Download NoN-sustaiNed, symptomatic VeNtricular tachycar

Taiwan Crit. Care Med.2011;12:182-192
Tzu Ming Ou et al.
Non-sustained, Symptomatic Ventricular Tachycardia: A case report and literatures review
Tzu Ming Ou1, Shih Chung Huang2, Jeng Chuan Shiang1, Yi Chen Wang2
Abstract
Non-sustained ventricular tachycardia (NSVT) is commonly seen but poorly
understood. Patients with NSVT might be asymptomatic or encountered sudden cardiac
death. The prognosis depends on what the concomitant heart disease is. Poor prognosis
were found in patient with NSVT during or post exercise; acute myocardial infarction
more than 24 hours; chronic ischemic heart disease with left ventricular ejection
fraction (LVEF) below 40% with/without inducible sustained ventricular tachycardia in
electrophysiology testing; and hypertrophic obstructive cardiomyopathy in the young.
Medical therapy including beta-blockers and class III antiarrhythmic agents, while
implantable cardiac defibrillators (ICD) and radiofrequency ablation are indicated
in certain patients. Here, we report a case that had near syncope and palpitation with
NSVT on 24-hours electrocardiography, finally received ablation and antiarrhythmic
therapy. No more arrhythmia was found during out patient department follow up.
Key Words: Non-sustained ventricular tachycardia (NSVT), Left ventricular ejection
fraction (LVEF), Right ventricular outflow tract (RVOT), Implantable
cardioveter defibrillator (ICD)
Introduction
2-weeks history of epigastric pain, chest tightness,
shortness of breath, near syncope, and palpitation.
The electrocardiography (Fig. 1) revealed sinus
tachycardia and complete right bundle branch
block. Initial vital signs showed that the blood
pressure was 202/73 mmHg, the pulse rate was
105 beats per minute, the respiratory rate was
18 breaths per minute and the body temperature
was 37.2°C. Physical examination revealed mild
pale conjunctivae, no jugular vein engorgement,
rapidly regular heart beat, no heart murmur, clear
breath sound, no legs edema. Laboratory data
showed that microcytic anemia, normal cardiac
NSVT is usually a benign cause, but it may
provoke malignant arrhythmia and then induce
sudden cardiac death. The symptoms of NSVT
vary from asymptomatic to heart failure. This report describes a 71-year-old woman with NSVT.
The symptoms were stabilized after antiarrhythmic agents and electrophysiology study plus ablation.
Case Report
A 71-year-old woman presented with a
Correspondence: Dr. Yi Chen Wang
Division of Cardiology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital; No. 2, Zhongzheng 1st
Road, Lingya District, Kaohsiung City 80284, Taiwan2
Phone: +886-7-749-4941; E-mail: [email protected]
Department of Internal Medicine, Kaohsiung Armed Forces General Hospital1
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Non-sustained, symptomatic ventricular tachycardia
enzymes (Hgb: 10.4 gm/dl, Hct.: 30.5%, MCV:
78.2 fl, CK: 35 U/L, CK-MB: 13.4 U/L). Traced
her past history, she has had hypertension with
medical control (unknown drugs) for 4 years. She
also received internal fixation for left femoral
fracture 2 years ago. Under the tentative diagnosis
of hypertensive emergency, conduction disorder,
anemia, peptic ulcer, she was admitted for further
management. The upper gastrointestinal panen-
doscopy revealed gastric ulcer, duodenal ulcers,
and gastroesophageal reflux disease. The 24-hours
electrocardiography showed 39 episodes of frequent NSVT (the longest duration was 4 seconds),
occasional premature ventricular contractions, and
no ischemic change (Fig. 2). The echocardiogram
disclosed no hypertrophic or dilated cardiomyopathy and normal left ventricular systolic function.
There is no prominent hemodynamic compromise
Fig. 1. Electrocardiography revealed sinus tachycardia and complete right bundle branch block.
Fig. 2. One episode of NSVT during 24-hours electrocardiography.
