Acute Hypotension After MitraClip Implantation due to Acute Left Ventricular Failure

Introduction

The MitraClip (Abbott Vascular, Menlo Park, CA) is a percutaneously implanted device approved for the treatment of symptomatic moderate-to-severe organic mitral regurgitation (MR) in patients at exorbitant risk for open mitral valve (MV) surgery.^1-7 Improved outcomes have been associated with MitraClip use for MR therapy; however, associated hemodynamic changes with the improvement of MR can impart increased work on the left ventricle (LV).^1,8-10 This acute excessive work on a chronically dysfunctional LV can cause cardiovascular deterioration postdeployment.^1,8-10 The expedient diagnosis and treatment of MitraClip-induced acute low cardiac output syndrome, described as afterload mismatch, which can mimic acute mitral stenosis (MS) echocardiographically, may improve patient outcomes.^1,8-10

The authors present a case of acute hypotension after MitraClip implantation due to acute LV failure. The timely and accurate diagnosis of afterload mismatch resulted in rapid hemodynamic correction and successful care of the patient. Written consent was obtained from the patient for the publication of this case report.

Case Report

An 86-year-old female with severe organic MR presented for MitraClip implantation. She was considered too high-risk for conventional MV surgery. A preoperative echocardiogram revealed moderate-to-severe MR due to posterior leaflet (P2) prolapse and an ejection fraction of 30%. On the procedure day, a radial arterial catheter was inserted for hemodynamic monitoring. General anesthesia was then induced uneventfully. A right internal jugular central venous catheter was inserted for additional hemodynamic monitoring and for administration of vasoactive medications. Pre-MitraClip implantation, a transesophageal echocardiogram (TEE) demonstrated severe MR, LV dilatation, and severe LV systolic dysfunction with a 30% to 35% ejection fraction. The MitraClip was implanted under TEE and fluoroscopic guidance to coapt the A2 and P2 segments of the MV leaflets. After successful implantation of the MitraClip, TEE examination revealed a well-positioned and stable MitraClip, significant improvement in the severity of the MR from severe to mild, normal pulmonary venous flow pattern on Doppler echocardiography (systolic flow dominance), and the absence of iatrogenic MS (mean transmitral pressure gradient of 3 mm Hg; normal <5 mm Hg). However, approximately 5 minutes post-MitraClip implantation, the patient became acutely hypotensive (blood pressure of 75/41 mm Hg). TEE examination demonstrated worsening of LV systolic function with an estimated ejection fraction of 15% to 20%, and spontaneous contrast formation in the LV. Spontaneous contrast formation in the left atrium is usually concerning for acute MS; however, a mean transmitral pressure gradient of 3 mm Hg performed immediately after MitraClip implantation allowed us to quickly make the alternative diagnosis of acute LV failure. Inotropic support was rapidly initiated with an epinephrine infusion (0.02 to 0.08 µg/kg/min), which resulted in a remarkable hemodynamic improvement (systolic blood pressure ≥100 mm Hg). The LV function improved using this strategy to achieve an ejection fraction of 30%. Additionally, the spontaneous echo contrast in the left atrium and the LV corrected as the LV contractility improved. The patient was transferred to the intensive care unit with stable hemodynamic parameters postprocedure. In the intensive care unit, a milrinone infusion (0.25 µg/kg/min) was initiated and the epinephrine infusion was subsequently weaned to 0.02 µg/kg/min This treatment strategy was implemented to unload the LV and provide inotropic support concurrently, due to the low cardiac output syndrome. Both inotropes were weaned off the next day. The patient was discharged home a few days later.

Discussion

The MitraClip device has demonstrated excellent safety and effectiveness in the treatment of hemodynamically significant organic MR compared with medical therapy in patients deemed at prohibitive risk for MV surgery.^1-9 As a result, the US Food and Drug Administration recently approved the treatment of MR of organic etiology with the MitraClip. ⁷ Although MitraClip implantation is considered a minimally invasive procedure, it has been associated with major complications including MS, injury to the MV complex, device embolization, cardiovascular injury, bleeding, cardiac tamponade, myocardial ischemia, and hypotension.^1,8 Hypotension after MitraClip deployment can be diagnostically challenging for the anesthesiologist and the culprit pathology needs to be determined in a timely fashion in order to initiate appropriate therapies. Although multiple conditions such as left atrial wall or pulmonary vein injury during transseptal access, cardiac tamponade, MV complex injury, and myocardial ischemia may cause hypotension, current evidence indicates that LV systolic failure and iatrogenic MS are the most common causes of acute hypotension after MitraClip implantation.^1,8,11-14 Identifying the exact cause of hypotension can be challenging, and TEE plays a key role in making an accurate diagnosis. More important, the aforementioned conditions require different treatment strategies: inotropic support for LV failure versus surgical removal of the MitraClip in MS.^1,8 Therefore, rapid differentiation of MitraClip therapy induced MS from LV failure is crucial.

