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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3737_Библиотеки_им_академика_М_И_Перельмана
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Part III
https://t.me/med1917
Interventions in Heart Failure

Interatrial Shunt Devices
https://t.me/med1917
TaimurSafder, SanjivShah, andAkhilNarang
Abstract
Heart failure with preserved ejection fraction
(HFpEF) remains difcult to manage while
contributing to high morbidity and mortality.
It is a complex disease state with a pathophysiology based in a multitude of contributing
factors. One common aspect of HFpEF is the
presence of increased LV end diastolic pressure (LVEDP) resulting in elevated left atrial
(LA) pressure. Increased LA pressure may
also be the best guide in assessing if dyspnea
is the result of elevated LA pressures leading
to pulmonary congestion. In this chapter, we
will discuss the evolving eld of interatrial
shunt devices (IASD) which target elevated
LA pressures as a possible therapeutic option
in patients with HFpEF.This chapter will discuss prevalence, morbidity and mortality of
HFpEF, along with the pathophysiology of
elevated left atrial pressures in HFpEF, and
treatment options using interatrial shunt
devices. Lastly, an example case of a patient
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 50740- 3_9.
T. Safder · S. Shah (*) · A. Narang
Bluhm Cardiovascular Institute, Northwestern
Memorial Hospital, Chicago, IL, USA
e-mail: Taimur.Safder@nm.org;
Sanjiv.Shah@northwestern.edu;
Akhil.Narang@nm.org
undergoing an IASD placement with pre, intra
and post procedural imaging guidance will be
reviewed.
Keywords
Heart failure with preserved ejection fraction
treatment · Heart failure with mild range
ejection fraction treatment · Interatrial shunt
device · Left atrial hypertension · Diastolic
dysfunction
Abbreviations
ACEi Angiotensin-converting enzyme
inhibitors
ARB Angiotensin II receptor blockers
ARNI Angiotensin receptor-neprilysin
inhibitor
CABG Coronary artery bypass graft
CAD Coronary artery disease
EF Ejection fraction
HF Heart failure
HFimrEF Heart failure with improved EF
HFmrEF Heart failure with mildly reduced
ejection fraction
HFrEF Heart failure with reduced ejection
fraction
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. M. Kelsey et al. (eds.), Cardiac Imaging in Structural Heart Disease Interventions,
https://doi.org/10.1007/978-3-031-50740-3_9
245

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IAS Interatrial septum
IASD Interatrial shunt device
KCCQ Kansas City Cardiomyopathy
Questionnaire
LA Left atrium
LV Left ventricle
LVEDP Left ventricle end diastolic pressure
MRA Mineralocorticoid receptor
antagonists
PA Pulmonary artery
PCWP Pulmonary capillary wedge
pressure
PVD Pulmonary vascular disease
PVR Pulmonary vascular resistance
RA Right atrium
RV Right ventricle
WU Wood units
Test your learning and check your understanding of this book’s contents: use the
“Springer Nature Flashcards” app to access
questions using ▶ https://sn.pub/ambACS.
To use the app, please follow the instructions in the chapter “Transcatheter Aortic
Valve Replacement.”
Learning Objectives
1. Review prevalence, morbidity and mortality
and the denitions of HFpEF.
2. Understand the interplay of HFpEF and left
atrial hypertension and how left atrial decom-
Background andDenitions
pression may be a viable and effective treatment option in patients with HFpEF.
3. Review the currently available literature in the
eld of interatrial shunts for HFpEF.
4. Understand the factors that are important to
identify in the pre-procedural stage that could
make the imaging and the procedure more
challenging.
5. Understand the key steps for a IASD proce-
dure and the optimal imaging needed to support it.
6. Understand post procedural imaging goals
and possible complications that can occur.
Despite signicant advances in the eld of heart
failure (HF) management, HF remains a challenging diagnosis for clinicians. The combined
prevalence of HFpEF and HFmrEF exceeds
HFrEF and possess a signicant challenge to clinicians [1–5]. HFpEF, and to a certain extent
HFmrEF, represent a distinct entity than HFrEF
[6] (Table2). HFpEF, in particular, is a complex
multiorgan syndrome that has layers of different
pathophysiological mechanisms that are built
upon the traditional diastolic heart failure paradigm. Despite this complex underpinning of
T. Safder et al.
Case Study
A 70-year-old male presents to clinic for
worsening dyspnea. He has a history of
CAD status post three vessel coronary
artery bypass graft, HFpEF, permanent
atrial brillation status post left atrial
appendage occlusion device, hypertension,
hyperlipidemia and obesity. Patient reports
he can only walk 1–2 blocks before having
signicant dyspnea that limits his activity.
Transthoracic echocardiogram was
notable for normal LV size and function
(LVEF 65%), mildly dilated RV, bi-atrial
enlargement, no signicant valvular abnormalities. LV global longitudinal strain
−15%.
For further evaluation of etiology of the
patient’s symptoms, a right heart catheterization (RHC) with exercise bike was done
with results noted in Table1.
Table 1 RHC with exercise bike results prior to
IASD
Rest Peak exercise
RA (mean, mmHg) 6 22
RV (mean, mmHg) 8
PA (mean, mmHg) 29 51
PCWP (mmHg) 11 32
CI (L/min/m
PVR (woods units) 3.5
2
) 2.5 3.6

