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_3723_Библиотеки_им_академика_М_И_Перельмана
.pdf
8 Pericardial Diseases
https://t.me/medicina_free
105
a bc
d
Fig. 8.3 A 53-year-old male referred with a history of
Behcet’s disease, mouth ulcers, and renal infarctions.
Whole-body FDG-PET (a) and axial FDG-PET/CT (b)
images demonstrate mild and focal increased uptake
(arrow) in the pericardium. On cardiac magnetic reso-
systemic inammatory disease itself or may be
precipitated by increased susceptibility to other
unrelated illnesses.
FDG-PET can play an important role in the
evaluation of patients with suspected autoimmune causes. In this setting, although PET can
detect pericardial inammation (Fig. 8.3), its
strength resides in its ability to assess areas of
inammation on whole-body imaging, which
may help reveal the underlying causative pathology and potentially guide biopsy. For example,
characteristic FDG-avid mediastinal lymph
nodes and lung lesions can point to the diagnosis
of sarcoidosis [14], while increased vascular
FDG uptake can conrm the presence of large
vessel vasculitis [15]. In addition, FDG-PET can
readily localize inammatory arthritis in patients
with suspected rheumatoid disease, which is typically symmetrical, FDG-avid, and present in
multiple small and large joints and can sometimes be accompanied by FDG-avid lymph nodes
[16]. In SLE and Sjögren’s syndrome, FDG-PET
can highlight areas of active inammation,
including in the pericardium, joints, lymph
nodes, salivary glands, and lungs [17–19].
nance, cine short axis images without contrast (c) and
viability sequences with contrast (d) demonstrate enhancing pericardium (arrowheads), compatible with pericarditis. The focal uptake is an unusual presentation of
pericarditis
Neoplastic Pericardial Diseases
Pericardial diseases associated with malignancy
are secondary to metastatic disease in the vast
majority of cases, including lung cancer, breast
cancer, lymphoma, and melanoma. Primary pericardial tumors, most commonly pericardial
mesothelioma, are infrequent. Pericardial mesothelioma is very rare, with an incidence of
0.0022% and represents less than 3% of primary
cardiac tumors (see Chap. 10) and may be associated with asbestos exposure [20, 21]. Conversely,
secondary pericardial involvement in malignancy
is not rare, affecting 1–20% of patients with cancer based on autopsy studies, but is often underdiagnosed [1, 22, 23]. Neoplastic pericardial
diseases may present as acute pericarditis, pericardial effusion with or without tamponade, and
constrictive pericarditis.
The role of FDG-PET is well established for
the diagnosis, staging, and response assessment
of neoplastic disease due to the increased FDG
uptake seen in most malignancies. Therefore, in
cases of suspected neoplastic pericardial disease,
FDG-PET with whole-body imaging can be help-
106
https://t.me/medicina_free
M. Pelletier-Galarneau and P. Martineau
ful to clarify the etiology of pericardial disease,
identify and assess the extent of underlying
malignancy, and guide biopsy (Fig. 8.4).
Neoplastic pericardial lesions (i.e. metastases)
often demonstrate intense and heterogeneous
a
d
b
FDG uptake with corresponding nodularity on
CT [24, 25]. In cases of direct spread from an
adjacent tumor (typically from a lung primary),
an FDG-avid mass involving the pericardium is
usually easily identied.
