Are all Non-sustained Ventricular Tachycardia the Same in
Hypertrophic Cardiomyopathy Risk Stratification for Sudden Cardiac
Death?
Mohamad Khaled Sabeh MD1, Marwan M. Refaat
MD2
1Cardiac Arrhythmia Service, Massachusetts General
Hospital, Boston, Massachusetts - USA
2Division of Cardiology, Department of Internal
Medicine, American University of Beirut Medical Center Beirut, Lebanon
Running Title: NSVT in HCM SCD Risk Stratification
Words (excluding references): 664
Disclosures: None
Funding: None
Keywords: Hypertrophic Cardiomyopathy, Non-sustained Ventricular
Tachycardia, Cardiac Arrhythmias, Cardiovascular Diseases
Correspondence:
Marwan M. Refaat, MD, FACC, FAHA, FHRS, FASE, FESC, FACP, FRCP
Associate Professor of Medicine
Director, Cardiovascular Fellowship Program
Department of Internal Medicine, Cardiovascular Medicine/Cardiac
Electrophysiology
Department of Biochemistry and Molecular Genetics
American University of Beirut Faculty of Medicine and Medical Center
PO Box 11-0236, Riad El-Solh 1107 2020- Beirut, Lebanon
Fax: +961-1-370814
Clinic: +961-1-350000/+961-1-374374 Extension 5800
Office: +961-1-350000/+961-1-374374 Extension 5353 or Extension 5366
(Direct)
Email: mr48@aub.edu.lb
Cardiomyopathies with reduced systolic function predispose to sudden
cardiac death (SCD) and many studies helped in decreasing that risk by
Implantable Cardioverter Defibrillator (ICD) implantation and
pharmacologic management (1-4). Many types of cardiomyopathies with
preserved systolic function, including hypertrophic cardiomyopathy
(HCM), can predispose to malignant ventricular arrhythmias and SCD. HCM
is the most common inherited cardiac disease that affects 1 in 200 live
births (5,6). SCD remains one of the main causes of death in HCM and the
SCD rate peaks in early adulthood (7-14). Data from ICDs suggest that
SCD in HCM is most commonly caused by ventricular fibrillation (VF)
(15). One major clinical challenge is identifying patients at risk for
SCD. Multiple studies showed that non-sustained ventricular tachycardia
(NSVT) is a risk actor for SCD (16,17). However the strength of the data
was variable across these studies due to difference in populations and
the low sensitivity of Holter ECG. Moreover, other studies looked at the
rate and duration of the ventricular arrhythmias and their relationship
to SCD in HCM (17-19) yet the effect of the morphology of NSVT on SCD
has not been well investigated.
In this single center study Adduci et al . explore the prognostic
impact of different NSVT morphologies in a cohort of 109 consecutive HCM
patients. The study included patients who had an ICD implanted in the
authors’ institution from January 2001 to December 2018. The ICDs were
mostly implanted for primary prevention in HCM patient with 1) one or
more risk factor including maximal LV thickness ≥30 mm, family history
of SD in at least 1 first-degree relative <50 years of age,
non-sustained ventricular tachycardia (NSVT), recent (≤ 6 months)
unexplained syncope, 2) hypotensive blood pressure during exercise with
at least one additional major risk factor for SD 3) end-stage HCM
regardless of other established risk markers of SCD. Devices were
interrogated on evaluation every 3 to 6 months and the data was assessed
for appropriate or inappropriate ICD therapies. Two independent
electrophysiologists analyzed the ICD near field and far field EGMs from
the ventricular tachycardia runs. They classified the VTs as either
monomorphic (MMVT) or polymorphic (PMVT).
During a mean follow up of 71+/- 48 months, 377 NSVT episodes of NSVT
were retrieved from ICD memory in 46 patients; of these episodes, 7(2%)
were polymorphic and 370 (98%) were monomorphic (MM). The mean HR of
The MM NSVT had an average HR of 171+/- 32 BPM and lasted for 17 +/- 12
beats while the PMVT were faster at 241BPM +/- and longer at 28+/- 16
beats. The appropriate intervention rate was 5.1% per year and
interestingly NSVT did not predict the occurrence of ICD therapy.
However patients with polymorphic NSVT had a statistically higher risk
for ICD intervention as compared to monomorphic NSVT. Further analysis
noted a trend for increased risk of ICD therapy with patients with
>1 NSVT morphology. Moreover 75% of the treated VTs had
been previously observed as NSVT.
Risk stratification is very important in this young patient population;
decreasing the risk threshold for ICD implants leads to missed
arrhythmias and bad outcomes while increasing it increases the risk for
complications from unnecessarily implanted devices. There are several
types of ICDs: Transvenous ICD, Subcutaneous ICD and Extravascular ICD.
The results of this study suggest that the risk of SCD in patients with
PMVT and/or NSVT with multiple morphologies is different from that of
patients with a MMVT, and that the presence of short MMVT doe not
predict the future ICD therapies. As such, one may consider a
conservative approach in low-risk patients with short bursts of slow MM
NSVT, and a more aggressive approach in patients with frequent, rapid
rate burst of PMVT. Although this study suggests that different NSVT
morphologies affect the prognosis in HCM patients, the low number of
events lacked the statistical power to redefine ICD candidacy. Larger
multicenter studies are needed to confirm these findings and to help
delineate the “at risk patients” who would truly benefit from ICDs.