Diastolic DysfunctionEdit

Diastolic dysfunction refers to a problem with the heart’s left ventricle relaxing and filling properly during the diastolic phase of the heartbeat. In this condition, the ventricle becomes stiff or less compliant, so filling pressures rise and the heart has to work harder to deliver blood to the circulation. It is a common finding in older adults and in people with conditions such as long-standing hypertension, obesity, and diabetes. When diastolic dysfunction progresses to clinically meaningful heart failure with preserved ejection fraction, the heart’s pumping function appears normal on standard measurements, but symptoms such as shortness of breath and exercise intolerance reflect the impaired filling and increased pressures inside the heart. For many patients, diastolic dysfunction exists on a spectrum from subclinical abnormalities detected on imaging to overt heart failure symptoms. See also Heart failure and Heart failure with preserved ejection fraction.

Pathophysiology

Relaxation, compliance, and filling

The left ventricle’s ability to relax quickly and fully during early diastole, and its overall compliance (how easily it stretches to accommodate incoming blood), are central to diastolic function. When relaxation is delayed or the ventricle becomes stiffer, filling occurs under higher pressures, which can back up into the atria and venous system. This can lead to symptoms and signs of congestion even if the heart’s pumping strength remains relatively preserved.

Contributing conditions

Several diseases and risk factors promote diastolic dysfunction, including: - long-standing hypertension that causes thickening of the heart muscle (left ventricular hypertrophy) - obesity and insulin resistance - aging-related changes to myocardial tissue and vasculature - ischemic heart disease and prior myocardial injury - valvular heart disease, especially mitral or aortic valve problems - atrial fibrillation and other rhythm disturbances - infiltrative or restrictive processes in rare cases

These factors can interact and create a phenotype sometimes described as HFpEF (heart failure with preserved ejection fraction), in which symptoms arise from elevated filling pressures and impaired diastolic reserve rather than an outright decline in systolic pumping capacity.

Diagnostic implications

Because diastolic dysfunction often coexists with other cardiac changes, clinicians rely on imaging and laboratory measures to characterize it. Echocardiography is central, with metrics such as the E/A ratio (early to late ventricular filling), E/e’ (a surrogate for filling pressures), and the size of the left atrium helping classify the degree of dysfunction. Natriuretic peptides (e.g., BNP or NT-proBNP) frequently rise with filling pressure and provide supporting information. In some cases, invasive hemodynamic assessment is used to define filling pressures more precisely.

Clinical presentation

Many patients with diastolic dysfunction experience exertional dyspnea, limited tolerance for activity, or signs of congestive symptoms such as peripheral edema. Because the ejection fraction is often normal, early recognition can be challenging. Symptoms may wax and wane with comorbid conditions, activity level, and volume status. The clinical picture frequently reflects the underlying contributors—uncontrolled hypertension, obesity, diabetes, and sleep-disordered breathing can all worsen diastolic function.

Diagnosis

Echocardiography is the standard noninvasive test. It evaluates relaxation, filling pressures, and chamber sizes, and helps distinguish isolated diastolic dysfunction from more complex heart failure phenotypes. See Echocardiography and Diastolic dysfunction grading for more detail.
Doppler and tissue Doppler measurements (including E/A and E/e’ ratios) inform estimates of filling pressures and stiffness.
Biomarkers such as BNP or NT-proBNP support the diagnosis and help gauge severity or the risk of deterioration.
Cardiac magnetic resonance imaging can provide high-resolution assessment of myocardial tissue and function in some cases.
In selected patients, invasive right heart catheterization offers definitive pressure measurements if noninvasive testing is inconclusive.

Management

Lifestyle and risk factor modification

Core strategies focus on addressing driving risk factors and preventing progression: - blood pressure control, often with a combination of therapies tailored to the individual - weight reduction and management of metabolic risk factors - sodium restriction and fluid management during decompensation - encouragement of physical activity and structured exercise programs - management of sleep-disordered breathing when present

Pharmacologic therapy

Diuretics are commonly used to relieve congestion and fluid overload during symptomatic episodes.
Treatments targeting the underlying conditions (e.g., antihypertensives, diabetes medications, lipid management) help reduce the burden on the heart.
The evidence for disease-modifying pharmacotherapy specifically for diastolic dysfunction or HFpEF has historically been limited, but recent trials suggest that certain agents may improve outcomes in selected patients. In particular, SGLT2 inhibitors used for diabetes care have shown benefit in some HFpEF populations and are being incorporated into evolving management strategies. See SGLT2 inhibitors and Dapagliflozin / Empagliflozin as examples of this approach.
Antiarrhythmic or rate-control strategies are important when atrial fibrillation or other rhythm problems are present, as these conditions can worsen diastolic filling.

Device and procedural considerations

In selected cases, management of comorbid valvular disease or consideration of pacing strategies may be appropriate.
Cardiac rehabilitation and multidisciplinary care improve quality of life and functional status for many patients with diastolic dysfunction.

Controversies and debates

Diagnostic criteria and the concept of diastolic dysfunction as a discrete disease versus a spectrum within HFpEF remain topics of discussion. Some clinicians emphasize hemodynamic measurements and imaging thresholds, while others view diastolic abnormalities as part of broader myocardial aging and cardiometabolic disease.
HFpEF is recognized as a heterogeneous syndrome with multiple phenotypes. This has led to debate over one-size-fits-all treatments and has spurred interest in phenotype-driven approaches to therapy rather than a single disease model.
The utility of diastolic dysfunction grading on routine echocardiography for predicting outcomes or guiding therapy has varied across studies and guidelines. Critics argue that emphasis should be on symptoms, functional status, and comprehensive risk factor management rather than strict grading alone.
Pharmacologic therapies specifically for HFpEF have historically produced inconsistent results. While newer evidence supports certain agents (notably SGLT2 inhibitors) in improving outcomes for some patients, the overall landscape remains nuanced, and clinicians tailor therapy to individual risk profiles and comorbidities. See Heart failure with preserved ejection fraction for a broader discussion of these challenges and evolving treatment approaches.