Successful Catheter Ablation of Hemodynamically Unstable Monomorphic Ventricular Tachycardia in a Patient with Hypertrophic Cardiomyopathy and Apical Aneurysm

Lim, Kiam Khiang; Maron, Barry J.; Knight, Bradley P.

doi:10.1111/j.1540-8167.2008.01366.x

Cited by 59 publications

(20 citation statements)

References 13 publications

(26 reference statements)

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“…Our results confirm a statistically significant association between the presence of apical aneurysm and %LGE (P = 0.013), in keeping with prior studies that have suggested that apical aneurysms are composed predominantly of fibrosis and may act as a substrate for ventricular tachyarrhythmias. 36,37 The presence of an apical aneurysm and the extent of LGE did not remain significant predictors of major adverse events in a multivariable model; however, this analysis was limited by the number of events and the fact that apical aneurysms are composed of fibrosis; therefore, these variables are not independent of each other. In our study, patients with both an apical aneurysm and >5% LGE on cardiac MRI had the highest combined risk for major adverse events (OR 6.7), suggesting that identification of both imaging findings may P-values in bold are statistically significant.…”

Section: Discussionmentioning

confidence: 89%

Cardiac Magnetic Resonance Imaging Findings Predict Major Adverse Events in Apical Hypertrophic Cardiomyopathy

Hanneman

Crean²,

Williams³

et al. 2014

Journal of Thoracic Imaging

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Section: Discussionmentioning

confidence: 89%

Cardiac Magnetic Resonance Imaging Findings Predict Major Adverse Events in Apical Hypertrophic Cardiomyopathy

Hanneman

Crean²,

Williams³

et al. 2014

Journal of Thoracic Imaging

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“…Currently, data pertaining to catheter ablation of monomorphic VT in this group are limited to a few case reports that have used a strictly endocardial approach. [3][4][5][6] In the present study, we report the acute and long-term results of a combined epicardial and endocardial approach to catheter ablation in a highly selected group of patients with HCM-related VT.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5][6] Furthermore, although myocardial scar has been implicated in the genesis of monomorphic VT in other disease states, few data characterize the arrhythmogenic substrate in patients with HCM. However, MRI data demonstrate the presence of myocardial scar as identified by delayed enhancement imaging in patients with HCM with manifest monomorphic MMVT, [7][8][9][10] suggesting that the substrate for monomorphic VT may be similar to that seen in patients postmyocardial infarction and, thus, may be amenable to catheter ablation.…”

Section: Clinical Perspective On P 194mentioning

confidence: 99%

Long-Term Outcomes of Combined Epicardial and Endocardial Ablation of Monomorphic Ventricular Tachycardia Related to Hypertrophic Cardiomyopathy

Dukkipati

d’Ávila

Soejima

et al. 2011

Circ: Arrhythmia and Electrophysiology

137

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Background-Monomorphic ventricular tachycardia (MMVT) is rare in patients with hypertrophic cardiomyopathy (HCM). There are limited data on the utility of catheter ablation for the treatment of MMVT in this population. This study details a series of case reports from multiple centers where combined epicardial-endocardial ablation was performed in a highly selected group of patients with HCM-related MMVT. Methods and Results-The cohort consisted of 10 patients with HCM-related MMVT. Pericardial access was achieved using the percutaneous subxyphoid approach. Epicardial and endocardial ventricular 3D bipolar voltage maps were generated. Ablation sites were identified using a combination of entrainment, activation, late/fractionated potential, and pace mapping. Electrophysiological-identified epicardial scar was present in 8 (80%) patients, endocardial scar in 6 (60%), and no scar in 1 (10%). In the 5 patients with inducible, stable MMVT, 3 cases were successfully terminated with ablation from the epicardium and 1 from the endocardium. The case that failed catheter ablation required surgical cryoablation to abolish the incessant VT. In the remaining 5 patients, 4 underwent epicardial and endocardial ablation of sites with good pace maps and late/fractionated potentials. No ablation was performed in the remaining patient because of noninducibility and lack of identifiable scar. After 37Ϯ17 months (limits, 2 to 62 months; median, 37 months), the freedom from recurrent implantable cardioverter-defibrillator shocks was 78% (7/9 patients) in those who underwent ablation. Conclusions-In

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“…Often, fi brosis can extend from the aneurysm to the periapical regions in the septum and free wall and may thus serve as a substrate for malignant dysrhythmias [ 38 ]. Patients should be considered for ICD implantation for primary prevention of sudden death, particularly those with extensive LGE [ 10 ].…”

Section: Apical Aneurysmsmentioning

confidence: 99%

Hypertrophic Cardiomyopathy

Chan¹,

Maron²

2013

Cardiac CT and MR for Adult Congenital Heart Disease

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Hypertrophic cardiomyopathy (HCM) is a common genetic cardiomyopathy caused by mutations in genes which encode for the myofi lament protein components of the sarcomere or the z-disc [ 1 -4 ]. It has a prevalence of 1 in 500 in the general population and is a global disease affecting patients in all continents [ 5 ] and of both genders [ 6 ]. It is the leading cause of sudden death in young people, with an annual mortality rate of 1 % [ 7 ]. Since its fi rst description over 50 years ago, the pathophysiology of the disease is still incompletely understood [ 8 ]. The disease is associated with tremendous heterogeneity with regard to its presentation, phenotype, and prognosis. The diagnosis for HCM is usually made clinically after symptom onset or cardiac events, but may also be found after routine 12-lead electrocardiogram (ECG), heart murmur on cardiac exam, or in family screening of probands. ImagingClinical diagnosis is confi rmed through imaging using 2D echocardiography and/or cardiac MRI (CMR) or CT by identifying an increase in left ventricular (LV) wall thickness ≥15 mm (mean ~22 mm [normal ≤12 mm]) without a dilated LV chamber in absence of other cardiac or systemic disease processes (e.g., aortic stenosis, chronic hypertension) capable of producing the magnitude of hypertrophy [ 9 ]. In certain instances, such as patients with a family history of HCM, a maximal wall thickness ≥13 mm may be compatible with the diagnosis of HCM. LV hypertrophy is most commonly asymmetric, with the most common location of increased wall thickness occurring in the contiguous area of the basal anterior septum and anterior wall [ 10 ] (Fig. 16.1 ), although there is tremendous heterogeneity in phenotypic expression, even in those with a common genotype. In addition, in close to 25 % of HCM patients, segments of LV hypertrophy can be separated by myocardial regions of normal thickness, i.e., noncontiguous pattern of LV hypertrophy. Concentric pattern of LV hypertrophy occurs very rarely in HCM (~1 %) [ 11 , 12 ] (Fig. 16.2 ).

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Successful Catheter Ablation of Hemodynamically Unstable Monomorphic Ventricular Tachycardia in a Patient with Hypertrophic Cardiomyopathy and Apical Aneurysm

Cited by 59 publications

References 13 publications

Cardiac Magnetic Resonance Imaging Findings Predict Major Adverse Events in Apical Hypertrophic Cardiomyopathy

Cardiac Magnetic Resonance Imaging Findings Predict Major Adverse Events in Apical Hypertrophic Cardiomyopathy

Long-Term Outcomes of Combined Epicardial and Endocardial Ablation of Monomorphic Ventricular Tachycardia Related to Hypertrophic Cardiomyopathy

Hypertrophic Cardiomyopathy

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