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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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D. B. Loriaux et al.
another, and mitral leaet elongation [52, 53].
These primary structural changes in the mitral
valve apparatus, even in the absence of signicant
septal hypertrophy, can result in SAM and LVOTO
[51]. There is a small number of HOCM patients
who have minimal LVH but severe LVOTO due to
prominent SAM from leaet elongation, papillary
muscle displacement, or a combination of both.
Surgical plication of an elongated MV leaet or
trans-aortic Aleri stich placement are feasible
interventions that may be used to reduce SAM
and alleviate the obstruction [54, 55].
Differentiating the mechanism of LVOTO is
essential in guiding therapy, as patients with
severe LVOTO attributed predominantly to these
mitral valve abnormalities may not have adequate
LVOTO reduction with ASA alone [56, 57].
Mitral valve regurgitation in patients with
HOCM must be carefully evaluated to determine
whether the MR is attributable predominantly to
SAM or other intrinsic MV pathologies. Intrinsic
MV pathologies might include leaet prolapse,
degeneration, chordal rupture, or stenosis. For
these patients, SRT alone is unlikely to be effective and surgical intervention is indicated [2]. For
the majority of patients with HOCM, intrinsic
mitral valve pathology is not present and reduction in LVOTG will alleviate MR due to SAM.A
retrospective analysis of over 2100 septal myectomies performed at the Mayo Clinic between
1993 and 2014 found that less than 5% of patients
undergoing myectomy required concomitant MV
repair or replacement and the percentage of
patients with MR grade≥3 decreased from 54.3
to 1.7% [58]. For patients who have primary MV
disease and require MV intervention during surgical myectomy, survival is superior for those
who undergo repair rather than replacement of
the mitral valve [58].
The recommended diagnostic algorithm for
HCM, adapted from the 2020 AHA/ACC
Guideline for the Diagnosis and Treatment of
Patients With Hypertrophic Cardiomyopathy, is
shown in Fig.9.
PATIENT WITH SUSPECTED HCM
• Personal History • Physical Examination • Family History • ECG
TTE
CMR
Screening first-degree family members of patients with HCM, using either genetic testing or an imaging/ECG surveillance protocol, can begin at any age and is influenced by the patient/family history and preference.
ADEQUATE STUDY?
NO
LVOTO (>30 mm Hg) AT REST?
YES
HOCM
YES
PROVOCABLE OBSTRUCTION
(>30 mm Hg) ON STRESS ECHO?
YES
HOCM
Fig. 9 HCM diagnostic algorithm [2, 21]. Recommended
screening algorithm for patients with suspected hypertrophic obstructive cardiomyopathy (HOCM) including electrocardiography (ECG), transthoracic echocardiography
Comprehensive Clinical Assessment
CLINICAL SUSPICION FOR HCM
G+ / P+
NO
NO
NON-OBSTRUCTIVE HCM
Genetic Counseling, Potential Testing*
PATHOGENIC MUTATION PRESENT?
YES
Screening of
Family Members
G+ / P-
Q12-Month
Surveillance
Medical
Management
Q12-Month
Surveillance
NO Screening of
Family Members
(TTE), cardiac magnetic resonance imaging (CMR), and
genetic testing. G+ presence of pathogenic genetic variants, P+ phenotype positive HOCM, P− phenotype negative HOCM, Q12 every 12months
NO
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Section 3: Pre-procedural
Management ofHCM
Early HCM Management
Selection of appropriate therapy for HCM is dictated by two factors: (1) the presence or absence
of symptoms; and (2) the presence and severity of
LVOTO measured on echocardiography, CMR,
or by invasive hemodynamic monitoring. It is
estimated that approximately two-thirds of
patients with newly diagnosed HCM will have
evidence of obstructive disease on initial
diagnostic imaging [39, 59]. The management
algorithm for HCM leading into septal reduction
therapy (Fig. 10) will be the focus of this
section.
