I have taken over a job of editor-in-chief, International Heart Journal since January 1st, 2013 from Dr. Ryozo Nagai.
International Heart Journal was first published bimonthly as The Japanese Heart Journal in 1960. International Heart Journal had published manuscripts on clinical and experimental cardiovascular research that originated mainly from Japan. Submissions from countries outside Japan have increased and exceeded those from Japan in 2001, and the percentage of foreign submissions reached 66% in 2004. To reflect the increasing international significance of the Journal, The Japanese Heart Journal has been renamed as the International Heart Journal since January 2005.
We are now planning to change the International Heart Journal to be a more international and high impact journal.
We are looking forward to your continued interest and support for the Journal.

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Previous studies based on coronary angiography or computed tomography coronary angiography have demonstrated a high prevalence of coronary stenosis in patients with cerebral infarction and no prior history of coronary artery disease (CAD). The purpose of the present study was to compare the coronary angiographic findings of patients with prior cerebral infarction with those of patients with no prior cerebral infarction. Consecutive patients (n = 126) who underwent a first coronary angiography for suspected CAD but had no prior history of CAD were classified into 2 groups, those with a clinical history of cerebral infarction (cerebral infarction group) and those without a clinical history of cerebral infarction (noncerebral infarction group). The incidences of diabetes mellitus, peripheral artery disease, coronary stenosis, and multivessel disease were significantly higher in the cerebral infarction group than in the noncerebral infarction group. Multiple logistic regression analysis relating to coronary stenosis identifi ed prior cerebral infarction (P = 0.0027, odds ratio = 4.414) and diabetes mellitus (P = 0.0446, odds ratio = 2.619) as explanatory factors. Thirty-four of 78 patients (44%) with coronary stenosis did not have angina symptoms. Multiple logistic regression analysis regarding the lack of angina symptoms identified motor dysfunction (modified Rankin scale ≥ 2) (P = 0.0028, odds ratio = 8.323) as an explanatory factor. The results of the present study suggest that compared with patients without cerebral infarction those with the disorder have a high prevalence of coronary stenosis, and indicate that the development of angina symptoms is influenced by the severity of motor dysfunction.

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Previous intravascular ultrasound studies have shown that echolucent neointimal hyperplasia occasionally appears after bare-metal stent (BMS) or sirolimus-eluting stent (SES) implantation. Optical coherence tomography (OCT) studies have also demonstrated that paclitaxel-eluting stent (PES) restenosis exhibited similar images showing low signal intensity areas (LSIA) surrounding stent struts and three-layer appearance (TLA). The aim of the present study was to investigate the clinical significance of LSIA on OCT images in various types of stents. Fifty nine consecutive patients who underwent scheduled follow-up coronary angiography and OCT were enrolled. There was no significant difference in the prevalence of LSIA among the 3 stent groups (BMS 30%, SES 19%, PES 28%, P = 0.70). LSIA thickness was larger in the PES group than in the other stent groups (BMS 0.51 ± 0.21 mm, SES 0.35 ± 0.06 mm, PES 0.87 ± 0.19 mm, P < 0.01). The ratio of LSIA thickness to the neointimal thickness was also larger in PES compared with other stents (BMS 53 ± 9 %, SES 57 ± 8 %, PES 77 ± 5 %, P < 0.01). Also, LSIA thickness in patients with in-stent restenosis (ISR) was significantly larger than in those without ISR (0.37 ± 0.37 mm versus 0.12 ± 0.26 mm, P = 0.048). Our results suggest that LSIA might be involved in excessive neointimal formation, and that the healing response after PES implantation might be different from BMS or SES.

