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Chapter 19. Impact of cardiac resynchronization therapy on mitral regurgitation

Chapter 19. Impact of cardiac resynchronization therapy on mitral regurgitation

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240 CARDIAC RESYNCHRONIZATION THERAPY



consistently reported that CRT is associated with

a significant decrease in functional MR, both

acutely16–18 and in long-term follow-up.19–28 To

understand the mechanisms responsible for this

CRT-related improvement in the severity of

functional MR, it is necessary to take a closer

look at the complex pathophysiology of this

phenomenon.

PATHOPHYSIOLOGY OF FUNCTIONAL MITRAL

REGURGITATION IN HEART FAILURE

The term ‘functional MR’ implies the presence of

MR in the absence of structural damage to the

mitral valve leaflets. In the presence of systolic

heart failure, the incomplete systolic closure

of the mitral leaflets is provoked by several

contributing factors:









LV remodeling (i.e., spherical dilatation)

regional wall motion abnormalities

depressed LV systolic function



The most frequently cited (and probably

somewhat overemphasized) responsible condition for the occurrence of functional MR is

progressive dilatation of the mitral annulus in

the failing heart. It has been postulated that the

mitral leaflet area is insufficient to compensate

for the dilatation of the mitral annulus in heart

failure patients,29 but anatomic studies have

demonstrated that the actual available mitral

leaflet area is theoretically large enough to



(a)

Papillary

muscle



compensate for an amount of annular dilatation

that is usually beyond the degree observed in

heart failure patients.30 Thus, mitral annular

dilatation alone cannot sufficiently explain the

occurrence of functional MR. Simultaneous with

the dilatation of the mitral annulus, the LV

undergoes spherical LV remodeling with a progressively increasing distance between the mitral

leaflets and the papillary muscles. Since the

chordal apparatus is inelastic, the increased distance will in turn lead to an increased tethering

force that drags on the leaflet edges during systole and delays or even completely prevents complete leaflet coaptation during systole (Figure

19.1).31,32 The amount of tethering can be quantified by measuring the outward displacement of

the mitral leaflets, the so-called ‘tenting’ area.31,33

These observations led to the experimental concept of selective chordal cutting to reduce the

tethering forces and thereby the severity of functional MR.34 Furthermore, it has been well documented not only that regional dysfunction in

the area of papillary muscle insertion after

myocardial infarction may cause or aggravate

functional MR,1 but also that an additional

isolated loss of papillary muscle contraction may

paradoxically reduce the amount of MR. While

any regional dysfunction of the myocardium

around the papillary muscle insertion may augment the tethering forces, the additional loss of

contractile function within the papillary muscle

itself will counterbalance the increased tethering



(b)



LV



LV

PM

Papillary muscle

displacement



Closing force



Tethering

force



LA



MR



LA



Figure 19.1 (a) Balance of forces acting on the mitral valve. (b) Left ventricular (LV) dilatation displaces the papillary muscle

(PM) and increases the mitral tethering forces. This restricts complete mitral valve closure and causes functional mitral regurgitation (MR). LA, left atrium. (Reproduced from Otsuji Y, Handschumacher MD, Schwammenthal E, et al. Insights from threedimensional echocardiography into the mechanism of functional mitral regurgitation: in vivo demonstration of altered leaflet

tethering geometry. Circulation. 1997; 96(6):1999–2008.31)



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IMPACT OF CRT ON MITRAL REGURGITATION 241



forces and cause less apical tenting and a

decrease in the effective orifice area.35

The increased tethering force is counterbalanced by the LV ‘closing force’, which is determined by the effective transmitral pressure

gradient. LV dilatation will not cause significant

functional MR as long as myocardial contractility is still preserved and as long as the LV

is able to generate enough force to overcome

the increased tethering force. An example is the

patient with severe aortic regurgitation and preserved LV function who develops LV dilatation

(eccentric remodeling) but no significant functional MR. However, if LV myocardial contractility is also depressed – as it is by definition in

patients with systolic heart failure – then the

pressure rise in the LV will be delayed and

diminished. Thus, the closing force that is

required to overcome the increased tethering

forces cannot be generated, and functional MR

will be further aggravated.36 This concept is

supported by the observations that inotropic

stimulation (e.g., by dobutamine stress) in a

patient with heart failure will decrease the severity of functional MR, while dynamic physical

exercise, with an increase in afterload but only a

modest increase in inotropy, will aggravate

functional MR.37,38 The dependence of the effective

(a)