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Tzu Ming Ou et al.
and syncope, so the patient was monitored at intensive care unit without anti-arrhythmic medication initially. The magnetic resonance imaging of
chest (Fig. 5) disclosed no evidence of arrhythmogenic right ventricular dysplasia (ARVD). The
coronary angiography disclosed insignificant coronary artery disease (Fig. 3) and the electrophysiology study disclosed right ventricular outflow tract
ventricular tachycardia. Radiofrequency catheter
ablation with anatomically guided linear ablation
of the anterior septum and posterior septum little
moving to free wall was performed with a 4-mmtip ablation catheter (Safire, St. Jude Medical,
Minnetonka, MN, USA) with the temperature
preset at 60°C and radiofrequency pulse duration of 120 seconds (Fig. 4). After discharged, the
oral medications included amiodarone 200mg po
daily after intravenous loading dose, plus atenolol
25mg po daily and adalat OROS 30mg po daily.
Another 24-hour electrocardiographic recording
that revealed no more ventricular tachycardia at
outpatient department two months later.
tive premature ventricular contractions, which
may be monomorphic or polymorphic, occurred
with rate above 120 beats per minute, lasting less
than 30 seconds.
Etiology of NSVT
The mechanisms of NSVT included: (1) increased automaticity, (2) reentry, and (3) triggered
automaticity. Increased automaticity (such as right
ventricular outflow tract ventricular tachycardia)
is often associated with autonomic tone, ischemia,
reperfusion, acidosis, hypokalemia, hypomagnesemia, or cardiotoxic factors.1 It may not have
sudden onset or termination. Reentry is usually
scar related. NSVT occur after acute myocardial
infarction is believed to result from the formation
of scar tissue. Monomorphic ventricular tachycardia typically occurs due to reentry or triggered
automaticity, while polymorphic ventricular tachycardia is caused by increased automaticity.2 The
most common form of right ventricular outflow
tract (RVOT) ventricular tachycardia is related to
triggered automaticity arising from delayed afterdepolarizations. It is thought to be dependent on
intracellular calcium overload and cyclic adenosine monophosphate.3-5 Other causes of triggered
automaticity are described in Table 1.
Discussion
Definition of NSVT
NSVT is defined as three or more consecu-
(A)
(B)
Fig. 3. Coronary angiography disclosed insignificant coronary artery disease: (A) Right coronary artery (B)
Left anterior descending artery & left circumflex artery.
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Non-sustained, symptomatic ventricular tachycardia
Fig. 4. Right ventricular outflow tract ventricular tachycardia was terminated during radiofrequency
catheter ablation.
Prevalence of NSVT
Using 24 to 48 hours electrocardiographic
recording, the prevalence in people without symptoms or history of cardiac disease ranged from 0 to
3%,7-11 approximately 20% of patients with hypertrophic cardiomyopathy,12,13 40 to 50% in patients
with dilated cardiomyopathy.14-17 The prevalence
of NSVT in patients with coronary artery disease
depend on the stage of disease. Within the first 24
hours of acute MI, the prevalence ranged from 45
to 75%18-20 and declined as time went on after the
event. The SPRINT study showed the incidence
of NSVT 48 hours post MI was 3%.21 In the 24-48
hours post infarction, the NSVT is usually due to
automaticity or triggered activity; however NSVT
is often due to reentry while more than 48 hours
post infarction.20,21 The symptoms of NSVT include palpitation, chest distress, pre-syncope, syncope, and heart failure. It is usually asymptomatic
but a risk factor for sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac
death, especially in patients with high frequency
or left ventricular systolic dysfunction. NSVT also
may lead to tachycardia-induced cardiomyopathy,
Fig. 5. Magnetic resonance imaging of chest
disclosed no sufficient evidence of arrhythmogenic right ventricular dysplasia
(ARVD).
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Tzu Ming Ou et al.
