Relationship between transcardiac gradient of endothelin-1 and left ventricular remodelling in patients with first anterior myocardial infarction
|
|
- Elijah Craig
- 5 years ago
- Views:
Transcription
1 European Heart Journal (2003) 24, Relationship between transcardiac gradient of endothelin-1 and left ventricular remodelling in patients with first anterior myocardial infarction T. Tsutamoto *, A. Wada, M. Hayashi, T. Tsutsui, K. Maeda, M. Ohnishi, M. Fujii, T. Matsumoto, T. Yamamoto, T. Takayama, C. Ishii, M. Kinoshita First Department of Internal Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu , Japan Received 23 May 2002; accepted 12 June 2002 KEYWORDS Acute myocardial infarction; Endothelin-1; Brain natriuretic peptide; Ventricular remodelling Aims To evaluate whether plasma endothelin-1 (ET-1) is extracted or produced through the heart in patients with acute myocardial infarction (AMI), and the relationship between transcardiac extraction of plasma ET-1 and left ventricular (LV) remodelling. Methods and results We measured the plasma level of ET-1 in the aortic root (Ao) and coronary sinus (CS) in 48 consecutive patients, who received successful revascularization and enalapril, for a first anterior AMI. In the acute phase the plasma ET-1 level was significantly higher both in the Ao and the CS compared to the control subjects. However, the plasma ET-1 level was significantly lower in the CS than in the Ao in the acute phase and after 1 month. There were significant correlations between transcardiac extraction of ET-1 in the acute phase and LV ejection fraction and LV end-diastolic volume index (LVEDVI) after 1 month. Stepwise multivariate analysis showed that maximal creatine phosphokinase and transcardiac extraction of plasma ET-1 during the acute phase were independently and positively correlated with the absolute change in LVEDVI after 1 month. Conclusions These results indicate that elevated circulating ET-1 is extracted through the heart in patients with a first anterior AMI and that the extracted ET-1 plays a significant role in modulating post-infarct LV remodelling The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved. Introduction Endothelin-1 (ET-1) is a potent endotheliumderived vasoconstrictor peptide, 1 and its long-term effects include stimulation of myocardial hypertrophy, 2 fibroblast proliferation, 3 interstitial fibrosis, 4 * Corresponding author. Tel.: ; fax: address: tutamoto@belle.shiga-med.ac.jp (T. Tsutamoto). and myocardial cell injury, 5 suggesting an important role in ventricular remodelling after acute myocardial infarction (AMI). In an experimental model of AMI, ET-1 systems including prepro ET-1 mrna and ET receptor mrna are activated in the heart, 6 8 and ET-1 receptor antagonists had beneficial effects on mortality and left ventricular remodelling. 6,9,10 In addition, a high plasma ET-1 is an important prognostic predictor in patients with X/03/$ - see front matter 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved. doi: /s x(02)
2 Transcardiac extraction of endothelin in AMI 347 AMI, 11 suggesting that endogenous ET-1 has an important role in the pathogenesis of AMI. Moreover, we recently demonstrated that suppression of plasma ET-1 during the acute phase of AMI prevented postinfarct left ventricular remodelling. 12 ET-1 is produced not only by the endothelial cells but also by ventricular myocytes, 13,14 especially in pathological states such as hypertrophy and myocardial infarction, 6,15,16 suggesting that the elevated circulating ET-1 is partly derived from the heart in patients with AMI. Recent reports, including ours, showed that elevated circulating ET-1 is extracted across the failing heart in patients with severe congestive heart failure (CHF). 17,18 Moreover, there was a significant correlation between the transcardiac gradient of plasma ET-1 and the left ventricular end-diastolic volume index (LVEDVI) 17 in patients with CHF. However, the cause and effect of the relation between the transcardiac gradient of plasma ET-1 and LVEDVI remains unknown because we could not repeatedly measure these parameters in the previous study. 