Takeshi Kondo

Showa University, Shinagawa, Tōkyō, Japan

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Publications (13)20.82 Total impact

  • 01/2012; 24(2):89-101. DOI:10.15369/sujms.24.89
  • 01/2012; 24(2):113-125. DOI:10.15369/sujms.24.113
  • 01/2009; 21(4):245-253. DOI:10.15369/sujms.21.245
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    ABSTRACT: Although angiotensin-converting enzyme inhibitors (ACEIs) have been shown to reduce left ventricular remodeling after acute myocardial infarction (AMI), the effects of angiotensin receptor blockers have yet to be established. This study was conducted to examine the effects of candesartan on left ventricular remodeling after AMI. Consecutive AMI patients were assigned to a candesartan group or ACEI group after successful coronary intervention. The patients in the candesartan group (n = 77, mean age, 62.8 +/- 1.3) received candesartan and the patients in the ACEI group (n = 80, mean age, 63.3 +/- 1.2) received lisinopril, enalapril, or trandolapril. Four mg was the most frequent dose in the candesartan group at 6 months. Lisinopril, enalapril, and trandolapril were administered to 52%, 27%, and 21% of the patients in the ACEI group, respectively. No significant differences in the incidences of cardiac death, nonfatal MI, or hospitalization for heart failure (P = NS) were found between the groups. The candesartan group exhibited a somewhat higher percent increase in left ventricular ejection fraction and significantly lower percent increases in left ventricular end-diastolic volume index and left ventricular end-systolic volume index compared to the ACEI group (P < 0.05, P < 0.05, respectively). Candesartan is more effective than ACEI in preventing left ventricular remodeling after AMI.
    International Heart Journal 09/2006; 47(5):715-25. DOI:10.1536/ihj.47.715 · 1.13 Impact Factor
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    ABSTRACT: Although small dense low-density lipoprotein (sd-LDL) has an established association with diabetic dyslipidemia, previous studies have failed to show an association between sd-LDL and diabetes among coronary heart disease patients. This study investigated the prevalence of sd-LDL and abnormal glucose regulation in acute coronary syndrome (ACS). LDL size at the onset of ACS was measured by nondenatured gradient gel electrophoresis in 314 of 429 consecutive patients. Sd-LDL was prevalent in 54% of the patients, irrespective of the presence of previously known diabetes (50% vs 60% in nondiabetes and diabetes, respectively). Diabetes was present in 122 (28%) of the patients, and 110 patients without diabetes underwent an oral glucose tolerance test. Impaired glucose tolerance (IGT) and newly detected diabetes were found in as many as 44% and 22% of the patients tested, even though their hemoglobinA1c levels were in the normal range (5.3+/-0.5%). The prevalence of sd-LDL was significantly higher in patients with glucose intolerance than in those with normal glucose tolerance (61% vs 42%). IGT and diabetes were far more common than normal glucose regulation in ACS patients, and the abnormal glycometabolism was closely associated with highly atherogenic sd-LDL.
    Circulation Journal 05/2006; 70(4):393-401. DOI:10.1253/circj.70.393 · 3.69 Impact Factor
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    ABSTRACT: Although cytokine elevation has been demonstrated in chronic heart failure, little attention has been focused on cytokine levels during the acute stage. We examined the changes of cytokine levels in patients with acutely decompensated heart failure to investigate their relationship with severity of heart failure. Patients with acutely decompensated heart failure (73 patients; 72+/-2 years) were included. Blood samples were taken from the peripheral vein on admission before the start of drug therapy, at 12, 24, 48 and 72 h as well as 1, 2 and 4 weeks after admission. Control data were obtained from age-matched normal patients who had no cardiovascular disease. Serum IL-6, IL-1beta and TNF-alpha levels were measured using the ELISA method. Mean IL-6, IL-1beta and TNF-alpha levels on admission were significantly higher than those in the control patients (p<0.001). IL-6 peaked at 12 h and declined thereafter, whereas IL-1beta and TNF-alpha remained unchanged throughout the duration of the study. Peak IL-6 significantly correlated with pulmonary wedge pressure on admission (r=0.332, p=0.0041). % change of IL-6 levels between peak (12 h after admission) and 24 h was significantly correlated with that of pulmonary wedge pressure between peak (on admission) and 24 h (r=0.308, p=0.0081). Peak IL-6 in patients treated with mechanical ventilation on admission was significantly higher than that in patients who underwent no mechanical ventilation (p<0.05). IL-6 levels possibly reflect the severity of heart failure and thus may be useful for the evaluation of disease status in acutely decompensated heart failure.
