Practical Heart Failure Guidance for Clinicians Treating Patients with Diabetes

Heart failure is emerging as one of the most overlooked cardiovascular threats facing people with type 2 diabetes, according to a new expert commentary that urges endocrinologists, primary-care physicians and other noncardiology clinicians to look for the disease before unmistakable symptoms appear. The warning is especially significant because heart failure may be the first manifestation of cardiovascular disease in diabetes, arriving without the classic history of a heart attack or obvious coronary artery disease. In a three-episode podcast series published in Diabetes Therapy, cardiologist Nihar R. Desai, endocrinologist Silvio E. Inzucchi and primary-care physician Eugene E. Wright Jr. outline a practical strategy for identifying patients at risk, using biomarkers to detect early cardiac stress and moving rapidly toward treatment. Their central message is simple but consequential: waiting for breathlessness, swelling or repeated hospitalizations may mean waiting until the disease is already advanced.

The scale of the problem is growing as populations age and the prevalence of obesity, hypertension, diabetes and chronic kidney disease rises. In the United States, total medical costs associated with heart failure are projected to exceed $70 billion by 2030. The condition already affects approximately 22 percent of people with type 2 diabetes—more than one in five patients. Diabetes itself is considered stage A heart failure under the contemporary staging system, meaning that it places a person at increased risk even in the absence of symptoms or detectable structural heart disease. That risk is amplified by high blood pressure, excess adiposity, coronary disease, smoking and impaired kidney function. The experts describe these conditions not as isolated diagnoses but as interconnected components of cardiovascular-kidney-metabolic syndrome, in which disturbances in glucose regulation, vascular biology, renal filtration and cardiac function reinforce one another.

Heart failure is not a single mechanical failure in which the heart simply stops pumping. It is a clinical syndrome in which the heart cannot meet the body’s demands without elevated filling pressures, leading to symptoms, fluid accumulation and progressive organ dysfunction. The disease is divided into stages that describe its evolution. Stage A includes people at risk, including those with type 2 diabetes but no symptoms. Stage B, often called pre-heart failure, refers to people who have structural or functional abnormalities of the heart or abnormal cardiac biomarkers without symptoms. Stage C is symptomatic heart failure, while stage D represents advanced disease, in which symptoms interfere with daily activities and hospitalizations may occur repeatedly. By the time a patient reports shortness of breath, ankle swelling or obvious congestion, the disease may already have crossed into stage C.

The clinical challenge is that early heart failure can look remarkably ordinary. Fatigue, reduced exercise capacity, breathlessness and swelling can be attributed to aging, obesity, chronic obstructive pulmonary disease, venous insufficiency, kidney disease or deconditioning. In people with multiple medical conditions, clinicians may have difficulty identifying which diagnosis is driving a change in symptoms. Heart failure is consequently missed or misdiagnosed, particularly in patients who also have lung disease or ischemic heart disease. An apparently simple complaint such as leg edema can reflect increased venous pressure caused by cardiac dysfunction, but it can also arise from cirrhosis, nephrotic syndrome, thyroid disease or chronic venous disease. The commentary argues that the first safeguard is a deliberate medical history and physical examination that treats these symptoms as possible clues to cardiac disease rather than automatically assigning them to a familiar comorbidity.

The authors also emphasize that heart failure associated with diabetes frequently occurs even when the heart’s pumping percentage appears normal. Clinicians classify heart failure partly by left ventricular ejection fraction, the proportion of blood expelled from the main pumping chamber with each contraction. Heart failure with reduced ejection fraction, or HFrEF, is defined by an ejection fraction of 40 percent or less. Heart failure with preserved ejection fraction, or HFpEF, generally involves an ejection fraction of at least 50 percent, while values between 40 and 50 percent fall into an intermediate category. In HFpEF, the ventricle may contract sufficiently but become stiff, preventing it from relaxing and filling normally. The resulting rise in pressure can force fluid backward into the lungs and tissues. Diabetes, obesity, hypertension and kidney disease are strongly associated with this form of heart failure, meaning that a “normal” ejection fraction does not rule out serious cardiac dysfunction.

