Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5212_Библиотеки_им_академика_М_И_Перельмана.pdf
10 M. Hamilton and Y. Manla
Hydralazine and Isosorbide Dinitrate
The combination of hydralazine and isosorbide
dinitrate (arterial and venodilators respectively)
is recommended, in addition to other GDMT,
for African Americans with NYHA Class III-IV
HFrEF, having demonstrated improved mortality
and quality of life in the A-HeFT Trial. The
benefit in non-African Americans is unclear,
but there is evidence to suggest that these
vasodilators are useful in reducing morbidity
and mortality in symptomatic HF patients who
are unable to tolerate ACEi or ARBs, or those
with persistent HF symptoms and adequate
blood pressure despite maximal titration of the
other GDMT [3].
Additional Medications
The role of digoxin in the care of HF patients
has diminished, now with only a 2B indication for symptomatic patients to reduce hospitalizations [3]. Since it has a narrow therapeutic
window, with increased mortality at serum levels > 1.0 ng/mL, it should be used cautiously in
patients with advanced HF and fluctuating
renal function. Ivabradine, a selective inhibitor of the cardiac pacemaker “funny” current
If that lowers heart rate without affecting contractility; in a European 6558-patient multicenter study—the SHIFT TRIAL [35], it was
found among patients in sinus rhythm with
a heart rate > 70 bpm on maximally tolerated
beta-blocker dosage to reduce the risk of HF
hospitalization. This has led to a 2A recommendation, but it is important that beta blockade
dosing has truly been maximized prior to considering Ivabradine. It is not indicated in atrial
fibrillation since it only acts on the sinus node
and actually increases the risk of de novo atrial
fibrillation. Vericiguat, an oral soluble guanylate
cyclase stimulator with vasodilatory properties and potential for fibrosis reduction has a
2B indication for HFrEF patients with worsening HF, based on the VICTORIA trial in which
it led to a small reduction in hospitalizations in
this high risk population [36]. Its ultimate role
for our advanced HF patients is not yet clear.
Other medications currently with 2B indications
include the potassium binders to allow upward
titration of ACEi/ARNI/MRA in patients with
hyperkalemia, and Omega-3 PUFA which
showed a 10% reduction in mortality in one trial
[37, 38]. Non-dihydropyridine calcium channel
blockers (dilitiazem and verapamil) and nonsteroidal anti-inflammatory agents should be
avoided in HF patients due to risk of worsening
symptoms.
Device Management of Advanced Heart Failure
Cardiac Resynchronization Therapy
Approximately one-third of HF patients demonstrate substantial prolongation of the QRS
interval on ECG, which is associated with dyssynchronous left and right ventricular contractility leading to further increased oxygen
demand, LV dilation and reduced contractility,
and ultimately worse outcomes [39]. In these
patients, left ventricular pacing (termed cardiac
resynchronization therapy (CRT) or biventricular pacing) can improve ventricular contractile
function, diminish secondary mitral regurgitation, reverse ventricular remodeling, and provide
sustained improvement in LVEF [40].
Thus, in patients with reduced LV function
(EF ⩽35%), sinus rhythm, left bundle branch
block and a QRS width ⩾
display NYHA class II, III or ambulatory IV
symptoms despite optimal medical treatment,
cardiac resynchronization therapy (CRT) is
recommended (Class 1A) to improve symptoms
and exercise capacity while decreasing
hospitalizations and mortality [3]. For those
patients who meet all the aforementioned
categories except for a shorter QRS width
within the 120–149 range, or without a typical
LBBB pattern, CRT may also be considered,
although evidence for a benefit is less clear
150 ms, who
111 Medical Therapy for Patients with End-Stage Heart Failure
(Class2A and 2B).CRT is also appropriate for
those patients with reduced LVEF and >40%
RV pacing which can further impair contractility
[3]. Importantly, CRT should not be considered
a “rescue therapy” and is not indicated for
patients who are functionally stage IV and not
ambulatory, are requiring inotropic support, or
have an expected life-expectancy of <1 year due
to comorbidities or frailty.
Implantable CardioverterDebrillator (ICD)
Patients who have systolic dysfunction are
at risk of sudden cardiac death (SCD) due to
ventricular tachyarrhythmias. For secondary
prevention of SCD, ICD implantation has been
demonstrated to reduce mortality in cardiac
arrest survivors and in patients with sustained
symptomatic ventricular tachyarrhythmias [41].
