Arrhythmias in Acute Pulmonary Embolism: Current Evidence and Unresolved Questions

Sara Sóñora-López ¹, Nuria Rivas-Gándara ^1,2,3, Gerard Oristrell-Santamaria ^1,2,3, Ignacio Ferreira-González ^1,3,4,5

¹Cardiology Department, Vall d’Hebron University Hospital (HUVH), Barcelona, Spain

²Biomedical Research Networking Centre on Cardiovascular Diseases (CIBERCV), Barcelona, Spain

³Vall d’Hebron Research Institute (VHIR), Barcelona, Spain

⁴Faculty of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain

⁵Epidemiology and Public Health Networking Biomedical Research Centre (CIBERESP), Madrid, Spain

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Abstract

Acute pulmonary embolism (PE) presents with a wide clinical spectrum ranging from asymptomatic cases to obstructive shock and sudden cardiac death. While supraventricular arrhythmias, particularly atrial fibrillation and sinus tachycardia, are well recognized and associated with worse outcomes, ventricular arrhythmias remain poorly defined and are not routinely included in clinical guidelines. Emerging evidence from case reports suggests that ventricular tachycardia (VT), often with a morphology suggestive of a right ventricular origin, may occasionally represent an initial manifestation of acute PE in patients without structural heart disease. Reported cases consistently show resolution of VT following anticoagulation and treatment of PE, supporting the concept of a transient and reversible arrhythmogenic trigger. Proposed mechanisms include acute right ventricular pressure overload, ischemia, sympathetic activation, hypoxemia, and mechanical stimulation. In contrast, syncope and cardiac arrest associated with PE are more commonly linked to non-shockable rhythms reflecting hemodynamic collapse rather than primary ventricular arrhythmia. Despite these observations, the true incidence and prognostic significance of ventricular arrhythmias in PE remain unknown. This narrative review summarizes current evidence, explores potential mechanisms, and discusses diagnostic and therapeutic implications, highlighting the need for further studies to better define this underrecognized clinical association.

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Introduction

Acute pulmonary embolism (PE) may present with a wide spectrum of clinical manifestations, ranging from asymptomatic cases to obstructive shock and sudden cardiac death. The most common symptoms include dyspnea (78–81%) and pleuritic chest pain (39–56%), although atypical presentations such as syncope (22–26%)¹ or cardiac arrest (0.4%) may also occur². In addition, incidental diagnosis on chest imaging has become increasingly frequent³.

Beyond these clinical manifestations, cardiac arrhythmias represent a relevant but incompletely characterized component of the PE spectrum. Sinus tachycardia is the most common electrocardiographic finding^4,5, while atrial arrhythmias, particularly atrial fibrillation (AF), are well recognized in this setting^4,6. In contrast, ventricular arrhythmias remain poorly defined and are rarely discussed in current clinical practice guidelines^4,7.

Nevertheless, emerging evidence from isolated case reports suggests that ventricular tachycardia (VT) may occasionally appear as the initial manifestation of acute PE, even in the absence of structural heart disease^{8,9,10,11,12,13}. Recognition of this association is clinically relevant because PE represents a potentially reversible trigger of malignant arrhythmias.

This narrative review summarizes current evidence regarding arrhythmias in acute PE, with special emphasis on ventricular arrhythmias, their potential pathophysiological mechanisms, and their diagnostic and therapeutic implications.

Supraventricular Arrhythmias

Supraventricular arrhythmias are relatively common in acute PE and can include AF, atrial flutter, unifocal or multifocal atrial tachycardia, atrioventricular reentrant tachycardia, and junctional tachycardia⁵. Among these, AF represents the most frequent subtype⁴, with a pooled prevalence of 13.2%, of which 4.7% were newly diagnosed, according to a recent meta-analysis⁶. A causal and prognostic relationship exists between both entities, with AF increasing PE risk and potentially complicating its acute clinical presentation^14,15. Likewise, sinus tachycardia is observed in up to 40% of patients with PE^4,5. Importantly, beyond their diagnostic value, supraventricular arrhythmias—particularly AF—have consistently been associated with worse outcomes, including right ventricular (RV) dysfunction¹⁶, hemodynamic decompensation^5,17, and mortality^6,16,17,18. Therefore, atrial arrhythmias in PE may represent not only epiphenomena of acute cardiopulmonary stress but also markers of disease severity.

