DiastoleEdit
Diastole is the relaxation phase of the heart’s pumping cycle during which the chambers fill with blood. It follows systole, the contraction that ejects blood, and is essential for maintaining adequate cardiac output across a range of heart rates. During diastole, the ventricles relax, their walls become more compliant, and the pressure within the chambers drops enough to allow incoming blood to flow from the atria. The diastolic portion of the left heart is particularly important for overall circulatory efficiency, and diastolic function can be influenced by age, blood pressure, metabolic health, and structural heart disease. For the broader circulation, diastole is intertwined with the entire Cardiac cycle and the mechanics of the left ventricle as it fills.
Diastole unfolds through a sequence of subphases that reflect both pressure changes and ventricular compliance. Shortly after the end of systole, the aortic and pulmonary valves close, and the ventricle begins isovolumetric relaxation as its muscle fibers lengthen while the volume remains momentarily constant. When the ventricular pressure falls below the atrial pressure, the atrioventricular valve opens and filling begins. This initiates the rapid passive filling phase as blood flows from the left atrium to the left ventricle driven by the pressure gradient. The heart then transitions into diastasis, a period of slower filling as pressures equilibrate. Finally, atrial contraction (atrial systole) contributes an additional volume—the so-called “atrial kick”—to complete ventricular filling just before the next cycle of systole.
Physiology and determinants of diastolic filling hinge on ventricular relaxation and compliance. Relaxation is an active, energy-requiring process that reduces ventricular pressure after systole, while compliance describes how readily the ventricle expands to accept incoming blood. Anything that impairs relaxation or makes the ventricle stiffer can reduce the rate or amount of filling, particularly at higher heart rates when diastolic time is shortened. Valve function, pericardial constraint, myocardial architecture, and atrial contribution all influence the efficiency of diastolic filling. Clinically, the state of diastolic function is most often assessed in the context of the left ventricle, with attention to how well the heart fills at a given preload and heart rate.
Physiological subphases and measurements
Isovolumetric relaxation: Immediately after systole, the ventricles relax with the valves closed, causing pressure to fall without a change in volume. This phase ends when the AV valves open and filling begins. See Isovolumetric relaxation for further detail.
Early rapid filling: When the mitral valve opens, a brisk flow of blood enters the ventricle, producing a characteristic early-systolic filling pattern.
Diastasis: As pressures approach equilibrium, filling slows and becomes gradual.
Atrial contraction (atrial kick): The atria contract to deliver a final bolus of blood into the noncompliant ventricle, contributing to end-diastolic volume and pressure.
Diastolic function indices: Clinicians use Doppler and tissue Doppler techniques to quantify filling dynamics. Common measures include the transmitral flow pattern and the E/A ratio, the deceleration time of early filling, and the isovolumetric relaxation time (IVRT). Tissue Doppler measurements (e.g., e′ velocity) and the E/e′ ratio help estimate filling pressures. See Echocardiography and Doppler ultrasonography for imaging modalities; see E/A ratio and E/e' ratio for specific indices.
Clinical significance
Diastolic dysfunction and diastolic heart failure: Impaired relaxation or reduced ventricular compliance can lead to diastolic dysfunction, which in some patients progresses to heart failure with preserved ejection fraction (HFpEF). HFpEF is characterized by symptoms of heart failure despite a normal or near-normal ejection fraction and is a major area of focus in contemporary cardiovascular care. See Diastolic dysfunction and Heart failure with preserved ejection fraction for more.
Etiologies and associations: Hypertension, aging, obesity, diabetes, coronary disease, and certain infiltrative or hypertrophic conditions (such as hypertrophic cardiomyopathy) can alter diastolic properties. Structural changes, including left atrial enlargement, may accompany chronic diastolic dysfunction. See hypertension, aging, obesity, and amyloidosis for related topics.
Diagnosis and management: Diagnosis rests on a combination of clinical symptoms (e.g., dyspnea on exertion, reduced exercise tolerance) and imaging findings that reflect filling dynamics. Management emphasizes risk factor modification (blood pressure control, weight management, physical activity), rhythm optimization, and symptom relief with diuretics when congestion is present. Pharmacologic strategies that improve diastolic function or outcomes in HFpEF remain nuanced and are guided by individual patient characteristics; see Echocardiography and Heart failure with preserved ejection fraction for current approach and debates.
Controversies and debates: A central area of discussion concerns how best to define and diagnose diastolic dysfunction and HFpEF, particularly in asymptomatic individuals or those with comorbidities. Some clinicians emphasize strict thresholds on Doppler indices, while others advocate for a more integrated, multi-parameter assessment that includes ventricular stiffness and atrial contribution. The predictive value of isolated diastolic abnormalities in the general population is imperfect, and there is ongoing debate about which patients benefit most from specific interventions. In HFpEF, several traditional heart-failure therapies have shown limited mortality benefits compared with heart failure with reduced ejection fraction, prompting discussion about targeting underlying mechanisms such as microvascular function, ventricular-arterial coupling, and systemic comorbidities. See Diastolic dysfunction, HFpEF, and E/e' ratio for related discussions.
Practical considerations: Diastolic function is sensitive to heart rate and loading conditions. At faster heart rates, diastolic time shortens and filling can become inadequate in some individuals, particularly those with stiff ventricles. Conversely, increased preload or systemic factors can transiently enhance filling, complicating interpretation. The balance of preload, afterload, and myocardial relaxation shapes the observed diastolic pattern on imaging and in clinical assessment.