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Background <p>Supporting data of exercise stress echocardiography (ESE) in patients with chronic aortic regurgitation (AR) was limited, and no reports have focused on the mechanisms of the impaired left ventricular contractile reserve (LVCR) in AR.</p> Methods <p>We retrospectively registered 44 consecutive asymptomatic or equivocally symptomatic patients undergoing ESE with more than moderate to severe chronic AR and a left ventricular ejection fraction (LVEF) of ≥ 50%. LVCR(+) is defined by ΔLVEF (peak workload − baseline) of ≥ 5%, and LVCR(−) by ΔLVEF of &lt; 5%. In the vector flow mapping analysis, energy loss (EL) and wall shear stress (WSS) were evaluated during exercise.</p> Results <p>Among the 44 patients, 32 were LVCR(−) and 12 were LVCR(+). At baseline, no differences were revealed in intraventricular EL and WSS between the two groups. During exercise, however, EL was higher in patients with LVCR(−) than LVCR(+) [16.2 (11.7–22.5) vs. 11.2 (9.3–15.6) mW/m, <i>p</i> = 0.015 at low workload; 17.8 (15.4–22.3) vs. 13.3 (9.6–18.0) mW/m, <i>p</i> = 0.027 at peak workload]. EL at low workload could predict patients with LVCR(−) (OR: 1.18, 95%CI: 1.02–1.37, <i>p</i> = 0.025). No differences in WSS were shown between the two groups during exercise.</p> Conclusions <p>In patients with chronic AR and LVCR(−), EL during exercise increased, and evaluation of EL at low workload was useful for predicting impaired LVCR.</p>

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Relationship between left ventricular contractile reserve and vector flow mapping analysis in chronic aortic regurgitation

  • 期刊论文

  • 发表日期：

    2026年3月7日

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  • Masashi Amano,
  • Yuki Kubota,
  • Kenji Moriuchi,
  • Hitomi Nishimura,
  • Yurie Tamai,
  • Ayaka Mizumoto,
  • Yoshiki Yanagi,
  • Yoshito Jo,
  • Shinichi Kurashima,
  • Yuki Irie,
  • Takahiro Sakamoto,
  • Atsushi Okada,
  • Makoto Amaki,
  • Hideaki Kanzaki,
  • Takeshi Kitai,
  • Satoshi Nakatani,
  • Chisato Izumi

摘要

Background

Supporting data of exercise stress echocardiography (ESE) in patients with chronic aortic regurgitation (AR) was limited, and no reports have focused on the mechanisms of the impaired left ventricular contractile reserve (LVCR) in AR.

Methods

We retrospectively registered 44 consecutive asymptomatic or equivocally symptomatic patients undergoing ESE with more than moderate to severe chronic AR and a left ventricular ejection fraction (LVEF) of ≥ 50%. LVCR(+) is defined by ΔLVEF (peak workload − baseline) of ≥ 5%, and LVCR(−) by ΔLVEF of < 5%. In the vector flow mapping analysis, energy loss (EL) and wall shear stress (WSS) were evaluated during exercise.

Results

Among the 44 patients, 32 were LVCR(−) and 12 were LVCR(+). At baseline, no differences were revealed in intraventricular EL and WSS between the two groups. During exercise, however, EL was higher in patients with LVCR(−) than LVCR(+) [16.2 (11.7–22.5) vs. 11.2 (9.3–15.6) mW/m, p = 0.015 at low workload; 17.8 (15.4–22.3) vs. 13.3 (9.6–18.0) mW/m, p = 0.027 at peak workload]. EL at low workload could predict patients with LVCR(−) (OR: 1.18, 95%CI: 1.02–1.37, p = 0.025). No differences in WSS were shown between the two groups during exercise.

Conclusions

In patients with chronic AR and LVCR(−), EL during exercise increased, and evaluation of EL at low workload was useful for predicting impaired LVCR.