Thoracic endografting increases cardiac afterload and leads to left ventricular hypertrophy in dogs

Yoshiyuki Yamashita, Yasuhisa Oishi, Yuma Motomatsu, Kazuto Hirayama, Takeaki Harada, Tomoki Ushijima, satoshi fujita, Satoshi Kimura, Hiromichi Sonoda, Hideki Tatewaki, Yoshihisa Tanoue, Genya Sunagawa, Takuya Nishikawa, Keita Saku, Akira Shiose

研究成果: ジャーナルへの寄稿記事

抄録

OBJECTIVES Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 μm vs 13.9 ± 1.5 μm, P = 0.02, respectively). CONCLUSIONS The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.

元の言語英語
ページ(範囲)618-625
ページ数8
ジャーナルEuropean Journal of Cardio-thoracic Surgery
55
発行部数4
DOI
出版物ステータス出版済み - 4 1 2019

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Left Ventricular Hypertrophy
Electric Impedance
Thorax
Dogs
Cardiac Myocytes
Compliance
Euthanasia
Ventricular Pressure
Thoracic Aorta
Cell Size
Heart Ventricles
Stents
Canidae
Arterial Pressure
Catheters
Body Weight
Transplants
Pressure
Weights and Measures

All Science Journal Classification (ASJC) codes

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

これを引用

Thoracic endografting increases cardiac afterload and leads to left ventricular hypertrophy in dogs. / Yamashita, Yoshiyuki; Oishi, Yasuhisa; Motomatsu, Yuma; Hirayama, Kazuto; Harada, Takeaki; Ushijima, Tomoki; fujita, satoshi; Kimura, Satoshi; Sonoda, Hiromichi; Tatewaki, Hideki; Tanoue, Yoshihisa; Sunagawa, Genya; Nishikawa, Takuya; Saku, Keita; Shiose, Akira.

:: European Journal of Cardio-thoracic Surgery, 巻 55, 番号 4, 01.04.2019, p. 618-625.

研究成果: ジャーナルへの寄稿記事

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abstract = "OBJECTIVES Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 μm vs 13.9 ± 1.5 μm, P = 0.02, respectively). CONCLUSIONS The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.",
author = "Yoshiyuki Yamashita and Yasuhisa Oishi and Yuma Motomatsu and Kazuto Hirayama and Takeaki Harada and Tomoki Ushijima and satoshi fujita and Satoshi Kimura and Hiromichi Sonoda and Hideki Tatewaki and Yoshihisa Tanoue and Genya Sunagawa and Takuya Nishikawa and Keita Saku and Akira Shiose",
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T1 - Thoracic endografting increases cardiac afterload and leads to left ventricular hypertrophy in dogs

AU - Yamashita, Yoshiyuki

AU - Oishi, Yasuhisa

AU - Motomatsu, Yuma

AU - Hirayama, Kazuto

AU - Harada, Takeaki

AU - Ushijima, Tomoki

AU - fujita, satoshi

AU - Kimura, Satoshi

AU - Sonoda, Hiromichi

AU - Tatewaki, Hideki

AU - Tanoue, Yoshihisa

AU - Sunagawa, Genya

AU - Nishikawa, Takuya

AU - Saku, Keita

AU - Shiose, Akira

PY - 2019/4/1

Y1 - 2019/4/1

N2 - OBJECTIVES Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 μm vs 13.9 ± 1.5 μm, P = 0.02, respectively). CONCLUSIONS The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.

AB - OBJECTIVES Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 μm vs 13.9 ± 1.5 μm, P = 0.02, respectively). CONCLUSIONS The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.

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DO - 10.1093/ejcts/ezy402

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SP - 618

EP - 625

JO - European Journal of Cardio-thoracic Surgery

JF - European Journal of Cardio-thoracic Surgery

SN - 1010-7940

IS - 4

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