As highlighted in the HCM management algorithm above, SRT is reserved for patients whose
symptoms remain refractory to pharmacologic
therapies. Negative inotropic agents (beta block-
ers, calcium channel blockers, and disopyramide)
are the centerpiece of medical management for
symptomatic HCM [60]. Tailoring medical management of HCM should also include elimination
of vasodilating medications (decreased systemic
vascular resistance may lead to increased outow
obstruction) and diuretics (decreased preload
may lead to decreased LV dimensions and greater
obstruction). Optimal medical management of
HCM augments LV preload and prolongs diastole, thereby reducing LVOTO, minimizing
microvascular ischemia, decreasing MR severity,
and reducing left atrial pressures.
In the six decades that have passed since
Braunwald and Morrow sparked the earliest
attempts to treat HCM with beta blockade, fewer
than 50 pharmacologic studies enrolling slightly
more than 2000 patients have been performed
[39, 61, 62]. Beta-blockers continue to remain
the rst-line agent for patients with obstructive
HCM [2]. For patients who do not respond to
Septal Reduction
(Class I)
SURGICAL CANDIDATE?
OTHER SURGICAL
NO
INDICATION?
YES
Myectomy
(Class I)
Septal Ablation
(Class I)
NO YES
Fig. 10 Hypertrophic obstructive cardiomyopathy treatment algorithm. Colors correspond to Class of
Recommendation from 2020 AHA/ACC Guideline for the
Diagnosis and Treatment of Patients with Hypertrophic
Cardiomyopathy. Mavacamten, FDA approved in April
Patient with HOCM
Avoid Vasodilators
Avoid High-Dose Diuretics
Beta Blockade
(Class I)
SYMPTOMS PERSIST
Verapamil or Diltiazem
(Class I)
SYMPTOMS PERSIST
Disopyramide
(Class I)
Mavacamten
2022, is included in algorithm as an alternative to disopyramide. GDMT guideline directed medical therapy,
HCM hypertrophic cardiomyopathy, HFrEF heart failure
with reduced ejection fraction, LVEF left ventricular ejection fraction
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D. B. Loriaux et al.
beta blockade, calcium channel blockers may be
considered. Although several studies have
demonstrated that non-dihydropyridine calcium
channel blockers are efcacious in alleviating the
symptoms of HCM, these agents must be used
with some caution due to the potential to rarely
worsen LVOTO by promoting peripheral vasodilation and decreasing LV preload [2, 40]. Finally,
in patients who have not responded to rst-line or
second-line therapies, disopyramide may be considered [40]. Disopyramide, a class 1A antiarrhythmic, possesses negative inotropic properties
and is an important therapeutic option (particularly in patients who are not candidates for SRT).
As disopyramide has the potential to enhance
conduction across the atrioventricular node, it
must be given in combination with atrioventricular nodal blockade [40]. Mavacamten, a small
molecule modulator of beta-cardiac myosin that
reversibly binds to myosin and reduces myocardial contractility, is an alternative to disopyramide in highly symptomatic patients with HOCM
[63]. A Study to Evaluate Mavacamten in Adults
with Symptomatic Obstructive HCM Who Are
Eligible for Septal Reduction Therapy (VALORHCM) randomized 112 patients with HOCM
(dened as LVOT gradient ≥50mmHg at rest or
with exertion) to mavacamten or placebo with a
primary endpoint of eligibility for SRT after
16 weeks of treatment [63]. After 16weeks of
therapy, 76.8% of patients in the placebo arm satised criteria for SRT compared to just 17.9% of
patients randomized to mavacamten (p<0.001)
[63]. Longer term freedom from SRT for symptomatic patients treated with mavacamten
remains to be determined.
Although the majority of patients with HCM
can achieve adequate symptom control using
medical treatment alone, responsiveness to pharmacotherapy for HCM can be highly variable [1].