17 Previous reports, including ours, showed that the main source of increased ET-1 is the pulmonary circulation in patients with CHF. 17,19 However, whether circulating ET-1 is spilled over or extracted across the heart, the role of endogenous ET-1 on left ventricular (LV) remodelling in patients with AMI remains unknown. In the present study, we evaluated (1) whether plasma ET-1 is extracted or produced through the heart during the acute-phase, and (2) if plasma ET-1 is extracted, whether the transcardiac extraction of plasma ET-1 during the acute phase is related to LV remodelling after 1 month in patients with a first anterior AMI, who received successful revascularization and enalapril. Method Study population We prospectively studied 54 patients, the study population, who were admitted to the coronary care unit of our institution with a first anterior AMI, and presented Thrombolysis in Myocardial Infarction (TIMI) grade 0 or 1 flow at initial coronary angiography. Admission criteria included prolonged chest pain (>30 min), an electrocardiographic ST segment elevation >2 mv in two or more adjacent precordial leads, successful reperfusion therapy within 24 h of the onset of chest pain documented by coronary angiography, and a more than threefold increase in serum creatine phosphokinase (CK) levels. Admission criteria was the same as previously reported. 12 The patients who had prior myocardial infarction; significant stenosis of a coronary artery not related to the infarcted area and residual stenosis (>70%) of the infarct-related coronary artery were excluded from this study. We also selected 14 age-matched normal subjects (age, 44 to 72, mean=58 years) who were admitted complaining of chest pain, whose hearts proved to be normal by coronary angiography. All patients gave informed consent, and the study was approved by the Committee on Human Investigation at our institution. Patients were classified into two groups; Remodelling ( ) group and Remodelling (+) group, based on the absolute change of LVEDVI. The cutoff level was the median value for the absolute change of LVEDVI after 1 month. Study design and protocol All patients underwent cardiac catheterization by the femoral approach. Patients with persistent occlusion of the infarct-related vessel underwent percutaneous transluminal coronary angioplasty following standard techniques. Patients who could not obtain more than 70% patency and/or TIMI 3 flow were excluded from this study. After obtaining revascularization (patency 70% and TIMI 3 flow) and assuring hemodynamic stability, right-sided cardiac catheterization using a 7F Swan-Ganz catheter and measurement of LV end-diastolic pressure (LVEDP) using a 5F pig tail catheter were performed. Blood samples for measuring plasma ET-1 were collected simultaneously from the Ao and CS as previously reported. 17 We also measured plasma levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and aldosterone in the Ao and CS. After angioplasty and blood sampling was done, contrast left ventriculography was performed. After admission to the coronary care unit, all patients received oral aspirin and/or ticlopidine. ACE inhibitors (enalapril) were administrated to all patients. Repeat cardiac catheterization and contrast left ventriculography were performed 1 month after the initial catheterization to determine culprit artery patency and LV function. Left ventriculography performed by contrast medium was analysed for LV ejection fraction (LVEF) and LV volume by cardiologists who were unaware of the patients' data at the acute-phase and after 1 month. Hemodynamic measurement using a Swan Ganz catheter, and blood sampling from the Ao and CS were also performed. Patients with significant
3 348 T. Tsutamoto et al. Table 1 Patient characteristics restenosis (>70%) of the culprit lesion were excluded from the study. Measurement of neurohumoral factors The plasma ET-1 level was determined using an antibody directed against synthetic ET-1 (Peninsula Laboratories, Inc., Belmont, CA, USA) and 125 I ET-1 (Amersham Japan, Tokyo, Japan) as previously reported. 20 Plasma concentrations of ANP and BNP were measured with a specific immunoradiometric assay using a commercial kit (Shionogi, Osaka, Japan) as previously reported. 21 Plasma aldosterone levels were measured using a commercial kit as previously reported. 