The present study evaluated the usefulness of 3-dimensional volume rendering (VR) images using electron-beam computed tomography (EBCT) in determining the possible causes of ischemia resulting from the anomalous origin of the right coronary artery (RCA) from the left sinus of Valsalva, which coursed between the ascending aorta and pulmonary trunk. Such anomalies could cause ischemia or sudden death without obstructive coronary artery disease. The suggested mechanism is either compression causing closure of the slit-like orifice of the anomalous artery as the aorta dilates with exertion or compression of the anomalous artery by the aorta and pulmonary trunk as it courses between these 2 arteries, which dilate with exercise. A 17-year-old male underwent EBCT coupled with a 100-ml intravenous injection of iodinated contrast medium. Data were reconstructed into 3-dimensional images through VR to evaluate the shape of the orifice and the spatial relationship of the RCA, ascending aorta and pulmonary trunk. Perspective VR showed the shape of the orifice of the left main trunk, which was not slit-like, and cut-plane VR showed the spatial relationship of both the lumen and the surface of the RCA, ascending aorta and pulmonary trunk, providing information on whether the ascending aorta or pulmonary trunk would compress the RCA and cause ischemia.
{"title":"Utility of three-dimensional volume rendering images using electron-beam computed tomography to evaluate possible causes of ischemia from an anomalous origin of the right coronary artery from the left sinus of valsalva.","authors":"N Funabashi, Y Kobayashi, G D Rubin","doi":"10.1253/jcj.65.575","DOIUrl":"10.1253/jcj.65.575","url":null,"abstract":"<p><p>The present study evaluated the usefulness of 3-dimensional volume rendering (VR) images using electron-beam computed tomography (EBCT) in determining the possible causes of ischemia resulting from the anomalous origin of the right coronary artery (RCA) from the left sinus of Valsalva, which coursed between the ascending aorta and pulmonary trunk. Such anomalies could cause ischemia or sudden death without obstructive coronary artery disease. The suggested mechanism is either compression causing closure of the slit-like orifice of the anomalous artery as the aorta dilates with exertion or compression of the anomalous artery by the aorta and pulmonary trunk as it courses between these 2 arteries, which dilate with exercise. A 17-year-old male underwent EBCT coupled with a 100-ml intravenous injection of iodinated contrast medium. Data were reconstructed into 3-dimensional images through VR to evaluate the shape of the orifice and the spatial relationship of the RCA, ascending aorta and pulmonary trunk. Perspective VR showed the shape of the orifice of the left main trunk, which was not slit-like, and cut-plane VR showed the spatial relationship of both the lumen and the surface of the RCA, ascending aorta and pulmonary trunk, providing information on whether the ascending aorta or pulmonary trunk would compress the RCA and cause ischemia.</p>","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"69 1","pages":"575-8"},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77503877","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}
T. Yasuda, K. Hashimura, Y. Matsu-ura, Y. Kato, T. Ueda, I. Mori, Y. Kijima
The human heart progressively becomes more tolerant to ischemia after repeated balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). The present study investigated whether nicorandil, a hybrid between nitrate and an ATP-sensitive potassium channel opener, affects this ischemic preconditioning. Sixteen patients with stable angina pectoris caused by left anterior descending artery lesions were subjected to 2 balloon inflations of 2-min duration with a 3-min reperfusion period. Seven of these patients served as the control group and in the remaining 9 patients, nicorandil was administered intravenously (6 mg/h) throughout the PTCA procedure (nicorandil group). The lactate extraction ratio (LER) was obtained at 30 s after each ischemic event (LERpost-1 and LERpost-2) in both groups. In the control group, LERpost-1 was more negative than LERpost-2 (-185.7+/-74.2 vs -98.0+/-37.3%, p<0.01). The ratio of the sum of the ST elevation in the precordial leads during the second inflation (sumST-2, 0.94+/-0.66 mV) to that during the first inflation (sumST-1, 1.43+/-1.17 mV) was 0.72+/-0.16 in the control group, which was less than the ratio in the nicorandil group (1.06+/-0.13, p<0.01). Nicorandil abolished the difference between the 2 ischemic events (LERpost-1, -45.1+/-41.6 vs LERpost-2, -43.5+/-51.1%; sumST-1, 1.38+/-0.80 vs sumST-2, 1.46+/-0.90 mV). LER was less negative in the nicorandil group than that in the control group (LERpost-1, -45.1+/-41.6 vs -185.7+/-74.2%, p<0.01; LERpost-2, -43.5+/-51.1 vs -98.0+/-37.3%, p<0.05). Thus, nicorandil improved lactate metabolism during PTCA without significantly influencing ST-elevation. In conclusion, intravenous pre-administration of nicorandil appears to precondition the human heart during PTCA.
