Ventricular Tachycardia In Hypertrophic Cardiomyopathy Research Articles

Reversed Septal Curvature Is Associated With Nonsustained Ventricular Tachycardia in Hypertrophic Cardiomyopathy

Sudden cardiac death (SCD) is associated with nonsustained ventricular tachycardia (NSVT) in patients with hypertrophic cardiomyopathy (HCM). Recently, differences regarding septal morphology have been reported, with an increased probability of sudden death in HCM patients who had reverse septal curvature (RSC). The aim of this study was to examine the relationship between RSC and NSVT in HCM. A total of 138 patients with HCM were enrolled. Of 138 patients, 47 (34.1%) were diagnosed with RSC and 42 patients (30.4%) had NSVT. Compared with the non-RSC group, those with RSC were much younger and had an increased incidence of NSVT, thicker septal thickness, larger mass, and a higher proportion of HCM or SCD family history. Furthermore, patients with RSC had a higher risk of SCD according to the European Society of Cardiology calculator (2.5 (1.6, 4.6) vs. 1.6(1.1, 2.3)(%/5 year), p <0.001). Multivariate analysis showed that RSC was a strong and independent risk factor for NSVT (odds ratio = 2.756, 95% confidence interval: 1.164-6.525, p = 0.021). In conclusion, the presence of RSC in HCM patients is independently associated with NSVT. Further studies are needed to evaluate the role of RSC as a risk factor for SCD in this population.

Ventricular Tachycardia in Hypertrophic Cardiomyopathy Complicated with Apical Aneurysm: About two cases

Ventricular Tachycardia in Hypertrophic Cardiomyopathy Complicated with Apical Aneurysm: About two cases

Positron emission tomography (15O-water, 11C-acetate, 11C-HED) risk markers and nonsustained ventricular tachycardia in hypertrophic cardiomyopathy

BackgroundThe objectives of the study were to describe positron emission tomography (PET) parameters, using the tracers 15O-water at rest/stress, 11C-acetate, and 11C-HED, with regard to nonsustained ventricular tachycardia (NSVT) in hypertrophic cardiomyopathy (HCM). PET offers quantitative assessment of pathophysiology throughout the left ventricular segments, including the endocardium/epicardium. The potential use PET in risk stratification remains to be elucidated. NSVT provides a marker for sudden cardiac death. MethodsPatients with a validated diagnosis of HCM who had an implantable cardioverter-defibrillator were interrogated at 12 months and independently of PET-examinations. ResultsIn total, 25 patients (mean age 56.8 ± 12.9 years, 76% males) were included and 10 reported NSVT. Mean myocardial blood flow (MBF) at rest was 0.91 ml/g/min and decreased at stress, 1.59 ml/g/min. The mean gradient (endocardium/epicardium quotient) at rest was 1.14 ± 0.09, while inverse at stress (mean 0.92 ± 0.16). Notably, MBF gradient at stress was significantly lower in patients with NSVT (p = 0.022) and borderline at rest (p = 0.059) while global MBF at rest and stress were not. Mean myocardial oxygen consumption (MVO2) was 0.088 ml/g/min (higher in NSVT, p = 0.023) and myocardial external efficiency 18.5%. Using 11C-HED, the mean retention index was 0.11 min−1 and a higher volume of distribution (p = 0.089) or transmural gradient of clearance rate (p = 0.061) or lower clearance rate (p = 0.052) showed a tendency of association of NSVT. ConclusionsThe endocardium/epicardium MBF gradient at stress is significantly lower in HCM patients with NSVT. This provides a novel approach to further refine risk stratification of sudden cardiac death.

2378Blunted stress myocardial oxygenation and not myocardial perfusion reserve is associated with arrhythmic risk in hypertrophic cardiomyopathy

