Lost in perfusion
Author(s) -
Fulvio Morello,
Peiman Nazerian,
Enrico Lupia
Publication year - 2016
Publication title -
european journal of cardio-thoracic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 133
eISSN - 1873-734X
pISSN - 1010-7940
DOI - 10.1093/ejcts/ezw097
Subject(s) - perfusion , cardiology , medicine
The recently published article by Conzelmann et al., based on the GERAADA registry, provides further multicentre evidence from a large number of patients that organ malperfusion represents a key factor for mortality in acute Stanford type A aortic dissection (AD), with death rates increasing proportional to the number of affected organs [1, 2]. This concept critically applies also to Stanford type B AD, where non-surgical options play a primary role. In our strive to continuously improve outcome, these findings primarily imply that tailored strategies to revert organ malperfusion should start as early as possible in conjunction with aortic repair, and should take advantage of an expert multidisciplinary ‘aortic team’. A major challenge in front of us, however, is represented by the unclear definition of organ malperfusion syndromes in AD. This negatively affects both clinical practice and research, and leads to poor recognition of the substantial clinical heterogeneity of patients with AD. Unfortunately, in spite of its leading role in identifying perfusion as a key pathophysiological and prognostic factor, the GERAADA registry itself does not provide any provisional definition of malperfusion syndromes applicable to clinical practice and to further studies, as the diagnosis of malperfusion was operator-/centre-specific [1–3]. In the current era, a large amount of data exploring organ perfusion threedimensionally can bemade available for patients with AD in a timely fashion and already in the Emergency Department. These data, awaiting systematic record and exploration, include objective assessment of neurological status (NIH Stroke Scale, Glasgow Coma Scale, Modified Rankin Scale), ECG findings, bedside ultrasonography of the heart and vessels, biomarkers exploring organ damage (myocardium: troponin; kidney: cystatin C, neutrophil gelatinase-associated lipocalin, creatinine; visceral organs: lactate dehydrogenase, amylase, transaminases; muscle: creatine kinase, lactate dehydrogenase), microperfusion (lactate), systemic inflammation (white blood cells, C-reactive protein), thrombotic burden (D-dimer, fibrinogen, platelets) and increasingly detailed imaging data. For standardization, these variables could be classified in predefined bundles of organ Acute Aortic Dissection Type A (GERAADA). Eur J Cardiothorac Surg 2016;
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