OLD WOMAN WITH SEVERE CORONARY HEART DISASE AND

OLD WOMAN WITH SEVERE CORONARY HEART DISASE AND

OLD WOMAN WITH SEVERE CORONARY HEART
DISASE AND LEFT BUNDLE BRANCH BLOCK
MULHER IDOSA COM DOENÇA CORONARIANA
SEVERA E BLOQUEIO COMPLETO DE RAMO
ESQUERDO
MUJER DE EDAD AVANZADA CON ENFERMEDAD
CORONARIA SEVERA Y BLOQUEO COMPLETO DE
RAMA IZQUIERDA
Case of Andrés Ricardo Pérez-Riera MD PhD
Chief of electrovectorcardiogram sector – Cardiology Discipline - ABC Medicine Faculty – Santo
André - São Paulo Brazil.
Contact [email protected]
Cell phone: (011) 84693388
Feminine, Caucasian, 74 yo, retired, severe coronary artery disease, (two clinical episodes of myocardial
infarctions at past), essential hypertension, type 2 diabetes mellitus, hyperlipoproteinemia type IIb
(increased blood levels of low density lipoproteins LDL and apoprotein B (ApoB) and centripetal obesity
android fat distribution. Absolute waist circumference 105cm and waist–hip ratio>0.85. (body
mass index >30 kg/m2 ).
BP 165/90, General: Breathless, moderately obese woman in acute distress sitting upright complaining "I
am going to die. Please help me."
Normocephalic. Eyes, ears, and throat normal.
Neck: Whit the patient positioned under 45° distended neck veins with visible large 'a' waves, The jugular
venous pressure JVP to 12cm. Sistolic bruit on left carotid reflecting turbulence of flow .
Chest: the point of maximal impulse (ictus cordis) palpated in the 6th intercostal space just al axilar line
and exceed a quarter size (24.26 mm). No thrill.
Normal HR, regular. Grade 3/6 systolic murmur at LSB, S3 gallop noted.
Lung: bilateral rales one third lower bases.
Abdome: Liver palpable painful two centimeters below right costal margin. HJR+ Non-tender to palpation,
+Bowel sounds 4 quadrants.
Genitalia: Exam deferred.
Extremities: minimal pitting edema of lower extremities to the knees. Nail beds acyanotic, no clubbing.
Pedis and posterior tibial pulse in retromalleolar decreased. Elevation of the left foot to 30º for 30
seconds caused pallor. (Buerger’s test).
Neurologic: No localized or sensory deficits. Mental status intact.
Which is the ECG/VCG diagnosis and why?
--------------------------------------------------------------------------------------------------------------------------
Paciente del sexo femenino, 74 años, jubilada, sabidamente portadora de severa enfermedad coronaria
(antecedente de dos episodios clinicos previos de infarto de miocardio). hipertensa esencial, diabética tipo 2,
dislipémica tipo IIb (aumento de LDL y Apo B) y obesa centrípeta (índice de masa corporal > 30)
distribuición androide: circunferencia abdominal 105cm y relación cintura/cadera >0.85 Indice de masa
corporal >30kg/m2. PA 165/90, respiración dificultosa, obesa, sentada y diciendo que estaba por morir. “Por
fabor me ayude”.
Cabeza: nada digno de nota
Cuello: con la paciente 45 grados se observa distensión de las yuguares con ondas “a” aumentadas.
Soplo sistólico en carótida izquierda refejando turbulencia al flujo sanguineo.
Tórax: choque de la punta palpable en el 6to espacio intercostal izquierdo en la linea axilar anterior y no se
cubre con una pulpa digital. Ausencia de frémito catário.
RCR, soplo sistólico 3/6 el el borde izquierdo del esternón y tercer ruido con cadencia de galope
Pulmones rales crepitantes bilaterales en el tercio inferior de ambos pulmones.
Abdomen: hígado palpable doloroso a dos centímetros del reborde costal derecho.
Ruidos hidroaereos pesentes en los cuatro cuadrantes
Genitales: no realizado.
Extremidades; fobea en la región maleolar de las extremidades inferiores, Lecho ungeal acianótico y sin
baqueteamiento digital. Pulso pedio y tibial posterior en la región retro-maleolar interna disminuido a la
izquierda. La maniobra de elevación del pie izquierdo a 30º por 30 segundos causó palidez del pie( test de
Buerger)
Neurológico: sin déficit neurologicos. Buen contacto.
Preguntas: Cual es el diagnóstico ECG/VCG y porque?
