P754Iron status indices (transferrin saturation, serum ferritin) in the course of acute myocarditis: relations with neurohormonal activation, cardiac dysfunction and clinical recovery
Abstract Introduction Acute myocarditis (MCD) can progress to post-myocarditis cardiomyopathy. Immune response is the major pathophysiological trigger leading to MCD. Optimal iron status is essential for the functioning of immune cells, cardiomyocytes and cardiofibroblasts. Therefore, there are prem...
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| creator | Franczuk, P Kosiorek, A Tkaczyszyn, M Drozd, M Zapolska, A Walczak, T Kulej-Lyko, K Sidorowicz, N Soltowska, A Banasiak, W Kosmala, W Przewlocka-Kosmala, M Jaroch, J Ponikowski, P Jankowska, E A |
| description | Abstract
Introduction
Acute myocarditis (MCD) can progress to post-myocarditis cardiomyopathy. Immune response is the major pathophysiological trigger leading to MCD. Optimal iron status is essential for the functioning of immune cells, cardiomyocytes and cardiofibroblasts. Therefore, there are premises to consider iron metabolism as a significant modulator of complex pathophysiology of MCD.
Purpose
We aimed to assess iron status in the course of MCD and relate it with clinical and laboratory measures.
Methods
We prospectively enrolled consecutive patients hospitalized for acute MCD in 2 tertiary referral cardiology centers during 2015–2018 and followed them up for 30 weeks. MCD was diagnosed based on the following criteria: 1) new onset symptoms suggestive of myocarditis (effort intolerance, dyspnea, palpitations or chest pain), 2) elevated high sensitivity cardiac troponin I (hs-cTnI), 3) exclusion of obstructive coronary artery disease.
Results
Study group comprised 41 patients with confirmed MCD [age: 31 (26–34) years, men: 95%] and 15 healthy age- and gender-matched subjects [age: 30 (28–33) years, men: 87%]. All patients survived hospitalization and follow-up, no subject needed ventricular assist device.
Patients with MCD had lower LVEF (56±10% vs. 69±14%) and higher CRP [32 (14–8754) vs. 3 (3–3) mg/l], NT-proBNP [452 (240–877) vs. 33 (18–46) pg/ml], hs-cTnI [7.3 (3.3–12.8) vs. 0,01 (0.01–0.01) μg/l] than the control group (all p |
| doi_str_mv | 10.1093/eurheartj/ehz747.0356 |
| format | Article |
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Introduction
Acute myocarditis (MCD) can progress to post-myocarditis cardiomyopathy. Immune response is the major pathophysiological trigger leading to MCD. Optimal iron status is essential for the functioning of immune cells, cardiomyocytes and cardiofibroblasts. Therefore, there are premises to consider iron metabolism as a significant modulator of complex pathophysiology of MCD.
Purpose
We aimed to assess iron status in the course of MCD and relate it with clinical and laboratory measures.
Methods
We prospectively enrolled consecutive patients hospitalized for acute MCD in 2 tertiary referral cardiology centers during 2015–2018 and followed them up for 30 weeks. MCD was diagnosed based on the following criteria: 1) new onset symptoms suggestive of myocarditis (effort intolerance, dyspnea, palpitations or chest pain), 2) elevated high sensitivity cardiac troponin I (hs-cTnI), 3) exclusion of obstructive coronary artery disease.
Results
Study group comprised 41 patients with confirmed MCD [age: 31 (26–34) years, men: 95%] and 15 healthy age- and gender-matched subjects [age: 30 (28–33) years, men: 87%]. All patients survived hospitalization and follow-up, no subject needed ventricular assist device.
Patients with MCD had lower LVEF (56±10% vs. 69±14%) and higher CRP [32 (14–8754) vs. 3 (3–3) mg/l], NT-proBNP [452 (240–877) vs. 33 (18–46) pg/ml], hs-cTnI [7.3 (3.3–12.8) vs. 0,01 (0.01–0.01) μg/l] than the control group (all p<0.001). Regarding iron status, MCD group presented higher serum ferritin [213 (121–386) vs. 135 (84–210) μg/l] and lower transferrin saturation (TSAT) [21±10 vs. 28±15%] (all p<0.05). In patients with MCD ferritin correlated with CRP (r=0.46, p<0.01), TSAT correlated neither with CRP nor with ferritin (all p>0.02).
Patients with MCD and NT-proBNP >1000 pg/ml had lower TSAT (16±8 vs. 23±9%; p<0.05) and LVEF (47±13 vs. 59±7%; p<0.001) than the remaining subjects. No difference in ferritin was observed (p>0.2). 46% of patients during acute phase of MCD had LVEF≤55% – these patients presented lower TSAT (17±8% vs. 24±10%) and higher NT-proBNP – [577 (436–1657) vs. 358 (167–499) pg/ml] (all p<0.05). After 30 weeks only in 13% patients LVEF≤55% persisted and related to lower baseline TSAT (9±1% vs. 21±9%) and higher CRP (147±113 vs. 52±40 mg/l) (all p<0.05). LVEF≤55% was not related to ferritin (both p>0.2).
