A Case Report of Hypertrophic cardiomyopathy and ventricular suicide: The danger of abrupt afterload reduction

A Case Report of Hypertrophic cardiomyopathy and ventricular suicide: The danger of abrupt afterload reduction | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report A Case Report of Hypertrophic cardiomyopathy and ventricular suicide: The danger of abrupt afterload reduction Kirtivardhan Vashistha, Akshat Banga, Ramzi Khalil, Jian Hu, Pietro Bajona, and 6 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5259342/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 01 Jun, 2025 Read the published version in The Egyptian Heart Journal → Version 1 posted 5 You are reading this latest preprint version Abstract Background We describe a patient with severe aortic stenosis (AS) developing obstructive shock immediately following transcatheter aortic valve replacement (TAVR) secondary to a unique phenomenon termed “ventricular suicide.” Abrupt withdrawal of chronically high afterload may lead to mid-ventricular systolic collapse +/- left ventricular outflow tract (LVOT) obstruction in the setting of hyperdynamic contractility, as seen in hypertrophic cardiomyopathy (HCM). Case Presentation An 88-year-old male with severe symptomatic AS presented with worsening dyspnea. Given his high surgical risk and frailty, he underwent TAVR. The patient had a history of persistent atrial fibrillation, hypertension, hyperlipidemia, prior cerebellar stroke, and severe AS. Post-TAVR, he experienced a significant blood pressure drop, leading to shock. Investigations revealed hyperdynamic left ventricular (LV) function, cavitary obliteration, and systolic anterior motion of the mitral valve. Management included intravenous fluids and phenylephrine, which stabilized his condition. He was discharged on a beta-blocker and remained asymptomatic with a normally functioning TAVR prosthesis one month post-discharge. Conclusion HCM and its phenocopies are associated with worse outcomes post-TAVR. Prophylactic beta-blockade and hydration may prevent hemodynamic collapse in patients with anatomic substrates for ventricular suicide. Hypertrophic cardiomyopathy left ventricular outflow tract obstruction TAVR Aortic stenosis ventricular suicide Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 LEARNING OBJECTIVES Identification of patients who may present with HCM-like physiology. To understand the physiology of obstructive shock in patients post-TAVR procedure. Outline the management of shock or “ventricular suicide” in post-TAVR patients. BACKGROUND Transcatheter aortic valve replacement (TAVR) has become a widely accepted treatment for patients with severe symptomatic aortic stenosis (AS), especially those at high surgical risk due to advanced age or comorbidities ( 1 ). However, despite the procedural benefits, TAVR can lead to unexpected complications, including a rare and critical condition termed "ventricular suicide” ( 2 ). This phenomenon is characterized by an abrupt drop in afterload, leading to mid-ventricular systolic collapse and possibly left ventricular outflow tract (LVOT) obstruction ( 3 ), particularly in patients with hypertrophic cardiomyopathy (HCM) or HCM-like physiology ( 4 ). HCM, a condition characterized by left ventricular (LV) hypertrophy without another causative cardiac or systemic condition, can present challenges during and after TAVR. When the chronically high afterload imposed by AS is suddenly relieved, the hyperdynamic contractile state of the hypertrophied left ventricle can precipitate severe hemodynamic instability ( 5 ). This instability is exacerbated by factors such as small ventricular cavity size, severe concentric hypertrophy, and systolic anterior motion (SAM) of the mitral valve, leading to dynamic LVOT obstruction and the potential for obstructive shock ( 6 ). In this case report, we present an 88-year-old male with severe AS who developed obstructive cardiogenic shock and hemodynamic collapse immediately following TAVR due to "ventricular suicide" and was found to have hyperdynamic LV function, cavitary obliteration, and SAM of the mitral valve, consistent with HCM. CASE PRESENTATION History of Presentation An 88-year-old male with severe symptomatic aortic stenosis (AS) presented with worsening exertional dyspnea and progressive fatigue over several weeks. On initial assessment, his vitals were: blood pressure (BP) 138/76 mmHg, heart rate (HR) 78 bpm (irregularly irregular due to atrial fibrillation), respiratory rate (RR) 18 breaths per minute, and oxygen saturation (SpO₂) 96% on room air. Physical examination revealed a frail-appearing male with a 3/6 harsh mid-systolic murmur at the upper right sternal border radiating to the neck. Given his high surgical risk, frailty, and worsening symptoms, he was deemed not a candidate for surgical valve replacement and was scheduled for an elective TAVR. Past medical history The patient had a past medical history of persistent atrial fibrillation, hypertension, hyperlipidemia, prior cerebellar stroke, and severe AS. Differential diagnosis The differential diagnosis for shock following the TAVR procedure included acute coronary syndrome, heart failure with preserved ejection fraction exacerbation, acute pulmonary embolism, and hypertrophic cardiomyopathy with acute shock from LVOT obstruction. Investigations Prior to undergoing the TAVR procedure, an electrocardiogram (EKG) showed chronic atrial fibrillation with a left bundle branch block. A transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 60–64%, grade III diastolic dysfunction, severe AS with a valve area 0.9 cm 2 , mean AV gradient (AVG) 37 mmHg, AV peak velocity 3.99 m/s, and trace aortic regurgitation (Fig. 1 ). There was severe concentric hypertrophy (basal anteroseptal segment 19 mm; a posterior wall of 18 mm) and a small LV cavity (LVEDD 35 mm). Cardiac catheterization revealed hemodynamic parameters of AO pressure 135/73 mmHg (mean 97 mmHg), LV pressure 178/5 mmHg with a left ventricular end-diastolic pressure (LVEDP) of 14 mmHg, and a peak-to-peak gradient of 56 mmHg between the LV and AO (Fig. 2 ) . The calculated body surface area was 1.82 m², with an estimated O₂ consumption of 242.3%. Computed tomography showed an Agatston valve score of 4,963, and coronary angiography demonstrated mild-to-moderate nonobstructive coronary