Unilateral pulmonary oedema after minimally invasive mitral valve surgery: a single-centre experience.

Objectives: Unilateral pulmonary oedema (UPE) is a rare but potentially life-threatening complication that has been described after minimally invasive mitral valve surgery (MICS). Over the last 8 years, we have witnessed, in our institution, several cases of severe UPE requiring immediate postoperative extracorporeal life support after MICS. Reviewing the available literature, data regarding this complication after MICS are rare. Consequently, we decided to retrospectively analyse patients scheduled for MICS in our institution.

Methods: After approval by our institutional review board, 256 MICS patients were analysed. As a primary end-point, we defined a newly developed UPE, radiographically evident within the first 24 h postoperatively. Secondary end-points were length of stay in the intensive care unit, length of stay in the hospital and in-hospital mortality. Chest radiographs were analysed by an independent consultant of radiology.

Results: Fifty-one (19.9%) patients showed increased right-sided pulmonary vascular congestion in the 1st postoperative chest radiography performed in the intensive care unit. Five (1.95%) patients immediately required extracorporeal life support after admission to the intensive care unit. Cardiopulmonary bypass time was significantly longer in the UPE group [UPE vs non-UPE 213 (49) vs 196 (43) min; P = 0.013]. More patients with UPE showed a preoperative increase of C-reactive protein >0.4265 mg/dl (P = 0.05). Logistic regression analysis identified a preoperative increase in C-reactive protein >0.4265 mg/dl as well as a prolonged cardiopulmonary bypass time (odds ratio 1.009, 95% confidence level 1.002-1.016; P = 0.014) independent risk factors, significantly associated with the development of UPE (odds ratio 2.583, 95% confidence interval 1.275-5.233; P = 0.008), a prolonged cardiopulmonary bypass time (odds ratio 1.009, 95% confidence interval 1.002-1.016; P = 0.014). The presence of pulmonary hypertension (odds ratio 0.273, 95% confidence interval 0.08-0.84; P = 0.02) seemed to be a protective factor regarding the genesis of UPE.

Conclusions: In accordance with the rarely available literature regarding UPE after MICS, our analysis led us to hypothesize the possibility of an inflammatory disposition for UPE. The role of pulmonary hypertension remains unclear in our patient population.

Clinical Trials Number: NCT02655094.