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transfusion-associated circulatory overload (TACO), and transfusion-associated lung injury (TRALI) due to blood
product transfusion
[70]. Acute respiratory distress syndrome (ARDS) may also occur in advanced liver failure in
the setting of multiorgan failure or sepsis
[71]. The threshold for mechanical ventilation as well as routine bron-
choscopy must be low for critically ill patients with advanced liver disease with multiorgan dysfunction.
In the course of preoperative diagnostic testing, the anesthesiologist should be aware of conditions that may
predispose a patient to pulmonary complications and that may require intervention in the perioperative period.
All of these pulmonary conditions can worsen throughout the pretransplant course, so continued therapies may
be necessary prior to transplant to maintain optimal pulmonary status.
Intraoperative pulmonary considerations
The anesthesiologist may encounter difficulties in oxygenation and ventilation depending on the pathology
encountered, starting from the induction of anesthesia. In patients with severe HPS or decreased functional resid-
ual capacity due to large volume ascites, a rapid sequence induction may be indicated, as hypoxemia may result
immediately after the induction of anesthesia. In addition, aspiration risk may also be high in these patients due
to emergent nature of the surgery and preexisting encephalopathy
[72]. In situations of decompensated liver fail-
ure with multiorgan failure, patients can present with acute lung injury (ALI) or ARDS and may pres ent to the
operating room on mechanical ventilation. Preoperatively, they also may require intubation for airway protection
due to severe encephalopathy. Depending on the severity of the respiratory failure, intraoperative bronchoscopy
may be required for the removal of secretions. Utilization of a mechanical ventilator separate from the anesthesia
machine may be necessary to maintain oxygenation and ventilation in some patients. Mechanical ventilation
should be optimized with tidal volumes of 6 mL/kg based on ideal body weight, optimal PEEP, and lowest FiO
2
for a SpO
2
of 88%90% [73].
During the dissection phase, surgical manipulation may impact the pulmonary physiology of the patient. The
placement of large abdominal retractors can result in atelectasis, increased airway pressures, hypoxemia, and hyper-
carbia depending on the baseline status of the patient. The diaphragm may be violated during the dissection phase
due to adhesions or intentional drainage of effusions. The resulting pneumothorax may impact ventilation-
necessitating chest tube placement. Trauma to lung tissue may result in hemothorax. It would be prudent to avoid
nitrous oxide in the setting of diaphragmatic violation as that may worsen pneumothorax and in turn potential for
intraoperative hypoxemia. In addition, with the sudden drainage of a long-standing effusion, the patient could
develop postexpansion pulmonary edema or “trapped lung” that may impact respiratory mechanics
[71]. During the
reperfusion phase, hypoxemia typically occurs due to cardiac issues such as arrhythmia, hypotension, right/LV dys-
function, and thromboembolism, however, there is the potential for primary pulmonary events like pulmonary edema
[72]. In patients with poor pulmonary function, hypercarbia may contribute to transient acidosis at graft reperfusion.
The potential for severe hypoxemia (noncardiac) during LT is always present. Pulmonary management strate-
gies in patients with severe HPS include drainage of effusions, diuresis in the setting of edema, maintaining tren-
delenburg position, and optimizing ventilatory parameters. Pharmacologic interventions including inhaled
pulmonary vasodilators and methylene blue have been described
[73]. In the setting of massive transfusion, the
anesthesiologist should be aware of the potential for the development of TACO/TRALI with resulting ALI and
ARDS. Lung protective ventilatory strategies should be employed in this situation
[71].
With persistent and worsening intraoperative hypoxemia unresponsive to conventional therapy, extracorporeal
membrane oxygenator support may be considered in selective patients
[73]. ECMO has been described in LT patients
for both cardiac and pulmonary pathologies and has been utilized in the pre-, intra-, and postoperative periods for
refractory hypoxemia. Unfortunately, evidence is limited to case reports and small series
[74,75]. Although further
research is needed in this area, there should be some consideration for ECMO in high-risk cases with significant
hypoxemia.