Name: E. G. A.; Date: 02/11/2009.; Age: 74 years old; Gender: Female; Ethnic group: Caucasian;
Weight: 81Kg.; Height:1.57m.; Biotype profile: Endomorphic.;
Medication in use: Metformine 850mg twice a day, glibenclamide 5mg twice a day, carvedilol 25mg twice a
day, enalapril maleate 20mg 2 twice a day, espironolactone 25mg/once a day, furosemide 40mg once a day,
Symvastatine 20mg once a day, AAS 100mg once a day.
aV
R
L
aV
X
T
aVF
III
Y
II
I
Z
X V6
V5
T
V1
V2
V3
V4
V2
Z
T
Y
aVF
COLLEAGES OPINION
Caro Andrés:O caso é realmente muito interessante. O diagnóstico eletrocardiográfico é de um
BRE mais BDAS. Ocorre que o supradesnivelamento do segmento ST está presente de V1 a V5 o
que não é habitual em presença de BRE isolado.
O Vectocardiograma revela área eletricamente inativa em face anterior.
Podemos concluir a partir destes dados, que houve uma obstrução da artéria descendente anterior
e poderíamos até elucubrar que durante a ocorrência do infarto que a anamnese já havia revelado,
tivesse se instalado o BRE (apenas elucubração, não nenhuma certeza). Por outro lado, tratandose de paciente diabética, com síndrome metabólica, não surpreenderia se a cinecoronariografia
revela-se uma coronariopatia difusa, com comprometimento das demais artérias coronárias.
Um grande abraço do Hélio Germiniani que o felicita pela sua linda Tese.
Prof. Hélio Germiniani Professor livre-docente de Cardiologia da UFPr.Professor Adjunto IV de
Farmacologia da UFPr.Coordenador do Curso de Pós-Graduação Mestrado em Cardiologia da
U.F.PrChefe do Serviço de Eletrocardiografia do Hospital de Clínicas da U.F.Pr.
Ex-presidente da Sociedade Brasileira de Cardiologia e da Sociedade Paranaense de
Cardiologia.
Dear Andrés,
The case is really very interesting. The electrocardiographic diagnosis is of LBBB plus
LSFB. It so happens that ST segment elevation is present from
V1 through V5, which is not usual in the presence of isolated LBBB.
The Vectorcadiogram reveals an electrically inactive area in the anterior wall.
We can conclude from these data, that there was an obstruction of the ADA, and we may
even present the hypothesis that during the infarction that the anamnesis had already
revealed that the LBBB had installed (just a hypothesis, with no certainty). On the other
hand, since this is a diabetic patient, with metabolic syndrome, I would not be surprised if
coronary angiography revealed a diffuse CAD, with involvement of the other coronary
arteries.
Warm regards from Hélio Germiniani, and congratulations for your great thesis.
Estimado Maestro Perez Riera: En el ECG presenta RS 76 por min con BAV de primer grado y
BCRI. En una paciente conoraria previa, que padece miocardiopatia diltada isquemico necrotica
segun lo referido, que se presenta con signos de falla cardiaca aguda.
1. La primera pregunta seria si el BCRI es agudo o lo padecia previamente?
Considerando el momento de aparición de los signos electrocardiográficos, en los ECG realizdos
previos a las 24 horas del ingreso, R decreciente de V1-V4, elevación del ST más de 5mm
oponente con los complejos QRS, melladura tardía en la S de V3-V5 (signo de CabreraFrieland). Es conocida la dificultad de asociar el IAM en presencia de BCRI
El diagnóstico de SCA o IAM en pacientes de edad avanzada, más la asociación de otras
patologías como Infartos previos, IC, DBT enfermedad arterial periferica y HTA presentes en los
pacientes con bloqueo de rama izquierda, ya que la presencia de la misma en pacientes con
avanzada edad hace mayor la mortalidad hospitalaria al sufrir un SCA o IAM,
Cabrera y Friedland describieron la melladura de la rama ascendente de la S en V3-V4 y la Q en
DI, aVl, V5 y V6. La incidencia de IAM en presencia de BCRI oscila entre un 4.5 y 5.5%,
otros reportan una incidencia entre 6 y 9%. En la serie de Melgarejo las mujeres presentaban
mayor prevalencia de IAm y BCRI con una incidencia de Killip.Kimball de I mayor de 64% en los
partadores de BCRI. Otras series reportan una mortalidad de 38% en pacientes portadores de
BCRI en el curso del IAM.
Considerando el momento de aparición de los signos electrocardiográficos se puede decir, en los
ECG realizados previos a las 24 horas del ingreso, R decreciente de V1-V4, elevación del ST más
de 5 mm oponente con los complejos QRS, cuatro pacientes con Q en DI, aVl, V5 y V6 (presente
en más de una derivación) y melladura tardía en la S de V3-V5 (signo de Cabrera).
En el estudio GUSTO-I valorando los pacientes con BCRI encontraron tres criterios con valor
independiente en el diagnóstico de infarto: la elevación del segmento ST a 1 mm en presencia de
un complejo QRS predominantemente positivo; un descenso del segmento ST a 1 mm en V1, V2 o
V3; y una elevación del segmento ST a 5 mm en presencia de un complejo QRS
predominantemente negativo.
