The findings of this study demonstrate that epicardial and endocardial activation can be discordant in specific regions and that discordance increases with abnormal activation sequences. Many of the differences in the epicardial and endocardial activation can be correlated with the heterogeneity of the anatomic architecture of the right atrium. The study also demonstrates that reentry can occur in a three-dimensional plane using the epicardial and endocardial surfaces connected by transmural muscle fibers.

NOGAMI A et al.(5) View the monitor during imaging During imaging, the heart rate must be continuously monitored using a pulse oximeter or an ECG monitor. (6) Prepare for unexpected situations It should be ensured that the room is equipped with an electrical defibrillator to be used in an emergency, if necessary. A hospital manual for handling unexpected situations should be established. In addition, it should be kept in mind that the threshold and lead resistance need to be re-measured after imaging and the mode needs to be returned to the original setting.Recommendations are shown in Table 6. Electrophysiology StudiesThe clinical significance of induced arrhythmia depends on the underlying heart disease, type of arrhythmia, and induction protocol. Electrophysiology studies are considered less useful in patients with frequent premature ventricular contraction (PVCs) without structural heart disease.

A bdominal aortic aneurysm (AAA) is a common vascular disease, which occurs in ≈4% to 8% of men aged 65 to 80 years.1 Aortic rupture is the most feared clinical consequence of AAA progression, resulting in mortality in ≈90% of cases. [2][3][4] Because AAA usually progresses without symptoms, AAA is often discovered in advanced stage. At present, surgical aortic replacement and endovascular stent graft repair are performed as standard definitive therapies for AAA. However, there is no effective medical therapy to prevent aortic rupture in AAA. Although several studies have reported the pathophysiology of AAA, the mechanisms of AAA formation are largely unknown. Therefore, it is necessary to investigate the molecular pathophysiology of AAA to find noninvasive strategies for the prevention of AAA.Iron is an essential element for maintaining physiological function. However, excess iron causes tissue damage by oxidative stress via the Fenton/Haber-Weiss reaction. 5Therefore, iron is involved in the pathophysiology of several diseases including cardiovascular diseases. In fact, we have previously shown that iron accumulation and superoxide production are observed in the renal tubules of a rat model of chronic kidney disease.6 Lee et al 7 have shown that iron accumulation is observed in the atherosclerotic lesions of apolipoprotein E knockout mice. Most recently, Martinez-Pinna et al 8 have demonstrated that iron is deposited in human AAA walls. Meanwhile, we have also reported that dietary iron restriction (IR) prevents the development of hypertension and proteinuria with inhibition of oxidative stress and inflammation in Dahl salt-sensitive hypertensive rats.9 Although oxidative stress and inflammation are well known to be involved in the development of AAA formation, it has not been investigated whether iron is associated with the pathophysiology of AAA through © 2015 American Heart Association, Inc. Objective-Although iron is an essential element for maintaining physiological function, excess iron leads to tissue damage caused by oxidative stress and inflammation. Oxidative stress and inflammation play critical roles for the development of abdominal aortic aneurysm (AAA). However, it has not been investigated whether iron plays a role in AAA formation through oxidative stress and inflammation. We, therefore, examined whether iron is involved in the pathophysiology of AAA formation using human AAA walls and murine AAA models. Approach and Results-Human aortic walls were collected from 53 patients who underwent cardiovascular surgery (non-AAA=34; AAA=19). Murine AAA was induced by infusion of angiotensin II to apolipoprotein E knockout mice. Iron was accumulated in human and murine AAA walls compared with non-AAA walls. Immunohistochemistry showed that both 8-hydroxy-2′-deoxyguanosine and CD68-positive areas were increased in AAA walls compared with non-AAA walls. The extent of iron accumulated area positively correlated with that of 8-hydroxy-2′-deoxyguanosine expression area and macrophage infiltration area in huma...

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The minimal cardiopulmonary bypass (mini-CPB) circuit, a closed system with neither cardiotomy suction nor an open venous reservoir and thus no air-blood interface, reportedly reduces blood loss and inflammatory reactions associated with coronary bypass surgery. We evaluated the inflammatory reactions in patients in whom coronary bypass operations were performed with conventional CPB or mini-CPB (n=15 each). Interleukin (IL)-6, IL-8, and neutrophil elastase levels; the neutrophil count; and the C-reactive protein value were measured before and immediately after surgery and on postoperative days 1 and 2. In addition, intraoperative blood loss and the transfusion volume were evaluated in these groups. Neutrophil elastase levels were lower in the mini-CPB group than in the conventional group on postoperative days 1 (127 +/- 52 vs. 240 +/- 100 microg/l, P=0.013) and 2 (107 +/- 17 vs. 170 +/- 45 micro/l, P=0.0001), as was the IL-8 level on postoperative day 1 (8.3 +/- 6.4 vs. 19 +/- 11 pg/ml, P=0.016). The intraoperative blood loss and transfusion volumes were significantly lower in the mini-CPB group than in the conventional group (510 +/- 244 vs. 1046 +/- 966 ml, P=0.012, and 691 +/- 427 vs. 1416 +/- 918 ml, P=0.0033). Thus, mini-CPB appears to attenuate neutrophil activation and cytokine release after coronary bypass surgery and, in addition, has some beneficial effects on blood conservation.

In patients with paroxysmal AF related to aortic valve disease and/or coronary artery disease, a dilated left atrium (≥45 mm) was associated with inferior AF- and event-free survival after PVI, accompanied by persistent abnormalities in cardiac and haemodynamic function. These findings may assist patient selection for PVI during AVR and/or CABG.

Background:In chronic aortic regurgitation, eccentric hypertrophy, with combined concentric hypertrophy of the left ventricle, is an important adaptive response to volume overload, which in itself is a compensatory mechanism for permitting the ventricle to normalize its afterload and to maintain normal ejection performance (physiologic hypertrophy). However, progressive dilatation of the left ventricle leads to depressed left ventricular 0.V) contractility and myocardial structural changes, including cellular hypertrophy and interstitial fibrosis (pathological hypertrophy).Hypothesis: The study was undertaken to determine the relationship between left ventricular myocardial structure and contractile function in 14 patients with chronic aortic regurgitation by cardiac catheterization and endomyocardial biopsies.Methods: Myocardial cell diameter and percent interstitial fibrosis were obtained from biopsy samples. Contractile function was evaluated from the ratio of end-systolic wall stress to end-systolic volume index (ESSESVI) and the ejection fraction-end-systolic stress (EF-ESS) relationship, which was obtained from 30 normal control subjects.Resulrs: Myocardial cell diameter correlated significantly with the ESVI (r = 0.72, p

Intraleaflet haemorrhage was frequently observed in the valve leaflets of degenerative AS and associated with a rapid progression of AS.