A case of percutaneous septal myocardial ablation in a patient with obstructive hypertrophic cardiomyopathy with accessory mitral valve tissue.

Accessory mitral valve tissue (AMVT) is a rare congenital anomaly that sometimes causes left ventricular outflow tract (LVOT) obstruction. We report the case of a 72-year-old woman with hypertrophic obstructive cardiomyopathy (HOCM) complicated by AMVT. The patient presented at our hospital with palpitations and shortness of breath. Transthoracic echocardiography revealed a diagnosis of HOCM and an abnormal structure inside the LVOT. Transesophageal echocardiography revealed an AMVT. We initially treated the patient with oral medication, but due to side effects, the patient could not take the target dose and her symptoms did not improve. We suggested surgical treatment, but the patient refused. By evaluating the relationship between AMVT and the surrounding tissues using three-dimensional transesophageal echocardiography, we determined that percutaneous septal myocardial ablation (PTSMA) might be successful. The first PTSMA was not effective, but the second procedure showed significant improvement in the pressure gradient and symptoms. The patient with HOCM and concomitant AMVT had a severe LVOT pressure gradient, and PTSMA was performed with excellent results. Since we experienced a rare case and were able to treat it percutaneously, we report our findings in relation to the literature. Learning objective: This case study highlights successful use of percutaneous septal myocardial ablation (PTSMA) in treating a patient with hypertrophic obstructive cardiomyopathy (HOCM) and accessory mitral valve tissue (AMVT). The key objective is to understand PTSMA can be an effective treatment option for HOCM with Type IIa AMVT, characterized by the attachment only to the mitral leaflets, when surgical intervention is not preferred, enhancing management of this rare condition.

Swallowing-induced Paroxysmal Atrial Tachycardia Causes Weight Loss and Fainting during Mealtime: A Case Report and Literature Review.

Swallow or deglutition syncope is an unusual disorder. We herein report an 80-year-old man with paroxysmal atrial tachycardia induced by swallowing, causing syncope. Initially, we suspected a digestive disorder and found no significant findings. Finally, a swallowing test with monitoring of the heart rate and blood pressure helped in the diagnosis. The patient was treated with antiarrhythmic drugs and catheter ablation. The mechanism underlying swallowing-induced tachycardia presumably involves mechanical stimulation of the esophagus and autonomic nervous system effects. However, few cases have been reported, and the exact mechanism remains unclear.

Pathophysiological characteristics and responsiveness to neurohormonal antagonism in idiopathic dilated cardiomyopathy patients with antihepatitis C virus antibody.

A high prevalence of hepatitis C virus (HCV) infection has been reported among idiopathic dilated cardiomyopathy (DCM) patients. We examined the prevalence of DCM patients with HCV antibody, and the pathophysiological characteristics and responsiveness to neurohormonal antagonism in DCM with HCV. HCV antibodies were determined in 540 patients with cardiac diseases. In 117 DCM patients, clinicopathologic data were evaluated before and 1 year after angiotensin converting enzyme inhibitor and/or beta-blocker (ACE-inhibitor/BB) administration and their prognosis was followed-up for a mean of 72 +/- 41 months. HCV antibodies were found in 12 of 135 DCM patients (8.9%) and in 37 of 405 patients without DCM (9.1%) (P = NS). At baseline, contrary to DCM without HCV, DCM with HCV was associated (P < 0.05) with greater left ventricular (LV) end-diastolic and end-systolic dimension, LV mass, and myocardial diameter in endomyocardial biopsy, and lower % fractional shortening. By multivariate analysis, HCV infection was independently associated with larger LV end-systolic dimension among DCM patients (P = 0.005). The advanced LV dilatation and hypertrophy in DCM with HCV decreased more in response to the ACE-inhibitor/BB therapy compared to DCM without HCV. There were no differences between DCM patients with and without HCV in survival and cardiac event-free rates. In summary, although HCV infection appears not to be the specific cause of DCM, HCV may enhance ventricular remodeling leading to heart failure among DCM patients. Nevertheless, the advanced ventricular remodeling with HCV was adequately reversed by neurohormonal antagonism, and did not lead to an unfavorable outcome.