Los mismos tenían una sensibilidad del 30% y una especificidad del 96%, con un valor predictivo
positivo del 88% y negativo del 61%.6
Haywood en un estudio observacional, plantea tres situaciones diferentes en que el ECG pudiera
presentar valor diferencial ante un paciente con clínica subjetiva de insuficiencia coronaria o
IAM: 1) la presencia de un BCRI de nueva aparición, en pacientes, con trazados previos con
ausencia de BCRI. 2) en pacientes con previo BCRI existirán criterios que indique la presencia de
un IAM y cuando un paciente ingresa a urgencias y presenta un BCRI que se desconoce si es
previo o no; es posible diferenciar si existen criterios que apoyen la presencia de IAM. El
autor valora los criterios de Sgarbossa, que estos criterios pudieran beneficiar a la disminución de
la mortalidad al favorecer a la terapia precoz en pacientes de grupos de alto riesgo. Además
comenta que el riesgo de mortalidad que confiere el BCRI está asociado a la edad y comorbilidad a
la hora de padecer un IAM.
En conclusion por lo que referi, compensar a la paciente y tratarla como un SCA de alto riesgo.
2. Si padecia previamente el BCRI con BAV de primer grado, mas deterioro de la FEY, lo indicado
hubiera sido terapia de resincronizacion cardiaca con CDI, como evidencian los estudios con una
disminucion de la morbimortalidad en este grupo de pacientes.
Mil disculpas a todos por lo extenso
Un cordial saludo
Martin Ibarrola
1.Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, et al: Correction: Electrocardiographic diagnosis of
evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med 1996; 334: 931.
2.Elena B. Sgarbossa, M.D., Sergio L. Pinski, M.D., Alejandro Barbagelata, M.D., Donald A. Underwood, M.D., Kathy B. Gates, Eric
J. Topol, M.D., Robert M. Califf, M.D., and Galen S. Wagner, M.D. for the GUSTO-1 (Global Utilization of Streptokinase and Tissue
Plasminogen Activator for Occluded Coronary Arteries) Investigators Electrocardiographic Diagnosis of Evolving Acute Myocardial
Infarction in the Presence of Left Bundle-Branch Block N Engl J Med 1996; 334:481-487February 22, 1996
Discutire el caso de bloqueo de rama izquierda ,enviado por nuestro maestro Profesor
Andrés Ricardo Pérez Riera MD PhD: este es un caso gravisimo, muy probable, bloqueo
bilateral LBBB + bloqueo AV de primer grado. El BCRI es muy ancho (casi 200 ms),
sugeriendo dilatación del VI muy probablemente como evolución de una HVI asociada a
isquemia severa. Las ondas S,s muy profundas en las precordiales indican predominancia
de los potenciales posteriores por remodelación de un infarto anterior y SVI sistólica y
diastólica La separacion en aVL, entre R1 y R2 de alrededor de 80 ms, sugiere fibrosis
severa del septo ventricular (normalmente R1-R2 del LBBB sin patologia es de ≤40ms)
El potencial que aparece como primer vector en II antecede al QRS en I
y aVL,
sugeriendo depolarizacion muy lenta del VD, probablemente por infarto de esta cámara,
que origina los signos de insuficiencia ventricular derecha y alta presion auticular.
La falta de progresion de las R hasta V6 que es muy infrecuente en BCRI , muy
probablemente sea consecuencia de infarto anteroseptal muy extenso (los bloqueos Q/S
hasta V6 se ven en marcapasos derechos o en infartos anteriores muy extensos ).
En conclusion este ECG indica dilatación de ambos ventriculos, por infartos muy extenso
anterior izquierdo y de VD, talvez con insuficiencia tricuspidea o mitral. En los. datos
clinicos falta la irradiacion del soplo, y si el higado late. Debo agregar que este BCRI es
troncular (frecuente en mujeres post-menopáusicas generalmente se acompaña de
calcificación del anillo valvular izquierdo) no relacionado al cuadro isquemico
Probablemente el bloqueo de primer grado tiene relacion con el infarto de VD. Estos
ECGs son bastante frecuentes actualmente debido a los tratamientos
médicos mas
eficaces o by-pass aorto coronario. Una chance probable de mejorar en algo el sufrimiento
de esta pobre mujer es cateterizarla y tratar de abrir cualquier arteria que aun pueda
suplir este miocardio
Un fraternal abrazo Samuel Sclarovsky
I will tried to report a very severe case in a 74 year old female with CLBBB, presented our good friend
Professor Dr Andrés Ricardo Pérez Riera MD PhD: From the electrical conduction point of view, it is a
case of CLBBB + first-degree A-V block suggesting a bilateral bundle branch block. From the
morphological point of view this is a very wide LBBB (near 200ms) suggesting severe left ventricular
dilatation.
