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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3781_Библиотеки_им_академика_М_И_Перельмана
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27 Hypertrophic Cardiomyopathy
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Fig. 27.2 Treatment algorithm for HCM.LVOT indicates left ventricular outow tract; NYHA
indicates NewYork Heart Association
309
• For patients who remain symptomatic despite maximal medical management,
septal reduction therapy by alcohol septal ablation or septal myectomy is indicated (Fig.27.1).
• Surgical intervention to alleviate LVOT obstruction is most performed via the
transaortic approach, although transatrial and transapical myectomy techniques
have been described.
• Percutaneous septal ablation is appropriate for patients who have failed medical
management but may be poor surgical candidates and have favorable coronary
anatomy.
• A single-chamber transvenous or subcutaneous implantable cardioverter-
debrillator (ICD) is indicated for all HCM patients who experience cardiac
arrest or sustained ventricular tachycardia. For HCM patients with LV wall
thickness>30mm, an apical aneurysm, a history of syncope, a family history of
SCD, or an ejection fraction <50%, placement of an ICD is recommended as a
Class II recommendation by the American Heart Association [4].
Transaortic Septal Myectomy
• Transaortic septal myectomy has been the standard surgical management for
patients symptomatic from septal hypertrophy since Morrow and colleagues
introduced it in the 1960s [5].
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• Patients with isolated LVOT obstruction or mid-cavitary obstruction are typi-
cally excellent candidates for this technique.
• Key steps of this approach include: [6] a low oblique aortotomy, taking care to
identify the origin of the right coronary artery to prevent inadvertent trauma, [7]
initiation of the myectomy just right of the nadir of the right coronary cusp,
avoiding the membranous septum, and carrying it leftward (for the right-handed
surgeon) to the commissure between right and left cusps, [8] the proximal extent
of the myectomy should remain 5mm below the surgical annulus of the aortic
valve, [1]. distally, it must extend well beyond the endocardial scar indicating the
mitral valve contact point. This may be 5–7cm into the ventricle. The thickness
resected will depend upon the thickness of the ventricle.
• Anomalous papillary muscle attachments to the septum are common and may
require division.
• Postoperatively, patients commonly develop left bundle branch block [9].
Complete heart block is uncommon unless a right bundle branch block (common
after prior septal ablation) is present.
• Postoperative care should focus on maintenance of atrial-ventricular synchrony.
• Symptom relief can be expected in 90% of cases. Recurrence is uncommon if
initial myectomy was adequate.
B. Kubi and T. M. Sundt
Transatrial Myectomy
• For HCM patients with concomitant mitral valve and sub-valvular apparatus
pathology, transatrial septal myectomy may be a more appropriate approach as it
offers a broader view of the ventricular septum and affords the opportunity for
intervention upon pathology of both the septum and the mitral valve and its apparatus [10].
• Compared to the transaortic approach, the transatrial approach reduces risk of
injury to the aortic valve cusps and associated coronary vessels.
• Characteristics of a successful repair for both approaches include achievement of
septal thickness of 8-10mm, absence of secondary ventricular septal defect, and
separation between the septum and the anterior leaet of the mitral valve throughout the cardiac cycle.
Benets andRisks ofSeptal Myectomy
• In experienced centers, perioperative mortality after isolated septal myectomy is
<1% [11].
• The residual inducible gradient across the LVOT should be less than
10mmHg [12].
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311
• Myectomy has been well demonstrated to be benecial to patients with obstruc-
tive HCM, with a superior overall survival than medically managed patients [13].
• Satisfactory myectomy should relieve mitral regurgitation secondary to SAM
among patients without primary mitral valve pathology.
• Patients who have had myectomy are less likely to have discharges from their
implantable cardioverter-debrillator (ICD), pulmonary hypertension, sudden
cardiac death, and have even been demonstrated in some studies to have reverse
myocardial remodelling [14, 15].
• Postoperative complications include ventricular septal perforation, conduction
abnormalities, and injury to the aortic or mitral valves [9–11, 16].
Alcohol Septal Ablation
• Alcohol septal ablation is another therapeutic option for symptomatic HCM
patients for whom surgery may be contraindicated, if their coronary anatomy is
favorable.