After 6 weeks of follow-up patients with MCD already presented higher LVEF (61±8%; p<0.05) and haemoglobin [14.7 (14.0–15.7) g/dl], lower CRP [3 (3–3) mg/l], NT-proBNP [34 (25–67) pg/ml], hs-cTnI [0.01 (0.01–0.01)], ferritin [124 (78–168) μg/l] and higher TSAT (26±7%) (all p<0.01). There was no further change in these parameters within the next 24 weeks (all p>0.2).
Conclusions
Iron status is deranged in acute MCD. Serum ferritin is an indicator of inflammatory response, whereas TSAT relates to neurohormonal activation and cardiac dysfunction. Iron status normalizes within 6 weeks after acute phase of MCD.
Acknowledgement/Funding
This research was financially supported by the National Science Centre (Poland) grant number 2014/13/B/NZ5/03146.]]></description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehz747.0356</identifier><language>eng</language><publisher>Oxford University Press</publisher><ispartof>European heart journal, 2019-10, Vol.40 (Supplement_1)</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com. 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1396-7de67470ea42d05f8161d565a807d9bee83a7f1a7ee93f02e031a04ffcd1ac423</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27903,27904</link.rule.ids></links><search><creatorcontrib>Franczuk, P</creatorcontrib><creatorcontrib>Kosiorek, A</creatorcontrib><creatorcontrib>Tkaczyszyn, M</creatorcontrib><creatorcontrib>Drozd, M</creatorcontrib><creatorcontrib>Zapolska, A</creatorcontrib><creatorcontrib>Walczak, T</creatorcontrib><creatorcontrib>Kulej-Lyko, K</creatorcontrib><creatorcontrib>Sidorowicz, N</creatorcontrib><creatorcontrib>Soltowska, A</creatorcontrib><creatorcontrib>Banasiak, W</creatorcontrib><creatorcontrib>Kosmala, W</creatorcontrib><creatorcontrib>Przewlocka-Kosmala, M</creatorcontrib><creatorcontrib>Jaroch, J</creatorcontrib><creatorcontrib>Ponikowski, P</creatorcontrib><creatorcontrib>Jankowska, E A</creatorcontrib><title>P754Iron status indices (transferrin saturation, serum ferritin) in the course of acute myocarditis: relations with neurohormonal activation, cardiac dysfunction and clinical recovery</title><title>European heart journal</title><description><![CDATA[Abstract
Introduction
Acute myocarditis (MCD) can progress to post-myocarditis cardiomyopathy. Immune response is the major pathophysiological trigger leading to MCD. Optimal iron status is essential for the functioning of immune cells, cardiomyocytes and cardiofibroblasts. Therefore, there are premises to consider iron metabolism as a significant modulator of complex pathophysiology of MCD.
Purpose
We aimed to assess iron status in the course of MCD and relate it with clinical and laboratory measures.
Methods
We prospectively enrolled consecutive patients hospitalized for acute MCD in 2 tertiary referral cardiology centers during 2015–2018 and followed them up for 30 weeks. MCD was diagnosed based on the following criteria: 1) new onset symptoms suggestive of myocarditis (effort intolerance, dyspnea, palpitations or chest pain), 2) elevated high sensitivity cardiac troponin I (hs-cTnI), 3) exclusion of obstructive coronary artery disease.
Results
Study group comprised 41 patients with confirmed MCD [age: 31 (26–34) years, men: 95%] and 15 healthy age- and gender-matched subjects [age: 30 (28–33) years, men: 87%]. All patients survived hospitalization and follow-up, no subject needed ventricular assist device.
Patients with MCD had lower LVEF (56±10% vs. 69±14%) and higher CRP [32 (14–8754) vs. 3 (3–3) mg/l], NT-proBNP [452 (240–877) vs. 33 (18–46) pg/ml], hs-cTnI [7.3 (3.3–12.8) vs. 0,01 (0.01–0.01) μg/l] than the control group (all p<0.001). Regarding iron status, MCD group presented higher serum ferritin [213 (121–386) vs. 135 (84–210) μg/l] and lower transferrin saturation (TSAT) [21±10 vs. 28±15%] (all p<0.05). In patients with MCD ferritin correlated with CRP (r=0.46, p<0.01), TSAT correlated neither with CRP nor with ferritin (all p>0.02).
