Mark P V Begieneman1, Reindert W Emmens2, Liza Rijvers3, Bela Kubat4, Walter J Paulus5, Alexander B A Vonk6, Lawrence Rozendaal7, P Stefan Biesbroek8, Diana Wouters9, Sacha Zeerleder10, Marieke van Ham9, Stephane Heymans11, Albert C van Rossum12, Hans W M Niessen13, Paul A J Krijnen7. 1. Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Dutch Forensic Institute, The Hague, the Netherlands. 2. Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Department of Immunopathology, Sanquin Research, Amsterdam, the Netherlands. Electronic address: r.emmens@vumc.nl. 3. Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands. 4. Dutch Forensic Institute, The Hague, the Netherlands. 5. ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Department of Physiology, VU University Medical Center, Amsterdam, the Netherlands. 6. Department of Cardiac Surgery, VU University Medical Center, Amsterdam, the Netherlands. 7. Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands. 8. Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands. 9. Department of Immunopathology, Sanquin Research, Amsterdam, the Netherlands. 10. Department of Immunopathology, Sanquin Research, Amsterdam, the Netherlands; Department of Hematology, Academic Medical Center, Amsterdam, the Netherlands. 11. Department of Cardiology, Maastricht University Medical Center, Maastricht, the Netherlands. 12. ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Department of Cardiology, VU University Medical Center, Amsterdam, the Netherlands. 13. Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Department of Cardiac Surgery, VU University Medical Center, Amsterdam, the Netherlands.
Abstract
INTRODUCTION: Atrial fibrillation (AF) is a common complication in myocarditis. Atrial inflammation has been suggested to play an important role in the pathophysiology of AF. However, little is known about the occurrence of atrial inflammation in myocarditis patients. Here, we analyzed inflammatory cell numbers in the atria of myocarditis patients without symptomatic AF. METHODS: Cardiac tissue was obtained postmortem from lymphocytic myocarditis patients (n=6), catecholamine-induced myocarditis patients (n=5), and control patients without pathological evidence of heart disease (n=5). Tissue sections of left and right ventricle and left and right atrium were stained for myeloperoxidase (neutrophilic granulocytes), CD45 (lymphocytes), and CD68 (macrophages). These cells were subsequently quantified in atrial and ventricular myocardium and atrial adipose tissue. RESULTS: In lymphocytic myocarditis patients, a significant increase was observed for lymphocytes in the left atrial adipose tissue. In catecholamine-induced myocarditis patients, significant increases were found in the atria for all three inflammatory cell types. Infiltrating inflammatory cell numbers in the atrial myocardium correlated positively with those in the ventricles, especially in catecholamine-induced myocarditis patients. CONCLUSIONS: To a varying extent, atrial myocarditis occurs concurrently with ventricular myocarditis in patients diagnosed with myocarditis of different etiology. This provides a substrate that potentially predisposes myocarditis patients to the development of AF and subsequent complications such as sudden cardiac death and heart failure.
INTRODUCTION:Atrial fibrillation (AF) is a common complication in myocarditis. Atrial inflammation has been suggested to play an important role in the pathophysiology of AF. However, little is known about the occurrence of atrial inflammation in myocarditispatients. Here, we analyzed inflammatory cell numbers in the atria of myocarditispatients without symptomatic AF. METHODS: Cardiac tissue was obtained postmortem from lymphocytic myocarditispatients (n=6), catecholamine-induced myocarditispatients (n=5), and control patients without pathological evidence of heart disease (n=5). Tissue sections of left and right ventricle and left and right atrium were stained for myeloperoxidase (neutrophilic granulocytes), CD45 (lymphocytes), and CD68 (macrophages). These cells were subsequently quantified in atrial and ventricular myocardium and atrial adipose tissue. RESULTS: In lymphocytic myocarditispatients, a significant increase was observed for lymphocytes in the left atrial adipose tissue. In catecholamine-induced myocarditispatients, significant increases were found in the atria for all three inflammatory cell types. Infiltrating inflammatory cell numbers in the atrial myocardium correlated positively with those in the ventricles, especially in catecholamine-induced myocarditispatients. CONCLUSIONS: To a varying extent, atrial myocarditis occurs concurrently with ventricular myocarditis in patients diagnosed with myocarditis of different etiology. This provides a substrate that potentially predisposes myocarditispatients to the development of AF and subsequent complications such as sudden cardiac death and heart failure.
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