Effect of nicorandil administration on cardiac burden and cardio-ankle vascular index after coronary intervention

Myocardial injury is a problem associated with percutaneous coronary intervention (PCI). This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecu...

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Veröffentlicht in:Heart and vessels 2020-12, Vol.35 (12), p.1664-1671
Hauptverfasser: Sato, Shuji, Takahashi, Mao, Mikamo, Hiroshi, Kawazoe, Masayo, Iizuka, Takuo, Shimizu, Kazuhiro, Noro, Mahito, Shirai, Kohji
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container_end_page 1671
container_issue 12
container_start_page 1664
container_title Heart and vessels
container_volume 35
creator Sato, Shuji
Takahashi, Mao
Mikamo, Hiroshi
Kawazoe, Masayo
Iizuka, Takuo
Shimizu, Kazuhiro
Noro, Mahito
Shirai, Kohji
description Myocardial injury is a problem associated with percutaneous coronary intervention (PCI). This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecutive patients, the first 20 patients received only saline infusion after PCI (control group); the other 38 patients received a continuous intravenous infusion of nicorandil and saline after PCI (nicorandil group). Troponin I and brain natriuretic peptide (BNP) levels were measured. Vascular parameters, such as blood pressure (BP), cardiac output, cardio-ankle vascular index (CAVI), and estimated systemic vascular resistance (eSVR), were measured. Troponin I of both groups increased 12 h after PCI. Changes in BNP levels between immediately after PCI and 12 h after PCI were significantly higher in the control than in the nicorandil group (10.8 ± 44.2 vs. − 2.6 ± 14.6 pg/ml, p  = 0.04). In the nicorandil group, BP, eSVR, and CAVI decreased significantly at 12 h after PCI compared with those immediately after PCI ( p  
doi_str_mv 10.1007/s00380-020-01650-9
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This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecutive patients, the first 20 patients received only saline infusion after PCI (control group); the other 38 patients received a continuous intravenous infusion of nicorandil and saline after PCI (nicorandil group). Troponin I and brain natriuretic peptide (BNP) levels were measured. Vascular parameters, such as blood pressure (BP), cardiac output, cardio-ankle vascular index (CAVI), and estimated systemic vascular resistance (eSVR), were measured. Troponin I of both groups increased 12 h after PCI. Changes in BNP levels between immediately after PCI and 12 h after PCI were significantly higher in the control than in the nicorandil group (10.8 ± 44.2 vs. − 2.6 ± 14.6 pg/ml, p  = 0.04). In the nicorandil group, BP, eSVR, and CAVI decreased significantly at 12 h after PCI compared with those immediately after PCI ( p  &lt; 0.0001), whereas no change was observed in the control group. In a single linear analysis, the change in BP ( r  = 0.36, p  &lt; 0.01) and nicorandil administration ( r  = − 0.47, p  &lt; 0.001) was significantly correlated with the change in CAVI, multiple regression analysis revealed that the changes in CO and eSVR were significant contributing factors for the changes in CAVI. PCI could result in myocardial injury and/or cardiac burden in patients with stable angina. 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This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecutive patients, the first 20 patients received only saline infusion after PCI (control group); the other 38 patients received a continuous intravenous infusion of nicorandil and saline after PCI (nicorandil group). Troponin I and brain natriuretic peptide (BNP) levels were measured. Vascular parameters, such as blood pressure (BP), cardiac output, cardio-ankle vascular index (CAVI), and estimated systemic vascular resistance (eSVR), were measured. Troponin I of both groups increased 12 h after PCI. Changes in BNP levels between immediately after PCI and 12 h after PCI were significantly higher in the control than in the nicorandil group (10.8 ± 44.2 vs. − 2.6 ± 14.6 pg/ml, p  = 0.04). 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This study aimed to clarify the role of nicorandil administration in preventing myocardial injury. This study included patients with stable angina who underwent PCI from November 2013 to June 2016. Of 58 consecutive patients, the first 20 patients received only saline infusion after PCI (control group); the other 38 patients received a continuous intravenous infusion of nicorandil and saline after PCI (nicorandil group). Troponin I and brain natriuretic peptide (BNP) levels were measured. Vascular parameters, such as blood pressure (BP), cardiac output, cardio-ankle vascular index (CAVI), and estimated systemic vascular resistance (eSVR), were measured. Troponin I of both groups increased 12 h after PCI. Changes in BNP levels between immediately after PCI and 12 h after PCI were significantly higher in the control than in the nicorandil group (10.8 ± 44.2 vs. − 2.6 ± 14.6 pg/ml, p  = 0.04). In the nicorandil group, BP, eSVR, and CAVI decreased significantly at 12 h after PCI compared with those immediately after PCI ( p  &lt; 0.0001), whereas no change was observed in the control group. In a single linear analysis, the change in BP ( r  = 0.36, p  &lt; 0.01) and nicorandil administration ( r  = − 0.47, p  &lt; 0.001) was significantly correlated with the change in CAVI, multiple regression analysis revealed that the changes in CO and eSVR were significant contributing factors for the changes in CAVI. PCI could result in myocardial injury and/or cardiac burden in patients with stable angina. Nicorandil administration after PCI may be effective in relieving the burden by decreasing arterial stiffness (CAVI).</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>32572567</pmid><doi>10.1007/s00380-020-01650-9</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6386-8670</orcidid><oa>free_for_read</oa></addata></record>
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subjects Aged
Angina
Angina pectoris
Angina, Stable - diagnostic imaging
Angina, Stable - physiopathology
Angina, Stable - therapy
Ankle
Biomedical Engineering and Bioengineering
Blood pressure
Brain natriuretic peptide
Calcium-binding protein
Cardiac output
Cardiac Surgery
Cardiology
Coronary Artery Disease - diagnostic imaging
Coronary Artery Disease - physiopathology
Coronary Artery Disease - therapy
Female
Heart
Heart Diseases - diagnostic imaging
Heart Diseases - etiology
Heart Diseases - physiopathology
Heart Diseases - prevention & control
Hemodynamics - drug effects
Humans
Infusions, Intravenous
Injury prevention
Intravenous administration
Intravenous infusion
Linear analysis
Male
Medicine
Medicine & Public Health
Middle Aged
Multiple regression analysis
Nicorandil - administration & dosage
Nicorandil - adverse effects
Original
Original Article
Percutaneous Coronary Intervention - adverse effects
Stiffness
Time Factors
Treatment Outcome
Troponin
Troponin I
Vascular Stiffness - drug effects
Vascular Surgery
Vasodilator Agents - administration & dosage
Vasodilator Agents - adverse effects
title Effect of nicorandil administration on cardiac burden and cardio-ankle vascular index after coronary intervention
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