Patients with MCD and NT-proBNP >1000 pg/ml had lower TSAT (16±8 vs. 23±9%; p<0.05) and LVEF (47±13 vs. 59±7%; p<0.001) than the remaining subjects. No difference in ferritin was observed (p>0.2). 46% of patients during acute phase of MCD had LVEF≤55% – these patients presented lower TSAT (17±8% vs. 24±10%) and higher NT-proBNP – [577 (436–1657) vs. 358 (167–499) pg/ml] (all p<0.05). After 30 weeks only in 13% patients LVEF≤55% persisted and related to lower baseline TSAT (9±1% vs. 21±9%) and higher CRP (147±113 vs. 52±40 mg/l) (all p<0.05). LVEF≤55% was not related to ferritin (both p>0.2).
After 6 weeks of follow-up patients with MCD already presented higher LVEF (61±8%; p<0.05) and haemoglobin [14.7 (14.0–15.7) g/dl], lower CRP [3 (3–3) mg/l], NT-proBNP [34 (25–67) pg/ml], hs-cTnI [0.01 (0.01–0.01)], ferritin [124 (78–168) μg/l] and higher TSAT (26±7%) (all p<0.01). There was no further change in these parameters within the next 24 weeks (all p>0.2).
Conclusions
Iron status is deranged in acute MCD. Serum ferritin is an indicator of inflammatory response, whereas TSAT relates to neurohormonal activation and cardiac dysfunction. Iron status normalizes within 6 weeks after acute phase of MCD.
Acknowledgement/Funding
This research was financially supported by the National Science Centre (Poland) grant number 2014/13/B/NZ5/03146.]]></description><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNqNkMFKJDEQhoOs4KzuIwg5rmBr0t1Jd-9NRHcFYfegsLemTCp0ZCaRSloZX8zXMzMjnj0V1P9_RfExdizFmRRDc44zTQiUH89xeu3a7kw0Su-xhVR1XQ26Vd_YQshBVVr3_w_Y95QehRC9lnrB3v51qr2hGHjKkOfEfbDeYOI_M0FIDol8yUpEkH0MpzwhzSu-DbIPJwXgeUJu4kwJeXQczJyRr9bRANnSSb844XJLJ_7i88RD-ThOkVYxwLL0s3_-OL5FwHC7Tm4OZrPkECw3Sx-8KWVCE5-R1kds38Ey4Y-Pecjur6_uLv9Ut39_31xe3FZGNoOuOou6GBEIbW2Fcr3U0iqtoBedHR4Q-wY6J6FDHBonahSNBNE6Z6wE09bNIVO7u4ZiSoRufCK_AlqPUowb--On_XFnf9zYL5zYcXF--iLyDp50k04</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Franczuk, P</creator><creator>Kosiorek, A</creator><creator>Tkaczyszyn, M</creator><creator>Drozd, M</creator><creator>Zapolska, A</creator><creator>Walczak, T</creator><creator>Kulej-Lyko, K</creator><creator>Sidorowicz, N</creator><creator>Soltowska, A</creator><creator>Banasiak, W</creator><creator>Kosmala, W</creator><creator>Przewlocka-Kosmala, M</creator><creator>Jaroch, J</creator><creator>Ponikowski, P</creator><creator>Jankowska, E A</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20191001</creationdate><title>P754Iron status indices (transferrin saturation, serum ferritin) in the course of acute myocarditis: relations with neurohormonal activation, cardiac dysfunction and clinical recovery</title><author>Franczuk, P ; Kosiorek, A ; Tkaczyszyn, M ; Drozd, M ; Zapolska, A ; Walczak, T ; Kulej-Lyko, K ; Sidorowicz, N ; Soltowska, A ; Banasiak, W ; Kosmala, W ; Przewlocka-Kosmala, M ; Jaroch, J ; Ponikowski, P ; Jankowska, E A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1396-7de67470ea42d05f8161d565a807d9bee83a7f1a7ee93f02e031a04ffcd1ac423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Franczuk, P</creatorcontrib><creatorcontrib>Kosiorek, A</creatorcontrib><creatorcontrib>Tkaczyszyn, M</creatorcontrib><creatorcontrib>Drozd, M</creatorcontrib><creatorcontrib>Zapolska, A</creatorcontrib><creatorcontrib>Walczak, T</creatorcontrib><creatorcontrib>Kulej-Lyko, K</creatorcontrib><creatorcontrib>Sidorowicz, N</creatorcontrib><creatorcontrib>Soltowska, A</creatorcontrib><creatorcontrib>Banasiak, W</creatorcontrib><creatorcontrib>Kosmala, W</creatorcontrib><creatorcontrib>Przewlocka-Kosmala, M</creatorcontrib><creatorcontrib>Jaroch, J</creatorcontrib><creatorcontrib>Ponikowski, P</creatorcontrib><creatorcontrib>Jankowska, E A</creatorcontrib><collection>CrossRef</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Franczuk, P</au><au>Kosiorek, A</au><au>Tkaczyszyn, M</au><au>Drozd, M</au><au>Zapolska, A</au><au>Walczak, T</au><au>Kulej-Lyko, K</au><au>Sidorowicz, N</au><au>Soltowska, A</au><au>Banasiak, W</au><au>Kosmala, W</au><au>Przewlocka-Kosmala, M</au><au>Jaroch, J</au><au>Ponikowski, P</au><au>Jankowska, E A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P754Iron status indices (transferrin saturation, serum ferritin) in the course of acute myocarditis: relations with neurohormonal activation, cardiac dysfunction and clinical recovery</atitle><jtitle>European heart journal</jtitle><date>2019-10-01</date><risdate>2019</risdate><volume>40</volume><issue>Supplement_1</issue><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract><![CDATA[Abstract
Introduction
Acute myocarditis (MCD) can progress to post-myocarditis cardiomyopathy. Immune response is the major pathophysiological trigger leading to MCD. Optimal iron status is essential for the functioning of immune cells, cardiomyocytes and cardiofibroblasts. Therefore, there are premises to consider iron metabolism as a significant modulator of complex pathophysiology of MCD.