Electrocardiographic Patterns

Characteristic electrocardiographic findings have also been described in PE, including S1Q3T3 pattern, QR pattern in V1, right bundle branch block or T-wave inversions in leads V1-V4^4,17. These abnormalities may raise diagnostic suspicion in the appropriate clinical context and generally reflect acute RV pressure overload, with potential prognostic implications¹⁷.

Ventricular Arrhythmias: Current Evidence

In contrast to supraventricular arrhythmias, the association between PE and ventricular arrhythmias remains poorly defined. Clinical practice guidelines do not include malignant ventricular arrhythmias as a potential presentation of PE^4,7, and available evidence is largely limited to isolated case reports^{8,9,10,11,12,13}, predominantly involving VT. Regarding ventricular fibrillation (VF), only a limited number of cases have been reported, suggesting that its occurrence in PE is rare. Most reported episodes have been observed in the setting of massive PE complicated by obstructive shock and cardiac arrest, making it challenging to determine whether VF represents a primary arrhythmic event triggered by acute RV strain and ischemia or, more commonly, a terminal rhythm arising from profound hemodynamic collapse. Overall, this limited evidence likely reflects not only true rarity but also potential under-recognition, given the transient nature of some events and the lack of systematic rhythm monitoring in this population.

To further illustrate the potential association and clinical relevance of ventricular arrhythmias in PE, we present a representative case previously reported by our group¹³ (Figure 1). A 63-year-old man arrived at the emergency department complaining of palpitations and was diagnosed with VT of RV outflow tract (RVOT) morphology, which progressed to an electrical storm. The diagnostic workup ruled out structural heart disease and revealed bilateral PE. Following anticoagulation and discontinuation of antiarrhythmic therapy, he remained free of arrhythmic recurrence, with no events detected on the implantable loop recorder during follow-up, suggesting PE as the trigger of the arrhythmic event and a potentially reversible cause. Following this clinical case, similar cases of concomitant VT and PE reported in the literature were reviewed^8,9,10,11,12. The main clinical characteristics of the published cases are summarized in Table 1.

Taken together, these reports suggest a heterogeneous clinical presentation consistent with the known variability of PE¹.  Despite heterogeneity, several common patterns emerge:

• Predominance of RV-origin VT: Although VT morphologies are diverse, there seems to be a predominance of ECG patterns compatible with RV origin across reported cases^10,11,12,13.
• Absence of structural heart disease.
• Resolution after PE treatment.
• Lack of recurrence during follow-up: while different acute interventions are often required to achieve initial rhythm control, no arrhythmic recurrences have been reported during follow-up after targeted treatment of PE⁹, even in cases where antiarrhythmic therapy was subsequently discontinued^10,11,12,13.

Overall, these findings support the hypothesis that PE may act as a transient and reversible arrhythmogenic trigger rather than reflecting primary electrical disease. However, these observations should be interpreted with caution due to small sample size, heterogeneous follow-up, and potential publication bias toward unusual or favorable cases.

Cardiac Arrest and Syncope

Syncope and cardiac arrest represent severe manifestations of acute PE and are typically associated with RV failure, obstructive shock, or profound hypoxemia¹⁹.

Cardiac arrest secondary to PE most commonly presents with non-shockable rhythms, particularly pulseless electrical activity or asystole (26%–75%)^20,21,22,23. Registry data consistently show that shockable rhythms, including VF, account for only a small proportion of cases (5-6%)^21,22,24,25.

The relationship between PE and syncope is more complex. Syncope occurs in a significant proportion of patients with acute PE and may result from transient hemodynamic collapse¹⁹, reflex mechanisms, or potentially unrecognized arrhythmic events. Importantly, studies evaluating patients hospitalized for syncope have reported a surprisingly high prevalence of PE²⁶, suggesting that PE-related arrhythmias may occasionally remain undiagnosed due to the transient nature of symptoms and the absence of rhythm monitoring at the time of the event. In this context, there may be a potential role for non-invasive monitoring systems during the acute phase of PE, such as continuous telemetry, Holter monitoring, or wearable devices, which could help better define and quantify the frequency of possible arrhythmic disorders in this clinical setting.

