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• A focused transthoracic echocardiogram is performed to examine for PVL, aor-
tic valve gradient, cardiac function, and the presence of pericardial effusion that
might suggest cardiac injury and bleeding.
• If there is a concern for PVL, or valve under-expansion causing a residual AV
gradient, balloon dilatation of the TAVR valve can be performed here.
W. Shi and T. Kaneko
Closure
• The right CFA sheath is removed, and the percutaneous closure devices are
deployed and secured.
• Angiography of the iliofemoral arterial system can be performed via the left CFA
pigtail catheter to conrm vessel patency, with any bleeding reected by contrast
extravasation during angiography.
• The left CFA and CFV catheters and sheaths are removed.
• Lower limb pulses are assessed manually and with a doppler to ensure limb
adequate perfusion.
Complications inTAVR
Like in open surgery, the risks of TAVR are dependent on patients’ clinical and
anatomical factors. In general, the risk of mortality after transfemoral TAVR is
approximately 1%. The risk of stroke is also approximately 1%. The risk of a major
vascular complication is around 5%. One disadvantage of TAVR is the heightened
risk of requiring a permanent pacemaker which is around 5–10%. This risk is
heightened in those with pre-existing conduction decits such as right bundle
branch block (RBBB). Fortunately, the risk of annular rupture and aortic injury with
the latest generation of TAVR devices is low at <1%.
Unlike in SAVR, TAVR valves are not sewn into the annulus, and as such, there
is an inherently increased risk of paravalvular leakage (PVL), though later- generation
devices have served to reduce these due to engineering improvements. Patients with
bicuspid aortic valve (BAV) stenosis pose a unique challenge, as these valves tend
to be more calcied and asymmetrical and in some cases, may limit the effective
expansion and sealing of a TAVR prosthesis, leading to residual gradients and
PVL.With the latest generation of TAVR valves, the risk of >mild PVL is approximately 5%. Most patients can be discharged on post-operative day 1 after TAVR.
Conclusions
The rise of transcatheter valve technology has changed the way structural heart
disease is treated. TAVR has become a popular, non-invasive way to manage aortic
stenosis, while the indications for transcatheter mitral and tricuspid procedures also
continue to grow. An appreciation of the full spectrum of treatment options for
structural heart disease ensures the utmost inpatient care.
17 Transcatheter Therapies forStructural Heart Disease
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203
References
1. Otto C, Nishimura R, Bonow R, Carabello B, Erwin J Jr, Gentile F, etal. ACC/AHA guideline
for the management of patients with valvular heart disease: a report of the American College
of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.
Circulation. 2020;2021(143):e72–227.
2. Carroll J, Mack M, Vemulapalli S, Herrmann H, Gleason T, Hanzel G, etal. STS-ACC TVT
registry of transcatheter aortic valve replacement. J Am Coll Cardiol. 2020;76:2492–516.
3. Smith C, Leon M, Mack M, Miller D, Moses J, Svensson L, etal. Transcatheter versus surgical
aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364:2187–98.
4. Mack M, Leon M, Thourani V, Makkar R, Kodali S, Russo M, et al. Transcatheter aortic-
valve replacement with a balloon-expandable valve in low-risk patients. N Engl J Med.
2019;380:1695–705.
5. Stone G, Lindenfeld J, Abraham WT, Kar S, Lim D, Mishell J, etal. Transcatheter mitral valve
repair in patients with heart failure. N Engl J Med. 2018;379:2307–18.
6. Bleiziffer S, Simonato M, Webb J, Rodés-Cabau J, Pibarot P, Kornowski R, etal. Long-term
outcomes after transcatheter aortic valve implantation in failed bioprosthetic valves. Eur Heart
J. 2020;41:2731–42.
7. Coylewright M, Mack M, Holmes DJ, O’Gara P.A call for an evidence-based approach to
the Heart Team for patients with severe aortic stenosis. J Am Coll Cardiol. 2015;65:1472–80.
Chapter 18
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Management ofEndocarditis
OritAbrahim, SaryAranki, andAshrafA.Sabe
Overview
• Infective endocarditis (IE) occurs when bacteria or fungi in the bloodstream
infect the inner lining of the heart (endocardium), typically of a heart valve [1].
It is a relatively rare disease with 2–10 cases per 100,000 people globally [2].