The S,s waves in the V2 ,V3 are very deep, suggesting that the prevalent electrotonic ventricular forces
are shifted to the posterior wall, indicating posterior remodeling due to extensive transmural anterior
wall infarction or LVH due diastolic and systolic overloading as well
The space between the first R and the second one in aVL is 80 ms , suggesting a severe delay in the
anterior wall of left ventricular , due to a repair fibrosis after extensive infarction ( in patient with
CLBBB without structural heart disease RR´ is 40 ms )
The positive vector witch appears in II and V6, precede the left vectors expressed in aVL and I, indicated
most probably very slow depolarization of right ventricle, suggesting a RV fibrosis due to an
old infarction.
The lack of R progression in CLBBB is not a frequent finding, The lack of R progression of CLBBB
pattern is found in right ventricle pacemaker excitation or in very extensive anterior wall MI with left
axis deviation
The clinics parameters indicate a severe mitral insufficiency with a tricuspide one ,too
In conclusion this patient in according to the electrical morphology suffers from a severe biventricular
dilatation, most probably the right ventricular dysfunction and tricuspide insuffiency relief the overflow
to the left one. This is a troncular CLBBB, no related to the the ischemic process, but very frequent in
post menopausal female, frequently accompanied with annulus calcification of the left valves. The left
conduction delay due to posterior and anterior infarction, is seen as atypical LBBB, due to a down
regulation of the conexin 43 due to
severe anterior and posterior ischemia in this pattern
mimicking LBBB is complete different fron the troncular. My opinion is this patient ,must be undergone
a hemodinamic study and try to open every artery possible , because in this severe cases still leaving ,
are many hibernated areas in the heart, and same time it is possible to get positive results. This
cases were very seldom in the past ( I survive 52 years as cardiologist ) but in the modern era , this
cases are more frequent due to the modern medical treatment ,aortic -coronary bypass and angioplasty
My best regard
Samuel Sclarovsky
Estimados amigos del Foro: en primer lugar quiero agradecer las conceptuosas palabras de
AB y del Profesor Pérez Riera hacia mi persona.
Con respecto al caso, obviamente tenemos un infarto de pared anterior y de pared libre del
ventrículo izquierdo porque no hay crecimiento de la onda R en las precordiales y en el
plano horizontal la porción final cruza el eje de Z hacia la derecha, lo que motiva las "S"
profundas en precordiales izquierdas.
Ademas el plano frontal es sugestivo la concomitancia de necrosis inferior.
El cuadro parece ser agudo porque la repolarización ventricular el bucle QRS no cierra en
0 sinó que deja un importante vector ST responsable por el desnivel de este segmento. Si
a eso le agregamos el del bucle de T es redondeado, podemos sospechar que el proceso es
isquémico. Cabe destacar el septum está indemne, porque el nacimiento del bucle QRS en
el PH está dirigido hacia delante y a izquierda, es decir preservado.
Saludos a todos
Carlos Lavergne Neuquén
Dear Friends Forum: First of all I want to thank the glowing words of AB and Professor
Pérez-Riera related myself
Regarding the case, we obviously have an anterior and left ventricular free wall MI because
there is no growth of the R wave in the horizontal plane and the end of QRS loop crosses
the orthognal Z axis to the right, what motivates the final "S" deep waves in left precordial
leads.
Besides the frontal plane is suggestive of inferior necrosis in association.
The picture seems to be acute because the QRS ventricular repolarization loop does not
close to 0 but leaves an important ST segment elevation. Additionally, the loop T is round,
suggestive of ischemic T-loop.
Notably the septum is intact, because the initial 10ms QRS loop in the PH is preserved
because it is directed forward and left.
Greetings to all. Carlos Lavergne MD Neuquén
Dear Andrés: This woman with severe ischemic cardiomyopathy and LBBB has ECG findings
compatible with several old myocardial infarctions. From the ECG perspective she is in sinus
rhythm with a first degree AV block (PR ~ 280 ms) and a very wide QRS (~180 ms) suggestive of
left ventricular hypertrophy. The QRS axis is left at approximately -30 degrees. The ST-T wave
findings are typical of the secondary ST-T changes seen with LBBB with the general direction of the
ST-T in the opposite direction from the QRS direction. I do not see primary (ischemic) ST-T
abnormalities. In lead V3 the take-off of the ST wave is ~5 mm above the baseline, but I think this
is unlikely to be primary ischemia. Several findings in the QRS complex suggest old myocardial
infarctions. In lead V5 the prominent notch in the upstroke of the S wave is the "sign of Cabrera"
and represents myocardial scar late in the left ventricular activation sequence (LV lateral wall). The
prominent S wave in lead V6, assuming accurate lead placement, is also likely a Q-wave equivalent
and an electrically silent area of myocardium in the basal-lateral wall of the LV. Also, in lead V6 as
well as lead II there is an "bite" taken out of the initial r-wave (? sign of Chapman) which also is a
Q-wave equivalent of old myocardial scar from an area of LV that is activated early in the LV
activation sequence.