c
Fig. 8.4 A 43-year-old male with a history of heart transplant presented with sepsis and diarrhea. Axial FDG-PET
(a), CT (b), fused PET/CT (c), and whole-body MPI (d)
demonstrate innumerable foci of intense FDG uptake projecting in lymph nodes as well as within the myocardium,
the pericardium (arrowhead), spleen, liver, and bones,
compatible with a lymphoproliferative process. The nal
diagnosis of post-transplant lymphoproliferative disorder
(PTLD) was established on biopsy
8 Pericardial Diseases
https://t.me/medicina_free
107
Other Non-Infectious Pericardial
Diseases
Post-cardiac injury syndrome, also called
Dressler’s syndrome, occurs in the presence of
myocardial or pericardial injury, which can be
seen following cardiac surgery, myocardial
infarction, penetrating injury, pacemaker
insertion, etc. It usually occurs within
1–6 weeks following injury [26]. Postmyocardial infarction syndrome became rare
following the advent of reperfusion treatments
a
d
[27]. Nonetheless, in the weeks following a
myocardial infarction, especially for patients
who did not undergo revascularization or for
those with delayed revascularization, symptoms including fever, generalized weakness,
and pleuritic chest pain should raise the suspicion of post-myocardial infarction syndrome.
On FDG-PET, post- myocardial infarction syndrome is indistinguishable from idiopathic
and viral pericarditis and demonstrates mild to
moderate, diffusely increased pericardial
uptake (Fig.8.5).
b
c
Fig. 8.5 A 57-year-old female referred for fever of
unknown origin. The patient had a ST-segment elevation
myocardial infarction (STEMI) 2 weeks prior to the study.
Axial FDG-PET (a), CT (b), fused PET/CT (c), and
whole-body MPI (d) images demonstrate mild and diffuse
increased uptake within a pericardial effusion, compatible
with post-myocardial infarction syndrome (Dressler
syndrome)
108
https://t.me/medicina_free
M. Pelletier-Galarneau and P. Martineau
Post-pericardiotomy syndrome occurs in the
References
weeks following cardiac surgery, with an incidence between 2% and 30% [28]. FDG-PET may
reveal diffusely increased pericardial uptake with
an associated effusion [29]. Importantly, it may
be difcult to differentiate post-operative changes
from pericarditis in this context. The distribution
of FDG uptake may help distinguish between
post-operative changes and post-pericardiotomy
syndrome, with the former being more focal and
anterior and the latter more diffuse and
circumferential.
An unusual cause of non-infectious pericardial
disease is IgG4-related disease, which is a rare,
multisystemic, immune-mediated, broinammatory disease often mimicking malignancy [30]. FDG-PET can identify areas of active
inammation and therefore be used for the assessment of organ involvement, therapy response
monitoring, and guiding intervention [31]. IgG4related pericarditis may appear as diffuse or heterogeneous uptake projecting in a pericardial
effusion [32]. Coronary involvement can also be
seen on occasion, with more focal activity noted
at the level of the affected epicardial vessels.
Whole-body imaging can be useful in patients
with suspected IgG4-related disease in order to
assess disease extent as additional, non- cardiac
sites of brosis and inammation can be present.
Conclusion
10. Eldin C, Melenotte C, Million M, Cammilleri S, Sotto
Pericardial diseases are relatively frequent and
clarifying the etiology is of paramount importance in order to administer the appropriate therapy and identify potential life-threatening
11. Barten DG, Delsing CE, Keijmel SP, Sprong T,
conditions. FDG-PET is emerging as a useful
tool for the evaluation of patients with pericardial
disease, as it allows for the identication and
12. Chang S-A, Choi JY, Kim EK, Hyun SH, Jang SY,
assessment of disease extent. It has been shown
to be especially useful for the assessment of
tuberculous pericarditis and neoplastic pericar-
13. Knockaert DC. Cardiac involvement in sys-
dial lesions. In addition, FDG-PET has shown
potential in predicting the response to therapy.
Further studies are required to assess the role of
14. Martineau P, Pelletier-Galarneau M, Juneau D, Leung
FDG-PET, particularly for non-infectious and
non-oncological pericardial diseases.
1. Adler Y, Charron P, Imazio M, Badano L, BarónEsquivias G, Bogaert J, etal. 2015 ESC guidelines for
the diagnosis and management of pericardial diseases.
Eur Heart J. 2015;36(42):2921–64.