12 Statistical analysis Remodelling ( ) group (n=24) Remodelling (+) group (n=24) P value Age (years) 61.8± ±2.3 ns Gender (male/female) 22/2 18/6 ns Symptom onset-reflow time (h) 4.6± ±0.9 ns Max CK (IUH ml 1 ) 1858± ±425 < Collateral (grade 2) 4 5 ns Risk factors Smoking ns Hypertension 9 9 ns Hyperlipidemia 11 7 ns Diabetes mellitus 5 5 ns Acute therapy Intravenous nitroglycerin ns Catecholamine 7 8 ns IABP 3 4 ns In-hospital therapy Oral nitrates ns Ca antagonists 7 5 ns Diuretics 0 3 ns Beta blockades 6 11 ns ACE inhibitor (enalapril) dose (mg) 6.2± ±0.53 ns ACE=angiotensin-converting enzyme, Ca=calcium, CK=creatine phosphokinase, IABP=intra aortic balloon pumping. 14 variables. A values of P<0.05 was considered significant. Results Clinical characteristics (Table 1) Fifty-four consecutive patients who met the entry criteria were enrolled. One patient died of lethal arrhythmia, two died of CHF. Three patients were excluded from this study due to restenosis of the culprit coronary artery. Therefore, 48 of 54 patients enrolled in the trial completed the entire protocol. There were no differences in baseline characteristics including the dose of ACE inhibitor (enalapril). However, maximal CK was significantly higher in the Remodelling (+) group than in the Remodelling ( ) group. All results are expressed as the mean±sem. Categoric data were compared against chi-squared distribution. Student's t test was used for continuous variables between groups, and paired t test was used for within group comparison. Linear regression analysis was used to determine the relation between continuous variables. To evaluate the contribution of ET-1 extraction at the acute-phase to LVEDVI 1 month after onset, univariate and stepwise multivariate analysis were used among the Difference between plasma concentration of ET-1 in the Ao and the CS In 14 age-matched control subjects, the plasma ET-1 level was significantly higher in CS than in Ao (1.7±0.1 vs 1.5±0.07 pg ml 1, P<0.05) (Fig. 1). In 48 patients with AMI in the acute phase, plasma ET-1 level was significantly higher both in the Ao and the CS compared to that in the control subjects, and plasma ET-1 level was significantly lower in CS than
4 Transcardiac extraction of endothelin in AMI 349 month after onset, absolute change in LVEF was significantly higher in the Remodelling ( ) group than in the Remodelling (+) group. Neurohumoral factors (Table 3) Fig. 1 Plasma endothelin-1 (ET-1) concentrations during the acute phase in the aortic root (Ao) and coronary sinus (CS) in patients with a first anterior acute myocardial infarction (AMI) compared with those of the control subjects. Open bars show the plasma ET-1 levels in the control subjects. Closed bars show the plasma ET-1 levels in the acute-phase in patients with AMI. *P<0.01 vs the value of the Ao in the control subjects, **P<0.001 vs the value of the Ao in patients with AMI. Ao in the acute phase (Fig. 1) and 1 month after onset of AMI. The transcardiac extraction of ET-1 in the acute phase was significantly higher in the Remodelling (+) group than in the Remodelling ( ) group (Fig. 2). Hemodynamic parameters, and LV function and volume (Table 2) In the acute phase, there were no significant differences in hemodynamic parameters such as mean blood pressure and mean pulmonary arterial pressure between the Remodelling (+) group and the Remodelling ( ) group. Pulmonary capillary wedge pressure and LV end-diastolic pressure in the Remodelling (+) group were higher than those in the Remodelling ( ) group. Regarding LV function and volumes in the acute phase, there was no difference in LVEDVI and the LV end-systolic volume index between the two groups. LVEF in the Remodelling (+) group was significantly lower than that in the Remodelling ( ) group. One In the acute phase, there were no significant differences in plasma levels of ANP, BNP, or ET-1 in the Ao and the CS between between the Remodelling (+) group and the Remodelling ( ) group. However, the transcardiac extraction of ET-1 was significantly higher in the Remodelling (+) group than in the Remodelling ( ) group. One month after onset, plasma BNP in the Ao and the transcardiac gradient of BNP in the Remodelling (+) were significantly higher group than those in the Remodelling ( ) group. There was no difference of the transcardiac extraction of ET-1 between the two groups. Relationship of plasma ET-1 extraction across the heart and LV remodelling Although there was no correlation between the transcardiac