I'm interested in other ideas from colleagues especially with regard to the VCG findings.
Best regards,
Yanowitz, Frank MD
Professor of Medicine
University of Utah School of Medicine
Medical Director, ECG Department
LDS Hospital Salt Lake City, Utah
8th Ave. and C Street
Salt Lake City, Utah 84143 USA
[email protected];
[email protected]
Querido Andrés: Esta mujer con cardiomiopatia isquémica severa y BCRI tiene hayazgos
compatibles con varios infartos antiguos.
El ECG muestra ritmo sinusal, bloqueo AV de primer grado (PR ≈ 280 ms) QRS muy
ancho(~180 ms) sugestivo de SVI. El eje del QRS se encuentra ≈ en -30º.
El ST/T tiene características secundárias observadas en los BRCI no complicados con
dirección totalmente opuesta a la del QRS. Yo no veo anormalidades primárias en el ST/T.
En la derivación V3 el supradesnivel del ST se encuentra ≈ 5mm arriba de la linea de base,
no obstante no pienso que esto sea alteración primarias de repolarización.
Vários hallazgos en el complejo QRS sugieren infartos antiguos de miocardio. En la
derivación V5 se observa una escotadura en la rampa ascendente de la S conocida como
signo de Cabrera y representa cicatrices que afectan la secuencia de la activación del VI
en la pared lateral.
La onda S profunda de V6 asumiendo que el electrodo esté en posición correcta, es
también un equivalente de una Q de necrosis y una area silente de miocardio en la región
basal-lateral del VI( signo de Chapman) el cual también es un equivalente de una Q de
cicatriz antigua en la secuencia de activación ventricular.
Estoy interesado en otras ideas de colegas especialmente en relación a los hayazgos
vectocardiográficos.
Estimados amigos: el analisis del ECG/VCG en contexto de la clinica "orientadora " se trata de :
BAV de 1er grado
Bloqueo De Rama Izquierda Disfrazado Precordial Con R En V1(por Necrosis Anterolateral
Extensa ) y fuerzas en cuadrante Ne Por Necrosis Inferior
Alteracion de R.V por discinecia anterior y apical
Todo esto explica el compromiso clinico y hemodinamico de la paciente choque punta difuso
ondas a en pulso venoso por dilatacion de VD mas htps soplo de insuficiencia tricuspidea
hepatomegalia tercer ruido galope
POR DILATACION MAS DISF
SIST.V.I mas ANEUR.hipoperfusionlecho ungueal palido
Posiblemente encontremos en el eco las alteraciones descriptas con una fraccion de eyeccion
severamente disminuida ( menor de 30 %) y disfuncion diastolica por alteracion de la
distensibilidad (patron tipo 3-4 ) y citerios de disincronia A-V ,inter e intra ventricular ,criterios que
sumados a falla tratamiento full para IC
BCRI
Potencial indicacion de terapia eléctrica de resincronizacion
Abrazos a todos
Juan José Sirena
OUR DIAGNOSIS AND
FINAL COMMENTS
Name: E. G. A.; Date: 02/11/2009.; Age: 74 years old; Gender: Female; Ethnic group: Caucasian;
Weight: 81Kg.; Height:1.57m.; Biotype profile: Endomorphic.;
Medication in use: Metformine 850mg twice a day, glibenclamide 5mg twice a day, carvedilol 25mg twice a
day, enalapril maleate 20mg 2 twice a day, espironolactone 25mg/once a day, furosemide 40mg once a day,
Symvastatine 20mg once a day, AAS 100mg once a day.
LAFB+ inferior MI (See next slide)
QRS loop rotation first CW and later CCW
QRS axis - 45º following
VCG criteria
aV
R
L
aV
CCW
CW
T
I
QRS axis - 30º following
ECG criteria: Isodiphasic
QRS complex in II
aVF
III
X
Y
II
QRS LOOPS IN THE FP: LAFB, DIAPHRAGMATIC INFARCTION AND
ASSOCIATION OF BOTH
C
CC
W
CC
W
W
CW
30 ms
30ms
10 ms
LAFB
CCW
INFERIOR
MIOCARDIAL
INFARCTION
CW
INFERIOR
MIOCARDIAL
INFARCTION
+
LAFB
First CW and later CCW
Comparison of QRS loops in the frontal plane in LAFB, in diaphragmatic infarction and in association of both.
