NDT Advance Access originally published online on March 30, 2006
Nephrology Dialysis Transplantation 2006 21(6):1549-1554; doi:10.1093/ndt/gfl127
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Clinical Nephrology
Acute myocardial infarction in thrombotic microangiopathies—clinical characteristics, risk factors and outcome
1 Department of Nephrology, 2 Department of Haematology and 3 Department of Cardiology, University Hospital, Essen, University of Duisburg-Essen, Germany
Correspondence and offprint requests to: Stefan Herget-Rosenthal, MD, Klinik für Nieren- und Hochdruckkrankheiten, Universitätsklinikum Essen, Hufelandstr. 55, D-45122 Essen, Germany. Email: stefan.herget-rosenthal{at}uni-essen.de
Background. Acute myocardial infarction (AMI) has been reported and is associated with poor outcome in the course of thrombotic microangiopathies (TMA). However, data are very limited in regard to the clinical characteristics, risk factors and outcome of AMI during TMA. Furthermore, current AMI definitions based on troponins are more sensitive and specific to detect myocardial injury.
Methods. We retrospectively analysed 74 consecutive patients with 78 TMA episodes. TMA was defined as platelets below 150 x 109/l, haemolytic anaemia, elevated lactate dehydrogenase (LDH) and increased red cell fragmentation, and AMI as serum troponin I above 1 ng/ml with symptoms of myocardial ischaemia and/or appropriate electrocardiography (ECG) alterations.
Results. AMI occurred in 14 TMA episodes (18%) (9 non- and 5 ST-segment elevation AMI). AMI occurred 5±3 days after TMA diagnosis, predominately in clinically suspected thrombotic thrombocytopenic purpura (TTP) as TMA subtype. Independent risk factors for subsequent AMI were TTP (RR 2.2; 95% CI 1.1–5.6), and serum LDH above 1000 U/l (RR 2.7; 95% CI 1.3–7.2) as well as serum troponin I above 0.20 ng/ml at TMA presentation (RR 13.5; 95% CI 2.6–86.8). LDH above 1000 U/l together with troponin I above 0.20 ng/ml had a sensitivity of 86% (95% CI 60–96%) and a specificity of 95% (95% CI 86–98%) to predict AMI in the later course of TMA. AMI contributed substantially to morbidity causing left ventricular dysfunction in three of eight survivors and potentially accounted for the death in five of six non-survivors.
Conclusions. AMI is an early, frequent and severe complication during TMA. AMI occurs especially in TTP, and serum LDH above 1000 U/l in combination with serum troponin I above 0.20 ng/ml at TMA presentation are excellent predictors of subsequent AMI.
Keywords: myocardial infarction; prediction; thrombotic microangiopathy; thrombotic thrombocytopenic purpura; troponin
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