• Risk factors for endocarditis include age greater than 60years, male sex, struc-
tural heart disease (valvular and congenital), prosthetic valves, intravenous drug
users (IVDU), chronic hemodialysis, intravascular catheters, indwelling cardiac
devices, skin infection, and oral/dental hygiene pathology [1].
• In-hospital mortality remains high, up to 40% in 1 year, with poor outcomes
related to left-sided or paravalvular involvement, prosthetic valve endocarditis,
multiple comorbidities, CNS involvement, advanced age, and Staphylococcal or
fungal infections [2].
O. Abrahim (*)
Department of Surgery, Massachusetts General Hospital, Harvard Medical School,
Boston, MA, USA
e-mail: oabrahim@mgb.org
S. Aranki · A. A. Sabe
Department of Surgery, Cardiac Surgery, Brigham and Women’s Hospital, Harvard Medical
School, Boston, MA, USA
e-mail: saranki@bwh.harvard.edu; asabe@bwh.harvard.edu
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_18
205© The Author(s), under exclusive license to Springer Nature
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O. Abrahim et al.
Common Organisms andEtiology
• The development of IE begins with endothelial damage, followed by the intro-
duction of a pathogen into the bloodstream, adherence of the pathogen to the
endothelium, and proliferation of the pathogen.
• Valves may be damaged mechanically (e.g., catheters or electrodes) or by auto-
antibodies, inammation, or the pathogen itself. Valves with compromised integ-
rity may be due to such things as mitral valve prolapse, rheumatic heart disease,
congenital cardiac malformations, or prosthetic valves.
• Once organisms are able to proliferate, vegetations may form which are infec-
tious mass composed of brin, platelets, red and white cells, and bacteria
(Fig.18.1).
• Up to 40–50% of IE cases are caused by Staphylococcal aureus [3]. Other com-
mon organisms include Viridans group streptococci and enterococci in those
with native heart valves. Coagulase-negative staphylococci are common among
those with prosthetic valves and cardiac devices. Rarely, endocarditis can be
caused by gram-negative bacteria (e.g., HACEK* organisms) and fungus.
• S. aureus is the predominant organism responsible for endocarditis among IVDU
though at higher proportions nearing 70%, partly attributed to higher rates of
colonization [2]. HACEK organisms, polymicrobial infections, and fungus are
also more common in these populations.
Fig. 18.1 Endocarditis of
the mitral valve, anterior
leaet
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Clinical Presentation
• The clinical manifestations of endocarditis are broad and multisystem. Fever
remains the most common symptom (90%) [4].
• From a cardiac perspective, there may be valvular incompetence from direct
destruction; rupture of papillary muscles and ventricular walls; pericarditis;
myocardial abscess formation; or complete heart block. Cardiac murmurs may
not always be heard.
• Septic emboli from vegetations may occur resulting in infarctions or abscess
formation in any organ, including the brain, kidney, spleen, mesentery, lung,
eyes, and skin. Renal involvement is often universal (i.e., abnormal renal biopsy),
even in the absence of clinically apparent disease [5].
• The most common site of embolic disease is the central nervous system. The
incidence of stroke has been shown to decline rapidly with the initiation of anti-
biotic therapy—from 4.82 per 1000 patient days in the rst week of therapy to
1.71 per 1000 patient days in the second week [6]. Hallmark physical exam nd-
ings suggesting IE may be noted, including Janeway lesions, Osler nodes, Roth’s
spots, petechiae, and subungual hemorrhages [7].
• IE may also be characterized as acute and subacute based on the virulence of the
causative pathogen, severity of infection, progression, and presence of underly-
ing cardiac disease [7]. Acute IE is typically caused by S. aureus and is highly
destructive to native heart valves with high early mortality if left untreated.
Subacute IE is indolent, caused by organisms such as S. viridans, and often
involves previously damaged valves.
• The side of valvular involvement (left vs. right) results in differences in cardiac
manifestations (e.g., heart failure), bacterial density, treatment duration, choice
of management (e.g., surgical intervention), and risk of embolus. Left-sided IE
accounts for 90% of all IE cases [8]. Of all right-sided IE, 90% are among
IVDU [9].
Diagnostic Criteria
• The modied Duke criteria provide a clinical framework for the diagnosis of IE
using major and minor criteria. It has a reported sensitivity between 70% and
79% (Table18.1) [10].