    International Journal of Cardiology 04/2005; 100(3):415-20. DOI:10.1016/j.ijcard.2004.08.041 · 6.18 Impact Factor
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    ABSTRACT: We evaluated the extent of reperfusion injury (RI) following successful coronary intervention quantitatively and non-invasively using technetium-99m pyrophosphate (Tc-PYP) /thallium-201 dual-isotope single photon emission computed tomography (SPECT) . Tc-PYP/thallium-201 SPECT was performed 48 hours after coronary intervention in 67 patients (62.6±12.1 yr) who had undergone successful coronary intervention (TIMI grade 3) in the infarct-affected left anterior descending coronary artery within 6 hours after acute anteroseptal myocardial infarction. The infarct-affected region, which was defined quantitatively by a>55% uptake of Tc-PYP, was considered as showing RI if the recovery of myocardial perfusion was defined quantitatively by <60% uptake of thallium-201. Left ventriculography was performed immediately after intervention and at the 6-month follow-up. These clinical parameters were compared between patients with and without RI. RI was presented in 32 of the 67 patients. Electrocardiographic ST-segment elevations did not return to normal immediately after intervention in the patients with RI as compared to the patients without RI (62.5% of 20 patients versus 25.7% of 9, P<0.01) . The patients with RI had larger infarcts (Unit/L) (5490±3002 versus 2506±2074, P<0.0001), more severe left ventricular function (43±11.8% versus 50.2±10.2%, P<0.05), and larger end-diastolic left ventricular dilatation at the 6-month follow-up (mL/m2) (101±27.2 versus 85.2±24.1, P<0.05) than the patients without RI. This study therefore demonstrates that RI occurring soon after successful coronary intervention following acute myocardial infarction can be detected quantitatively by overlap SPECT images of Tc-PYP/thallium-201.
    01/2004; 16(2):117-126. DOI:10.15369/sujms1989.16.117
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    ABSTRACT: The small dense low-density lipoprotein (LDL) phenotype (pattern B), high concentrations of remnant-like particles (RLPs), and postprandial lipemia are newly recognized risk factors for coronary heart disease (CHD). However, the associations of these lipoprotein abnormalities remain unclear. The aim of this study was to investigate the relationships among LDL phenotype, very-low-density lipoprotein (VLDL) subclasses, and postprandial lipoprotein metabolism in CHD patients. We performed an oral fat tolerance test in 32 patients with acute myocardial infarction and compared the following parameters between patients characterized by either large buoyant LDL (pattern A) versus pattern B: lipids and apolipoproteins (apo) in the plasma and Svedberg flotation rates (Sf) >400 (chylomicron), Sf 60-400 (large VLDL), and Sf 20-60 (small VLDL) fractions. Fasting levels of triglyceride, RLP-cholesterol and RLP-triglyceride were slightly higher in the pattern B patients. Postprandial increases of RLP-cholesterol and the cholesterol and triglyceride of large VLDL fractions were significantly greater in the pattern B patients. The areas under the curves of cholesterol, triglyceride, and apo-B in large VLDL fractions were significantly higher in pattern B, while those in small VLDL were not. RLP-cholesterol and RLP-triglyceride in fasting and fed states correlated very highly with the corresponding cholesterol and triglyceride concentrations in large VLDL fractions. These results suggest that postprandial increase of large VLDL fractions and RLPs contribute to the formation of small dense LDL in CHD patients.
    Atherosclerosis 09/2003; 170(1):131-40. DOI:10.1016/S0021-9150(03)00245-4 · 3.97 Impact Factor
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    ABSTRACT: Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors, but the production of these growth factors in cardiomyocytes has also been demonstrated. However, there have been no reports focusing their attention on the changes in these growth factors after coronary intervention. We investigated the time-course changes of the serum VEGF and HGF levels in angina pectoris (AP) and acute myocardial infarction (AMI). The serum HGF and VEGF levels were measured in 60 patients with AP, in 62 patients with AMI (AP, before heparin administration, and at 24 and 48 hours, and one week after intervention; AMI, before heparin, and at 48 and 72 hours, and one, two, three and four weeks) and in 56 patients with neurocirculatory asthenia as controls. We defined the patients with remodelling who showed an increase in left ventricular end-diastolic volume index (LVEDVI) in the sub-acute phase of AMI. Hepatocyte growth factor levels in the AP and AMI were significantly higher than that in the control (p<0.0001). The AMI level was also significantly higher than AP (p<0.001). In the AMI and AP, HGF peaked at 48 hours. Vascular endothelial growth factor level in the AMI was significantly higher than that in the control and AP (p<0.0001). In the AMI, VEGF peaked at two weeks. There was a significant positive correlation between the peak VEGF and LVEDVI in the sub-acute phase of AMI (p=0.0089, r=0.436). Peak VEGF in the remodelling (+) group was significantly higher than that in the remodelling (-) group (p<0.001). In the AP, VEGF was unchanged. While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.
