Dynamic LVOT Obstruction as a Cause of Hemodynamic Instability in Takotsubo Syndrome

Abstract

Takotsubo syndrome (TTS) frequently presents with chest pain, ST-segment elevation, and troponin elevation, closely mimicking acute coronary syndrome, and can be complicated by acute heart failure and cardiogenic shock. In a subset of patients, dynamic left ventricular outflow tract obstruction (LVOTO) with systolic anterior motion (SAM) of the mitral valve contributes to hemodynamic instability and requires a distinct therapeutic approach. We report a 79-year-old woman admitted for evaluation of biliary and pancreatic ductal dilation who developed acute chest pain followed by dizziness and hypotension during hospitalization. Electrocardiography demonstrated anterolateral ST-segment elevations, and HS troponin I peaked at 7,594 ng/L. Emergent coronary angiography revealed mild, non-obstructive coronary artery disease, while left ventriculography demonstrated apical akinesis with basal hyperkinesis consistent with TTS. Persistent hypotension despite intravenous fluids prompted bedside echocardiography, which demonstrated severe left ventricular systolic dysfunction with basal hypercontractility and SAM. Transthoracic echocardiography confirmed severe dynamic LVOTO (peak gradient 126 mmHg) with moderate mitral regurgitation and reduced ejection fraction (25%–30%). Phenylephrine was initiated with prompt improvement in blood pressure and symptoms, while inotropes and afterload-reducing agents were avoided. With cautious volume resuscitation and beta-blockade after stabilization, serial echocardiography demonstrated reduction in LVOT gradient and improvement in mitral regurgitation. This case highlights the importance of early echocardiography in hypotensive patients with suspected TTS, the need for mechanism-directed management when dynamic LVOTO is present, and suggests that the distribution of regional wall motion abnormalities may influence the development of obstructive physiology.

Introduction

Takotsubo syndrome (TTS), also termed stress-induced cardiomyopathy, is an acute syndrome characterized by transient left ventricular systolic dysfunction that often presents with chest pain, electrocardiographic abnormalities (including ST-segment elevation), and troponin elevation, closely mimicking acute myocardial infarction.^1,2 Although previously regarded as benign, contemporary evidence demonstrates that acute complications, including heart failure, arrhythmias, and cardiogenic shock, can occur during the index hospitalization. ¹

Dynamic LVOTO is an important, physiology-defining complication in a subset of patients with TTS.^3,4 In this setting, LVOTO is typically related to basal hypercontractility, reduced ventricular cavity size, and systolic anterior motion (SAM) of the mitral valve, often accompanied by functional mitral regurgitation. ⁴ Recognition is critical because conventional therapies for shock, particularly inotropes and afterload reduction, may exacerbate obstruction and worsen hemodynamics.^3-5

We report a case of TTS complicated by severe dynamic LVOTO presenting as refractory hypotension, emphasizing the importance of early echocardiographic diagnosis and mechanism-directed management.

Case Presentation

A 79-year-old woman with a history of hypertension, hyperlipidemia, hypothyroidism, prior myocardial infarctions, chronic back pain, opioid use disorder on methadone, remote pharyngeal cancer, and chronic pancreatic and biliary ductal dilation presented with nausea and recurrent non-bloody, non-bilious vomiting. She denied abdominal pain, fevers, or chills. On initial examination, she was alert and oriented ×4, hemodynamically stable with blood pressure 156/98 mmHg, heart rate 78 bpm, respiratory rate 16/min, and SpO₂ 98% on room air. Physical examination was notable for a soft, non-tender abdomen without organomegaly, and regular heart sounds without murmurs, rubs, or gallops.

Laboratory evaluation on admission revealed potassium 3.2 mmol/L [normal: 3.5–5.0 mmol/L], BNP 161 pg/mL [normal: <100 pg/mL], hemoglobin 15.3 g/dL [normal: 12.0–16.0 g/dL], and white blood cell count 5.7 ×10³/µL [normal: 4.5–11.0 ×10³/µL]. Electrocardiography demonstrated sinus rhythm with prolonged PR interval, borderline left axis deviation, incomplete right bundle branch block, and QTc 449 ms. Imaging including CT abdomen demonstrated diffuse intrahepatic and extrahepatic bile duct dilation and a distended gallbladder with multiple gallstones.