2. Gerardin C, Mageau A, Benali K, Jouan F, Ducrocq
G, Alexandra J-F, et al. Increased FDG-PET/
CT pericardial uptake identies acute pericarditis patients at high risk for relapse. Int J Cardiol.
2018;271:192–4.
3. Imazio M.Contemporary management of pericardial
diseases. Curr Opin Cardiol. 2012;27(3):308–17.
4. Noubiap JJ, Agbor VN, Ndoadoumgue AL, Nkeck
JR, Kamguia A, Nyaga UF, et al. Epidemiology of
pericardial diseases in Africa: a systematic scoping
review. Heart. 2019;105(3):180–8.
5. Melenotte C, Protopopescu C, Million M, Edouard
S, Carrieri MP, Eldin C, et al. Clinical features and
complications of Coxiella burnetii infections from the
French National Reference Center for Q fever. JAMA
Netw Open. 2018;1(4):e181580.
6. James OG, Christensen JD, Wong TZ, Borges-Neto
S, Koweek LM.Utility of FDG PET/CT in inammatory cardiovascular disease. Radiogr Rev Publ
Radiographics. 2011;31(5):1271–86.
7. Hyeon CW, Yi HK, Kim EK, Park S-J, Lee S-C,
Park SW, etal. The role of 18F-uorodeoxyglucosepositron emission tomography/computed tomography
in the differential diagnosis of pericardial disease. Sci
Rep. 2020;10(1):21524.
8. Martineau P, Grégoire J, Harel F, Pelletier-Galarneau
M.Assessing cardiovascular infection and inammation with FDG-PET.Am J Nucl Med Mol Imaging.
2021;11(1):46–58.
9. Pelletier-Galarneau M, Martineau P, Zuckier LS,
Pham X, Lambert R, Turpin S. 18F-FDG-PET/CT
imaging of thoracic and extrathoracic tuberculosis in
children. Semin Nucl Med. 2017;47(3):304–18.
A, Elsendoorn A, etal. 18F-FDG PET/CT as a central tool in the shift from chronic Q fever to Coxiella
burnetii persistent focalized infection. Medicine
(Baltimore). 2016;95(34):e4287.
Timmermans J, Oyen WJ, etal. Localizing chronic
Q fever: a challenging query. BMC Infect Dis.
2013;13(1):413.
Choi J-O, et al. [18F] Fluorodeoxyglucose PET/CT
predicts response to steroid therapy in constrictive
pericarditis. J Am Coll Cardiol. 2017;69(6):750–2.
temic inammatory diseases. Eur Heart J.
2007;28(15):1797–804.
E, Birnie D, Beanlands RSB.Molecular imaging of
cardiac sarcoidosis. Curr Cardiovasc Imaging Rep.
2018;11(3):6–17.
8 Pericardial Diseases
https://t.me/medicina_free
109
15. Pelletier-Galarneau M, Ruddy TD.PET/CT for diagnosis and management of large-vessel vasculitis. Curr
Cardiol Rep. 2019;21(5):34.
16. Hotta M, Minamimoto R, Kaneko H, Yamashita
H.Fluorodeoxyglucose PET/CT of arthritis in rheumatic diseases: a pictorial review. Radiographics.
2020;40(1):223–40.
17. Curiel R, Akin EA, Beaulieu G, DePalma L, Hashe
M. PET/CT imaging in systemic lupus erythematosus. Ann N Y Acad Sci. 2011;1228:71–80.
18. Cohen C, Mekinian A, Uzunhan Y, Fauchais A-L,
Dhote R, Pop G, et al. 18F-uorodeoxyglucose
positron emission tomography/computer tomography as an objective tool for assessing disease
activity in sjögren’s syndrome. Autoimmun Rev.
2013;12(11):1109–14.
19. Sharma P, Chatterjee P. 18F-FDG PET/CT in
multisystem sjögren syndrome. Clin Nucl Med.
2015;40(5):e293–4.
