K. Hirooka, Y. Yasumura, Y. Ishida, A. Hanatani, S. Nakatani, K. Komamura, M. Hori, M. Yamagishi, K. Miyatake
The efficacy of treating dilated cardiomyopathy with metoprolol was compared with that of carvedilol. Metoprolol was administered to 29 patients, and carvedilol to 62. Patients who could not be dosed with up to 40 mg daily of metoprolol or 20 mg daily of carvedilol were defined as intolerant. As well as the tolerability of these beta-blockers, the effects on left ventricular end-diastolic dimension (LVDd), fractional shortening (FS), plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations, the delayed heart and mediastinum (H/M) ratio determined from metaiodobenzylguanidine imaging were compared. Drug intolerance occurred in 24% of patients in the metoprolol group and 19% in the carvedilol group. Among the drug-tolerant patients, LVDd, FS and plasma BNP concentration improved in both groups and to the same degree. Only 25% of drug-tolerant patients in the metoprolol group had a delayed H/M ratio below 1.9 compared with 57% in the carvedilol group. Both metoprolol and carvedilol, when tolerated, improve cardiac function and neurohumoral factors to the same degree. However, carvedilol is preferable to metoprolol for patients with a low delayed H/M ratio.
{"title":"Comparative left ventricular functional and neurohumoral effects of chronic treatment with carvedilol versus metoprolol in patients with dilated cardiomyopathy.","authors":"K. Hirooka, Y. Yasumura, Y. Ishida, A. Hanatani, S. Nakatani, K. Komamura, M. Hori, M. Yamagishi, K. Miyatake","doi":"10.1253/JCJ.65.931","DOIUrl":"https://doi.org/10.1253/JCJ.65.931","url":null,"abstract":"The efficacy of treating dilated cardiomyopathy with metoprolol was compared with that of carvedilol. Metoprolol was administered to 29 patients, and carvedilol to 62. Patients who could not be dosed with up to 40 mg daily of metoprolol or 20 mg daily of carvedilol were defined as intolerant. As well as the tolerability of these beta-blockers, the effects on left ventricular end-diastolic dimension (LVDd), fractional shortening (FS), plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations, the delayed heart and mediastinum (H/M) ratio determined from metaiodobenzylguanidine imaging were compared. Drug intolerance occurred in 24% of patients in the metoprolol group and 19% in the carvedilol group. Among the drug-tolerant patients, LVDd, FS and plasma BNP concentration improved in both groups and to the same degree. Only 25% of drug-tolerant patients in the metoprolol group had a delayed H/M ratio below 1.9 compared with 57% in the carvedilol group. Both metoprolol and carvedilol, when tolerated, improve cardiac function and neurohumoral factors to the same degree. However, carvedilol is preferable to metoprolol for patients with a low delayed H/M ratio.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"26 1","pages":"931-6"},"PeriodicalIF":0.0,"publicationDate":"2001-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77105823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kazuya Akiyama, N. Taniyasu, Jun Hirota, Yutaka Iba, K. Maisawa
Gemella morbillorum (G. morbillorum) is part of the commensal flora of the oropharynx and intestinal tract, and on rare occasions causes infective endocarditis. A 55-year-old man with massive aortic regurgitation caused by recurrent infective endocarditis with G. morbillorum had a history of prior endocarditis caused by alpha-hemolytic streptococcus and multiple antibiotic allergies 5 years prior, and was successfully treated by aortic valve replacement. Almost all the reported cases of endocarditis caused by G. morbillorum have been bacteriologically cured with antibiotics and this is the first reported case of recurrent endocarditis caused by G. morbillorum in which the initial infection was bacteriologically cured by antibiotics and the secondary infection treated with valve replacement. This organism can be one of the causes of infective endocarditis and prompt surgical repair is mandatory if the infection is refractory or there is progression of congestive heart failure under antibiotic cover.
