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Objective: To examine the effects of eplerenone, a selective aldosterone blocker, on cardiac function after myocardial infarction (MI) and myocardial remodelling related transcriptional factors and mRNA expression in non-infarcted myocardium. Methods: MI was induced by ligation of the coronary artery in Wistar rats. Rats were randomly assigned to a vehicle treated group or an eplerenone treated group (100 mg/kg/day). Results: At four weeks after MI, left ventricular (LV) end diastolic pressure, LV weight, and LV end diastolic dimension were increased in MI rats. Eplerenone significantly reduced the increase in LV end diastolic pressure, LV weight, and LV end diastolic dimension. In the MI rats the decreased ejection fraction indicated systolic dysfunction and the increased E wave to A wave ratio and E deceleration rate indicated diastolic dysfunction. Eplerenone significantly attenuated this systolic and diastolic dysfunction. Myocardial interstitial fibrosis, transcriptional activities of activator protein 1 and nuclear factor κB, and mRNA expression of monocyte chemoattractant protein 1, plasminogen activator inhibitor 1, atrial natriuretic peptide, brain natriuretic peptide, and collagen types I and III were significantly increased at four weeks after MI. Eplerenone significantly attenuated interstitial fibrosis and suppressed transcriptional activity and mRNA expression of these genes. Conclusions: When administered after MI, eplerenone prevents cardiac remodelling accompanied by systolic and diastolic dysfunction and inhibits abnormal myocardial transcriptional activities and gene expression.

Background: It is well known that angiotensin converting enzyme (ACE) inhibitors and angiotensin II type 1 (AT1) receptor blockers (ARBs) prevent left ventricular (LV) remodelling after myocardial infarction (MI). However, it is still not clear whether inhibition of the AT1 receptor is enough to prevent LV remodelling after MI. Objective: To elucidate the effects of ACE inhibitors that are not mediated by the AT1 receptor on LV remodelling, MI was experimentally induced in wild-type (WT-MI) mice and AT1 receptor knockout (KO-MI) mice. Methods: Mice were divided into six groups: WT-control, KO-control, WT-MI, KO-MI, WT-MI treated with an ACE inhibitor, and KO-MI treated with an ACE inhibitor. Four weeks after MI, cardiac function was assessed by Doppler echocardiography and non-infarcted myocardial mRNA expression by northern blot analysis. Results: Cardiac function decreased significantly in the MI groups compared with the sham operated groups. Additionally, in the MI groups end diastolic dimension, E wave velocity, the ratio of peak velocity of E wave to A wave, deceleration rate of E wave, and mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, and collagens I and III increased significantly compared with the sham groups. LV remodelling after MI was prevented in KO-MI mice compared with WT-MI mice. ACE inhibitor administration significantly attenuated progressive LV remodelling in both WT and KO-MI groups. Conclusion: ACE inhibitors can prevent the LV remodelling process that accompanies cardiac dysfunction after MI, even in AT1 KO mice. These findings suggest that ACE inhibitors prevent LV remodelling after MI by mechanisms other than inhibition of angiotensin AT1 receptor mediated effects.

Objectives: To clarify the value of cycle dependent variation of myocardial integrated backscatter (CV-IB) analysis, which non-invasively measures acoustic properties of the myocardium, for early detection of cardiac involvement in patients with sarcoidosis. Methods: The study population consisted of 22 consecutive patients with biopsy proven sarcoidosis who did not have any abnormal findings on conventional two dimensional echocardiogram. Cardiac sarcoidosis was diagnosed by radionuclide testing including thallium-201 scintigraphy, gallium-67 scintigraphy, and cardiac fluorine-18-deoxyglucose positron emission tomography. The magnitude and delay of the CV-IB were analysed in the basal mid septum and the basal mid posterior wall of the left ventricle of all patients. Results: The patients were divided into two groups: 8 patients with cardiac involvement and 14 patients without cardiac involvement. In the basal septum, a major reduction in the magnitude (mean (SD) 1.8 (4.4) v 6.6 (1.3), p = 0.012) and an increase in the time delay (1.3 (0.5) v 1.0 (0.1), p = 0.038) of CV-IB were observed in patients with cardiac sarcoidosis even in the absence of two dimensional echocardiographic abnormalities. The sensitivity for detecting cardiac involvement was such that the magnitude of CV-IB in the basal septum discriminated 75% of patients with cardiac sarcoidosis from those with non-cardiac sarcoidosis, whereas two dimensional echocardiographic parameters did not discriminate between these two groups. Conclusions: The CV-IB is decreased in the basal septum in patients with cardiac sarcoidosis even in the absence of two dimensional echocardiographic abnormalities. Analysis of CV-IB may be a useful method to detect early myocardial involvement in patients with sarcoidosis.

