Myocarditis in patients with subarachnoid hemorrhage: A histopathologic study

Ivo A. C. van der Bilt, Jean-Paul Vendeville, Tim P. van de Hoef, Mark P. V. Begieneman, Wim K. Lagrand, Johan M. Kros, Arthur A. M. Wilde, Gabriel J. E. Rinkel, Hans W. M. Niessen

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Cardiac abnormalities after subarachnoid hemorrhage (SAH) such as electrocardiographic changes, echocardiographic wall motion abnormalities, and elevated troponin levels are independently associated with a poor prognosis. They are caused by catecholaminergic stress coinciding with influx of inflammatory cells into the heart. These abnormalities could be a sign of a myocarditis, potentially giving insight in pathophysiology and treatment options. These inflammatory cells are insufficiently characterized, and it is unknown whether myocarditis is associated with SAH. Myocardium of 25 patients who died of SAH and 18 controls was stained with antibodies identifying macrophages (CD68), lymphocytes (CD45), and neutrophil granulocytes (myeloperoxidase). Myocytolysis was visualized using complement staining (C3d). CD31 was used to identify putative thrombi. We used Mann-Whitney U testing for analysis. In the myocardium of SAH patients, the amount of myeloperoxidase-positive (P < .005), CD45-positive (P < .0005), and CD68-positive (P < .0005) cells was significantly higher compared to controls. Thrombi in intramyocardial arteries were found in 22 SAH patients and 1 control. Myocytolysis was found in 6 SAH patients but not in controls. Myocarditis, consisting of an influx of neutrophil granulocytes, lymphocytes, and macrophages, coinciding with myocytolysis and thrombi in intramyocardial arteries, occurs in patients with SAH but not in controls. These findings might explain the cardiac abnormalities after SAH and may have implications for treatment.

Original languageEnglish
Pages (from-to)196-200
Number of pages5
JournalJournal of Critical Care
Volume32
DOIs
Publication statusPublished - Apr 2016

Cite this

van der Bilt, I. A. C., Vendeville, J-P., van de Hoef, T. P., Begieneman, M. P. V., Lagrand, W. K., Kros, J. M., ... Niessen, H. W. M. (2016). Myocarditis in patients with subarachnoid hemorrhage: A histopathologic study. Journal of Critical Care, 32, 196-200. https://doi.org/10.1016/j.jcrc.2015.12.005
van der Bilt, Ivo A. C. ; Vendeville, Jean-Paul ; van de Hoef, Tim P. ; Begieneman, Mark P. V. ; Lagrand, Wim K. ; Kros, Johan M. ; Wilde, Arthur A. M. ; Rinkel, Gabriel J. E. ; Niessen, Hans W. M. / Myocarditis in patients with subarachnoid hemorrhage : A histopathologic study. In: Journal of Critical Care. 2016 ; Vol. 32. pp. 196-200.
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abstract = "Cardiac abnormalities after subarachnoid hemorrhage (SAH) such as electrocardiographic changes, echocardiographic wall motion abnormalities, and elevated troponin levels are independently associated with a poor prognosis. They are caused by catecholaminergic stress coinciding with influx of inflammatory cells into the heart. These abnormalities could be a sign of a myocarditis, potentially giving insight in pathophysiology and treatment options. These inflammatory cells are insufficiently characterized, and it is unknown whether myocarditis is associated with SAH. Myocardium of 25 patients who died of SAH and 18 controls was stained with antibodies identifying macrophages (CD68), lymphocytes (CD45), and neutrophil granulocytes (myeloperoxidase). Myocytolysis was visualized using complement staining (C3d). CD31 was used to identify putative thrombi. We used Mann-Whitney U testing for analysis. In the myocardium of SAH patients, the amount of myeloperoxidase-positive (P < .005), CD45-positive (P < .0005), and CD68-positive (P < .0005) cells was significantly higher compared to controls. Thrombi in intramyocardial arteries were found in 22 SAH patients and 1 control. Myocytolysis was found in 6 SAH patients but not in controls. Myocarditis, consisting of an influx of neutrophil granulocytes, lymphocytes, and macrophages, coinciding with myocytolysis and thrombi in intramyocardial arteries, occurs in patients with SAH but not in controls. These findings might explain the cardiac abnormalities after SAH and may have implications for treatment.",
keywords = "Subarachnoid hemorrhage, Myocarditis, Inflammation, Takotsubo, Cardiac abnormalities, Outcome",
author = "{van der Bilt}, {Ivo A. C.} and Jean-Paul Vendeville and {van de Hoef}, {Tim P.} and Begieneman, {Mark P. V.} and Lagrand, {Wim K.} and Kros, {Johan M.} and Wilde, {Arthur A. M.} and Rinkel, {Gabriel J. E.} and Niessen, {Hans W. M.}",
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van der Bilt, IAC, Vendeville, J-P, van de Hoef, TP, Begieneman, MPV, Lagrand, WK, Kros, JM, Wilde, AAM, Rinkel, GJE & Niessen, HWM 2016, 'Myocarditis in patients with subarachnoid hemorrhage: A histopathologic study' Journal of Critical Care, vol. 32, pp. 196-200. https://doi.org/10.1016/j.jcrc.2015.12.005

Myocarditis in patients with subarachnoid hemorrhage : A histopathologic study. / van der Bilt, Ivo A. C.; Vendeville, Jean-Paul; van de Hoef, Tim P.; Begieneman, Mark P. V.; Lagrand, Wim K.; Kros, Johan M.; Wilde, Arthur A. M.; Rinkel, Gabriel J. E.; Niessen, Hans W. M.

