Interpreting Diastolic Dynamics and Evaluation through Echocardiography

Figures

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  Figure 1. Simplified schematic diagram of Ca2+ regulation channels during the myocardial cell contraction and relaxation phases. The sarcoendoplasmic reticulum calcium ATPase (SERCA-ATPase) pump is vital for absorbing Ca2+ and storing it in the sarcoplasmic reticulum (SR). This absorption reduces the Ca2+ concentration in cytoplasm, contributing to the initiation of the myocyte’s relaxation phase. Importantly, SERCA-ATPase remains active throughout the relaxation process. In parallel, ryanodine receptors (RyR), stimulated by external Ca2+ from L-type Ca2+ channels, release stored Ca2+ from the SR. This increases the concentration of Ca2+ in the cytoplasm, ultimately triggering myocyte contraction.

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  Figure 2. Schematic representation of left ventricular pressure (LVP), left atrial pressure (LAP), and LV filling rate during the relaxation phase. The cardiac cycle consists of six phases: isovolumetric relaxation (phase 1), LV active relaxation (early rapid filling in phase 2 and inflow deceleration in phase 3), diastasis (phase 4), and LA contraction (the A wave upstroke in phase 5 and the A wave downstroke in phase 6). The initial pressure crossover marks the conclusion of isovolumic relaxation and the commencement of early rapid filling. which begins with the opening of the mitral valve. During this phase, LAP surpasses LVP, hastening mitral flow, and peak mitral E aligns with the second crossover. Subsequently, LVP surpasses LAP, slowing mitral flow and demarcating the early rapid filling phase and inflow deceleration phase. These phases are succeeded by diastasis, characterized by minimal pressure differentials. During LA contraction, LAP once again surpasses LVP, and an A wave appears. E: mitral peak velocity of early filling; A: mitral peak velocity of late filling.

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  Figure 3. Schematic representation of left ventricular (LV) strain, strain rate, and left atrial (LA) strain (LAS). SRivr: strain rate during isovolumic relaxation; SRe: strain rate during early diastole; SRa: diastolic peak longitudinal strain rate; ECG: electrocardiogram.

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  Figure 4. Diverse schematic patterns of left ventricular diastolic dysfunction (LVDD) illustrated through transmitral flow (top) and tissue Doppler at the level of the mitral annulus (bottom). As LVDD worsens, the peak value of e′ progressively decreases and is reached later in the cycle than the E wave peak (vertical dashed lines). E: mitral peak velocity of early filling; A: mitral peak velocity of late filling; e′: mitral annular peak velocity of early filling; a′: mitral annular peak velocity of late filling.

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  Figure 5. Algorithm A for diagnosis of LV diastolic dysfunction (LVDD) in subjects with normal LV ejection fraction (LVEF). E: mitral peak velocity of early filling; e′: mitral annular velocity of early filling by tissue Doppler; TR: tricuspid valve regurgitation; LA: left atrium; Vmax: maximum velocity.

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  Figure 6. Algorithm B aims to estimate left ventricular (LV) pressure and grade LV diastolic dysfunction (LVDD) in patients with reduced LV ejection fraction (LVEF) and those with myocardial disease but normal LVEF. ⬆ and ⬆⬆ indicate a mild increase and a greater increase, respectively, in left atrial (LA) pressure. E/A: ratio of mitral peak velocities of early and late filling; e′: mitral annular velocity of early filling by tissue Doppler; TR max: peak velocity of tricuspid regurgitation; LA: left atrial; LAP: LA pressure.