artery disease. The patient underwent an elective TAVR placement with Edward Sapien Ultra 26 mm valve. The hemodynamic profile following valve implantation showed an interval decrease in mean AVG from 56 mmHg to 6 mmHg while LVEDP remained stable around 12–14 mmHg. There was no significant gradient between the LVOT and ascending aorta (Figs. 2 and 3 ). Immediately following valve deployment, the patient developed hypotension with BP dropping from 135/73 mmHg to 86/42 mmHg. Heart rate increased to 120–130 bpm, and he became increasingly agitated with increased respiratory rate and worsening dyspnea. Intra-procedural echocardiography demonstrated a well-seated valve prosthesis with normal leaflet motion and no transvalvular or significant paravalvular aortic regurgitation. There was hyperdynamic LV function with cavitary obliteration, worsened mitral regurgitation, and new SAM of the mitral valve (Fig. 4 , Video 1 and 2 ). Invasive LV pressure tracing showed the Brockenbrough-Braunwald-Morrow sign with a peak-to-peak gradient of 25 mmHg (Fig. 3 ). The gradient was thought to be intraventricular with no significant LVOT obstruction based on a peak LVOT gradient of 10 mmHg ( Fig. 5 ). Laboratory evaluation during the shock phase revealed early signs of end-organ hypoperfusion. Serum creatinine increased from 1.2 mg/dL pre-procedure to 1.8 mg/dL post-TAVR. Serum lactate was elevated at 3.8 mmol/L, liver enzymes were mildly elevated, with an AST of 80 U/L and ALT of 70 U/L, and urine output decreased to 0.3 mL/kg/hr. Clinically, the patient appeared lethargic and disoriented. To rule out coronary obstruction as a potential cause of post-TAVR hemodynamic collapse, a coronary angiogram was performed intraoperatively and demonstrated no evidence of coronary ostial compromise from valve deployment. This evaluation was preceded by careful preprocedural CT planning, which guided optimal valve sizing and confirmed adequate coronary ostial height, thereby reducing the procedural risk of coronary obstruction. Additionally, there were no dynamic ST-T changes on intraoperative ECG, and TTE revealed a hyperdynamic left ventricle with no regional wall motion abnormalities. No valvular or paravalvular regurgitation was observed. Rather, findings of SAM severe hyperdynamic ejection fraction, and intracavitary obliteration were noted, consistent with dynamic midventricular obstruction rather than ischemic collapse. Management Given the LV systolic collapse following acute afterload reduction, the patient was promptly managed with 1.5L of intravenous fluids and was initiated on phenylephrine infusion. His blood pressure, which had dropped to 80/50 mmHg, subsequently improved to 110/65 mmHg. Heart rate decreased from 120–130 bpm to 80–90 bpm, and peripheral perfusion improved. With fluid resuscitation and vasoconstrictor support, urine output improved to > 0.5 mL/kg/hr, liver enzymes normalized, and serum lactate trended down to 1.8 mmol/L gradually. The patient was successfully weaned off phenylephrine within 24 hours, maintaining stable hemodynamics and organ perfusion. Follow up He was discharged on a beta-blocker aimed at decreasing the heart rate and increasing ventricular filling time. A follow-up TTE one month later revealed a normal LVEF (55–60%), improved diastolic function (grade I), and a well-seated bioprosthetic aortic valve with normal leaflet motion. Aortic valve Doppler measurements showed a peak velocity of 2.1 m/s, mean gradient of 8 mmHg, and calculated aortic valve area (AVA) of 1.4 cm². The patient remained asymptomatic with no signs of recurrent obstruction or heart failure. DISCUSSION Ventricular suicide is a rare but potentially life-threatening complication following TAVR, particularly in patients with underlying HCM or HCM-like physiology. This case report aims to emphasize the importance of preoperative risk stratification to identify patients at risk, recognizing predisposing factors, and implementing targeted management strategies to mitigate hemodynamic instability. In this case, an 88-year-old male with severe AS developed obstructive cardiogenic shock immediately following TAVR due to abrupt afterload reduction. The resultant hyperdynamic left ventricular function, cavitary obliteration, and SAM of the mitral valve led to hemodynamic collapse. Prompt recognition and hemodynamic optimization, including volume expansion, vasoconstrictor support, and heart rate modulation, are essential to preventing severe complications. TAVR is a widely accepted treatment for severe symptomatic AS, particularly in patients with advanced age, suboptimal surgical risk, and underlying LV dysfunction ( 7 ). However, its associated complications include coronary occlusion, heart block, device embolization, LV perforation and tamponade, aortic dissection, aortic regurgitation, and ventricular suicide ( 8 ). The rare phenomenon of ventricular suicide results from acute afterload reduction in a predisposed hypertrophic LV with a small cavity, leading to cardiovascular collapse due to dynamic intraventricular gradients ± LVOT obstruction ( 9 ). Risk factors include hyperdynamic ventricular systolic function, a small, obliterated LV cavity due to hypertrophy, asymmetrical septal thickening leading to HCM-like physiology, narrowed LVOT, anterior mitral leaflet displacement, and elevated baseline LVOT gradients ( 10 ). A sudden reduction in afterload post-TAVR can precipitate a hyperdynamic state, inducing the Venturi effect on the anterior mitral leaflet and leading to acute hemodynamic collapse. Post-TAVR systolic obstruction is usually midventricular due to concentric hypertrophy secondary to chronic pressure overload in AS ( 11 ). Some patients may have underlying HCM or develop HCM-like physiology due to chronic pressure overload, resulting in a septal bulge and SAM of the anterior mitral leaflet ( 12 ). Ventricular suicide physiology is often anticipated based on the presence or absence of baseline LVOT obstruction, severe basal LV hypertrophy (LVH), a long anterior mitral valve leaflet, or evidence of SAM. Preprocedural assessment is therefore critical in identifying patients at risk. While the majority of such patients can be managed conservatively with preload optimization, beta-blockers, and non-dihydropyridine calcium channel blockers ( 13 ), alcohol septal ablation (ASA) may be