20. Godar M, Liu J, Zhang P, Xia Y, Yuan Q.Primary pericardial mesothelioma: a rare entity. Case Rep Oncol
Med. 2013;2013:283601.
21. Gössinger HD, Siostrzonek P, Zangeneh M, Neuhold
A, Herold C, Schmoliner R, etal. Magnetic resonance
imaging ndings in a patient with pericardial mesothelioma. Am Heart J. 1988;115(6):1321–2.
22. Klatt EC, Heitz DR. Cardiac metastases. Cancer.
1990;65(6):1456–9.
23. Maisch B, Ristic A, Pankuweit S. Evaluation and
management of pericardial effusion in patients
with neoplastic disease. Prog Cardiovasc Dis.
2010;53(2):157–63.
24. Yi J-E, Yoon HJ, JH O, Youn H-J.Cardiac and pericardial 18F-FDG uptake on oncologic PET/CT: compar-
ison with echocardiographic ndings. J Cardiovasc
Imaging. 2018;26(2):93–102.
25. Martineau P, Dilsizian V, Pelletier-Galarneau
M.Incremental value of FDG-PET in the evaluation
of cardiac masses. Curr Cardiol Rep. 2021;23(7):78.
26. Leib AD, Foris LA, Nguyen T, Khaddour K.Dressler
Syndrome. In: Stat pearls [internet]. Treasure Island,
FL: Stat Pearls; 2021. http://www.ncbi.nlm.nih.gov/
books/NBK441988/.
27. Shahar A, Hod H, Barabash GM, Kaplinsky E,
Motro M. Disappearance of a syndrome: Dressler’s
syndrome in the era of thrombolysis. Cardiology.
1994;85(3–4):255–8.
28. Gabaldo K, Sutlić Ž, Mišković D, Knežević Praveček
M, Prvulović Đ, Vujeva B, etal. Postpericardiotomy
syndrome incidence, diagnostic and treatment strategies: experience AT two collaborative centers. Acta
Clin Croat. 2019;58(1):57–62.
29. Salomäki SP, Hohenthal U, Kemppainen J, Pirilä L,
Saraste A.Visualization of pericarditis by uorodeoxyglucose PET. Eur Heart J Cardiovasc Imaging.
2014;15(3):291.
30. Stone JH, Zen Y, Deshpande V.IgG4-related disease.
N Engl J Med. 2012;366(6):539–51.
31. Zhang J, Chen H, Ma Y, Xiao Y, Niu N, Lin W, etal.
Characterizing IgG4-related disease with 18F-FDG
PET/CT: a prospective cohort study. Eur J Nucl Med
Mol Imaging. 2014;41(8):1624–34.
32. Matsumiya R, Hosono O, Yoshikawa N, Uehara
M, Kobayashi H, Oda A, et al. Elevated serum
IgG4 complicated by pericardial involvement with
a patchy (18) F-FDG uptake in PET/CT: atypical
presentation of IgG4-related disease. Intern Med.
2015;54(18):2337–41.