Characteristics of Frontal QRS loop, ST vector and T -loop in uncomplicated LBBB
1. Size: the frontal QRS loop tends to be smaller and more irregular in contour that that in the HP and SP,
because the QRS loop is directed almost perpendicular to the FP
2. Initial deflection: directed to left and inferiorly and continues in this direction as the afferent limb.
3. QRS-loop rotation: Counter Clock Wise Rotation (CCW) or figure in eight.
4. The Maximal QRS vector: is directed to the left and inferiorly or superiorly in the range of
– 705º to +50º
5. Conduction delay: Conduction delay noted in the mid and terminal portion.
6. The ST vector and T-loop: with opposite polarity related to QRS loop. Both are discordant 180º
directed rightward. Additionally efferent limb slower inscription related afferent one.
Efferent limb:
with mid and terminal conduction delay
The ST vector
and T-loop
Directed
rightward
CCW rotation
Afferent limb
Uncomplicated LBBB
The current case
QRS and T loop in
Uncomplicated LBBB
The current case
CW
Efferent limb
Afferent limb
conduction
delay
T
V6
R
T
•The QRS loop duration is ≥ 120ms
•The QRS loop shape is elongated and narrow
•The main body of the QRS loop is inscribed posteriorly
and to the left within the range - 90 to - 40 degree.
•The main body of QRS loop is inscribed clockwise (CW)
•The magnitude of the max QRS vector is increased above
normalexceeding 2mV.
•The afferent limb is located rightward,
•Conduction delay noted in the mid and terminal portion
RS
The afferent limb is dislocated to right of the efferent limb
conduction delay noted in the mid and terminal portion.
T wave is not totally ellogated (normal) rouded
insinuation.
The secondary T-loop is elongated or elliptical
LBBB ASSOCIATED TO LV FREE WALL MIOCARDIAL NFARCTION
The afferent limb is dislocated to right
of the efferent limb conduction delay
noted in the mid and terminal portion
Z
X
V5
T
When electrocardiography was starting,
Wilson postulated that the broad final S
wave of V6 in the LBBB associated to
lateral infarction was due to the sensing
by the exploring electrode of V6 of
intracavitary potential of the LV (RS): it is
called the “electric window” of Wilson.
Today we know that the afferent limb is
dislocated to right of the efferent limb.
V6
V4
V1
V2
V3
Notch
Cabrera’s sign
Secondary alteration of
ventricular repolarization
is observed:
QRS/ST-T angle near 180º.
V2
Z
Afferent limb with middle
and final conduction delay
T
aVF
Y
PRIMARY REPOLARIZATION PATTERN
Normal T loop
Primary T-loop
The secondary normal T-loop is
Allocated, asymmetrical with the afferent
Limb slower inscription related the
Efferent limb.
The T-loop is symmetrical in afferent
and efferent limbs.
Rounded T-loop shape
Prolonged
PR interval
Very wide QRS duration = 180ms
suggesting severe LV enlargement
The mean patient age at LBBB diagnosis was relatively elderly, and the LBBB incidence increased
progressively with advancing age. Hypertension, coronary artery disease, left ventricular
hypertrophy, ST-T abnormalities, and an increased cardiothoracic ratio were associated with
LBBB.
LBBB predicted for mortality from heart failure but not for all-cause mortality, independent of age,
gender, and underlying disease1.
1.
Imanishi R, Seto S, Ichimaru S, et al. Prognostic significance of incident complete left bundle branch block
observed over a 40-year period. Am J Cardiol. 2006; 98: 644-648.
ECG/VCG final diagnosis
1) Prolonged PR interval: First degree AV block
2) Extreme left axis deviation: ECG -30º VCG -45º
3) Left Anterior Fascicular Block (LAFB)
4) Inferior Myocardial infarction
Extreme left axis deviation with
the first portion of QRS loop with
CW rotation and later CCW
5) Complete Left Bundle Branch Block
6) Left Ventricular Enlargement or Hypertrophy (LVE or LVH); Wide QRSd
7) Free wall Myocardial Infarction: final S wave V6, Cabrera signal, Chapman signal,
and afferent limb dislocated to right.
8) Secondary repolarization pattern. Minimally Primary?
Elderly patients (aged 60-85 years) with chronic heart failure (NYHA class II-IV CHF)
and LBBB had statistically significant increases of end diastolic and systolic
dimensions, end diastolic and systolic volumes, sphericity index, long axis,
decreases of relative thickness of the left ventricle, interventricular septum, and left
low ventricular ejection fraction. Pronounced mitral regurgitation also was more
frequent in patients with LBBB. During follow up 14/34 patients (41.2%) with LBBB
and 19/74 patients (25.7%) without LBBB died. There were 10 and 9 sudden deaths
among patients with and without LBBB, respectively1.
The reports in the literature indicate a large increase in mortality when LBBB develops in
patients over 44 years of age2.
1.
2.
Larina VN, Bart BIa.Structural-functional peculiarities of the heart and survival of elderly patients with chronic
heart failure and left bundle branch block Kardiologiia. 2009;49:16-21.
