International Heart Journal
Online ISSN : 1349-3299
Print ISSN : 1349-2365
ISSN-L : 1349-2365
Volume 50, Issue 4
Displaying 1-13 of 13 articles from this issue
Clinical Studies
  • Sherif A. Sakr, Tarek M. Abbas, Maged Z. Amer, Eid M. Dawood, Nader El ...
    2009 Volume 50 Issue 4 Pages 407-419
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    Microvascular angina is a condition characterized by angina-like chest pain and normal coronary angiography. Endothelial dysfunction and systemic inflammation with elevated serum high-sensitive C-reactive protein (hsCRP) levels play a role in its pathogenesis. This study aimed to explore the possible relation between CRP, brachial flow-mediated dilatation (FMD), and microvascular angina.
    We included 21 patients with attacks of chest pain diagnosed as microvascular angina (study group) and 10 normal asymptomatic subjects (control group). Patients and controls were thoroughly examined clinically and by echocardiography, electrocardiography, and brachial FMD (using external brachial ultrasonography). Serum hsCRP and uric acid levels were assessed in all subjects.
    A significantly higher mean hsCRP level was found in the study group compared to controls (11.5 ± 3.8 versus 3.34 ± 1.5 mg/L; P < 0.001). FMD of the brachial artery showed significant impairment in patients with microvascular angina compared to controls (0.16 ± 0.06 versus 0.76 ± 0.09 mm; P < 0.001). There were significantly higher total cholesterol (196.1 ± 44.4 versus 159.8 ± 14.5 mg/dL; P = 0.018) and triglyceride levels (185.0 ± 103.2 versus 113.0 ± 17.6 mg/dL; P = 0.038) in the patients compared to controls; but there was a statistically insignificant difference in mean serum uric acid levels between these two groups. There were no significant correlations between the brachial FMD and any of the clinical variables studied (apart from ankle/brachial index).
    Microvascular angina may have an inflammatory element (reflected as a higher serum hsCRP level), together with a contribution by endothelial dysfunction (reflected as impaired brachial artery FMD); while serum uric acid is possibly not associated with microvascular angina.
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  • Wilfried Dinh, Reiner Füth, Thomas Scheffold, Lars Bansemir, Till ...
    2009 Volume 50 Issue 4 Pages 421-431
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    It has been suggested that matrix-metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of metalloproteinases (TIMPs) play a major role in the regulation of myocardial remodeling. Myocardial extracellular matrix (ECM) is highly susceptible to ischemic injury in acute myocardial infarction (AMI).
    We measured serum levels of TIMP-1 in the early hours of AMI to study the kinetics of these enzymes in an early ischemic phase.
    TIMP-1 was measured in 25 patients with AMI and 116 healthy controls. Blood samples were obtained during the first 12 hours after hospital admission. Left ventricular function (LVF) and hemodynamic data were collected during coronary intervention.
    TIMP-1 was significantly elevated in patients with AMI within the first hours compared to controls (P < 0.05). No significant difference was observed between patients with preserved LVF and with impaired LVF. Elevated TIMP-1 levels did not correlate with increased levels of CK or CK-MB band during the first hours after AMI.
    Increased TIMP-1 can be detected within 12 hours in patients with AMI, suggesting early onset of remodeling. Elevation of TIMP-1 may be a surrogate marker for increased ECM-turnover. The prognostic relevance needs to be proved in long-term studies.
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  • Li-Tang Kuo, Shih-Jen Chen, Wen-Jin Cherng, Ning-I Yang, Chen-Chin Lee ...
    2009 Volume 50 Issue 4 Pages 433-444
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    After acute myocardial infarction (AMI), reopening of a totally occluded infarct-related artery (IRA) at a subacute stage is still controversial in symptom-free patients. However, in patients with persistent ischemic symptoms and inadequate collaterals to the in-farct area, recanalization is thought to provide beneficial effects. In addition to augmenting myocardial perfusion, we hypothesized that the benefit of recanalization involves the manipulation of circulating stem cell-mobilizing cytokines. This study included 30 patients with a totally occluded IRA and ongoing ischemic symptoms (the study group) and 30 patients with a partially occluded IRA (the control group). All patients underwent successful angioplasty and/or stenting. Before and immediately after the coronary intervention, blood granulocyte-colony-stimulating factor (G-CSF), stem-cell factor (SCF), vascular endothelial growth factor (VEGF), and stroma-derived factor-1 (SDF-1α) were measured. After recanalization, G-CSF levels significantly increased in the study group compared to the control group (P = 0.03). SDF-1α levels in the study group decreased relative to the controls (P = 0.02). However, no significant changes in VEGF or SCF levels between the two groups were found. In the multivariate analysis, reopening of a totally occluded IRA was independently and significantly associated with changes in G-CSF and SDF-1α levels after recanalization. In conclusion, our data suggest that the benefits of late reperfusion of a totally occluded IRA in patients with ongoing myocardial ischemia may involve mechanisms associated with stem cell-mobilizing and plaque-stabilizing cytokines. This study provides the rationale to investigate serial changes in cytokines and the numbers of circulating progenitors after reperfusion in the future.