Ventricular Arrhythmias
https://t.me/medicina_free
DanieleMuser, AbassAlavi,
andPasqualeSantangeli
9
Introduction
Ventricular arrhythmias (VA) include a wide
spectrum of clinical entities ranging from idiopathic premature ventricular contractions (PVC)
to malignant sustained ventricular tachycardia
(VT) or ventricular brillation (VF). The mechanisms behind VA are heterogeneous and include
triggered activity or exacerbated automaticity in
the absence of structural heart disease as well as
reentry mechanisms related to the presence of
myocardial scar associated with structural heart
diseases (SHD) such as ischemic heart disease
and non-ischemic cardiomyopathies. Myocardial
inammation may also play a role in the genesis
and maintenance of VT in several conditions
such as myocarditis, cardiac sarcoidosis (CS),
and Chagas cardiomyopathy either by determining cell loss and reparative brosis able to sustain
reentrant arrhythmias as well as triggered activity
and exacerbated automaticity within inamed
areas [1–3]. Recently, a potential role of subclinical myocardial inammation in patients present-
D. Muser · P. Santangeli (*)
Cardiac Electrophysiology, Cardiovascular Medicine
Division, Hospital of the University of Pennsylvania,
Philadelphia, PA, USA
e-mail: pasquale.santangeli@uphs.upenn.edu
A. Alavi
Nuclear Medicine Division, Radiology Department,
Hospital of the University of Pennsylvania,
Philadelphia, PA, USA
ing with VA of unexplained origin has been also
reported [4]. Cardiac 18F-uorodeoxyglucose
(18F-FDG) positron emission tomography (PET)
is the gold standard for evaluation of myocardial
inammation and may be used to improve
arrhythmic substrate characterization, risk stratication and identication potential therapeutic
targets in patients presenting with VA [5]. In the
present chapter, we present the principles and
main clinical applications of 18F-FDG PET imaging in the setting of VA.
Mechanistic Bases
Myocardial inammation contributes to the genesis of VA in several ways [1]. First of all, active
inammation is responsible for direct cell injury
leading to myocyte death and consequent replacement brosis. The presence of surviving myocardial bers within brous tissue leads to the
formation of slow conduction pathways, dispersion of activation and refractoriness which all
together create the pathophysiologic basis for
reentrant circuits (Fig.9.1) [6]. Systemic inammatory response may also promote myocardial
electrical instability through cytokine release,
electrical remodeling, and sympathetic hyperactivity [7]. Finally, myocardial ischemia as a result
of microvascular dysfunction and demand/supply
imbalance within the inamed myocardium can
further increase arrhythmogenicity [8].
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
M. Pelletier-Galarneau, P. Martineau (eds.), FDG-PET/CT and PET/MR in Cardiovascular
Diseases, https://doi.org/10.1007/978-3-031-09807-9_9
111
112
https://t.me/medicina_free
Fig. 9.1 Schematic representation of a reentry circuit as
originally described by Stevenson etal. in 1993. In this
model, two activation wavefronts propagate around two
lines of conduction block sharing a common pathway
(central isthmus). Areas of dense scar (blue) cannot be
excitable during tachycardia. Bystander pathways can be
attached to any point in the circuit and represent areas of
tissue activated by the wavefront but not playing an active
role in the reentrant circuit
General Principles of18F-FDG PET/
CT Imaging intheSetting
ofVentricular Arrhythmias
The possibility to identify myocardial inammation by the use of 18F-FDG PET relies on the preferential accumulation of 18F-FDG in areas of
active inammation compared to healthy
myocardium, thanks to the higher metabolic
activity (glucose demand) of inammatory cells.
Considering that in normal circumstances, cardiac metabolism may rely on glucose consumption, physiologic myocardial glucose uptake may
represent a major source of false positive results
making its suppression of pivotal importance to
identify areas of true pathologic involvement [9].
Several strategies have been proposed to
achieve adequate suppression of physiologic 18FFDG uptake including prolonged fasting (≥18h)
preceded by a low-carbohydrate/high-fat content
diet to shift cardiac metabolism from a glucose to
a free fatty acid one and administration of unfractionated heparin (intravenous bolus of 50IU/kg
15 min prior to 18F-FDG injection) in order to
increase circulating free fatty acid levels [10, 11].