• Denitive endocarditis may also be diagnosed from culture of microorganisms
or histologic evidence of active endocarditis from pathologic lesions, vegeta-
tions, or intracardiac abscess.
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Table 18.1 Modied Duke criteria [1]
Denite IE Possible IE Rejected IE
2 major criteria 1 major and
1–2 minor
criteria
1 major and≥3 minor criteria 3–4 minor
criteria
5 minor criteria
Major criteria
1. Blood culture positive for IE
• Typical microorganism for infective endocarditis from two separate blood cultures:
Viridans streptococci, Staphylococcus aureus, Streptococcus bovis, HACEK group
(Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis,
Eikenella spp., and Kingella kingae) or community-acquired enterococci, in the absence of a
primary focus
• Microorganisms consistent with infective endocarditis from persistently positive blood
cultures, dened as follows:
– At least 2 positive cultures of blood samples drawn more than 12h apart
– All of 3 or a majority of 4 or more separate cultures of blood (with rst and last
sample drawn ≥1h apart)
– Single positive blood culture for Coxiella burnetii or phase I antibody titer >1:800
2. Evidence of endocardial involvement
• Echocardiogram supportive of infective endocarditis
• Denition of positive ndings: Oscillating intracardiac mass, on valve or supporting
structures, or in the path of regurgitant jets, or on implanted material, in the absence of an
alternative anatomic explanation or myocardial abscess or new partial dehiscence of
prosthetic valve
• New valvular regurgitation (increase or change in preexisting murmur not sufcient)
Minor criteria
Predisposing heart condition or intravenous drug use
Fever ≥38 °C (100.4°F)
Vascular phenomena: Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions
Immunologic phenomena: Glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor
Positive blood culture not meeting major criterion as noted previously (excluding single
positive cultures for coagulase-negative staphylococci and organisms that do not cause
endocarditis) or serologic evidence of active infection with organism consistent with infective
endocarditis
O. Abrahim et al.
0 major and
1–2 minor
criteria
1 major and
0 minor
criteria
Antimicrobial Management
• Treatment of IE begins with empiric antibiotic therapy, ideally after blood cultures are collected if it does not result in signicant delays in therapy. Selection
of organism specic antibiotic therapy is complex.
• Antibiotic therapy is typically prolonged and dependent on resistance proles,
native vs. prosthetic valves, and type of pathogen.
• Antibiotic selection and duration recommendations are summarized in a set of
guidelines by the AHA [11].
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Surgical Intervention
• Factors determining whether to operate include the patient’s hemodynamic status, left vs. right-sided pathology, risk of thromboembolic complication, and
likelihood of source control with non-invasive treatments [2, 12].
• Surgical candidacy and timing can be further complicated by recent stroke/
mycotic aneurysms, abscesses/source control, psychosocial issues including IV
drug use and non-compliance, and center expertise.
Timing andIndications forOperation onLeft-Sided Valves
• Surgical repair of left-sided valves (aortic and mitral) serves to address hemodynamic status/heart failure, obtain source control, and prevent thromboembolic
complications.
• Early surgical intervention (within 48h) for patients with IE and severe valve
disease has been shown to be associated with lower rates of death, embolic
events, recurrence of IE, and repeat hospitalizations due to the development of
CHF [13].
• Several guidelines (AHA, European Society of Cardiology, American Association
for Thoracic Surgery (AATS)) exist to guide operative decision-making [12,
14, 15].
• The 2014 AHA guidelines recommend early surgery (dened as during the initial
hospitalization before completion of full therapeutic antibiotic course) for otherwise good operative candidates and patients with valve dysfunction resulting in
heart failure symptoms, heart block, annular or aortic abscess, destructive penetrating lesions, left-sided IE with highly resistant organisms or persistent infection, prosthetic valve endocarditis, and relapsing infection.
• The AATS emphasizes early operation and minimizing delays before heart failure symptoms are evident [15].
Timing andIndications forOperation onRight-Sided Valves
• Right-sided disease has lower risk of severe sequelae (i.e., lower risk of thromboembolic events and is typically subacute disease).
• Surgery is considered for persistent bacteremia, right heart failure due to tricuspid regurgitation that is refractory to diuresis, and vegetations on the tricuspid
valve >20mm that persist after recurrent pulmonary embolism.
