Interventricular Delay

Optimal inter- and intraventricular coupling is more important than AV coupling for maximum ventricular pumping function. Normal ventricular electrical activation is rapid and homogeneous with minimal temporal dispersion throughout the wall. This elicits a synchronous mechanical activation and ventricular contraction. Exploration of the link between the sequence of cardiac electrical activation and mechanical function is one of the most exciting contemporary areas of research in heart failure but recognition of the importance of normal ventricular activation patterns for optimal pumping function dates back 75 years. Wiggers observed that asynchronous delayed activation of the ventricular musculature induced by electrical stimulation had adverse hemody-namic consequences in mammals and proposed that the more muscle activated before excitation of the Purkinje system, the greater the asynchrony and the weaker the resulting contraction.7 Forty years later, Schlant reached similar conclusions and concluded that asynchronous ventricular activation imposed by significant interventricular conduction delay (LBBB) was hemodynamically disadvantageous due to loss of the "idioventricular kick."8 This is a term applied to improved systolic function resulting from coordinated myocardial segment activation. This was attributed to the greater stretch and increased contractility

Mitral Regurgitation Wigger

Figure 9.1. Events of the cardiac electrical cycle. Atrial contraction followed by relaxation produces a negative pressure gradient, causing a surge of blood in the LV at end diastole. Reversal of the atrioventricular pressure gradient initiates mitral valve (MV) closure because of a rapid decrease in pressure between the MV cusps pulling them into apposition. A brief period of isovolumetric contraction exists after MV closure and before AV opening during which the maximal rate of pressure change (peak + dP/dt) occurs. Rapid ejection occurs during ventricular systole and is terminated when ventricular pressure falls below aortic pressure, closing the aortic valve (AV). A brief period of isovolu-mic relaxation follows during which the maximal rate of pressure decline (peak - dP/dt) occurs. As the left ventricular (LV) pressure continues to decline and fall below atrial pressure, the MV opens and diastolic ventricular filling begins. Normal diastolic filling is characterized by an initial rapid increase in ventricular filling during early diastole followed by a slow phase of filling during mid-diastole. A second rapid increase in ventricular filling occurs in late diastole as a result of atrial contraction.

Figure 9.1. Events of the cardiac electrical cycle. Atrial contraction followed by relaxation produces a negative pressure gradient, causing a surge of blood in the LV at end diastole. Reversal of the atrioventricular pressure gradient initiates mitral valve (MV) closure because of a rapid decrease in pressure between the MV cusps pulling them into apposition. A brief period of isovolumetric contraction exists after MV closure and before AV opening during which the maximal rate of pressure change (peak + dP/dt) occurs. Rapid ejection occurs during ventricular systole and is terminated when ventricular pressure falls below aortic pressure, closing the aortic valve (AV). A brief period of isovolu-mic relaxation follows during which the maximal rate of pressure decline (peak - dP/dt) occurs. As the left ventricular (LV) pressure continues to decline and fall below atrial pressure, the MV opens and diastolic ventricular filling begins. Normal diastolic filling is characterized by an initial rapid increase in ventricular filling during early diastole followed by a slow phase of filling during mid-diastole. A second rapid increase in ventricular filling occurs in late diastole as a result of atrial contraction.

(by Starling's law) of later contracting areas that is imparted by earlier contraction of other areas.

Chronic DCM is often accompanied by delayed ventricular electrical activation manifest as prolonged QRS duration (QRSd), most commonly in the form of left bundle branch block (LBBB).The prevalence of prolonged QRSd in heart failure associated with DCM varies between studies but appears to be

Doppler Mitral Inflow

Figure 9.2. Doppler mitral inflow patterns. This figure shows left ventricular (LV) filling velocities from a normal subject, recorded at the level of the mitral leaflet tips (apical window) with pulsed-wave Doppler. The mitral flow velocity curve is composed of the peak initial velocity (E wave) and the velocity at atrial contraction (A wave). This comprises the diastolic filling period, which is the interval from the onset of the E velocity to the cessation of the A velocity. In the first diastolic complex, the periods of rapid filling (RF), diastasis (D), and atrial systole (AS) are labeled. In the second complex, early diastolic (E) and atrial systolic (A) maximum velocities are indicated. The dashed line denotes the slope of decay of the peak early diastolic velocity and the arrowheads mark the deceleration time. The third complex shows how planimetry of the diastolic velocity curve as a function of time yields the velocity-time integral (VTI), which indicates diastolic "stroke distance."