在经皮腔内冠状动脉成形术(PTCA)中反复球囊膨胀后，人类心脏对缺血的耐受性逐渐增强。本研究调查了硝酸和atp敏感的钾通道打开剂之间的杂交种尼可地尔是否影响这种缺血预处理。对16例由左前降支病变引起的稳定型心绞痛患者行2次球囊充气术，持续时间2 min，再灌注时间3 min。其中7例患者作为对照组，其余9例患者在PTCA过程中静脉注射尼可地尔(6 mg/h)(尼可地尔组)。在每次缺血后30s测定两组乳酸提取比(LERpost-1和LERpost-2)。对照组LERpost-1阳性比LERpost-2阴性(-185.7+/-74.2 vs -98.0+/-37.3%， p<0.01)。对照组第二次充气时(sumST-2, 0.94+/-0.66 mV)与第一次充气时(sumST-1, 1.43+/-1.17 mV)心前导联ST抬高之和之比为0.72+/-0.16，低于尼可地尔组(1.06+/-0.13,p<0.01)。尼可地尔消除了两种缺血性事件之间的差异(LERpost-1， -45.1+/-41.6 vs LERpost-2， -43.5+/-51.1%;sumST-1, 1.38 + / - -0.80 vs sumST-2, 1.46 + / - -0.90 mV)。尼可地尔组的LER阴性程度低于对照组(LERpost-1， -45.1+/-41.6 vs -185.7+/-74.2%， p<0.01;LERpost-2 -43.5 + / - -51.1 vs -98.0 + / - -37.3%, p < 0.05)。因此，尼可地尔改善PTCA期间的乳酸代谢，但不显著影响st段抬高。总之，静脉预给药尼可地尔似乎在PTCA期间对人类心脏有前置作用。
{"title":"Nicorandil, a hybrid between nitrate and ATP-sensitive potassium channel opener, preconditions human heart to ischemia during percutaneous transluminal coronary angioplasty.","authors":"T. Yasuda, K. Hashimura, Y. Matsu-ura, Y. Kato, T. Ueda, I. Mori, Y. Kijima","doi":"10.1253/JCJ.65.526","DOIUrl":"https://doi.org/10.1253/JCJ.65.526","url":null,"abstract":"The human heart progressively becomes more tolerant to ischemia after repeated balloon inflations during percutaneous transluminal coronary angioplasty (PTCA). The present study investigated whether nicorandil, a hybrid between nitrate and an ATP-sensitive potassium channel opener, affects this ischemic preconditioning. Sixteen patients with stable angina pectoris caused by left anterior descending artery lesions were subjected to 2 balloon inflations of 2-min duration with a 3-min reperfusion period. Seven of these patients served as the control group and in the remaining 9 patients, nicorandil was administered intravenously (6 mg/h) throughout the PTCA procedure (nicorandil group). The lactate extraction ratio (LER) was obtained at 30 s after each ischemic event (LERpost-1 and LERpost-2) in both groups. In the control group, LERpost-1 was more negative than LERpost-2 (-185.7+/-74.2 vs -98.0+/-37.3%, p<0.01). The ratio of the sum of the ST elevation in the precordial leads during the second inflation (sumST-2, 0.94+/-0.66 mV) to that during the first inflation (sumST-1, 1.43+/-1.17 mV) was 0.72+/-0.16 in the control group, which was less than the ratio in the nicorandil group (1.06+/-0.13, p<0.01). Nicorandil abolished the difference between the 2 ischemic events (LERpost-1, -45.1+/-41.6 vs LERpost-2, -43.5+/-51.1%; sumST-1, 1.38+/-0.80 vs sumST-2, 1.46+/-0.90 mV). LER was less negative in the nicorandil group than that in the control group (LERpost-1, -45.1+/-41.6 vs -185.7+/-74.2%, p<0.01; LERpost-2, -43.5+/-51.1 vs -98.0+/-37.3%, p<0.05). Thus, nicorandil improved lactate metabolism during PTCA without significantly influencing ST-elevation. In conclusion, intravenous pre-administration of nicorandil appears to precondition the human heart during PTCA.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"19 1","pages":"526-30"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77733858","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}
I. Nishi, K. Iida, S. Kawano, T. Masumi, I. Yamaguchi
