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_3651_Библиотеки_им_академика_М_И_Перельмана
.pdf
Contributors
https://t.me/medicina_free
xxiii
ThomasRobein
Biosense Webster, Mulhouse, France
Johnson & Johnson, Mulhouse, France
OlivierRoth, MD
Cardiology Department, “Emile Muller” Hospital, Mulhouse, France
SerbanSchiau, MD
Cardiology Department, “Emile Muller” Hospital, Mulhouse, France
xxiv
https://t.me/medicina_free
BergamotteThinotSerbanSchiau, MD
Biosense Webster, Mulhouse, France
MaximTissier
Contributors
Biosense Webster, Mulhouse, France
Johnson & Johnsson, Mulhouse, France
Jean-YvesWiedemann, MD
Cardiology Department, “Emile Muller” Hospital, Mulhouse, France
Abbreviations
https://t.me/medicina_free
AF Atrial brillation
AP Antero-posterior
ASD Atrial septal defect
AT Atrial tachycardia
AV Atrio-ventricular
AVN Atrio-ventricular node
AVNRT Atrio-ventricular node reentry tachycardia
AVRT Atrio-ventricular reentry tachycardia
BMI Body mass index
BP Blood pressure
BUN Blood urea nitrogen
CABG Coronary artery bypass graft
CFAE Complex fractionated atrial electrograms
COPD Chronic obstructive pulmonary disease
cTnI Cardiac troponin I
CX Circumex (coronary artery)
EDD End diastolic diameter
EF Ejection fraction
EP Electrophysiology
EPS Electrophysiological study
ESD End systolic diameter
Hb Hemoglobin
Hct Hematocrit
HFpEF Heart failure with preserved ejection fraction
HFrEF Heart failure with reduced ejection fraction
HR Heart rate
ICD Implantable cardioverter debrillator
ISV Internal saphenous vein
IVC Inferior vena cava
IVS Interventricular septum
LA Left atrium
LAD Left anterior descending (coronary artery)
LAO Left anterior oblique
LBBB Left bundle branch block
LIMA Left internal mammary artery
LPSV Left superior pulmonary vein
LIPV Left inferior pulmonary vein
xxv
xxvi
https://t.me/medicina_free
LL Left lateral
LV Left ventricle
MI Myocardial infarction
NT-pro BNP N-terminal pro-brain natriuretic peptide
ORT Orthodromic reciprocating tachycardia
PA Postero-anterior
PAC Premature atrial contraction
PAF Paroxysmal atrial brillation
PFO Patent foramen ovale
PV Pulmonary vein
PVC Premature ventricular contraction
RA Right atrium
RAO Right anterior oblique
RBBB Right bundle branch block
RCA Right coronary artery
RIMA Right internal mammary artery
RL Right lateral
RSPV Right superior pulmonary vein
RIPV Right inferior pulmonary vein
RV Right ventricle
SCD Sudden cardiac death
sPAP Systolic pulmonary artery pressure
SVC Superior vena cava
TAPSE Tricuspid annulus plane systolic excursion
TSH Thyroid stimulating hormone
VT Ventricular tachycardia
WPW Wolf-Parkinson-White
Abbreviations
Case 1
https://t.me/medicina_free
RonanLe Bouar, FrédéricHalbwachs,
JacquesLevy, Jean-YvesWiedemann,
CrinaMuresan, andLaurentDietrich
1
Case Presentation
A 45-year-old female patient with no signicant
past medical history was diagnosed by her family
physician with an irregular pulse. The patient had
been complaining of dyspnea on exertion that
had progressively aggravated during the past several months. A cardiology consultation was organized and performed, which diagnosed frequent,
predominantly monomorphic PVC, with a high
ventricular arrhythmia burden at 24-h Holter
ECG (50,017 PVC, of which 46,435 isolated
PVC, 1838 couplets, and 2 runs, representing
36.7% of the total QRS complexes/24h).
Her 12-lead ECG is presented in Fig.1.1. The
result of her 24-h Holter ECG is presented in
Fig.1.2.