Postoperative pulmonary considerations
With improvement in surgical technique, perioperative blood administration, and anesthetic management over
the past two decades, some centers advocate operating room extubation of patients at the completion of a LT pro-
cedure. Several studies have reaffirmed that a large percentage of LT recipients can be extubated in the operating
room with low rates of pulmonary complications
[7678]. While early extubation allows for minimization of
ventilator-associated complications, subsets of patients have risk factors for prolonged mechanical ventilation
304 18. Cardiopulmonary considerations for the anesthetic management of liver transplantation
III. Cardiovascular system in liver failure
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after transplantation. One single-center study demonstrated that advanced age, high hemoglobin level, high
MELD score, and long-term pretransplant mechanical ventilation were risk factors
[79]. Graft malfunction may
also prolong postoperative mechanical ventilation
[80]. Early tracheostomy may be beneficial to reduce depen-
dence on mechanical ventilation, although there is no evidence for this practice specifically in LT recipients.
In patients with HPS liver transplantation is curative, however, some patients may require oxygen after sur-
gery. Depending on their preoperative severity of hypoxemia, they may also require prolonged mechanical venti-
lation, tracheostomy, and in rare cases extracorporeal membrane oxygenator support. However, most patients
improve rapidly unless they have a large burden of intrapulmonary arteriovenous shunts
[81].
Pulmonary infectious complications, most commonly pneumonia, are common in LT recipients
[82]. Although
the rate of this complication is low, mortality in LT patients with pneumonia is high if not diagnosed appropri-
ately
[83]. Early and frequent bronchoscopy may be beneficial. The most common noninfectious complications
are atelectasis and pleural effusions. In one study of 333 LT recipients, 86. 7% of postoperative pulmonary compli-
cations were represented by those two groups
[84]. In addition, pulmonary edema is a complication that is of a
multifactorial etiology in the postoperative period. Noncardiogenic causes are most commonly due to excess
fluid administration, although TRALI can also contribute
[85,86].
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CHAPTER
19
Cardiovascular assessment before liver
transplantation
Iliana Doycheva
1,
*, Manhal Izzy
2,
* and Kymberly D. Watt
1
1
Division of Gastroenterology & Hepatology, The Mayo Clinic, Rochester, MN, United States
2
Division of
Gastroenterology, Hepatology, and Nutritions, Vanderbilt University, Nashville, TN, United States
Introduction
Cardiovascular diseases (CVDs) are the main cause of morbidity and mortality in the United States accounting
for more than 900,000 deaths in 2016
[1]. In the setting of this high burden of CVD in the general population,
patients with advanced liver disease awaiting liver transplantation (LT) are a special subgroup that carries het-
erogeneous CVD risk factors and has unique clinical characteristics. Cardiovascular assessment of LT candidates
aims to ascertain intraoperative endurance and immediate postoperative survi val as well as to determine long-
term CAD risk and its potential impa ct on survival. CVD remains the leading cause of early mortality (, 1 year)
post-LT and it is one of the top causes for late post-LT deaths
[25]. This results in high-cost hospitalizations and
significant healthcare utilization
[6]. A systematic review of cardiovascular events post-LT reported an incidence
rate of 12.8% within 30 days of LT, 22.6% for events # 6 months, and 11.8% for events . 6 months
[7]. The stron-
gest and most consistent independent predictors of cardiovascular events after LT were older age and a history
of CVD before transplant followed by pre-LT echocardiographic findings and asymptomatic elevation of serum tropo-
nin in cirrhotic patients
[5,7]. highlighting the importance of comprehensive cardiovascular evaluation pre-LT.
Assessment of coronary artery disease
Prevalence of coronary artery disease in liver transplant candidates
Clinical studies dating more than four decades ago has reported a lower prevalence of coronary artery disease
(CAD) in patients with cirrhosis
[8,9]. However, subsequent evidence has shown that CAD prevalence in patients
awaiting LT could be equal to that of the general population (7.2% vs 7.9%, respectively P 5 .646)
[10].orevenhigher
among cirrhotic patients matched to healthy controls by age, gender, and smoking habits (20% vs 12%, P 5 .001)
[11].
The reported prevalence in different studies varies widely mainly due to small sample size
[1214], use of noninva-
sive methods for CAD assessment
[1518], broad definition of positive results [19,20], and preselected studied popu-
lation
[21,22]. When coronary angiography was used as a gold standard for diagnosis of CAD, any coronary artery
stenoses were noted in 27%36%
[12,23], the prevalence was 17%33% for $ 50% stenosis [2228],and5%27% for
$ 70% stenosis
[1214,19,22,25,27,28] (Table 19.1). Among asymptomatic LT candidates over the age of 45 years,
angiographically proven CAD prevalence was 13%26%
[12,22]. Importantly, more recent studies reported CAD by
invasive coronary angiography (ICA) in more than one-third of the studied cohorts (33%37%)
[23,26].Possible
explanations for the heterogeneity of these data are different modalities for detecting CAD, increasing age of LT can-
didates, and increasing rates of nonalcoholic steatohepatitis (NASH) as an indication for LT.