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Together with aging of the Japanese population, aortic valve replacement (AVR) for aortic stenosis (AS) is now becoming more and more common in the elderly. When the aortic annulus is too small to allow an adequate sized prosthetic valve, aortic root enlargement is required to avoid prosthesis-patient mismatch (PPM). However, age-related comorbidities including aortic root calcification bring significant risk in performing aortic root enlargement. In the present study, 40 patients aged 75 years or more who underwent AVR for AS were reviewed to determine whether moderate PPM has a negative impact on the long-term results. Operative mortality occurred in 2 patients (5%) and moderate PPM occurred in 8 patients. There was no significant difference in survival between cases with and without PPM (P = 0.87). Both aortic pressure gradient (PG) and left ventricular mass index (LVMI) measured by echocardiography were signifi cantly decreased in patients with and without PPM. Reduction of PG was significantly greater in patients with PPM than without PPM (P = 0.02). Reduction of LVMI was not different between the groups (P = 0.58). Moderate PPM did not negatively influence survival or reduction of PG or LVMI in patients aged 75 years or older who underwent AVR for AS.

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The effect of beta-blockers in treating Japanese heart failure (HF) patients with preserved left ventricular (LV) ejection fraction (EF) is unclear. This prospective observational study enrolled 1,682 Japanese HF patients who received carvedilol for the first time. Patients were followed for a mean of 1.6 years. The 1,492 patients with baseline LVEF measurements were allocated to the following groups: reduced EF (LVEF < 40%; n = 724), borderline EF (LVEF 4050%; n = 355), and preserved EF (LVEF ≥ 50%; n = 413). Baseline characteristics, New York Heart Association (NYHA) class, change in B-type natriuretic peptide (BNP) level, and long-term outcome were compared among the groups. Patients with preserved EF were more likely to be older, female, and have ischemic etiology and hypertension than patients with reduced EF. Carvedilol maintenance dosage was lower in patients with preserved EF (7.9 mg/day versus 6.6 mg/ day). NYHA class and BNP level were lower in patients with preserved EF at baseline but improved to the same level in all groups at 6 months. After adjusting for baseline characteristics, the hazard ratio for death or hospitalization due to cardiovascular disease in patients with preserved EF versus those with reduced EF was 1.031 (P = 0.847). This study elucidated the characteristics of HF patients given carvedilol in “real world” clinical settings. A comparative controlled study is necessary to elucidate whether the improvements in NYHA and BNP as well as the outcome profile observed in patients with preserved EF were caused by the favorable effects of carvedilol.

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Marfan syndrome (MFS) is an inherited connective tissue disorder mainly caused by the fibrillin-1 mutation. Deficient fibrillin-1 is thought to result in the failed sequestration of transforming growth factor β (TGFβ) and subsequent activation of the TGFβ signaling pathway, suggesting that the circulating TGFβ level may be elevated in MFS, although its accurate measurement is complex due to ex vivo release from platelet stores upon platelet activation. We measured the plasma TGFβ1 levels of 32 Japanese MFS patients (22 medically untreated, 10 treated, 20 males, 30.1 ± 9.6 years old) and 30 healthy volunteers (19 males, 29.5 ± 5.8 years old) by ruthenium-based electrochemiluminescence platform (ECL). PF4 was also measured by enzyme immunoassay (EIA) as a platelet degranulation marker. There was no significant difference in the mean plasma TGFβ1 level between the MFS group (1.31 ± 0.40 ng/mL) and controls (1.17 ± 0.33 ng/mL) (P = 0.16, NS). Also, there was no significant difference between the untreated (1.24 ± 0.37 ng/mL) and treated (1.46 ± 0.45 ng/mL) MFS patients (P = 0.15, NS). We also measured PF4, which showed wide deviations but no significant difference between the two groups (P = 0.50). A difference in circulating TGFβ1 levels between MFS patients and controls was not detected in this Japanese population. Circulating TGFβ1 is not a diagnostic and therapeutic marker for Japanese MFS patients, although our findings do not eliminate the possible association of TGFβ with the pathogenesis of MFS.