Her transthoracic echocardiography demon-
strated severe LV systolic dysfunction (LVEF of
30%). She was referred to the cardiology department for detailed cardiovascular investigations
and treatment. Her cardiovascular risk factors
R. Le Bouar (*) · J. Levy · J.-Y. Wiedemann ·
C. Muresan · L. Dietrich
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr; levyj@ghrmsa.fr;
wiedemannjy@ghrmsa.fr; crina.muresan@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr
F. Halbwachs
Biosense Webster, Mulhouse, France
were represented by active smoking. Her medication at home consisted of bisoprolol 2.5mg, prescribed by her cardiologist.
Her transthoracic echocardiography showed
severe LV systolic dysfunction, with an EF% of
26% (Fig.1.3). It also showed global hypokinesia, with a dilated LV (EDD of 63 mm), nonelevated LV lling pressure, cardiac index of
2.9 L/min/m2, mild aortic regurgitation, nondilated left atrium, non-dilated right ventricle,
mild tricuspid regurgitation, absence of pulmonary hypertension, sPAP of 33 mmHg, and
absence of pericardial effusion.
An exercise stress test did not show any signs
of myocardial ischemia. It demonstrated disappearance of PVCs during effort, with reappearance after the end of the effort.
Given the ECG aspect of the PVC, suggesting
an origin in the RVOT, a cardiac MRI was performed, searching for arguments in favor of
arrhythmogenic cardiomyopathy (Fig.1.4).
Her biological workup showed a Hb level of
12.1 g/dL, leukocytes 4.81 × 109/L, platelets
214×109/L, CRP<3mg/L, BUN 4.5mmol/L,
creatinine 68μmol/L, glycemia 4.5mmol/L, Na+
141 mmol/L, K+ 3.7 mmol/L, NT pro-BNP
1080pg/mL, and TSH 2.3IU/L.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
L. Muresan (ed.), Clinical Cases in Cardiac Electrophysiology: Ventricular Arrhythmias,
https://doi.org/10.1007/978-3-031-35579-0_1
1
2
https://t.me/medicina_free
R. Le Bouar et al.
Fig. 1.1 A 12-lead ECG at admittance to the cardiology department
Question 1: Where is the origin of the
PVCs presented in Fig. 1.1?
A. RVOT
B. LVOT
Question 3: Is there a possible relation-
ship between the PVCs and the systolic
LV dysfunction?
A. Yes. The PVCs are the most likely cause
C. LV summit
D. Right coronary cusp
B. Yes. The severe systolic dysfunction
E. Left coronary cusp
C. No. This is a simple coincidence.
D. No. Both are expression of the same
Question 2: How would you consider the
E. I don’t know.
ventricular arrhythmia burden of this
patient on the 24-h Holter ECG?
A. Insignicant.
B. Mild.
C. Moderate.
D. Important.
E. I don’t know.
Question 4: What is the best treatment
option for this patient’s PVCs?
A. Beta blockers
B. Flecainide
C. Amiodarone
D. Sotalol
E. Catheter ablation
of the LV systolic dysfunction.
determined the appearance of PVCs.
unidentied inherited arrhythmia
syndrome.
1 Case 1
https://t.me/medicina_free
3
Fig. 1.2 A 24-hour Holter ECG recording showing frequent, predominantly monomorphic PVC, with a high ventricular arrhythmia burden, representing 36.7% of the total QRS complexes/24h