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  • Yasuko Tanabe, Yuichiro Kawamura, Naka Sakamoto, Nobuyuki Sato, Kenjir ...
    2009 Volume 50 Issue 4 Pages 445-456
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    The purpose of this study was to investigate whether the ideal control of atrial fibrillation (AF) associated with hypertensive patients depends on the usage of renin-angiotensin system (RAS) inhibitors or whether it occurs regardless of the kind of antihypertensive agents used. The control of AF was compared in 112 outpatients between 1) those with or without the administration of RAS inhibitors, and 2) those with an ideal or poor control of the blood pressure (BP) regardless of the kind of antihypertensive therapy used.
    The therapies with or without RAS inhibitors did not yield any significant difference in the AF control states, even though RAS inhibitors had been administered to the patient group with a high proportion of organic heart disease. The ideal BP control group exhibited a significantly better AF control in comparison to the poor BP control group. The former group had a significantly smaller left atrial diameter determined by ultrasonic echocardiography. BP control itself may essentially be important for preventing AF in the general patient population. Poor BP control seemed to have an affect on worsening AF possibly via left ventricular diastolic dysfunction, followed by left atrial overload.
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  • Masahide Minami, Yasuki Kobayashi, Satoshi Toyokawa, Kazuo Inoue, Yasu ...
    2009 Volume 50 Issue 4 Pages 457-464
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    The current study aimed to identify risk factors for atrial fibrillation (AF) detected during routine medical checkups of male workers in Japan. A nested case-control study was conducted using retrospective data from January 1998 to December 2006 collected at a hospital in Ishikawa Prefecture. Cases were those first diagnosed with AF with no record of AF events during the preceding 3 years. For each case, 2 controls were matched for age and time of medical checkup, randomly selected from among those who had not been diagnosed with AF during the same 3 years. Logistic regression was used to identify risk factors in the 3 years prior for new-onset AF. Sixty-nine cases and 138 controls were recruited; their average ages were 57.6 (SD 6.7) and 57.4 years (SD 6.7), respectively. In the logistic models, new-onset AF was associated with systolic blood pressure and drinking habits in the 3 years prior.
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  • Takashi Komatsu, Hideaki Tachibana, Yoshihiro Sato, Mahito Ozawa, Fusa ...
    2009 Volume 50 Issue 4 Pages 465-476
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    The long-term efficacy of upstream therapy to prevent occurrence of paroxysmal atrial fibrillation (AF) in Japanese patients remains unclear. We retrospectively assessed the long-term efficacy of combination therapy with pravastatin (10 mg/day) and enalapril (5 mg/day) in addition to antiarrhythmic drugs (AAD) for maintaining sinus rhythm in patients with AF. This study included 319 patients (221 men, 98 women, mean age, 68 ± 10 years, mean follow-up period, 50 ± 34 months) who were divided into 4 groups: group I (n = 191) without combination therapy - namely pravastatin(-) and enalapril(-); group II (n = 81) with combination therapy - pravastatin (-) and enalapril (+) (n = 81); group III (n = 29) with combination therapy - pravastatin (+) and enalapril (-); and group IV (n = 18) with combination therapy - pravastatin (+) and enalapril (+). The percentages of patients free from conversion to permanent AF at 12, 36, 60, 90, and 120 months were as follows: group I 88, 83, 78, 75, and 73%, respectively; group II 96, 88, 79, 77, and 75%, respectively; group III 100, 97, 91, 91, and 86%, respectively; group IV 100, 100, 100, 94, and 94%, respectively. The actuarial rate free from conversion to permanent AF at 120 months was significantly higher in group IV than in group I (P < 0.05). The results suggest that in patients with paroxysmal AF, the addition of both pravastatin and enalapril to AAD was more effective for maintaining sinus rhythm in terms of an upstream therapy.
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  • Kimie Ohkubo, Ichiro Watanabe, Yasuo Okumura, Sonoko Ashino, Masayoshi ...