Trials have demonstrated that carvedilol can produce hemodynamic, symptomatic, and prognostic improvements in dilated cardiomyopathy (DCM), but some DCM patients have deteriorated after carvedilol, developing congestive heart failure. The present study investigated the use of isoproterenol (ISP) stress echocardiography to select those patients with DCM who would respond to carvedilol. ISP was infused intravenously in 22 patients with DCM and they were classified into 2 groups based on the left ventricular systolic response: good response to ISP [change in fractional shortening (FS) with ISP > 0.05, n=13] and poor response to ISP (change < or = 0.05, n=9). In the good response group, FS significantly increased from 0.12+/-0.04 to 0.17+/-0.08 (mean+/-SD, p<0.05) with carvedilol, and 7 patients improved symptomatically (New York Heart Association class). However, in the poor response group, no significant difference was observed between FS at baseline and that at the end of follow-up. Moreover, only 1 patient in the poor response group improved symptomatically. ISP stress echocardiography can assist in selecting patients with DCM who will respond positively to carvedilol.
{"title":"Using isoproterenol stress echocardiography to predict the response to carvedilol in patients with dilated cardiomyopathy.","authors":"I. Nishi, K. Iida, S. Kawano, T. Masumi, I. Yamaguchi","doi":"10.1253/JCJ.65.514","DOIUrl":"https://doi.org/10.1253/JCJ.65.514","url":null,"abstract":"Trials have demonstrated that carvedilol can produce hemodynamic, symptomatic, and prognostic improvements in dilated cardiomyopathy (DCM), but some DCM patients have deteriorated after carvedilol, developing congestive heart failure. The present study investigated the use of isoproterenol (ISP) stress echocardiography to select those patients with DCM who would respond to carvedilol. ISP was infused intravenously in 22 patients with DCM and they were classified into 2 groups based on the left ventricular systolic response: good response to ISP [change in fractional shortening (FS) with ISP > 0.05, n=13] and poor response to ISP (change < or = 0.05, n=9). In the good response group, FS significantly increased from 0.12+/-0.04 to 0.17+/-0.08 (mean+/-SD, p<0.05) with carvedilol, and 7 patients improved symptomatically (New York Heart Association class). However, in the poor response group, no significant difference was observed between FS at baseline and that at the end of follow-up. Moreover, only 1 patient in the poor response group improved symptomatically. ISP stress echocardiography can assist in selecting patients with DCM who will respond positively to carvedilol.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"1 1","pages":"514-8"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76724966","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}
Using data from a survey of a white-collar working population in Taiwan (438 women, 526 men), the relation between job strain status and cardiovascular risk factors (high serum total cholesterol, low serum high-density lipoprotein (HDL) cholesterol, and high plasma fibrinogen) was examined. Job strain indicators, defined by Karasek's model, included psychological demand and decision latitude. Blood pressure, cholesterol and fibrinogen were analyzed as continuous variables, whereas psychological demand and decision latitude were dichotomized into 2 levels and job strain into 4 exposure categories. Plasma fibrinogen was significantly and positively associated with job strain status in both male and female workers and also with decision latitude in female workers only. No consistent association between job strain status and total serum and HDL cholesterol was detectable. In conclusion, plasma fibrinogen is a possible intermediate factor linking occupational stress to elevated cardiovascular risk.
