A case of Left Ventricular Apical Aneurysm with Ventricular Tachycardia and Congestive Heart Failure Detected 17 Years after the Diagnosis of Apical Hypertrophic Cardiomyopathy.

Background: Increasing penetration of high spatial resolution cardiovascular magnetic resonance (CMR) imaging into routine cardiovascular practice has resulted in more frequent identification of a subset of hypertrophic cardiomyopathy (HCM) patients with thin-walled, scarred left ventricular (LV) apical aneurysms. Prior experience involved relatively small numbers of patients with short follow-up and therefore the risk associated with this subgroup remains incompletely defined. Therefore, we assembled a large HCM cohort with LV apical aneurysms and long-term follow-up in order to clarify clinical course and prognosis. Methods and Results: Of 2,400 HCM patients, 60 (2.5%) were identified by CMR with LV apical aneurysm, 24 to 86 years of age, including 19 (32%) <45 years old; 70% male, and followed for 5.6 ± 3.5 years. Over the follow-up period, 24 patients experienced 31 adverse disease-related complications including: appropriate implantable cardioverter-defibrillator discharge for VT/VF (n=11), received or listed for heart transplant (n=6), heart failure death (n=5), nonfatal thromboembolic events (n=4), resuscitated out-of-hospital cardiac arrest (n=3), and sudden death (n=2). In addition, an intracavitary thrombus was identified in the apical aneurysm in 9 patients without a thromboembolic history. Combined HCM-related death and aborted life threatening event rate was 8.6% per year, nearly 6-fold greater than the 1.5% annual mortality rate reported in the general HCM population. Conclusions: Patients with LV apical aneurysms represent a high-risk subgroup within the diverse HCM spectrum, associated with substantial increased risk for disease-related morbidity and mortality, including advanced heart failure, thromboembolic stroke and sudden death. Identification of this unique HCM phenotype should prompt consideration for primary prevention ICD, and anticoagulation for stroke prophylaxis.

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Sustained Ventricular Tachycardia in Apical Hypertrophic Cardiomyopathy, Midcavitary Obstruction, and Apical Aneurysm

Pacing and Clinical Electrophysiology ◽

10.1111/j.1540-8159.2007.00753.x ◽

2007 ◽

Vol 30 (6) ◽

pp. 799-803 ◽

Cited By ~ 12

Author(s):

NEIL K SANGHVI ◽

CYNTHIA M TRACY

Keyword(s):

Ventricular Tachycardia ◽

Hypertrophic Cardiomyopathy ◽

Sustained Ventricular Tachycardia ◽

Apical Hypertrophic Cardiomyopathy ◽

Apical Aneurysm

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Ventricular tachycardia and heart failure in a patient of mid‑ventricular obstructive hypertrophic cardiomyopathy with apical aneurysm: A case report

Experimental and Therapeutic Medicine ◽

10.3892/etm.2019.7796 ◽

2019 ◽

Author(s):

Xin Zhang ◽

Xingbin Liu

Keyword(s):

Heart Failure ◽

Ventricular Tachycardia ◽

Case Report ◽

Hypertrophic Cardiomyopathy ◽

Obstructive Hypertrophic Cardiomyopathy ◽

Apical Aneurysm

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Myocardial infarction complicating management of congestive heart failure in a dog

Journal of the American Animal Hospital Association ◽

10.5326/15473317-32-1-68 ◽

1996 ◽

Vol 32 (1) ◽

pp. 68-72 ◽

Cited By ~ 3

Author(s):

TC DeFrancesco ◽

CE Atkins ◽

BW Keene

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Congestive Heart Failure ◽

Ventricular Tachycardia ◽

Mitral Valve Regurgitation ◽

Sudden Onset ◽

Left Ventricular ◽

Mixed Breed ◽

Rare Diagnosis ◽

Echocardiographic Evidence

A 7.5-kg, 10-year-old, spayed female, mixed-breed dog was evaluated for sudden onset of weakness, tachypnea, and an irregular cardiac rhythm. Congestive heart failure secondary to mitral valve regurgitation had been diagnosed six weeks earlier. The dog was stable on furosemide, enalapril, and hydralazine. Complex ventricular tachycardia, altered QRS conformation of sinus complexes, echocardiographic evidence of a hypokinetic left-ventricular free wall, and elevated creatine kinase suggested a diagnosis of myocardial infarction. Despite antiarrhythmic therapy, the dog developed ventricular fibrillation and died 36 hours after admission. Postmortem examination confirmed the myocardial infarction. Although a rare diagnosis in the veterinary patient, myocardial infarction must be considered in the differential diagnosis for sudden onset of weakness, tachypnea, and ventricular tachycardia.

