71.272, - 26.174], p < 0.001）、z波（β = - 31.047, 95% CI [- 53.596, - 8.498], p = 0.007）扩增相关。结构性CMD与钝化a （β = - 76.938, 95% CI [- 113.125, - 40.751], p < 0.001）和j （β = 24.787, 95% CI [1.361, 48.213], p = 0.039）相关。结论：心外膜疾病的严重程度与静息dU/dt模式的改变相关性很小，而CMD内分型与明显改变的心内搏动特征相关。静止时更强的加速度并不表明微循环更健康或没有CMD。临床试验注册网站（NCT02328820）
Coronary Microvascular Dysfunction Alters the Pulsatile Behavior of the Resting Coronary Blood Flow
Background
Variations in resting pulsatile coronary flow velocity acceleration/deceleration characteristics (dU/dt) with respect to epicardial lesions and coronary microvascular dysfunction (CMD) remain incompletely understood.
Method
The coronary dU/dt pattern was extracted from the first derivative of the intracoronary Doppler velocity signal. Univariable and multivariable models evaluated the relationships between the dU/dt amplitudes, epicardial disease as well as CMD, defined by a blunted coronary flow reserve (CFR) adjusted for the concomitant epicardial disease severity (fractional flow reserve, FFR) yielding the microvascular resistance reserve (MRR). Functional CMD was defined by a blunted MRR (≤ 3.0) but normal hyperemic microvascular resistance (hMR < 2.5) whereas structural CMD was defined by a blunted MRR (≤ 3.0) combined with increased hMR (≥ 2.5). Six major acceleration or deceleration peaks were identified in each cardiac cycle; these were a (amplitude of peak diastolic acceleration), b (amplitude of early diastolic deceleration nadir), c (amplitude of peak diastolic re-acceleration), j (amplitude of end-diastolic deceleration nadir), x (amplitude of peak systolic acceleration), and z (amplitude of end-systolic deceleration nadir) waves.
Results
Functional CMD was associated with amplification of a (β = 55.944, 95% CI [21.112, 90.777], p = 0.002) and × (β = 44.069, 95% CI [20.182, 67.955], p < 0.001), b (β = −34.019, 95% CI [−50.865, −17.173], p < 0.001), j (β = −48.723, 95% CI [−71.272, −26.174], p < 0.001), and z (β = −31.047, 95% CI [−53.596, −8.498], p = 0.007) waves. Structural CMD was associated with blunted a (β = −76.938, 95% CI [−113.125, −40.751], p < 0.001) and j (β = 24.787, 95% CI [1.361, 48.213], p = 0.039).
Conclusion
Epicardial disease severity is minimally associated with alterations in the resting dU/dt pattern, whereas CMD endotypes are associated with distinctively altered intrabeat pulsatility characteristics. Stronger acceleration magnitudes at rest do not indicate a healthier microcirculation or absence of CMD.
期刊介绍：
The journal features original contributions that are the result of investigations contributing significant new information relating to the vascular and lymphatic microcirculation addressed at the intact animal, organ, cellular, or molecular level. Papers describe applications of the methods of physiology, biophysics, bioengineering, genetics, cell biology, biochemistry, and molecular biology to problems in microcirculation.
Microcirculation also publishes state-of-the-art reviews that address frontier areas or new advances in technology in the fields of microcirculatory disease and function. Specific areas of interest include: Angiogenesis, growth and remodeling; Transport and exchange of gasses and solutes; Rheology and biorheology; Endothelial cell biology and metabolism; Interactions between endothelium, smooth muscle, parenchymal cells, leukocytes and platelets; Regulation of vasomotor tone; and Microvascular structures, imaging and morphometry. Papers also describe innovations in experimental techniques and instrumentation for studying all aspects of microcirculatory structure and function.
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