considered in select cases with significant baseline LVOTO. ASA, typically reserved for patients with demonstrable obstruction prior to TAVR, reduces septal thickness and LVOT gradients but carries procedural risks such as complete heart block and the need for permanent pacemaker implantation ( 14 , 15 ). In our case, the patient did not exhibit LVOTO or intraventricular gradients on preprocedural imaging. The gradient that developed post-deployment was intraventricular rather than subaortic, and thus not amenable to ASA. However, for patients who develop refractory obstructive physiology post-TAVR despite optimal medical management, urgent ASA remains a viable intervention to relieve dynamic obstruction and restore hemodynamic stability. Treatment of ventricular suicide is aimed at increasing diastolic filling time and expanding the LV cavity. Initial management involves beta-blockers to slow the heart rate and improve ventricular filling, along with intravenous fluids to maintain preload. Vasoconstrictors such as phenylephrine are beneficial in increasing afterload and stabilizing LV end-diastolic pressure ( 16 ). Our case had an underlying conduction defect (LBBB) and may have also benefited from prophylactic transvenous pacing post-TAVR to mitigate LVOT gradients. HCM is strongly associated with senile calcific AS and has been linked to higher in-hospital mortality and post-TAVR complications ( 17 ). Olsen et al. reported a case of hemodynamic collapse in a 56-year-old male with undiagnosed HCM undergoing TAVR, where intraoperative transesophageal echocardiography revealed SAM of the anterior mitral valve leaflet and asymmetric septal hypertrophy. Similar to our case, the patient experienced acute hemodynamic deterioration following valve deployment, attributed to unrecognized dynamic obstruction, though specific details of end-organ hypoperfusion were not reported. They noted that in patients with severe AS, the high LV afterload and arterial impedance often mask subvalvular gradients, making the condition difficult to detect preoperatively ( 18 ). Another case by Suh et al. described an 82-year-old woman undergoing TAVR who developed obstructive shock due to SAM and asymmetric septal hypertrophy (29). Both cases share key physiologic features with our patient, including septal hypertrophy, hyperdynamic left ventricular function, and SAM-induced obstruction, and like ours, they were managed with intravenous fluids, beta-blockers, and vasoconstrictors to stabilize hemodynamics. Collectively, these cases highlight the need for vigilant pre-procedural risk assessment for latent obstruction and emphasize the importance of rapid recognition and hemodynamic management to prevent life-threatening outcomes following TAVR. CONCLUSION This case report highlights ventricular suicide as a rare but critical complication following TAVR in a patient with severe AS and HCM. Abrupt afterload reduction led to mid-ventricular systolic collapse, hyperdynamic left ventricular function, and obstructive shock. Prompt recognition and intervention were crucial in stabilizing our patient following hemodynamic collapse post-TAVR. Immediate management with intravenous fluids and phenylephrine effectively restored hemodynamic stability, preventing further deterioration, and beta-blockade was initiated to prevent recurrence. Given the predisposition of HCM and its phenocopies to adverse outcomes post-TAVR, identifying high-risk patients preoperatively is essential. Preemptive strategies such as echocardiographic assessment for small left ventricular cavity size, pre-existing SAM, and latent LVOT obstruction should be incorporated into preprocedural planning. In high-risk patients, prophylactic measures such as preoperative beta-blockade, volume loading, and consideration of temporary pacing to reduce LVOT gradient may prevent post-TAVR hemodynamic collapse and ventricular suicide. Abbreviations Aortic Stenosis – AS Transcatheter Aortic Valve Replacement – TAVR Left Ventricular Outflow Tract Obstruction – LVOT Electrocardiogram – EKG Transthoracic Echocardiography – TTE Alcohol Septal Ablation – ASA Declarations Ethics approval and consent to participate We confirm that the ethical approval for the study was waived by the International Review Board. Consent for publication Written informed consent was obtained from the patient’s parents for the publication of this case report and accompanying images. Funding The authors report no involvement in the research by the sponsor that could have influenced the outcome of this work. Author Contribution Kirtivardhan Vashistha worked towards conception and manuscript drafting. Akshat Banga, Ramzi Khalil, Jian Hu, Pietro Bajona, Jennifer Keeley, Srinivas Murali, Craig Alpert, Robert Biederman, and Victor Farah worked toward drafting the manuscript. Vinh Nguyen was responsible for the conception, revising the manuscript critically for important intellectual content, and approval of the manuscript submitted. Acknowledgement Not applicable References Lindman BR, Alexander KP, O’Gara PT, Afilalo J. Futility, Benefit, and Transcatheter Aortic Valve Replacement. JACC Cardiovasc Interv. 2014;7:707–16. https://doi.org/10.1016/j.jcin.2014.01.167 . Koliastasis L, Drakopoulou M, Latsios G, Apostolos A, Ktenopoulos N, Katsaros O, et al.. Overcoming the Obstacle of Suicide Left Ventricle After Transcatheter Aortic Valve Replacement Phenomenon. 