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PVCs in Patients Without Heart Disease: Risks and Treatments
1. Are PVCs in patients without
structural heart disease really safe?
Ventricular Arrhythmias in Patients
With Normal Hearts
(Ventricular Arrhythmias in the
Absence of Structural Heart Disease)
Prof. Samir Morcos Rafla, FACC, FESC, FHRS
Alexandria Univ.
2. Ventricular tachycardia in patients without
apparent structural heart disease
• Idiopathic ventricular tachycardia (IVT), a term that
has been used for ventricular tachycardia (VT) in the
absence of clinically apparent structural heart disease
, accounts for around 10% of all VTs. Several types
have been reported according to their clinical
presentation, ventricular origin, response to drugs,
electrocardiographic pattern, among others. The most
common type is the so called ventricular outflow tract
(VOT-T) or adenosine-sensitive tachycardia while
other monomorphic forms of IVT, include
intrafascicular verapamil-sensitive reentrant
tachycardia and ventricular tachycardia in patients
with structural heart disease.
5. • Correlation of the site of origin of ventricular
ectopy with the electrocardiogram (ECG)
morphology in V1. The anatomy of the outflow
tract region is such that areas on the right and left
sides of the heart can be in close proximity to each
other. This can give similar ECG patterns in several
leads. However, note that in V1, there is a gradual
increase in the amplitude of the r-wave as the site
of origin of the ventricular ectopy moves leftward.
Ao = aorta; LA = left atrium; LV = left ventricle;
RVOT = right ventricular outflow tract.
9. • 12-Lead ECG of PVCs
• A 12-lead electrocardiogram (ECG) of premature
ventricular contractions (PVCs) originating in the
left coronary cusp/aortic sinus of Valsalva (ASV).
Note that the QRS morphology in the limb leads is
nearly the same as in the example in Figure 2.
However, the precordial ECG leads are markedly
different. There is a broad but small r-wave in
V1 and V2, and the transition from small to large R-
wave is from V2 to V3. Although that could still be
from the right side, a left-sided site is more likely,
and intracardiac mapping and ablation confirmed a
left ASV site.
10. • Table 1 Classification of Ventricular Arrhythmias in
the Absence of Structural Heart Disease
• I. Non–life-threatening (typically monomorphic)
• A. Outflow tract
• Right ventricular outflow
• Left ventricular outflow
• Aortic sinus of Valsalva
• Peri His bundle
• B. Idiopathic left ventricular tachycardia
• Left posterior fascicle
• Left anterior fascicle
• High septal fascicle
11. • C. Other
• Mitral annulus
• Tricuspid annulus
• Papillary muscle
• Perivascular epicardial
• II. Life-threatening (typically polymorphic)
• A. Genetic syndromes
• Long QT
• Brugada
• Catecholaminergic polymorphic ventricular
tachycardia
• Short QT
• B. Idiopathic ventricular fibrillation
12.
13.
14.
15. • Patients presenting in sustained VT may respond acutely
to carotid sinus massage, Valsalva maneuvers, or
intravenous adenosine or verapamil . Long-term oral
therapy with either beta-adrenergic blockers or calcium-
channel blockers may control arrhythmias . Patients
nonresponsive to beta-blockers and calcium-channel
blockers may respond to class I or III antiarrhythmic
agents .
• Radiofrequency catheter ablation may be considered in
cases where medical therapy is ineffective or not
tolerated. Excellent outcomes for ablation of OTAs.
Ablation of epicardial or aortic sinuses of Valsalva sites is
also highly effective, but can be technically challenging
and carries higher risks due to these sites' proximity to
coronary arteries.
16.
17. COMPLEMENTARY TESTS AND DIFFERENTIAL
DIAGNOSIS
• Electrocardiogram:
• Blood tests: Plasma brain natriuretic peptide (BNP) levels have been proposed to
distinguish VOT-T from ARVC.
• Echocardiography:
• Exercise test: It is frequently used to evaluate and
initiate VOT-T .
• Myocardial perfusion scintigraphy:
• Magnetic resonance imaging (MRI):
• Holter Monitor:
• Right ventricular biopsy:
23. Key Points
• Although most patients with idiopathic ventricular
arrhythmias do not require treatment, some
patients will experience severe symptoms. In
addition, treatment is warranted for patients with
PVC-related myopathy and the malignant form of
idiopathic VT, which can trigger episodes of PMVT.
• Treatment for idiopathic VT includes
pharmacologic agents (i.e., beta-blockers, calcium
channel antagonists, class IC antiarrhythmic drugs)
and catheter ablation.
24. • Inherited arrhythmogenic diseases constitute an expanding
field with a wide spectrum of electrocardiographic
manifestations.
• Mutations in the same gene may cause different
phenotypes according to the functional consequences of
mutations and are often associated with variable
penetrance and incomplete expressivity.
• Both tachyarrhythmias and bradyarrhythmias in the
structurally normal heart may be genetically determined.
• Gene-specific electrocardiographic features have been
identified in LQTS and BrS. In LQTS, the underlying genotype
modulates both the clinical outcome and the response to
therapy.
25. Key Points
Amiodarone is the major antiarrhythmic drug
option for symptomatic ventricular arrhythmias in
patients with depressed ventricular function, but
the drug has significant toxicities.
Sustained polymorphic VT is usually due to an
acute coronary syndrome or QT prolonging factors
causing torsade de pointes.
26. RECOMMEND
ATION CLASS
Catheter ablation is useful in patients with structurally normal hearts
with symptomatic, drug-refractory VT arising from the RV or LV or
in those who are drug intolerant or who do not desire long-term drug
therapy.
I
EP testing is reasonable for diagnostic evaluation in patients with
structurally normal hearts with palpitations or suspected outflow
tract VT.
IIa
Drug therapy with beta blockers and/or calcium channel blockers
(and/or IC agents in RVOT VT) can be useful in patients with
structurally normal hearts with symptomatic VT arising from the RV.
IIa
ICD implantation can be effective therapy for the termination of
sustained VT in patients with normal or near normal ventricular
function and no structural heart disease who are receiving chronic
optimal medical therapy and who have reasonable expectation of
survival for more than 1 y
IIa