For primary prevention of SCD in HF patients
with optimal pharmacological treatment,
guidelines [3] specify a 1A indication for ICD
therapy in selected patients with LVEF ⩽35%
at least 40 days after myocardial infarction and
in patients with ischemic and non‐ischemic HF
(NYHA class II–III) with LVEF ⩽35% to reduce
mortality [42]. ICDs also have a 1A indication
for patients with an ischemic cardiomyopathy
with LVEF less than 30%, even if asymptomatic.
The data supporting primary prevention ICDs
is strongest in those with an ischemic etiology.
The DANISH Trial demonstrated a reduction
in cardiac, but not overall, mortality, in patients
with nonischemic cardiomyopathy, which
was seen primarily in younger patients [43].
Primary prevention of ICD, therefore, requires
shared decision-making on an individual basis
for patients with dilated cardiomyopathy
and reduced LVEF. ICDs may be considered
(2A indication) now for high risk genetic
arrhythmogenic cardiomyopathy patients
with LVEF as high as 45%, and we can likely
anticipate further changes in guidelines for
primary prevention as our genetic understanding
of cardiomyopathies becomes more refined.
Subcutaneous defibrillators rather than
transvenous devices may also be considered in
younger patients for whom anti tachycardia or
bradycardia pacing is not anticipated, avoiding
vascular and endocarditis risks [44].
Since many patients with HFrEF have indications for both CRT and ICD, these devices are
often implanted together, sharing a generator
(CRT-D). Similar to CRT, ICD’s should not be
implanted in patients with Class IV symptoms
and/or predicted survival of less than 1 year.
Other implantable electrical devices are under
investigation, including baroreceptor and vagal
nerve stimulation and His and left bundle pacing
[3]. Cardiac contractility modulation, in which
an impulse is applied to the RV septal wall during the refractory period to improve contractility, has been FDA approved for Class III HFrEF
patients to improve quality of life, but does not
yet have positive outcomes data [45]. Class 1C
antiarrhythmics and donadrenone should be
avoided in HF patients due to increased risk of
sudden death and worsening HF.
Transcatheter Mitral Valve Edge-ToEdge Repair (TEER)
Functional secondary mitral regurgitation (MR)
in HF patients can contribute to worsening
symptoms, left ventricular dilation and contractility, as well as pulmonary hypertension. In the
COAPT Trial [46], patients with LVEF as low
as 20%, NYHA Class III symptoms, with persistent severe MR despite maximally tolerated
GDMT, had a significant reduction in mortality
and hospitalizations after TEER. Of note for the
advanced HF population, there was also a reduction in need for cardiac transplantation. A trial
of TEER in HF patients with relatively less MR
compared to the degree of left ventricular dilation (MITRA-FR) did not show similar benefits,
suggesting optimal candidates for the procedure
are those with disproportionately more MR [47].
Since functional MR can be dynamic, TEER
should only be considered if it remains severe
after GDMT has been optimized and CRT performed (if indicated).
12 M. Hamilton and Y. Manla
Indwelling Pulmonary Artery Pressure Sensors
The CardioMEMS implanted pulmonary
artery (PA) sensor was shown to reduce
hospitalizations in Class III HFrEF and HFpEF
patients in the Champion Trial [48], but was not
confirmed in the Guide-HF Trial [49], leaving
this device with a 2B indication. Other remote
monitoring devices are being investigated,
awaiting the findings.
Treatment of the Hospitalized Patient with Acute Decompensation
As stated in the guidelines, the goal of treatment for patients hospitalized with decompensated HF (Class 1C indication) should address
reversible factors, establish optimal volume
status, and advance GDMT toward targets for
outpatient therapy. Unless the patient has cardiogenic shock or substantial creatinine rise,
withholding GDMT during a hospitalization
for decompensated HF may be detrimental, and
both initiation and upward titration of GDMT
during a HF admission appear to have long-term
benefits [50]. Diuresis should be complete and
not be withheld for small increases of creatinine
(<0.3), as persistent congestion at discharge is
a poor prognostic factor. Bedside ultrafiltration
and addition of low dose dopamine to iv diuresis have not improved outcomes [51]. Persistent
hypotension or hypoperfusion require administration of inotropic support; management of cardiogenic shock is reviewed in Chap. 2.
References
1. Members WC, Bozkurt B, Ahmad T, Alexander
KM, Baker WL, Bosak K, et al. Heart failure epidemiology and outcomes statistics: a report of
the Heart Failure Society of America. J Card Fail.
