Casos
Clínicos
Hugo R. Ramos1,2,3, Marcelo
Sagripanti1, Ángel Sandrín1, Lorena C. Balestrini1,
Víctor R. Balestrini1, Valeria Balestrini1, Verónica
Celorrio1, Adriana Gigena1, Marcelo Coll1,
Félix Zelaya1, Walter Quiroga Castro1, Eduardo C. Conci1.
DATOS DE AUTORES
1. Instituto Modelo de Cardiología. División Cardiología.
2. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas
3. ORCID: https://orcid.org/0000-0001-6772-903X. E-mail de contacto: mbelen93@gmail.com.
CONCEPTOS CLAVE:
Qué se sabe sobre el tema.
A frequent presentation of
Amyloid Transthyretin Cardiomyopathy wild type (ATTR-CMwt) is heart failure and
arrhythmias, but the prevalence of sustained ventricular tachycardia as the
first manifestation is unknoun and is considered uncommon.
Qué aporta este trabajo.
We report an uncommom case of
a 71 y-old man without heart failure who had a severe sustained ventricular
tachycardia (SVT) as the first presentation of ATTR-CMwt. This case highlights
that any type of life-threatening arrhytmia could be find and the mechanisms of
SVT and the current indications for ICD are reviewed.
Divulgación
ATTR-CM is a toxic-infiltrative
disease affecting the myocardial interstitium. Regular symptoms are related
with heart failure, atrio-ventricular block, any type of arrhythmias or aortic
stenosis. Life-threatening sustained ventricular tachycardia (SVT) is
considered uncommon and its prevalence is unknoun, despite data from some
registries. However, patients with this arrhythmia can suffer sudden cardiac
death or they are not considered for ATTR-CM. In patients with SVT and septal
thickness >12 mm ATTR-CM should be considered as a possible diagnosis.
Abstract
Transthyretin Amyloid Cardiomyopathy (ATTR-CM) was considered an uncommon
disease until a few years ago, but advances in the epidemiology and
non-invasive diagnostic tests have increased its timely detection. We report a
71 years-old man with history of hypertension and an incidental carcinoma of
the left kidney detected 6 years ago, without heart failure who was performed
cardiac magnetic resonance images (MRI) by suspicion of hypertrophic
cardiomyopathy. Before his cardiologist be aware of the result, he suffered a
severe sustained ventricular tachycardia (SVT) that required emergency
cardioversion. Echocardiogram and cardiac MRI were suggestive for cardiac
amyloidosis and the diagnosis was confirmed by scintigraphy with 99mTc-PYP
(Perugini +3). Serum levels of light chains kappa and lambda were normal, and
serum and urine immunofixation were negative; a genetic test had no variants,
so supporting an ATTR-CM wild type. PET-CT did not detect metastasis of the
renal tumor, but showed cardiac hypermetabolism and pericardial effusion. An
implantable cardioverter defibrillator (ICD) was placed and after nine days a
shock was delivered by the ICD due to a new event of SVT; in addition a Holter
monitoring registered runs of asymptomatic atrial fibrillation. Etiologic
treatment for ATTR-CM with Tafamidis 61 mg was started, amiodarone and
rivaroxaban were added for control of arrhythmias and prevention of systemic embolism,
respectively. After 14 months of follow-up, he is stable in class I NYHA.
ATTR-CM is a complex disease, and the treatments should be indicated by a
multidisciplinary team that consider the risks, benefits, and costs of each
intervention.
Keywords:
amyloidosis; heart; tachycardia; arrhythmia.
Resumen
Cardiomiopatía Amiloide por Transtiretina (ATTR-CM)
fue considerada hasta hace poco tiempo una enfermedad poco frecuente, pero los
avances en el conocimiento de su epidemiología y de los tests no invasivos han
aumentado su diagnóstico oportuno. Presentamos un hombre de 71 años con
historia de hipertensión arterial y un tumor renal a células claras operado 6
años antes, sin insuficiencia cardíaca a quien se realizó una resonancia
magnética cardiaca por sospecha de miocardiopatía hipertrófica; antes de que su
cardiólogo viera el resultado, presentó una taquicardia ventricular sostenida
(TVS) severa que requirió cardioversión eléctrica de urgencia. Ecocardiograma y
resonancia magnética cardiaca fueron sugestivos y el diagnóstico fue confirmado
por centellografía con PYPTc99m (Perugini +3). Cadenas livianas kappa y lambda
en suero e inmunofijación en sangre y orina fueron negativas y el test genético
no mostró variantes, confirmando ATTR-CMwt. PET-CT no mostró metástasis del
tumor renal pero detectó hipermetabolismo miocárdico y derrame pericárdico. Se colocó
un cardio-desfibrilador implantable (CDI) y nueve días después tuvo una nueva
TVS que fue detectada y tratada adecuadamente por el CDI. Además, el monitoreo
Holter detectó eventos asintomáticos de fibrilación auricular. Se inició
tratamiento etiológico de ATTR-CM con Tafamidis 61 mg y se agregó amiodarona
para prevenir nuevos eventos de TVS y rivaroxaban para prevención de embolismo
sistémico. A 14 meses de seguimiento el paciente permanece en clase I de NYHA.