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Catheterization and Cardiovascular Interventions 2010;76:616–20. https://doi.org/10.1002/ccd.22609 . Additional Declarations No competing interests reported. Supplementary Files Video1.mp4 Video 1-Baseline 3 chamber view cine Video2.mp4 Video 2 -Post TAVR parasternal long-axis view Angio1.mov Angio2.mov Angio3.mov Angio4.mov Cite Share Download PDF Status: Published Journal Publication published 01 Jun, 2025 Read the published version in The Egyptian Heart Journal → Version 1 posted Editorial decision: Accepted 11 May, 2025 Reviewers agreed at journal 30 Apr, 2025 Reviewers invited by journal 28 Apr, 2025 Submission checks completed at journal 28 Apr, 2025 First submitted to journal 26 Apr, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-5259342","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":449341513,"identity":"8dd103e0-6c1d-4757-a91b-941bdd4631cc","order_by":0,"name":"Kirtivardhan Vashistha","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA+0lEQVRIie3PMWrDMBSAYQmBvcidX3GhV7AxhIam6Co2hk7uFYpAoCxq53TKLUJHG4GnHCBBl7C3uGSobLp0qJVuheofHjx43/AQ8vn+YEltB+aAEGBed3YJQgdJ+RehQJpmMxLiIBmaCLIkKDUdNxdZQJX2w/sdY7FK9Opjd3tFEO766meygiqLoz0U6maf6KdXk0qCyPXbbobQNo+xhJxCZYky2JKARDNkQdtyGCSwiSyVYU6ShaKFSAJW8JhrdDKFk6Rr0d5bUqhDWTcv3JSSYDH7S6KxOA7ymYWbQnSns3nYrkXT9TPke1hOk196P3b+zbHP5/P9lz4BbGpRE/XQ4CYAAAAASUVORK5CYII=","orcid":"","institution":"Mount Sinai Morningside","correspondingAuthor":true,"prefix":"","firstName":"Kirtivardhan","middleName":"","lastName":"Vashistha","suffix":""},{"id":449341514,"identity":"8482bc1e-850b-4587-ac1b-26487e2b5ff6","order_by":1,"name":"Akshat Banga","email":"","orcid":"","institution":"Mount Auburn Hospital","correspondingAuthor":false,"prefix":"","firstName":"Akshat","middleName":"","lastName":"Banga","suffix":""},{"id":449341515,"identity":"66c124c2-a840-4600-92d1-038f2420035f","order_by":2,"name":"Ramzi Khalil","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Ramzi","middleName":"","lastName":"Khalil","suffix":""},{"id":449341516,"identity":"f62509ca-c84f-4047-a950-727d2c084f59","order_by":3,"name":"Jian Hu","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Jian","middleName":"","lastName":"Hu","suffix":""},{"id":449341517,"identity":"5a70ebcf-1c8b-4ade-8732-23d3e28bd8bd","order_by":4,"name":"Pietro Bajona","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Pietro","middleName":"","lastName":"Bajona","suffix":""},{"id":449341518,"identity":"ba0e651c-d1c1-400d-84ec-2fd2a6753a56","order_by":5,"name":"Jennifer Keeley","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Jennifer","middleName":"","lastName":"Keeley","suffix":""},{"id":449341519,"identity":"8cb4afe4-0a4e-4cfc-8014-0a15209265a0","order_by":6,"name":"Srinivas Murali","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Srinivas","middleName":"","lastName":"Murali","suffix":""},{"id":449341520,"identity":"f0771343-cb1d-49ae-9764-52b31f6f4c90","order_by":7,"name":"Craig Alpert","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Craig","middleName":"","lastName":"Alpert","suffix":""},{"id":449341526,"identity":"4f5ca0d5-ed0a-46b0-9cfd-747d8eff9fd0","order_by":8,"name":"Robert Biederman","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Robert","middleName":"","lastName":"Biederman","suffix":""},{"id":449341528,"identity":"77a6f661-0859-4343-b5fc-fffb2f9f3db6","order_by":9,"name":"Victor Farah","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Victor","middleName":"","lastName":"Farah","suffix":""},{"id":449341530,"identity":"d7e73dae-6a5e-4091-95f4-16c729b4d7ad","order_by":10,"name":"Vinh Nguyen","email":"","orcid":"","institution":"Allegheny General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Vinh","middleName":"","lastName":"Nguyen","suffix":""}],"badges":[],"createdAt":"2024-10-14 08:23:28","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-5259342/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-5259342/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s43044-025-00650-2","type":"published","date":"2025-06-01T15:57:57+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":82030880,"identity":"43f6e265-cb43-4d2d-8bc4-15820affa155","added_by":"auto","created_at":"2025-05-06 07:19:07","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":537704,"visible":true,"origin":"","legend":"\u003cp\u003eBaseline LVOT spectral Doppler showing late peaking Doppler waveform (left). Transaortic continuous Doppler indicates severe aortic stenosis by peak velocity 399 cm/s.\u003c/p\u003e","description":"","filename":"Figure1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/afe12df769e3e52ebd1997eb.jpg"},{"id":82029972,"identity":"c4c3282c-7ce7-4a8d-a4cd-771e3b21ced7","added_by":"auto","created_at":"2025-05-06 07:11:07","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":156359,"visible":true,"origin":"","legend":"\u003cp\u003eInvasive hemodynamic tracing pre-TAVR demonstrating elevated LV-Ao gradient consistent with severe aortic stenosis.\u003c/p\u003e","description":"","filename":"Figure2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/99a79da02de4cfebab910e53.jpg"},{"id":82029971,"identity":"cd2bef15-2f97-4000-bf8b-3517015de4e8","added_by":"auto","created_at":"2025-05-06 07:11:07","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":120889,"visible":true,"origin":"","legend":"\u003cp\u003ePost-TAVR\u003cstrong\u003e \u003c/strong\u003eInvasive LV pressure tracing showed the Brockenbrough-Braunwald-Morrow sign with a peak-to-peak pressure ~25 mmHg.\u003c/p\u003e","description":"","filename":"Figure3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/4460dc0f6a567a3ce023a37c.jpg"},{"id":82029980,"identity":"e5da9210-0962-4073-9d94-697cb6241b3e","added_by":"auto","created_at":"2025-05-06 07:11:07","extension":"jpg","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":408809,"visible":true,"origin":"","legend":"\u003cp\u003eStatic systolic frame showing baseline trace mitral regurgitation (left) and moderate-severe 3+ mitral regurgitation (right).\u003c/p\u003e","description":"","filename":"Figure4.jpg","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/a5277e7954475c2b83e02d1f.jpg"},{"id":82030884,"identity":"27d0e720-cf7d-4606-ab13-36b1027d6370","added_by":"auto","created_at":"2025-05-06 07:19:07","extension":"jpg","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":73971,"visible":true,"origin":"","legend":"\u003cp\u003eContinuous Doppler showed no significant LVOT obstruction. The peak and mean LVOT gradient were 10 mmHg and 5 mmHg, respectively.