Purpose
We aimed to assess iron status in the course of MCD and relate it with clinical and laboratory measures.
Methods
We prospectively enrolled consecutive patients hospitalized for acute MCD in 2 tertiary referral cardiology centers during 2015–2018 and followed them up for 30 weeks. MCD was diagnosed based on the following criteria: 1) new onset symptoms suggestive of myocarditis (effort intolerance, dyspnea, palpitations or chest pain), 2) elevated high sensitivity cardiac troponin I (hs-cTnI), 3) exclusion of obstructive coronary artery disease.
Results
Study group comprised 41 patients with confirmed MCD [age: 31 (26–34) years, men: 95%] and 15 healthy age- and gender-matched subjects [age: 30 (28–33) years, men: 87%]. All patients survived hospitalization and follow-up, no subject needed ventricular assist device.
Patients with MCD had lower LVEF (56±10% vs. 69±14%) and higher CRP [32 (14–8754) vs. 3 (3–3) mg/l], NT-proBNP [452 (240–877) vs. 33 (18–46) pg/ml], hs-cTnI [7.3 (3.3–12.8) vs. 0,01 (0.01–0.01) μg/l] than the control group (all p<0.001). Regarding iron status, MCD group presented higher serum ferritin [213 (121–386) vs. 135 (84–210) μg/l] and lower transferrin saturation (TSAT) [21±10 vs. 28±15%] (all p<0.05). In patients with MCD ferritin correlated with CRP (r=0.46, p<0.01), TSAT correlated neither with CRP nor with ferritin (all p>0.02).
Patients with MCD and NT-proBNP >1000 pg/ml had lower TSAT (16±8 vs. 23±9%; p<0.05) and LVEF (47±13 vs. 59±7%; p<0.001) than the remaining subjects. No difference in ferritin was observed (p>0.2). 46% of patients during acute phase of MCD had LVEF≤55% – these patients presented lower TSAT (17±8% vs. 24±10%) and higher NT-proBNP – [577 (436–1657) vs. 358 (167–499) pg/ml] (all p<0.05). After 30 weeks only in 13% patients LVEF≤55% persisted and related to lower baseline TSAT (9±1% vs. 21±9%) and higher CRP (147±113 vs. 52±40 mg/l) (all p<0.05). LVEF≤55% was not related to ferritin (both p>0.2).
After 6 weeks of follow-up patients with MCD already presented higher LVEF (61±8%; p<0.05) and haemoglobin [14.7 (14.0–15.7) g/dl], lower CRP [3 (3–3) mg/l], NT-proBNP [34 (25–67) pg/ml], hs-cTnI [0.01 (0.01–0.01)], ferritin [124 (78–168) μg/l] and higher TSAT (26±7%) (all p<0.01). There was no further change in these parameters within the next 24 weeks (all p>0.2).
Conclusions
Iron status is deranged in acute MCD. Serum ferritin is an indicator of inflammatory response, whereas TSAT relates to neurohormonal activation and cardiac dysfunction. Iron status normalizes within 6 weeks after acute phase of MCD.
Acknowledgement/Funding
This research was financially supported by the National Science Centre (Poland) grant number 2014/13/B/NZ5/03146.]]></abstract><pub>Oxford University Press</pub><doi>10.1093/eurheartj/ehz747.0356</doi></addata></record> |
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| title | P754Iron status indices (transferrin saturation, serum ferritin) in the course of acute myocarditis: relations with neurohormonal activation, cardiac dysfunction and clinical recovery |
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