Table 1. The etiologies of NSVT
Triggered automaticity6
Early afterdepolarization
1.Drugs (sotalol, N-acetylprocainamide,
terfenadine, erythromycin), cesium,
barium, low potassium
2.Acquired long-QT syndrome and
associated ventricular arrhythmia
Increased automaticity
Autonomic tone
Ischemia
Reperfusion
Acidosis
Hypokalemia
Hypomagnesemia
Cardiotoxic factors
Delay afterdepolarization
1. Gain-of- function mutation in the gene
encoding RyR2
2. Catecholaminergic polymorphic
ventricular tachycardia
Reentry
Abnormalities of myocardium or Purkinje
fibers (Same as increased automaticity or scar
formation post-myocardial infarction)
which is reversible. Ventricular tachycardia is the
most common manifestation of arrhythmogenic
right ventricular dysplasia that is a familial disease causing sudden cardiac death. Idiopathic
right ventricular tachycardia commonly presents
as non-sustained or repetitive monomorphic ventricular tachycardia. Ventricular tachycardia arising from the RVOT in the absence of structural
heart disease is common, accounting up to 10%
of all ventricular tachycardias.22 The symptoms of
idiopathic RVOT ventricular tachycardia occurred
typically between the age of 20 and 40 years,
more commonly in women.23 Idiopathic right ventricular tachycardia that is most often arising from
the septal region of the right ventricular outflow
tract is a benign course.
physiology study in risk stratification for arrhythmic death is influenced by the LVEF. Patients with
LVEF between 30 % and 40% were suggested for
electrophysiology study. In ischemic heart disease
with LVEF >40%, the role of electrophysiology
study is not yet established. 25 In patients with
coronary artery disease, the two and five years
rate of sudden death were 18 and 32 percent if not
treated in NSVT and induced sustained monomorphic VT.24 Without induced sustained monomorphic VT, the two & five years rate of sudden death
were 12 and 24 percent in patients with coronary
artery disease and NSVT.26 The ACC/AHA/ESC
guidelines suggested electrophysiology testing is
reasonable for risk stratification in patients with
remote myocardial infarction, NSVT, and LVEF
equal to or less than 40% ( Class IIa; Level of Evidence: B).27
Diagnosis of NSVT
Diagnosis of NSVT is typically based on the
finding of ambulatory 24-hour Holter electrocardiography. It can establish the frequency, duration,
and morphology of the NSVT. Echocardiography
can provide the left ventricular function and identify other underlying cardiomyopathy. Patients
with suspected coronary heart disease may require
coronary angiography. Besides, the MUSTT study
suggested inducibility of tachyarrhythmia-identified patients whose death was significantly more
likely to be arrhythmic.24 The utility of electro-
Treatment of NSVT
The goals of treatment are prevention of
malignant arrhythmia, sudden cardiac death and
elimination of symptoms. Treatments included antiarrhythmic medications, implantable cardioveter
defibrillator (ICD) and catheter ablation.
1. Anti-arrhythmic medications
According to the CAST trial,28 class I antiarrhythmic drugs are not advised due to associated
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Non-sustained, symptomatic ventricular tachycardia
with increased mortality in patients with history of
myocardial infarction. The safe & effective antiarrhythmic medications are commonly beta-blocker
and amiodarone. Beta-blocker can reduce the
mortality of patients with ischemic heart disease
who both have LVEF below 40% and NSVT. 29
Amiodarone is effective in suppressing ventricular
arrhythmias and has a trend toward reduces mortality among those with nonischemic cardiomyopathy, but it cannot reduce the incidence of sudden death or prolong survival among patients with
heart failure.30 Another study showed amiodarone
is associated with a reduction in the incidence of
sudden death in adult HCM patients (including
young adults) with NSVT.31 The Canadian Myocardial Infarction Amiodarone Trial (CAMIAT)
disclosed that amiodarone reduces the incidence of
ventricular fibrillation or arrhythmic death among
survivors of acute myocardial infarction with frequent VPCs or NSVT, but no significant reduction
in overall mortality was found.32 Amiodarone in
combination with beta blockers significantly reduced both arrhythmic and nonarrhythmic cardiac
death.32
received ICD implantation. In patients without diminished ejection fraction, further studies will be
needed to determine whether those patients would
benefit from ICD therapy. The ACC/AHA/HRS
2008 guidelines suggested ICD therapy is indicated in patients with NSVT due to prior myocardial
infarction, LVEF less than or equal to 40%, and
inducible ventricular fibrillation or sustained ventricular tachycardia at electrophysiological study
(Class I; Level of Evidence: B).36
3. Catheter ablation
ICD can terminate ventricular tachycardia
episodes but does not prevent them. Catheter ablation offers a cure for ventricular tachycardia,
which is resistant to antiarrhythmic medications.