\u003c/p\u003e","description":"","filename":"Figure5.jpg","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/8177dbae558c8bd221423a5a.jpg"},{"id":83783656,"identity":"9dfe9dc5-fedd-450e-a254-8833536827a4","added_by":"auto","created_at":"2025-06-02 16:12:21","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1811663,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/2e5fb481-a152-4d55-8a79-502bbdee60ff.pdf"},{"id":82032097,"identity":"491d928e-6e1f-40eb-ac0f-7fa0c17d4518","added_by":"auto","created_at":"2025-05-06 07:27:07","extension":"mp4","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":1722219,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eVideo 1-\u003c/strong\u003eBaseline 3 chamber view cine\u003c/p\u003e","description":"","filename":"Video1.mp4","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/bfcee873b60b48a428418398.mp4"},{"id":82032100,"identity":"4d7209ad-7951-47ed-9ecc-f80880c8108c","added_by":"auto","created_at":"2025-05-06 07:27:07","extension":"mp4","order_by":2,"title":"","display":"","copyAsset":false,"role":"supplement","size":1863863,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eVideo 2 -\u003c/strong\u003ePost TAVR parasternal long-axis view\u003c/p\u003e","description":"","filename":"Video2.mp4","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/d602bca03f9129e9c411c5f0.mp4"},{"id":82030888,"identity":"bd2e4ade-4802-4046-aef9-08fa9de652f2","added_by":"auto","created_at":"2025-05-06 07:19:07","extension":"mov","order_by":3,"title":"","display":"","copyAsset":false,"role":"supplement","size":3393365,"visible":true,"origin":"","legend":"","description":"","filename":"Angio1.mov","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/48c84f804bebe98ebc468c36.mov"},{"id":82030899,"identity":"51a7d492-c47d-4a63-939c-b525b13cbc91","added_by":"auto","created_at":"2025-05-06 07:19:07","extension":"mov","order_by":4,"title":"","display":"","copyAsset":false,"role":"supplement","size":2619443,"visible":true,"origin":"","legend":"","description":"","filename":"Angio2.mov","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/f93c3f74b99fea8c3b6fd140.mov"},{"id":82030898,"identity":"87470099-1232-49c5-ae2c-caef048876d9","added_by":"auto","created_at":"2025-05-06 07:19:07","extension":"mov","order_by":5,"title":"","display":"","copyAsset":false,"role":"supplement","size":5373532,"visible":true,"origin":"","legend":"","description":"","filename":"Angio3.mov","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/4def7e8736668e296a83a219.mov"},{"id":82032102,"identity":"6ada6b11-6264-4eb2-99ac-cacff30445bc","added_by":"auto","created_at":"2025-05-06 07:27:07","extension":"mov","order_by":6,"title":"","display":"","copyAsset":false,"role":"supplement","size":4954591,"visible":true,"origin":"","legend":"","description":"","filename":"Angio4.mov","url":"https://assets-eu.researchsquare.com/files/rs-5259342/v1/f63c18faac6e4fe552338857.mov"}],"financialInterests":"No competing interests reported.","formattedTitle":"A Case Report of Hypertrophic cardiomyopathy and ventricular suicide: The danger of abrupt afterload reduction","fulltext":[{"header":"LEARNING OBJECTIVES ","content":"\u003cul\u003e\n \u003cli\u003eIdentification of patients who may present with HCM-like physiology.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eTo understand the physiology of obstructive shock in patients post-TAVR procedure.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eOutline the management of shock or \u0026ldquo;ventricular suicide\u0026rdquo; in post-TAVR patients.\u0026nbsp;\u003c/li\u003e\n\u003c/ul\u003e"},{"header":"BACKGROUND","content":"\u003cp\u003eTranscatheter aortic valve replacement (TAVR) has become a widely accepted treatment for patients with severe symptomatic aortic stenosis (AS), especially those at high surgical risk due to advanced age or comorbidities (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). However, despite the procedural benefits, TAVR can lead to unexpected complications, including a rare and critical condition termed \"ventricular suicide\u0026rdquo; (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). This phenomenon is characterized by an abrupt drop in afterload, leading to mid-ventricular systolic collapse and possibly left ventricular outflow tract (LVOT) obstruction (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e), particularly in patients with hypertrophic cardiomyopathy (HCM) or HCM-like physiology (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eHCM, a condition characterized by left ventricular (LV) hypertrophy without another causative cardiac or systemic condition, can present challenges during and after TAVR. When the chronically high afterload imposed by AS is suddenly relieved, the hyperdynamic contractile state of the hypertrophied left ventricle can precipitate severe hemodynamic instability (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). This instability is exacerbated by factors such as small ventricular cavity size, severe concentric hypertrophy, and systolic anterior motion (SAM) of the mitral valve, leading to dynamic LVOT obstruction and the potential for obstructive shock (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn this case report, we present an 88-year-old male with severe AS who developed obstructive cardiogenic shock and hemodynamic collapse immediately following TAVR due to \"ventricular suicide\" and was found to have hyperdynamic LV function, cavitary obliteration, and SAM of the mitral valve, consistent with HCM.\u003c/p\u003e"},{"header":"CASE PRESENTATION","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eHistory of Presentation\u003c/h2\u003e \u003cp\u003eAn 88-year-old male with severe symptomatic aortic stenosis (AS) presented with worsening exertional dyspnea and progressive fatigue over several weeks. On initial assessment, his vitals were: blood pressure (BP) 138/76 mmHg, heart rate (HR) 78 bpm (irregularly irregular due to atrial fibrillation), respiratory rate (RR) 18 breaths per minute, and oxygen saturation (SpO₂) 96% on room air.\u003c/p\u003e \u003cp\u003ePhysical examination revealed a frail-appearing male with a 3/6 harsh mid-systolic murmur at the upper right sternal border radiating to the neck. Given his high surgical risk, frailty, and worsening symptoms, he was deemed not a candidate for surgical valve replacement and was scheduled for an elective TAVR.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003ePast medical history\u003c/h3\u003e\n\u003cp\u003eThe patient had a past medical history of persistent atrial fibrillation, hypertension, hyperlipidemia, prior cerebellar stroke, and severe AS.\u003c/p\u003e\n\u003ch3\u003eDifferential diagnosis\u003c/h3\u003e\n\u003cp\u003eThe differential diagnosis for shock following the TAVR procedure included acute coronary syndrome, heart failure with preserved ejection fraction exacerbation, acute pulmonary embolism, and hypertrophic cardiomyopathy with acute shock from LVOT obstruction.