Figure 9.2. Doppler mitral inflow patterns. This figure shows left ventricular (LV) filling velocities from a normal subject, recorded at the level of the mitral leaflet tips (apical window) with pulsed-wave Doppler. The mitral flow velocity curve is composed of the peak initial velocity (E wave) and the velocity at atrial contraction (A wave). This comprises the diastolic filling period, which is the interval from the onset of the E velocity to the cessation of the A velocity. In the first diastolic complex, the periods of rapid filling (RF), diastasis (D), and atrial systole (AS) are labeled. In the second complex, early diastolic (E) and atrial systolic (A) maximum velocities are indicated. The dashed line denotes the slope of decay of the peak early diastolic velocity and the arrowheads mark the deceleration time. The third complex shows how planimetry of the diastolic velocity curve as a function of time yields the velocity-time integral (VTI), which indicates diastolic "stroke distance."

in the range of 25% to 50%. Prolonged QRSd is a potent predictor of mortality in heart failure associated with DCM. In the VEST study, which assessed the efficacy of vesnarinone in patients with DCM and class II-IV heart failure, age, creatinine, ejection fraction, heart rate, and QRSd were found to be independent predictors of mortality. Cumulative survival from all-cause mortality decreased proportionally with QRSd. The relative risk of the widest QRSd group was five times greater than the narrowest.9 The association between LBBB in DCM and increased risk of sudden death and total mortality in DCM has subsequently been demonstrated in large population studies.10

Interventricular coupling refers to coordinated contraction of the right ventricle (RV) and LV Interventricular delay refers to a relative delay in mechanical activation of each ventricle, most commonly LBBB where the RV begins its contraction before the LV. The delay in onset of left ventricular activation results in reversal of the normal sequence between right and left ventricular

Figure 9.3. Schematic representation of hemodynamic effects of prolonged native AV conduction on left ventricular performance. The absence of the "a" wave before ventricular contraction may result in suboptimal ventricular filling and diastolic mitral regurgitation.

mechanical events that persists throughout the cardiac cycle.11 Asynchronous ventricular contraction and relaxation results in dynamic changes in ventricular pressures and volumes throughout the cardiac cycle. This results in abnormal septal deflections that alter the regional contribution to global ejection fraction. Earliest ventricular depolarization is recorded over the anterior surface of the RV and latest at the basal-lateral LV12 In canine models with induced LBBB, increasing the delay between RV and LV contraction increases the delay between the upslope of LV and RV systolic pressure. The increase in interventricular delay was associated with decreased LV + dP/dt and decreased stroke work, presumably the result of ventricular interdependence and impairment of the septal contribution to LV ejection due to displacement after onset of RV ejection.13 Pacing models can be used to induce asynchronous ventricular activation, with early activation occurring at the pacing site.14'15 Regions of late activation are subject to greater wall stress and develop local myocyte hypertrophy accompanied by reductions in sarcoplasmic reticulum calcium-ATPase and pho-spholamban.16 Chronic asynchronous ventricular activation redistributes the mechanical load within the ventricular wall and leads to reduction of blood flow and myocardial wall thickness over the site of early activation.15'17 This ventricular remodeling may contribute to progression of heart failure. In addition to these effects, delayed, sequential activation of papillary muscles may aggravate mitral regurgitation.18

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Responses

  • Allan
    Does isovolumic contraction exist?
    7 years ago

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