{"title":"Recurrent aortic valve endocarditis caused by Gemella morbillorum--report of a case and review of the literature.","authors":"Kazuya Akiyama, N. Taniyasu, Jun Hirota, Yutaka Iba, K. Maisawa","doi":"10.1253/JCJ.65.997","DOIUrl":"https://doi.org/10.1253/JCJ.65.997","url":null,"abstract":"Gemella morbillorum (G. morbillorum) is part of the commensal flora of the oropharynx and intestinal tract, and on rare occasions causes infective endocarditis. A 55-year-old man with massive aortic regurgitation caused by recurrent infective endocarditis with G. morbillorum had a history of prior endocarditis caused by alpha-hemolytic streptococcus and multiple antibiotic allergies 5 years prior, and was successfully treated by aortic valve replacement. Almost all the reported cases of endocarditis caused by G. morbillorum have been bacteriologically cured with antibiotics and this is the first reported case of recurrent endocarditis caused by G. morbillorum in which the initial infection was bacteriologically cured by antibiotics and the secondary infection treated with valve replacement. This organism can be one of the causes of infective endocarditis and prompt surgical repair is mandatory if the infection is refractory or there is progression of congestive heart failure under antibiotic cover.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"109 1","pages":"997-1000"},"PeriodicalIF":0.0,"publicationDate":"2001-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80944397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K. Yoshida, M. Yoshiyama, T. Omura, Y. Nakamura, S. Kim, K. Takeuchi, H. Iwao, J. Yoshikawa
As one of the signal transduction pathways related to myocardial remodeling, mitogen-activated protein kinases (MAPKs) possibly play an important role in ischemic heart disease, but it is still unknown whether myocardial MAPKs are activated in the non-ischemic region of an acute myocardial infarction (AMI). Therefore, the present study investigated the myocardial activity of extracellular signal-regulated kinases (ERKs), c-Jun NH2 terminal kinases (JNKs) and p38MAPK during the acute phase of an infarction of the rat heart, and measured the geometrical ventricular changes by echocardiography. All MAPKs were significantly activated in the ischemic myocardium (IM), non-ischemic septal wall (SW), and right ventricular wall (RV). Furthermore, the activation patterns of MAPKs differed in each region. The activation of p44ERK, JNKs and p38MAPK in the IM occurred rapidly after myocardial ischemia, followed by those in the SW and RV. The activator protein-1 DNA binding activities of the IM, SW and RV increased significantly at I day after coronary ligation. Echocardiography showed increased SW motion and RV dilatation. In conclusion, this is the first in vivo evidence that myocardial MAPKs are activated in the non-ischemic region of an AMI. Echocardiographic results suggest that acceleration of workload and/or stretch may partially induce the activation of MAPKs.
{"title":"Activation of mitogen-activated protein kinases in the non-ischemic myocardium of an acute myocardial infarction in rats.","authors":"K. Yoshida, M. Yoshiyama, T. Omura, Y. Nakamura, S. Kim, K. Takeuchi, H. Iwao, J. Yoshikawa","doi":"10.1253/JCJ.65.808","DOIUrl":"https://doi.org/10.1253/JCJ.65.808","url":null,"abstract":"As one of the signal transduction pathways related to myocardial remodeling, mitogen-activated protein kinases (MAPKs) possibly play an important role in ischemic heart disease, but it is still unknown whether myocardial MAPKs are activated in the non-ischemic region of an acute myocardial infarction (AMI). Therefore, the present study investigated the myocardial activity of extracellular signal-regulated kinases (ERKs), c-Jun NH2 terminal kinases (JNKs) and p38MAPK during the acute phase of an infarction of the rat heart, and measured the geometrical ventricular changes by echocardiography. All MAPKs were significantly activated in the ischemic myocardium (IM), non-ischemic septal wall (SW), and right ventricular wall (RV). Furthermore, the activation patterns of MAPKs differed in each region. The activation of p44ERK, JNKs and p38MAPK in the IM occurred rapidly after myocardial ischemia, followed by those in the SW and RV. The activator protein-1 DNA binding activities of the IM, SW and RV increased significantly at I day after coronary ligation. Echocardiography showed increased SW motion and RV dilatation. In conclusion, this is the first in vivo evidence that myocardial MAPKs are activated in the non-ischemic region of an AMI. Echocardiographic results suggest that acceleration of workload and/or stretch may partially induce the activation of MAPKs.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"182 8 1","pages":"808-14"},"PeriodicalIF":0.0,"publicationDate":"2001-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82750765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Y. Mukai, H. Tsutsui, K. Todaka, M. Mohri, N. Hirai, H. Arai, A. Takeshita
Behçet's disease frequently involves the venous system, usually affecting small vessels, but sometimes large vessels such as the vena cava. Antiphospholipid antibody syndrome is associated with an increased incidence of arterial and venous thrombosis. A 29-year-old male with Behçet's disease developed bilateral leg edema secondary to thrombotic occlusion of the inferior vena cava. Laboratory tests revealed positive antiphospholipid antibodies and lupus anticoagulant. Treatment with steroid and warfarin subsequent to intravenous administration of uro-kinase resulted in improvement of symptoms. The association of antiphospholipid antibody syndrome and Behçet's disease may have caused the total thrombotic occlusion of the vena cava in this case.