In: Journal of Critical Care, Vol. 32, 04.2016, p. 196-200.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Myocarditis in patients with subarachnoid hemorrhage

T2 - A histopathologic study

AU - van der Bilt, Ivo A. C.

AU - Vendeville, Jean-Paul

AU - van de Hoef, Tim P.

AU - Begieneman, Mark P. V.

AU - Lagrand, Wim K.

AU - Kros, Johan M.

AU - Wilde, Arthur A. M.

AU - Rinkel, Gabriel J. E.

AU - Niessen, Hans W. M.

N1 - Copyright © 2015 Elsevier Inc. All rights reserved.

PY - 2016/4

Y1 - 2016/4

N2 - Cardiac abnormalities after subarachnoid hemorrhage (SAH) such as electrocardiographic changes, echocardiographic wall motion abnormalities, and elevated troponin levels are independently associated with a poor prognosis. They are caused by catecholaminergic stress coinciding with influx of inflammatory cells into the heart. These abnormalities could be a sign of a myocarditis, potentially giving insight in pathophysiology and treatment options. These inflammatory cells are insufficiently characterized, and it is unknown whether myocarditis is associated with SAH. Myocardium of 25 patients who died of SAH and 18 controls was stained with antibodies identifying macrophages (CD68), lymphocytes (CD45), and neutrophil granulocytes (myeloperoxidase). Myocytolysis was visualized using complement staining (C3d). CD31 was used to identify putative thrombi. We used Mann-Whitney U testing for analysis. In the myocardium of SAH patients, the amount of myeloperoxidase-positive (P < .005), CD45-positive (P < .0005), and CD68-positive (P < .0005) cells was significantly higher compared to controls. Thrombi in intramyocardial arteries were found in 22 SAH patients and 1 control. Myocytolysis was found in 6 SAH patients but not in controls. Myocarditis, consisting of an influx of neutrophil granulocytes, lymphocytes, and macrophages, coinciding with myocytolysis and thrombi in intramyocardial arteries, occurs in patients with SAH but not in controls. These findings might explain the cardiac abnormalities after SAH and may have implications for treatment.

AB - Cardiac abnormalities after subarachnoid hemorrhage (SAH) such as electrocardiographic changes, echocardiographic wall motion abnormalities, and elevated troponin levels are independently associated with a poor prognosis. They are caused by catecholaminergic stress coinciding with influx of inflammatory cells into the heart. These abnormalities could be a sign of a myocarditis, potentially giving insight in pathophysiology and treatment options. These inflammatory cells are insufficiently characterized, and it is unknown whether myocarditis is associated with SAH. Myocardium of 25 patients who died of SAH and 18 controls was stained with antibodies identifying macrophages (CD68), lymphocytes (CD45), and neutrophil granulocytes (myeloperoxidase). Myocytolysis was visualized using complement staining (C3d). CD31 was used to identify putative thrombi. We used Mann-Whitney U testing for analysis. In the myocardium of SAH patients, the amount of myeloperoxidase-positive (P < .005), CD45-positive (P < .0005), and CD68-positive (P < .0005) cells was significantly higher compared to controls. Thrombi in intramyocardial arteries were found in 22 SAH patients and 1 control. Myocytolysis was found in 6 SAH patients but not in controls. Myocarditis, consisting of an influx of neutrophil granulocytes, lymphocytes, and macrophages, coinciding with myocytolysis and thrombi in intramyocardial arteries, occurs in patients with SAH but not in controls. These findings might explain the cardiac abnormalities after SAH and may have implications for treatment.

KW - Subarachnoid hemorrhage

KW - Myocarditis

KW - Inflammation

KW - Takotsubo

KW - Cardiac abnormalities

KW - Outcome

U2 - 10.1016/j.jcrc.2015.12.005

DO - 10.1016/j.jcrc.2015.12.005

M3 - Article

VL - 32

SP - 196

EP - 200

JO - Journal of Critical Care

JF - Journal of Critical Care

SN - 0883-9441

ER -

van der Bilt IAC, Vendeville J-P, van de Hoef TP, Begieneman MPV, Lagrand WK, Kros JM et al. Myocarditis in patients with subarachnoid hemorrhage: A histopathologic study. Journal of Critical Care. 2016 Apr;32:196-200. https://doi.org/10.1016/j.jcrc.2015.12.005