* Both authors equally contributed.
309
Cardio-Hepatology.
DOI:
https://doi.org/10.1016/B978-0-12-817394-7.00005-X © 2023 Elsevier Inc. All rights reserved.
https://t.me/medicina_free

Risk factors
The burden of traditional cardiovascular risk factors and liver disease etiology is the most important compo-
nents that play a role for CAD stratification of LT candidates. Based on the last guidelines for cardiac evaluation
of LT candidates of the American Heart Association (AHA) and the American College of Cardiology Foundation
(ACCF) from 2012, a noninvasive stress test was recommended for patients without active cardiac conditions
based on the burden of CAD risk factors
[29]. The most pertinent risk fact ors for considerations were aging, type
2 diabetes mellitus (T2DM), hypertension, dyslipidemia, smoking, history of CVD, and left ventricular hypertro-
phy. Due to lac k of sufficient evidence, no specific number of factors was strongly recommended to prompt test-
ing, and guidelines suggested a threshold of three or more factors to be considered significant. A recent study
showed that having $ 3 risk factors had good sensitivity and specificity (75% and 77%, respectively) for detection
of severe CAD and was associated with adverse cardiac outcomes in post-LT [hazard ratio (HR) 2.39, P 5 .044]
[30]. Other studies have shown that the presence of $ 2 risk factors [22,31] and even $ 1 factor [28] was associ-
ated with a higher likelihood of severe angiographically proven CAD. Various combinations of these risk factors
have been identified in different studies (
Table 19.1). Out of all, T2DM has been identified as the strongest inde-
pendent risk factor of CAD with odds ratio (OR) 1.75.5
[1012,23].
LT candidates ($65 years) encompassed up to 22.9% of the listed patients in 2017, in both the United States
and Europe
[32,33]. Up to one-third of the older adults have concomitant T2DM [34] and more than a half of the
people $ 60 years have metabolic syndrome (54.9%)
[35] that further increases CAD risk.
TABLE 19.1 Prevalence and risk factors for CAD in LT candidates.
References #Patients
Mean age,
range/SD
#Patients
with known
CAD (%) Definition of CAD
Prevalence of
CAD Risk factors for CAD or for post-LT mortality
[12] 37 Median 61
(5071)
7 (19%) Mild , 30% stenosis;
moderate 30%70%;
severe . 70%
27% total
16.2% severe
DM for moderate or severe CAD
[13] 40 — — Stenosis $ 70% 5% —
[19] 83 56 (3573) 0 Stenosis $ 70% 23% —
[22] 161 57.0 6 7.0 0 $ 50%; severe $ 70% 26%20%
severe
—
[14] 64 61.06 8.0 0 Stenosis $ 70% 27% —
[20] 93 — 0 Severe:
stenosis . 70% or
.50% and positive
stress test
6.5% Alcohol-associated cirrhosis, reversible perfusion
defects on MPI, LV systolic dysfunction, high
LDL-cholesterol, triglyceride level
[24] 83 56.06 9.0 — Mild, 50% stenosis;
moderate 50%70%;
severe . 70%
24.1%
moderate to
severe
—
[28] 420 56.0 6 7.0 0 Mild , 30% stenosis;
moderate 30%70%;
severe . 70%
30%
moderate to
severe 15%
severe
Age, DM, hypertension, hyperlipidemia, alcohol-
associated cirrhosis
[25] 630 — — Stenosis $ 50%;
severe . 70%
23.8%15.2%
severe
—
[27] 414 60.0 6 7.6 — Significant . 50%;
severe . 70%
17%13%
severe
Age . 60, hypertension, DM, hyperlipidemia,
smoking, family h/o CAD
[26] 87 57.56 7.3 — Stenosis. 50% 33.3% Cardiac events within 90 days of LT predict
decreased survival after LT
[23] 228 57.0 6 6.0 9 (11%) Any stenosis,
obstructive . 50%
36.8%19.3%
obstructive
DM, dyslipidemia, current or h/o hypertension;
NASH
CAD, Coronary artery disease; DM, diabetes mellitus; LDL, low-density lipoprotein; LT, liver transplantation; LV, left ventricle; MPI, myocardial perfusion
imaging; NASH, nonalcoholic steatohepatitis.