When symptoms remain refractory to optimal
medical management, involvement of the Heart
Team for consideration of septal reduction strategies (surgical myectomy or alcohol septal
ablation) should be considered. Invasive management of HCM with septal reduction therapy will
be the focus of the next section.
Section 4: Procedural Management
ofHCM
Overview ofSeptal Reduction
Therapies
It has been less than 70years since the rst septal
reduction procedure was performed and less than
30years since the rst septal ablation. Over this
relatively short timeframe, the utilization of septal reduction therapies has grown exponentially.
Thousands of septal reduction procedures are
now performed each year worldwide. Surgical
septal myectomy continues to be regarded as the
gold standard treatment for symptomatic HCM
refractory to medical management [64]. However,
annual rate of ASA is increasing while that of SM
is slowly decreasing [65]. The use of ASA as an
alternative to surgery has continued to rise and
ASA has now become the primary septal reduction strategy in many parts of the world [64].
There are no randomized clinical trials comparing the efcacy and safety of septal ablation
relative to surgical myectomy. Current guideline
statements continue to rely solely on expert opinion and observational data, which have demonstrated similar short-term and long-term
outcomes between ASA and SM (Table7) [66].
The Hypertrophic Cardiomyopathy Guideline
Statements published in 2011 and 2014 differed
signicantly with respect to recommendations
for septal reduction therapy [57]. In 2011, surgical myectomy (receiving a Class IIa recommendation) was decisively favored over alcohol septal
ablation (Class IIb) [57]. In the 2011 version of
the guidelines, ASA was only recommended
when surgery was either deemed to be contraindicated or high risk [57]. In the 2014 and 2020
guidelines, equal Class I status is given to each
strategy for the management of adult patients
with symptoms refractory to medical management [2, 3]. Shared decision-making between the
patient and Heart Team with dialogue that
includes full disclosure of all available treatment
options, risks, benets, and patient goals is essential in choosing the most appropriate management strategy for HCM.
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Long term
mortality
general
population
general
population
Operative
mortality
Reoperation
rate
Any procedural
complication
215
Permanent
pacemaker
placement LOS
Primary
ECG
change
Mass of
myocardium
affected
Estimated
healthcare
costs
US
prevalence
First
case
15–20% 3days 20–30% 15–20% <1–5% Equal to
RBBB
(60%)
16 +/− 7g
15–20k
annual SRT
cases
1994 40–50%
5–10% 5–7days 20–30% 1–2% <1–5% Equal to
LBBB
(50%)
6 +/− 4g
40–50k
annual SRT
cases
1958 50–60%
Procedure
Alcohol
septal
ablation
Surgical
Table 7 Clinical comparison of ASA vs SM [3, 4, 66–68]
myectomy
Clinical comparison of alcohol septal ablation (ASA) versus surgical myectomy (SM) including history, prevalence, cost, mass of myocardium affected by the procedure, percent
procedural complications including complete heart block requiring permanent device placement, average hospital length of stay (LOS) following the procedure, reoperation rate,
and mortality (in-hospital and long-term)
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D. B. Loriaux et al.
ASA Technical Considerations
Alcohol septal ablation entails injecting 1–2mL
of 96% ethanol into a septal perforator artery
supplying the hypertrophied ventricular septum
to produce a myocardial infarction, induce septal
thinning, and alleviate outow obstruction [64].
Studies evaluating lower (1–2mL) versus higher
(>2mL) doses of ethanol have shown no difference in ASA safety and efcacy [69]. Candidacy
for ASA must be carefully considered. Factors
favoring ASA include advanced age, extensive
comorbidities, high surgical risk, prior sternotomy, and patient preference. Septal myectomy is
recommended in patients who have other indications for surgery (CABG, MVR, etc), severe septal hypertrophy (>3 cm), or coronary anatomy
that does not allow for successful ablation. The
interventricular septum is the most heavily vascularized area of the left ventricle, receiving
blood supply from all perforator branches as well
as the posterior descending artery.