Pathophysiological Mechanisms

The mechanisms underlying arrhythmogenesis in acute PE are likely multifactorial and may include acute RV pressure overload, myocardial ischemia, sympathetic activation, hypoxemia or mechanical irritation.

Acute RV pressure overload. Acute pulmonary arterial obstruction leads to a sudden increase in RV afterload, leading to RV pressure overload and strain. RV strain is a well-established marker of disease severity in acute PE and is incorporated into risk stratification tools such as the Bova and Composite PE Shock (CPES) scores, as well as the American Heart Association/American College of Cardiology (AHA/ACC) and European Society of Cardiology (ESC) guidelines^4,7. These assessments combine cardiac biomarkers (e.g., NT-proBNP and cardiac troponin) with imaging findings, including RV dilation, dysfunction, and free-wall hypokinesis. A potential consequence of acute RV pressure overload is the development of electrical instability, as RV dilation and increased wall stress can alter myocardial electrophysiological properties^27,28. Whether ventricular arrhythmias in this context reflect a primary arrhythmogenic mechanism or instead represent an epiphenomenon of more severe RV strain and hemodynamic compromise, remains unclear. In either case, their occurrence might reflect greater disease severity.

Myocardial ischemia. Acute RV pressure overload may compromise coronary perfusion and increase myocardial oxygen demand, leading to subendocardial ischemia even in the absence of coronary artery disease⁴. This ischemic environment may increase heterogeneity of depolarization and repolarization, thereby facilitating ventricular arrhythmias.

Sympathetic activation and triggered activity. Acute PE is associated with significant neurohormonal and sympathetic activation. Catecholamine surge may enhance automaticity and promote triggered activity, particularly within the RVOT, a region known to be highly susceptible to arrhythmogenesis due to its unique anatomical and electrophysiological characteristics²⁹.

Hypoxemia and metabolic disturbances. Hypoxemia, acidosis, and metabolic stress may further contribute to electrical instability and lower the threshold for ventricular arrhythmias³⁰.

Mechanically induced arrhythmias. Another speculative mechanism involves direct mechanical stimulation caused by thrombus migration through the right-sided cardiac chambers or RVOT. Although evidence supporting this hypothesis remains very limited, it has been proposed in isolated case reports¹³.

The lack of strong evidence in this field precludes a clear distinction between association and causation, as current observations have not been systematically validated in clinical studies. Even when apparent structural heart disease has been excluded in the reported cases, the presence of an underlying arrhythmogenic substrate or occult myocardial disease cannot be ruled out as alternative explanations for susceptibility to ventricular arrhythmias. However, it is reasonable to consider that some of the proposed mechanisms may interact synergistically, leading to a transient proarrhythmic substrate during the acute phase of PE.

Clinical Implications

Recognition of PE as a potential trigger of ventricular arrhythmias has important clinical implications.

First, PE should be considered in the differential diagnosis of unexplained VT, particularly in patients without structural heart disease and in those with features suggestive of RV origin. Clinical clues such as dyspnea, pleuritic chest pain, hypoxemia, syncope, or thromboembolic risk factors may support suspicion.

Second, identification of PE as the underlying cause may significantly modify therapeutic decision-making. In contrast to primary electrical disorders or scar-related VT, ventricular arrhythmias associated with PE may resolve completely after treatment of the embolic event.

Consequently, recognition of a potentially reversible trigger may lead to a different management approach compared with ventricular arrhythmias of well-established etiology, for which long-term antiarrhythmic therapy, catheter ablation, or implantable cardioverter-defibrillator implantation are more routinely considered. However, given the absence of guideline-directed recommendations and limited clinical experience in this setting, a shared decision-making approach may be appropriate to ensure individualized management integrating all clinical and diagnostic data.

