A diagnosis of heart failure (HF) has never been established based on a single test alone. Nevertheless, clinical practice continues to be dominated by a fragmented approach focused tightly on threshold ejection fraction (EF) values, elevated natriuretic peptide concentrations, or “dysfunction” noted in an imaging report. In the face of a rising incidence of Heart Failure with Preserved Ejection Fraction (HFpEF) and ongoing technological advancements, this diagnostic habit is becoming increasingly inadequate.
Today, clinicians routinely encounter contradictory findings: patients with elevated natriuretic peptides but no structural pathology; normal biomarkers despite clearly manifest HFpEF; or Artificial Intelligence (AI) generated alerts in asymptomatic individuals. The challenge today is no longer simply detecting heart failure, but determining which piece of evidence should carry decisive weight.
The Second Universal Definition of Heart Failure is viewed as an effort to overcome these contradictions. It returns heart failure to the center of a clinical syndrome, where a diagnosis is established not by isolated parameters that validate or rule out the disease, but by pathophysiologically consistent, cumulative evidence.
This update reminds clinicians that heart failure cannot be reduced to a single laboratory or imaging result. In an era of increasing fragmentation of diagnostic data, the consensus directly defends the principle of integrated clinical reasoning.
Prevention Begins Before Symptoms Appear
The majority of individuals with heart failure do not yet exhibit symptoms. They are in the early stages of the disease—either at-risk or pre-HF stages—where structural anomalies already exist but a distinct clinical syndrome has not yet manifested. The updated definition relies precisely on these stages, reinforcing the principle that the greatest benefit to the patient is achieved through prevention rather than merely managing established disease.
Traditional Stage A factors, such as arterial hypertension and coronary artery disease, continue to hold a central place, but the document goes beyond simply reformulating these elements. One significant update is that social determinants are no longer viewed merely as secondary circumstances. Poverty, low education levels, adverse living environments, and cumulative social inequalities are brought directly into the conceptual framework of heart failure; they are recognized as direct risk factors for the disease, rather than just barriers to accessing medical services.
Concurrently, cardiometabolic pathologies—obesity, diabetes, and chronic kidney disease—are defined as direct therapeutic targets. Alongside providing glycemic or nephroprotective effects, SGLT2 inhibitors, GLP-1 receptor agonists, and finerenone serve to prevent heart failure in high-risk groups. In this way, a preventive strategy based on a risk gradient adapts to the individual needs of the patient from Stage A to Stage B (pre-HF).
Beyond Traditional Screening
Detecting hidden and slowly progressing heart failure is notably difficult. Patients frequently attribute fatigue, mild exertional dyspnea, and fluid retention-related weight gain to aging and its natural processes. Consequently, in the primary care setting, many of them remain on chronic diuretic therapy without an accurate diagnosis.
This consensus tackles early detection with a multicomponent approach. Screening natriuretic peptides, in combination with clinical risk factors, allows for the identification of pre-HF patients who will benefit from therapy long before symptoms surface.
In specific populations, additional markers (troponin and urinary albumin-to-creatinine ratio) provide risk refinement. Furthermore, AI-supported ECG analysis offers a major advantage: it enables the prediction of left ventricular dysfunction and structural pathologies. Crucially, it manages to link abnormal patterns to the risk of developing heart failure, even against a backdrop of normal systolic function.
While this may seem like a subtle shift in emphasis, its implications extend beyond terminological boundaries. The primary value of the update lies not in the additional recommendations it provides, but in what it asks clinicians to stop doing—relying on a single test to screen for heart failure. The document does not view screening as a simplified procedure yielding a binary “yes/no” answer, but defines it as a synthetic diagnostic process.
Rethinking Ejection Fraction
For years, ejection fraction (EF) served as the axis around which heart failure categories and treatment decisions revolved. Reduced, mildly reduced, and preserved ejection fractions were separated by strictly enforced thresholds. This approach is problematic because “normal” varies by age, sex, and ethnicity, and the measurement process itself is imperfect.
The Second Universal Definition proposes a fundamentally new approach, deliberately moving away from imperative EF thresholds. Instead of rigid numerical categories, the document groups heart failure into three clinically relevant categories: reduced, preserved, and improved EF. Within this framework, the exact EF value determining a “reduced” status is subject to clinical judgment based on normative data and therapeutic response, rather than traditional dogma.
