Abstract
Transcatheter aortic valve replacement (TAVR) is becoming the standard of care in the management of severe aortic stenosis for patients in all risk stratifications. Many causes have been identified for acute drop in blood pressure during TAVR. Mitral regurgitation (MR) is a rare, but important acute intraprocedural complication that requires rapid assessment and treatment. Two important reasons for acute MR during TAVR include entanglement of the guide wire in papillary muscles and extension of the guidewire into the left atrium. Here, we report a case of acute reversible MR which was assessed using an echocardiogram and rapidly reversed by removing the stiff preshaped Safari2 wire from the left ventricle post valve deployment.
Keywords: interventional cardiology, valvar diseases, radiology (diagnostics)
Background
Over the past decade, transcatheter aortic valve replacement (TAVR) has become the standard of care for the treatment of severe aortic stenosis (AS) in both low risk and high-risk patients because of its minimal invasiveness and good short-term and mid-term outcomes.1 2 With the increased use of this procedure, various complications are being noted. Prompt assessment and treatment of these complications are essential for the success of the procedure and the survival of the patient. We would like to discuss a unique complication of TAVR and elucidate the strategy used to manage the patient.
Case presentation
A 78-year-old woman was referred to the cardiology clinic with worsening shortness of breath and increasing exercise intolerance. She denied exertional chest pain, dizziness, palpitations or syncope. She was diagnosed with mild AS 6 years ago, which gradually worsened to severe AS. She had a medical history of atrial fibrillation treated with ablation 5 years ago, type 2 diabetes mellitus, essential hypertension, hypothyroidism, hyperlipidaemia, obstructive sleep apnea and major depression. On physical examination, her temperature was 97.3°F, pulse rate was 64 beats/min, blood pressure was 140/66 mm Hg and oxygen saturation was 97% under room air. She had diminished S1, S2, crescendo-decrescendo systolic murmur, 4/6 in intensity, best heard in the right second intercostal space, radiating towards carotid arteries. After the preoperative assessment, the patient was scheduled for the TAVR procedure. During the procedure, the patient had an acute drop in blood pressure to 80/40 mm Hg. To assess the causative factor for the shock a rapid bedside transthoracic echocardiography (TTE) was performed, which showed severe mitral regurgitation (MR) (video 1) that was new and absent preoperatively (video 2).
Video 1.
Video 2.
Investigations
ECG showed sinus bradycardia. TTE showed moderate to severe AS with aortic valve area 1.0 cm2, mean gradient of 26 mm Hg and peak velocity of 3.42 m/s, with a left ventricular ejection fraction 55%–60%. However, it was felt that peak velocity, gradient and aortic valve area were underestimated because of suboptimal echocardiographic images secondary to patient body habitus. The patient subsequently underwent left and right cardiac catheterisation and haemodynamic assessment of the aortic valve, which showed severe AS with a mean transaortic gradient of 44 mm Hg, cardiac output of 3.24 L/min and a calculated valve area of 0.5 cm2. The patient also had non-obstructive plaque involving the mid left anterior descending artery and mid right coronary artery, normal right and left sided filling pressures. The patient was found to have an STS score of 2.6%, on surgical evaluation she was deemed intermediate risk and elective trans-aortic valve replacement (TAVR) was planned. The patient underwent TAVR with a 26 mm Edward Sapien 3 valve via left femoral artery access. The valve was delivered and deployed over a stiff preshaped small Safari wire. Starting immediately before the valve deployment, the patient was observed to have sudden hypotension with a blood pressure level as low as 80/40 mm Hg, and the valve was rapidly deployed. Immediately post deployment, intravenous norepinephrine infusion and vasopressin infusion began augmenting the blood pressure, but only increased the level to 90/50 mm Hg without improvement in haemodynamics. TTE analysis showed moderate to severe MR, which was new, compared with the preprocedural TTE, which showed trace to mild MR. TTE showed that safari guidewire had extended into the left atrium and also entangled in the subvalvular apparatus (video 2).
Differential diagnosis
Acute intraprocedural drop in blood pressure or shock during TAVR can be due to a variety of causes, broadly classified as cardiac and non-cardiac. Cardiac complications include paravalvular leakage, myocardial ischaemia, cardiac tamponade and conduction abnormalities requiring pacemaker placement. A rare cardiac cause of shock includes MR. Some of the non-cardiac complications are bleeding related to vascular access, retroperitoneal bleed.3 An intraprocedural echocardiogram helps to rapidly assess the cardiac causes.
Treatment
Intraprocedural TTE was performed, which showed severe MR. It was quickly recognised that the mechanism behind the acute severe MR was likely due to the interaction of the Safari wire in the LV cavity with the chordae tendineae and impingement of the mitral leaflets because the guidewire extending into left atrium causing acute MR. The Safari wire was retrieved and removed from the LV cavity, following which hypotension was resolved and the blood pressure in the patient acutely elevated to 210/100 mm Hg. Norepinephrine and vasopressin infusions were stopped. Repeat transthoracic echocardiogram showed that with the removal of the wire, the severe MR had resolved (video 3). Over the next few minutes, her blood pressure decreased to 153/59 mm Hg and remained stable in the range of 140/50 to 150/60 mm Hg.
Video 3.
Outcome and follow-up
A TTE was performed 1 day later, which showed trace MR. The blood pressure in the patient remained stable with a reading of 140/60 mm Hg. She was discharged from the hospital 1 day after TAVR. She was followed up in the cardiology clinic 1 week later when metoprolol dose was decreased due to bradycardia, but no other complications were reported.