extraction of ET-1 in the acute phase and LV function in the acute phase, such as LVEF and LVEDVI, there were significant correlations between the transcardiac extraction of ET-1 in the acute phase, and LVEF (r K0.51, P ) and LVEDVI (r 0.463, P ) after 1 month (Fig. 3). Moreover, there were significant positive correlations between the plasma ET-1 in the Ao and the transcardiac gradient of ET-1 (Fig. 4A), and between the transcardiac gradient of ET-1 in the acute phase and the absolute change in LVEDVI after 1 month (Fig. 4B). Table 4 shows the results of univariate and multivariate analysis among 14 variables related to the acute phase to assess factors regulating the absolute change in LVEDVI 1 month after onset. According to stepwise multivariate analysis, high levels of transcardiac extraction of ET-1 (P ) and aldosterone in the acute phase (P ) and maximal CK (P ) were significant independent predictors of the absolute change in LVEDVI after 1 month. Discussion The results of this study demonstrated that (1) plasma ET-1 is extracted through the heart in the acute phase and 1 month after onset of the first anterior AMI, and (2) the transcardiac gradient of plasma ET-1 in the acute phase correlates with the absolute change in LVEDVI 1 month after onset, independent of maximal CK. These results indicated that elevated circulating ET-1 is extracted
5 350 T. Tsutamoto et al. Fig. 2 Comparison of the transcardiac gradient of endothelin-1 (ET-1) between the Remodelling ( ) group and the Remodelling (+) group in patients with a first anterior acute myocardial infarction (AMI). Closed bars show the transcardiac gradient of ET-1 during the acute phase and open bars showed the transcardiac gradient of ET-1 after 1 month in patients with AMI. Ao=aortic root; CS=coronary sinus. *P<0.05 vs the value of the remodelling ( ) group. through the heart and that the transcardiac extraction of ET-1 is a significant predictor of postinfarct remodelling independent of infarct size and plasma aldosterone levels in patients with a first anterior AMI, who received successful revascularization and enalapril. Plasma ET-1 difference between the Ao and CS in patients with AMI ET-1 systems, including ET receptors, are activated and ET-1 antagonists had beneficial effects on mortality in the experimental model of AMI In addition, a high plasma ET-1 is an important prognostic predictor in patients with AMI, 11 suggesting that endogenous ET-1 plays an important role in the pathogenesis of AMI. ET-1 is produced not only by endothelial cells but also by ventricular myocytes, especially in pathological states such as hypertrophy and myocardial infarction, suggesting that the elevated circulating ET-1 is partly derived from the heart in patients with AMI. Previous reports, including ours, showed that the main source of the increased ET-1 is pulmonary circulation in patients with CHF. 19,20 To our knowledge, there were no reports on whether plasma ET-1 is a spillover or extracted across the human heart after an AMI. In the present study, the plasma ET-1 level was significantly higher both in the Ao and the CS compared to the control subjects, and was significantly lower in CS than Ao in patients with AMI in the acute phase. Therefore, we demonstrated for the first time, that elevated circulating plasma ET-1 is extracted through the heart in the acute phase of AMI. These findings were similar to those of our previous report 17 and the recent study by Azevedo et al. 18 in patients with CHF, suggesting that plasma ET-1 is also extracted through the heart in patients with AMI and that the increase in ET-1 concentration in the heart with AMI is partly due to the extraction of circulating ET-1 through the heart. Possibility of upregulation of ET-1 receptors in the heart of patients with AMI The present findings suggest that ET receptors are upregulated after ischemia and reperfusion in patients with AMI, which is supported by the experimental study. 6,8,22 As described for beta adrenoreceptors, where ischemia causes an increase in cardiac beta adrenoreceptor density despite raised plasma levels of catecholamines, 23 we speculate