Prior echocardiography demonstrated mild concentric left ventricular hypertrophy with a septal knuckle/sigmoid septum, fluctuating regional wall motion abnormalities, and variable left ventricular systolic function across serial studies, including transient anterolateral wall motion abnormalities on earlier examinations. Baseline Doppler assessment demonstrated no significant left ventricular outflow tract gradient (Figure 1), and echocardiography showed no evidence of systolic anterior motion or dynamic obstruction (Video 1).

Figure 1.

Baseline LVOT Doppler without significant obstruction. Pulsed-wave Doppler interrogation of the left ventricular outflow tract at baseline demonstrating a peak velocity of 124 cm/s and a maximum pressure gradient of 6 mmHg, consistent with the absence of hemodynamically significant obstruction.

During hospitalization, the patient developed acute-onset chest pain accompanied by dizziness and hypotension (MAP 51 mmHg, HR 82 bpm, SpO₂ 96% on room air). Electrocardiography revealed anterolateral ST-segment elevations, and HS troponin I was elevated to 7,594 ng/L [normal: <6 ng/L]. STEMI protocol was activated, and emergent coronary angiography demonstrated mild, non-obstructive coronary artery disease. Left ventriculography revealed apical akinesis with basal hyperkinesis, consistent with stress-induced (Takotsubo) cardiomyopathy.

Following the procedure, hypotension persisted despite intravenous fluid administration. Bedside point-of-care echocardiography demonstrated basal hyperkinesis with systolic anterior motion (SAM) of the mitral valve, raising concern for obstructive physiology. Formal transthoracic echocardiography subsequently confirmed severe dynamic left ventricular outflow tract obstruction (peak gradient 126 mmHg) with moderate mitral regurgitation, basal septal hypertrophy, a small left ventricular cavity, and severely depressed systolic function (LVEF 25%–30%) (Figure 2, Video 2). The inferior vena cava was dilated with less than 50% inspiratory collapse. The patient was upgraded to the intensive care unit.

Figure 2.

Severe dynamic LVOT obstruction during acute Takotsubo syndrome. Continuous-wave Doppler interrogation demonstrating a late-peaking, dagger-shaped systolic velocity profile characteristic of dynamic left ventricular outflow tract obstruction. Peak velocity exceeds 5 m/s, corresponding to a calculated peak pressure gradient greater than 100 mmHg, in the setting of systolic anterior motion of the mitral valve and basal hypercontractility.

Management focused on mechanism-directed hemodynamic support. Phenylephrine infusion was initiated, resulting in prompt improvement in blood pressure and resolution of dizziness. Inotropic agents and afterload-reducing medications were avoided. The patient received cautious volume resuscitation and beta-blockade after hemodynamic stabilization. Serial transthoracic echocardiography demonstrated interval reduction in LVOT gradient and improvement in mitral regurgitation (Figure 3, Video 3). The patient remained hemodynamically stable and was eventually downgraded from the ICU without recurrence of hypotension. She was subsequently discharged in stable condition with close outpatient cardiology follow-up.

Figure 3.

Interval resolution of dynamic LVOT obstruction following targeted therapy. Follow-up pulsed-wave Doppler interrogation of the left ventricular outflow tract after initiation of phenylephrine, cautious volume resuscitation, and beta-blockade, demonstrating marked reduction in peak systolic velocity to approximately 195 cm/s (approximately 2 m/s) and a maximum pressure gradient of 15 mmHg, consistent with near-resolution of dynamic obstruction compared with the index presentation.

Discussion

TTS is characterized by acute, typically reversible ventricular systolic dysfunction with regional wall motion abnormalities extending beyond a single coronary territory and modest biomarker elevation in the absence of obstructive coronary disease.^1,2 Although ventricular recovery is common, acute complications, including cardiogenic shock, are well recognized. ¹

Dynamic LVOTO represents a treatable mechanism of hemodynamic compromise in a subset of patients with TTS.^3,4 Reported prevalence varies by cohort and methodology, with registry-based analyses demonstrating LVOTO in 7%–13% of cases. ⁴

The pathophysiology of LVOTO in TTS is attributed to basal hypercontractility, reduced ventricular cavity size, and predisposing anatomic features such as a sigmoid septum, resulting in systolic anterior motion (SAM) of the mitral valve and secondary mitral regurgitation.^3,4 Mechanistic insights into SAM demonstrate that flow drag forces and ventricular geometry play central roles in the development of dynamic obstruction. ⁶