Discussion
Iatrogenic MR has been reported in percutaneous mitral valvotomy for rheumatic mitral stenosis, intracardiac left ventricular assist devices but less commonly for TAVR.4 In a study reported by López-Aguilera et al, out of 129 patients undergoing TAVR, the incidence of significant MR was noted to be 8.5%. In this study, significant MR was defined as new grade >IIa MR or worsening of pre-existing <IIa grade MR to >IIa grade.5 Another study by Ito et al showed the development of haemodynamically significant MR in 7.8% of 64 patients who underwent TAVR. In this study, haemodynamically significant acute MR was defined as a sudden onset of massive MR with persistent hypotension (systolic blood pressure <80–90 mm Hg or mean arterial pressure 30 mm Hg lower than baseline), a severe reduction in cardiac index (<1.8 L/min/m2 without support or <2.0–2.2 L/min/m2 with support), and adequate or elevated filling pressures.6
MR can cause cardiogenic shock and/or pulmonary oedema and has been noted to be an independent predictor of poor response during TAVR signifying the importance of early detection of the cause.7 Acute MR is often missed in conditions of severe haemodynamic instability, due to equalisation of pressures between left atrium and left ventricle, leading to a soft or absent murmur.4 Transthoracic or transesophageal echocardiogram must be used to help confirm the diagnosis in suspected cases. Intraprocedural TEE is not routinely performed and is only used when a possible complication is suspected, such as haemodynamic instability or appearance of significant mitral or aortic regurgitation on postimplant angiography. TEE has been observed to be superior compared with other studies in detecting TAVR related MR. In the study by López-Aguilera et al, angiography was performed in all cases of TAVR related acute MR, but could not detect their aetiology, while TEE detected the aetiology in all such cases.5
Multiple mechanisms have been observed to cause MR during TAVR. Organic damage to mitral valvular/subvalvular apparatus by the guidewire or prosthetic valve, especially via transapical approach has been noted, although reversible usually within a week. In some cases, direct impingement on the anterior mitral leaflet has been observed to occur due to low implantation of the prosthesis, leading to severe MR, which can be treated by repositioning the valve before releasing.5 Secondary mechanisms leading to MR during TAVR include significant new onset left bundle branch block, systolic anterior motion of mitral valve leaflets, cardiac tamponade and relative myocardial ischaemia induced by right ventricular pacing leading to posterior papillary muscle dysfunction.5 7–9 The use of catecholamines, reduced circulating blood volume, and septal hypertrophy have also been identified as risk factors for acute MR during TAVR.10
Entanglement of the guidewire in the mitral apparatus or protrusion of guidewire into left atrium has been observed to cause malcoaptation of the mitral valve leaflets, leading to acute MR.11 Ito et al reported haemodynamically significant acute MR due to wire entanglement in 7.8% of patients undergoing TAVR. The incidence of this complication may vary depending on the operator experience. Impingement of the oversized guidewire when it extends into the left atrium interferes with the closure of mitral valve leading to acute MR. Oversized wire, calcified mitral apparatus (assessed as Wilkins score) and smaller left ventricular end-systolic diameter (LVESD) have been reported as significant risk factors for development of intraprocedural acute MR.6 In small LVESDs, the chordae tendineae and papillary muscles are close to each other, thus increasing the chances of wire entrapment in sub valvular apparatus or extension of guidewire into left atrium, leading to temporary incomplete closure of mitral valves. This anatomy, along with wire oversizing can contribute to development of reversible acute iatrogenic MR. Calcified mitral leaflets or chordae tendineae can occasionally make it difficult to manoeuvre the guide wire because of decreased capacity to coapt, causing the mitral valves to remain stuck in an open position.
Based on preoperative echocardiography, our patient had a low LVESD of 2.6 cm. Additionally, we used the small 4.2 cm curve-width guidewire. Based on the evidence, using an extra-small guidewire, of 2.9 cm curve-width, may have prevented the interaction of the wire with the mitral subvalvular apparatus and wire would remain in the left ventricular cavity without extending into the left atrium causing acute MR and the sudden drop in blood pressure observed in this patient. These factors make it important to understand the importance of pre-TAVR echocardiogram to identify LVESD, calcification in mitral apparatus, and determining the appropriate size of the guidewire to be used. Performing intraoperative echocardiography is equally important to promptly identify the severity and morphology of mitral regurgitation in patients undergoing TAVR and treat the condition appropriately.
Patient’s perspective.
Following surgery, I was not as tired as I had been previously. I have resumed normal activities such as shopping and have had no pain. Recovery was a breeze, no ill effects from surgery.
Learning points.
Mitral regurgitation (MR) can be seriously exaggerated by various complicated mechanisms during transcatheter aortic valve replacement and should be rapidly assessed and appropriately managed depending on the aetiology.
TEE/transthoracic echocardiography during the procedure can be an important tool to assess the cause of MR.
Preoperative echocardiogram to assess left ventricular end systolic diameter and calcification of mitral apparatus can help predict the risk of MR and suggest the use of a smaller guidewire.
Footnotes
Contributors: SKA, PM, AN and NA were equally involved in managing the patient during the hospitalisation. SKA contributed in acquiring data, analysis and interpretation of data, drafting the case report and revising it critically for important intellectual content. SKA was helped by PM and AN to do all the aforementioned tasks. Final approval of this version was provided by NA. SKA takes the responsibility for the overall content.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed.
Ethics statements
Patient consent for publication
Obtained.
References
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