To investigate whether concentrations of plasma adiponectin constitute a significant coronary risk factor, with particular focus on the relation between plasma concentrations of adiponectin and the development of acute coronary syndrome (ACS).Plasma concentrations of adiponectin were measured in 123 patients with coronary artery disease (CAD) and in 17 control participants. Patients were divided into three groups according to condition type: acute myocardial infarction (AMI) group (n = 59), unstable angina pectoris (UAP) group (n = 28), and stable angina pectoris (SAP) group (n = 36).Plasma concentrations of adiponectin correlated negatively with body mass index (r = -0.18, p0.05), serum triglyceride (r = -0.25, p0.01), and fasting glucose concentrations (r = -0.21, p0.05), but correlated positively with age (r = 0.26, p0.01), high density lipoprotein cholesterol concentrations (r = 0.35, p0.01), and low density lipoprotein particle size (r = 0.37, p0.01). Plasma concentrations of adiponectin in patients with ACS, in both the AMI and UAP groups, were significantly lower than those in patients with SAP and in the control group (ACS, 6.5 (3.0) microg/ml; SAP, 11.3 (5.9) micro g/ml; control 12.8 (4.3) microg/ml; p0.01). Additionally, plasma concentrations of adiponectin in patients with CAD (7.9 (4.6) microg/ml, p0.01) were significantly lower than in the control group. There were, however, no significant differences between patients with SAP and the control group (p = 0.36). Multiple logistic regression analysis showed that smoking, fasting glucose concentration, and low log adiponectin concentration correlated independently with the development of an ACS.The findings suggest that measurement of plasma concentrations of adiponectin may be of use for assessing the risk of CAD and may be related to the development of ACS.

Objective: To evaluate the acute effects on haemodynamic variables of biatrial pacing in comparison with high right atrial (HRA) pacing and left lateral atrial pacing. Patients and design: 23 patients were paced from the HRA site, the lateral site of the coronary sinus (CS), and both sites on two fixed atrioventricular delays (100 and 150 ms) during atrioventricular sequential pacing at 80 and 100 beats/min in random order. Main outcome measures: After five minute pacing, the maximum P wave duration on a 12 lead ECG, cardiac output, pulmonary capillary wedge pressure, and the transmitral flow pattern by transthoracic echocardiography were measured. Results: Biatrial pacing delivered the shortest P wave duration (133 (25) ms, 133 (27) ms, and 96 (15) ms during HRA, CS, and biatrial pacing, respectively; p < 0.001), and the most improvement in cardiac output and pulmonary capillary wedge pressure (3.71 (0.93) l/min and 15 (7) mm Hg, 3.79 (0.97) l/min, and 14 (6) mm Hg, and 4.09 (1.01) l/min and 13(6) mm Hg during HRA, CS, and biatrial pacing, respectively; p < 0.01). Biatrial pacing most significantly decreased the intervals between the atrial pacing spike and the peak and end of the atrial filling wave (186 (16) ms and 250 (22) ms, 172 (19) ms and 242 (24) ms, and 153 (15) ms and 227 (23) ms during HRA, CS, and biatrial pacing, respectively; p < 0.001). It also significantly increased the mitral flow time velocity integral and peak atrial filling wave velocity (7.5 (3.4) cm and 63.8 (17.6) cm/s, 7.8 (3.0) cm and 62.4 (16.6) cm/s, and 8.3 (3.4) cm and 67.8 (19.3) cm/s during HRA, CS, and biatrial pacing, respectively; p < 0.05). The improvements in haemodynamic variables were especially remarkable in patients who had a longer interatrial conduction delay. Conclusions: Biatrial pacing yielded the most significant improvements in haemodynamic variables. These haemodynamic benefits may play a part in reducing intra-atrial pressure and preventing atrial fibrillation.