• Common operations in right-sided IE include tricuspid valvectomy, tricuspid
valve repair, and tricuspid valve replacement [2].
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O. Abrahim et al.
Complex Multi-Valve Endocarditis
• Complicated endocarditis may require replacement or repair of multiple valves
after extensive debridement.
• Commonly, a drop lesion from the aortic valve may infect the anterior leaet of
the mitral valve, or erosive abscesses can invade the intervalvular brous body
(IFB). [16].
• Replacement or repair of both valves and reconstruction of the IVF can be done
through procedures such as the Commando (double-valve replacement with IFB
reconstruction) or Hemi-Commando (aortic-valve replacement and mitral valve
repair).
• Such procedures are complex, associated with high morbidity and mortality
rates, and are typically performed at tertiary care facilities [17–19].
• Similarly, the use of homografts (human tissue grafts) over xenografts or
mechanical prostheses requires higher technical expertise. However, the use of
homografts has not been shown to be more resistant to reinfection in IE [20].
Timing ofOperative Intervention After Acute Stroke
• Cardiac surgeons must balance urgent operation with the risk of converting ischemic stroke to hemorrhagic stroke, worsening existing hemorrhagic stroke, causing hypotension or embolization with cardiopulmonary bypass [21].
• Recently, it was found that early surgery for IE after stroke was not associated
with an increased risk of new post-operative stroke and not all operations should
be delayed [22–24].
• Patients with intracerebral hemorrhage (ICH), though, may have increased risk
of mortality after early surgery.
• Current AATS guidelines recommend (1) early surgery for patients with nonhemorrhagic stroke and cardiac indications for urgent surgery, (2) delaying operations for 3+ weeks for patients with recent ICH, and (3) a neurology consultation
for patients with severe or multiple strokes [15].
Special Considerations
Prosthesis Selection
• Prosthesis selection (mechanical vs. tissue) for native valve endocarditis requiring simple valve replacement should be based on normal criteria including age,
compliance with anticoagulation, life expectancy, and presence of comorbidities
[15, 25].
• Several studies have shown no difference in reinfection rates between patients
receiving mechanical vs. tissue prosthetic valves [26–28].
• Recent stroke may limit post-operative anticoagulation mandating a tissue valve.
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Prosthetic Valve Endocarditis
• IE can occur in 3–6% of those with prosthetic valves [29].
• PVE is separated into early (rst 60days after surgery), intermediate (60daysrst year after surgery), and late-onset (greater than 1year) [12].
• Nearly 50% of PVE cases require surgery, though PVE is associated with high
mortality and morbidity after surgical intervention [30].
• Surgical debridement and replacement of infected prosthetic valves are associated with improved mortality compared to medical treatment.
• Select cases of PVE—such as patients without signs of congestive heart failure,
conduction abnormalities, valvular complications, or annular abscesses or stulas— may be treated with antibiotic therapy alone [31–34].
Intravenous Drug Use
• Short-term outcomes in patients with IE related to intravenous drug use have
been shown to be better than non-IVDU (likely due to age, fewer comorbidities,
and selection bias for healthier operative candidates); but, there are high rates of
reinfection and re-operation leading to poor long-term outcomes and increased
risk of death [35–37].
• Re-do surgeries are complex and costly prompting debate on resource allocation
and futility [38].
• IVDUs are a vulnerable population at risk of delayed care, sub-standard care, or
refusal of care stemming in part from surgeon bias and stigma within the medical
system and greater society [39].
• Coupling addiction treatment with surgical intervention for IE may reduce recidivism and improve outcomes [40]. Psychiatric services including addiction medicine therapy, after-care programs, and medical adjuncts (i.e., buprenorphine,
methadone, naltrexone) may be used to reduce the risk of relapse and support
IVDUs pre-and post-operatively [41].
• Multi-disciplinary care with cardiac surgery, infectious disease, social work, and
addiction medicine is an important part of caring for these populations.
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9. Moreillon P, Que YA.Infective endocarditis. Lancet Br Ed. 2004;363(9403):139–49.
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of Duke criteria for diagnosis of denite infective endocarditis: a cohort study. Open Forum
Infect Dis. 2017;4:S550–1.
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