    Coronary Artery Disease 06/2003; 14(4):301-7. DOI:10.1097/01.mca.0000073431.02845.a1 · 1.30 Impact Factor
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    ABSTRACT: It remains unclear how closely the small dense low-density lipoprotein (LDL) (diameter < or =25.5 nm) is associated with various types of coronary heart disease (CHD) in Japanese patients, an ethnic group with lower serum cholesterol levels and less massive obesity compared with Western populations. We measured mean LDL particle diameter by gradient gel electrophoresis in 571 patients with CHD and in 263 healthy subjects who served as control patients. Patients with CHD were classified into acute coronary syndrome (ACS), stable CHD and vasospastic angina. High-density lipoprotein cholesterol and apolipoprotein-A1 and -B were significantly different between patients with CHD and controls. LDL size in patients with CHD was markedly smaller than that in controls in both men and women (25.5 +/- 0.7 vs 25.9 +/- 0.4 and 25.7 +/- 0.7 vs 26.0 +/- 0.5 nm, respectively). LDL cholesterol was significantly higher in patients with ACS than in other groups. Plasma levels of high-density lipoprotein cholesterol decreased as the number of diseased vessels or angiographic coronary severity evaluated by Gensini score increased, but the LDL size was comparable irrespective of the type of CHD and the extent and severity of the lesions. Multiple logistic regression analysis revealed that small dense LDL was independently associated with the incidence of CHD in both sexes (odds ratio [OR] 3.5, 95% CI 2.1-5.7, and OR 2.9, 95% CI 1.5-5.6, P <.005). Our study suggests that the small dense LDL is strongly associated with various types of CHD, independent of traditional and nontraditional coronary risk factors, but is not related to the severity and extent of the coronary lesions.
    American heart journal 12/2002; 144(6):1026-35. DOI:10.1067/mhj.2002.126119 · 4.56 Impact Factor
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    ABSTRACT: Coronary spasm can be induced by acetylcholine (ACh) in many patients without a past history of rest angina. However, the low specificity of ACh for diagnosing coronary spastic angina is a controversial aspect of the ACh stress test. We investigated the clinical significance of the ACh stress test following isosorbide dinitrate (ISDN) administration. In addition, to elucidate the relationship between coronary vasospasm and endothelin (ET), we determined plasma ET-1 levels in patients with vasospastic angina pectoris. Twenty-six (81.3%) out of thirty-two patients (Group P) who developed vasospasm induced by ACh following administration of ISDN, had rest angina, while only seventeen (37.8%) out of forty-five patients (Group N ) who did not develop vasospasm induced by ACh following administration of ISDN, had rest angina. The frequency of subjective chest pain at rest was significantly higher in Group P than in Group N (81.3% vs. 37.8%: p<0.01) . Therefore, the post-ISDN ACh stress test may be useful in detecting true vasospastic angina pectoris. Plasma ET-1 levels in the coronary sinus increased significantly from a basal value of 3.13 to 3.78 pg/ml in patients who developed ACh induced vasospasm following injection of ISDN (p<0.05) . These patients exhibited symptoms to the clinical symptoms of rest angina, but there was no change in the other patients. Elevated plasma levels of ET-1 might directly or indirectly increase the level of vascular smooth muscle contraction. This study suggests that the development of ACh-induced vasospasm following administration of ISDN might be due not only to injury of vascular endothelial cells but also to the increased contractility of vascular smooth muscle cells.
    01/2001; 13(2):101-109. DOI:10.15369/sujms1989.13.101
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    ABSTRACT: This study retrospectively examined prognostic factors for acute myocardial infarction in 150 patients with cardiogenic shock among 1, 200 patients who developed acute myocardial infarction. The mortality was 35.3%. A history of old myocardial infarction, multi-vessel coronary lesions, unsuccessful reperfusion therapy, and infarction of the left main coronary trunk significantly influenced prognosis. In patients in whom circulatory reconstruc-tion led to discharge without residual ischemia, the prognosis was similar to that in patients with usual myocardial infarction. The prognosis of acute myocardial infarction with cardiogenic shock may be improved by performing reperfusion therapy earlier. If necessary, residual ischemia should be treated by additional circulatory reconstruction.
    01/2000; 12(2):175-180. DOI:10.15369/sujms1989.12.175
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    ABSTRACT: Current treatment guidelines for hypertension in both Europe and the USA stress the importance of aggressive blood pressure control. When monotherapy is not enough to reach treatment targets, there is a need for combination regimens that have both high efficacy and good tolerability. The aim of this study is to evaluate the efficacy and tolerability of the combination therapy candesartan and amlodipine in patients with hypertension not satisfactorily controlled by mono-therapy. Patients with uncomplicated essential hypertension not satisfactorily controlled by monotherapy, which is candesartan 8 mg or amlodipine 5 mg, were eligible. Candesartan 8 mg and amlodipine 5 mg were given for 12 weeks. 13 patients who received candesartan 8 mg previoursly were assigned to the candesartan group and 8 patients who received amlodipine 5 mg previoursly were assigned to the amlodipine group. Sitting systolic blood pressure (SBP) at baseline was 151.9 ± 11.6 mmHg in the candesartan group, and 154.6 ± 7.6 mmHg in the amlodipine group. Sitting diastolic blood pressure (DBP) was 93.2 ± 13.1 in the candesartan group, and 80.4 ± 14.7 in the amlodipine group. DBP in the amlodipine group was lower than that in the cadesartan group (P = 0.036). After the combination therapy, SBP was significantly reduced in the two groups. DBP showed significant reduction in the amlodipine group. The rate of achieving blood pressure goals was 4% at baseline and significantly increased to 58% after the combination therapy. These results showed that candesartan 8 mg/amlodipine 5 mg are effective lowering blood pressure after 12 weeks in patients not adequately controlled by monotherapy.