Author + information
- Mayooran Namasivayam, MBBS, BSc(Med),
- Michael P. Feneley, MBBS, MD,
- Christopher S. Hayward, BMed, MD,
- Martin Shaw, MBBS,
- Sriram Rao, MBBS,
- Paul Jansz, MBBS, PhD and
- David W.M. Muller, MBBS, MD∗ ()
- ↵∗Department of Cardiology, St. Vincent’s Hospital, 390 Victoria Street, Darlinghurst, New South Wales, 2010, Australia
Mitral valve replacement (MVR) for mitral regurgitation (MR) acutely increases left ventricular (LV) afterload due to elimination of low afterload regurgitant flow. In high-risk patients, this may cause cardiac decompensation, but this is difficult to test due to the confounding effects of cardioplegia and cardiopulmonary bypass. A novel transcatheter approach (1) provided a unique opportunity to study the acute hemodynamic response to MVR in beating human hearts for the first time.
Nine consecutive high-risk surgical candidates recruited into the Tendyne (Tendyne Holdings, Roseville, Minnesota) transcatheter mitral valve replacement (TMVR) Global Feasibility Study (1) (Expanded Clinical Study of the Tendyne Mitral Valve System; NTC02321514) were included in a substudy evaluating intraprocedural hemodynamics. Inclusion and exclusion criteria have been described previously (1). Patients provided written informed consent, and studies were approved by the St. Vincent’s Hospital Research Ethics Committee.
TMVR was performed via apical access through a 4- to 5-cm thoracotomy. The valve was seated in the mitral annulus and secured to the LV apex with a tensioned tether. Technical details have been described previously (1). We measured invasively LV and aortic pressures and right heart catheter indices. LV volumes were determined by 3-dimensional transesophageal echocardiography (EpiQ7/QLab, Philips Healthcare, Eindhoven, the Netherlands). The transesophageal echocardiography probe remained in a stable mid-esophageal position throughout the procedure. Data were recorded at 3 intraoperative time points: baseline, immediate post-valve (median time 1 min), and late post-valve (median time 17 min).
LV contractility was measured with pressure–volume analysis. Single-beat end-systolic elastance (Ees) was calculated as: Ees = (LV end-systolic pressure)/(LV end-systolic volume [LVESV]) (2). LV pressures and volumes were correlated at 4 stages of the cardiac cycle (end-diastole, end-isovolumetric contraction, end-systole, and end-isovolumetric relaxation) to reconstruct pressure–volume loops. Stroke work (SW) was determined by the area of the pressure–volume loops using the surveyor’s formula. Single-beat preload recruitable SW relationship slope (Mw) was determined by dividing SW by LV end-diastolic volume, to provide another load-insensitive measure of LV contractility (3). We used the Wilcoxon signed rank test with post hoc Bonferroni correction for pairwise comparisons across the time points studied (SPSS-24, IBM Corporation, Armonk, New York).
The age of our cohort was 75.8 ± 10.2 years (range 55 to 91 years). All patients had grade 4+ secondary MR (predominantly due to ischemic leaflet tethering). The Society of Thoracic Surgeons predicted risk of mortality (STS-PROM) cohort score for surgery was 9.4 ± 6.3%.
MR was abolished in all patients following TMVR. There were no significant intraoperative changes in LV end-diastolic pressure, coronary perfusion pressure, central venous pressure, mean pulmonary artery pressure, cardiac index (CI), or mixed venous oxygen saturation (Svo2). Mean ± SD and median baseline values were LV end-diastolic pressure 17.8 ± 4.3 mm Hg, median 17.2 mm Hg; coronary perfusion pressure 39.7 ± 11.8 mm Hg, median 39.4 mm Hg; central venous pressure 15.7 ± 3.8 mm Hg, median 17.0 mm Hg; mean pulmonary artery pressure 32.3 ± 8.6 mm Hg, median 28.0 mm Hg; CI: 1.7 ± 0.5 l/min/m2, median 1.9; and Svo2 78.8 ± 7.2%, median 82.0%. There was an immediate increase in absolute and indexed LVESV following TMVR (absolute LVESV [121 ± 46.2 ml, median 113.2 ml] vs. [144.1 ± 46.3 ml, median 135.9 ml]; p < 0.05), but LVESV returned to baseline such that there was no significant difference between baseline and late post-deployment values. As expected, due to cessation of regurgitant volume, there was a significant reduction in ejection fraction from baseline to immediate and late post-deployment time points (ejection fraction [32.2 ± 10.1%, median 31.0%] vs. [26.9 ± 11.1%, median 26.8%] vs. [24.4 ± 9.2%, median 25.5%]; p < 0.05 at immediate and late time points compared with baseline), but forward stroke volume was preserved throughout (baseline 46.5 ± 18.7 ml, median 41.1 ml). Ees decreased immediately after valve replacement (Ees [0.8 ± 0.5 mm Hg/ml, median 0.6 mm Hg/ml] vs. [0.6 ± 0.3 mm Hg/ml, median 0.5 mm Hg/ml]; p < 0.05) as did Mw (Mw [17.1 ± 6.9 mm Hg, median 14.1 mm Hg] vs. [13.7 ± 6.8 mm Hg, median 12.9 mm Hg]; p < 0.05), but these parameters subsequently stabilized such that there were no significant differences between baseline and late post-deployment values for either measure. Intraoperative pressure–volume changes are summarized in Figure 1.
In a high-risk series, TMVR resulted in acute LV dilatation and reduction in contractility, but these changes returned to baseline after a median time of 17 min. Left and right heart pressures, forward stroke volume, CI, and Svo2 were preserved. The acute hemodynamic effects of TMVR were tolerated and adapted to quickly in this study, the first study to our knowledge of LV hemodynamic responses to mitral valve replacement in the off-pump, beating human heart setting.
The authors thank Mr. Marinos Christofi, St. Vincent’s Hospital, for technical assistance with data recording, and Dr. Zhixin Liu, University of New South Wales, for statistical advice.
Please note: This study was funded in part by Tendyne Holdings LLC, Roseville, Minnesota (a subsidiary of Abbott Vascular, Chicago, Illinois). However, the company had no involvement in study design, data collection or analysis, or manuscript writing. Dr. Namasivayam is supported by an Australian Government Research Training Program Scholarship. Dr. Muller has been an advisory board member for Medtronic and Boston Scientific; has been a consultant to Abbott Vascular, Medtronic, Tendyne Holdings, and Cephea; has received research grant support from Tendyne Holdings, Abbott Vascular, and Medtronic; and is a proctor for Medtronic and Abbott Vascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
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- on behalf of the Tendyne Global Feasibility Trial Investigators
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