CM-ATTR es una enfermedad compleja y los tratamientos deberían ser indicados
por un equipo multidisciplinario que considere los riesgos, beneficios y costos
de cada intervención.
Palabras
clave:
amiloidosis;
corazón; taquicardia; arritmia.
Resumo
A Cardiomiopatia Amiloide por Transtiretina
(ATTR-CM) foi considerada até há pouco tempo, uma doença pouco frequente, mas
os avanços no conhecimento da sua epidemiologia e dos testes não invasivos
aumentaram o diagnóstico oportuno. Apresentamos um caso de um homem de 71 anos
com antecedentes de hipertensão arterial e tumor renal a células claras com
cirurgia de 6 anos de data, sem insuficiência cardíaca. Realizou-se ressonância
magnética cardíaca por suspeita de miocardiopatia hipertrófica. Antes da
revisão do estudo pelo seu cardiologista, o paciente apresentou taquicardia
ventricular sustentada (TVS) severa que exigiu cardioversão eléctrica de
emergência. Ecocardiograma e ressonância magnética foram sugestivas e o
diagnostico foi confirmado com cintilografia com PYPTc99m (Perugini +3).
Correntes claras kappa e lambda em souro e imunofixação em sangue e urina foram
negativos e o teste genético não amostrou variações, confirmando ATTR-CM wild
type. O PET-CT não mostraram metátese do tumor renal, mas detecto hipermetabolismo
miocárdico e derrame pericárdico. Colocou-se um cardio-desfibrilador
implantável (CDI) e nove dias depois apresentou uma nova TVS que foi detectada
e tratada adequadamente pelo CDI. Além disso, o monitoreo-Holter detectou
eventos assintomáticos de fibrilação auricular. Começou-se um tratamento
etiológico de ATTR-CM com Tafamidis 61 mg e se adicionou amiodarona para
prevenir novos eventos de TVS e rivaroxaban para prevenção de embolismo
sistémico. Após 14 meses de seguimento, o paciente continua em tipo I de NYHA.
CM-ATTR e uma doença complexa e os tratamentos deveriam ser indicados por uma
equipe multidisciplinar que considere os riscos, benefícios e custos de cada
intervenção.
Palavras-chave:
amiloidose;
coração; taquicardia; arritmia.
Transthyretin
Amyloidosis Cardiomyopathy (ATTR-CM) is currently considered much more common
than previously thought, mainly due to advances in its knowledge and in
non-invasive cardiac imaging(1,2). The clinical spectrum of ATTR-CM
ranging from asymptomatic to autonomic dysfunction and syncope, heart failure
with preserved ejection fraction, aortic stenosis, atrial fibrillation (AF) and
conduction system disease, advanced atrioventricular block, and ventricular
arrhythmias, but sustained ventricular tachycardia (SVT) are quite uncommon(1).
We report a patient without any previous symptom of ATTR-CM with a SVT as the
initial presentation.
The patient provided written informed consent
for this report.
A 71-years-old man woke up feeling unwell,
pale, sweating, with neck pain and weakness, so his wife called the emergency
service. On examination at home, blood pressure was 60/40 mmHg, and ECG showed
sustained monomorphic ventricular tachycardia originated from the inferior wall
of the right ventricle at 211 bpm. A biphasic electrical cardioversion was
performed with 200 joules, resulting in sinus rhythm of 115 bpm with
first-degree atrioventricular block and left bundle branch block, with a QTc of
333 ms (Figure 1).
A
B
Figure N°1. ECG at home. A. Sustained ventricular tachycardia
from the inferior wall of the right ventricle. B. Sinus rhythm after biphasic
cardioversion with 200 joules emerging with first-degree atrioventricular
block and left bundle branch block.
He was admitted to the hospital with a heart
rate of 65 bpm, blood pressure 115/70 mmHg, oxygen saturation 97%, and
respiratory rate 14 bpm. He had a history of hypertension and past smoking, but
no chest pain or dyspnea.