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Premature arteriosclerosis may be one of the mechanisms linking pre-diabetes mellitus (pre-DM) and cardiovascular disease. We sought to characterize premature arteriosclerosis in pre-DM using different arterial stiffness indices and to find the independent contributors of this process. We recruited 33 patients without DM, 53 patients with pre-DM, and 34 subjects with DM. Both the compliance index (CI) and stiffness index (SI) were measured. Patients with pre-DM and DM had lower CI (3.8 ± 2.1 versus 5.2 ± 3.0 units; P < 0.05 and 3.6 ± 1.8 versus 5.2 ± 3.0 units; P < 0.05, respectively) and higher SI (8.0 ± 2.0 versus 6.7 ± 1.6 m/s; P < 0.01 and 9.4 ± 2.3 versus 6.7 ± 1.6 m/s; P < 0.001, respectively) than patients without DM. Using multivariate linear regression analysis, age, heart rate, and HOMA index were independent determinants for SI (whole model: R² = 0.47, P < 0.001), whereas male gender, hsCRP, and HOMA index were independent determinants for CI (whole model: R² = 0.34, P < 0.01). The HOMA index was an independent determinant for arterial stiffness. Increased insulin resistance may associate with increased arterial stiffness at peripheral arteries in pre-DM patients.

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This paper describes a subanalysis of the JART Study comparing rosuvastatin and pravastatin treatment. A total of 314 subjects were analyzed in this subanalysis, 282 of whom were eligible for evaluation of the relationship between LDL-C and carotid mean-IMT change. In the subanalysis, we evaluated the extent to which intensive lipid-lowering therapy slowed the mean-IMT progression by a correlation analysis between LDL-C and mean-IMT change after 12 months of statin treatment. Nearly half were male (49.4%) and elderly (49.7%). The majority (84.4%) were treated for primary prevention. Patients with hypertension and diabetes mellitus accounted for 65.3% and 44.0%, respectively. At the 12-month measurement point, mean-IMT change was correlated with LDL-C (R = 0.187; P = 0.0016), LDL-C/ HDL-C ratio (R = 0.152; P = 0.0105), and non-HDL-C (R = 0.132; P = 0.0259). Mean-IMT after 12 months was divided into 4 subgroups by LDL-C at 12 months; < 80, ≥ 80 to < 100, ≥ 100 to < 120, and ≥ 120 mg/dL. A trend analysis using the Jonckheere–Terpstra test showed statistical signifi cance (P = 0.0002). Even for prevention in Japanese patients who have lower risk of atherosclerotic disease than Western patients, lowering the LDL-C level to below the therapeutic target prevented mean-IMT progression after 12 months more strongly. These findings suggest that more intensive control of LDL-C to levels lower than those in current JAS guidelines should be required to achieve slowing of progression as well as induction of regression of atherosclerosis.

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Cardiac fibroblasts (CFs) produce extracellular matrix (ECM) which is a potent regulator of heart cell function and growth, and provides a supportive microenvironment for heart cells. Therefore, CF-derived ECM produced in vitro is very suitable for heart-cell culturing and cardiac tissue engineering. The aim of this study was to investigate the effect of CF-derived ECM produced in vitro on the growth and metabolism of cultured ventricular cells. CF-derived ECM-coated cell culture dishes were prepared by culturing rat CFs and then decellularizing the cultures. Isolated neonatal rat ventricular cells were seeded on ECM-coated, collagen I-coated or uncoated dishes, and the growth of cells after 1-5 days of culture was assayed with MTT reagent. In addition, cellular metabolic activity was analyzed by spectrophotometric methods and protein levels of sarco(endo)plasmic reticulum Ca²⁺-ATPase type 2a (SERCA2a) by Western blotting. The relative growth of ventricular cells was better on ECM-coated than on uncoated or collagen I-coated dishes. Furthermore, the glucose consumption ratio, lactic acid production ratio, Na⁺/K⁺-ATPase activity, SERCA activity and protein levels of SERCA2a were all higher in cells on the ECM-coated dishes. In conclusion, cardiac fi broblast-derived ECM produced in vitro stimulates the growth and metabolism of cultured ventricular cells. This study indicates that the bioactivity of the ECM supports heart cell growth in vitro, and this might be useful for cardiac tissue engineering.