MR orifice area on the LV pressure rise also

explains the dynamic changes of the effective

regurgitant orifice area (EROA) during systole.39

Delayed, asynchronous electrical activation of

the LV as is typically seen in patients with left

bundle branch block (LBBB) is another independent cause of functional MR mediated

by the delayed LV pressure rise.40 A prolonged

atrioventricular interval further delays the onset

of LV contraction and pressure rise. In the

presence of an abnormally tethered mitral valve,

this situation predisposes to incomplete mitral

valve closure with the occurrence of pre-systolic

(diastolic) MR (Figure 19.2a).41 The end-diastolic

pressure reversal may not exert enough force to

close the restricted mitral leaflets (Figure 19.3).42

The critical value for the PR interval for the

appearance of diastolic MR has been determined

to be around 0.23 s.43

In summary, the progressive spherical remodeling of the LV during the evolutionary process

of systolic heart failure increases the mitral

annulus diameter and the distance between the

mitral leaflets and the papillary muscles. Both

effects will decrease the mitral leaflet coaptation

area and increase the tethering forces on the

leaflets, thereby increasing the EROA. Severe

regional wall motion abnormalities around the

(b)



LBBB



CRT



Figure 19.2 (a) A patient with left bundle branch block, showing a prolonged PR interval of 280 ms and pre-systolic mitral regurgitation (MR) on continuous-wave (CW) Doppler (arrow). (b) Cardiac resynchronization therapy (CRT) with atrioventricular delay

optimization eliminates pre-systolic MR, and LV dP/dtmax increases from 530 mmHg/s to approximately 1000 mmHg/s, as

indicated by the steeper slope of the regurgitant signal during CRT (dashed lines in (a) and (b)). Note that CW Doppler tends

to overestimate the improvement in LV dP/dtmax. Reprinted from The American Journal of Cardiology: Vol 97: Nof E, Glikson M,

Bar-Lev D, et al. Mechanism of Diastolic Mitral Regurgitation in candidates for Cardiac Resynchronization therapy. Issue II, pages

1611–1614. (2006). With permission from Elsevier.



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242 CARDIAC RESYNCHRONIZATION THERAPY



(a)



(b)



Restricted diastolic

leaflet motion



Normal



LV

LVEDP

LVEDP

LA



Post A-wave

pressure



Post A-wave

pressure



Figure 19.3 The effect of the left ventricular end-diastolic pressure (LVEDP) gradient on a normally (a) and abnormally

(b) tethered mitral valve. If diastolic leaflet motion is restricted due to increased tethering forces, the end-diastolic reversal of

the left ventricular (LV) – left atrial (LA) pressure gradient may not exert enough force to close the leaflets sufficiently.

(Reproduced from Am J Cardiol. Vol 97. Nof E, et al. Mechanism of diastolic mitral regurgitation in candidates for cardiac resynchronization therapy. Pages 1611–14 (2006). With permission from Elsevier. 42)



papillary muscles will further aggravate the

severity of MR, but papillary dysfunction in

itself will not further contribute to functional MR.

Electrical conduction delays as in first-degree

atrioventricular (AV) block and bundle branch

block contribute independently to the problem.

The volume overload of the LV contributes

further to LV dilatation and the progressive

deterioration in LV function, which in turn again

increases MR severity. Thus, it is often quoted

that ‘MR begets MR’.44

EFFECTS OF CRT ON FUNCTIONAL

MITRAL REGURGITATION

On the basis of the pathophysiology described

above, it becomes evident that any therapy that

improves global LV systolic function and that

simultaneously reduces wall motion abnormalities will also help to decrease the severity

of functional MR. CRT is such a therapy, and



has been shown to improve LV systolic function

as measured by an acute increase in LV dP/dtmax

and pulse pressure45,46 mediated by an improved

synchrony of myocardial contraction.22,47–49

The diastolic (pre-systolic) component of

functional MR is mainly dependent on delayed

AV coupling, which can be identified by a prolonged PR interval. It is eliminated by pacing

with a short (optimized) AV delay, independent

of the ventricular pacing site (Figure 19.2b).