\u003c/p\u003e\n\u003ch3\u003eInvestigations\u003c/h3\u003e\n\u003cp\u003ePrior to undergoing the TAVR procedure, an electrocardiogram (EKG) showed chronic atrial fibrillation with a left bundle branch block. A transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 60\u0026ndash;64%, grade III diastolic dysfunction, severe AS with a valve area 0.9 cm\u003csup\u003e2\u003c/sup\u003e, mean AV gradient (AVG) 37 mmHg, AV peak velocity 3.99 m/s, and trace aortic regurgitation (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). There was severe concentric hypertrophy (basal anteroseptal segment 19 mm; a posterior wall of 18 mm) and a small LV cavity (LVEDD 35 mm). Cardiac catheterization revealed hemodynamic parameters of AO pressure 135/73 mmHg (mean 97 mmHg), LV pressure 178/5 mmHg with a left ventricular end-diastolic pressure (LVEDP) of 14 mmHg, and a peak-to-peak gradient of 56 mmHg between the LV and AO (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e. The calculated body surface area was 1.82 m\u0026sup2;, with an estimated O₂ consumption of 242.3%. Computed tomography showed an Agatston valve score of 4,963, and coronary angiography demonstrated mild-to-moderate nonobstructive coronary artery disease.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThe patient underwent an elective TAVR placement with Edward Sapien Ultra 26 mm valve. The hemodynamic profile following valve implantation showed an interval decrease in mean AVG from 56 mmHg to 6 mmHg while LVEDP remained stable around 12\u0026ndash;14 mmHg. There was no significant gradient between the LVOT and ascending aorta (Figs.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e and \u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). Immediately following valve deployment, the patient developed hypotension with BP dropping from 135/73 mmHg to 86/42 mmHg. Heart rate increased to 120\u0026ndash;130 bpm, and he became increasingly agitated with increased respiratory rate and worsening dyspnea. Intra-procedural echocardiography demonstrated a well-seated valve prosthesis with normal leaflet motion and no transvalvular or significant paravalvular aortic regurgitation. There was hyperdynamic LV function with cavitary obliteration, worsened mitral regurgitation, and new SAM of the mitral valve (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003e, \u003cb\u003eVideo 1 and 2\u003c/b\u003e). Invasive LV pressure tracing showed the Brockenbrough-Braunwald-Morrow sign with a peak-to-peak gradient of 25 mmHg (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). The gradient was thought to be intraventricular with no significant LVOT obstruction based on a peak LVOT gradient of 10 mmHg \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eLaboratory evaluation during the shock phase revealed early signs of end-organ hypoperfusion. Serum creatinine increased from 1.2 mg/dL pre-procedure to 1.8 mg/dL post-TAVR. Serum lactate was elevated at 3.8 mmol/L, liver enzymes were mildly elevated, with an AST of 80 U/L and ALT of 70 U/L, and urine output decreased to 0.3 mL/kg/hr. Clinically, the patient appeared lethargic and disoriented.\u003c/p\u003e \u003cp\u003eTo rule out coronary obstruction as a potential cause of post-TAVR hemodynamic collapse, a coronary angiogram was performed intraoperatively and demonstrated no evidence of coronary ostial compromise from valve deployment. This evaluation was preceded by careful preprocedural CT planning, which guided optimal valve sizing and confirmed adequate coronary ostial height, thereby reducing the procedural risk of coronary obstruction. Additionally, there were no dynamic ST-T changes on intraoperative ECG, and TTE revealed a hyperdynamic left ventricle with no regional wall motion abnormalities. No valvular or paravalvular regurgitation was observed. Rather, findings of SAM severe hyperdynamic ejection fraction, and intracavitary obliteration were noted, consistent with dynamic midventricular obstruction rather than ischemic collapse.\u003c/p\u003e\n\u003ch3\u003eManagement\u003c/h3\u003e\n\u003cp\u003eGiven the LV systolic collapse following acute afterload reduction, the patient was promptly managed with 1.5L of intravenous fluids and was initiated on phenylephrine infusion. His blood pressure, which had dropped to 80/50 mmHg, subsequently improved to 110/65 mmHg. Heart rate decreased from 120\u0026ndash;130 bpm to 80\u0026ndash;90 bpm, and peripheral perfusion improved.\u003c/p\u003e \u003cp\u003eWith fluid resuscitation and vasoconstrictor support, urine output improved to \u0026gt;\u0026thinsp;0.5 mL/kg/hr, liver enzymes normalized, and serum lactate trended down to 1.8 mmol/L gradually. The patient was successfully weaned off phenylephrine within 24 hours, maintaining stable hemodynamics and organ perfusion.\u003c/p\u003e \u003cdiv id=\"Sec8\" class=\"Section2\"\u003e \u003ch2\u003eFollow up\u003c/h2\u003e \u003cp\u003eHe was discharged on a beta-blocker aimed at decreasing the heart rate and increasing ventricular filling time. A follow-up TTE one month later revealed a normal LVEF (55\u0026ndash;60%), improved diastolic function (grade I), and a well-seated bioprosthetic aortic valve with normal leaflet motion. Aortic valve Doppler measurements showed a peak velocity of 2.1 m/s, mean gradient of 8 mmHg, and calculated aortic valve area (AVA) of 1.4 cm\u0026sup2;. The patient remained asymptomatic with no signs of recurrent obstruction or heart failure.\u003c/p\u003e \u003c/div\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eVentricular suicide is a rare but potentially life-threatening complication following TAVR, particularly in patients with underlying HCM or HCM-like physiology. This case report aims to emphasize the importance of preoperative risk stratification to identify patients at risk, recognizing predisposing factors, and implementing targeted management strategies to mitigate hemodynamic instability. In this case, an 88-year-old male with severe AS developed obstructive cardiogenic shock immediately following TAVR due to abrupt afterload reduction. The resultant hyperdynamic left ventricular function, cavitary obliteration, and SAM of the mitral valve led to hemodynamic collapse. Prompt recognition and hemodynamic optimization, including volume expansion, vasoconstrictor support, and heart rate modulation, are essential to preventing severe complications.