2023;29(10):1412.
2. Tsao CW, Aday AW, Almarzooq ZI, Anderson
CAM, Arora P, Avery CL, et al. Heart disease
and stroke statistics—2023 update: a report from
the American Heart Association. Circulation.
2023;147(8):e93-621.
3. Heidenreich PA, Bozkurt B, Aguilar D, Allen LA,
Byun JJ, Colvin MM, et al. 2022 AHA/ACC/HFSA
guideline for the management of heart failure: a
report of the American College of Cardiology/
American Heart Association Joint Committee on
Clinical Practice Guidelines. J Am Coll Cardiol.
2022;79(17):e263-421.
4. Yancy CW, Jessup M, Bozkurt B, Butler J,
Casey DE, Drazner MH, et al. 2013 ACCF/AHA
guideline for the management of heart failure:
a report of the American College of Cardiology
Foundation/American Heart Association Task
Force on Practice Guidelines. J Am Coll Cardiol.
2013;62(16):e147-239.
5. Lewsey SC, Breathett K. Racial and ethnic
disparities in heart failure: current state and future
directions. Curr Opin Cardiol. 2021;36(3):320–8.
6. Savarese G, Lund LH. Global public health burden
of heart failure. Card Fail Rev. 2017;3(1):7.
7. Folsom AR, Shah AM, Lutsey PL, Roetker NS,
Alonso A, Avery CL, et al. American Heart
Association’s Life’s Simple 7: avoiding heart failure
and preserving cardiac structure and function. Am J
Med. 2015;128(9):970–6.
8. Aggarwal M, Bozkurt B, Panjrath G, Aggarwal B,
Ostfeld RJ, Barnard ND, et al. Lifestyle modifications for preventing and treating heart failure. J Am
Coll Cardiol. 2018;72(19):2391–405.
9. Lara KM, Levitan EB, Gutierrez OM, Shikany
JM, Safford MM, Judd SE, et al. Dietary pat terns
and incident heart failure in US adults without
known coronary disease. J Am Coll Cardiol.
2019;73(16):2036–45.
10. Simon T, Mary-Krause M, Funck-Brentano C,
Jaillon P. Sex differences in the prognosis of
congestive heart failure: results from the Cardiac
Insufficiency Bisoprolol Study (CIBIS II).
Circulation. 2001;103(3):375–80.
11. Packer M, Fowler MB, Roecker EB, Coats AJS,
Katus HA, Krum H, et al. Effect of carvedilol on
the morbidity of patients with severe chronic
heart failure: results of the carvedilol prospective
randomized cumulative survival (COPERNICUS)
study. Circulation. 2002;106(17):2194–9.
12. Investigators* S. Effect of enalapril on survival in
patients with reduced left ventricular ejection
fractions and congestive heart failure. N Engl J Med.
1991;325(5):293–302.
13. Garg R, Yusuf S. for the Collaborative Group on
ACE Inhibitor Trials. Overview of randomized
trials of angiotensin-converting enzyme inhibitors
on mortality and morbidity in patients with heart
failure. JAMA. 1995;273(18):1450–6.
14. McMurray JJV, Packer M, Desai AS, Gong J,
Lefkowitz MP, Rizkala AR, et al. Angiotensin–
neprilysin inhibition versus enalapril in heart failure.
N Engl J Med. 2014;371(11):993–1004.
15. Pitt B, Zannad F, Remme WJ, Cody R, Castaigne
A, Perez A, et al. The effect of spironolactone on
131 Medical Therapy for Patients with End-Stage Heart Failure
morbidity and mortality in patients with severe heart
failure. N Engl J Med. 1999;341(10):709–17.
16. Zannad F, McMurray JJV, Krum H, van Veldhuisen
DJ, Swedberg K, Shi H, et al. Eplerenone in patients
with systolic heart failure and mild symptoms. N
Engl J Med. 2011;364(1):11–21.
17. McMurray JJV, Solomon SD, Inzucchi SE, Køber L,
Kosiborod MN, Martinez FA, et al. Dapagliflozin in
patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381(21):1995–2008.
18. Packer M, Anker SD, Butler J, Filippatos G, Pocock
SJ, Carson P, et al. Cardiovascular and renal outcomes with empagliflozin in heart failure. N Engl J
Med. 2020;383(15):1413–24.