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It is important for myocardial infarction patients to undergo immediate reperfusion of the affected coronary artery. In order to improve the prognosis, efforts to shorten the door to balloon time to within 90 minutes have been made. However, conventional methods such as faxing electrocardiograms (ECG) have not become widespread due to their high cost and lack of sharpness of the ECG. The “Doctor Car” (rapid response car system) of Kitasato University Hospital is now equipped with a Mobile Cloud ECG system. With this system, 12-lead ECG data obtained in the field are transmitted to the cloud server via a standard mobile telephone network. Since it uses an existing phone network, the cost of this system is low and it is fairly reliable. Cardiologists at the hospital read the ECG waveforms on the cloud server and decide whether emergency cardiac catheterization is necessary. In our fi rst case using this Mobile Cloud ECG system, the door to balloon time could be shortened.

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Chronic kidney disease (CKD) is often complicated with advanced heart failure because of not only renal congestion and decreased renal perfusion but also prolonged use of diuretics at higher doses, which sometimes results in hyponatremia. Preoperative CKD is known to be associated with poor prognosis after heart transplantation (HTx). We experienced a stage D heart failure patient with CKD and hyponatremia who was switched from trichlormethiazide to tolvaptan. His hyponatremia was normalized, and his renal function was improved after conversion to tolvaptan. In patients with stage D heart failure, it may be useful to administer tolvaptan with a concomitant reduction in the dose of diuretics in order to preserve renal function and avoid hyponatremia before HTx.

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A 67-year-old woman with asthma visited our hospital with increasing dyspnea and new-onset paresthesia and purpura in her legs. Physical examination showed a wheeze, pretibial edema, and surrounding purpura. Chest X-rays showed cardiac decompensation and an electrocardiogram revealed a new ST-T change. Laboratory data showed leukocytosis, hypereosinophilia (10,450/μL), troponin T(+), elevated BNP, and markedly elevated eosinophil cationic protein (ECP) (> 150 ng/mL). Echocardiography revealed diffuse left ventricular hypokinesis (ejection fraction 30%) with increased wall thickness. Coronary angiography was normal. Cardiac magnetic resonance imaging implied diffuse myocardial edema and subendocardial late gadolinium enhancement. Skin biopsy of purpura showed superfi cial perivascular dermatitis with remarkable eosinophilic infiltrations. No evidence of drug allergies, parasitic infection, or myeloproliferative disorder was detected. Based on these findings, a diagnosis of eosinophilic myocarditis due to Churg-Strauss syndrome was considered. She was administered prednisolone at a dose of 1 mg/kg, cyclophosphamide, and diuretics. Several markers of eosinophilic myocarditis and heart failure gradually improved, including ECP. She was discharged 30 days later with no cardiac event. Eosinophilic myocarditis is characterized by predominantly eosinophilic infi ltration. Eosinophilic granule proteins, such as ECP and major basic protein, play important roles in the pathogenesis of eosinophilic myocarditis. We experienced a rare case of eosinophilic myocarditis due to Churg-Strauss syndrome. Markedly elevated ECP played an important role in the early diagnosis and subsequent reduction in ECP served as a marker of monitoring. In an asthmatic patient with dyspnea, hypereosinophilia, and vasculitis, Churg-Strauss syndrome with eosinophilic myocarditis should be considered.

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Simulation studies have been performed in attempts to elucidate the signifi cance of shear and tissue stresses in the progression and rupture of coronary artery plaques, but few studies have analyzed both stresses simultaneously. We analyzed the distributions of shear stress and tissue stress in a model of coronary artery plaque based on intravascular ultrasound data by fluid-structure interaction finite element analysis under physiological pressure and flow. As shown in previous studies, the region of peak shear stress was observed at the proximal side of the plaque where flow velocity was high but its value was at most 10 Pa. On the other hand, 1000−10,000 times greater tissue stress was located in the stenotic region but the location of peak tissue stress was different from that of shear stress. We also found that stenting not only stabilizes the stented segment but also reduces the stress in the adjacent region. Fluid-structure interaction analysis revealed discordance in the distribution of shear and tissue stresses. These two stresses exert distinct influences on the coronary plaque, rupture of which may occur where tissue stress exceeds the plaque strength, which is weakened by pathological processes triggered by shear stress.

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