{"title":"Total occlusion of inferior vena cava in a patient with antiphospholipid antibody syndrome associated with behçet's disease.","authors":"Y. Mukai, H. Tsutsui, K. Todaka, M. Mohri, N. Hirai, H. Arai, A. Takeshita","doi":"10.1253/JCJ.65.837","DOIUrl":"https://doi.org/10.1253/JCJ.65.837","url":null,"abstract":"Behçet's disease frequently involves the venous system, usually affecting small vessels, but sometimes large vessels such as the vena cava. Antiphospholipid antibody syndrome is associated with an increased incidence of arterial and venous thrombosis. A 29-year-old male with Behçet's disease developed bilateral leg edema secondary to thrombotic occlusion of the inferior vena cava. Laboratory tests revealed positive antiphospholipid antibodies and lupus anticoagulant. Treatment with steroid and warfarin subsequent to intravenous administration of uro-kinase resulted in improvement of symptoms. The association of antiphospholipid antibody syndrome and Behçet's disease may have caused the total thrombotic occlusion of the vena cava in this case.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"1 1","pages":"837-8"},"PeriodicalIF":0.0,"publicationDate":"2001-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79956151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
K. Kimura, Kengo Tsukahara, Takashi Usui, J. Okuda, Yutaka Kitamura, M. Kosuge, Toshio Sano, Shinnichi Tohyama, Osamu Yamanaka, Y. Yoshii, S. Umemura
The time from admission to reperfusion in patients with acute myocardial infarction (AMI) was compared according to the type of hospital and treatment strategy. A total of 164 patients with a first AMI within 12h of onset were enrolled at one tertiary emergency center (TEC) and 6 community hospitals (CHs). The subjects were randomly assigned to receive either primary percutaneous transluminal coronary angioplasty (PTCA) (TEC-primary PTCA and CHs-primary PTCA groups) or 800,000 units of intravenous monteplase, half the standard dose of a mutant tissue plasminogen activator (t-PA), followed by rescue PTCA if the Thrombolysis in Myocardial Infarction (TIMI) flow grade was 2 or less (TEC-monteplase and CHs-monteplase groups) on the first coronary angiogram. Sixty minutes after admission, TIMI flow grade 3 rates of the study groups were as follows, in descending order: TEC-monteplase group, CHs-monteplase group, TEC-primary PTCA group, and CHs-primary PTCA group (56%, 41%, 36%, and 8%, respectively; p<0.01). However, there was no significant difference in the final TIMI flow grade 3 rate among the 4 groups. In the CHs, the peak creatine kinase tended to be lower in the monteplase group than in the primary PTCA group. The results suggest that low-dose monteplase followed by rescue PTCA is an effective strategy for promoting early reperfusion in patients with AMI, especially those who are treated at CHs.