{"title":"Association between job strain status and cardiovascular risk in a population of Taiwanese white-collar workers.","authors":"C. Su","doi":"10.1253/JCJ.65.509","DOIUrl":"https://doi.org/10.1253/JCJ.65.509","url":null,"abstract":"Using data from a survey of a white-collar working population in Taiwan (438 women, 526 men), the relation between job strain status and cardiovascular risk factors (high serum total cholesterol, low serum high-density lipoprotein (HDL) cholesterol, and high plasma fibrinogen) was examined. Job strain indicators, defined by Karasek's model, included psychological demand and decision latitude. Blood pressure, cholesterol and fibrinogen were analyzed as continuous variables, whereas psychological demand and decision latitude were dichotomized into 2 levels and job strain into 4 exposure categories. Plasma fibrinogen was significantly and positively associated with job strain status in both male and female workers and also with decision latitude in female workers only. No consistent association between job strain status and total serum and HDL cholesterol was detectable. In conclusion, plasma fibrinogen is a possible intermediate factor linking occupational stress to elevated cardiovascular risk.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"2 1","pages":"509-13"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81157875","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}
mammals, have resident smooth muscle cells in the tunica intima underneath the endothelial monolayer, even before atherosclerotic changes begin.1,2 The thickness of the intimal layer increases progressively as humans age from fetus to child to young adult, and its complex structure probably favors the formation of atheroma. When atherogenesis begins, the artery wall becomes host to inflammatory cells, including macrophages and T lymphocytes,3 and an excess of risk factors accelerates the pathological changes in the artery. Presently, the most understood risk factor is low-density lipoprotein (LDL). Epidemiological and clinical studies suggest that elevated levels of plasma cholesterol, especially LDL particles, increase the risk of acute coronary events.4,5 Beginning with Anitschkow and Chalatow’s description in 1913 of a diet rich in cholesterol that induced atherosclerosis in rabbits, 6 a number of animal studies have linked hypercholesterolemia to atherosclerosis. 7–9 In vitro studies, however, suggested that native LDL itself does not induce vascular cell activation and foam cell formation, the features that are related to atherosclerosis. In the late 1980s, the ‘oxidized LDL’ hypothesis postulated the missing link between hypercholesterolemia and atherosclerosis;10 that is, excess LDL in the artery wall can be modified, which instigates an inflammatory response on the endothelial surface of the artery.11 Endothelial activation, in turn, causes an infiltration of macrophages, one of the hallmarks of the atherosclerotic lesion. 12–15 Macrophage-rich atheroma, which are prone to rupture and thrombus formation, result in the onset of acute coronary syndromes such as unstable angina and myocardial infarction.16–19 Recent clinical and preclinical studies have repeatedly suggested that lipid lowering can stabilize these vulnerable plaques and improve clinical outcomes.20 This review will discuss the current understanding of the biology of vascular inflammation, the pathophysiolgy of acute thrombotic complications, and the likely mechanisms responsible for the effects of lipid-lowering therapy.
