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.

Increased expression of endothelial lipase in rat models of hypertension.

OBJECTIVE: To gain a better understanding of the involvement of endothelial lipase (EL) in vascular disease, we examined whether the EL expression is regulated in animal models of hypertension. METHODS: The rat cDNA homologue of EL was identified using reverse transcription-polymerase chain reaction. Cultured rat aortic smooth muscle cells were stimulated with angiotensin II (Ang II) and phorbol 12-myristate 13-acetate (PMA), and EL mRNA expression was analyzed by Northern blotting. EL mRNA levels in tissues from stroke-prone spontaneously hypertensive rats (SHR-SP) and Ang II-induced hypertensive rats were evaluated using RNase protection assays. RESULTS: Rat EL cDNA encoded a protein containing 493 amino acid residues including a signal peptide, and shares 91.9% and 80.9% sequence homology with murine and human EL, respectively. Northern blotting revealed that EL was expressed in a wide range of rat tissues. In cultured rat aortic smooth muscle cells, Ang II and PMA increased EL mRNA levels by 2.9- and 3.3-fold, respectively. In Ang II-induced hypertensive rats, EL expression was upregulated in the aorta, heart, and lung. In SHR-SP, EL expression was upregulated in the aorta and heart. CONCLUSION: EL expression is increased in rat models of hypertension. Thus, EL might have a role in the local pathophysiology of vascular diseases.

Endothelial lipase modulates monocyte adhesion to the vessel wall. A potential role in inflammation.

Endothelial lipase (EL), a new member of the lipoprotein lipase gene family, plays a central role in high density lipoprotein metabolism. Previous studies indicated that EL is expressed in endothelial cells, macrophages, and smooth muscle cells in atherosclerotic lesions in human coronary arteries. However, the functional role of EL in the local vessel wall remains obscure. In this study, we evaluated the ability of EL to modulate monocyte adhesion to the endothelial cell surface. EL mRNA and protein levels were markedly increased in tissues of the mouse model of inflammation induced by lipopolysaccharide injection. Adhesion assays in vitro revealed that overexpression of EL in COS7 or Pro5 cells enhanced monocyte bindings to the EL-expression cells. Heparin or heparinase treatment inhibited EL-mediated increases of monocyte adhesion in a dose-dependent manner. Moreover, ex vivo adhesion assays revealed that the number of adherent monocytes on aortic strips was significantly increased in EL transgenic mice and decreased in EL knock-out mice as compared with wild-type mice. These results suggest that EL on the endothelial cell surface can promote monocyte adhesion to the vascular endothelium through the interaction with heparan sulfate proteoglycans. Thus, the up-regulation of EL by inflammatory stimuli may be involved in the progression of inflammation.