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CASE REPORT
Year : 2022 | Volume
: 11
| Issue : 1 | Page : 33-35
Migrating obstruction posttranscatheter aortic valve replacement
Ata Firouzi1, Seifollah Abdi1, Mohammad Javad Alemzadeh-Ansari1, Zahra Hosseini1, Tayebe Mohamad Gholizad2, Amir Abdi3, Ehsan Khalilipur1
1 Cardiovascular Intervention Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
2 Rajaie Cardiovascular Medical and Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
3 Student Research Committee Member, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Correspondence Address:
Dr. Ehsan Khalilipur
Cardiovascular Intervention Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran
Iran
Source of Support: None, Conflict of Interest: None
DOI: 10.4103/rcm.rcm_68_21
In tanscatheter aortic valve replacement (TAVR) era, knowing complications related to the procedure guides interventional cardiologist in predicting the obstacles and helps them in manage these infirmities. We describe a case of TAVR which deploying the valve resulted in left ventricle outlet tract (LVOT) obstruction which was perfectly managed pacing and medical therapy.
Keywords: LVOT obstruction, pacemaker, transcatheter aortic valve replacement
Transcatheter aortic valve implantation (TAVI) is substantially superior to medical therapy for inoperable high-risk patients. In addition, it may be beneficial in individuals with a high surgical risk, although TAVI is not inferior to surgery in individuals with moderate risk.[1] Dynamic intraventricular obstruction following TAVI has been observed to be similar to that following surgical aortic valve replacement (SAVR).[2],[3]
We describe a patient who was effectively treated with dual-chamber pacing and medication and then recovered from severe hemodynamic collapse with temporary pacing from the right ventricular (RV) apex.
Case ReportWe assessed a 72-year-old diabetic woman who presented to our clinic with dyspnea (New York Heart Association Functional Class III). Physical examination revealed and confirmed several characteristics of severe aortic valve stenosis, including normal systolic function, concentric mild left ventricular (LV) hypertrophy (11 mm) without sigmoid septum, and a calcified and thick tricuspid aortic valve. The aortic valve area was 0.9 cm2 by the continuity equation and 0.7 cm2 by two-dimensional planimetry, with a peak gradient of 73 mmHg and a mean transvalvular gradient of 46 mmHg, respectively [Figure 1]. There was no evidence of obstruction of the left ventricle outflow tract (LVOTO), systolic anterior mitral (SAM) valve motion, asymmetric septal hypertrophy, or intraventricular gradient. The annular circumference was predicted to be 72 mm and the annular area to be 393 mm2.
Figure 1: Preprocedural echocardiography showing aortic valve area by two-dimensional planimetry and peak aortic valve gradient (a and b). Transcatheter aortic valve replacement steps with final deployment demonstrating the acceptable depth and no paravalvular leakage (c-e). Postprocedural echocardiography showing LVOT gradient with dagger-shaped Doppler trace (f) and patient's chest X-ray (g) with permanent pacemaker implantationA cardiothoracic surgeon determined that the patient was at intermediate risk for conventional surgery (the Society of Thoracic Surgery evaluated the probability of death to be 3.6%), and transfemoral transcatheter aortic valve replacement (TAVR) was recommended. Under general anesthesia, a balloon-expandable Myval prosthetic valve (Meril Life Sciences Pvt Ltd., India) size 23 was implanted. Immediate refractory hypotension occurred following implantation [Figure 1]. Transesophageal echocardiography indicated normal valve function in the absence of aortic regurgitation or early valve thrombosis, and it revealed no paravalvular leak or cusp rupture. A “continuous-wave dagger-shaped” Doppler trace was observed with a peak gradient of 55 mmHg, which is indicative of dynamic LVOT obstruction. Then, LVOT obstruction was discovered as a result of mitral valve SAM caused by severe mitral regurgitation (MR), which was not noticed preprocedurally. Other hypertrophic cardiomyopathy characteristics were not detected. The idealized indexed valve area for the manufacturer-supplied prosthesis was 1.1 cm2/m2. Unlikely, this resulted in the patient's prosthesis being mismatched in this circumstance. Due to the ineffectiveness of the fluid infusion, the patient developed a complete heart block. The LVOT obstruction and MR grade were then eased, followed by temporary pacing at 60 beats/min from the RV apex. The patient's hemodynamics was eventually stabilized, and she was transferred to the intensive care unit and she was subsequently a candidate for permanent pacemaker because of complete heart block [Figure 1].
DiscussionThe development of LVOTO is well documented in the SAVR (post-SAVR) population. Around 15% of individuals undergoing SAVR for aortic stenosis (AS) have been observed to have dynamic intraventricular obstruction.[4] Asymmetrical hypertrophy (septal to ventricular free wall ratio >1.4), small LV diameter, increased basal septal thickness (>15 mm), narrow LVOT (<18 mm), high valve gradients, high ejection fraction, and a ratio of anterior/posterior mitral valve leaflet length <1.3 were all associated with increased risk.[5],[6] There is little information on the mechanism underpinning LVOTO, SAM, and TAVR. Chronic aortic stenosis increases intraventricular pressures, splinting the septum, and inhibiting inward motion. As a result, both midventricular and LVOTO are averted. After AVR, a rapid drop in this LV pressure results in a smaller LVOT area. In addition, increased flow across the LVOT results in a Venturi effect, which draws the anterior mitral valve leaflet into the LVOT through the dynamic obstruction.[7]
Managing the dynamic LVOTO following AVR is challenging. Certain variables, including increasing LV preload with fluid boluses and decreasing LV contractility by weaning inotropes, and increasing beta-blockade, may help minimize obstruction in the acute setting. In addition, dual-chamber pacing has been considered for individuals with severe shock.[6] According to the postulated mechanism, ventricular pacing modifies the activation pattern of myocardial depolarization by initiating ventricular depolarization at the right ventricular apex. Furthermore, pacing-induced left bundle branch block leads the septum to shift away from the front mitral valve leaflet, therefore minimizing dynamic outflow obstruction. The gradient is decreased by maintaining AV synchronization while increasing the LV filling pressure. Thus, when a single RV pacing does not enhance hemodynamics, dual-chamber pacing may be considered.
Due to the potential for additional deterioration of hemodynamics due to LVOT obstruction, bail-out therapy may be necessary for some situations, coupled with concurrent septal myectomy, in high-risk patients undergoing SAVR.[8] Although surgical excision may be impossible in individuals receiving TAVI for their fragility and comorbidities. Alcohol septal ablation is less intrusive than surgical resection. Nonetheless, more than 20% of the individuals may lack proper septal circulation.[3] In addition, alcohol septal ablation requires specialized equipment and trained operators.
Leya et al. claimed success in treating severe LVOT blockage with the implantation of a second self-expanding valve (“valve in valve”). Retaining the radial force at the LVOT may provide a solution for LVOT obstruction.[3] Prophylactic MitraClip (Abbott, Davis, CA, USA) implantation before TAVI has been shown to be beneficial in preventing exacerbation of LVOT obstruction caused by SAM.[9]
Additional research is necessary to demonstrate the efficacy of such novel techniques. It is critical to detect and recognize probable LVOT obstruction, which should be treated after TAVI. Pacing from the RV apex, as well as dual-chamber pacing, provides a less intrusive and realistic therapeutic approach.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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