He was being treated for lithiasis in the left
renal pelvis with complete fragmentation of the calculus by flexible
ureteroscopy and placement of a pigtail. Six years earlier, he had undergone a
partial nephrectomy of the left kidney for incidental clear cell papillary
carcinoma (Grade II Furham), and periodic follow-up showed no evidence of
recurrence. The patient had a recent cardiac magnetic resonance imaging (MRI)
suspected by his cardiologist of hypertrophic cardiomyopathy performed before
his SVT, which showed wall thickening of the left ventricle (LV), late
gadolinium enhancement with diffuse subendocardial signal increase with nearly
transmural extension at the basal segments, preserved systolic function (LVEF
55%), normal morphology and motility of the right ventricle (RV) (RVEF 58%)
with diffuse signal intensity increased in all its walls, left atrial dilation
with signal increased in both the right and left atrium and in the interatrial
septum, consistent with amyloid infiltration (Figure 2).
Figure N°2. Cardiac magnetic resonance imaging showing severe
thickness of interventricular septum (left), and late gadolinium enhancement
with increased diffuse subendocardial signal at the basal segments of the left
and right ventricles and interatrial septum
Admission laboratory showed creatinine 5 mg/dL,
which decreased to 1.5 mg/dL within 48 hours, hemoglobin 13.8 g/dL, hs-cTnT 98
ng/L, NT-proBNP 2622 pg/mL, sodium 134 mmol/L, potassium 4.5 mmol/L, and
chloride 98 mmol/L. Echocardiogram showed interventricular septum thickness of
22 mm, left ventricular posterior wall thickness 14 mm, LVEF 61%, grade II
diastolic dysfunction, average global longitudinal strain -11% with
"cherry-on-top" pattern, biatrial dilation, and moderate pericardial
effusion (Figure 3). A cardiac scintigraphy with 99mTc-PYP showed Perugini
grade 3, without vascular pool confirming the diagnosis of cardiac amyloidosis
(Figure 4).
Figure N° 3. Echocardiogram. A. Parasternal long axis showing
severe thickness of interventricular septum and posterior wall. B. Four chamber
view showing interventricular septum thickened, biatrial dilation and moderate
pericardial effusion. C. Global longitudinal strain -11% with
"cherry-on-top" pattern.
Figure N° 4. Cardiac scintigraphy with 99mTc-PYP. A. Planar
whole-body bone scan in the anterior and posterior projection demonstrating
intense cardiac uptake. B. 99mTc-PYP imaged at 1 hour after injection showing
myocardial uptake greater than ribs (visual score grade 3). C. Additional scan
was conducted at 3 hours to assess for blood pool washout.
Coronary angiography showed no obstructive
lesions, only a muscular bridge in the middle third of the anterior descending
artery with moderate reduction of the lumen during systole. A PET-CT with
FDG-F18 looking for metastasis of the renal tumor was negative, but diffuse
hypermetabolism in the myocardium and pericardial effusion was detected (Figure
5). Serum and urine immunofixation tests were negative, and serum measurement
of light chains was: kappa 35.81 mg/L (reference range 3.3-19.4) and lambda
17.79 mg/L (reference range 5.71-26.3 mg/L), with a kappa/lambda ratio of 2.01 (reference
range 0.37 to 3.1 for chronic renal failure). The hematologist concluded that
the values did not correspond to light-chain amyloidosis (AL), and the genetic
test did not detect sequence variants, so ATTR-CM wild-type was confirmed.
Figure N° 5. Positron emission tomography-computed tomography
(PET-CT) scan with FDG-F18 showing diffuse hypermetabolism in the myocardium
and pericardial effusion.
An implantable cardioverter-defibrillator (ICD) was
placed, and Tafamidis 61 mg was started. The patient was discharged in stable
condition, and nine days later had another SVT recorded and treated with an
appropriate ICD shock; amiodarone was added and after that he did not have any
further VT episodes. Before starting Tafamidis a 6-minute walk test was
performed, and he covered 76% of the theoretical distance with a score of 0 on
the Borg scale and O2 sat 98% without significant changes. On the 24-hour Holter
monitoring, the patient had sinus rhythm with supraventricular extrasystoles
and self-limited asymptomatic AF episodes, without ventricular ectopic
activity, so oral anticoagulation with Rivaroxaban 20 mg was initiated. After
fourteen months of follow-up, he is stable without new shocks from the ICD and
NYHA class I.