19. Flather MD, Yusuf S, Køber L, Pfeffer M, Hall
A, Murray G, et al. Long-term ACE-inhibitor
therapy in patients with heart failure or leftventricular dysfunction: a systematic overview
of data from individual patients. The Lancet.
2000;355(9215):1575–81.
20. Pitt B, Remme W, Zannad F, Neaton J, Martinez F,
Roniker B, et al. Eplerenone, a selective aldosterone
blocker, in patients with left ventricular dysfunction
after myocardial infarction. N Engl J Med.
2003;348(14):1309–21.
21. Cr M. Effect of metoprolol CR/XL in chronic heart
failure. Lancet. 1999;353:2001–7.
22. Ezekowitz JA, McAlister FA. Aldosterone blockade
and left ventricular dysfunction: a systematic
review of randomized clinical trials. Eur Heart J.
2009;30(4):469–77.
23. McCullough PA, Mehta HS, Barker CM, Van
Houten J, Mollenkopf S, Gunnarsson C, et al.
Mortality and guideline-directed medical therapy
in real-world heart failure patients with reduced
ejection fraction. Clin Cardiol. 2021;44(9):1192–8.
24. Braun LT, Grady KL, Kutner JS, Adler E, Berlinger
N, Boss R, et al. Palliative care and cardiovascular
disease and stroke: a policy statement from the
American Heart Association/American Stroke
Association. Circulation. 2016;134(11):e198-225.
25. Friedrich EB, Böhm M. Management of end stage
heart failure. Heart. 2007;93(5):626–31.
26. Mahtani KR, Heneghan C, Onakpoya I, Tierney S,
Aronson JK, Roberts N, et al. Reduced salt intake
for heart failure: a systematic review. JAMA Intern
Med. 2018;178(12):1693–700.
27. McMurray JJV, Östergren J, Swedberg K,
Granger CB, Held P, Michelson EL, et al. Effects
of candesartan in patients with chronic heart
failure and reduced left-ventricular systolic
function taking angiotensin-converting-enzyme
inhibitors: the CHARM-added trial. The Lancet.
2003;362(9386):767–71.
28. Velazquez EJ, Morrow DA, DeVore AD, Duffy
CI, Ambrosy AP, McCague K, et al. Angiotensin–
neprilysin inhibition in acute decompensated heart
failure. N Engl J Med. 2019;380(6):539–48.
29. Brophy JM, Joseph L, Rouleau JL. β-Blockers in
congestive heart failure: a Bayesian meta-analysis.
Ann Intern Med. 2001;134(7):550–60.
30. Poole-Wilson PA, Swedberg K, Cleland JGF,
Di Lenarda A, Hanrath P, Komajda M, et al.
Comparison of carvedilol and metoprolol on clinical
outcomes in patients with chronic heart failure
in the Carvedilol Or Metoprolol European Trial
(COMET): randomised controlled trial. The Lancet.
2003;362(9377):7–13.
31. Pitt B, Remme W, Zannad F ft, Neaton J, Martinez
F, Roniker B, et al. Eplerenone post-acute
myocardial infarction heart failure efficacy and
survival study investigators. Eplerenone, a selective
aldosterone blocker, in patients with left ventricular
dysfunction after myocardial infarction. 2003.
32. Zannad F, Ferreira JP, Pocock SJ, Anker SD,
Butler J, Filippatos G, et al. SGLT2 inhibitors in
patients with heart failure with reduced ejection
fraction: a meta-analysis of the EMPERORreduced and DAPA-HF trials. The Lancet.
2020;396(10254):819–29.
33. Butler J, Packer M, Filippatos G, Ferreira JP,
Zeller C, Schnee J, et al. Effect of empagliflozin
in patients with heart failure across the spectrum
of left ventricular ejection fraction. Eur Heart J.
2022;43(5):416–24.
34. Zelniker TA, Braunwald E. Mechanisms of
cardiorenal effects of sodium-glucose cotransporter
2 inhibitors: JACC state-of-the-art review. J Am Coll
Cardiol. 2020;75(4):422–34.
35. Swedberg K, Komajda M, Böhm M, Borer JS,
Ford I, Dubost-Brama A, et al. Ivabradine and
outcomes in chronic heart failure (SHIFT): a
randomised placebo-controlled study. The Lancet.
2010;376(9744):875–85.
36. Armstrong PW, Pieske B, Anstrom KJ, Ezekowitz J,
Hernandez AF, Butler J, et al. Vericiguat in patients
with heart failure and reduced ejection fraction. N
Engl J Med. 2020;382(20):1883–93.