Deharo JC.Left bundle branch block. Electrocardiographic and prognostic aspectsArch Mal Coeur Vaiss. 2000
Apr;93:31-37.
Patients with LBBB and concomitant coronary artery disease (CAD) have a worse prognosis than
those with LBBB without CAD. In addition, subjects with CAD and concomitant LBBB have a higher
cardiovascular mortality than those with a similar extent of CAD but without LBBB. Because the
presence of LBBB makes the noninvasive identification of CAD problematic, patients with LBBB
often are referred for coronary angiography to assess the presence and severity of CAD. Those
with CAD were likely to be older, Caucasian, and men; they were more likely to have angina
pectoris, MI, and diabetes mellitus; and they were more likely to have a left ventricular ejection
fraction (LVEF) <0.50. In contrast, patients with heart failure (HF) were less likely to have CAD1.
In survivors of myocardial infarction (MI), new LBBB is associated with adverse outcomes, In postMI survivors with left ventricular (LV) systolic dysfunction and/or heart failure (HF), new LBBB was
an independent predictor of all major adverse cardiovascular outcomes during long-term follow-up.
This readily available ECG marker should be considered a major risk factor for long-term
cardiovascular complications in high-risk patients after MI2.
The presence of LBBB on admission ECG in patients who have AMI is an independent predictor of
in-hospital mortality. Because 85% of deaths in patients who have LBBB occur within the first week,
these patients should be recognized early and receive prompt and aggressive treatment
(thrombolysis)3.
1.
2.
3.
Abrol R, Trost JC, Nguyen K,et al. Predictors of coronary artery disease in patients with left bundle branch block
undergoing coronary angiography. Am J Cardiol. 2006;98:1307-1310.
Stephenson K, Skali H, McMurray JJ, et al. Long-term outcomes of left bundle branch block in high-risk survivors of
acute myocardial infarction: the VALIANT experience. Heart Rhythm. 2007; 4:308-313.
Guerrero M, Harjai K, Stone GW, et al. Comparison of the prognostic effect of left versus right versus no bundle
branch block on presenting electrocardiogram in acute myocardial infarction patients treated with primary angioplasty
in the primary angioplasty in myocardial infarction trials. Am J Cardiol. 2005; 96: 482-488
In case of AMI and a BBB major diagnostic and prognostic issues should be addressed with
different considerations, depending on the presence of a LBBB or a RBBB, distinguishing new
or presumably new BBB, considering the possibility that the BBB masks ECG features of MI with
ST-segment elevation.
Wong et al. analysis of HERO-2 trial demonstrates that in the setting of an anterior STEMI, the
presence of an RBBB, whatever its onset, is associated with a higher risk of death. The same
analysis shows as RBBB associated with an inferior infarction does not portend a worse
prognosis independently of its onset.
Patients with LBBB already present at randomization were found to have worse pre-infarction
characteristics, responsible, by itself, for the worst prognosis. However, the occurrence of an
LBBB after randomization indicates a 'true' ischaemic conduction damage, thus carrying an
independent negative prognostic value due to the large percentage of myocardium involved.
HERO-2 trial, showing prognostic differences between different clinical presentations, underlines
the importance to be familiar with the mechanisms related to BBBs and with the prognostic
implications of BBBs in the setting of an AMI.
Patients with LBBB, RBBB, or indeterminate ventricular conduction disturbances show longer
repolarization duration than patients without these conduction disturbances, and QT (RR,QRS)
and JT(RR) intervals reflect better than QTc repolarization duration in patients with conduction
disturbances. QT(RR) and JT(RR) intervals significantly and independently predict mortality in
patients after MI with conduction disturbances1.
1.
Piotrowicz K, Zareba W, McNitt S, et al. Repolarization duration in patients with conduction disturbances
after myocardial infarction. Am J Cardiol. 2007; 99:163-168.
The prognostic implications in HF with preserved systolic function (HF-PSF) are less well
understood. The simple clinical finding of BBB is a powerful independent predictor of worse clinical
outcomes in patients with HF and reduced LVEF. It is less frequent, with a more modest predictive
effect, in patients with preserved systolic function1.
Criteria of cardiac resynchronization therapy (CRT) from American College of Cardiology
and American Heart Association guidelines are:
LVEF ≤ 0.35;]
Functional class III or IV(NYHA). Patients with class III or IV HF are candidates for CDT regardless
of underlying etiology if cardiac recompensation to class III is at least temporarily successful. CRT
has a beneficial effect on clinical symptoms, exercise capacity, and systolic LV performance in
patients with HF. HF in functional state NYHA II should be regarded as a CRT indication is currently
being investigated in the randomized RAFT and MADIT-CRT trials.
