• German Study: Closing iASD After TMVR Leads to Decline in Heart Failure Symptoms at 1 Month

    Closing an iatrogenic atrial septal defect (iASD) following transcatheter mitral valve edge-to-edge repair (TMVR) leads to a volume shift from the right ventricle (RV) to the left ventricle (LV), with a reduction in pulmonary cardiac index but increase in systemic cardiac index and with favorable biventricular interaction at unchanged LV filling pressure, all resulting in a decline in heart failure symptoms at 1-month follow-up, according to a study released Monday.

    Stephan Blazek, MD, of Heart Center Leipzig, University of Leipzig and Leipzig Heart Institute, Germany, and co-investigators reported their findings in a manuscript published in the Jan. 11 issue of JACC: Cardiovascular Interventions.

    Persistent iASD following a transseptal puncture during TMVR is frequently observed. The potential hemodynamic and clinical consequences of an iASD following TMVR are currently subject to controversial debates. The prognostic role of iASD is controversial, and there are only a scarcity of data on if and when to close an iASD and the hemodynamic implications thereof.

    Blazek and colleagues sought to assess the acute hemodynamic effects of iASD closure following TMVR. They performed a single-center retrospective study (Heart Center Leipzig at University of Leipzig) in 21 patients who underwent  percutaneous closure of an iASD following TMVR using the MitraClip system (Abbott Laboratories) between June 2015 and December 2019. These patients had a relevant left-to-right shunt flow (50% [interquartile range: 38% to 60%] of systemic perfusion volume) across an iASD following TMVR. The patients underwent interventional closure, and recordings of LV and RV pressure-volume loops were performed during iASD occlusion.

    The authors’ analysis found that iASD occlusion led to a volume shift from the RV to the LV with reduced RV but increased LV cardiac index. Although RV end-diastolic pressure decreased, LV end-diastolic pressure remained unchanged. LV transmural pressure increased and LV eccentricity index decreased (p < 0.001). The change in LV transmural pressure correlated significantly with the change in LV-to-RV end-diastolic volume ratio (r = 0.674; p = 0.018). Right heart failure symptoms declined at 1-month follow-up (71% vs. 35%; p = 0.003), as did New York Heart Association functional class (≥III: 48% vs. 25%; p < 0.001).

    The authors concluded that successful closure of an iASD following TMVR leads to a volume shift from the RV to the LV, with reduced pulmonary cardiac index and increased systemic cardiac index, and is associated with a favorable biventricular interaction at unchanged LV filling pressure, resulting in a decline in heart failure symptoms at 1-month follow-up.

    Limitations included the analysis being a single-center study and retrospective in nature. In addition, the follow-up was short term and, overall, a relatively small sample size. Thus, the interpretation of results and conclusions should be considered only hypothesis-generating. Prospective randomized clinical trials would determine whether the beneficial hemodynamic effects of iASD closure translate into long-term improved outcomes and symptom amelioration.

    Accompanying this study was an editorial from Jeffrey S. Borer, MD, State University of New York Downstate Health Sciences University. He was cautious, outlining the study’s limitations.

    Furthermore, he stated: “Taken together, these considerations indicate that Blazek’s conclusions may be slightly premature, i.e., there remain important gaps in our knowledge of the natural history of myocardial function after TMVR to enable firm conclusions about whether and when to close iASDs created during catheter-based repair of MR. A relatively large, carefully designed randomized controlled trial with clinical outcomes as endpoints will be needed and, with the increasing application of TMVR, the importance of such a trial is increasing. The anticipated report of the MITHRAS trial will be very important in this regard.”

     

    Sources:

    Blazek S, Unterhuber M, Rommel K-P, et al. Biventricular Physiology of Iatrogenic Atrial Septal Defects Following Transcatheter Mitral Valve Edge-to-Edge Repair. JACC Cardiovasc Interv 2021;14:54–66.

    Borer JS. Iatrogenic Atrial Septal Defect after Mitral Valve Repair for Mitral Regurgitation: To Close or Not to Close – That is the Question. JACC Cardiovasc Interv 2021 Jan 4 (Article in press).

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