310 19. Cardiovascular assessment before liver transplantation
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Other well-recognized factors associated with CAD include male sex and famil y history of CAD [10,27].In
addition, renal impairment has been shown to be an independent predictor of sign ificant CAD in cirrhotic
patients
[36] and was associated with cardiac events in post-LT [HR 2.19, 95% confidence interval (CI) 1.253.85].
[37]. Renal impairment has also been noted to be the strongest predictor of post-LT cardiovascular mortality in
patients with NASH cirrhosis
[38].
Nonalcoholic fatty liver disease (NAFLD) is a major risk factor of CVD among LT candidates. The growing
prevalence of NAFLD over the last three decades mirrors the epidemic of obesity and T2DM in the United States
[39]. Based on the 2017 annual report of the organ procurement transplant network/scientific registry of trans-
plant recipients, 35.9% of the adult LT recipients were obese [body mass index (BMI) . 30 kg/m
2
] and 14% had
morbid obesity (BMI $ 35 kg/m
2
) [32], a significant increase from 29% and 9.2%, respectively in 2002 [40].Itis
projected that by 2030, one in two US adults will be obese and almost one in four will have severe obesity, which
will further impact LT candidates’ profile in the coming years
[41]. Patients with NASH cirrhosis were noted to
have higher prevalence of metabolic risk factors and more prevalent CAD when compared to patients with other
etiologies of cirrhosis (21.6% vs 3.3%, P , .05)
[42]. The suggested pathogenic mechanisms through which
NAFLD and NASH potentiate CVD development are systemic inflammation, oxidative stress, hepatic insulin
resistance, alterations in lipid metabolism, and endothelial dysfunction
[43]. Meta-analyses have demonstrated
that NAFLD is independently associated with subclinical atherosclerosis
[44] and any coronary artery calcium
score (CACS) assessed by cardiac computed tomograph y (CT), including with CACS of 0
[45], has increased risk
of prevalent and incident CAD
[46], carries higher risk of clinical cardiovascular events [47] and increased risk of
fatal and nonfatal CVD events when compared to those without NAFLD
[48]. Severity of liver disease among
NASH patients was associated with increased cardiovascular events and higher incident CVD when compared to
those without NASH
[46,48]. Currently, NASH is the most rapidly rising indication for LT and is the second
leading etiology for LT
[49]. A recent study noted that more than a half of patients with NASH cirrhosis undergo-
ing LT evaluation had CAD (52.8%) with the highest extent and severity of disease when compared to alcohol-
associated and hepatitis C cirrhosis etiologies
[23].
Some studies have shown that not only NAFLD but also patients with alcohol-associated liver diseases have
an increased risk of prevalent subclinical atherosclerosis even after adjustment for traditional CVD risk factors
[50]. Alcohol-associated cirrhosis was identified as a risk factor for obstructive CAD in several studies [10,11,20].
Alcohol-associated cirrhosis and NASH had significantly higher CAD prevalence than all other etiologies in one
study (31% vs 27% vs 2.4%)
[11] while another study showed that patients with alcohol-associated cirrhosis had
significantly lower prevalence of severe CAD ( . 70% stenosis) when compared to other etiologies (2% vs 13%,
P , .05)
[28].
Among other etiologies of cirrhosis, it should be noted that a recent meta-analysis based on 36 studies from 51
countries demonstrated that hepatitis C virus (HCV) infection is associated with an increased risk of cardiovascu-
lar events (pooled risk ratio 1.28, 95% CI 1.181.39)
[51]. In support of this finding, both HCV and NASH have
been identified as independent risk factors for the presence of angiographically proved CAD in cirrhotic patients
[23]. However, successful treatment of hepatitis C has been associated with a decreased risk of CVD events [52].
LT candidates with cholestatic liver disease etiology do not appear in increased risk of CAD
[12,53].
Screening tests for coronary artery disease in liver transplantation candidates
AHA/ACCF guidelines advise on noninvasive stress test in patients with $ 3 risk factors but does not specify
which test is preferred (class IIb, level of evidence C)
[29], whereas American Association for the Study of Liver
Diseases recommends risk stratification and pharmacological stress echocardiography as an initial test in all LT
candidates (strength 1, quality of evidence B)
[54]. The medium strength and low level of evidence of these
recommendations indicate that the data on efficacy of suggested tests are insufficient and additional studies are
needed.