Equally important is how “improved EF” is formulated. The document does not view it as a complete restoration of health, but as a form of remission. Ejection fraction may normalize, symptoms may decrease, and biomarkers may stabilize—yet the clinical risk profile remains. Consequently, de-escalation of therapy does not happen automatically, and clinical supervision is not discontinued.
A Universal Definition for a Non-Universal Disease
The concept of a “universal” definition of heart failure runs the risk of overshadowing the fact that this disease lacks a uniform clinical picture and identical underlying mechanisms.
While ischemic and hypertensive heart diseases dominate the etiology of heart failure in high-income regions, completely different pathologies take the lead elsewhere: rheumatic carditis in parts of Africa and Asia, Chagas disease in Latin America, chronic obstructive pulmonary disease in South and East Asia, and alcoholic cardiomyopathy in Eastern Europe. In migrant populations, fixed pathologies—such as endomyocardial fibrosis, tuberculous pericarditis, or peripartum cardiomyopathy—present a challenge to local medical personnel, as these conditions are rarely encountered in their daily practices.
The authors note that in low- and middle-income countries, heart failure manifests at an earlier age and with different phenotypes—for example, a lean type of diabetic HFpEF in Southeast Asia, and hypertensive and peripartum cardiomyopathy in Africa. Furthermore, the problem of the global validity of research is highlighted: clinical trials include only a small fraction of patients from these regions, which limits the generalizability of the results.
In the context of managing heart failure in Georgia, cardiologist Vazha Agladze notes:
“No specific characteristics regarding the manifestation of heart failure have been established in Georgia. The only aspect we can emphasize is the relatively high prevalence of arterial hypertension across all regions of Georgia. As is well known, this pathology (especially in cases of inadequate treatment) is one of the most critical causative factors in the development of heart failure.”
Regarding critical surges in hypertension, Professor Agladze explains that they frequently provoke acute diastolic failure, even when the cardiac ejection fraction is completely preserved. In such instances, the cornerstone of the therapeutic strategy, alongside improving blood rheological parameters, is the optimal control of blood pressure.
Differential Diagnosis
Dyspnea, edema, and abnormal instrumental findings are integral to cardiovascular practice, but they do not always point to heart failure. The consensus dedicates a significant section to HF mimics—conditions that symptomatically resemble heart failure but are driven by different palthophysiological mechanisms.
Chronic coronary syndromes may manifest solely as exertional dyspnea or may coexist with heart failure. Chronic kidney disease can cause fluid overload, dyspnea, and structural changes like left ventricular hypertrophy, where high filling pressures are driven by renal mechanisms rather than primary myocardial failure.
In late pregnancy, dyspnea and edema are common; therefore, distinguishing physiological changes from peripartum or previously hidden cardiomyopathy requires the careful use of natriuretic peptides and echocardiography. Obesity and low physical activity complicate the presentation and reduce the diagnostic value of both physical examination and natriuretic peptides, sometimes requiring invasive exercise hemodynamic testing, particularly in cases of HFpEF.
The essence of this section lies not just in the specific clinical examples, but in its fundamental message: similar symptoms do not automatically imply an identical syndrome. Thus, against a backdrop of increasing comorbidities and refined technology, diagnosing the condition using oversimplified approaches is becoming increasingly risky.
Redefining the Disease Trajectory
The dynamic nature of heart failure (its improvement and worsening) has always been clear to clinicians, but the terminology describing these processes remained somewhat vague. Words like “stable,” “compensated,” “decompensated,” and “worsening” were used interchangeably across various contexts, often even as synonyms.
The consensus unifies the terminology and offers the following definitions:
“Improvement” denotes positive dynamics in ejection fraction or symptoms, against a backdrop of persistent underlying pathology.
“Remission” implies a normalization of EF, minimal symptoms, and stable biomarkers, while explicitly recognizing the patient’s elevated ongoing risk.
“Recovery” refers only to those clinical cases where structural, functional, symptomatic, and biochemical parameters have stabilized within normal ranges over a prolonged observation period.
Parallel to these positive trajectories, the document clearly distinguishes “worsening heart failure” from “decompensated heart failure.” The former implies a progressive deterioration of clinical and biochemical markers on the background of already established disease, while the latter is characterized by an acute worsening of the condition that creates a need for intensive or emergency therapy, and frequently, hospitalization.
At first glance, this appears to be merely a terminological refinement, but its actual impact encompasses research methodology, clinical outcome criteria, and patient communication. This classification is essential to clearly separate acute, life-threatening complications from the dynamic, progressive nature of heart failure.
The full consensus can be found at the following link: AHA|ASA Journals