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Cardiac remodelling and heart failure symptoms in patients with apical hypertrophic cardiomyopathy

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jeaa356.391 ◽

2021 ◽

Vol 22 (Supplement_1) ◽

Author(s):

M Rosca ◽

D Ciuperca ◽

L Mandes ◽

M Trofin ◽

A Calin ◽

...

Keyword(s):

Heart Failure ◽

Hypertrophic Cardiomyopathy ◽

Mitral Regurgitation ◽

Wall Thickness ◽

Contractile Function ◽

Left Ventricular ◽

Cardiac Remodelling ◽

Apical Hypertrophic Cardiomyopathy ◽

Significant Difference ◽

The Impact

Abstract Funding Acknowledgements Type of funding sources: None. Background Although earlier publications suggested a more benign clinical course for patients (pts) with apical hypertrophic cardiomyopathy (ApHCM), recent studies report increased morbidity and mortality, comparable to the prognosis of other HCM variants. Moreover, information regarding cardiac remodelling and its relationship with symptoms in pts with ApHCM is scarce. The aim of our study was to assess left ventricular (LV), right ventricular (RV) and left atrial (LA) remodelling in pts with ApHCM in comparison with non-apical variants of HCM (nonApHCM), and the impact of cardiac remodelling on heart failure symptoms. Methods One hundred fifty-one consecutive pts with HCM (52 ± 16 yrs, 47% men) in sinus rhythm and with preserved LV ejection fraction (16 pts with ApHCM and 135 pts with nonApHCM), were prospectively enrolled. Comprehensive echocardiography was performed in all, including the measurement of maximal LV wall thickness (LVWT), RV free wall thickness (RVWT) and maximal LA volume indexed to body surface area (LAVi). Global LV strain (ɛ), RVɛ, LAɛ and end-diastolic LA strain rate (ASr) were measured using speckle-tracking echocardiography (STE). The ratio of E to average e’ was used to estimate LV filling pressure. The degree of mitral regurgitation (1/2/3) has also been assessed. Heart failure symptoms were defined according to the New York Heart Association (NYHA) classification. Results Forty-eight pts in nonApHCM group had intraventricular obstruction. There were no significant differences between pts with and without ApHCM regarding: age (58 ± 20 vs 52 ± 16 yrs), gender distribution, RVWT, LVɛ (-14.9 ± 2.7 vs -13.9 ± 3.5 %), RVɛ (-19.6 ± 3.6 vs -10.0 ± 5.0%), LAɛ (19.2 ± 5.8 vs 16.4 ± 7.1%)(p > 0.05 for all). Pts with ApHCM had lower values for LVWT (17.2 ± 1.9 vs 21.4 ± 5.2 mm, p = 0.002), E/e’ (12.0 ± 5.8 vs 17.6 ± 8.5, p = 0.02) and LAVi (48 ± 16 vs 61 ± 25, p = 0.03) compared to pts with nonApHCM. Pts with ApHCM had slightly better LA contractile function as assessed by ASr (-1.23 ± 0.50 vs -0.97 ± 0.49 sec-1, p = 0.05). Mitral regurgitation was more often severe in nonApHCM pts (56/42/31 vs 10/4/0, p < 0.001). There was no significant difference between the percentage of symptomatic pts (NYHA class ≥2) in ApHCM vs nonApHCM group (p = 0.3). In the ApHCM group, symptomatic pts had significantly lower ASr compared to asymptomatic pts (-0.98 ± 0.35 vs -1.61 ± 0.46 sec-1, p = 0.01). Conclusions Despite of lower LVWT values, less severe MR and no obstruction, pts with apical HCM have similar prevalence of heart failure symptoms, and similar LV, RV and LA dysfunction compared to pts with non-apical HCM. Symptomatic pts with apical HCM have worse LA contractile function compared to asymptomatic pts.

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