Afterload Mismatch After Mitral Valve Edge‐to‐Edge Repair: Echocardiographic Evaluation and Clinical Implications

Much discussion has been going on in the recent period about the selection of the patient candidate for mitral transcatheter edge-to-edge repair (M-TEER) procedure. In particular, dilatation and left ventricular systolic dysfunction may lead to futility of the procedure in clinical and prognostic terms; besides, in terms of periprocedural time, it can lead to the lengthening of hospitalization. Strictly procedurally, indeed, a dilated and dysfunctional ventricle may have labile hemodynamic compensation mechanisms, and the clip procedure may reduce the left atrium ventricular venting capacity, leading in the acute setting to an abrupt increase in afterload, leading to acute left ventricular ejection fraction reduction (LVEFR). The hemodynamic mechanisms that lead to this acute systolic dysfunction are only partially known, and in this recent paper, Hashimoto et al. [1] sought to understand what are the changes in hemodynamic parameters after M-TEER, specifically, using noninvasive echocardiographic assessment of ventricular arterial (V/A) coupling, the end systolic elastance (Ees) and arterial elastance (Ea). A significant proportion of patients undergoing M-TEER may experience a LVEFR [2-7]. Recent studies have emphasized the relevance of LVEFR in predicting long-term outcomes after mitral valve TEER. This phenomenon, often referred to as “afterload mismatch,” is thought to result from the immediate loss of the low-resistance regurgitation into the left atrium, leading to a sudden alteration in left ventricular loading. However, clear clinical evidence linking “afterload mismatch” to the development of LVEFR after M-TEER is still lacking. Moreover, predictor of LVEFR in primary mitral regurgitation could be baseline left ventricular ejection fraction (LVEF), left atrial pressure V waves > 30 mm Hg, right ventricular dysfunction, and systolic blood pressure > 120 mm Hg at presentation [6]. Arterial elastance is a measure of the stiffness of the arterial system. It represents the relationship between the pressure in the arteries and the stroke volume. Arterial elastance reflects how much pressure the arterial system exerts for a given volume of blood ejected by the heart. High arterial elastance indicates stiff or less compliant arteries, often seen in conditions like hypertension. End-systolic elastance is a measure of the contractility of the left ventricle, specifically at the end of systole, when the heart has contracted fully. It reflects the ability of the ventricle to generate pressure for a given volume of blood remaining in the ventricle at the end of contraction. End-systolic elastance is a key indicator of ventricular function and contractility, and it can be used to assess the heart's ability to generate pressure. V/A elastance refers to the relationship between the properties of the ventricle and the arteries. It essentially combines the concepts of ventricular elastance and arterial elastance to describe the overall interaction between the heart's pumping function and the resistance of the vascular system. This ratio gives an indication of the efficiency of the heart in pumping blood against the arterial load. The closer this value is to 1, the more coupled and therefore efficient the system is. A higher value suggests that the heart is working harder to pump against the arterial resistance, which could be indicative of increased afterload or a compromised cardiovascular system. Ea and Ees can be calculated noninvasively with the formula of Chen et al. [8]. From a practical point of view, the useful parameters for the calculation of elastance are the measurement of systolic and diastolic pressure and on the echocardiographic side the ejection fraction, stroke volume, pre-ejection time, and total ejection time. Hashimoto et al. [1] retrospectively analyzed serial transthoracic echocardiography studies before and after M-TEER in 49 patients (25 men, average age 81 ± 9 years). Cardiomechanical parameters were evaluated using a modified single-beat method by Chen et al. [8]. LVEFR was defined as a decrease in LVEF of ≥ 5 points post-procedure, observed in 18 patients. Those with LVEFR had a longer hospitalization (5.5 days) compared to those without ARD (4 days, p = 0.031). After improvement in mitral regurgitation, Ea increased from 1.54 ± 0.49 mm Hg/mL to 1.84 ± 0.55 mm Hg/mL (p = 0.004). Linear regression analysis showed a significant correlation between changes in total stroke volume (SV) and changes in Ea (r = 0.614, p < 0.0001). Moreover, the increase in Ea was more pronounced in patients with LVEFR compared to those without LVEFR (0.60 ± 0.73 mm Hg/mL vs. 0.14 ± 0.39 mm Hg/mL, p = 0.006). The data found in this work are very interesting because they open the perspective on the best evaluation of hemodynamics after percutaneous mitral valve repair procedures, especially in already dilated and dysfunctional left ventricles, opening to new evidence which could lead to a better patient selection. As we know, in fact, in recent years so much has been debated about the selection of the candidate patient for M-TEER; in particular the analysis of the COAPT [9] and MITRA-FR [10] trials have brought attention to a selection of the patient at a clinical stage when the ventricle is not too far ahead in terms of dilatation and dysfunction. This obviously, in terms of clinical impact, on hospitalizations and prognosis, however, in light of this evidence, it would be very interesting to analyze the perioperative time, in prospective terms, the impact of hemodynamics and changes in Ea and V/A coupling in patients undergoing mitral valve clipping. In conclusion, the impact of the M-TEER procedure may result in acute LVEFR also conditioned by the loss of atrial ventricular outflow from an already overloaded ventricle. This is evidenced by increased Ea in terms of acute left ventricular overload. In the future, it would be very interesting to prospectively analyze hemodynamic changes and, in particular, the Ea variations, in patients undergoing M-TEER to better understand individual patient behavior in relation to the starting conditions of left ventricular dilatation and systolic dysfunction. The author has nothing to disclose regarding potential conflicts of interest or relationships with industry.