Objective: To evaluate the feasibility of quantifying low temperature radiofrequency catheter ablation (RFCA) lesions using a phased array intracardiac echocardiography (ICE) catheter—with better tissue penetration and in a deflectable device—in the canine model. Intervention: Low temperature radiofrequency (RF) energy (50–60°C at up to 40 W) was delivered to the left ventricle in 11 beagles for 60 seconds, using an 8 French catheter with a deflectable tip and a 4 mm distal electrode. Main outcome measures: Comparison of the width and depth of RFCA lesions measured by ICE with pathological findings. Results: 33 RF energies were delivered in 11 dogs. 31 lesions (94%) were confirmed at necropsy. 27 of 31 ablation lesions (87%) were detected by ICE. The mean (SD) width and depth of the ICE detected lesions were 10.4 (2.6) mm and 5.7 (1.9) mm, respectively. Pathological findings showed that RFCA lesions consisted of inner and outer layers. Macroscopically, the mean (SD) width and depth of the inner layers were 7.6 (2.3) mm and 3.6 (1.2) mm and those for the whole layers were 10.0 (2.8) mm and 5.3 (1.5) mm, respectively. Microscopically, the inner and outer layers corresponded to necrotic and oedematous areas, respectively. The ICE detected lesion size had better correlation with the pathological measurements of the whole layers in width (r = 0.911) and in depth (r = 0.756). Conclusion: The real time evaluation of RFCA lesion size using the phased array ICE is feasible, even with a low temperature RF application. However, ICE slightly overestimates RFCA lesion size compared with pathological necrotic lesion size.

Objective To investigate the specificity and sensitivity of the combination of redistribution in exercise thallium-201 single photon emission computed tomography (SPECT) and exercise induced ST elevation for detecting the viable myocardium in patients with acute myocardial infarction. Design 37 patients were studied within seven weeks of onset of Q wave myocardial infarction (anterior in 22, inferior in 15). All patients underwent exercise four hour redistribution thallium-201 SPECT and positron emission tomography using fluorine-18-fluorodeoxyglucose (FDG) and nitrogen-13 ammonia under fasting conditions. Results Sixteen patients showed exercise induced ST elevation ⩾ 1.5 mm, and 15 of these had increased FDG uptake in the infarct region. Eleven of 16 patients (10 of 11 patients with anterior infarctions) with irreversible thallium-201 defects and increased FDG uptake showed exercise induced ST elevation. The sensitivity, specificity, and predictive accuracy of redistribution, exercise induced ST segment elevation, or both for detecting increased FDG uptake were 82%, 75%, and 67% (94%, 75%, and 91% for anterior infarctions), respectively. Conclusions In patients with acute Q wave myocardial infarction, the combination of redistribution in exercise thallium-201 SPECT and exercise induced ST elevation can detect the viable myocardium in the infarct region with high sensitivity and specificity, especially in patients with anterior infarctions.

Objective—To investigate the relations between myocardial metabolism and the kinetics of thallium-201 in myocardial scintigraphy. Methods—46 patients within six weeks after the onset of acute myocardial infarction underwent resting myocardial dual isotope, single acquisition, single photon emission computed tomography (SPECT) using radioiodinated 15-iodophenyl 3-methyl pentadecaenoic acid (BMIPP) and thallium-201, exercise thallium-201 SPECT, and positron emission tomography (PET) using nitrogen-13 ammonia (NH3) and [F18]fluorodeoxyglucose (FDG) under fasting conditions. The left ventricle was divided into nine segments, and the severity of defects was assessed visually. Results—In the resting SPECT, less BMIPP uptake than thallium-201 uptake was observed in all of 40 segments with reverse redistribution of thallium-201, and in 21 of 88 segments with a fixed defect of thallium-201 (p

Recently, the relation between coronary arterial remodelling and ischaemic coronary disease has become a focus of investigation.1 Positive coronary arterial remodelling has been shown to be more frequent in acute coronary syndromes, including acute myocardial infarction (AMI), whereas negative remodelling has been shown to be more frequent in stable angina.2 However, in the case of AMI, preceding clinical presentations of the onset vary among patients and it is well known that patients often undergo episodes of unstable or stable angina.3 Furthermore, no studies have correlated remodelling and the presence of prodromal symptoms. In this study intravascular ultrasound (IVUS) was performed before coronary intervention to evaluate the possible correlation between the arterial remodelling at the culprit lesion site of AMI and the prodromal symptoms. Ninety four consecutive patients presenting with their first AMI were considered for entry into this study. AMI was diagnosed on the basis of coronary angiography, ECG, prolonged chest pain (> 30 minutes), and subsequent elevation of creatine kinase. Twenty two of these patients were excluded because of either an inability to make the IVUS catheter pass across the lesion before angioplasty (n = 5), no proximal reference site defined due to a large side branch (n = 4), or poor ultrasound image quality (n = 13). Finally, 72 patients (60 men, …