Thus, diastolic MR can theoretically also be

effectively treated by conventional right ventricular (RV) pacing; however, this approach might

aggravate mechanical LV dyssynchrony and

thereby the systolic MR component.

As explained above, the systolic MR component is mainly determined by the imbalance

between the tethering and closing forces on

the leaflets. This led to the assumption that the

CRT-related acute improvement in LV systolic

function will augment the closing force on the



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IMPACT OF CRT ON MITRAL REGURGITATION 243



mitral leaflet and thereby immediately produce

a more rapid and more effective closure of the

valves. This was tested in an acute experiment

with reprogramming of the CRT device at rest

to on-and-off pacing in 24 patients with an

implanted CRT device.17 The severity of MR

was quantified with echocardiography by the

proximal isovelocity surface area (PISA) method

and compared with the non-invasively determined changes in LV systolic function (LV

dP/dtmax by continuous-wave Doppler). As

postulated, a linear correlation between the

EROA and LV dP/dtmax was observed in this

small study, demonstrating the close relationship between the accelerated rise in the systolic

closing force and the severity of functional MR

(Figure 19.4 and 19.5). This is in good agreement

with the observations by Fukuda et al,28 who

showed in a detailed color flow Doppler analysis



(a)



(b)



CRT off



CRT off



of the dynamic behavior of functional MR that

CRT reduced only the amount of earlysystolic MR, but not the late-systolic MR fraction

(Figure 19.6).

Kanzaki et al26 were able to confirm the relationship between the increase in LV dP/dtmax

and severity of MR. In addition, they analyzed

the deformation sequence of the papillary

muscles by strain rate imaging and found a relationship between the interpapillary muscle activation time delay and the improvement in the

degree of MR by CRT (Figures 19.7 and 19.8).

Similar observations were made by Porciani

et al,50 who demonstrated that the improvement

in MR was mainly related to the improved ventricular synchrony in the midventricular level.

Thus, the immediate reduction in severity of MR

can be attributed to an improved coordination of

ventricular contraction, including resynchronized



(c)



(d)



CRT on



CRT on



Figure 19.4 Effect of CRT on functional mitral regurgitation. Color Doppler shows moderate mitral regurgitation during no pacing

(LBBB) (a), and the estimated LV dP/dtmax <400 mmHg/s (b). During CRT, the mitral regurgitant velocity is smaller, corresponding to mild mitral regurgitation (c). The simultaneously acquired LV dP/dtmax by continuous-wave Doppler has improved significantly, as indicated by the faster rise of the regurgitant velocity (d). (Reprinted from J Am Coll Cardiol. Vol 46. Bax JJ et al.

Part 2–Issues During And After Device implantation and Unresolved Questions. Pages 2168–82 (2005). With permission from

American College of Cardiology Foundation.)



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244 CARDIAC RESYNCHRONIZATION THERAPY

Transmitral pressure



Normalized values



1.0



(a)



0.5



0



1.0



(b)

Time



0.5



OFF



0



CRT

Time



Effective regurgitant

orifice area



LA and LV pressure

EROA



Figure 19.5 Schematic representation of the relationship between the increase in transmitral pressure (TMP, the instantaneous difference between left ventricular (LV) and left atrial (LA) pressure) and the decrease in effective regurgitant orifice area (EROA). During

no pacing (a), LV contractility is low and results in a slow rise in the LV pressure curve and TMP, with a relatively late systolic maximum. Due to the slow LV pressure rise with delayed development of an effective transmitral closing force (~TMP), EROA remains

large for a relatively long period until it finally reaches its minimum value. In contrast, during CRT (b) LV contractility improves, TMP

rises faster and to a higher maximum value, which is also reached earlier. Consequently, the reduction in EROA occurs earlier, and

EROA reaches lower values and for a prolonged period of time. The shaded area represents the time in systole during which EROA

is <50% of its initial value. Note that in the example chosen here, the reduction in the height of the V-wave following a decrease in

the initial mitral regurgitation will contribute to a preserved TMP during the latter half of systole. (Reprinted from J Am Coll

