Altered aortic stiffness associated with stress cardiomyopathy in patients with aneurysmal subarachnoid haemorrhage

Introduction

We investigated whether possible alterations in aortic stiffness were associated with stress cardiomyopathy (SC) in patients with subarachnoid haemorrhage (SAH).

Methods

Thirty-seven patients with SAH (aged 42.65 ± 13.07, 23 males) were included in the study. The severity of SAH was estimated by Hunt-Hess and Fisher scales, respectively. The left ventricular ejection fraction (LVEF) was measured by the Simpson's biplane method of disks; aortic stiffness was assessed by sonographic measurements of the carotid to femoral pulse wave velocity (PWV). The above sonographic measurements along with BNP measurements were obtained upon admission and repeated measurements were performed 20 ± 2 days following the acute phase of SAH. All patients were mechanically ventilated under the same conditions during all measurements.

Results

Patients with severe SAH showed depressed LV function and increased aortic stiffness. Both Hunt-Hess and Fisher scales were associated with LVEF (r = -0.460, P = 0.004 and r = -0.512; P = 0.001, respectively) and PWV values (r = 0.359, P = 0.029 and r = 0.363; P = 0.027, respectively). On admission, 14 patients (38%) manifested SC with increased BNP values as compared with those without cardiac alterations (841.43 ± 561.04 vs 145.04 ± 106.02 pg/ml, P < 0.001). These subjects exhibited increased PWV as compared with patients with normal LV function (12.79 ± 2.02 vs 9.63 ± 2.89 m/second, P = 0.001). PWV correlated to BNP values (r = 0.489, P = 0.002). Follow-up measurements revealed a significant increase in LVEF and decrease in PWV as compared with baseline measurements (62.64 ± 9.18 vs 57.94 ± 12.55%, P = 0.005 and 9.37 ± 2.07 vs 10.71 ± 2.96 m/second, P = 0.001, respectively). In this series, brain death was documented clinically in seven cases. An ongoing study including a larger number of patients with SAH analyzes the prognostic value of echocardiographic and BNP measurements.

Conclusions

Alterations of the heart-vessel coupling may be due to catecholamine-induced mechanisms. Stress cardiomyopathy associated with altered aortic stiffness during the acute phase of SAH may be transient phenomena.