Publications by authors named "Hisaaki Komaki"

Background: Progranulin is a secreted glycoprotein that regulates inflammation and wound healing. However, plasma progranulin levels in the acute phase and their clinical significance in patients with acute myocardial infarction (AMI) remain to be elucidated.

Objective: We aimed to investigate the relationship between the increase in plasma progranulin levels in the acute phase and the recovery of left ventricular function in the chronic phase in AMI patients.

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Article Synopsis
  • * In patients with lower left ventricular ejection fraction (LVEF < 50%), plasma levels of miR-143 and miR-145 were even higher, indicating a possible relationship between these microRNAs and heart function deterioration.
  • * There was an inverse correlation between miR-143 and miR-145 levels and LVEF, while both microRNAs were positively correlated with features of heart dysfunction, such as LV dilation and elevated BNP levels, suggesting they may play a role in heart disease progression.
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Bow hunter syndrome is a rare condition characterized by repetitive syncope, which is reflected in brain stem ischaemia due to vertebral compression induced by head rotation. We herein report a rare presentation of bow hunter syndrome due to severe stenosis of the left subclavian artery with a thoracic aortic aneurysm. Disease, hypoplasia of the vertebral artery, or degenerative bone disease as well as congenital foraminal narrowing can be causative.

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Article Synopsis
  • MicroRNA-143 and -145 are non-coding RNAs found in heart muscle cells, and their roles in acute myocardial infarction (AMI) patients were studied for the first time.
  • In a study involving 25 AMI patients and 20 controls, researchers measured plasma levels of these microRNAs on admission (Day 0) and again on Day 7 post-admission, finding significant increases in AMI patients.
  • The rise in microRNA-143 levels from Day 0 to Day 7 was linked to better recovery of heart function, suggesting it could serve as a biomarker for recovery in AMI patients.
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Objective: This study aimed to investigate the effect of combination of high-salt intake and hypertension on renal functional and histological damage, associated with renal (pro)renin receptor [(P)RR] and AT1 receptor in rats.

Methods: Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) received regular rat chow (normal-salt diet 0.9%) or high-salt rat chow (high-salt diet 8.

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We describe a 41-year-old man with a prior history of myocardial infarction, whose surface 12-lead electrocardiogram did not show typical left bundle-branch block pattern or wide QRS complex. However, electrophysiological study showed distinct left ventricular electrical conduction delays. The surface 12-lead electrocardiogram modified to the paper at 50 mm/s and double standard (20 mm equals 1 mV) revealed obvious notches of the terminal forces of the QRS in leads II, III, aVL, aVF, V3, V4, V5, and V6, these might be partially consistent with left ventricular electrical conduction delay in the scar lesion of the infero-posterior of the ventricle.

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We examined whether the stimulation of the angiotensin II AT1 receptor increases the expression of the cardiac (pro)renin receptor ((P)RR) and its downstream signals and whether the blockade of the angiotensin II AT1 receptor by azilsartan decreases the expression of the cardiac (P)RR and its signaling in spontaneously hypertensive rats (SHRs) with a high-salt intake. Rats received normal-salt (0.9%) chow, high-salt (8.

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In some patients with Kawasaki disease, a prior myocardial infarction causes ventricular tachycardia in the chronic post-myocardial infarction phase. We report the case of a 41-year-old man with symptomatic and haemodynamically unstable ventricular tachycardia in whom substrate ablation was performed for the ventricular tachycardia before insertion of an implantable cardioverter-defibrillator.

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Objective: A high salt intake causes hypertension and leads to cardiovascular disease. Therefore, a low salt diet is now recommended to prevent hypertension and cardiovascular disease. However, it is still unknown whether an excessively low salt diet is beneficial or harmful for the heart.

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Objective: It has not yet been fully elucidated whether cardiac tissue levels of prorenin, renin and (P)RR are activated in hypertension with a high salt intake. We hypothesized that a high salt intake activates the cardiac tissue renin angiotensin system and prorenin-(pro)renin receptor system, and damages the heart at an early stage of hypertension.

Methods: Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) received regular (normal-salt diet, 0.

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