Successful ASA is contingent upon several
factors: the injected volume of ethanol must be
able to reach the area of obstruction within the
LVOT, cause a focal infarct, resulting in a myocardial scar with subsequent thinning of this territory [64, 66]. When assessing patient candidacy
for ASA, septal hypertrophy should be within the
range of 18–30 mm. Patients with less than
18mm of septal hypertrophy are at risk of excessive wall thinning, and those with greater than
30mm hypertrophy are unlikely to achieve adequate reduction in septal wall thickness and outow tract gradient [70]. Signicant abnormalities
within the mitral valve apparatus contributing to
the outow gradient, such as elongated leaets
and anomalous insertion of papillary muscles,
should be absent in patients undergoing ASA
[64] to achieve optimal reduction in LVOT
obstruction. Patients less than 21 years of age
should not undergo ASA (Class III indication)
and the procedure is discouraged in patients
younger than 40 [2, 3]. The anatomic, pathophysiologic, and clinical proles that warrant consideration when assessing candidacy for ASA are
outlined in Fig.11.
For patients with medication refractory HCM
who satisfy the above selection criteria, ASA is a
safe and effective treatment strategy.
Echocardiography guided ASA has greatly
improved procedural success, decreased intervention time, and minimized complication rates
[2, 13]. Utilizing echocardiography guidance and
a perutren lipid microsphere contrast agent or
agitated saline via an over the wire coronary bal-
Fig. 11 Clinical features to guide selection of septal reduction therapy. Overview of variables impacting candidacy for
alcohol septal ablation versus surgical myectomy. LVOTO left ventricular outow tract obstruction
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loon selectively placed in the septal perforator of
interest, the septal artery supplying the portion of
the basal septum can be conrmed prior to injection of ethanol [40]. Contrast opacication occurs
from epicardium to endocardium, so slow injection of contrast with imaging over several minutes may be needed to fully assess septal
perfusion. When perfusion of the basal septum
endocardium is deemed inadequate, the contrast
agent appears predominantly in the right ventricular endocardium, or another cardiac structure
such as the RV free wall or a papillary muscle is
opacied, the procedure is aborted
(Supplementary Fig.4).
When the contrast agent conrms perfusion of
the basal septum (particularly endocardium of
septum) at the site of SAM-septal contact
(Supplementary Fig.5), ASA is performed using
approximately 1cc of absolute ethanol per 1cm
septal thickness [3]. The ethanol is slowly administered via the over the inated wire balloon over
10min. During this time, the cardiac rhythm is
Table 8 Procedural overview of ASA
Step Description
Consent
closely monitored, and infusion slowed with the
development of frequent premature ventricular
contractions and/or with PR prolongation or transient AV block. In addition, frequent evaluation
of the endoator is performed to ensure that the
baseline atmospheres of pressure that inated the
coronary balloon in the septal perforator are
maintained. Similarly, periodic uoroscopy to
ensure the balloon remains inated and in the
correct position is performed.
A full overview of the ASA procedure is pro-
vided in Table8.
It cannot be overstated that optimization of
the interventional management of HCM requires
a dedicated multidisciplinary team working at a
comprehensive HCM center of excellence where
a high volume of septal reduction therapies are
performed annually [2]. In this setting, the outcomes of septal reduction therapies are excellent. A summary of outcomes and complications
of ASA in comparison to SM is provided in
Table9.