{"title":"Low-dose tissue plasminogen activator followed by planned rescue angioplasty reduces time to reperfusion for acute myocardial infarction treated at community hospitals.","authors":"K. Kimura, Kengo Tsukahara, Takashi Usui, J. Okuda, Yutaka Kitamura, M. Kosuge, Toshio Sano, Shinnichi Tohyama, Osamu Yamanaka, Y. Yoshii, S. Umemura","doi":"10.1253/JCJ.65.901","DOIUrl":"https://doi.org/10.1253/JCJ.65.901","url":null,"abstract":"The time from admission to reperfusion in patients with acute myocardial infarction (AMI) was compared according to the type of hospital and treatment strategy. A total of 164 patients with a first AMI within 12h of onset were enrolled at one tertiary emergency center (TEC) and 6 community hospitals (CHs). The subjects were randomly assigned to receive either primary percutaneous transluminal coronary angioplasty (PTCA) (TEC-primary PTCA and CHs-primary PTCA groups) or 800,000 units of intravenous monteplase, half the standard dose of a mutant tissue plasminogen activator (t-PA), followed by rescue PTCA if the Thrombolysis in Myocardial Infarction (TIMI) flow grade was 2 or less (TEC-monteplase and CHs-monteplase groups) on the first coronary angiogram. Sixty minutes after admission, TIMI flow grade 3 rates of the study groups were as follows, in descending order: TEC-monteplase group, CHs-monteplase group, TEC-primary PTCA group, and CHs-primary PTCA group (56%, 41%, 36%, and 8%, respectively; p<0.01). However, there was no significant difference in the final TIMI flow grade 3 rate among the 4 groups. In the CHs, the peak creatine kinase tended to be lower in the monteplase group than in the primary PTCA group. The results suggest that low-dose monteplase followed by rescue PTCA is an effective strategy for promoting early reperfusion in patients with AMI, especially those who are treated at CHs.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"48 1","pages":"901-6"},"PeriodicalIF":0.0,"publicationDate":"2001-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73759363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Acute necrotizing eosinophilic myocarditis is the most severe form of eosinophilic myocarditis, or hypersensitivity myocarditis, and is characterized by rapidly progressive congestive heart failure followed by fulminant clinical deterioration that is nearly always fatal. A 55-year-old previously healthy patient with acute necrotizing eosinophilic myocarditis was diagnosed by early myocardial biopsy and successfully treated with corticosteroids. Throughout his hospitalization, the eosinophil count in the peripheral blood remained normal (56-201/mm3). Early stage corticosteroid therapy can have dramatic effects in acute necrotizing eosinophilic myocarditis and early diagnosis by endomyocardial biopsy is recommended.
{"title":"Acute necrotizing eosinophilic myocarditis successfully treated by high dose methylprednisolone.","authors":"Nozomi Watanabe, Susumu Nakagawa, Takashi Fukunaga, Shuji Fukuoka, Kinta Hatakeyama, Tohru Hayashi","doi":"10.1253/JCJ.65.923","DOIUrl":"https://doi.org/10.1253/JCJ.65.923","url":null,"abstract":"Acute necrotizing eosinophilic myocarditis is the most severe form of eosinophilic myocarditis, or hypersensitivity myocarditis, and is characterized by rapidly progressive congestive heart failure followed by fulminant clinical deterioration that is nearly always fatal. A 55-year-old previously healthy patient with acute necrotizing eosinophilic myocarditis was diagnosed by early myocardial biopsy and successfully treated with corticosteroids. Throughout his hospitalization, the eosinophil count in the peripheral blood remained normal (56-201/mm3). Early stage corticosteroid therapy can have dramatic effects in acute necrotizing eosinophilic myocarditis and early diagnosis by endomyocardial biopsy is recommended.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"19 1","pages":"923-6"},"PeriodicalIF":0.0,"publicationDate":"2001-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85464854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Minatoguchi, T. Kariya, Y. Uno, M. Arai, Y. Nishida, K. Hashimoto, N. Wang, T. Aoyama, G. Takemura, T. Fujiwara, H. Fujiwara
