Neurogenic Stress Cardiomyopathy in Heart Donors

Takotsubo cardiomyopathy and its relevance to anesthesiology: a narrative review

“…Although often global, it is likely a variant of stress cardiomyopathy. 202 Blocking the sympathetic storm associated with brain death may reduce the incidence of cardiac dysfunction in donors, 203 but if it occurs, given time and hormonal therapy (e.g., thyroid, corticosteroids), the heart may recover and be acceptable for transplantation. These hearts may even be successfully transplanted before fully recovered, with subsequent recovery in the recipient.…”

“Neurogenic stress cardiomyopathy in heart donors” is a form of Takotsubo syndrome

“…Recovery of heart function in patients with ABI may take occasionally many days to weeks, but it is meaningful to evaluate serially only for a few hours the hearts of cardiac donors in an effort to declare them suitable for transplantation. Although experience showing improvement is usually based on 2 ECHO examinations, extending from 3 to 36 h [4,5], or at no specified time intervals [8], it is advisable that ECHO be implemented very frequently, akin to what is advised for patients with TTS [10]. An important issue is to provide appropriate management (hemodynamic and metabolic) to the patient-donor, in an effort to enhance and speed-up recovery of the heart, and to this goal there are guidelines issued [4][5][6][7], although the matter is still under consideration [8].…”

“…The scarcity of donor hearts for cardiac transplantation is further compounded by the fact that only a small fraction of potentially available hearts for procurement are deemed suitable during evaluation [4][5][6][7]. The unsuitable donor hearts reveal on ECHO a low LVEF, which by many is felt to be due to NSC, consequent to the ABI [4][5][6][7], with evidence that at follow-up ECHO a few hours later [4,5,8], or at low dose dobutamine stress ECHO [9], there is considerable improvement, or even normalization of the LVEF. Recovery of heart function in patients with ABI may take occasionally many days to weeks, but it is meaningful to evaluate serially only for a few hours the hearts of cardiac donors in an effort to declare them suitable for transplantation.…”

“…It is exemplified by an illustrated case report, in a recent comprehensive review on the topic [4], of a 23-year-old man, a gunshot wound victim, who suffered acute brain injury (ABI), and whose heart revealed on echocardiography (ECHO) a left ventricular ejection fraction (LVEF) of 30%; on a follow-up ECHO 10 h later, the patient's LVEF was 50%, the heart was successfully procured and transplanted, and immediate postoperative ECHO of the recipient showed a LVEF of 60%, with subsequent normal ECHO findings. The scarcity of donor hearts for cardiac transplantation is further compounded by the fact that only a small fraction of potentially available hearts for procurement are deemed suitable during evaluation [4][5][6][7]. The unsuitable donor hearts reveal on ECHO a low LVEF, which by many is felt to be due to NSC, consequent to the ABI [4-7], with evidence that at follow-up ECHO a few hours later [4,5,8], or at low dose dobutamine stress ECHO [9], there is considerable improvement, or even normalization of the LVEF.…”

“…An important issue is to provide appropriate management (hemodynamic and metabolic) to the patient-donor, in an effort to enhance and speed-up recovery of the heart, and to this goal there are guidelines issued [4][5][6][7], although the matter is still under consideration [8]. Vasopressors are often employed to sustain adequate heart perfusion [4][5][6][7][8][9], and this is required, while the procuring team monitors the heart for improvement of its LVEF. Although data on pressor employment revealed that exogenously administered catecholamines did not cause improvement or worsening in the LVEF [5], one wonders whether such drugs used for hemodynamic support, could act as mediators of further NSC, similar to the one seen in patients developing TTS from iatrogenic administration of epinephrine or dobutamine [1], or found in resuscitated victims of cardiac arrest, in whom epinephrine has been repeatedly used during resuscitation [11].…”