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HFpEF, one common thread that binds these
patients is elevated LVEDP and LA pressure at
rest and/or with exercise [7]. Elevated LVEDP
leads to an increased LA pressure and remodeling, which further leads to increased pulmonary
pressures and lung gas exchange abnormalities
resulting in the characteristic symptom of dyspnea [8]. With modest success of medical therapies, one new focus of treatment in HFpEF and
HFmrEF patients has become ways to help
reduce the elevated LA pressure.
Left atrial decompression by a way of an iatrogenic interatrial shunt is one strategy currently
being investigated. This strategy developed from
historical observations of patients with left sided
valvular disease and atrial septal defects (ASD),
such as Lutembacher syndrome. These patients
Table 2 Denitions of HF by LVEF, adapted from ACC/
AHA/HFSA 2022 HF guidelines
HF types Denition
HF with reduced EF
HF with improved
EF
HF with mildly
reduced EF
HF with preserved
EF
LVEF ≤40%
Previous LVEF ≤40% but now
LVEF ≥40%
LVEF 41–49%
LVEF ≥50%
were found to tolerate their valvular disease better than patients with valvular disease but no
ASD.In addition, closure of ASDs has shown to
result in abrupt increases of LA pressure and HF
exacerbations [1] (Fig.1). Utilizing this framework, this novel device-based treatment strategy
of iatrogenic interatrial shunt is currently being
pursued and several shunt devices are in various
stages of development for patients with HF
(Fig.2).
Data from clinical trials using the Corvia
IASD device has been promising (Fig.3). Phase
I data from the REDUCE LAP-HF trials demonstrated safety and efcacy of the Corvia IASD
device in patients with LVEF ≥40% (Table3).
Although the overall phase 3 randomized control
trial failed to show an overall difference in the
primary end point (CVD death or non-fatal ischemic stroke at 12months, total HF events up to
24 months, and change in KCCQ overall summary score at 12 months) between sham and
treatment arm, the study did note a positive signal
of benet in patients without PVD (PVR <1.8
WU). This may represent a subsegment of
patients that may benet from IASD therapy [9].
At this stage, IASD therapy remains promising
and further studies are needed to establish it as an
evidence based therapy for HF patients.
Fig. 1 Left atrial
pressure tracing showing
increased LA pressures
when ASD is occluded
and decrease of LA
pressures when ASD is
opened
ECG
Left atrial
pressure
ASD occluded ASD open
1 sec
v
a
v
a
60
[mmHg]
30
0

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T. Safder et al.
Fig. 2 List of the current interatrial shunt devices/procedures under investigation

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Fig. 3 Proposed mode of action for Corvia device: dynamic decompression of overloaded LA chamber by shunting blood from LA ➔ RA (Qp:Qs 1.2–1.3)

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Summary of REDUCE LAP-HF trials
Table 3
Shah etal. REDUCE
LAP-HF II (2022)
Baseline characteristics
N 314 (treatment arm)
Age (years) 73 (median)
Male (%) 36
LVEF (%) 60 (median)
PCWP at rest (mmHg)
Baseline
Post-procedure
Functional status outcomes
NYHA
Baseline
Post-procedure
Median change in KCCQ
(IQR) from baseline to
12months
*Not statistically signicant
**Statistically signicant
Percent of patients
with:
PCWP <15 ➔ 30%
PCWP >15 ➔ 70%
Change in median
NYHA
−0.5 (−1 to 0)**
10.2 (−1.8 to 26.8)*
Diagnosis andPre-procedural
Assessment
When patients with suspected HFpEF are evaluated for IASD, their symptoms must be interrogated fully as to delineate the etiology from other
comorbidities that may be present in this patient
population (i.e. anemia, COPD). Exercise stress
echocardiogram can be a helpful tool in assessing
diastolic dysfunction in patients presenting with
unexplained dyspnea. After a comprehensive
T. Safder et al.
evaluation which excluded ischemia, anemia, or
pulmonary disease in our patient, a RHC with
exercise was obtained.
RHC with exercise is an important and often
underutilized test for HFpEF. When done correctly and interpreted accurately, the information
can be revealing. Resting measurements of cardiac lling pressures alone often lack sensitivity
for diagnosing HFpEF.Left sided cardiac lling
pressures (i.e. PCWP) measured during exercise
is likely to yield much better HF diagnostic and
prognostic information [10]. Occasionally elevated left atrial pressures are only elicited during
exercise with the patient having normal pressures
at rest (Fig. 4). Exercise hemodynamics in
patients with HFpEF can help classify their disease phenotype and one such classication system is proposed in Fig.5.
The notable nding from our patients RHC
notes a resting PCWP of 13 mmHg, which
increases signicantly to 32mmHg at peak exercise (Table1). This nding of exercised induced
LA hypertension categorizes our patient as type I
HFpEF (Fig.5). Type I, and to a smaller extent
type II, HFpEF patients represent the ideal candidate for an IASD (Fig.6). Patients with signicant right heart failure and/or pulmonary arterial
hypertension are unlikely to benet from an
IASD and are poor candidates for shunt based
therapy (these patients were also excluded from
REDUCE LAP-HF II trials).

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a
b
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Fig. 4 Hemodynamic measurements at rest (Panel a) showing normal values and the same patient undergoing exercise
with hemodynamic measurements (Panel b), showing signicant increase in the PCWP

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T. Safder et al.
Fig. 5 Phenotype guided approach to HFpEF

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Fig. 6 Device based therapeutics for HFpEF
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