Some infarcted myocytes undergo caspase-dependent DNA fragmentation, but serine protease-dependent DNA fragmentation may also be involved. There is controversy regarding whether caspase inhibitors can reduce infarct size, so the present study investigated whether serine protease inhibitor can reduce the DNA fragmentation of infarcted myocytes and whether serine protease or caspase inhibitors attenuates myocardial infarct size in Japanese white rabbits without collateral circulation. Rabbits were subjected to 30-min coronary occlusion followed by 48-h reperfusion. A vehicle (dimethylsulfoxide, control group, n=8) or Z-Val-Ala-Asp(Ome)-CH2F (ZVAD-fmk, a caspase inhibitor, ZVAD group, 0.8 mg/kg iv at 20 min before coronary occlusion and 0.8 mg/kg at 90 min after reperfusion, n=8) or 3,4-dichloroisocoumarin (DCI, a serine protease inhibitor, 2 mg/kg iv at 20 min before coronary occlusion, DCI group, n=8) was administered. Animals were killed at 48h after reperfusion for the detection of myocardial infarct size and at 4h after reperfusion for the detection of dUTP nick end-labeling (TUNEL)-positive myocytes, the electrophoretic pattern of DNA fragmentation and ultrastructural analysis. The left ventricle (LV) was excised and sliced. The myocardial infarct size as a percentage of the area at risk was assessed by triphenyltetrazolium chloride staining. DNA fragmentation was assessed by in situ TUNEL at the light microscopic level. ZVAD and DCI significantly reduced the mean blood pressure during reperfusion without affecting heart rate. There was no significant difference in the % area at risk (AAR) of LV among the 3 groups (control: 26.3+/-3.0%; ZVAD: 25.6+/-2.6%; DCI: 25.6+/-2.0%). The % infarct size as a percentage of the AAR in the ZVAD group (41.3+/-4.5%) and the DCI group (50.4+/-3.8%) was not significantly different from the control group (43.5+/-4.5%). However, the percent DNA fragmentation in the infarcted area in the ZVAD (3.5+/-0.8%) and DCI groups (4.2+/-0.9%) was significantly reduced compared with the control group (10.7+/-1.9%). The DNA ladder pattern observed in the control group was attenuated in both the ZVAD and DCI groups. There was no difference in electron microscopic changes among the 3 groups. Serine protease-dependent DNA fragmentation is present in infarcted myocytes, in addition to caspase-dependent DNA fragmentation, but an infarct-size reducing effect was not observed with either of these inhibitors.
{"title":"Caspase-dependent and serine protease-dependent DNA fragmentation of myocytes in the ischemia-reperfused rabbit heart: these inhibitors do not reduce infarct size.","authors":"S. Minatoguchi, T. Kariya, Y. Uno, M. Arai, Y. Nishida, K. Hashimoto, N. Wang, T. Aoyama, G. Takemura, T. Fujiwara, H. Fujiwara","doi":"10.1253/JCJ.65.907","DOIUrl":"https://doi.org/10.1253/JCJ.65.907","url":null,"abstract":"Some infarcted myocytes undergo caspase-dependent DNA fragmentation, but serine protease-dependent DNA fragmentation may also be involved. There is controversy regarding whether caspase inhibitors can reduce infarct size, so the present study investigated whether serine protease inhibitor can reduce the DNA fragmentation of infarcted myocytes and whether serine protease or caspase inhibitors attenuates myocardial infarct size in Japanese white rabbits without collateral circulation. Rabbits were subjected to 30-min coronary occlusion followed by 48-h reperfusion. A vehicle (dimethylsulfoxide, control group, n=8) or Z-Val-Ala-Asp(Ome)-CH2F (ZVAD-fmk, a caspase inhibitor, ZVAD group, 0.8 mg/kg iv at 20 min before coronary occlusion and 0.8 mg/kg at 90 min after reperfusion, n=8) or 3,4-dichloroisocoumarin (DCI, a serine protease inhibitor, 2 mg/kg iv at 20 min before coronary occlusion, DCI group, n=8) was administered. Animals were killed at 48h after reperfusion for the detection of myocardial infarct size and at 4h after reperfusion for the detection of dUTP nick end-labeling (TUNEL)-positive myocytes, the electrophoretic pattern of DNA fragmentation and ultrastructural analysis. The left ventricle (LV) was excised and sliced. The myocardial infarct size as a percentage of the area at risk was assessed by triphenyltetrazolium chloride staining. DNA fragmentation was assessed by in situ TUNEL at the light microscopic level. ZVAD and DCI significantly reduced the mean blood pressure during reperfusion without affecting heart rate. There was no significant difference in the % area at risk (AAR) of LV among the 3 groups (control: 26.3+/-3.0%; ZVAD: 25.6+/-2.6%; DCI: 25.6+/-2.0%). The % infarct size as a percentage of the AAR in the ZVAD group (41.3+/-4.5%) and the DCI group (50.4+/-3.8%) was not significantly different from the control group (43.5+/-4.5%). However, the percent DNA fragmentation in the infarcted area in the ZVAD (3.5+/-0.8%) and DCI groups (4.2+/-0.9%) was significantly reduced compared with the control group (10.7+/-1.9%). The DNA ladder pattern observed in the control group was attenuated in both the ZVAD and DCI groups. There was no difference in electron microscopic changes among the 3 groups. Serine protease-dependent DNA fragmentation is present in infarcted myocytes, in addition to caspase-dependent DNA fragmentation, but an infarct-size reducing effect was not observed with either of these inhibitors.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"101 1","pages":"907-11"},"PeriodicalIF":0.0,"publicationDate":"2001-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76224725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Kawamura, T. Yoshikawa, T. Takahashi, T. Hayashi, E. Takahashi, T. Anzai, T. Sato, S. Ogawa
