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Non-contrast T1 hypointense infarct cores (ICs) within infarcted myocardium detected using cardiac magnetic resonance imaging (CMR) T1 mapping may help assess the severity of left ventricular (LV) injury. However, because the relationship of ICs with chronic LV reverse remodeling (LVRR) is unknown, this study aimed to clarify it.Methods and Results: We enrolled patients with reperfused AMI who underwent baseline CMR on day-7 post-primary percutaneous coronary intervention (n=109) and 12-month follow-up CMR (n=94). Correlations between ICs and chronic LVRR (end-systolic volume decrease ≥15% at 12-month follow-up from baseline CMR) were investigated. We detected 52 (47.7%) ICs on baseline CMR by non-contrast-T1 mapping. LVRR was found in 52.1% of patients with reperfused AMI at 12-month follow-up. Patients with ICs demonstrated higher peak creatine kinase levels, higher B-type natriuretic peptide levels at discharge, lower LV ejection fraction at discharge, and lower incidence of LVRR than those without ICs (26.5% vs. 73.3%, P0.001) at follow-up. Multivariate logistic regression analysis showed that the presence of ICs was an independent and the strongest negative predictor for LVRR at 12-month follow-up (hazard ratio: 0.087, 95% confidence interval: 0.017-0.459, P=0.004). Peak creatine kinase levels, native T1 values at myocardial edema, and myocardial salvaged indices also correlated with ICs.ICs detected by non-contrast-T1 mapping with 3.0-T CMR were an independent negative predictor of LVRR in patients with reperfused AMI.

The 4-Fr catheter system is not recommended for invasive functional assessment of coronary artery stenosis, because it tends to distort the aortic waveform. This study aimed to identify the incidence of aortic waveform distortion and a feasible method for correct diagnosis of coronary artery stenosis with a 4-Fr catheter. We retrospectively investigated 178 lesions with intermediate coronary artery stenosis. Non-hyperemic distal coronary artery pressure (Pd) and aortic pressure (Pa) were measured with a 4-Fr diagnostic or 6-Fr guiding catheter before and after saline flush. The mean Pd/mean Pa (Pd/Pa) and instantaneous wave-free ratio (iFR) were calculated before and after flushing. We compared the effect of flushing on the changes in Pd/Pa and iFR between the 4-Fr diagnostic and 6-Fr guiding catheters. Using the 4-Fr diagnostic catheter, there was a significant decrease in incidence of aortic waveform distortion from 42.0% (47 lesions) before flushing to 1.8% (2 lesions) after flushing (p 0.001); the incidence was only 3.0% before saline flush and decreased to 0% after saline flush when using the 6-Fr guiding catheter. The presence of aortic waveform distortion influenced the iFR when the 4-Fr system was used. Functional measurements with the 4-Fr diagnostic catheter require adequate saline flush to remove the influence of aortic waveform distortion.

The purpose of this study was to clarify the characteristics of black-blood echo-planar imaging (BB-EPI) in the assessment of infarct-related myocardial edema (IRME), compared with T2-weighted imaging (T2WI). Thirteen acute myocardial infarction (MI) patients after reperfusion and 11 old MI patients underwent BB-EPI and T2WI, excluding those with posterior MI. In acute MI patients, signal intensity ratio (SI ratio) of edema to normal myocardium was measured. Black-blood echo-planar imaging revealed hyperintensity in the same region identified as IRME on T2WI in all acute MI patients, and SI ratio was significantly higher in BB-EPI (2.66 +/- 1.58) than in T2WI (1.44 +/- 0.22) (P0.05). However, BB-EPI showed hyperintensity in posterior wall, where there is no clinical evidence of acute MI, in 2 out of 13 acute MI patients. Both T2WI and BB-EPI detected no IRME in known old infarct area of all old MI patients, but BB-EPI showed hyperintensity in the posterior wall of 4 out of 11 old MI patients. Black-blood echo-planar imaging can depict IRME with sufficient suppression of background and blood flow signals, and with excellent edema-to-normal myocardium contrast resolution. However, BB-EPI sometimes shows an inconsistent signal area with T2WI specifically in posterior wall. The wide practical use of BB-EPI requires the solution to this serious problem.

Background Placental growth factor (PlGF), a homolog of vascular endothelial growth factor, is reported to stimulate angiogenesis and arteriogenesis in pathological conditions. It was recently demonstrated that PlGF is rapidly produced in myocardial tissue during acute myocardial infarction (MI). However, the effects of exogenous PlGF administration on the healing process after MI are not fully understood. The purpose of the present study was to examine whether PlGF treatment has therapeutic potential in MI. Methods and results Recombinant human PlGF (rhPlGF: 10 microg) was administered continuously for 3 days in a mouse model of acute MI. rhPlGF treatment significantly improved survival rate after MI and preserved cardiac function relative to control mice. The numbers of CD31-positive cells and alpha-smooth muscle actin-positive vessels in the infarct area were significantly increased in the rhPlGF group. Endothelial progenitor cells (Flk-1(+)Sca-1(+) cells) were mobilized by rhPlGF into the peripheral circulation. Furthermore, rhPlGF promoted the recruitment of GFP-labeled bone marrow cells to the infarct area, but only a few of those migrating cells differentiated into endothelial cells. Conclusions Exogenous PlGF plays an important role in healing processes by improving cardiac function and stimulating angiogenesis following MI. It can be considered as a new therapeutic molecule.