The first step in cardiovascular assessment of LT candidates shou ld be to obtain medical his tory for risk fac-
tors stratification, followed by a physical examination that includes functional status assessment. A 12-lead elec-
trocardiogram (ECG) to assess for baseline abnormalities should be done. Standard exercise test is rarely used in
cirrhotic patients due to their poor functional capacity, which has reflected in the main use of pharmacological
stress testing.
Dobutamine stress echocardiogram
Although initial studies in assessing accuracy of dobutamine stress echocardiogram (DSE) have demonstrated
good sensitivity (75%100%)
[13,21], more recent analyses have challenged these findings by suggesting that this
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method is not sensitive enough to detect obstructive CAD (Table 19.2) [14,28,55]. A pooled analysis of four accu-
racy studies that included 110 patients consistently showed low sensitivity of 32% and moderate specificity of
78% with 37% positive predictive value (PPV) and 75% negative predictive value (NPV)
[58]. There was no differ-
ence in DSE accuracy when patients were stratified based on risk factors
[55], although other reports showed
excellent specificity and 100% PPV with persistently low sensitivity (13%) and moderate NPV (68%) in patients
with $ 3 risk factors
[14] and NPV of 98%100% in the absence of any cardiovascular risk factors [28]. To this
end, a recent single-center study showed that stress echocardiography in this patient population has a sens itivity
of only 37% for detecting significant CAD
[59].
The major disadvantage of DSE is the inability of 5%49% of the patients to achieve 85% of the maximum age-
predicted heart rate (220 2 age 3 0.85), which makes the test nondiagnostic
[14,15,53,55,6062]. This could be
explained with the common use of nonselective beta-blockers (NSBBs) in cirrhotic patients used for prevention of
variceal bleeding. Chronotropic incompetence with blunted response to stress is another possible reason, which
could be a marker of cirrhotic cardiomyopathy (CCM)
[63]. Overall, 50%81% of the patients with nondiagnostic
DSE test were on NSBBs [14,60,62] and they were more likely to fail achieving target heart rate compared to those
not on NSBBs (64% vs 27%, P , .05)
[62]. Severity of liver disease was not a risk factor for failing to achieve target
heart rate
[62]. Withholding beta-blocker therapy for up to 48 hours before the DSE did not affect maximum
achieved heart rate and heart rate reserve (marker inversely associated with CVD and death in the general popula-
tion)
[61]. One study proposed a new prediction model called “modified heart rate reserve” (a formula using as a
numerator is the relative increase from resting to peak heart rate instead the absolute difference between these
values) that was not affected by NSBB therapy with low values of the model predicting post-LT myocardial infarc-
tion (MI) and heart failure (HF)
[61]. No studies have assessed DSE accuracy after withholding NSBB for more than
2 days, although a prospective study reported no episodes of variceal bleeding and no hemodynamic rebound in 25
patients who discontinued beta-blockers for a median duration of 4 days
[64]. Other complications requiring early
termination of DSE have been reported in up to 28% and include hypotension, arrhythmias, and chest pain
[15,62].
Several studies have assessed the predictive value of DSE for early and late cardiovascular events post-LT
[15,53,56,57,60]. Positive DSE did not correlate with perioperative cardiac events while normal test had good NPV
[15,56,57]. Similar results were noted for late cardiac events [53,58]. A rate blood pressure product at peak DSE, another
TABLE 19.2 Diagnostic performance of dobutamine stress echocardiogram.
References #Patients #Inconclusive (%) Sensitivity (%) Specificity (%) PPV (%) NPV (%)
DSE compared to coronary angiography CAD definition
[21] 18 — 75 57 33 89 Stenosis$ 50%
[13] 21 — 100 100 100 100 Stenosis$ 70%
[14] 64 27/105 (25.7%) 13 85 22 75 Stenosis$ 70%
[28] 65 alcoholl-
associated liver
disease
0 33 84 9 96 Stenosis . 70%
140 patients
with other
etiologies
64 61 23 90
[55] 66 3/66 (4.5%) 41 47 40 48 Stenosis $ 50%
DSE for prediction of post-LT cardiovascular events Definition of events
[56] 73 — 17 91 38 77 Elevated troponin post-LT
[57] 403
a
— 14 95 27 89 Nonfatal MI, death, or
combined outcome within 30
days post-LT
[53] 195 82/278 (29.9%) 9 98 33 89 ACS, new HF, arrhythmia,
CVA, PVD, resuscitated
cardiac arrest
a
89% underwent DSE for preoperative assessment, the rest had other stress tests.
