scholarly journals Extensive Myocardial Fibrosis in a Patient With Hypertrophic Cardiomyopathy and Ventricular Tachycardia Without Traditional High-Risk Features

2009 ◽  
Vol 2 (4) ◽  
pp. 349-350 ◽  
Author(s):  
Sergio Bongioanni ◽  
Paolo Spirito ◽  
Andrea Sibona Masi ◽  
Amedeo Chiribiri ◽  
Rodolfo Bonamini ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Hypertrophic Cardiomyopathy ◽  
High Risk ◽  
Myocardial Fibrosis

scholarly journals Myocardial fibrosis detected by cardiac CT predicts ventricular fibrillation/ventricular tachycardia events in patients with hypertrophic cardiomyopathy

2013 ◽  
Vol 7 (3) ◽  
pp. 173-181 ◽  
Author(s):  
Afonso Akio Shiozaki ◽  
Tiago Senra ◽  
Edmundo Arteaga ◽  
Martino Martinelli Filho ◽  
Cristiane Guedes Pita ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Hypertrophic Cardiomyopathy ◽  
Ventricular Fibrillation ◽  
Myocardial Fibrosis ◽  
Cardiac Ct

Predictors of sudden cardiac death and ventricular tachyarrhythmias in patients with hypertrophic cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
N Rineiska ◽  
E Zakharava ◽  
S Komissarova ◽  
I Haidel
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
High Risk ◽  
Sudden Cardiac Death ◽  
Myocardial Fibrosis ◽  
Cardiac Death ◽  
T1 Mapping ◽  
Adverse Outcome ◽  
Low Risk ◽  
Ventricular Tachyarrhythmias ◽  
Risk Patients

Abstract Background Determining additional predictors that allow more accurate identification of patients who need primary prevention of sudden cardiac death (SCD) and ventricular tachyarrhythmias (VT) in patients with hypertrophic cardiomyopathy (HCM) is one of the most important tasks. High-risk patients can be more accurately identified using modern non-invasive research methods. Purpose Identification of new risk predictors for SCD and ventricular tachyarrhythmias based on cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) and T1-mapping in patients with hypertrophic cardiomyopathy. Materials and methods Clinical data of 98 HCM subjects (58 males and 40 females, median age 46.5 [35.2; 54.7] treated in our centre in the period between 2013 and 2017 have been studied. All patients underwent CMR with LGE and T1-mapping. Results According to the existing ESC-2014 scale, 45 (46%) of the 98 patients included in the study had a low risk, an intermediate risk was identified in 26 (26%) patients and a high risk of SCD in 27 (28%). During the follow-up period 16 episodes of sudden cardiac death were recorded. Of these, only 8 (50%) patients had a high risk on the ESC-2014 scale. High-risk patients show significantly greater myocardial fibrosis (Me 28.5%; [21.9; 44.1]) compared with patients with intermediate (Me 17.6% [8.0; 22.5]) and low risk of SCD (Me 11.7%; [5.8; 17.6]), p<0.001. A threshold level of fibrosis volume associated with an adverse outcome was determined, which was 15% (based on determining the maximum rank of statistics). For patients with 15% fibrosis volume, the cumulative survival rate on the Kaplan-Mayer curve over the observation period was 96% (95% CI 88.6–100), while for patients with fibrosis volume ≥15% - 72.4% (95% CI 60.6–86.4). The study showed that in 15 (93.7%) patients out of 16 who had an adverse outcome, the volume of myocardial fibrosis was ≥15%. Episodes of nonsustained ventricular tachycardia were detected in 48 patients (48.7%) according to daily ECG monitoring. To identify patients with ventricular tachyarrhythmias by ROC analysis, the threshold value of extracellular myocardial volume was determined using CMR with LGE and T1 mapping, which was 32.5% (sensitivity 74% and specificity 86%). According to multivariate analysis, one of the independent predictors of ventricular tachyarrhythmias was the level of extracellular myocardial volume ≥32.5% (HR 1.2; 95% CI 1.03–1.4). Conclusion Predictors detected by CMR with LGE and T1 mapping can identify patients with HCM with a high risk of sudden cardiac death and ventricular tachyarrhythmias. Funding Acknowledgement Type of funding source: None

Ventricular tachycardia/fibrillation early after defibrillator implantation in patients with hypertrophic cardiomyopathy is explained by a high-risk subgroup of patients

Heart Rhythm ◽  
2013 ◽  
Vol 10 (2) ◽  
pp. 214-218 ◽  
Author(s):  
Alawi A. Alsheikh-Ali ◽  
Mark S. Link ◽  
Christopher Semsarian ◽  
Win-Kuang Shen ◽  
N.A. Mark Estes ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Hypertrophic Cardiomyopathy ◽  
High Risk

scholarly journals Myocardial extracellular space expansion is related to burden of premature ventricular contractions in patients with hypertrophic cardiomyopathy without non-sustained ventricular tachycardia

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
H Chung ◽  
CH Park ◽  
YJ Kim ◽  
JY Kim ◽  
PK Min ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Hypertrophic Cardiomyopathy ◽  
Myocardial Fibrosis ◽  
Extracellular Space ◽  
Premature Ventricular Contraction ◽  
Sustained Ventricular Tachycardia ◽  
Premature Ventricular Contractions ◽  
Funding Sources ◽  
Space Expansion ◽  
Current Guidelines

Abstract Funding Acknowledgements Type of funding sources: None. Background Current guidelines suggest the presence of non-sustained ventricular tachycardia (NSVT) as a risk factor of sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). However, high burden of premature ventricular contraction (PVC) may reflect myocardial fibrosis although the absence of NSVT. Purpose We investigated the association between PVC burden and myocardial extracellular space expansion in HCM patients without NSVT. Methods Of the 212 patients prospectively enrolled to the HCM registry of genetics, 84 patients were evaluated with both cardiac magnetic resonance and 24hr holter. Among them, 71 patients (58 males, mean age: 71 ± 13 years) have not been diagnosed with NSVT. Results Patients with NSVT (n = 13) showed more impaired LA functional indices and higher myocardial fibrosis burden compared with patients without NSVT (n = 71). Among patients who have not been diagnosed with NSVT, patients with late gadolinium enhancement (LGE, n = 46) had a higher total beats (109 ± 332 vs. 7 ± 13 beats per a day, p = 0.003) and burden (0.114 ± 0.225 vs. 0.008 ± 0.014 %, p = 0.003) of PVC during 24-hour compared with patients without LGE (n = 25). %LGE was correlated with total beats of PVC (r = 0.358, p = 0.002) and PVC burden (r = 0.377, p = 0.001). ECV also correlated with total beats of PVC (r = 0.387, p = 0.001) and PVC burden (r = 0.401, p = 0.001). The optimal cutoff value for PVC number was 45 (37.0% of sensitivity and 100% of specificity) with 0.733 of the area under the ROC curve (p < 0.001). Pathogenic or likely pathogenic sarcomere mutation was higher in NSVT group than no NSVT group (p < 0.05), and had a higher tendency in higher PVC burden group (0.05 < p < 0.1) than lower PVC burden group. Conclusions Total beats and burden of PVC are significantly related to increase in myocardial fibrosis in HCM patients without NSVT. Abstract Figure. Mechanism of ventricular arrhythmia

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