The aim of the present study is to clarify the roles of circulating ADAMTS13 and von Willebrand factor (VWF) in the formation of coronary artery thrombi in acute myocardial infarction (AMI). Twenty-six AMI patients, 37 age-matched healthy controls, and 20 young controls were studied. Plasma ADAMTS13 activity and levels of VWF antigen (VWF: Ag) and unusually large VWF multimer (UL-VWFM) were measured in the femoral vein (FV), aortic root (Ao), and coronary sinus (Cs) immediately before percutaneous coronary intervention (PCI) during the acute phase of AMI, as well as 6 months later. During the acute phase of AMI, plasma levels of VWF: Ag were similar in FV, Ao, and Cs, and were higher than those of age-matched control. In contrast, ADAMTS13 activity in three sampling points in AMI patients was similar to that of age-matched controls. Thus, the ratio of VWF: Ag to ADAMTS13 activity in the acute phase of AMI was significantly higher in all three sampled sites than that of age-matched controls. In the chronic phase, plasma levels of VWF: Ag, ADAMTS13 activity, and the ratio of VWF: Ag to ADAMTS13 activity were similar to those of age-matched controls. UL-VWFM was detected in the acute phase of AMI but not in the chronic phase. The present study showed that the plasma VWF: Ag levels are increased and ADAMTS13 activity is relatively decreased in both systemic and coronary circulation during the acute phase of AMI, suggesting that an imbalance between the enzyme and its substrate may play a role in the formation of occlusive thrombi in a coronary artery.

2015 AHA Effectiveness of Ethanol Infusion in the Vein of Marshall for Bidirectional Mitral Isthmus Block in Unsuccessful Cases with Conventional Ablation [Introduction] Treatment of mitral isthmus dependent atrial tachycardia (AT) requires bidirectional mitral isthmus (MI) block. It is usually difficult to achieve bidirectional MI block by endocardial linear ablation. When MI block is incomplete, additional ablation inside the coronary sinus (CS) is often required. The vein of Marshall (VOM) is located in the epicardial aspect of MI. The purpose of this study is to determine whether complete bidirectional MI block is obtained by ethanol infusion in the VOM in cases with incomplete MI block by conventional ablation. [Method] This study consisted of 38 consecutive patients who underwent conventional ablation to obtain bidirectional MI block from October 2013 to September 2014. [Results] In 24 patients (63%), bidirectional MI block was achieved by conventional ablation. In 11 patients (29%) of the other 14 patients, the CS venogram was performed to assess the presence or absence of the VOM. The VOM was imaged in 9 patients (24%), into which 100% ethanol was injected (2ml, 2-3times). After ethanol infusion in the VOM, bidirectional MI block was obtained in all cases (Figure). [Conclusion] Ethanol infusion in the VOM is an effective treatment in cases with incomplete MI block by conventional ablation.

Objectives Our aim was to investigate cardiac expression of placental growth factor (PlGF) and its clinical significance in patients with acute myocardial infarction (AMI). Background Placental growth factor is known to stimulate wound healing by activating mononuclear cells and inducing angiogenesis. The clinical significance of PlGF in AMI is not yet known. Methods Fifty-five AMI patients and 43 control subjects participated in the study. Peripheral blood sampling was performed on days 1, 3, and 7 after AMI. Blood was also sampled from the coronary artery (CAos) and the coronary sinus (CS), before and after acute coronary recanalization. Cardiac expression of PlGF was analyzed in a mouse AMI model. Results In AMI patients, peripheral plasma PlGF levels on day 3 were significantly higher than in control subjects. Plasma PlGF levels just after recanalization were significantly higher in the CS than the CAos, which indicates cardiac production and release of PlGF. Peripheral plasma levels of PlGF on day 3 were negatively correlated with the acute phase left ventricular ejection fraction (LVEF), positively correlated with both acute phase peak peripheral monocyte counts and chronic phase changes in LVEF. Placental growth factor messenger ribonucleic acid expression was 26.6-fold greater in a mouse AMI model than in sham-operated mice, and PlGF was expressed mainly in endothelial cells within the infarct region. Conclusions Placental growth factor is rapidly produced in infarct myocardium, especially by endothelial cells during the acute phase of myocardial infarction. Placental growth factor might be over-expressed to compensate the acute ischemic damage, and appears to then act to improve LVEF during the chronic phase.

