Is stress cardiomyopathy the underlying cause of ventricular dysfunction associated with brain death?

Brain death causes significant right ventricular (RV) dysfunction and power loss, which further deteriorates after graft preservation and transplantation. (A) RV pre-load-recruitable stroke work (PRSW) and (B) total power (TP) changes in controls (CTL), brain-dead donor transplant group (BD-Tx), and the chronic pulmonary hypertension recipient group (PHTN-Tx) before and 4 hours after induction of brain death (Post-BD) and after cardiac transplantation (Post-Tx). Compared with the control group, RV PRSW and TP decreased significantly after brain death and transplantation. In the group with a normal donor heart and recipients with pulmonary hypertension, there was a significant increase in RV PRSW and TP. Data are presented with the standard deviation.

Brain death causes a significant decrease in left (LV) and right ventricular (RV) function. The injury to the RV is more prominent than the LV. Pressure volume loops plotted for (A) the LV and (B) RV in consecutive cardiac cycles during occlusion of both vena cava. Left graph; x-axis shows the intracavitary ventricular volume (ml); y-axis shows the intracavitary pressure (mm Hg). Right graph; x-axis shows the intracavitary ventricular volume (ml); y-axis shows the stroke work (area of pressure volume loop) plotted for each cardiac cycle (erg 10³). The slope of this graph equals the pre-load independent recruitable stroke volume (PRSW).

Relationship of brain death and left (LV) and right ventricular (RV) function. Pre-load-recruitable stroke work increased acutely from baseline values (LV, 74.5 ± 4.1 erg 10³; RV, 21.9 ± 1.4 erg 10³) at time 0 immediately after induction of brain death. On average, LR and RV function decreased significantly, by 19% and 35%, respectively, after induction of brain death and over the course of 2 to 6 hours after brain death. No recovery potential of LV or RV function was observed. Data are presented with the standard deviation.

Right ventricular involvement is shown in Takotsubo cardiomyopathy. (A) Diastolic and (B) systolic cine cardiographic magnetic resonance images in the horizontal long axis-axis view demonstrate right and left ventricular ballooning (arrows). Mild right-sided pleural effusion (asteric) and significant left-sided pleural effusion (hash) are also present.

Right ventricular (RV) involvement in Takotsubo cardiomyopathy. (A) End-diastolic and (B) end-systolic frames of the left ventricle (LV) and (C) end-diastolic and (D) end-systolic frames of the RV demonstrate the extent of LV and RV dysfunction (arrows).

(A) Effect of increased intracranial pressure (ICP) and brain death on left ventricular myocardial histologic features. Increased ICP resulted in pronounced contraction band necrosis and myocytolysis. (B) In contrast, brain death ameliorated with central sympathetic blockade (ICP-CSB) abrogates these effects with sparse lesions and minimal contraction banding. Hematoxylin and eosin stain, original magnification 300x.