D. Muser et al.
Regrettably, a high variability in myocardial 18FFDG uptake is still observed even after all the
aforementioned precautions, leading to a rate of
false positive results of up to 30% [10]. In order
to optimize scan reliability, specic criteria have
been developed for image interpretation. In particular, diffuse 18F-FDG uptake should always be
looked at very suspiciously as a possible result of
inadequate suppression, while focal or focal on
diffuse uptake patterns are generally regarded as
more signicant [11]. To further complicate the
interpretation of 18F-FDG/PET results, selective
uptake of 18F-FDG in the inferolateral wall, even
in the presence of a complete suppression of the
remaining myocardium, has been reported as a
normal physiologic pattern [12, 13]. In this
regard, the comparison between 18F-FDG/PET
nding and other imaging modalities such CMR
with T2-weighted imaging to detect myocardial
inammation and late gadolinium enhancement
to detect necrosis/brosis may improve its specicity [14]. Other possible sources of false results
are represented by misalignment issues due to
patient movement or abnormal 18F-FDG uptake
surrounding pacemaker (PM) or implantable cardioverter debrillator (ICD) leads [15, 16].
Recently, the development of new radiotracers
which do not physiologically accumulate within
healthy myocardium such as Gallium-68 (68Ga)
DOTATATE may potentially overcome 18F-FDG
limitations. 68Ga-DOTATATE targets somatostatin receptors on activated macrophages which are
absent on normal myocardial cells making
68
Ga-DOTATATE a selective marker of myocar-
dial inammation [17].
Cardiac Sarcoidosis
Sarcoidosis is a systemic inammatory disease
characterized by lymphocyte CD4+ mediated
formation of non-necrotizing granulomas [18].
Overt cardiac involvement is relatively rare being
found in about 5–10% of the patients [19].
Cardiac sarcoidosis is characterized by patchy
areas of myocardial inammation and brosis
which, depending on the location and severity,
may be clinically silent or lead to atrio- ventricular
9 Ventricular Arrhythmias
https://t.me/medicina_free
113
conduction block, supra-ventricular arrhythmias,
VA, and progressive heart failure [18]. In the
pathophysiologic process of CS there is always a
coexistence of lesions at different stages of the
disease with areas of active inammation overlapping areas of dense, metabolically inactive
scar (Fig.9.2) [20, 21]. In patients with CS presenting with recurrent VT, characterization of the
arrhythmogenic substrate helps the detection of
potential targets for substrate-based ablation but
also provides important diagnostic elements and
information to identify patients at high risk of
recurrence after catheter ablation (CA) that may
benet from more aggressive medical therapy
with immunosuppressive drugs [22]. Interestingly,
areas of unipolar voltage abnormality on invasive
electroanatomic voltage mapping have been correlated with the presence of active inammation
in areas without a signicant amount of scar representing optimal targets for endomyocardial
biopsy (EMB), thus improving its sensitivity and
specicity which is typically limited by the
ab
cd
Fig. 9.2 Imaging and electroanatomic ndings of a
patients with cardiac sarcoidosis and recurrent ventricular
tachycardia. Positron emission tomographic (PET) scan
(a–e) showing active inammation of the mid-basal
inferoseptum (a, red arrowhead), basal (a, asterix) and
apical (a, red arrow) anterolateral wall, basal inferior (e,
red arrow), and anterior (e,
enhanced magnetic resonance imaging (b–f) of the same
patient showing diffuse myocardial scar involving the distal anterolateral wall (b, green arrow), the anterior wall (f,
green arrows), and the inferior wall (f, green arrowheads).
red arrowhead) walls. Contrast-
The septum and the basal anterolateral wall do not show
scar although they are involved by active inammation.
Left ventricular (LV) endocardial electroanatomic map
(EAM; (c), (d), (g), and (h)) showing a small area of low
bipolar voltage (≤1.5mV) on the midapical inferior wall
(g, inferior view) and a more diffuse area of low unipolar
voltage (≤8.3) on the basal septum (d, right anterior
oblique [RAO] view) and inferior wall (h, inferior view);
unipolar EAM showed areas of abnormal voltage consistent with both scar and inammation. (Reprinted with permission from Muser etal. [22])