Abstract Background In hypertrophic cardiomyopathy (HCM), myocardial ischaemia is believed to play a role in fatal life-threatening ventricular arrhythmias and caused by microvascular dysfunction manifesting as impaired myocardial perfusion. However, previous studies suggest that myocardial oxygenation during vasodilator stress may also be blunted when perfusion is normal, due to increased metabolic demands conferred by energy-costly sarcomeric mutations, left ventricular hypertrophy and outflow obstruction. Whether or not impaired myocardial perfusion reserve or blunted stress oxygenation on cardiac magnetic resonance (CMR) predict the risk of ventricular arrhythmia in HCM is unknown. Purpose We sought to investigate if impaired myocardial perfusion reserve or stress oxygenation is associated with an increased risk of ventricular arrhythmia in HCM. Methods 103 genotyped HCM patients (mean age 47±15 years) and 32 age- and sex-matched healthy controls underwent adenosine stress blood oxygen level dependent (BOLD) imaging, first pass perfusion and late gadolinium imaging (LGE) on CMR to assess stress oxygenation (BOLD ΔSI), myocardial perfusion reserve index (MPRI), and fibrosis respectively. All HCM patients were monitored for ventricular tachycardia (≥3 beats, ≥120 beats per minute) on a 24-hour Holter. Results As expected, MPRI was significantly reduced in HCM (1.5±0.4 vs 2.0±0.3, p&lt;0.0001) compared to controls. Stress oxygenation response was blunted in HCM versus controls (9.1±4.1% vs 17.0±1.6%, p&lt;0.0001, Figure 1B). Twenty-six (25%) patients developed ventricular tachycardia on Holter monitoring. On univariate analysis, only stress oxygenation and not MPRI associated with ventricular tachycardia. The prevalence of ventricular tachycardia in HCM increased with decreasing quartiles of stress oxygenation (Figure 1D). HCM patients in the lowest quartile of oxygenation (BOLD ΔSI &lt;6.5%) were at a three-fold risk of ventricular tachycardia (OR 3.04, 95% confidence interval 1.02–9.05, p=0.04) on multivariable analysis (after adjusting for sudden cardiac death risk factors and LGE mass) compared to other patients. Sarcomeric mutation status was an independent determinant of stress oxygenation on multivariable analysis. Stress oxygenation was impaired in phenotype-negative sarcomeric mutation carriers (Sarc+P-, n=16) despite normal perfusion (Figure 1C, E). Sarcomeric HCM (Sarc+HCM) had more severe impairment in stress oxygenation than genotype negative HCM (G-HCM) and controls (Figure 1E). Figure 1 Conclusion In HCM, blunted stress-induced oxygenation is associated with an increased risk of ventricular arrhythmia and may represent a novel biomarker of arrhythmic risk. Sarcomeric mutation status is an important determinant of stress oxygenation response. Acknowledgement/Funding National Institute for Health Research Oxford Biomedical Centre and British Heart Foundation.

The relationship between the quantitative extent of late gadolinium enhancement and burden of nonsustained ventricular tachycardia in hypertrophic cardiomyopathy: A delayed contrast-enhanced magnetic resonance study.

To examine the relationship between late gadolinium enhancement (LGE) extent and nonsustained ventricular tachycardia (NSVT) characteristics in patients with hypertrophic cardiomyopathy (HCM). NSVT has been shown to be independently associated with sudden cardiac death (SCD) in HCM. Previous studies have found LGE on cardiac magnetic resonance (CMR) to be independently associated with NSVT. Seventy-three patients who had 14-day Holter monitoring for either risk stratification for SCD (n = 62) or evaluation of atrial fibrillation (n = 11) on a CMR study were included. Areas of LGE in left ventricle (LV) were visually identified and analyzed quantitatively for both high (≥6 SD above the mean signal intensity of normal myocardium) and intermediate (≥4 but <6 SD) LGE signal intensity. Patients with more extensive LGE had longer (P = 0.0028) and more frequent (P = 0.02) episodes of NSVT. In univariate analyses, frequency of NSVT was associated with LGE extent (rs = 0.43, P = 0.001), LV ejection fraction (rs = -0.38, P < 0.001), LV mass (rs = 0.32, P = 0.005), LV maximal wall thickness (rs = 0.28, P = 0.016), and left atrium diameter (rs = 0.29, P = 0.001); maximal length of NSVT was associated with LGE extent (rs = 0.52, P < 0.001), LV ejection fraction (rs = -0.44, P < 0.001), LV mass (rs = 0.37, P = 0.001), and left atrium diameter (rs = 0.3, P < 0.001). In multivariable analyses, LGE extent remained the sole variable independently associated with frequency (P = 0.001) and maximal length of episodes of NSVT (P = 0.001). No significant association was found between the rate of NSVT and LGE extent. LGE extent is independently associated with a greater burden and longer episodes of NSVT in HCM. These findings support the association between myocardial fibrosis as represented by LGE and ventricular tachyarrhythmias in HCM.

P3701Analysis of myocardial fibrosis using cardiac magnetic resonance T1 imaging and late gadolinium enhancement: Association with ventricular tachycardia in hypertrophic cardiomyopathy

P3701Analysis of myocardial fibrosis using cardiac magnetic resonance T1 imaging and late gadolinium enhancement: Association with ventricular tachycardia in hypertrophic cardiomyopathy

Associaton of elevated troponin levels with increased heart rate and higher frequency of nonsustained ventricular tachycardia in hypertrophic cardiomyopathy.

Associaton of elevated troponin levels with increased heart rate and higher frequency of nonsustained ventricular tachycardia in hypertrophic cardiomyopathy.

