LVADs reverse pulmonary hypertension secondary to left heart disease
Left ventricular assist devices (LVADs) can reverse pulmonary hypertension secondary to left heart disease (WHO group 2) regardless of baseline pulmonary vascular resistance (PVR), according to a new study.
“In our study, we showed that pulmonary hypertension with advanced pulmonary vascular disease can benefit significantly from LVAD placement. Most importantly, we showed that the normalization of mean pulmonary artery pressure (mPAP) and PVR persists after cardiac transplantation is performed,” said researchers.
Researchers reviewed the medical records of 258 LVAD patients with elevated mPAP (>25 mm Hg) and PVR (≥3 Wood units). Fifty-one patients were eligible and subsequently included in the analysis (mean age, 56±13 years; 75 percent male). Of the participants, 29 had moderately elevated PVR and the remaining 22 showed significant elevations. Both groups were comparable in terms of baseline demographic variables. [Heart Lung Circ 2019;28:946-952]
There was a significant drop towards normalization in mPAP, PVR, transpulmonary gradient (TPG) and pulmonary capillary wedge pressures after placement of LVAD in both groups.
For instance, pre-LVAD TPG (18±5 vs 14±3; mm Hg p=0.001) and PVR (6.3±1.2 vs 3.8±0.5 Wood units; p<0.001) values were markedly higher in those with significant vs moderate PVR elevations. Notably, after device placement, readings dropped to levels comparable to that in patients with only moderate PVR elevation (p=0.52 and p=0.94 for TPG and PVR, respectively).
Linear regression modelling also showed a strong and significant correlation between baseline PVR and subsequent decline after LVAD placement (r, 0.87; p<0.001).
Dividing the participants into tertiles of PVR yielded similar results. There were significant improvements in mPAP, pulmonary wedge pressure, TPG and PVR across all tertiles after LVAD placement. Kaplan-Meier analysis, used to compare time to PVR normalization, further showed no significant differences among all three tertiles.
Fourteen patients, all with significant PVR elevation, subsequently underwent cardiac transplant after LVAD. PVR remained normal in all patients at the 1-year follow-up.
“In our study, we tried to answer a clinically-relevant question by investigating the effect of LVAD on patients with severely elevated PVR; a group of patients that used to be excluded from consideration or cardiac transplantation before the era of LVAD,” said researchers.
The findings show “study also shows that the relationship between the baseline PVR and the drop in PVR post-LVAD is linear, which indicates a full recovery regardless of the degree of pulmonary vascular bed remodelling, and suggests that baseline PVR could be taken completely out of the equation as a risk factor for cardiac transplantation once LVAD is used for bridging,” they continued.
There are several important limitations that need to be considered, researchers pointed out. Chief of these is the retrospective design, which constrains the availability and uniformity of the information included in the analysis.
“We believe a prospective study should be planned to confirm these findings, and to investigate the long-term outcomes after LVAD placement in patients with significant pulmonary vascular disease,” they added.