\u003c/p\u003e \u003cp\u003eTAVR is a widely accepted treatment for severe symptomatic AS, particularly in patients with advanced age, suboptimal surgical risk, and underlying LV dysfunction (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). However, its associated complications include coronary occlusion, heart block, device embolization, LV perforation and tamponade, aortic dissection, aortic regurgitation, and ventricular suicide (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). The rare phenomenon of ventricular suicide results from acute afterload reduction in a predisposed hypertrophic LV with a small cavity, leading to cardiovascular collapse due to dynamic intraventricular gradients\u0026thinsp;\u0026plusmn;\u0026thinsp;LVOT obstruction (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). Risk factors include hyperdynamic ventricular systolic function, a small, obliterated LV cavity due to hypertrophy, asymmetrical septal thickening leading to HCM-like physiology, narrowed LVOT, anterior mitral leaflet displacement, and elevated baseline LVOT gradients (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). A sudden reduction in afterload post-TAVR can precipitate a hyperdynamic state, inducing the Venturi effect on the anterior mitral leaflet and leading to acute hemodynamic collapse. Post-TAVR systolic obstruction is usually midventricular due to concentric hypertrophy secondary to chronic pressure overload in AS (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). Some patients may have underlying HCM or develop HCM-like physiology due to chronic pressure overload, resulting in a septal bulge and SAM of the anterior mitral leaflet (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eVentricular suicide physiology is often anticipated based on the presence or absence of baseline LVOT obstruction, severe basal LV hypertrophy (LVH), a long anterior mitral valve leaflet, or evidence of SAM. Preprocedural assessment is therefore critical in identifying patients at risk. While the majority of such patients can be managed conservatively with preload optimization, beta-blockers, and non-dihydropyridine calcium channel blockers (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e), alcohol septal ablation (ASA) may be considered in select cases with significant baseline LVOTO. ASA, typically reserved for patients with demonstrable obstruction prior to TAVR, reduces septal thickness and LVOT gradients but carries procedural risks such as complete heart block and the need for permanent pacemaker implantation (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn our case, the patient did not exhibit LVOTO or intraventricular gradients on preprocedural imaging. The gradient that developed post-deployment was intraventricular rather than subaortic, and thus not amenable to ASA. However, for patients who develop refractory obstructive physiology post-TAVR despite optimal medical management, urgent ASA remains a viable intervention to relieve dynamic obstruction and restore hemodynamic stability.\u003c/p\u003e \u003cp\u003eTreatment of ventricular suicide is aimed at increasing diastolic filling time and expanding the LV cavity. Initial management involves beta-blockers to slow the heart rate and improve ventricular filling, along with intravenous fluids to maintain preload. Vasoconstrictors such as phenylephrine are beneficial in increasing afterload and stabilizing LV end-diastolic pressure (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). Our case had an underlying conduction defect (LBBB) and may have also benefited from prophylactic transvenous pacing post-TAVR to mitigate LVOT gradients.\u003c/p\u003e \u003cp\u003eHCM is strongly associated with senile calcific AS and has been linked to higher in-hospital mortality and post-TAVR complications (\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). Olsen et al. reported a case of hemodynamic collapse in a 56-year-old male with undiagnosed HCM undergoing TAVR, where intraoperative transesophageal echocardiography revealed SAM of the anterior mitral valve leaflet and asymmetric septal hypertrophy. Similar to our case, the patient experienced acute hemodynamic deterioration following valve deployment, attributed to unrecognized dynamic obstruction, though specific details of end-organ hypoperfusion were not reported. They noted that in patients with severe AS, the high LV afterload and arterial impedance often mask subvalvular gradients, making the condition difficult to detect preoperatively (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). Another case by Suh et al. described an 82-year-old woman undergoing TAVR who developed obstructive shock due to SAM and asymmetric septal hypertrophy (29). Both cases share key physiologic features with our patient, including septal hypertrophy, hyperdynamic left ventricular function, and SAM-induced obstruction, and like ours, they were managed with intravenous fluids, beta-blockers, and vasoconstrictors to stabilize hemodynamics.\u003c/p\u003e \u003cp\u003eCollectively, these cases highlight the need for vigilant pre-procedural risk assessment for latent obstruction and emphasize the importance of rapid recognition and hemodynamic management to prevent life-threatening outcomes following TAVR.\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eThis case report highlights ventricular suicide as a rare but critical complication following TAVR in a patient with severe AS and HCM. Abrupt afterload reduction led to mid-ventricular systolic collapse, hyperdynamic left ventricular function, and obstructive shock. Prompt recognition and intervention were crucial in stabilizing our patient following hemodynamic collapse post-TAVR. Immediate management with intravenous fluids and phenylephrine effectively restored hemodynamic stability, preventing further deterioration, and beta-blockade was initiated to prevent recurrence.\u003c/p\u003e \u003cp\u003eGiven the predisposition of HCM and its phenocopies to adverse outcomes post-TAVR, identifying high-risk patients preoperatively is essential. Preemptive strategies such as echocardiographic assessment for small left ventricular cavity size, pre-existing SAM, and latent LVOT obstruction should be incorporated into preprocedural planning. In high-risk patients, prophylactic measures such as preoperative beta-blockade, volume loading, and consideration of temporary pacing to reduce LVOT gradient may prevent post-TAVR hemodynamic collapse and ventricular suicide.