• In this technique, approximately 1 to 3cc of ethanol is injected into the septal
branches supplying the hypertrophied aspects of the myocardium. Through this
iatrogenic chemical necrosis, contractile dysfunction of the injected portion of
the myocardium is induced and the septum atrophies over time.
• While current studies have not demonstrated any differences in overall survival
between patients undergoing alcohol ablation and those undergoing myectomy,
freedom from reintervention and sustained reduction of LVOT gradient is greater
in the myectomy group [17].
References
1. Maron BJ.The electrocardiogram as a diagnostic tool for hypertrophic cardiomyopathy: revisited. Ann Noninvasive Electrocardiol. 2001;6(4):277–9.
2. Shirani J, Dilsizian V. Nuclear cardiac imaging in hypertrophic cardiomyopathy. J Nucl
Cardiol. 2011;18(1):123–34.
3. Authors/Task Force members, Elliott PM, Anastasakis A, Borger MA, Borggrefe M, Cecchi
F, etal. 2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy:
the Task Force for the diagnosis and Management of Hypertrophic Cardiomyopathy of the
European Society of Cardiology (ESC). Eur Heart J. 2014;35(39):2733–79.
4. Ommen SR, Mital S, Burke MA, Day SM, Deswal A, Elliott P, etal. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: A report of
the American College of Cardiology/American Heart Association joint committee on clinical
practice guidelines. J Am Coll Cardiol. 2020;76(25):e159–240.
5. Morrow AG, Brockenbrough EC. Surgical treatment of idiopathic hypertrophic subaortic stenosis: technic and hemodynamic results of subaortic ventriculomyotomy. Ann Surg.
1961;154:181–9.
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6. Maron MS, Hellawell JL, Lucove JC, Farzaneh-Far R, Olivotto I.Occurrence of clinically diagnosed hypertrophic cardiomyopathy in the United States. Am J Cardiol. 2016;117(10):1651–4.
7. Maron BJ, Maron MS. A discussion of contemporary nomenclature, diagnosis, imaging, and management of patients with hypertrophic cardiomyopathy. Am J Cardiol.
2016;118(12):1897–907.
8. Maron BJ, Maron MS, Semsarian C.Genetics of hypertrophic cardiomyopathy after 20 years:
clinical perspectives. J Am Coll Cardiol. 2012;60(8):705–15.
9. Ralph-Edwards A, Vanderlaan RD, Bajona P. Transaortic septal myectomy: techniques and
pitfalls. Ann Cardiothorac Surg. 2017;6(4):410–5.
10. Wehman B, Ghoreishi M, Foster N, Wang L, D'Ambra MN, Maassel N, etal. Transmitral
septal Myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg.
2018;105(4):1102–8.
11. Maron BJ, DearaA OSR, Maron MS, Schaff HV, Nishimura RA, et al. Low operative mortality achieved with surgical septal Myectomy: role of dedicated hypertrophic cardiomyopathy centers in the Management of Dynamic Subaortic Obstruction. J Am Coll Cardiol.
2015;66(11):1307–8.
12. Kotkar KD, Said SM, Dearani JA, Schaff HV.Hypertrophic obstructive cardiomyopathy: the
Mayo Clinic experience. Ann Cardiothorac Surg. 2017;6(4):329–36.
13. Orme NM, Sorajja P, Dearani JA, Schaff HV, Gersh BJ, Ommen SR.Comparison of surgical
septal myectomy to medical therapy alone in patients with hypertrophic cardiomyopathy and
syncope. Am J Cardiol. 2013;111(3):388–92.
14. Wang J, Sun X, Xiao M, Zhang M, Chen H, Zhu C, etal. Regional left ventricular reverse remodeling after Myectomy in hypertrophic cardiomyopathy. Ann Thorac Surg. 2016;102(1):124–31.
15. Smedira NG, Lytle BW, Lever HM, Rajeswaran J, Krishnaswamy G, Kaple RK, etal. Current
effectiveness and risks of isolated septal myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg. 2008;85(1):127–33.