Increased neurohormone and cytokine concentrations are associated with adverse outcome in patients with congestive heart failure, so minimizing these increases may improve outcome, even in the acute phase of decompensated heart failure. The present study was designed to test the hypothesis that phosphodiesterase inhibitors, but not catecholamines, could favorably affect neurohormone and cytokine profiles in patients with acutely decompensated heart failure. Twenty-nine patients underwent monitoring using a Swan-Ganz catheter and were randomly allocated to receive phosphodiesterase inhibitors (PDEI group, n=19) or catecholamines (CA group, n=10). Pulmonary capillary wedge pressure decreased significantly in both groups and cardiac output showed a slight, but not statistically significant increase, in both groups. There was a significant decrease in plasma brain natriuretic peptide concentration in the PDEI group, but not in the CA group, whereas plasma interleukin-6 concentration increased in the CA group, but not in the PDEI group. Phosphodiesterase inhibitors favorably affect neurohormone and cytokine concentrations in patients with acutely decompensated heart failure.
{"title":"Randomized trial of phosphodiesterase inhibitors versus catecholamines in patients with acutely decompensated heart failure.","authors":"A. Kawamura, T. Yoshikawa, T. Takahashi, T. Hayashi, E. Takahashi, T. Anzai, T. Sato, S. Ogawa","doi":"10.1253/JCJ.65.858","DOIUrl":"https://doi.org/10.1253/JCJ.65.858","url":null,"abstract":"Increased neurohormone and cytokine concentrations are associated with adverse outcome in patients with congestive heart failure, so minimizing these increases may improve outcome, even in the acute phase of decompensated heart failure. The present study was designed to test the hypothesis that phosphodiesterase inhibitors, but not catecholamines, could favorably affect neurohormone and cytokine profiles in patients with acutely decompensated heart failure. Twenty-nine patients underwent monitoring using a Swan-Ganz catheter and were randomly allocated to receive phosphodiesterase inhibitors (PDEI group, n=19) or catecholamines (CA group, n=10). Pulmonary capillary wedge pressure decreased significantly in both groups and cardiac output showed a slight, but not statistically significant increase, in both groups. There was a significant decrease in plasma brain natriuretic peptide concentration in the PDEI group, but not in the CA group, whereas plasma interleukin-6 concentration increased in the CA group, but not in the PDEI group. Phosphodiesterase inhibitors favorably affect neurohormone and cytokine concentrations in patients with acutely decompensated heart failure.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"22 1","pages":"858-62"},"PeriodicalIF":0.0,"publicationDate":"2001-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75069254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hongmei Song, H. Tasaki, A. Yashiro, K. Yamashita, H. Taniguchi, Y. Nakashima
Elevated levels of acute-phase proteins, a systemic marker for inflammation, predict coronary events; Chlamydia pneumoniae (C. pneumoniae) infection is associated with coronary atherosclerosis. The present study investigated whether inflammation or infection is involved in the pathogenesis of acute coronary syndrome (ACS) and which one has the more important role. The study group comprised 49 patients with angiographically diagnosed ACS, 48 cases of chronic coronary heart disease (CCHD), and 44 subjects with a normal coronary profile. The levels of serum C-reactive protein (CRP), fibrinogen and anti-C. pneumoniae IgG antibody were measured. The IgG antibody against C. pneumoniae was higher in the ACS and CCHD groups compared with the control group after adjusting for age and gender. The levels of CRP and fibrinogen were significantly increased in patients with ACS compared with controls and CCHD patients. Multiple stepwise logistic regression analysis revealed that C. pneumoniae IgG antibody is an independent risk factor for both ACS and CCHD (odds ratio 2.3 and 2.1, respectively), but the CRP level is a risk factor only for ACS (odds ratio 6.9). The inflammatory response, as indicated by acute-phase proteins, especially CRP, rather than C. pneumoniae infection, may contribute more to the clinical course of ACS.
