Reverse redistribution (RR) of 99mTc-sestamibi is observed after direct percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI). The purpose of this study was to clarify the functional characteristics of myocardial segments with RR after direct PTCA in AMI. Thirty patients with AMI who had undergone direct PTCA were examined. Myocardial perfusion tomography with 99mTc-sestamibi and low dose dobutamine echocardiography were performed within 2 weeks of the onset. The 99mTc-sestamibi images were obtained 1 and 3 h after tracer administration. The left ventricle was divided into nine segments, and regional 99mTc-sestamibi uptake and clearance were quantitatively evaluated in each segment. RR was defined as a decrease in 99mTc-sestamibi uptake of >10% on 3 h delayed images compared with the 1 h early images. The left ventricle in the echocardiographic images was also divided into nine segments corresponding to the scintigraphic images, and regional wall motion was assessed in the resting condition as the baseline and during dobutamine administration (5-10 microg x kg(-1) x min(-1)). Out of a total of 270 myocardial segments, 111 segments were perfused by the culprit coronary artery and were defined as ischaemic segments. There were 25 segments with RR and 86 segments without RR in the ischaemic myocardium. Enhanced clearance of 99mTc-sestamibi was observed in ischaemic segments with RR (P<0.001). Echocardiography demonstrated that 24 out of 25 segments with RR and 61 out of 86 segments without RR had wall motion abnormalities. Dobutamine infusion improved wall motion in 20 (83%) of the 24 dysfunctional segments with RR and 33 (54%) of the 61 dysfunctional segments without RR (P<0.02). These findings suggest that RR indicates reversible functional abnormalities associated with preserved contractile reserve in response to dobutamine. The early and delayed imaging of 99mTc-sestamibi provides useful information regarding the residual viability of the dysfunctional myocardium in AMI patients.

SUMMARYDespite a variety of biological roles for nitric oxide (NO) in the cardiovascular system, little is known about whether NO is involved in cardiac hypertrophy. We hypothesized that NO production following a sustained increase in shear stress by volumeoverload modifies the level of cardiac hypertrophy independent of hemodynamic changes. Volume-overload was induced by shunt formation between the left common carotid artery and the external jugular vein in 21 rabbits. These shunt rabbits were randomly assigned to 3 groups: shunt with no treatment (n=8), shunt treated with a low dose of N G -nitro-Larginine methyl ester (L-NAME, 0.5 g/L in drinking water, n=8), and shunt with a high dose of L-NAME (1.5 g/L, n=5). Eight sham operated rabbits were used as controls. Treatments were started immediately after operation and were continued for 6 weeks. Chronic volume-overload by shunt formation caused left ventricular dilatation and arterial enlargement proximal to the fistula. The relative wall thickness of the left ventricle was decreased, indicating eccentric cardiac hypertrophy. L-NAME elevated mean arterial blood pressure (P<0.01) and reduced the increment of cardiac output (P<0.05). L-NAME attenuated ventricular weight (P<0.01), ventricular cavity dilatation (P<0.01), and arterial enlargement (P<0.05). The re-capitulation of atrial natriuretic factor mRNA in the hypertrophied left ventricular myocardium by volume-overload was attenuated with L-NAME. In this model with chronic volume-overload, NO plays a pivotal role in the progression of cardiovascular remodeling by regulating the loading conditions of the heart. (Jpn Heart J 2003; 44: 127-137)

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Background Heart failure with preserved ejection fraction (HFpEF) is increasing with aging of the population, whereas the mechanisms of HFpEF remain poorly understood. It was reported that systemic inflammation is associated with pathophysiology of HFpEF. Lymphocyte-to-monocyte ratio (LMR) is a marker of systemic inflammation, which predicts clinical outcomes in various cancers. However, the prognostic value of LMR has not yet been elucidated in patients with HFpEF. Purpose The aim of this study was to investigate the impact of LMR on clinical outcomes in patients with HFpEF. Methods and results We prospectively analyzed 414 consecutive patients with HFpEF. Preserved EF was defined as an EF ≥50%. During a median follow-up period of 740 days, there were 111 major adverse cardiovascular events (MACE). When patients were divided into tertiles according to LMR, Kaplan-Meier analysis demonstrated that the low LMR was associated with the greatest risk for MACE. Multivariate Cox proportional hazard regression analysis showed that the low LMR was significantly associated with MACE after adjustment for confounding factors. Conclusions Low LMR could predict poor clinical outcomes in patients with HFpEF. LMR is a feasible marker for predicting MACE in patients with HFpEF.

Introduction Serum carboxy-terminal telopeptide of type I collagen (I-CTP) is a collagen degradation product of type I collagen in the extracellular matrix of the heart, blood vessels, and bone. The serum levels of I-CTP were reportedly a predictive marker for cardiac remodeling after acute myocardial infarction. However, it remains unclear whether I-CTP can predict poor clinical outcome in patient with acute coronary syndrome (ACS). Purpose The aim of this study was to investigate the association between serum levels of I-CTP and clinical outcome in patients with ACS. Methods Serum levels of I-CTP were measured in 200 patients with ACS who underwent percutaneous coronary intervention (PCI). All patients were prospectively followed during the median follow-up period of 1312 days with the end point of major adverse cardiovascular events (MACE). We divided the patients into tertiles according to serum I-CTP level: low I-CTP group (≤4.4 ng/ml, n=72), middle I-CTP group (4.4–6.4 ng/ml, n=65), and high I-CTP group (≥6.5 ng/ml, n=63). Results There were 44 MACE, including 24 all-cause death and 9 rehospitalization due to heart failure. I-CTP was significantly higher in patients with MACE than those without (4.90 [interquartile range (IQR): 3.80–6.38] ng/ml vs. 6.65 [IQR: 5.00–10.08] ng/ml, p&lt;0.001). Kaplan-Meier analysis demonstrated that patients in the highest tertile of I-CTP had the greatest risk of MACE. In a univariate analysis, age, Albumin, estimated glomerular filtration rate (eGFR), low-density lipoprotein cholesterol (LDL-C), brain natriuretic peptide (BNP), high-sensitivity C-reactive protein (hsCRP) and I-CTP were significant predictors of MACE. A multivariate Cox proportional hazard analysis showed that the high I-CTP group had a higher risk for MACE (Hazard ratio [HR] 2.6, p=0.049) compared with the low I-CTP group after adjusting for confounding factors. Conclusions I-CTP was significantly associated with MACE, suggesting that I-CTP could be a reliable marker for clinical outcome in patients with ACS who underwent PCI. Figure 1 Funding Acknowledgement Type of funding source: None