• Candidacy:
– Septal thickness >16 mm, <30mm [13, 57]
– Advanced age, extensive comorbidities, or patient
preference
– High operative risk with no concomitant surgical
indications
• Risks:
– Vascular access complications
– Contrast dye reactions
– Extravasation of alcohol beyond target vessel
– Guide catheter complications (dissection, CVA)
– Heart block requiring permanent pacemaker
placement (10–20% general risk, up to 50% in
those with baseline LBBB) [2, 3, 71]
– Need for repeat ablation or surgical myectomy
(10–20%) [2, 3, 71]
• Benets:
– Reduction of LVOTO and alleviation of symptoms
– Improved long-term mortality free of cardiac
events
– Shorter duration recovery relative to surgical
myectomy
(continued)
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Table 8 (continued)
Step Description
TVP placement
Identication of septal perforator • Preferably right radial arterial access
• Transvenous pacemaker placement:
– Required in the absence of PPM or transvenous
ICD in situ
– Preferably via IJ access
– Capture threshold <1.0 mA
– Conrmation of placement in RV apex by
uoroscopy, CXR
– Placement maintained for 24–48 h post-procedure
• 6 Fr guide catheter introduced into left main coronary
artery
• Baseline angiogram in the RAO 30° and cranial 30°
projection for optimal visualization of the septal
perforator branches
• 0.014 inch coronary guidewire (300 cm) is advanced
via the guide catheter into rst septal perforator
– Unfractionated heparin given for ACT >250–300
prior to advancing guidewire
D. B. Loriaux et al.
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Table 8 (continued)
Step Description
Balloon positioning
a
• Over-the-wire (OTW) coronary balloon (slightly
larger in diameter than septal branch) is advanced
into the proximal portion of the vessel over the
coronary guidewire
• Balloon positioned to ensure placement entirely
within the septal branch without encroachment on
LAD
• Inate OTW balloon to nominal pressure per specic
balloon ATM chart
• Test injection of angiographic contrast dye with
OTW balloon inated to conrm absence of contrast
reux into native LAD while balloon is inated
• Injection of denity echo contrast to conrm
opacication of basal septum without other LV or RV
opacication
219
b
(continued)
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Table 8 (continued)
Step Description
Echocardiography guidance
• TTE performed to assess baseline wall motion, LVOT
gradient, SAM, and MR
• Coronary wire is removed, balloon inated, and
small volume of echocardiographic contrast dye is
injected via the OTW balloon to highlight area of
myocardium subtended by septal branch
• Echocardiographic images are acquired in the short
axis, parasternal long axis, and apical 3-chamber
views to conrm the presence of contrastenhancement of the basal septum at the location of
SAM
• If the region supplied by septal branch does not
correspond to area of obstruction on chest wall echo,
another septal branch should be evaluated, or the
procedure aborted
D. B. Loriaux et al.
Ethanol injection
• 1–2 cc 100% ethanol injected slowly over 10min
• OTW balloon remains inated for duration of EtOH
infusion to ensure no reux into LAD
• Balloon cleared with 0.5 cc bolus of normal saline,
deated, and removed
• Angiography to conrm 100% occlusion of septal
with intact and unchanged LAD
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Table 8 (continued)
Step Description
Post-injection echocardiogram
• Intraprocedural transthoracic echocardiogram is
performed
– Conrmation of basal septum akinesis
– Reassessment of LVOT gradient
– Ensure preserved wall motion in the anterior wall
and apex
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Post-procedural monitoring
Discharge
Step-by-step procedural overview of alcohol septal ablation
ACT activated coagulation time, ASA alcohol septal ablation, CHB complete heart block, CICU cardiac intensive care
unit, CVA cerebrovascular accident, CXR chest X-ray, ICD implantable cardioverter debrillator, IJ internal jugular,
LAD left anterior descending artery; LBBB, left bundle branch block; LVOTO, left ventricular outow tract obstruction;
MR mitral regurgitation, OTW
echocardiogram, TTE transthoracic echocardiogram, VT ventricular tachycardia, WMA wall motion abnormality
over-the- wire, SAM systolic anterior motion of the mitral valve, TEE transesophageal
• Overnight monitoring in Cardiac Intensive Care Unit
• Continuous telemetry to assess for arrhythmia (CHB,
VT)
• Continuation of transvenous temporary pacemaker
backup via IJ
• If no pacing, AV block, or pauses, discontinue
transvenous pacemaker the next morning and transfer
from the CICU to a telemetry unit
• Discharge on postprocedural day 3–4 if clinically
appropriate
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