From the Guidelines
A pulmonary embolism (PE) can indeed cause a hyperdynamic left ventricle, although this is not the most common cardiac manifestation of PE. In most cases of PE, right ventricular dysfunction occurs due to increased pulmonary vascular resistance and right ventricular pressure overload, as described in the 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism 1. However, in some situations, particularly with smaller PEs that don't significantly compromise pulmonary blood flow, the left ventricle may appear hyperdynamic on echocardiography.
This phenomenon can be attributed to several factors, including:
- The underfilled left ventricle demonstrating increased contractility as a compensatory mechanism
- The catecholamine surge that accompanies PE as part of the body's stress response, which can increase left ventricular contractility
- The potential for PE-induced vasoconstriction, mediated by the release of thromboxane A2 and serotonin, to contribute to the initial increase in pulmonary vascular resistance (PVR) after PE, as noted in the guidelines 1
The hyperdynamic left ventricle in PE is often transient and resolves with appropriate treatment of the underlying embolism. Treatment typically includes anticoagulation with heparin initially, followed by oral anticoagulants such as direct oral anticoagulants (DOACs) or warfarin. It's essential to recognize that while a hyperdynamic left ventricle can occur with PE, other cardiac findings such as right ventricular dilation, right ventricular hypokinesis, and interventricular septal flattening are more characteristic of significant pulmonary embolism, as outlined in the guidelines 1.
Key points to consider in the management of PE and its effects on the left ventricle include:
- Early recognition and treatment of PE to prevent long-term cardiac complications
- Monitoring for signs of right ventricular dysfunction and left ventricular hyperdynamic function
- Adjustment of anticoagulation therapy as needed to prevent recurrence of PE and minimize cardiac risk
- Consideration of the patient's overall clinical context, including the presence of comorbidities and risk factors for venous thromboembolism, as outlined in the guidelines 1
From the Research
Left Ventricle Response to Pulmonary Embolism
- A pulmonary embolism (PE) can cause hemodynamic compromise, leading to disparate ventricular conditions, with the left ventricle (LV) being under-filled and contracting vigorously, while the right ventricle (RV) is failing and dilated 2.
- The proximate cause of LV preload deprivation is thrombus-induced pulmonary vascular obstruction, which induces acute RV systolic dysfunction and further compromises trans-pulmonary flow 2.
- However, the role of the left ventricle in acute PE is not well defined, and its response can vary, with some patients experiencing LV systolic dysfunction 3.
Hyperdynamic Left Ventricle in PE
- In some cases, the left ventricle can become hyperdynamic, contracting vigorously due to the under-filled state caused by the pulmonary vascular obstruction 2.
- This hyperdynamic response can be seen in patients with acute PE, particularly those without a history of cardiac disease, who may experience a massive PE and have a higher BMI and less hypertension 3.
- The hyperdynamic left ventricle can lead to improved systemic hemodynamics, but it can also be associated with increased stress and potential long-term complications 2, 4.
Clinical Implications
- The diagnosis and treatment of PE should take into account the potential for LV systolic dysfunction and hyperdynamic response, particularly in patients without a history of cardiac disease 3.
- The use of direct oral anticoagulants, thrombolytics, and aspiration thrombectomy can improve systemic hemodynamics and reduce the risk of long-term complications 5, 2.
- Further research is needed to understand the mechanisms underlying the hyperdynamic left ventricle response in PE and to develop optimal treatment strategies for patients with this condition 4, 3.