For patients at elevated risk, the experts highlight blood tests that can reveal cardiac stress before severe symptoms develop. Natriuretic peptides—principally B-type natriuretic peptide, or BNP, and its inactive precursor N-terminal pro-BNP, or NT-proBNP—are released when the heart muscle is stretched by pressure or volume overload. BNP is produced from a precursor molecule and acts hormonally, promoting the excretion of sodium and water and encouraging blood-vessel relaxation; NT-proBNP is biologically inactive but remains useful because its concentration reflects the same underlying stress. The commentary identifies BNP levels above 50 picograms per milliliter and NT-proBNP levels above 125 picograms per milliliter as useful risk thresholds, while high-sensitivity cardiac troponin above the 99th percentile for a healthy population may indicate myocardial injury or stress. The authors recommend at least annual measurement of a natriuretic peptide or high-sensitivity troponin in high-risk patients, with more frequent testing when clinical status changes.

These biomarkers are not crystal balls, and their interpretation requires physiological context. NT-proBNP and BNP can rise with age, atrial fibrillation and chronic kidney disease even when worsening heart failure is not the immediate cause. Reduced kidney filtration slows the removal of circulating molecules and reflects broader changes in fluid balance and vascular health. Conversely, obesity can suppress natriuretic peptide concentrations, potentially masking significant cardiac dysfunction and producing a deceptively reassuring result. For that reason, the experts caution against treating a single laboratory value as a diagnosis. Trends may be more informative than isolated measurements. In the EXAMINE trial, which included people with type 2 diabetes, two NT-proBNP measurements taken six months apart helped distinguish risk: patients with persistently elevated values had the greatest likelihood of developing heart failure, while an increase from baseline was itself associated with rising risk. Serial testing effectively turns a snapshot into a trajectory.

When biomarkers or symptoms raise concern, echocardiography is the next important investigation. An echocardiogram uses ultrasound waves to generate moving images of the heart, allowing clinicians to assess chamber size, wall motion, valve function, filling patterns and pumping performance. It can reveal structural remodeling caused by long-standing hypertension, evidence of prior ischemic injury or abnormalities consistent with diabetic cardiomyopathy. It also helps distinguish HFrEF from HFpEF and can identify conditions that require different treatment strategies. The clinicians do not recommend echocardiography for every person with diabetes solely because diabetes confers risk. Rather, they describe a targeted sequence: identify high-risk patients, examine them carefully, measure biomarkers and arrange imaging when results or clinical findings suggest cardiac dysfunction. Importantly, they stress that potentially beneficial intervention should not necessarily be postponed while waiting for an echocardiogram, particularly when the overall clinical picture is compelling.

Risk-prediction tools such as the TIMI Heart Failure Risk Score and the Health ABC Heart Failure Risk Model may help clinicians understand how age, diabetes, hypertension and other variables combine to influence prognosis, but the specialists present them as aids rather than replacements for clinical judgment. The most urgent opportunity lies in the period before repeated decompensations, emergency visits and hospital admissions begin. Heart failure often has an initially stable phase followed by episodes in which fluid accumulates, symptoms worsen and the risk of hospitalization and death rises. Earlier recognition can lengthen the period of relative stability and preserve quality of life. The commentary therefore calls for a coordinated approach in which primary-care practices and diabetes clinics participate directly in cardiovascular surveillance. Patient conversations should explain why heart failure is being assessed, while prevention efforts address weight management, smoking cessation, physical activity and adherence to prescribed medication. The podcast’s later episodes are intended to discuss guideline-directed drug therapy and lifestyle modification, but the first episode’s message is that detection is the gateway to every subsequent intervention.

The experts’ appeal reflects a broader shift in cardiovascular medicine: diabetes care can no longer focus only on blood glucose, retinal disease, neuropathy and atherosclerotic events while treating heart failure as a specialist problem. The biological links between insulin resistance, inflammation, adipose-tissue dysfunction, arterial stiffening, renal injury and myocardial remodeling make heart failure a core complication of metabolic disease. A patient who appears stable in an endocrinology or primary-care waiting room may already have stage B disease, with changes that are detectable through biomarkers or imaging but not yet severe enough to cause obvious symptoms. Recognizing that hidden phase could be decisive, because treatment and risk-factor control are more likely to prevent deterioration before the heart enters a cycle of congestion and hospitalization. The commentary, developed by Desai, Inzucchi and Wright as the first installment of a clinical podcast series, does not report a new clinical trial or newly generated dataset. Instead, it translates existing evidence into an urgent clinical signal: in people with diabetes, the search for heart failure should begin before the heart failure announces itself.