Cardiol. Vol 41. Breithart OA, et al. Acute effects of cardiac resynchronization therapy on functional mitral regurgitation in advanced

systolic heart failure. Pages 765–70 (2003). With permission from American College of Cardiology Foundation.17)



(a)



End-diastolic



(b)



End-systole



Figure 19.6 Dynamic behavior of the mitral regurgitant (MR) jet throughout systole. (a) Before CRT, the mitral jet area and the

proximal flow convergence zone are much larger during early systole compared with late systole. (b) CRT reduces the total

amount of MR and reverses this pattern, with a late systolic peak of the MR jet. (Reproduced from Fukuda S et al. J Am Coll

Cardiol 2005;46:2270–6.28)



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IMPACT OF CRT ON MITRAL REGURGITATION 245



(a)

(c)



(d)



Baseline



After CRT



Strain (%)

0

−5



(b)

−10

−15



Mid-lateral site

Mid-inferior site



−20

0



1.0



2.0



Time (s)



0



1.0



2.0



Time (s)



Figure 19.7 (a, b) Parametric strain images from the apical four-chamber and two-chamber views. (c, d) Time–strain plots from

the LV myocardial segments adjacent to the papillary muscles, showing the extent of segmental shortening before and during

CRT. At baseline (c), clear dyssynchrony is observed, with delayed peak shortening of the mid-inferior segment. After CRT (d),

both segments shorten simultaneously. (Reprinted from American College of Cardiology Foundation. Vol 44. Kanzaki H, et al. A

mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy: insights from mechanical activation.Pages 1619–25 (2004). With permission from American College of Cardiology Foundation.26)



papillary muscle activation, which results in

improved systolic function and reduced mitral

leaflet tethering forces.

The effect of CRT on MR is largely independent of the underlying disease, and is found both

in ischemic and non-ischemic cardiomyopathy

patients.25 The immediate reduction of the MR

volume approaches about 30–40% on average

at rest.17,22,26 A further 10–20% improvement can

be observed in the long term after some months

of CRT, and is probably partly related to LV

reverse remodeling,22 although a direct relationship between reverse remodeling and MR reduction has not yet been demonstrated.51 However,

even a modest decrease in the MR volume

will improve the volume load to the LV and

contribute to long-term LV reverse remodeling.

Recent studies have also demonstrated that

the improvement in functional MR is not limited

to resting conditions, but can also be observed

during exercise. Lafitte et al52 found that about

30–40% of heart failure patients with a normal

QRS width (<120 ms) and 60–70% of patients



with a prolonged QRS width (>120 ms) demonstrate significant echocardiographic dyssynchrony at rest. Of those patients, about 30–40%

show a deterioration of the degree of dyssynchrony during exercise, which is accompanied

by a worsening of the severity of their MR. The

exercise-related increase in MR can be reduced

by appropriate biventricular pacing, as demonstrated by Lancellotti et al18 (Figure 19.9). It was

concluded that the inadequate rise in the mitral

closing force (i.e., LV dP/dtmax) during bicycle

exercise was the main determinant for the

increase in MR in non-synchronized patients

(CRT off at rest and during exercise). In alreadyresynchronized patients (CRT on at rest and

during exercise), the residual increase in MR

was mainly determined by geometrical factors

(namely the residual tenting area) and independent

of the increase in LV dP/dtmax.

The acute beneficial effects of CRT on MR are

sustained during mid- and long-term follow-up

and contribute significantly to the observed longterm benefit of CRT. Yu et al22 demonstrated that



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246 CARDIAC RESYNCHRONIZATION THERAPY



After CRT

Mild MR

Anterior



Baseline: LBBB

Moderate MR

Anterior



AL P



AL P



Lateral

Septal



300

ms



Septal



520

ms



300

ms



400

ms

Posterior



PM P



Posterior



PM P

Inferior



Inferior



(a)



250 ms



650 ms

After CRT

Trace MR

Anterior



Baseline: RV PACED

Moderate MR

Anterior



AL P



AL P



Lateral



Lateral

Septal



300

ms



Septal



520

ms



300

ms



300

ms

Posterior



PM P



Posterior



PM P

Inferior



Inferior



(b)



