Author + information
- Guido Tavazzi, MD, PhD∗ (, )
- Gabriele Via, MD,
- Giorgio Iotti, MD,
- on behalf of Marinella Zanierato, MD, and Francesco Procaccio, MD
- ↵∗Department of Anesthesia and Intensive Care, Fondazione IRCCS Policlinico San Matteo, Piazzale Golgi 19, Pavia 27110, Italy
We appreciate Prof. Madias’s insightful comments on our paper and strong endorsement of our hypotheses (1). He suggests additional potential solutions for better management of donors with dysfunctional hearts, including sympathetic activity monitoring, donor heart “nursing” with cardiac mechanical support, and ultimately, donor centralization in dedicated “donor ICUs.” These approaches, although stimulating and promising, are likely to pose remarkable logistical, organizational, economic, and resource-allocation challenges; however, we will have to accept these challenges if we aim to determine which transiently dysfunctional hearts are suitable for transplantation. Furthermore, as donor management teams do not currently include professionals specifically trained in the complex and evolving field at the boundary between cardiology and critical care, we believe that the development of a new set of medical skills and competences in “donor cardiology and critical care” would now be required. The increasing awareness of the complexity of this field needs to be matched by a growing specialization in a multimodal diagnostic and therapeutic strategy, aiming at a comprehensive, individually tailored donor approach. This is likely to represent an additional task for the expanding domain of acute cardiac care.
The topic discussed by Dr. Woronow and colleagues is extremely interesting and largely under-reported. The interaction between neurohormones/catecholamine (both exogenous and endogenous) on the cardiovascular system and other organs is a matter of daily debate in clinical and scientific settings, and especially in intensive care (2,3).
One thought, which has already been discussed elsewhere (4), is that Takotsubo syndrome is likely a well codified clinical entity, part of a wider “family” of cardiomyopathy that can be caused by an incredibly variety of triggers.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
- Tavazzi G.,
- Zanierato M.,
- Via G.,
- Iotti G.A.,
- Procaccio F.
- Tarvasmäki T.,
- Lassus J.,
- Varpula M.,
- et al.,
- for the CardShock Study Investigators
- Sarapultsev P.A.,
- Sarapultsev A.P.