QRS interval > 130 ms particularly if LBBB is present. Patients with CLBBB and a QRS duration of
120-130 ms seem to benefit if echocardiographic criteria demonstrate ventricular dyssynchrony.
Since a multiplicity of echocardiographic criteria of ventricular dyssynchrony exists which is neither
standardized nor evaluated in large-scale randomized trials, ventricular dyssynchrony on
echocardiography alone cannot be regarded as an established indication for CRT without a QRS
complex ≥120 ms. whether Sinus rhythm. In addition, available data also suggest an indication for
CRT in patients with atrial fibrillation if the other criteria listed above are met.
1.
Hawkins NM, Wang D, McMurray JJ, et al. Prevalence and prognostic impact of bundle branch block in patients with
heart failure: evidence from the CHARM programme. Eur J Heart Fail. 2007; 9:510-517.
CRT is possible using biventricular pacing or ICD systems has to be highly differentiated to
optimize the proportion of patients who derive significant symptomatic benefit from this therapy,
on the one hand, and to avoid this invasive treatment in patients with a low probability of clinical
success of CRT, on the other hand.
In patients with nonischaemic cardiomyopathy, the LVEF was improved from 28% to 37%, and in
patients with ischaemic cardiomyopathy, the LVEF was improved from 30% to 36%. No
significant difference of the improvement was found between the two groups. CRT could
significantly improve cardiac function in patients with chronic HF regardless of the underlying
heart disease1.
ECG abnormalities that were associated with postoperative MI were a RBBB and a LBBB.
Similar results were found for all-cause mortality. Bundle branch blocks identified on the
preoperative ECG were related to prediction of postoperative MI and death but did not improve
prediction beyond risk factors identified on patient history2.
Cardiac resynchronization therapy (CRT) provides a therapeutic option for patients with CHF
NYHA class III or IV, sinus rhythm, and LBBB with QRS ≥120ms( CLBBB). Some authors do not
consider QRS pattern. Studies show that only patients with LBBB benefit form CRT, and not
patients with RBBB or nonspecific intraventricular conduction delay. Additionally, approximately
30% diagnosed with LBBB by ECG criteria may not have true complete LBBB , but likely have a
combination of LVH and LAFB. Stricter criteria for CRT for Complete LBBB must include QRS
duration ≥ 140ms for men and ≥ 130ms for women and with mid-QRS notching or slurring in ≥
2mm contiguous leads.
1.
2.
3.
Hua W, Niu HX, Wang FZ, et al. Short-term effect of cardiac resynchronization therapy in patients with ischaemic or
nonischaemic cardiomyopathy. Chin Med J (Engl). 2006; 119:1507-1510.
van Klei WA, Bryson GL, Yang H,et al. The value of routine preoperative electrocardiography in predicting
myocardial infarction after noncardiac surgery. Ann Surg. 2007;246:165-170.
Strauss, DG, Selvester RH, Galen S, et al. Defining Left Bundle Branch Block in the Era of Cardiac
Resynchronization Therapy. Am J Cardiol 2011; 107: 927-934.
The results of MADIT-CRT, as well as the extended follow-up of the REVERSE substudy of the
European patient cohort, have shown that prevention of HF progression can be well
accomplished with CRT and implantable cardioverter-defibrillator (ICD) backup (CRT-D). HF
events and death occurred significantly less often in patients with CRT-D than in those with an
ICD only. A clinically important reversal of ventricular remodeling with reduced ventricular
volumes and increased LVEF was found in the CRT-D-treated patients. CRT in asymptomatic
or mildly symptomatic HF patients.( NYHA class I or II HF) the most benefit was demonstrated
in patients showing a "classic" LBBB ECG pattern and in female patients1.
Structural myocardial remodelling due to CRT has been described extensively. CRT results in
an electrical remodelling with a reduction of the intrinsic QRS duration. A significant decrease
in intrinsic QRS duration was observed in responders, only a slight decrease was seen in nonresponders2.
In hyper responder patients (they fulfilled concurrently the two following criteria: functional
recovery (NYHA class I or II) and normalization of LV ejection fraction (LVEF).), "normalization"
of LV function after CRT persists as long as pacing is maintained with an excellent survival3.
1.
2.
3.
Klein HU. Cardiac resynchronization therapy in asymptomatic or mildly symptomatic heart failure patients. Curr Treat
Options Cardiovasc Med. 2010 Oct;12(5):431-42.
Mischke K, Knackstedt C, Fache K, et al.. Electrical remodelling in cardiac resynchronization therapy: decrease in
intrinsic QRS duration. Acta Cardiol. 2011 Apr;66(2):175-80.
Castellant P, Orhan E, Bertault-Valls V, Is "hyper response" to cardiac resynchronization therapy in patients with
nonischemic cardiomyopathy a recovery, a remission, or a control? Ann Noninvasive Electrocardiol. 2010
Oct;15(4):321-7.