{"title":"Evolution and stabilization of vulnerable atherosclerotic plaques.","authors":"P. Libby, M. Aikawa","doi":"10.1253/JCJ.65.473","DOIUrl":"https://doi.org/10.1253/JCJ.65.473","url":null,"abstract":"mammals, have resident smooth muscle cells in the tunica intima underneath the endothelial monolayer, even before atherosclerotic changes begin.1,2 The thickness of the intimal layer increases progressively as humans age from fetus to child to young adult, and its complex structure probably favors the formation of atheroma. When atherogenesis begins, the artery wall becomes host to inflammatory cells, including macrophages and T lymphocytes,3 and an excess of risk factors accelerates the pathological changes in the artery. Presently, the most understood risk factor is low-density lipoprotein (LDL). Epidemiological and clinical studies suggest that elevated levels of plasma cholesterol, especially LDL particles, increase the risk of acute coronary events.4,5 Beginning with Anitschkow and Chalatow’s description in 1913 of a diet rich in cholesterol that induced atherosclerosis in rabbits, 6 a number of animal studies have linked hypercholesterolemia to atherosclerosis. 7–9 In vitro studies, however, suggested that native LDL itself does not induce vascular cell activation and foam cell formation, the features that are related to atherosclerosis. In the late 1980s, the ‘oxidized LDL’ hypothesis postulated the missing link between hypercholesterolemia and atherosclerosis;10 that is, excess LDL in the artery wall can be modified, which instigates an inflammatory response on the endothelial surface of the artery.11 Endothelial activation, in turn, causes an infiltration of macrophages, one of the hallmarks of the atherosclerotic lesion. 12–15 Macrophage-rich atheroma, which are prone to rupture and thrombus formation, result in the onset of acute coronary syndromes such as unstable angina and myocardial infarction.16–19 Recent clinical and preclinical studies have repeatedly suggested that lipid lowering can stabilize these vulnerable plaques and improve clinical outcomes.20 This review will discuss the current understanding of the biology of vascular inflammation, the pathophysiolgy of acute thrombotic complications, and the likely mechanisms responsible for the effects of lipid-lowering therapy.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"13 1","pages":"473-9"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91343108","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}
T. Hitsumoto, K. Yoshinaga, H. Noike, M. Kanai, K. Shirai
The present study investigated the clinical significance of preheparin serum lipoprotein lipase (LPL) mass in coronary vasospasm by examining its relationship with the acetylcholine-induced coronary artery response in patients without angiographically demonstrable atherosclerotic coronary artery disease (CAD). The subjects were 39 men who had suspected CAD and who underwent coronary angiography. Coronary vasospasm was defined as a marked luminal narrowing or total occlusion provoked by the intracoronary administration of acetylcholine. Preheparin LPL mass was lower (p<0.05) in 25 subjects in whom vasospasm was induced by the acetylcholine provocation test than in the 14 subjects with a negative response. As regards preheparin LPL mass, the subjects with multiple vessel spasm had significantly low concentrations (p<0.05) compared with single vessel spasm, although serum lipid levels were not significantly different. Multiple regression analysis revealed only preheparin LPL mass had a significant absolute t-value (2.016) among the coronary risk factors. Low preheparin LPL mass is interpreted as reflecting an impaired acetylcholine-induced coronary relaxation in coronary vasospasm and preheparin LPL mass may be useful as a marker of early stage coronary atherosclerosis that is not detectable by angiography.
{"title":"Clinical significance of preheparin serum lipoprotein lipase mass in coronary vasospasm.","authors":"T. Hitsumoto, K. Yoshinaga, H. Noike, M. Kanai, K. Shirai","doi":"10.1253/JCJ.65.539","DOIUrl":"https://doi.org/10.1253/JCJ.65.539","url":null,"abstract":"The present study investigated the clinical significance of preheparin serum lipoprotein lipase (LPL) mass in coronary vasospasm by examining its relationship with the acetylcholine-induced coronary artery response in patients without angiographically demonstrable atherosclerotic coronary artery disease (CAD). The subjects were 39 men who had suspected CAD and who underwent coronary angiography. Coronary vasospasm was defined as a marked luminal narrowing or total occlusion provoked by the intracoronary administration of acetylcholine. Preheparin LPL mass was lower (p<0.05) in 25 subjects in whom vasospasm was induced by the acetylcholine provocation test than in the 14 subjects with a negative response. As regards preheparin LPL mass, the subjects with multiple vessel spasm had significantly low concentrations (p<0.05) compared with single vessel spasm, although serum lipid levels were not significantly different. Multiple regression analysis revealed only preheparin LPL mass had a significant absolute t-value (2.016) among the coronary risk factors. Low preheparin LPL mass is interpreted as reflecting an impaired acetylcholine-induced coronary relaxation in coronary vasospasm and preheparin LPL mass may be useful as a marker of early stage coronary atherosclerosis that is not detectable by angiography.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"10 1","pages":"539-44"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77025121","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. Matsukida, Y. Otsuji, S. Hamasaki, S. Yoshifuku, T. Kumanohoso, C. Fujiyama-Koriyama, A. Kisanuki, S. Minagoe, C. Tei
When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r2=0.73), LV peak +dP/dt (p<0.05, r2=0.37), peak (+dP/dt)/P (p<0.01, r2=0.71), peak -dP/dt (p<0.05, r2=0.25), and tau (p<0.05, r2=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation.