Finally, current evidence remains limited and several unresolved questions persist. The true incidence of ventricular arrhythmias in PE is unknown, as continuous rhythm monitoring is not routinely performed in many patients. Likewise, the prognostic significance of ventricular arrhythmias in this setting remains uncertain. Future studies are needed to clarify whether ventricular arrhythmias merely reflect severe RV strain or identify a distinct high-risk subgroup.

Conclusions

Acute PE is well known to be associated with supraventricular arrhythmias, particularly AF, which has consistently been linked to worse clinical outcomes. In contrast, ventricular arrhythmias remain an uncommon and likely underrecognized manifestation.

Although available evidence is limited to isolated reports and may be influenced by publication bias favoring unusual presentations, published cases suggest several recurring patterns, including a predominance of RV-origin VT, absence of structural heart disease, and complete arrhythmic resolution following treatment of PE.

These observations support the concept that acute PE may act as a transient and reversible arrhythmogenic trigger, either through a hypothetical arrhythmogenic substrate or as a manifestation of hemodynamic compromise. Accordingly, PE should be considered in the differential diagnosis of unexplained VT, particularly in patients presenting with RV-origin arrhythmias and no identifiable structural substrate. In this context, systematic cardiac monitoring in selected patients may help further clarify this hypothesis in future studies.

Overall, further research is warranted to better define the incidence, mechanisms, and prognostic significance of ventricular arrhythmias in acute PE.

Table 1: Reported cases of ventricular arrhythmias in pulmonary embolism

Author, year	Patient characteristics (sex, age)	Chief complaint	Thrombus location	Severity of PE (AHA/ACC, ESC)a	RV strain	VT morphology (origin)	Treatment	Outcome	Cardiac medicacion at discharge	Follow-up
Sóñora-López et al., 2025	Male, 63	Palpitations, chest pain	Bilateral. RPA, left lobar branches	Intermediate-low, C1	No	LBBB, inferior axis, V4 transition (RVOT)	Procainamide, esmolol, LMWH	Progression to electrical storm and instability	Betablockers	Insertable cardiac monitor without arrhythmias
Zhou et al., 2025	Male, 71	Syncope	Bilateral. RPA, LPA and lobar branches	Intermediate-high, C3	Yes (dilation + mild dysfunction)	N/A	Amiodarone, UFH, mechanical thrombectomy, catheter-directed thrombolysis	Spontaneous termination	No AAD	N/A
Ohn et al., 2025	Male, 40	Dyspnea, chest pain	Bilateral. Lobar and segmental branches	High, E1+R	Yes (dilation + hypocinetic wall motion)	LBBB, left axis, V5-V6 transition (RV free wall / tricuspid annulus)	Vasopressor therapy, Amiodarone, UFH	Initially recurrent, termination with amiodarone	No AAD	1-week follow-up: no recurrence
Gomez et al., 2024	Male, 71	Presyncope	Bilateral. Saddle pulmonary embolus	Intermediate-high, C2+R	Yes (dilation + mild dysfunction)	LBBB, inferior axis, V4 transition (RVOT)	Amiodarone, metoprolol, heparin	Initially incessant, termination with metoprolol	Amiodarone, betablockers	Amiodarone discontinuation, no recurrence
Mendoza et al., 2022	Female, 66	Chest pain	RPA	Intermediate-low, C1	No	RBBB, superior axis, V3 transition (left posterior fascicle)	ECV, UFH	Successful ECV	Amiodarone	EPS scheduled
Birchak et al., 2021	Male, 64	Dyspnea, leg swelling	Bilateral. RPA, left lobar branch	Intermediate-high, C3+R	Yes (dilation)	LBBB, superior axis, negative concordance (RV apex)	ECV, amiodarone, UFH, catheter-directed thrombolysis, IVC filter, vein trhombectomy and stenting	Successful ECV (2 VT episodes)	Amiodarone	LifeVest monitor without arrhythmias, amiodarone discontinuation, negative EPS

Acknowledgements: No specific funding was received for this work. The authors thank the Department of Cardiology for their support and contribution to this work, with a special mention to Electrophysiology and Coronary Care Units.

Conflicts of interest: The authors declare no conflicts of interest related to this work.

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