37. Tavazzi L, Maggioni AP, Marchioli R, Barlera S,
Franzosi MG, Latini R, et al. Effect of n-3
polyunsaturated fatty acids in patients with chronic
heart failure (the GISSI-HF trial): a randomised,
double-blind, placebo-controlled trial. Lancet.
2008;372(9645):1223–30.
38. Pitt B, Anker SD, Bushinsky DA, Kitzman DW,
Zannad F, Huang IZ. Evaluation of the efficacy and
safety of RLY5016, a polymeric potassium binder,
in a double-blind, placebo-controlled study in
patients with chronic heart failure (the PEARL-HF)
trial. Eur Heart J. 2011;32(7):820–8.
39. Young JB, Abraham WT, Smith AL, Leon
AR, Lieberman R, Wilkoff B, et al. Combined
cardiac resynchronization and implantable
cardioversion defibrillation in advanced chronic
14 M. Hamilton and Y. Manla
heart failure: the MIRACLE ICD trial. JAMA.
2003;289(20):2685–94.
40. Bristow MR, Saxon LA, Boehmer J, Krueger
S, Kass DA, De Marco T, et al. Cardiacresynchronization therapy with or without an
implantable defibrillator in advanced chronic heart
failure. N Engl J Med. 2004;350(21):2140–50.
41. Lee DS, Green LD, Liu PP, Dorian P, Newman
DM, Grant FC, et al. Effectiveness of implantable
defibrillators for preventing arrhythmic events
and death: a meta-analysis. J Am Coll Cardiol.
2003;41(9):1573–82.
42. Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL,
Boineau R, et al. Amiodarone or an implantable
cardioverter–defibrillator for congestive heart
failure. N Engl J Med. 2005;352(3):225–37.
43. Køber L, Thune JJ, Nielsen JC, Haarbo J, Videbæk
L, Korup E, et al. Defibrillator implantation in
patients with nonischemic systolic heart failure. N
Engl J Med. 2016;375(13):1221–30.
44. Al-Khatib SM, Stevenson WG, Ackerman MJ,
Bryant WJ, Callans DJ, Curtis AB, et al. 2017 AHA/
ACC/HRS guideline for management of patients
with ventricular arrhythmias and the prevention
of sudden cardiac death: a report of the American
College of Cardiology/American Heart Association
Task Force on Clinical Practice Guidelines and
the Heart Rhythm Society. J Am Coll Cardiol.
2018;72(14):e91-220.
45. Abraham WT, Kuck KH, Goldsmith RL, Lindenfeld
J, Reddy VY, Carson PE, et al. A randomized
controlled trial to evaluate the safety and efficacy
of cardiac contractility modulation. Heart Fail.
2018;6(10):874–83.
46. Stone GW, Lindenfeld J, Abraham WT, Kar S, Lim
DS, Mishell JM, et al. Transcatheter mitral-valve
repair in patients with heart failure. N Engl J Med.
2018;379(24):2307–18.
47. Grayburn PA, Sannino A, Packer M. Proportionate
and disproportionate functional mitral regurgitation:
a new conceptual framework that reconciles the
results of the MITRA-FR and COAPT trials. JACC
Cardiovasc Imaging. 2019;12(2):353–62.
48. Givertz MM, Stevenson LW, Costanzo MR, Bourge
RC, Bauman JG, Ginn G, et al. Pulmonary artery
pressure-guided management of patients with heart
failure and reduced ejection fraction. J Am Coll
Cardiol. 2017;70(15):1875–86.
49. Lindenfeld J, Zile MR, Desai AS, Bhatt
K, Ducharme A, Horstmanshof D, et al.
Haemodynamic-guided management of heart failure
(GUIDE-HF): a randomised controlled trial. The
Lancet. 2021;398(10304):991–1001.
50. Tran RH, Aldemerdash A, Chang P, Sueta CA,
Kaufman B, Asafu-adjei J, et al. Guideline-directed
medical therapy and survival following hospitalization
in patients with heart failure. Pharmacother J Hum
Pharmacol Drug Therapy. 2018;38(4):406–16.
51. Wan SH, Stevens SR, Borlaug BA, Anstrom KJ,
Deswal A, Felker GM, et al. Differential response to
low-dose dopamine or low-dose nesiritide in acute
heart failure with reduced or preserved ejection
fraction: results from the ROSE AHF Trial (Renal
Optimization Strategies Evaluation in Acute Heart
Failure). Circ Heart Fail. 2016;9(8):e002593.