{"title":"Monophasic transmitral flow pattern with less increase in heart rate indicates left ventricular dysfunction.","authors":"K. Matsukida, Y. Otsuji, S. Hamasaki, S. Yoshifuku, T. Kumanohoso, C. Fujiyama-Koriyama, A. Kisanuki, S. Minagoe, C. Tei","doi":"10.1253/JCJ.65.545","DOIUrl":"https://doi.org/10.1253/JCJ.65.545","url":null,"abstract":"When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r2=0.73), LV peak +dP/dt (p<0.05, r2=0.37), peak (+dP/dt)/P (p<0.01, r2=0.71), peak -dP/dt (p<0.05, r2=0.25), and tau (p<0.05, r2=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"14 1","pages":"545-9"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84581373","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. Tomita, Yoshio Arakaki, Yasuo Ono, Osamu Yamada, T. Yagihara, S. Echigo
The Doppler echocardiograms of the aortic valve and associated aortic regurgitation (AR) were reviewed in 72 patients with a ventricular septal defect (VSD). Group I comprised 13 patients without any deformity of the aortic cusp for > or = 10 years, group 2 included 35 patients who did not develop AR for > or = 10 years after right coronary cusp prolapse (RCCP) was first detected, group 3 comprised 11 patients with RCCP and AR in whom the AR remained subclinical for > or = 10 years, and group 4 was 13 patients who underwent surgical treatment because of moderate to severe AR. The cusp imbalance index [width of right (R) or non- (N) coronary cusp/width of left coronary cusp (L)] was compared among the 4 groups. R/L or N/L was larger in group 4 than in groups 1-3; R/L exceeded 1.30 in all the patients in group 4, whereas it was less than 1.30 in all the atients in groups 1-3. Two patients in group 4 with non-coronary cusp prolapse had an N/L greater than 1.50. No other patients in any group had an N/L larger than 1.20. An imbalance of cusp width may predict possible progressive deterioration of AR.
{"title":"Imbalance of cusp width and aortic regurgitation associated with aortic cusp prolapse in ventricular septal defect.","authors":"H. Tomita, Yoshio Arakaki, Yasuo Ono, Osamu Yamada, T. Yagihara, S. Echigo","doi":"10.1253/JCJ.65.500","DOIUrl":"https://doi.org/10.1253/JCJ.65.500","url":null,"abstract":"The Doppler echocardiograms of the aortic valve and associated aortic regurgitation (AR) were reviewed in 72 patients with a ventricular septal defect (VSD). Group I comprised 13 patients without any deformity of the aortic cusp for > or = 10 years, group 2 included 35 patients who did not develop AR for > or = 10 years after right coronary cusp prolapse (RCCP) was first detected, group 3 comprised 11 patients with RCCP and AR in whom the AR remained subclinical for > or = 10 years, and group 4 was 13 patients who underwent surgical treatment because of moderate to severe AR. The cusp imbalance index [width of right (R) or non- (N) coronary cusp/width of left coronary cusp (L)] was compared among the 4 groups. R/L or N/L was larger in group 4 than in groups 1-3; R/L exceeded 1.30 in all the patients in group 4, whereas it was less than 1.30 in all the atients in groups 1-3. Two patients in group 4 with non-coronary cusp prolapse had an N/L greater than 1.50. No other patients in any group had an N/L larger than 1.20. An imbalance of cusp width may predict possible progressive deterioration of AR.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"6 1","pages":"500-4"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85364309","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. Ito, K. Takahashi, H. Sasaki, H. Akiho, Y. Katahira, H. Saito, T. Ishibashi
A 52-year-old woman suffered from acute massive myocardial infarction in association with a large thrombus in the ascending aorta. She was a moderate smoker and was taking hormone supplement therapy for menopausal hormone insufficiency and the contraceptive pill for endometriosis. Cardiac angiography revealed a large mobile filling defect close to the orifice of the left coronary artery, but the left coronary artery could not be visualized. Her hemodynamic condition was impaired so greatly that intraarterial counterpulsation and intravenous thrombolysis was immediately performed. The thrombus dissolved in 1 h and recanalization of the left coronary artery was achieved without serious systemic thromboembolism. She has been doing well with no cardiac events for 7 years. This is the second report of a large thrombus in ascending aorta being the cause of acute myocardial infarction in the whole territory of the left coronary artery, and the first to diagnose such a thrombus antemortem and treat it successfully.