ACS, Acute coronary syndrome; CAD, coronary artery disease, CVA, cerebrovascular acciden t; DSE, dobutamine stress echocardiogram; HF, heart failure; LT,
liver transplantation; MI, myocardial infarction; NPV, negative predictive value; PPV, positive predictive value; PVD, peripheral vascular disease.
312 19. Cardiovascular assessment before liver transplantation
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marker of chronotropic incompetence, was associated with an increased risk of atrial fibrillation (AF) post-LT when
,12,000
[53]. Failure to achieve rate blood pressure product . 16,333 along with model for end-stage liver disease
(MELD) .24 or submaximal heart rate on DSE predicted serious cardiac adverse events within 4 months post-LT
[60].
A downside to DSE is the risk of precipitating hepatic encephalopathy using atropine to facilitate reaching the
target heart rate. This risk can be minimized by lowering the maximum atropine dose used
[65].
In summary, although widely used, DSE does not reliably identify patients with CAD. A negative DSE in a
patient with low risk is strongly predictive of low risk of early and late cardiac events post-LT. The major limita-
tion of DSE is the large number of nondiag nostic tests in this population.
Myocardial perfusion imaging with real-time myocardial contrast echocardiography
This is a test that examines both regional wall motion abnormalities and microvascular capillary blood flow at
rest and during stress and has improved capacity of detecting CAD. Two studies have evaluated its prognostic
value for post-LT cardiac outcomes
[17,66]. All patients with inducible wall motion abnormalities also had micro-
vascular perfusion defects, but some patients had inducible perfusion defects only [66]. Presence of abnormal
microvascular perfusion defects was an independent predictor of post-LT cardiac events (HR 7.7)
[66] and
increased the risk of death after transplant 2.4 times
[17].
Single-photon emission computed tomographyMyocardial perfusion imaging
Single-photon emission computed tomography (SPECT) is a nuclear test that provides information on myocar-
dial perfusion and regional and global left ventricle (LV) function. Different protocols exist that use exercise or
various coronary vasodilators as pharmacological stressors: adenosine, regadenoson, dipyridamole, or dobuta-
mine. Most studies examining the accuracy of SPECTMyocardial perfusion imaging (MPI) for the diagnosis of
CAD in LT candidates have demonstrated low sensitivity (35%62%)
[19,27] except one study that showed a sen-
sitivity of 100%, but low specificity and high number of false-positive results (
Table 19.3) [20]. The low sensitivity
of SPECTMPI has been attributed to baseline low systemic vascular resistance in cirrhosis and inability to
achieve additional vasodilation under stress, while the high number of false-positive results has been attributed
to cardiac microvascular dysfunction and attenuation artifacts in the inferior cardiac wall that can be seen in the
presence of ascites and/or splenomegaly
[67,68]. The negative prognostic value of SPECTMPI for early and late
post-LT cardiac events is excellent with NPV of 91%99% for early
[68,69] and 96% for late events [68].
Coronary artery calcium score and coronary computed tomography angiography
CACS is a non-contrast, ECG-gated, and CT-based method for quantification of calcified plaques in the coro-
nary arteries calculated based on the Agatston scoring method. In the general population, CACS progression has
been strongly associated with an increased risk of major cardiovascular events even after the adjustment for tra-
ditional risk factors
[70]. It significantly improves risk stratification of asymptomatic patients when added to the
TABLE 19.3 Diagnostic performance of single-photon emission computed tomography.
Reference # Patients Sensitivity (%) Specificity (%) PPV (%) NPV (%)
SPECT compared to coronary angiography CAD definition
[19] 83 37 63 22 77 Stenosis $ 70%
[20] 93 100 61 15 100 Stenosis . 70%
[27] 293 adenosine scan 54 82 32 92 Stenosis . 50%
62 82 30 95 Stenosis . 70%
180 regadenoson scan 35 88 27 91 Stenosis . 50%
35 88 23 93 Stenosis . 70%
SPECT for prediction of post-LT cardiovascular events Definition of events
[53] 47 57 75 28 91 ACS, new HF, arrhythmia,
CVA, PVD, resuscitated cardiac
arrest
ACS, Acute coronary syndrome; CAD, coronary artery disease, CVA, cerebrovascular acciden t; HF, heart failure; LT, liver transplantation; NPV, negative
predictive value; PPV, positive predictive value; PVD, peripheral vascular disease; SPECT, single-photon emission computed tomography.
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