According to the World Health Organization (WHO), heart failure (HF) is defined as a complex syndrome in which the heart is unable to pump sufficient blood to meet the body's metabolic needs1. This condition can result from systolic dysfunction, where the heart fails to contract properly, or diastolic dysfunction, where the heart does not fill adequately2. HF is classified into two main categories: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF)3. In HFrEF, the left ventricular ejection fraction (LVEF) is <40%, indicating decreased pumping capacity, while in HFpEF, the LVEF is normal or near-normal, but the heart exhibits increased stiffness, preventing adequate filling4. The methods commonly used to evaluate cardiac function include standard echocardiography, tissue Doppler imaging (TDI), and magnetic resonance imaging (MRI)5.
Standard echocardiography is a non-invasive technique that allows visualization of cardiac structures and real-time assessment of ventricular and valvular functions6. It uses ultrasound to create images of the heart, enabling observation of the cardiac wall movements, blood flow through the valves, and the size of the cardiac chambers7. Standard echocardiography is essential for diagnosing various cardiac conditions such as cardiomyopathies, valvular diseases, and congenital anomalies8.
TDI, an advanced echocardiographic modality, measures myocardial velocities, providing detailed information on diastolic and systolic function9. TDI is particularly useful for assessing myocardial relaxation and stiffness, as well as detecting subtle ventricular dysfunctions that may not be apparent on standard echocardiography5.
Cardiac MRI offers a precise evaluation of cardiac function, volumes, myocardial masses, and scar tissues10. This technique uses magnetic fields and radio waves to produce detailed images of the heart without using ionizing radiation11. Cardiac MRI is considered the gold standard for volumetric and functional assessment of the heart12. Additionally, it can identify the presence of fibrosis or myocardial scars, providing crucial information for treatment planning13,14.
These evaluations are often performed at rest, which may not fully reveal potential cardiac dysfunctions15. For this reason, stress echocardiography (SE) was introduced as a crucial complementary method16. SE differs from rest echocardiography in its ability to evaluate the hemodynamic response of the heart to exertion. By simulating physical exercise or using pharmacological agents to induce cardiac stress, SE can uncover potential dysfunctions that remain invisible at rest15.
Exercise induction: During SE, the patient may be required to perform physical activity, such as walking or running on a treadmill, or pedaling on an ergometer bike17. Alternatively, medications like dobutamine or adenosine can be administered to increase heart rate and simulate exertion18. This approach evaluates the heart's ability to respond to increased demand for oxygen and nutrients, revealing functional and structural abnormalities not detectable at rest19,20,21.
Hemodynamic measurements: SE provides a more complete view of cardiac function, allowing cardiologists to measure how cardiac output, volumes, and diameters (end-systolic and end-diastolic) adapt to exertion17. For example, it allows tracking changes in the diameter of cardiac chambers and measuring ejection fraction under stress22. This technique is particularly useful for detecting myocardial ischemia, dynamic valvular insufficiencies, and abnormal increases in intracardiac pressures22.
More precisely, exercise stress aims at targeting a heart rate ≥ 85% of age-predicted maximum. While pedaling on a semi-supine bicycle ergometer, SE allows the analysis of cardiac responses to exercise from rest to peak exercise and recovery following generally the Bruce protocol. Thus, SE offers the potential to detect ischemia and delayed abnormalities. However, key contraindications must be considered, including acute decompensated heart failure, severe aortic stenosis, or uncontrolled arrhythmias, while limitations such as poor acoustic windows or chronotropic incompetence may reduce test sensitivity. This approach balances comprehensive functional assessment with careful risk stratification in high-risk populations like heart failure patients.
By evaluating these parameters under stress, SE significantly improves clinical diagnosis by offering a more comprehensive understanding of heart behavior15. It helps identify patients at increased risk of cardiovascular events and tailor therapeutic strategies15.
For patients suffering from HF, SE offers the advantage of enabling more precise treatment tailored to the severity of their condition22. By accurately identifying cardiac dysfunctions, doctors can customize treatment and training programs, thereby improving quality of life and clinical outcomes16. The SE's ability to provide detailed information on the heart's response to exertion helps target therapeutic interventions better, reducing the risk of complications and repeated hospitalizations15.
The overall goals of this methodological article are to present the SE protocol, report on the practical and clinical applications of this technique in patients with HFrEF16 and discuss the clinical relevance of SE and present previous studies conducted in HF patients22. Stress echocardiography represents a powerful diagnostic tool that reveals cardiac dysfunctions not detectable at rest16. By providing a more complete view of the heart's response to exertion, it enhances clinical diagnosis and allows for more personalized treatments15. This article aims to demonstrate the importance of SE in the management of HF, particularly in patients with HFrEF, and to highlight its practical clinical applications22.
In addition, while the use of SE in HFrEF is well established, its methodological relevance to HFpEF and mildly reduced ejection fraction (HFmrEF) is also recognized23. In these populations, SE can reveal impaired cardiac reserve and stress-induced elevations in left ventricular filling pressures (e.g.,via E/e′ ratio) and pulmonary artery systolic pressure, which may remain within normal limits at rest.
Thus, SE offers a reproducible and physiologically relevant methodology for unmasking latent cardiac dysfunction across the spectrum of heart failure phenotypes, with significant diagnostic and prognostic implications. Moreover, SE enables dynamic evaluation of systolic and diastolic function, myocardial strain, and contractile reserve, offering valuable insights into disease mechanisms and therapeutic responses in mice24. Its ability to detect early or subtle impairments in cardiac performance makes SE a powerful tool in translational cardiovascular research, bridging experimental findings with clinical relevance. We hope that this method will be used routinely by clinicians in the future.