Lateral



250 ms



650 ms



Figure 19.8 Bull’s-eye plots of myocardial shortening from representative heart failure patients before and during CRT:

(a) a patient with LBBB; (b) a patient with RV pacing. The time to peak systolic strain is color-coded with lines representing

isochrones of mechanical shortening (activation) times at 50 ms intervals. The ‘X’ indicates the site of lead placement and

the arrow indicates the direction of the propagating mechanical shortening. The time to peak strain is shown for sites adjacent

to the anterolateral (AL P) and posteromedial (PM P) papillary muscles. (Reprinted from J Am Coll Cardiol. Vol 44. Kanzaki H,

et al. A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy: insights from mechanical activation strain mapping. Pages 1619–25 (2004). With permission from American College of Cardiology Foundation.26)



brief cessation of CRT after 3 months of active

pacing led to a return of MR to baseline levels

(Figure 19.10). Even after more than 1 year,

abrupt cessation of active CRT will worsen the

severity of MR, indicating that the clinical and

hemodynamic benefit of CRT persists over time.27



In general, the reduction in MR seems to be independent of the etiology of heart failure (ischemic

vs non-ischemic).25 However, in another series of

169 patients, the magnitude of the CRT response,

defined as an increase in LVEF, was larger in

non-ischemic patients with a lesser extent of scar



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IMPACT OF CRT ON MITRAL REGURGITATION 247



No pacing



Pacing

Difference −15 mm2



Rest



Difference +23 mm2



Difference +9 mm2

Difference −29 mm2



Exercise



Figure 19.9 Proximal flow convergence zone in a representative patient with pacing during rest (upper row) and exercise (lower

row) without CRT (left) and with active CRT (right). CRT reduced MR at rest (calculated effective regurgitant orifice area (ERO)

from 39–24 mm2) and diminished the relative increase during exercise. (Reprinted from Am J Cardiol. Vol 94. Lancellotti P,

et al. Effect of cardiac resynchronization therapy on functional mitral regurgitation in heart failure. Pages 1462–5 (2004). With

permission from Elsevier. 18)



(a)



(b)



1000



*







35



800





700







600







500



Mitral regurgitation (%)



900

dP/dtmax (mmHg/s)



40



*



*†



*†



30



*



25



*



*



20

15

10



400

Baseline



1wk



1mo



3mo



off–immed off–1wk



off–4wk



Baseline



1wk



1mo



3mo off–immed off–1wk off–4wk



Figure 19.10 Changes in LV dP/dtmax (a) and MR (expressed as the percentage of the MR jet in relation to LA size) (b) over time

during CRT. Both parameters improve with CRT and return towards baseline levels after cessation of CRT after 3 months of active

pacing. *Significant difference versus baseline. †Significant difference versus 3 months. (Reproduced from Yu CM et al. Tissue

Doppler echocardiographic evidence of reverse remodeling and improved synchrony by simultaneously delaying regional contraction after biventricular pacing therapy in heart failure. Circulation 2002;40:111–18.22)



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248 CARDIAC RESYNCHRONIZATION THERAPY



segments and a lower wall motion score

index.53 Patients with a marked response (LVEF

increase >10%) showed a greater improvement

in severity of MR than moderate responders

(LVEF increase 4–10%), while LVEF nonresponders (LVEF increase ഛ4%) experienced

no change in MR.

SUMMARY

It has become evident that the clinical long-term

benefit of CRT is closely related to its acute and

long-term effects on mitral valve competence.

The most impressive improvement is observed

in patients with non-ischemic cardiomyopathies

and with mild to moderate functional MR.

Preliminary evidence suggests that the response

to CRT might be more dubious in patients

with very severe MR. These patients usually

respond less to pacing, and should probably

also be evaluated for reconstructive mitral valve

surgery. Among the multiple clinical and

procedural factors that determine the success of

CRT, the effects on the mitral valve are of utmost

clinical and prognostic importance. A patient

with a CRT-related improvement in functional

MR is also likely to experience a significant

clinical and prognostic long-term benefit.

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Chapter 19. Impact of cardiac resynchronization therapy on mitral regurgitation

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