6 Transcardiac extraction of endothelin in AMI 351 Table 2 Hemodynamics and LV function, at the acute phase and after 1 month that the possible increase in ET-1 binding sites is caused by an acute phase reactant response to severe cellular stress induced by ischemia and reperfusion. Liu et al., reported that 125 I-ET-1 binding sites in rat cardiomyocytes were increased after ischemia and reperfusion, 22 suggesting the upregulation of ET-1 receptors in the rat heart with AMI in the acute phase. There was no data on whether ET-1 receptors are upregulated in the human heart with AMI just after revascularization. However, our findings suggest that ET-1 receptors are upregulated in the heart of AMI patients in the acute phase, which is consistent with the experimental data. 22 Indeed, Liu et al. 22 commented that the ischemia and reperfusion induced increase in ET-1 binding sites is caused by externalization of latent receptors. Remodelling ( ) group (n=24) Remodelling (+) group (n=24) P value Hemodynamics Heart rate (beats min 1 ) Acute 74.5± ±3.8 ns 1 month 67.9± ±2.5 ns MBP (mmhg) Acute 93.6± ±3.7 ns 1 month 87.6± ±3.1 ns MPA (mmhg) Acute 17.7± ±1.3 ns 1 month 12.3± ±0.6 ns RA (mmhg) Acute 4.3± ±1.3 ns 1 month 2.8± ±0.4 ns PCWP (mmhg) Acute 14.5± ± month 7.1± ±0.5 ns LVEDP (mmhg) Acute 17.0± ± month 9.5± ± Cardiac index (l min 1 m 2 ) Acute 2.6± ±0.1 ns 1 month 3.0± ±0.1 ns LV function LVEF (%) Acute 47.2± ± month 56.8± ±1.3 < Absolute change 9.6± ± LVEDVI (ml m 2 ) Acute 87.6± ±2.2 ns 1 month 86.5± ±4.0 < Absolute change 1.0±2.4 45±4.0 < LVESVI (ml m 2 ) Acute 46.4± ±2.1 ns 1 month 37.8± ±3.3 < Absolute change 8.5± ±2.9 < Absolute change=(value at 1 month) (value during the acute phase), LVEDP=left ventricular end-diastolic pressure, LVEDVI=left ventricular end-diastolic volume index, LVEF=left ventricular ejection fraction, LVESVI=left ventricular end-systolic volume index, MBP=mean arterial blood pressure, MPA=mean pulmonary arterial pressure, PCWP=pulmonary capillary wedge pressure, RA=mean right atrial pressure. Transcardiac extraction of ET-1 and LV remodelling in patients with AMI The transcardiac extraction of ET-1 in the acute phase and after 1 month were significantly higher in the Remodelling (+) group than in the Remodelling ( ) group. In addition, we demonstrated a significant positive correlation of the transcardiac ET-1 gradient at the acute-phase with LVEDVI after 1 month and a significant positive correlation between the transcardiac extraction of ET-1 in the acute phase and the absolute change in LVEDVI, indicating that circulating ET-1 is extracted through the heart and promotes LV remodelling via ET-1 receptors in these patients. Recently, we reported that elevated circulating ET-1 is extracted across the failing heart with a significant correlation
7 352 T. Tsutamoto et al. Table 3 Neurohumoral factors Remodelling ( ) group (n=24) Remodelling (+) group (n=24) P value ANP level at Ao (pg ml 1 ) Acute 108.4± ±21 ns 1 month 55.5± ±13.6 ns (CS-Ao) ANP (pg ml 1 ) Acute 259±49 413±72 ns 1 month 284±55 413±69 ns BNP level at Ao (pg ml 1 ) Acute 82.1±22 109±28 ns 1 month 60.1± ± (CS-Ao) BNP (pg ml 1 ) Acute 128±28 173±47 ns 1 month 104±23 198± ET-1 level at Ao (pg ml 1 ) Acute 3.0± ±0.2 ns 1 month 2.5± ±0.1 ns ET-1 level at CS (pg ml 1 ) Acute 2.9± ±0.2 ns 1 month 2.2± ±0.1 ns (Ao-CS) ET-1 (pg ml 1 ) Acute 0.10± ± month 0.25± ±0.1 ns ANP=atrial natriuretic peptide, Ao=aortic root, ET=endothelin, BNP=brain natriuretic peptide, CS=coronary sinus. Fig. 3 Correlation between the transcardiac gradient of endothelin-1 (ET-1) during the acute phase and left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume index (LVEDVI) after 1 month in patients with a first anterior acute myocardial infarction. Ao=aortic root; CS=coronary sinus. between the transcardiac gradient of plasma ET-1 and LVEDVI, 17 suggesting that ET receptors are upregulated in the failing ventricle and that the elevated circulating ET-1 might stimulate the process of left ventricular remodelling in patients with severe CHF. However, the cause and effect of the relation between the transcardiac gradient of plasma ET-1 and LVEDVI remains unknown because we could not repeatedly measure these parameters in the previous study. 17 In the present study, we repeatedly evaluated the relationship between the transcardiac gradient of plasma ET-1 and LVEDVI in patients with AMI. Taken together with the findings of the present study, sustained ET-1 extraction may cause post infarct LV remodelling.
