Response to Letter Regarding Article, “Posttraumatic Cardiac Contrecoup: In Vivo Evidence by Cardiac Magnetic Resonance Imaging”
We thank Hamilton-Craig et al for their remarks on our recent article1 about a young subject with hypothetical posttraumatic myocardial damage. We respectfully disagree with some points, and we present the following additional arguments.
Hamilton-Craig et al suggest that the presented clinical and cardiac magnetic resonance imaging (CMRI) findings could be referred to acute myocarditis and subsequent ventricular dysrhythmia causing the motorcycle accident. We acknowledge that this hypothesis could be taken into account, although in our opinion this seems to be a highly unlikely explication in our patient. The medical history in a completely asymptomatic healthy sportsman who remained conscious before, during, and after the motorcycle accident is inconsistent with the hypothesis of myocarditis. The detailed analysis of the dynamics of the accident assisted by a third person proved that the patient was forced to rapidly change the direction of his motorbike to avoid another vehicle. The relatively rapid normalization of the Troponin I values does not favor myocarditis. Our CMRI findings with a transmural myocardial edema on T2-weighted images and a midwall late Gadolinium enhancement are, in our opinion, most likely related to the important thoracic trauma causing in addition a rib fracture. Typical changes of acute myocarditis on CMRI are subepicardial with late Gadolinium enhancement in the lateral free wall2 and less frequently associated with midmyocardial late enhancement, as in our case, although overlap may occur. CMRI has the potential to show the extension of acute myocardial damage with the presence of edema on T2-weighted images and to exclude posttraumatic myocardial infarction by the absence of subendocardial late Gadolinium enhancement.
In contrast to the statement of Hamilton-Craig et al, the most likely pattern of blunt cardiac trauma is not only ventricular, arterial, and valvular rupture but also the spectrum of cardiac trauma ranging from injuries with no cellular damage (cardiac concussion) to cardiac chamber rupture.3 The clinical history, the sequence of events, and the CMRI presentation are much more in favor of a posttraumatic cause. However, we agree with the authors that the denomination of a “contrecoup” injury to the heart remains, as stated in our article, somewhat hypothetical. The future role of CMRI in cardiac trauma has to be established by prospective studies.
Sources of Funding
Dr Wyttenbach and Dr Gallino are supported by a Swiss Heart Foundation grant. Dr Corti is supported by a Swiss National Science Foundation grant.
Moccetti M, Wyttenbach R, Santini P, Previsdomini M, Corti R, Gallino A. Posttraumatic cardiac contrecoup: in vivo evidence by cardiac magnetic resonance imaging. Circulation. 2009; 119: 1538–1540.
Mahrholdt H, Goedecke Ch, Wagner A, Meinhardt G, Athanasiadis A, Vogelsberg H, Fritz P, Klingel K, Kandolf R, Sechtem U. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation. 2004; 109: 1250–1258.