Physiologically, acute MS and acute LV failure after MitraClip placement have subtle differences in presentation. The reduction in EROA (effective regurgitant orifice area) with MitraClip can reduce the mitral valve area as well, causing acute MS.^1,8 This can result in hypotension due to arrhythmia or sudden loss of LV preload (± acute right ventricle [RV] dysfunction). If not treated expeditiously, LV failure can ensue following prolonged hypotension due to coronary malperfusion and myocardial ischemia.^1,8,12,13 Left ventricular systolic failure may subsequently develop from myocardial ischemia if hemodynamic support is not rapidly initiated in patients who develop MS. Echocardiographic findings suggestive of MitraClip-induced MS may include the following: spontaneous echo contrast formation in the left atrium, an increase in mean transmitral pressure gradient, and an empty LV.^1,8 It is important to note that the gradient across the MV has to be measured immediately after the MitraClip is deployed to ensure accurate assessment of MV area. Measuring the MV gradient after the development of LV dysfunction from MS may be inaccurate because LV failure increases diastolic pressures and would cause an overestimation in the MV area (low transmitral pressure gradient).

Concerning LV failure, optimal MR correction may cause an increment in the “effective afterload” of the LV, and may cause acute systolic failure.^1,8-11 Aortic impedance is predominantly composed of arterial systemic vascular resistance and the compliance of the aorta, and this is considered the LV afterload. In the setting of MR, the LA provides a low-pressure/low-resistance relief system that allows the LV to not eject against its true afterload, but a lower “effective” afterload. When the MitraClip is deployed, this acutely eliminates the LA relief system, forcing the LV to acutely eject against its full afterload, resulting in afterload mismatch.^1,8-11 For normally functioning LVs this change in hemodynamic demand is not a concern; however, this becomes problematic for patients with poor systolic LV function. The MitraClip therefore exposes the LV to previously “hidden” afterload. Echocardiographically, the low cardiac output state may cause a spontaneous contrast formation in the left atrium and LV, different from MS. However, the mean gradient across the MV will remain normal in the setting of LV failure.

The patient presented was at an elevated risk for LV failure after optimal MR correction with the MitraClip, due to the preprocedure LV ejection fraction of 30%. Immediately after MitraClip deployment, the mean transmitral pressure gradient was normal and demonstrated the absence of MS; the patient developed hemodynamic instability rapidly thereafter. TEE examination demonstrated deterioration in LV function with a 15% to 20% ejection fraction, and attendant spontaneous echo contrast formation in the left atrium and LV—afterload mismatch. The rapid initiation of inotropic therapy using epinephrine resulted in marked improvement in hemodynamics and LV function. Epinephrine helped improve LV contractility and ejection along with improvements in coronary perfusion pressure, thus making it a good first-line therapy for suspected LV failure due to afterload mismatch. ¹ Strict vasopressor support with phenylephrine or vasopressin would not be advised as this could worsen the LV failure; as such, a correct diagnosis of LV systolic failure rather than acute MS is vitally important to guide pharmacologic therapy. Although epinephrine can augment aortic pressure, this is often outweighed by the benefit of having improved LV and RV contractile support. ¹ Furthermore, in the setting of significant hypotension, epinephrine may help support coronary perfusion pressure as LV contractile function is restored. A milrinone infusion was subsequently added to provide afterload reduction, inotropy, and enabled rapid weaning of the epinephrine infusion. More important, both inotropic agents were weaned off within 24 hours. The LV regained contractile function and the low cardiac output state resolved. The increase in work after the correction of MR requires an inotrope that improves LV contractility. Milrinone and dobutamine may not be the best first-line drugs to administer following acute LV decompensation and hypotension as they can decrease coronary perfusion leading to further deterioration of LV function. The choice of inotrope should factor in the blood pressure at the time of therapy; if the patient is severely hypotensive, epinephrine may be a better choice to ensure adequate coronary perfusion while increasing LV contractility. Administering dobutamine or milrinone for afterload mismatch treatment in a hypotensive patient can lead to catastrophic hypotension.

Summary

MitraClip therapy has been shown to be both safe and efficacious, but can acutely cause hemodynamic instability in the setting of LV dysfunction. Promptly distinguishing afterload mismatch from MS, using echocardiography, and the treatment of afterload mismatch with inotropic support can affect patient outcomes. As MitraClip use continues to expand, clinicians should be aware of the presentation and treatment of afterload mismatch.