    2009 Volume 50 Issue 4 Pages 477-487
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    This study was designed to evaluate whether the right ventricular outflow tract (RVOT) is the arrhythmogenic focus in Brugada syndrome. We enrolled 45 patients with Brugada-type ECG who underwent programmed ventricular stimulation and inducible ventricular fibrillation (VF). In 25 of these 32 patients, repetitive VT was observed before degeneration into VF. The QRS morphology of surface ECG and intracardiac electrograms were evaluated to determine the origin of the ventricular tachycardia (VT) that degenerated into VF. The VT morphology was a left bundle branch block pattern with an inferior axis in 22 of 28 VTs and the intracardiac conduction sequence during VT revealed activation from the RVOT to the RV apex in these 22 VTs. The majority of the patients with Brugada syndrome showed repetitive VT originating from the RVOT that degenerated into VF. The RVOT may be an arrhythmogenic focus in patients with Brugada syndrome.
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  • Teruo Shiraki, Kazuhiro Osawa, Hideyuki Suzuki, Masatoki Yoshida, Nats ...
    2009 Volume 50 Issue 4 Pages 489-500
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    The aim of the present study was to evaluate the factors related to poor prognosis of out-of-hospital cardiac arrest patients in one local area of Japan. From May 1, 2002 to April 30, 2008, a total of 442 patients with cardiopulmonary arrest were transferred for resuscitation to the National Hospital Organization, Iwakuni Clinical Center. Of 325 patients with cardiopulmonary arrest of cardiac etiology, 126 patients were witnessed by a bystander. However, only 37 received bystander cardiopulmonary resuscitation, 13 had shockable cardiac rhythm, 3 survived 1 month, and 2 had a good neurological discharge. Multivariate analysis of overall cardiac arrest showed that 1-month survival and neurologically favorable discharge were associated with bystander cardiopulmonary resuscitation (P = 0.049 and 0.013) and initial shockable cardiac rhythm (P = 0.001 and 0.007). In this region, the survival rate for patients with cardiopulmonary arrest was lower than that reported in other areas, probably because fewer patients received bystander CPR or had shockable cardiac rhythm. This may result from CPR being less popularized in this region than in other areas, suggesting that raising the awareness of CPR would improve the survival rate.
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  • Tetsuya Nakamura, Kenji Kawachi, Yuichiro Saito, Tomoko Saito, Koujuro ...
    2009 Volume 50 Issue 4 Pages 501-512
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) γ. Stimulation of PPAR γ has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.
    Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.
    A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9 ± 5.6 to 58.1 ± 5.4 pg/mL) and perindopril (74.1 ± 4.7 to 64.7 ± 5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9 ± 4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.
    Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR γ stimulating activity is equivalent to ACE-I for the treatment of hypertension.
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  • Takeyoshi Kunieda, Norifumi Nakanishi, Hiromi Matsubara, Tohru Ohe, Yo ...
    2009 Volume 50 Issue 4 Pages 513-529
    Published: 2009
    Released on J-STAGE: July 16, 2009
    JOURNAL FREE ACCESS
    The long-acting beraprost preparation TRK-100STP is formulated to provide sustained release of an orally active prostacyclin derivative to maintain the optimal plasma concentration for a longer period of time compared with the currently used conventional beraprost sodium. In the present study, we evaluated the efficacy of this newly developed formulation for pulmonary arterial hypertension (PAH).
    An open-label, 12-week multicenter clinical trial was performed in 46 patients with PAH. They were initially treated with 120 μg of TRK-100STP divided into 60 μg twice daily, followed by a stepwise increase to 360 μg given as 180 μg twice daily. The 6-minute walking distance showed a significant increase by 33.4 ± 66.0 m (95% confidence interval [CI], 13.4 to 53.5) from the baseline measurement. Mean pulmonary artery pressure, total pulmonary vascular resistance, and pulmonary vascular resistance decreased by –2.8 ± 5.5 mmHg (95% CI, –4.6 to –1.0), by –0.92 ± 2.63 mmHg•L–1•min (95% CI, –1.78 to –0.05), and by –0.89 ± 2.81 mmHg•L–1•min (95% CI, –1.84 to 0.06), respectively, from the baseline measurements. A higher efficacy was observed in patients with a maximum tolerated dose of 360 μg daily than those of 240 μg daily or less.
    Treatment with TRK-100STP for a 12-week period improved the exercise capacity, mean pulmonary artery pressure, and total pulmonary vascular resistance. TRK-100STP was effective for Japanese patients with PAH.
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