A case of ATTR-CMwt with SVT as the first clinical presentation with no
history of heart failure or arrhythmias, was initially suspected of having
hypertrophic cardiomyopathy, but cardiac MRI performed before the event had
suggestive signs of amyloidosis. Before his cardiologist be aware of MRI, the
patient suffered a SVT that threated his life and the diagnosis was confirmed
during hospitalization. Cardiac amyloidosis typically presents with nonspecific
symptoms and heart failure, conduction disorders or low QRS voltage on the ECG,
in people over 60 years-old(1-3). However, severe arrhythmias
may be key for the diagnosis. In addition, the PET-CT showed cardiac
hypermetabolism and pericardial effusion supporting the toxic-infiltrative
nature of the amyloid fibers on the myocardium. Westin et al. reported an
increase in the incidence of cardiac amyloidosis (CA) in people over
65 years from 0.88 per 100,000 persons/year (p/y) in the period from 1998
to 2002 to 3.6 per 100,000 p/y in 2013-2017, and 62% had heart failure, cardiomyopathy,
atrial fibrillation, or pacemaker placement as their first diagnosis(4).
Chen et al. reported on 12,139 patients diagnosed with amyloidosis, an
incidence of 6.54 per 100,000 p/y and CA of 0.61 per 100,000 p/y. The risk of
developing VT in the amyloidosis group compared to those without amyloidosis
was 7.9 ([HR: hazard ratio] 95% CI 4.49-13.9), while the risk of developing VT
in the CA group compared to those without amyloidosis was 153.3 ([HR] 95% CI
54.3-432.7), and in patients with CA, the incidence of VT was significantly
higher than in patients with amyloidosis without cardiac involvement (HR 53.9;
95% CI 19.9-146.4, P <0.001); they also had a higher risk of cardiovascular
death(5). In the multivariable analysis, new-onset VT was
an independent predictor of cardiovascular death in patients with amyloidosis
(HR 1.50; 95% CI 1.07-2.12, P <0.02)(6). It is noteworthy that no ICD was placed during the follow-up of more than
10 years(5). Higgins et al. reported 47.5% of VT in 472
patients with CA, and it was significantly associated with mortality(6).
Of 5,585 inpatients, Thakkar et al. reported that 36.1% were hospitalized with
arrhythmias, atrial fibrillation being the most frequent (72.2%) followed by VT
(14.9%)(7). No CA registry with VT events differentiated between
ATTR-CMwt and AL, so the exact prevalence of VT in each of them is unknown(8-10).
Cases of SVT have been reported especially for AL, and there are few reported
in ATTR-CMwt. Oladiran et al. reported a similar case to ours in a 71-year-old man
with ATTR-CMwt who presented with SVT, which is considered less frequent than
non-sustained VT(11). The severity of the progression and mortality
of AL is greater than ATTR-CM, and although the cause is not yet clear, it
could be attributed to the rapid deposition of fibrils and the toxic effects of
amyloid light chain that produce an increase in reactive oxygen species,
oxidative stress with alterations in intracellular calcium, impairing the
contraction and relaxation of myocytes, lysosomal, mitochondrial and
microvascular dysfunction(12). In ATTR-CM, the same
process is probably similar but slower. The possible arrhythmogenic substrate
was studied combining ECG images with cardiac MRI: the ventricular conduction
is slow and spatially heterogeneous, repolarization is slow and spatially
dispersed, and epicardial potentials are of low amplitude. Patients with AL
have a lower total amyloid volume than ATTR-CM, electrophysiological
abnormalities are more notable: lower epicardial signal voltage, higher degree
of signal fragmentation, and greater dispersion of repolarization. In all
patients with CA, an inverse correlation between T1 and signal amplitude was
observed, and the higher the extracellular volume, the greater signal and
repolarization time fragmentation(13).
The indication for ICD for primary prevention is controversial: the
European Consensus does not routinely recommend ICD for primary prevention, but
it is recommended for secondary prevention(3). The American
Guidelines for the prevention of Sudden Death recommend an individualized
decision due to the shortage of data to make a recommendation(14)
and the Heart Rythm Society recommends the placement of an ICD for those who
survived a cardiac arrest if a survival of >1 year is expected, without
differentiating ATTR-CM from AL; on the other hand, for AL in which
non-sustained VT was confirmed, prophylactic ICD is recommended if a survival
of >1 year is expected(15).
In our patient, the indication for ICD was based on the presence of SVT
with severe hemodynamic deterioration that could evolve to ventricular
fibrillation (VF) and sudden death. In fact, the event recurred after the ICD
placement, and an appropriate discharge was provided by the device. The
combination of an antiarrhythmic (amiodarone), a transthyretin stabilizer
(tafamidis), an oral anticoagulant (rivaroxaban) for prevention of systemic
embolism, and ICD for additional episodes of VT/VF, are treatments that should
be indicated by a team that considers the risks, benefits, and costs of each intervention(2).
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Recibido: 2024-05-13 Aceptado: 2024-09-12
DOI:
http://dx.doi.org/10.31053/1853.0605.v81.n4.44893
©Universidad Nacional de Córdoba