Omentin Prevents Myocardial Ischemic Injury Through AMP-Activated Protein Kinase- and Akt-Dependent Mechanisms

ObjectivesThis study examined the impact of omentin on myocardial injury in a mouse model of ischemia/reperfusion (I/R) and explored its underlying mechanisms.BackgroundObesity is a major risk factor for ischemic heart disease. Omentin is a circulating adipokine that is down-regulated by obesity.MethodsIn patients who underwent successful reperfusion treatment after acute myocardial infarction, cardiac function and perfusion defect were assessed by using scintigraphic images. Mice were subjected to myocardial ischemia followed by reperfusion.ResultsThis study found that high levels of plasma omentin were associated with improvement of heart damage and function after reperfusion therapy in patients with acute myocardial infarction. Systemic administration of human omentin to mice led to a reduction in myocardial infarct size and apoptosis after I/R, which was accompanied by enhanced phosphorylation of AMP-activated protein kinase (AMPK) and Akt in the ischemic heart. Fat-specific overexpression of human omentin also resulted in reduction of infarct size after I/R. Blockade of AMPK or Akt activity reversed omentin-induced inhibition of myocardial ischemic damage and apoptosis in mice. In cultured cardiomyocytes, omentin suppressed hypoxia/reoxygenation-induced apoptosis, which was blocked by inactivation of AMPK or Akt.ConclusionsOur data indicate that omentin functions as an adipokine that ameliorates acute ischemic injury in the heart by suppressing myocyte apoptosis through both AMPK- and Akt-dependent mechanisms

Adenosine-Sensitive Focal Reentrant Atrial Tachycardia Originating From the Mitral Annulus-Aorta Junction

Adenosine-sensitive reentrant atrial tachycardia (AT) has been recognized to originate from the confined area of either the right or left atiroventricular nodal regions. We describe a case with adenosine-sensitive focal AT which was successfully ablated at the uncommon focus located at the mitral annulus-aorta junction. The mode of AT initiation during the atrial extrastimulus suggested as the mechanism tachycardia reentry; AT was terminated by a bolus of 2 mg of adenosine 5’-triphosphate. These electrophysiological features are possibly associated with a substrate involved in the mitral annulus-aorta junction with node-like properties that is responsive to adenosine

Left Ventricular Dyssynchrony in Patients with Moderate Coronary Stenosis and Border Line Fractional Flow Reserve

The cutoff values of fractional flow reserve (FFR) to detect physiological myocardial ischemia are still controversial. Some studies have reported that left ventricular (LV) dyssynchrony occurs in patients with coronary artery disease (CAD). The purpose of this study was to investigate LV dyssynchrony in patients with moderate coronary stenosis and borderline FFR, using stress electrocardiographically-gated myocardial perfusion single-photon emission computed tomography (SPECT). The study population comprised 10 patients with moderate (50–75% diameter) stenosis and an FFR in the range 0.75–0.90, who were compared to 10 control subjects. All underwent stress myocardial 99mTc-sestamibi (MIBI) or tetrofosmin SPECT imaging. The regional time to end systole (TES), time to peak ejection (TPE), and time to peak filling (TPF) were obtained as indexes of perfusion and function, using gated SPECT (pFAST) in combination with Cardio Gated SPECT Regional Assessment for LV Function (cardioGRAF). The dyssynchrony index (DI) was also calculated. The DI of post-stress TES was significantly greater than that of rest in patients with moderate CAD (4.8 ± 2.8 vs. 2.7 ± 1.5, P = 0.01), but there were no significant differences in the control subjects (3.0 ± 1.7 vs. 2.9 ± 1.9, P = 0.99). There were no significant differences in TPE and TPF between the groups. In conclusion, LV dyssynchrony may occur after stress in patients with coronary stenosis and borderline FFR, even without a significant reduction in perfusion

Novel Technique to Facilitate Defibrillator Lead Implantation via Cephalic Vein Cutdown by Means of a Reference Catheter and a Specially Designed Long Sheath

The cephalic vein is recommended as the access route for an implantable cardioverter defibrillator lead to avoid complications associated with subclavian vein puncture; however, cephalic vein cutdown is not necessarily preferred, mainly because of procedural complexity. To facilitate cephalic vein cutdown, we have devised the following method. An 8 Fr catheter is placed in the cephalic vein over a guidewire inserted percutaneously from the left peripheral cephalic vein. The catheter, which is palpable beneath the skin prior to incision, indicates the location of the cephalic vein, facilitating its isolation. A specially designed 9 Fr tear-away sheath-dilator unit is used to place leads. With its long-tapered and curved tip, the unit is easy to insert, even when the cephalic vein is stenotic or tortuous. The 30-cm-long sheath reaches the right atrium, and thus the lead is advanced directly to the right atrium without risk of vascular injury. This technique may be feasible in the majority of patients and can even be used by inexperienced implanters

Percutaneous Cardiopulmonary Support System for the Treatment of Fulminant Myocarditis

We have developed a simple percutaneous cardiopulmonary support (PCPS) system. The circuit of the system is set up and sterilized beforehand and can be used promptly in an emergency situation. We used the PCPS on three patients with fulminant myocarditis and treated them successfully. Case 1 was a 53-yr-old man and Case 2 was a 12-yr-old girl. They had failed to respond to treatment of their circulatory states with conventional therapy. Their circulatory states improved dramatically after application of PCPS with 2 L/min blood flow. They were weaned from PCPS after 107 and 227 hours use, respectively. Case 3 was a 37-yr-old woman who developed ventricular fibrillation which was resistant to drug therapy and cardioversion. After starting PCPSwith4 L/min blood flow, arrhythmia disappeared and her circulatory state improved. She was successfully weaned after 39-hour of PCPS. Patients with fulminant myocarditis fall into circulatory collapse which is resistant to conventional therapy, but there is a possibility that cardiac function will recover after the acute phase of myocarditis. Therefore, PCPS can be the only treatment of the circulatory collapse of fulminant myocarditis, which is refractory to conventional therapy