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eAortic Stenosis \u0026ndash; AS\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTranscatheter Aortic Valve Replacement \u0026ndash; TAVR\u003c/p\u003e\n\u003cp\u003eLeft Ventricular Outflow Tract Obstruction \u0026ndash; LVOT\u003c/p\u003e\n\u003cp\u003eElectrocardiogram \u0026ndash; EKG \u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTransthoracic Echocardiography \u0026ndash; TTE\u003c/p\u003e\n\u003cp\u003eAlcohol Septal Ablation \u0026ndash; ASA\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003ch2\u003eEthics approval and consent to participate\u003c/h2\u003e \u003cp\u003eWe confirm that the ethical approval for the study was waived by the International Review Board.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eConsent for publication\u003c/strong\u003e \u003cp\u003eWritten informed consent was obtained from the patient\u0026rsquo;s parents for the publication of this case report and accompanying images.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eThe authors report no involvement in the research by the sponsor that could have influenced the outcome of this work.\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eKirtivardhan Vashistha worked towards conception and manuscript drafting. Akshat Banga, Ramzi Khalil, Jian Hu, Pietro Bajona, Jennifer Keeley, Srinivas Murali, Craig Alpert, Robert Biederman, and Victor Farah worked toward drafting the manuscript. Vinh Nguyen was responsible for the conception, revising the manuscript critically for important intellectual content, and approval of the manuscript submitted.\u003c/p\u003e\u003ch2\u003eAcknowledgement\u003c/h2\u003e\u003cp\u003eNot applicable\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eLindman BR, Alexander KP, O\u0026rsquo;Gara PT, Afilalo J. Futility, Benefit, and Transcatheter Aortic Valve Replacement. 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Catheterization and Cardiovascular Interventions 2010;76:616\u0026ndash;20. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1002/ccd.22609\u003c/span\u003e\u003cspan address=\"10.1002/ccd.22609\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"the-egyptian-heart-journal","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"tehj","sideBox":"Learn more about [The Egyptian Heart Journal](https://tehj.springeropen.com)","snPcode":"43044","submissionUrl":"https://submission.springernature.com/new-submission/43044/3","title":"The Egyptian Heart Journal","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Hypertrophic cardiomyopathy, left ventricular outflow tract obstruction, TAVR, Aortic stenosis, ventricular suicide","lastPublishedDoi":"10.21203/rs.3.rs-5259342/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5259342/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eWe describe a patient with severe aortic stenosis (AS) developing obstructive shock immediately following transcatheter aortic valve replacement (TAVR) secondary to a unique phenomenon termed \u0026ldquo;ventricular suicide.\u0026rdquo; Abrupt withdrawal of chronically high afterload may lead to mid-ventricular systolic collapse +/- left ventricular outflow tract (LVOT) obstruction in the setting of hyperdynamic contractility, as seen in hypertrophic cardiomyopathy (HCM).\u003c/p\u003e\u003ch2\u003eCase Presentation\u003c/h2\u003e \u003cp\u003eAn 88-year-old male with severe symptomatic AS presented with worsening dyspnea. Given his high surgical risk and frailty, he underwent TAVR. The patient had a history of persistent atrial fibrillation, hypertension, hyperlipidemia, prior cerebellar stroke, and severe AS. Post-TAVR, he experienced a significant blood pressure drop, leading to shock. Investigations revealed hyperdynamic left ventricular (LV) function, cavitary obliteration, and systolic anterior motion of the mitral valve. Management included intravenous fluids and phenylephrine, which stabilized his condition. He was discharged on a beta-blocker and remained asymptomatic with a normally functioning TAVR prosthesis one month post-discharge.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eHCM and its phenocopies are associated with worse outcomes post-TAVR. Prophylactic beta-blockade and hydration may prevent hemodynamic collapse in patients with anatomic substrates for ventricular suicide.\u003c/p\u003e","manuscriptTitle":"A Case Report of Hypertrophic cardiomyopathy and ventricular suicide: The danger of abrupt afterload reduction","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-05-06 07:11:02","doi":"10.21203/rs.3.rs-5259342/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Accepted","date":"2025-05-11T09:41:59+00:00","index":"","fulltext":""},{"type":"reviewerAgreed","content":"325582374528623230347040899149352036175","date":"2025-04-30T22:16:56+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-04-28T22:10:36+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-04-28T09:48:05+00:00","index":"","fulltext":""},{"type":"submitted","content":"The Egyptian Heart Journal","date":"2025-04-26T19:55:02+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"the-egyptian-heart-journal","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"tehj","sideBox":"Learn more about [The Egyptian Heart Journal](https://tehj.springeropen.com)","snPcode":"43044","submissionUrl":"https://submission.springernature.com/new-submission/43044/3","title":"The Egyptian Heart Journal","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"52c09fd9-b41b-456f-a359-343e143d2039","owner":[],"postedDate":"May 6th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2025-06-02T16:10:57+00:00","versionOfRecord":{"articleIdentity":"rs-5259342","link":"https://doi.org/10.1186/s43044-025-00650-2","journal":{"identity":"the-egyptian-heart-journal","isVorOnly":false,"title":"The Egyptian Heart Journal"},"publishedOn":"2025-06-01 15:57:57","publishedOnDateReadable":"June 1st, 2025"},"versionCreatedAt":"2025-05-06 07:11:02","video":"","vorDoi":"10.1186/s43044-025-00650-2","vorDoiUrl":"https://doi.org/10.1186/s43044-025-00650-2","workflowStages":[]},"version":"v1","identity":"rs-5259342","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-5259342","identity":"rs-5259342","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}