Mechanical and Surgical Options for Patients with End-Stage Heart Failure
Robert M. Cole, Jaime D. Moriguchi, and Yosef Manla
2
Abstract
While the introduction of novel heart failure
(HF) therapeutics has improved the quality
of life and survival in advanced HF patients,
overall morbidity and mortality are still
high. Patients with refractory end-stage HF
may ultimately require either short or longterm mechanical circulatory support (MCS)
or heart transplantation. Once the patient is
deemed to have advanced HF and likely to
benefit from advanced therapies, the optimal strategy for implantation should include
selecting the most appropriate MCS device
with the best durability and lowest incidence
of adverse events and which provides adequate cardiac output for either one or both
failing ventricles. This chapter provides an
overview of the current indications and outcomes of MCS devices used in patients with
advanced HF.
R. M. Cole (*) · J. D. Moriguchi · Y. Manla
Cedars-Sinai Smidt Heart Institute, Los Angeles,
CA, USA
e-mail: Robert.Cole@cshs.org
J. D. Moriguchi
e-mail: MoriguchiJ@csmns.org
Y. Manla
e-mail: Yosef.manla@cshs.org;
Yosef.manla1@gmail.com
Keywords
Heart failure · Mechanical circulatory
support · Ventricular assist devices · Heart
transplantation
Clinical Pearls
• General indications for referral for advanced
heart failure therapies include left ventricular
ejection fraction ≤ 25%, persistent New York
Heart Association class III or IV symptoms,
recurrent atrial fibrillation or ventricular tachycardia with implantable cardioverter defibrillator shocks, and inotrope dependence.
• Patient selection for mechanical circula-
tory support should be a multidisciplinary
decision involving advanced heart failure/
transplantation cardiologists, cardiothoracic
surgeons, nurses, social workers, and palliative care clinicians, amongst others.
• Ventricular assist devices may be used as
bridge-to-transplant, bridge-to-candidacy,
bridge-to-recovery, or as a destination
therapy.
• Relative contraindications to left ventricular
assist device implantation include acute cardiogenic shock with uncertain neurological
status, active severe bleeding, uncontrolled
systemic infection, severe right ventricular
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
J. Kobashigawa (ed.), Clinical Guide to Heart Transplantation, https://doi.org/10.1007/978-3-031-88290-6_2
15
16 R. M. Cole et al.
dysfunction, severe uncorrected aortic insufficiency or mechanical aortic valve.
• The INTERMACS profile is useful for perioperative risk assessment and stratification for
future outcomes post-implant, including mortality and complications. INTERMACS 1–3
may be considered for bridge-to-transplant
or destination therapy using a durable, longterm continuous flow device.
• Mechanical circulatory support devicerelated adverse events include device
thrombosis, driveline infection, stroke, and
gastrointestinal bleeding.
•
Short-term mechanical circulatory support
methods are indicated in the setting of acute
refractory cardiogenic shock, including intraaortic balloon pump, Impella, TandemHeart
and veno-arterial extracorporeal membrane
oxygenation support.
Introduction
While the introduction of novel heart failure
(HF) therapeutics has improved the quality of
life and survival in advanced HF patients, overall morbidity and mortality are still high [1];
refractory end-stage HF patients may ultimately
require either short or long-term mechanical
circulatory support (MCS) or heart transplantation (HTx) [1, 2]. The paucity of available
donor hearts and the prevalence of significant
comorbidities, which may be contraindications
to transplantation, has led to the increasing use
of MCS devices [3]. Furthermore, patients with
advanced HF considered too unstable to await
a suitable donor organ may require univentricular or biventricular ventricular assist devices as
bridge‐to‐transplantation therapy, and have been
shown to improve quality of life, survival‐to‐
transplantation rates, and post‐transplant survival [4, 5].
Numerous clinical clues can help identify
patients with advanced HF and trigger consideration of referral for evaluation of advanced
therapies, including but not limited to inotrope dependence, left ventricular ejection
fraction ≤ 25%, persistent New York Heart
Association class III or IV symptoms, and
recurrent atrial fibrillation or ventricular tachycardia with implantable cardioverter defibrillator shocks (Table 2.1) [6]. Generally, patient
selection for MCS should be a multidisciplinary
decision involving advanced HF/transplantation
cardiologists, cardiothoracic surgeons, advanced
practice providers, nurses, social workers, and
palliative care clinicians, amongst others. Once
the patient is determined to have advanced
HF, the likelihood of benefit from referral to
advanced therapies should also be assessed.