Left ventricular mechanical dispersion is associated with nonsustained ventricular tachycardia in hypertrophic cardiomyopathy

Objective: We assessed the value of speckle tracking two-dimensional (2D) strain echocardiography (2DSE) measured mechanical dispersion (MD) with other imaging and electrocardiographic parameters in differentiating hypertrophic cardiomyopathy (HCM) patients with and without nonsustained ventricular tachycardia (NSVT) on 24-h ambulatory ECG monitoring.Methods and results: We studied 31 patients with HCM caused by the Finnish founder mutation MYBPC3-Q1061X and 20 control subjects with comprehensive 2DSE echocardiography and cardiac magnetic resonance imaging (CMRI). The presence of NSVT was assessed from ambulatory 24-h ECG monitoring.NSVT episodes were recorded in 11 (35%) patients with HCM. MD was significantly higher in HCM patients with NSVT (93 ± 41 ms) compared to HCM patients without NSVT (50 ± 18 ms, p = 0.012) and control subjects (41 ± 16 ms, p < 0.001). MD was the only variable independently associated with the presence of NSVT (OR: 1.60, 95% CI: 1.05–2.45, p = 0.030). Assessed by ROC curves, MD performed best in differentiating between HCM patients with and without NSVT (AUC = 0.81).Conclusions: Increased mechanical dispersion was associated with NSVT in HCM patients on 24-h ambulatory ECG monitoring. Key messagesThe prediction of sudden cardiac death in hypertrophic cardiomyopathy remains a challenge and novel imaging methods are required to identify individuals at risk of malignant ventricular arrhythmias.Mechanical dispersion by speckle tracking echocardiography is associated with NSVT on 24-h ambulatory ECG monitoring in patients with hypertrophic cardiomyopathy

Ventricular tachycardia in hypertrophic cardiomyopathy with apical aneurysm successfully treated with left ventricular aneurysmectomy and cryoablation

A 64-year-old woman with type II diabetes mellitus was admitted to our institution with incessant ventricular tachycardia. She reverted to sinus rhythm after treatment with intravenous amiodarone, but the tachyarrhythmia recurred days later. Coronary angiography showed unobstructed coronary arteries. Left ventriculography ( Panel A , Supplementary material online, Video S1 ) revealed apical ballooning with mid-ventricular obstruction, suggestive of either large left ventricular (LV) apical aneurysm or stress (Takotsubo) cardiomyopathy. Transthoracic …

Non Sustained Ventricular Tachycardia in Hypertrophic Cardiomyopathy and New Ultrasonic Derived Parameters

The mechanism of sudden death in hypertrophic cardiomyopathy (HCM) is ventricular tachyarrhythmia emanating from myocyte disarray, fibrosis, and inhomogeneity in intramyocardial activation. Tissue synchronization imaging (TSI) allows the measurement of regional delay, while two-dimensional strain can be used to identify myocardial fibrosis. The aim of this study was to assess the relationship between new ultrasonically derived parameters and nonsustained ventricular tachycardia (NSVT) in patients with HCM. Ninety-three patients with HCM (mean age, 36 +/- 16 years) and 30 patients with hypertension with secondary left ventricular (LV) hypertrophy (mean age, 42 +/- 10 years; 65% men) were studied. All underwent standard echocardiographic, TSI, and two-dimensional strain examinations. Patients were followed every 3 months for 2 years. Holter monitoring was performed every 3 months. The primary endpoint was the occurrence of NSVT. Twenty-four patients (26%) had >or=1 episode of NSVT. Patients with NSVT had a higher value of maximal LV thickness (22 +/- 6 vs 19 +/- 5 mm, P = .04). There were no significant associations between NSVT on Holter monitoring and LV outflow gradient, New York Heart Association class, syncope, and medical therapy. N-terminal pro-brain natriuretic peptide values were significantly (P = .01) higher in patients with NSTV (1034 +/- 1088 vs 561 +/- 593 pg/mL). Patients with HCM and NSVT had (1) similar values on TSI-studied parameters to patients without NSVT, (2) significant reductions in basal and mid septal strain and in basal anterior-septal strain, and (3) more frequently peak systolic strain >or= -10% (P < .0001). In multivariate analysis, the presence of >3 LV segments with longitudinal two-dimensional strain >or= -10% (sensitivity, 81%; specificity, 97.1%; area under the curve, 0.944; P < .0001) was an independent predictor of NSVT. Using a simple, inexpensive, easily available, and bedside-usable tool, it was possible to recognize with good sensitivity and specificity patients with HCM at higher risk for NSVT.

Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients

Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients

Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients

ObjectivesThe aim of this study was to examine the characteristics of non-sustained ventricular tachycardia (NSVT) episodes during Holter monitoring and to determine their relationship to age and prognosis. BackgroundIt has been suggested that NSVT is only of prognostic importance in patients with hypertrophic cardiomyopathy (HCM) when repetitive, prolonged, or associated with symptoms. MethodsWe studied 531 patients with HCM (323 male, 39 ± 15 years). All underwent ambulatory electrocardiogram monitoring (41 ± 11 h). ResultsA total of 104 patients (19.6%) had NSVT. The proportion of patients with NSVT increased with age (p = 0.008). Maximum left ventricular wall thickness and left atrial size were greater in patients with NSVT. Mean follow-up was 70 ± 40 months. Sixty-eight patients died, 32 from sudden cardiac death (SCD). Twenty-one patients received an implantable cardioverter defibrillator (ICD). There were four appropriate ICD discharges. In patients ≤30 years (but not >30), five-year freedom from sudden death was lower in those with NSVT (77.6% [95% confidence interval (CI): 59.8 to 95.4] vs. 94.1% [95% CI: 90.2 to 98.0]; p = 0.003). There was no relation between the duration, frequency, or rate of NSVT runs and prognosis at any age. The odds ratio of sudden death in patients ≤30 years of age with NSVT was 4.35 (95% CI: 1.54 to 12.28; p = 0.006) compared with 2.16 (95% CI: 0.82 to 5.69; p = 0.1) in patients >30 years of age. ConclusionsNon-sustained ventricular tachycardia is associated with a substantial increase in sudden death risk in young patients with HCM. A relation between the frequency, duration, and rate of NSVT episodes could not be demonstrated.

Influence of left ventricular hypertrophy and function on the occurrence of ventricular tachycardia in hypertrophic cardiomyopathy.

Sixty-nine patients with hypertrophic cardiomyopathy were studied by 2-dimensional and Doppler echocardiography and 72-hour Holter monitoring to examine the relation between the degree of left ventricular (LV) hypertrophy and dysfunction and the occurrence of ventricular tachycardia (VT). Episodes of nonsustained VT were detected in 20 patients (29%). Maximal wall thickness was not different between patients with (22 +/- 5 mm) and without (21 +/- 5 mm) VT. Total hypertrophy score, calculated as the sum of 10 segmental wall thicknesses, was also similar in both groups (157 +/- 22 and 153 +/- 32 mm, respectively; p = not significant). Furthermore, no significant differences were found between the 2 groups in LV end-diastolic dimension (41 +/- 7 vs 40 +/- 6 mm), fractional shortening (33 +/- 7 vs 34 +/- 10%) and left atrial size (40 +/- 10 vs 41 +/- 11 mm). An LV outflow tract gradient was detected in 25% of patients with and 35% without VT (p = not significant). One or more Doppler indexes of diastolic function were abnormal in 70% of patients, but no difference in any of these indexes was found between those with and without VT. In summary, the occurrence of VT in hypertrophic cardiomyopathy is not related to the degree of LV hypertrophy, outflow tract gradient or dysfunction. This finding suggests a dissociation between the arrhythmogenic substrate and echocardiographic features of the disease.

Relation between extent of left ventricular hypertrophy and occurrence of ventricular tachycardia in hypertrophic cardiomyopathy

This study was undertaken to determine whether the occurrence of ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HC) is related to the magnitude and extent of left ventricular (LV) hypertrophy. Extent of LV hypertrophy was assessed using 2-dimensional echocardiography in 30 patients with HC in whom VT had been documented on 24-hour ambulatory electrocardiographic (ECG) monitoring, and the extent of LV hypertrophy in these patients was compared with that of a control group of 61 patients with HC who had normal ambulatory ECG recordings. Severe LV hypertrophy, involving at least 3 of the 4 LV segments, occurred significantly more often in patients with documented VT (16 of 30, 53%) than in those with normal ambulatory ECG findings (13 of 61, 21%; p < 0.002). Conversely, mild LV hypertrophy, involving only 1 LV segment, occurred significantly less often in patients with VT (5 of 30, 17%) than in the control subjects (32 of 61, 52%; p < 0.001). Moderate LV hypertrophy, involving 2 of the 4 LV segments, occurred about as frequently in patients with VT (9 of 30, 30%) as in patients with normal ambulatory ECG findings (16 of 61, 26%; p > 0.05). In addition, the LV wall thickness index, a quantitative measure of overall extent of LV hypertrophy, was also significantly higher (thereby indicating a greater magnitude of hypertrophy) in patients with documented VT (72 ± 17 mm) than in those with normal ambulatory ECG recordings (61 ± 14 mm; p < 0.005). It is concluded that data from this study show a strong association between magnitude of LV hypertrophy and occurrence of VT in patients with HC; these findings provide new insights into the components of the disease process associated with VT.