Ischemic mitral regurgitation (IMR) is a distinct form of valvular disorder, wherein the left ventricular abnormalities arising as a result of coronary artery disease (CAD) are the primary cause of valve dysfunction. Excluding cases of papillary muscle rupture, IMR is a secondary form of mitral regurgitation (MR) characterized by structurally normal leaflets, though with restricted motion and apical tethering causing displacement of the coaptation zone from the mitral annulus toward the apex of the left ventricle, and leading to incomplete systolic closure of the mitral valve [1].
In the study by Ładzinski et al. [2], the authors present compelling evidence that severe MR following acute myocardial infarction (MI) is associated with a statistically significant increase in mortality and major adverse cardiovascular and cerebrovascular events (MACCE) in patients diagnosed with ST-segment elevation MI (STEMI) and non-ST-segment elevation MI (NSTEMI), during 12-month follow-up. Furthermore, severe MR was identified as an independent risk factor of all-cause death [2]. The incidence of severe MR in the current population is unknown. The study evaluated the prevalence and impact on prognosis of severe MR in a cohort of patients presenting with STEMI. Previously published studies also noted the adverse prognosis associated with MR following MI. Notably, Lamas et al. [3] demonstrated that, after a follow-up of 3.5 years, patients with IMR were more likely to experience cardiovascular mortality (29% vs. 12%; P <0.001), severe heart failure (HF) (24% vs. 16%; P = 0.015), and the combined endpoint of cardiovascular mortality, severe HF, or recurrent MI (47% vs. 29%; P <0.001). The presence of MR was an independent predictor of cardiovascular mortality (relative risk [RR], 2.00; 95% confidence interval [CI], 1.28–3.04) [3]. Moreover, Grigioni et al. [4] showed that after 5 years, total and cardiac mortalities for patients with IMR (62 ± 5% and 50 ± 6%, respectively) were higher than for those without IMR (39 ± 6% and 30 ± 5%, respectively) (both P <0.001). In multivariate analysis, independently of all baseline characteristics, the adjusted RRs of total and cardiac mortality associated with the presence of IMR were 1.88; P = 0.003, and 1.83; P = 0.014, respectively [4]. Nonetheless, despite the extensive evidence already available on the poor prognosis associated with IMR, Ładzinski et al. [2] add to the growing body of literature by examining a large patient population (n = 8062) and categorizing them based on the type of myocardial infarction (MI) (STEMI vs. NSTEMI) and focusing solely on severe MR patients.
Interestingly, it is worth noting that in the NSTEMI subgroup, patients with severe MR were more likely to have HF, a previously implanted pacemaker, atrial fibrillation (AF), chronic kidney disease (CKD), and a history of CAD or coronary artery bypass graft (CABG). In the STEMI subgroup, severe MR patients were more likely to be older and have AF. When interpreting outcomes, it is crucial to consider that these variables are likely associated with increased mortality. Nonetheless, even when adjusting for ejection fraction (EF), age, and CKD by multivariate analysis, severe MR remained an independent factor for mortality.
It is important to also highlight the dynamic nature of IMR. Nishino et al. [5] evaluated the course of IMR in MI patients following PCI. They found that degrees of IMR changed in the early and chronic phases after primary PCI. Specifically, MR was identified in 193 of 546 (35%) patients upon arrival at the emergency room. Following PCI, in the acute phase, IMR showed improvement in 63 patients while it worsened in 78 patients. In the chronic phase (6–8 months later), IMR got better in 79 patients, while it got worse in 36 patients [5]. The considerable variability in MR severity makes drawing conclusions more challenging. Furthermore, detailed information on the management of the patients is of utmost importance. Kang et al. [6] compared outcomes in patients with MI and IMR who underwent PCI vs. CABG. For the 45 propensity score-matched pairs, the risk of cardiac events was significantly lower in the surgical group than in the PCI group (hazard ratio [HR], 0.499; 95% CI, 0.251–0.990; P = 0.043), though this was before the era of widespread use of transcatheter edge-to-edge repair (TEER). Compared with patients who underwent CABG alone, event-free survival rates were significantly higher in those who underwent additional mitral annuloplasty [6], suggesting that additional mitral intervention could be beneficial. However, this was disputed by Mihaljevic et al. [7] who found that, in patients with moderate/severe IMR, CABG plus MV annuloplasty reduced postoperative MR and improved early symptoms compared to CABG alone but did not improve long-term functional status or survival.
Data show that revascularization on its own can decrease the severity of ischemic MR in patients experiencing an acute MI, and faster reperfusion time correlates with a more significant reduction in MR severity. However, IMR may persist or even worsen in conjunction with detrimental left ventricular remodeling, even when PCI is successful [8, 9]. Surgical management of IMR is controversial. Some studies suggest that adding mitral annuloplasty to CABG can improve functional capacity, LV reverse remodeling, and reduce MR severity [6, 10]. However, other studies have shown no significant difference in primary or secondary endpoints between CABG with or without mitral valve annuloplasty [7]. Data comparing approaches of MV repair and MV replacement (MVR) for IMR are largely limited to small, non-randomized retrospective studies. The only randomized trial data examining this issue indicated no difference in mortality between MVR and MV repair; however, MVR was consistently associated with higher rates of MR recurrence. Certain echocardiographic features have been reported to predict poor outcomes with MVR and may help refine the selection of the surgical approach for individual patients [11, 12].
TEER and transcatheter mitral valve replacement (TMVR) are emerging, less-invasive methods for treating select patients with chronic mitral regurgitation. However, numerous recent reports have shown that transcatheter mitral valve repair is a viable option to manage acute severe mitral regurgitation and cardiogenic shock, including cases involving papillary muscle rupture [13–15]. Although surgical intervention is typically the primary treatment for acute severe mitral regurgitation, transcatheter repair has been proposed as a “rescue” procedure for patients with worsening condition following PCI [13–15].
Thus, it would be valuable to stratify patients depending on the management (PCI ± TEER or CABG ± mitral annuloplasty/replacement) as outcomes could differ.
Our proposed management for severe MR complicating acute myocardial infarction is presented in Figure 1.
In conclusion, Ładzinski et al.’s [2] study adds valuable insights to our understanding of the impact of severe MR on STEMI and NSTEMI patients. The large patient cohort and stratification based on MI type provide a robust basis for the findings.
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