Diastolic dysfunction is a relatively new clinical diagnosis being made in patients where the observed echocardiographic findings are deemed to be consistent with abnormalities of left ventricular (LV) filling. Left ventricular filling is dependent on the complex interaction of three processes: LV relaxation, LV compliance, and left atrial (LA) contraction. Left ventricular relaxation is an active process involving the uptake of Ca into the sarcoplasmic reticulum by the sarcoendoplasmic reticulum Ca ATPase pump and removal of Ca from the cell by way of the sodium-calcium exchanger. Sarcoendoplasmic reticulum Ca ATPase pump expression and activity is reduced in the cardiomyocyte (and diastolic function is altered) with the onset of senescence, hypertrophy, and heart failure. Left ventricular compliance is a measure of the relationship between LV volume and LV pressure development during LV filling (dV/dp). Left ventricular compliance is influenced by: 1) the presence of ventricular hypertrophy; 2) the functional state of the right ventricle (direct diastolic ventricular interaction), since both ventricles share the septum as a common wall; and 3) the properties of the pericardium. Abnormal LV compliance is a feature of longstanding poorly-controlled hypertension, right ventricular dysfunction, and pericardial disease. In the presence of abnormal LV relaxation and/or compliance, LA contraction assumes a key role in maintaining LV filling. Under physiological conditions in youthful individuals, atrial contraction contributes approximately 20% of the total filling volume of the LV; whereas, in patients with LV diastolic dysfunction, LA contraction may account for over 50% of LV volume at enddiastole. Absence of LA contraction, as occurs with the development of atrial fibrillation, is a harbinger of heart failure and is a marker of an increased risk of premature death. The occurrence of abnormal LV relaxation and compliance, as a consequence of hypertensive heart disease, is one of the most common determinants of LA enlargement, poor LA contractile function, and LA dysrhythmia development. It is difficult, if not impossible, to individually assess the components of LV filling in humans; however, relatively precise global estimates of diastolic function can be performed following cardiac catheterization. This approach is invasive, time consuming, and not without risk. In reality, both our knowledge of diastolic function in the broader clinical environment and our interest in the topic did not materialize until the introduction of pulse wave Doppler echocardiography. Pulse wave Doppler echocardiography allows the timing and amplitude of the blood flow and tissue velocity profiles within the heart to be ascertained and graphically displayed. Extensive research has determined which blood flow/tissue velocity profile patterns are considered normal and which appear to be characteristic of diastolic dysfunction. The mitral inflow velocity profile, one of the earliest patterns studied, offers a relatively simple example of the deductive reasoning underlying the evolution of Doppler derived diastolic function assessment. Under ‘‘normal’’ circumstances, flow velocity across the mitral valve is biphasic, i.e., greater during early diastole (E wave) than during subsequent atrial contraction (A wave). In the presence of mild diastolic dysfunction associated with impaired ventricular relaxation, the early diastolic passive flow velocity is reduced while the flow velocity associated with atrial contraction is enhanced (reversed E/A ratio). It is clear, however, that many factors B. A. Finegan, MB (&) Department of Anesthesiology and Pain Medicine, University of Alberta, 8-120 Clinical Sciences Building, Edmonton, AB T6G 2G3, Canada e-mail: chassist@ualberta.ca
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May 17, 2009
W A Jaber + 3
Open Access