Efonidipine can block both L- and T- type Ca2+ channels. In a previous in vitro study, we clarified that efonidipine dramatically suppresses aldosterone secretion from human adrenocortical tumor cells during angiotensin II (Ang II)- and K+-stimulation, whereas nifedipine, a dominant L-type Ca2+ channel antagonist, does not. This study was conducted to assess the in vivo effects of efonidipine and nilvadipine on the plasma aldosterone concentration. Placebo, 40 mg of efonidipine, or 2 mg of nilvadipine was administered to five healthy male volunteers. Hemodynamic parameters (pulse rate [PR] and blood pressure [BP]), plasma concentrations of neurohormonal factors (plasma renin activity, Ang II, aldosterone, and adrenocorticotropic hormone [ACTH]), and serum concentrations of Na+ and K+ were measured before and 6 h after administration of the agents. All three agents had little effect on PR and BP. Efonidipine and nilvadipine significantly increased plasma renin activity and Ang II. Both had little effect on ACTH, Na+, and K+. The plasma aldosterone concentration was significantly decreased after efonidipine treatment (88.3 +/- 21.3 to 81.6 +/- 24.9 pg/ml, p = 0.0407), whereas it was significantly increased after nilvadipine treatment (66.5 +/- 12.2 to 82.17 +/- 16.6 pg/ml, p = 0.0049). Placebo had little effect on neurohormonal factors. Efonidipine decreased plasma aldosterone concentration despite the increase in plasma renin activity and Ang II, suggesting that T-type Ca2+ channels may also play an essential role in the secretion of aldosterone in healthy human volunteers.

Background Although multislice spiral computed tomography (MSCT) is a promising technique for non-invasive coronary angiography, its usefulness in patients with stent implantation remains unclear. The aim of the present study was to compare the usefulness of MSCT with that of invasive coronary angiography for evaluating coronary stent patency. Methods and Results Thirty-one patients were enrolled after coronary stent implantation. Sixteen-slice MSCT scans were performed (39.0±21.8 days) before follow-up coronary angiography. After assigning an image score based on luminal visibility (1= poor, 2= fair, 3= good), factors determing image quality were analyzed. Among 42 implanted stents, 33 (78%) were assigned an image score of 3, 2 (5%) a score of 2, and 7 (17%) a score of 1. Image scores among stents with diameters ≥3.5 mm were significantly (p

Background— Renal dysfunction is commonly accompanied by a worsening of atherosclerosis; however, the underlying molecular mechanism is not fully understood. We examined the role played by soluble fms-like tyrosine kinase-1 (sFlt-1), an endogenous antagonist of the proatherogenic cytokine placental growth factor (PlGF), in the worsening of atherosclerosis in patients with renal dysfunction and in an animal model of renal failure. Methods and Results— In this study, 329 patients who received cardiac catheterization and 76 patients who underwent renal biopsy were enrolled. Both plasma sFlt-1 levels and renal sFlt-1 mRNA expression were positively correlated with estimated glomerular filtration rate ( P P Conclusions— The present study demonstrates that a reduction in the circulating levels of sFlt-1 is associated with the worsening of atherosclerosis that accompanies renal dysfunction.

Placental growth factor and vascular endothelial growth factor increase angiogenesis and promote healing after acute myocardial infarction (MI), but the significance of soluble Fms-like tyrosine kinase-1 (sFlt-1), an antagonist of placental growth factor and vascular endothelial growth factor, in the setting of acute MI has not been elucidated. The development of acute heart failure in the immediate period after MI is a dreaded complication, but there are no useful biomarkers that identify patients at risk of acute heart failure. We wished to investigate the clinical significance of circulating sFlt-1 during acute MI. We enrolled 174 patients with acute MI, and arterial blood sampling was performed. Plasma levels of sFlt-1 were measured by enzyme-linked immunosorbent assay and their relation to clinical parameters was analyzed. Circulating levels of sFlt-1 on admission were significantly increased in patients with acute MI compared to controls (528.1 +/- 290.9 vs 355.7 +/- 205.0 pg/ml, p

Placental growth factor (PlGF) is known to stimulate peripheral monocyte recruitment and enhance wound healing by inducing: arteriogeesis. However, clinical significance of PlGF in myocardial infarction (MI) has not been understood. We investigated the impact of PlGF on the clinical course in patients with acute MI. Methods and Results: 55 patients with acute MI were enrolled. Blood samples were collected from peripheral vein, coronary artery, and coronary sinus. Transcardiac gradient of PlGF was significantly higher just after coronary reperfusion (RC) than before RC (14.1 10.6 vs 0.0 1.1pg/ml p 0.01), indicating cardiac production and release of PlGF from acute infarct heart. Peak PlGF levels of MI patients were significantly higher than those of controls (35.1 26.5 vs 13.4 5.7 pg/ml, p 0.001), and positively correlated with peak monocyte counts (r 0.42, p 0.005). Furthermore, multiple regression analysis revealed that PlGF was the strongest independent predictor for the restoration of LVEF examined at 6-month follow-up study (p 0.0098). In mouse models of MI, tissue PlGF mRNA expression increased 26.6 fold compared with sham operated heart. Immunohistochemical staining showed that PlGF protein was over-expressed mainly in endothelial cells in the infarct region. CONCLUSION: PlGF is rapidly produced in the infarct myocardial tissue during acute phase of MI, and overexpressed PlGF seems to be involved in the improvement of left ventricular function in chronic phase probably by recruiting monocyte from bone marrow.