{"title":"Large thrombus in the ascending aorta successfully treated by thrombolysis--an unusual cause of acute massive myocardial infarction.","authors":"H. Ito, K. Takahashi, H. Sasaki, H. Akiho, Y. Katahira, H. Saito, T. Ishibashi","doi":"10.1253/JCJ.65.572","DOIUrl":"https://doi.org/10.1253/JCJ.65.572","url":null,"abstract":"A 52-year-old woman suffered from acute massive myocardial infarction in association with a large thrombus in the ascending aorta. She was a moderate smoker and was taking hormone supplement therapy for menopausal hormone insufficiency and the contraceptive pill for endometriosis. Cardiac angiography revealed a large mobile filling defect close to the orifice of the left coronary artery, but the left coronary artery could not be visualized. Her hemodynamic condition was impaired so greatly that intraarterial counterpulsation and intravenous thrombolysis was immediately performed. The thrombus dissolved in 1 h and recanalization of the left coronary artery was achieved without serious systemic thromboembolism. She has been doing well with no cardiac events for 7 years. This is the second report of a large thrombus in ascending aorta being the cause of acute myocardial infarction in the whole territory of the left coronary artery, and the first to diagnose such a thrombus antemortem and treat it successfully.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"39 1","pages":"572-4"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87510435","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}
M. Miyamoto, C. Kishimoto, K. Shioji, H. Nakamura, S. Toyokuni, Y. Nakayama, M. Kita, J. Yodoi, S. Sasayama
Redox regulating mechanisms may be involved in the pathogenesis of viral myocarditis and thioredoxin (TRX) is a small multifunctional protein that contains a redox active sequence. The present study investigated the histopathology and characteristics of TRX expression in acute coxsackievirus B3 myocarditis in inbred strains of mice (severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice and mild myocarditis in C57BL/6 mice). Thioredoxin was upregulated and its expression correlated with the severity of the disease. In addition, 8-hydroxy-2'-deoxyguanosine, which is an established marker for oxidative stress, was concominantly positive in damaged myocytes. Thus, TRX may be specifically induced by the acute inflammatory stimuli in murine viral myocarditis, and the severity and development of acute viral myocarditis may be regulated by the cellular redox state.
{"title":"Difference in thioredoxin expression in viral myocarditis in inbred strains of mice.","authors":"M. Miyamoto, C. Kishimoto, K. Shioji, H. Nakamura, S. Toyokuni, Y. Nakayama, M. Kita, J. Yodoi, S. Sasayama","doi":"10.1253/JCJ.65.561","DOIUrl":"https://doi.org/10.1253/JCJ.65.561","url":null,"abstract":"Redox regulating mechanisms may be involved in the pathogenesis of viral myocarditis and thioredoxin (TRX) is a small multifunctional protein that contains a redox active sequence. The present study investigated the histopathology and characteristics of TRX expression in acute coxsackievirus B3 myocarditis in inbred strains of mice (severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice and mild myocarditis in C57BL/6 mice). Thioredoxin was upregulated and its expression correlated with the severity of the disease. In addition, 8-hydroxy-2'-deoxyguanosine, which is an established marker for oxidative stress, was concominantly positive in damaged myocytes. Thus, TRX may be specifically induced by the acute inflammatory stimuli in murine viral myocarditis, and the severity and development of acute viral myocarditis may be regulated by the cellular redox state.","PeriodicalId":14544,"journal":{"name":"Japanese circulation journal","volume":"20 1","pages":"561-4"},"PeriodicalIF":0.0,"publicationDate":"2001-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77178660","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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