4
https://t.me/medicina_free
R. Le Bouar et al.
Fig. 1.3 Left panel: Echocardiography image in apical
four-chamber view, showing a severely depressed LV
EF% of 26% (quantied by Simpson single-plane
60 mm
Fig. 1.4 Left panel: Cardiac MRI image (cine SSFP
four-chamber view) showing an end-diastolic diameter of
60mm and no global or localized dilation of the right ventricle. Right panel: Three-chamber view showing absence
method). Right panel: Echocardiography image in apical
two-chamber view, showing a severely depressed LV 31
EF% (quantied by Simpson biplane method)
of late gadolinium enhancement at the level of the right
and left ventricle. No major or minor criteria in favor of
arrhythmogenic cardiomyopathy
1 Case 1
https://t.me/medicina_free
5
Figure 1.1 explained. A 12-lead ECG showing sinus rhythm with a heart rate of 84bpm, QRS
axis at +60°, absence of LV hypertrophy, absence
of ischemia, frequent monomorphic PVC, and
one polymorphic ventricular couplet, normal QT
interval. The PVC morphology is “QS” in lead I,
“R” in leads II, III, and aVF with LBBB morphology, and a precordial transition in V4, in favor of
a RVOT origin. Of note, the PVC QRS transition
in precordial leads (V4) takes place later than the
QRS transition in sinus rhythm (V3), argument in
favor of a RVOT origin.
Given the high arrhythmia burden demonstrated by the 24-h Holter ECG (more than
26,000/24h) and the likely arrhythmic cause of
her dilated cardiomyopathy (no structural
abnormality was found by transthoracic echocardiography, coronary angiography, and cardiac
MRI), a catheter ablation procedure was offered
and accepted by the patient. Of note, long-term
antiarrhythmic drugs were not desired by the
patient.
Electrophysiological Study andRF
Catheter Ablation Procedure
The ablation procedure was performed under
local anesthesia and conscious sedation. Vascular
access was obtained using the modied Seldinger
technique, under Doppler ultrasound guidance. A
6F bipolar non-steerable catheter (Viking, Boston
Scientic®) was introduced in a 6F 20cm vascular sheath and was subsequently advanced via the
right common femoral vein up to the right ventricular apex. A Biosense Webster
SF open-irrigated 3.5mm tip with double curve
D/F was used as the roving/ablation catheter,
which was introduced in a 9F 20 cm vascular
sheath at the level of the right common femoral
vein and advanced at the level of the right
ventricle.
The CARTO® 3 electro-anatomic mapping
system (Biosense Webster, Johnson & Johnson)
was used to guide mapping and ablation of the
accessory pathway.
®
SmartTouch
6
https://t.me/medicina_free
R. Le Bouar et al.
Ventricular pacing was carried out at twice the
diastolic threshold using the EP-4™ Cardiac
Stimulator (Abbott®) system. Surface ECG and
intracavitary ECGs were recorded by the
WorkMate Claris™ System (Abbott®).
Given the 12-lead aspect of the PVC (“QS” in
lead I, “R” in leads II, III, and aVF with a LBBB
morphology, and a precordial transition in V4),
an origin at the level of the RVOT was suspected.
Mapping of the PVC was therefore commenced
in the RVOT.
An anatomical map of the RVOT was initially
created.
Next, an activation map of the RVOT during
the frequent PVCs was created. This showed the
presence of an early activation site at the level of
the high posterior and lateral RVOT, just below
the pulmonary valve, from where the activation
of the RVOT spread in a radial manner, suggesting a focal activation pattern (Fig.1.5). The local
bipolar electrogram preceded the onset of the
QRS complex on the surface ECG by 17ms. At
this site, the unipolar electrogram recorded by the
roving/ablation catheter had a “QS” aspect.
A pacemap was subsequently created by pacing from the distal electrode of the roving/ablation catheter at a xed coupling interval of
600ms in several areas of the RVOT, with emphasis on the area of the earliest activation during the
PVCs. The PASO module of the CARTO system
Fig. 1.5 CARTO image of the right ventricular outow
tract (RVOT) in left lateral view 100°. Activation map of
the RVOT during PVCs, showing an area of early endocardial activation, preceding the onset of the QRS onset
on the surface ECG, with a “QS” aspect of the local unipolar electrogram. The area is situated in the upper lateral
and slightly posterior part of the RVOT.The orange dots
represent the bundle of His. The right part of the image
shows the 12-lead ECG, together with the distal bipolar
electrode of the ablation catheter (MAP 1–2) and the unipolar recording of the distal electrode (MAP 1). The unipolar electrogram recorded by the ablation catheter has a
“QS” aspect
Соседние файлы в папке Библиотека им академика М.И. Перельмана