114
https://t.me/medicina_free
D. Muser et al.
ef
gh
Fig. 9.2 (continued)
patchy distribution of the disease and the presence of areas with dense scar (nonspecic nding
on histology) (Fig. 9.3) [5]. The available evidence strongly supports the critical role of scar
compared to active inammation in sustaining
VA. In a study including 50 patients with CS,
14% developed VA during follow-up: none
among those with LGE-/FDG+, 19% among
those with LGE+/FDG+, and 21% among those
with LGE+/FDG- [23]. In a series of 42 patients
with CS and VT referred for CA who underwent
preprocedural 18F-FDG PET and CMR, evidence
of active inammation was found in 48% of the
cases, while areas of LGE were almost ubiquitous (90% of the cases) [5]. Interestingly, after
quantication of myocardial inammatory activity in terms of metabolic volume (MV—volume
of the 18F-FDG-avid myocardium) and metabolic
activity (MA—product between SUV and MV),
myocardial areas showing the presence of abnormal electrograms (representing potential targets
for CA) had a higher degree of scar transmurality
on CMR and a lower MV and MA compared to
those without evidence of abnormal electrograms
(Fig.9.3). Moreover, critical sites for VA determined by electrophysiological mapping appeared
more strongly associated with LGE on CMR than
with increased 18F-FDG uptake on PET (abnormal electrograms present in 70% of LGE+/PET−
myocardial segments vs. 27% of LGE− /PET+
segments) [5]. All the aforementioned data suggest that reentrant VT circuits are strongly associated with presence of scar even in patients with
active disease and are located in areas with more
9 Ventricular Arrhythmias
https://t.me/medicina_free
80
60
40
CMA (g glucose)
20
115
Normal Unipolar/Normal Bipolar
Low Unipolar/Normal Bipolar
Low Unipolar/Low Bipolar
0
02040
a
100
80
60
40
% Scar Transmurality
20
0
Abnormal EGMs
p<0.001
Absence of
% Scar Transmurality
Presence of
Abnormal EGMs
60
b
20
15
10
5
Cardiac Metabolic Volume, ml
0
Absence of
Abnormal EGMs
Fig. 9.3 Correlation among presence of scar, inammation, and electroanatomic ndings in patients with cardiac
sarcoidosis undergoing ventricular tachycardia ablation
Top Panel: Scatter plot representing the distribution of
myocardial segments according to imaging and electroanatomic ndings. Segments with both normal unipolar
and bipolar voltage (green dots) represent the “healthy
myocardium” without either scar or inammation.
Segments with low unipolar voltage but normal bipolar
voltage (orange dots) represent sites of “active disease”
with absence/few scar and presence of active inammation in which no or only few abnormal electrograms are
recorded. Those sites represent potential good targets for
c
100
80
p<0.001
60
40
20
Cardiac Metabolic Ativity, g glucose
0
Presence of
Abnormal EGMs
Absence of
Abnormal EGMs
endomyocardial biopsy. Segments with both low unipolar
and bipolar voltage (blue dots) represent sites of
“advanced disease” with high scar transmurality and no/
few inammatory activity. In such sites, abnormal electrograms are frequently recorded representing potential good
targets for substrate modication. Bottom Panel: Boxplots demonstrating the higher degree of scar transmurality on CMR (a) and the lower degree of inammation
quantied by cardiac metabolic volume (b) and cardiac
metabolic activity (c) within myocardial segments showing the presence of abnormal electrograms (critical sites
of VT circuits) compared to those without. (Modied with
permission from Muser etal. [5])
p<0.001
Presence of
Abnormal EGMs
extensive brous replacement and less inammation stressing the central role of brosis in the
genesis of VA.Inammation still plays an important causative role in VA as the primary source of
myocardial damage, cell loss, and brotic
replacement. To that end, in patients undergoing
repeated CA after a rst attempt, a signicant
scar progression has been found only in those
with persistent inammatory activity detected by
FDG-PET (Fig. 9.4) [5]. Correspondingly, lack
Соседние файлы в папке Библиотека им академика М.И. Перельмана