It can also reduce ICD shock and reversing tachycardia-induced cardiomyopathy. 37 Ablation was
recommended in the ACC/AHA/ESC guidelines
as useful therapy in patients who are otherwise
at low risk for sudden cardiac death and have
symptomatic nonsustained monomorphic VT
that is drug resistant, who are drug intolerant or
who do not wish long-term anti-arrhythmic drugs
therapy(Class IIa; Level of Evidence: C).27 The
success rate of catheter ablation for ventricular
tachycardia ranges from 83%-100%, while recurrence rates from 0%-31% on a variable follow-up
period.38-41 Ablation for RVOT ectopy was more
likely to fail as opposed to RVOT ventricular
tachycardia (sustained or non-sustained).42 The
predictors of failed ablation included presence of
QRS morphologic variation, wider mean QRS,
and taller R wave amplitude in lead II.42 Ablation
of ventricular tachycardia is often challenging and
lower success rates than ablation of supraventricular tachycardias. The reasons included: (1) large
infarct region. (2) Hemodynamically unstable and
poorly tolerated. (3) Epicardial or intramural in
location. (4) Several reentrant circuits.33 It is controversial that anti-arrhythmic medications needed
after successful catheter ablation. Overall, catheter
ablation of ventricular tachycardia in the setting of
structural heart disease can only be considered an
adjunctive therapy, which in general, will require
ICD therapy.33
2. Implantable cardioveter defibrillator (ICD)
ICD is first-line therapy in patients with ventricular tachycardia who also have structural heart
disease with impaired LVEF. It is also superior to
medical therapy in primary and secondary prevention of sudden cardiac arrest. In the patients who
received ICD implantation as primary prevention of sudden cardiac death, 20% of them would
experience at least one ventricular tachycardia
episode within 3-5 years after ICD implantation.33
The MUSTT trial disclosed ICD reduced arrhythmic death in patients with asymptomatic NSVT,
LVEF≤ 40%, and induced sustained ventricular
tachycardia, comparing with no therapy or antiarrhythmic drugs.24,34 The MADIT I study proved
the benefit of ICD for improved survival in patient
with asymptomatic NSVT and symptomatic ischemic heart disease with LVEF<35%.35 According
to the MUSTT and MADIT I results, patients with
LVEF below 40%, NSVT, and inducible ventricular tachycardia in electrophysiology study should
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Tzu Ming Ou et al.