For instance, advanced therapies could be less
beneficial in patients whose goal of care is to
avoid a multipart medical or surgical regimen,
as well as in those with a severely limited lifespan or functional status due to other non-cardiac
conditions [6]. Contemporary MCS includes
both temporary and durable (long-term) forms.
Durable support primarily consists of ventricular
assist devices (VADs) and total artificial hearts
(TAHs), the latter of which will be discussed
in Chap. 28. Overall, the optimal strategy for
implantation should include selecting the most
appropriate MCS device with the best durability and lowest incidence of adverse events and
which provides adequate cardiac output for
either one or both failing ventricles. This chapter
provides an overview of MCS devices and indications for their usage in end-stage HF patients.
Ventricular Assist Device Categories: A Generational History
More than 50 years ago, the first successful
VAD was implanted by Dr. Michael DeBakey
with the aim of acting as a bridge to cardiac
recovery [8]. VADs are mechanical circulatory
pumps that partially or completely take over
ventricular function in order to assist systemic
circulation and improve end-organ perfusion. A
VAD may be used as a left ventricular (LVAD),
right ventricular (RVAD), or as a biventricular
assist device (BiVAD).
Initially introduced in the 1980s, the first
generation of long-term LVADs consisted
of large para-corporeal devices such as the
2 Mechanical and Surgical Options for Patients with End-Stage Heart Failure
Table 2.1 Clinical clues to help identify patients with advanced HF
• Inotrope dependence
• LVEF ≤ 25%, particularly with high-risk features on echocardiogram (grade III or IV diastolic dysfunction; signifi-
cant RV dysfunction; high pulmonary artery pressures or severe MR despite attempts at decongestion)
• ≥
2 Hospitalizations or emergency department visits for decompensated HF in 12 month
• Persistent NYHA class III or IV symptoms, including fatigue and confusion
• High-risk biomarker profile (e.g., hyponatremia, very elevated natriuretic peptides or troponin)
• Escalating doses of diuretics (e.g., >160 mg/d furosemide) or persistent edema despite escalating diuretic doses
• Down titration of GDMT as a result of hemodynamic intolerance such as hypotension (SBP < 90 mm Hg), dizziness,
excessive fatigue, or nausea
• Discontinuation of ACE inhibitor/ARB/ARNI because of hypotension or renal intolerance
• Progressive renal failure with rising creatinine/BUN
• Recurrent atrial fibrillation or VT with ICD shocks
• Nonresponse to cardiac resynchronization therapy
• Cardiac cachexia (i.e., unintentional loss of >5% of body weight attributable to HF)
• High mortality risk from validated risk prediction models or calculators
ACE indicates angiotensin-converting enzyme; ARB, angiotensin II receptor blocker; ARNI, angiotensin receptor–
neprilysin inhibitor; BUN, blood urea nitrogen; GDMT, guideline-directed medical therapy; HF, heart failure; ICD,
implantable cardioverter defibrillator; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; NYHA, New
York Heart Association; RV, right ventricular; SBP, systolic blood pressure; and VT, ventricular tachycardia. Reprinted with permission: Alanna A. Morris, Prateeti Khazanie, Mark H. Drazner, Nancy M. Albert, et al., Guidance for
Timely and Appropriate Referral of Patients With Advanced Heart Failure: A Scientific Statement From the American
Heart Association, Circulation, 144 (7), e238–e250. https://doi.org/10.1161/CIR.0000000000001016; American Heart
Association
17
Thoratec PVAD and Abiomed BVS 5000 (and
subsequently the AB 5000). Intracorporeal
devices included the HeartMate I IP/VE
(Thoratec Inc., Pleasanton, California, USA)
and the Novacor N100 (WorldHeart Inc., Salt
Lake City, Utah, USA). All of these functioned
on the basis of pulsatile systemic perfusion,
otherwise known as “pulsatile-flow” devices.
However, their bulkiness, lack of durability,
and proclivity to malfunction and complications meant that patients were often bedridden
and had less than optimal outcomes, including
high stroke rates [9]. Subsequent miniaturization
of the control and power-supply components
resulted in smaller versions of these first-generation pulsatile VADs that could be implanted
intra-abdominally [10, 11]. While these enabled
patients to mobilize, these devices still remained
restricted to patients with a large body surface
area; device failure rates remained high, infections continued to be problematic, and durability
remained poor [12].