16. Kwon DH, Smedira NG, Thamilarasan M, Lytle BW, Lever H, Desai MY.Characteristics and
surgical outcomes of symptomatic patients with hypertrophic cardiomyopathy with abnormal
papillary muscle morphology undergoing papillary muscle reorientation. J Thorac Cardiovasc
Surg. 2010;140(2):317–24.
17. Nguyen A, Schaff HV, Hang D, Nishimura RA, Geske JB, Dearani JA, etal. Surgical myectomy versus alcohol septal ablation for obstructive hypertrophic cardiomyopathy: A propensity score-matched cohort. J Thorac Cardiovasc Surg. 2019;157(1):306–315.e3.
B. Kubi and T. M. Sundt
Chapter 28
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Temporary Mechanical Circulatory
Support
StanleyB.Wolfe andEribertoMichel
Intra-Aortic Balloon Pump
Intra-aortic balloon pump is a catheter with a balloon on the tip that is placed in the
descending thoracic aorta (Fig.28.1). The balloon inates during diastole to increase
coronary artery perfusion and deates during systole to decrease left ventricular
afterload [1].
Indications
• Stabilize patients awaiting heart transplant (i.e., bridge to transplant).
• Bridge to durable left ventricular assist device.
• Congestive heart failure exacerbation with hemodynamic instability.
• Myocardial infarction with hemodynamic instability.
• Prophylactic placement before high-risk coronary angioplasty.
• Acute severe mitral valve regurgitation.
S. B. Wolfe (*) · E. Michel
Division of Cardiac Surgery, Massachusetts General Hospital, Boston, MA, USA
e-mail: stanleywolfe@icloud.com; EMICHEL2@mgb.org
Switzerland AG 2024
J. P. Bloom, T. M. Sundt (eds.), Cardiac Surgery Clerkship, Contemporary
Surgical Clerkships, https://doi.org/10.1007/978-3-031-41301-8_28
313© The Author(s), under exclusive license to Springer Nature
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Fig. 28.1 Intra-aortic
balloon pump inserted
through the right femoral
artery
S. B. Wolfe and E. Michel
Placement/Positioning
• The balloon catheter is inserted through the common femoral artery into the
descending thoracic aorta under uoroscopic guidance. Care must be taken to
ensure the catheter is distal to the left subclavian artery but proximal to the renal
arteries to prevent malperfusion.
• Alternatively, in patients who will need support for a more extended period, it
can be inserted through a graft into the axillary artery.
• The catheter is connected to the console and electrocardiogram (ECG) leads.
• Heparin is not required but is often used, especially when decreasing ination
frequency.
Settings andAugmentation Assessment
• Triggering ination: The balloon is inated during diastole as determined by the
T wave and deated at the start of systole, which is indicated by the peak of the
R wave. When the ECG quality is poor or not available, aortic pressure is used as
a backup to trigger ination and deation of the balloon.
• Augmentation ratio: This is the ratio of supported cardiac cycles to total cardiac
cycles. 1:1 augmentation indicates the balloon inates during diastole of each
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cardiac cycle. 1:2 augmentation indicates the balloon inated during diastole of
every second cardiac cycle.
• Augmentation is assessed when set to a 1:2 augmentation ratio. The arterial
waveform is evaluated for the following features:
– Diastolic augmentation wave: The tallest wave indicating ination of the bal-
loon. Should start just following the peak of the previous unassisted systole wave.
– Assisted systole wave: Peak immediately following diastolic augmentation
wave. It should be lower than the unassisted systole peak.
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Weaning
• Decrease the augmentation ratio from 1:1 to 1:2 for 30 min and monitor the
patient for ECG changes, hypotension, and reduced cardiac index.
• If the patient tolerates 1:2, a second trial further decreasing the augmentation
ratio to 1:3 can be attempted.
• The intra-aortic balloon pump should never be turned off and back on due to the
risk of clot formation and subsequent embolization.
Removal
• Once the patient passes a weaning trial, the balloon catheter can be removed.
This should be done with the patient in the supine position. If the balloon is
inserted via the axillary approach, the axillary incision must be reopened and the
graft ligated.