sudden death43 (see Table 2). In post-myocardial
infarction patients with LVEF less than 40%, the
risk of sudden death is increased more than fivefold.48, 49 The MUSTT study also disclosed patients with coronary artery disease, left ventricular
dysfunction and asymptomatic NSVT in whom
sustained ventricular tachycardia can be induced
in electrophysiology testing have a higher risk of
sudden death or cardiac arrest and higher overall
mortality than similar patients without inducible
sustained ventricular tachycardia.26
Prognosis of NSVT
Spontaneous NSVT in apparently healthy
individuals does not imply an adverse prognosis,
but long-term follow up is advisable. NSVT in
the presence of structural heart disease carries a
more serious prognosis than NSVT in the absence
of structural heart disease. It is adverse prognostic significance for NSVT attacks during or post
exercise, in patient with acute myocardial infarction more than 24 hours, chronic ischemic heart
disease with LVEF below 40%, and hypertrophic
obstructive cardiomyopathy in the young.43,44 In
patients with congestive heart failure, NSVT is an
independent marker for increased overall mortality rate and sudden death.45 In adult patients with
hypertrophic obstructive cardiomyopathy, NSVT
is a sensitive marker for increased risk of sudden
death.46 NSVT is an insensitive and nonspecific
predictor of sudden death in idiopathic dilated
cardiomyopathy patients. 47 However, NSVT in
patients with primary ventricular fibrillation, congenital long-QT, Brugada syndrome, arrhythmogenic right ventricular dysplasia, repaired congenital abnormalities, valvular heart disease, hypertension were unknown prognostic significance for
Conclusion
NSVT is frequently encountered in clinical
practice. It may increase the risk for malignant arrhythmia and sudden cardiac death. The prognosis
depends on the etiologies. Clinical approach to the
patient with NSVT should always be considered
what the coexisted heart disease is. In the absence
of heart disease, spontaneous NSVT does not
carry any adverse prognostic significance. NSVT
with adverse prognostic significance were found
in patients with some conditions. Treatment to
the NSVT included antiarrhythmic medications,
Table 2.Prognostic significance of non-sustained ventricular tachycardia with
different underlying heart condition.43-49
Adverse prognostic significance
1.NSVT during or post exercise
2.Acute myocardial infarction more than 24 hours
3.Chronic ischemic heart disease with LVEF below 40%
with/without inducible sustained ventricular
tachycardia in electrophysiology testing
4.Hypertrophic obstructive cardiomyopathy in the young
No Adverse prognostic significance
Idiopathic dilated cardiomyopathy
Unknown prognostic significance
1.Primary ventricular fibrillation
2.Congenital long-QT
3.Brugada syndrome
4.Arrhythmogenic right ventricular dysplasia
5.Repaired congenital abnormalities
6.Valvular heart disease
7.Hypertension
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Non-sustained, symptomatic ventricular tachycardia
ICD implantation and catheter ablation. Betablocker and amiodarone are safe and effective
anti-arrhythmic medications. ICD implantation is
convinced as first line therapy to terminate ventricular tachycardia episode. In patients who have
structural heart disease, catheter ablation is recommended as adjunctive therapy if frequent episodes
of VT and ICD shocks. Anti-arrhythmic medications therapy after successful catheter ablation is
controversial.
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非持續性具症狀之心室心搏過速:病例報告及文
獻回顧
1
2
1
2
歐子銘 , 黃世鐘 , 項正川 , 王怡誠
摘要
非持續性心室心搏過速臨床上很常見，但了解的人卻不多。具有非持續
性心室心搏過速的病人輕微者可以無症狀，嚴重者卻有猝死的可能。預後跟
合併的心臟疾病有關。不良的預後常見於運動誘發之非持續性心室心搏過速、
急性心肌梗塞 24 小時過後、慢性缺血性心臟病及左心室射出分率小於 40%
合併有或無於心臟電生理檢查誘發出非持續性心室心搏過速、年輕人之肥厚
性阻塞性心肌病變。藥物治療包含乙型交感神經阻斷劑及 amiodarone，而植
入式心臟整流去顫器及射頻燒灼術適用於某些病人。我們報告一個 71 歲女性
合併有暈厥及心悸的症狀，24 小時心電圖診斷非持續性心室心搏過速。經射
頻燒灼術及藥物治療後病情獲得穩定控制。希望藉由這個病例讓大家更加認
識這個疾病。
關鍵詞：非持續性心室心搏過速，左心室射出分率
聯絡人：王怡誠醫師
802 高雄市苓雅區中正一路 2 號；國軍高雄總醫院心臟內科 2
電話：07-749-4941；E-mail：[email protected]
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國軍高雄總醫院內科部
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