Pacemaker Treatment for Apical Hypertrophic Cardiomyopathy in the Setting of an Apical Ventricular Aneurysm

Toyoda, Shigeru; Ida, Keitaro; Kitagawa, Yusuke; Kamijima, Toru; Saito, Ikuta; Nishino, Seiji; Sakuma, Masashi; Ohki, Gaku; Naito, Shigeto; Inoue, Teruo

doi:10.1016/j.jaccas.2021.06.006

Cited by 1 publication

(1 citation statement)

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“…Since the last outpatient echocardiogram four years ago, untreated apical stress likely prompted the development of a left ventricular (LV) aneurysm in our patient. Novel techniques like guidewire measurement of high intracavitary pressure gradients have been proposed as a possible diagnostic tool for myocardial degeneration, aneurysm formation, and arrhythmogenic changes in apHCM [ 6 ]. Medical management for apHCM and aneurysm prevention are uniform, constituting beta-blockers as a first-line option and non-dihydropyridine calcium channel blockers as the second-line option [ 3 ].…”

Section: Discussionmentioning

confidence: 99%

Apical Hypertrophic Cardiomyopathy Prompting Aneurysm, Thrombus, and Cardiac Arrest in a 56-Year-Old Female

Biskupski¹,

Osella²,

Bhaskaran³

et al. 2022

Cureus

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Hypertrophic cardiomyopathy (HCM) is the most prevalent genetic cardiac disease while apical hypertrophic cardiomyopathy (apHCM) is a rare subset of HCM. The significance of this case report is to present apHCM, its chronological course, and its association with left ventricular aneurysm, thrombosis, and cardiac arrest. We present the case of a 56-year-old female with a past medical history of apHCM who was admitted for substernal chest pain, developed a ventricular storm (VT), and subsequently suffered cardiac arrest; resuscitation of spontaneous circulation (ROSC) was eventually achieved after 10 minutes. It was initially thought that her arrhythmia and hemodynamic decompensation were purely secondary to cocaine use at a party six hours prior to her presentation. During hospitalization, cardiac magnetic resonance imaging demonstrated a severe apHCM apical aneurysm, thrombosis, and a re-entrant circuit as a likely cause of this patient’s decompensation and eventual cardiac arrest. After several days of hemodynamic stability and decreased dependence on intravenous antiarrhythmic medication infusions, she was extubated and transitioned to oral amiodarone and beta-blocker therapy with the implantation of a cardioverter-defibrillator (ICD). In this case, we analyze the continuum of apHCM, a rare subset of HCM once thought to be benign but with the emergence of complications, including aneurysm, thrombus formation, resistant ventricular tachycardia, and cardiac arrest. Recognition and management of apHCM with medical and/or surgical intervention are therefore critical to prevent the aforementioned sequela.

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Section: Discussionmentioning

confidence: 99%