{"title":"Acute-phase proteins and Chlamydia pneumoniae infection: which one is more important in acute coronary syndrome?","authors":"Hongmei Song, H. Tasaki, A. Yashiro, K. Yamashita, H. Taniguchi, Y. Nakashima","doi":"10.1253/JCJ.65.853","DOIUrl":"https://doi.org/10.1253/JCJ.65.853","url":null,"abstract":"Elevated levels of acute-phase proteins, a systemic marker for inflammation, predict coronary events; Chlamydia pneumoniae (C. pneumoniae) infection is associated with coronary atherosclerosis. The present study investigated whether inflammation or infection is involved in the pathogenesis of acute coronary syndrome (ACS) and which one has the more important role. The study group comprised 49 patients with angiographically diagnosed ACS, 48 cases of chronic coronary heart disease (CCHD), and 44 subjects with a normal coronary profile. The levels of serum C-reactive protein (CRP), fibrinogen and anti-C. pneumoniae IgG antibody were measured. The IgG antibody against C. pneumoniae was higher in the ACS and CCHD groups compared with the control group after adjusting for age and gender. The levels of CRP and fibrinogen were significantly increased in patients with ACS compared with controls and CCHD patients. Multiple stepwise logistic regression analysis revealed that C. pneumoniae IgG antibody is an independent risk factor for both ACS and CCHD (odds ratio 2.3 and 2.1, respectively), but the CRP level is a risk factor only for ACS (odds ratio 6.9). The inflammatory response, as indicated by acute-phase proteins, especially CRP, rather than C. pneumoniae infection, may contribute more to the clinical course of ACS.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"16 1","pages":"853-7"},"PeriodicalIF":0.0,"publicationDate":"2001-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77075745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Matsui, S. Negoro, S. Nishida, Y. Saito, K. Kunisada, K. Yamauchi-Takihara
Severe right-side heart failure developed in a 47-year-old Japanese woman who suffered from hypoalbuminemia and a massive right side chylous pleural effusion. She had been diagnosed as having protein-losing enteropathy with right ventricular cardiomyopathy. Autopsy showed congenital anomalies of the lymph ducts and abnormal deposition of fibrous and fatty tissue in the right ventricular myocardium. The clinical and pathological findings are consistent with the nonarrythmogenic form of the arrythmogenic right ventricular dysplasia.
{"title":"Right ventricular cardiomyopathy accompanied by protein-losing enteropathy and chylous effusion.","authors":"H. Matsui, S. Negoro, S. Nishida, Y. Saito, K. Kunisada, K. Yamauchi-Takihara","doi":"10.1253/JCJ.65.912","DOIUrl":"https://doi.org/10.1253/JCJ.65.912","url":null,"abstract":"Severe right-side heart failure developed in a 47-year-old Japanese woman who suffered from hypoalbuminemia and a massive right side chylous pleural effusion. She had been diagnosed as having protein-losing enteropathy with right ventricular cardiomyopathy. Autopsy showed congenital anomalies of the lymph ducts and abnormal deposition of fibrous and fatty tissue in the right ventricular myocardium. The clinical and pathological findings are consistent with the nonarrythmogenic form of the arrythmogenic right ventricular dysplasia.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"22 10 1","pages":"912-4"},"PeriodicalIF":0.0,"publicationDate":"2001-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86231263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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