• Conrm that the patient is not anticoagulated prior to removal.
• Turn off the system console and disconnect the catheter.
• Ensure complete deation of the balloon by aspirating the balloon ination port
with a syringe.
• Remove the balloon catheter and sheath together (balloon will not t through
sheath after initial ination).
• Apply direct pressure to the femoral artery just proximal to the puncture site for
30min to ensure hemostasis.
• The patient should remain on bed rest for 6hours (or per institutional policy).
Impella
Impella® is a type of temporary left ventricular assist device (tLVAD). They are
catheter-based continuous ow pumps placed into the left ventricle via the aorta [2].
They function similar to an Archimedes screw by pumping blood from the distal
®
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insertion
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S. B. Wolfe and E. Michel
Fig. 28.2 The Impella®
pump is sitting across the
aortic valve with the distal
end in the left ventricle and
proximal end in the
ascending aorta. Both
axillary and femoral artery
insertion approaches are
demonstrated
Axillary graft
Femoral artery
end of the catheter, which sits in the left ventricle, to the proximal end of the pump
portion of the catheter, which sits in the aorta (Fig.28.2).
Indications
• Left ventricular failure.
• Bridge to heart transplant.
• Bridge to durable left ventricular assist device.
• Congestive heart failure exacerbation with hemodynamic instability.
• Myocardial infarction with hemodynamic instability.
• Elevated left ventricular end-diastolic pressure in patients on ECMO.
• Procedural or peri-procedure support for high-risk coronary interventions in the
catheterization lab or cardiac surgery patients with depressed LV function.
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317
Placement/Positioning
• There are four different types of Impella®, and placement approach varies by
device. Fluoroscopic and echocardiographic guidance is used during the placement of all devices.
• Impella® 2.5 (2.5L/min) and CP (3.5L/min): Percutaneous access of the femo-
ral artery.
– The femoral artery is accessed using the Seldinger technique, and a sheath
is placed.
– A guidewire is advanced into the apex of the left ventricle.
– The Impella® is advanced over the guidewire into the femoral artery, through
the aortic valve, and into the middle of the left ventricle.
– The guidewire is removed, and placement is conrmed via uoroscopy.
• Impella® 5.0 (5.0L/min) and 5.5 (5.5L/min): Surgical cutdown on the axillary
artery or central insertion directly into the ascending aorta.
– The axillary artery is exposed, and a vascular graft is anastomosed to its side.
– An introducer is inserted in and secured to the graft.
– A guidewire is advanced through the introducer and into the left ventricle.
– The Impella® is advanced over the guidewire into the graft, through the axil-
lary artery, and into the middle of the left ventricle.
– The guidewire and sheath are removed, and placement is conrmed via uo-
roscopy and echocardiography.
– The Impella® is secured to the vascular graft, the wound is closed, and the
Impella® is secured to the skin.
• Patients are anticoagulated while on Impella® support, both via a device purge
system and systemically.
Settings
• Impella® devices can provide varying levels of support.
• P levels indicate the level of ow provided by the device, with P-0 being 0L/min
and P-9 being the highest ow supported by that device.
• The lowest level of support to provide the desired cardiac output should be used
as higher ow levels result in more hemolysis.
• Power settings below P2 may not overcome the amount of aortic insufciency
created by the catheter and lead to patient decompensation.
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S. B. Wolfe and E. Michel
Weaning
• Reduce the level of support by incrementally decreasing the P level while monitoring for stability in the patient’s hemodynamic prole.
• Do not decrease the level of support lower than P2 until the Impella® is ready to
be removed.
Removal
• Decrease the level of support to P1 and pull the catheter out of the ventricle into
the aorta.
• Reduce the level of support to P0.
• The Impella® device is carefully removed and the arteriotomy repaired.
Protek Duo/LifeSparc® System
Protek Duo® cannula and LifeSparc® pump are a system that can be used as a right
ventricular assist device that pumps blood from the right atrium into the pulmonary
artery (Fig.28.3) [3].
Fig. 28.3 The Protek Duo
cannula is inserted through
the right internal jugular
vein with the tip of the
catheter terminating in the
pulmonary artery
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