The second generation of LVADs consisted
of smaller, continuous axial flow pump systems
that allowed considerably less extensive surgery
(thus reducing the risk of complications, see
Fig. 2.1) and conferred improved durability, the
ability to use in a wider range of patients due to
smaller size, and reduced thrombogenicity. The
increase in durability arose in part from the fact
that there was only one moving part. The prototypic second-generation LVAD is the HeartMate
II (HM II; Thoratec Inc., Pleasanton, California,
USA) (Fig. 2.2). Second-generation VADs suc-
cessfully demonstrated superior survival and
less organ failure in patients when compared to
patients on first-generation pulsatile VADs. The
1-year survival for these more modern devices
has been reported at 81% for bridge-to-transplantation and 73% for destination therapy [13,
14], which was significantly improved from the
first generation of LVADs. Furthermore, the
introduction of continuous flow devices led to
significantly improved quality of life, general
18 R. M. Cole et al.
Fig. 2.1 A visual overview of left ventricular assist
devices (LVAD). Panel a shows a first-generation pulsatile flow left ventricular assist device (LVAD). Panel b
shows a second-generation continuous flow LVAD. Both
mechanical pumps are placed in the abdominal wall.
The inflow cannula of the LVAD is placed in the apex of
the left ventricle. The outflow cannula is subsequently
anastamosed with the ascending aorta. A percutaneous
well-being, and ability to perform self-care postLVAD implantation [14, 15]. This improvement
meant that LVAD patients were able to engage in
daily life as outpatients relatively unperturbed.
The subsequent and most contemporary
third generation of LVADs have sought to
further refine the continuous-flow concept,
lead connects the LVAD pump with an external system controller and the battery pack. From [The New
England Journal of Medicine, Mark S. Slaughter, Joseph
G. Rogers, Carmelo A. Milano, et al., Advanced Heart
Failure Treated with Continuous-Flow Left Ventricular
Assist Device, 361 (16), 2241–2251, Copyright © (2009)
Massachusetts Medical. Reprinted with permission from
Massachusetts Medical Society
typically utilizing centrifugal rather than axial
flow through the device. There have also been
continued improvements in pump technology
to optimize hemocompatibility and minimize
adverse events through the development of
hydrodynamic or magnetic levitation technology and programmed pulsatility. Furthermore,
2 Mechanical and Surgical Options for Patients with End-Stage Heart Failure
19
Fig. 2.2 Overview of commonly used mechanical
circulatory support devices. First-generation device a
Thoratec HeartMate XVE: pulsatile flow LVAD (left
ventricular assist device) (reprinted with the permission of Thoratec Incorporation). Second-generation
LVAD b Thoratec HeartMate II (reprinted with the permission of Thoratec Incorporation). Third-generation
LVAD c HeartWare HVAD (reprinted with the permission of HeartWare). Approved TAH d SynCardia
CardioWest TAH (courtesy: SynCardia.com). Short-term
smaller pumps can be implanted within the
pericardium, thus further reducing postoperative complications. The most prominent examples of third-generation LVADs include the
HeartWare HVAD centrifugal pump (HeartWare
International Inc., Framingham, Massachusetts,
USA) (Fig. 2.1) and the HeartMate 3 LVAD
(Abbott, St Paul, MN, USA). However, it should
be noted that the HeartWare LVAD system has
been discontinued due to significant adverse
events and inferior clinical outcomes [7].
MCS devices with e Levitronix CentriMag extracorporeal RVAD (reprinted with the permission of
Thoratec Incorporation), and the f AbioMed Impella
5.0 (reprinted with the permission of Abiomed).
RVAD, right ventricular assist device; TAH, total artificial heart. Reprinted with permission from Hadi
Toeg, Talal Al-Atassi, Jose Garcia, et al., An update on
mechanical circulatory support for heart failure therapy, Current Opinion in Cardiology, 29, 2, 167–173;
https://doi.org/10.1097/hco.0000000000000037
The five-year follow-up to the MOMENTUM
3 trial evaluated the composite endpoints of survival to transplant, cardiac recovery, or LVAD
support free of debilitating stroke or need for
reoperation to replace the pump by comparing patients who had received HeartMate II
and HeartMate 3 LVAD devices. The 5-year
Kaplan–Meier estimate of these endpoints was
54.0% in the HeartMate 3 group versus 29.7%
in the HeartMate II group. Furthermore, serious adverse events, including stroke, bleeding,