The sigmoid septum is an age-related anatomical variant characterized by focal hypertrophy of the basal interventricular septum, with an overall echocardiographic prevalence of approximately 1.5%–7% that rises substantially with advancing age.^7,8 In community-based studies, prevalence increases markedly with age, reaching 17.8% in individuals aged 85 years and above, with age identified as the sole independent predictor on multivariate analysis. ⁸ At the structural level, the sigmoid septum narrows the subaortic space, reduces the mitral-to-septal distance, and creates geometric conditions that predispose to SAM and dynamic LVOTO — particularly when ventricular loading conditions are altered, as occurs in TTS with basal hypercontractility and volume depletion.^5,7 Current evidence does not clearly establish a septal thickness threshold above which alpha-agonists should be preferentially chosen over conventional vasopressors; however, the presence of sigmoid morphology in a patient with TTS and hemodynamic instability should prompt early echocardiographic evaluation for LVOTO prior to initiating vasoactive therapy, given the risk of paradoxical hemodynamic deterioration with inotropes or vasodilators in this context.^3,5

Notably, this patient had prior imaging evidence of a septal knuckle/sigmoid septum and intermittent transient left ventricular dysfunction, suggesting a pre-existing predisposition to dynamic obstructive physiology. Serial echocardiographic studies in this case demonstrated that different patterns of regional wall motion abnormalities were associated with distinct hemodynamic manifestations. Earlier imaging showed transient anterolateral wall motion abnormalities without development of LVOT obstruction. In contrast, during the current presentation, inferoseptal and apical hypokinesis with preserved basal contractility was accompanied by severe dynamic LVOTO with systolic anterior motion and a peak gradient of 126 mmHg. These findings suggest that the distribution of ventricular dysfunction may influence the likelihood of developing obstructive physiology in TTS. When basal segments remain hypercontractile in the setting of apical or inferoseptal dysfunction, the resulting ventricular geometry and flow dynamics may promote systolic anterior motion of the mitral valve and dynamic LVOT obstruction (Video 2).

Recognition of this physiology is essential because routine therapies for shock may worsen obstruction. Inotropes and catecholaminergic agents can increase basal contractility and exacerbate SAM/LVOTO, whereas afterload augmentation may reduce intraventricular gradients and stabilize blood pressure.^3,5 Similar physiology has been described in other shock states complicated by dynamic LVOTO, in which reduction of adrenergic burden and afterload support improved gradients and hemodynamics.^9,10

In our patient, persistent hypotension prompted immediate bedside echocardiography, which identified severe LVOTO. Afterload augmentation with phenylephrine resulted in rapid hemodynamic improvement, followed by cautious volume resuscitation and beta-blockade after stabilization.

This case highlights the dynamic, load-sensitive nature of LVOTO and underscores the importance of echocardiography-guided management in unstable patients with TTS.

Conclusion

Dynamic LVOTO is an important and potentially reversible cause of hypotension in patients with TTS.^3,4 Management differs fundamentally from non-obstructive shock physiology: inotropes and afterload reduction may worsen obstruction, whereas afterload augmentation, cautious preload optimization, and beta-blockade after stabilization can improve outcomes.^3,5 Early echocardiographic recognition and mechanism-directed therapy are essential to prevent clinical deterioration.

Supplemental Material

Video 1. Baseline echocardiography without LVOT obstruction. Transthoracic echocardiography demonstrating preserved ventricular function with no evidence of systolic anterior motion or dynamic left ventricular outflow tract obstruction.

Video 2. Takotsubo cardiomyopathy with systolic anterior motion and LVOT obstruction. Transthoracic echocardiography demonstrating apical and inferoseptal hypokinesis with preserved basal hypercontractility and systolic anterior motion of the mitral valve, consistent with dynamic left ventricular outflow tract obstruction.

Video 3. Recovery with resolution of LVOT obstruction. Follow-up transthoracic echocardiography demonstrating improvement in ventricular function with resolution of systolic anterior motion and dynamic left ventricular outflow tract obstruction after targeted therapy.

ORCID iDs

Simran Tanna https://orcid.org/0009-0008-2230-4757

Jonathan Kutcher https://orcid.org/0009-0002-3592-6551

Ethical Considerations

Our institution does not require ethical approval for reporting individual cases or case series.

Consent to Participate

Written informed consent was obtained from the patient for their anonymized information to be published in this article.

Data Availability Statement

This case report is based on clinical data obtained during routine medical care. The echocardiographic images and video clips supporting the findings of this study are included as figures and supplementary videos within the manuscript. No additional datasets, samples, or models were generated. Patient data cannot be made publicly available due to patient privacy and confidentiality requirements.*