8 Transcardiac extraction of endothelin in AMI 353 Fig. 4 (A): Correlation between the plasma endothelin-1 (ET-1) in the aortic root (Ao) and transcardiac gradient of ET-1 during the acute phase in patients with a first anterior acute myocardial infarction. (B): Correlation between the transcardiac gradient of endothelin-1 (ET-1) during the acute phase and absolute change in left ventricular end-diastolic volume index (LVEDVI) after 1 month in patients with a first anterior acute myocardial infarction. Ao=aortic root; CS=coronary sinus. Table 4 Univariate and multivariate linear model of the absolute change of LVEDVI 1 month after onset in 48 patients with first anterior AMI Variable Univariate correlation P value Multivariate beta P value coefficient coefficient (SE) Age (years) Max CK (IU dl 1 ) < (0.001) Heart rate (beats min 1 ) MBP (mmhg) Cardiac index (l min 1 m 2 ) LVEDP (mmhg) LVEF (%) LVEDVI (ml m 2 ) Aldosterone in Ao (pg ml 1 ) Aldosterone in CS (pg ml 1 ) (CS-Ao) Aldosterone (pg ml 1 ) < (1.143) ET-1 in Ao (pg ml 1 ) ET-1 in CS (pg ml 1 ) (Ao-CS) ET-1 (pg ml 1 ) (3.99) All variables were measured during the acute phase. Abbreviations are explained in Tables 1, 2 and 3. LV remodelling was shown to be regulated by multiple factors, including mechanical, neurohumoral and therapeutic factors. Recently, we reported that plasma aldosterone is extracted through the heart and that the extracted aldosterone plays an important role in modulating post-infarct LV remodeling. 24 According to stepwise multivariate analysis, high transcardiac gradient levels of plasma ET-1 and aldosterone in the acute phase and a high level of maximal CK among the 14 acute-phase variables were significant independent predictors of a large LVEDVI at 1 month, suggesting that the extraction of ET-1 during the acute phase, along with infarct size and the extraction of aldosterone plays a significant role in modulating LV remodelling after AMI. Clinical implications MI is one of the major etiological factors leading to CHF. The evidence of increased cardiac ET systems
9 354 T. Tsutamoto et al. after AMI and the fact that ET-1 receptor antagonists had beneficial effects on mortality and left ventricular remodelling of rat AMI have important pathophysiological implications. Increased plasma ET-1 in patients with AMI has been shown to be a strong and independent predictor of 1-year mortality. In the present study, there was a significant positive correlation between plasma ET-1 in the Ao and the transcardiac extraction of ET-1 in patients with AMI. Moreover, ET receptor antagonists can reduce the degree of myocardial fibrosis in experimental MI. In the present study, we demonstrated that transcardiac extraction of plasma ET-1 in the acute phase correlates with the absolute change in LVEDVI after 1 month of onset in AMI patients who received ACE inhibitors. Our data suggest that therapy to decrease the plasma levels of ET-1 and aldosterone 12 and ET-1 receptor antagonists could prevent LV remodelling in patients with a first anterior AMI. However, further studies are needed to clarify the role of endogenous ET-1 on postinfarct LV remodelling. Study limitation In this clinical study, we could not clearly demonstrate that ET-1 extracted through the heart plays a causal role in modulating postinfarct LV remodelling and we cannot deny the possibility that the transcardiac extraction of ET-1 is one of the markers of the extent of LV remodelling. However, treatment to decrease plasma ET-1, which correlated with the transcardiac extraction of ET-1, in combination with ACE inhibitors 12 prevented LV remodelling in patients with a first anterior AMI. Furthermore, in an experimental model of AMI, ET-1 receptor antagonists had beneficial effects on mortality and left ventricular remodeling. 6,9,10 Therefore, these findings seem to support our hypothesis. In this study, patients with multivessel and prior myocardial infarction were excluded from this study. This study also excluded patients with restenosis of the culprit lesion because significant stenosis (>70%) might reduce coronary flow and perfusion. To verify the effect of ET-1 extraction under such complex conditions, further studies are needed. Being unable to measure the total amount of ET-1 extraction, because CS flow was not measured, is also a limitation of this study. However, in the present study, patients with a significant coronary stenosis were excluded when the blood samplings indicated that the transcardiac gradient of ET-1 reflected the amount of ET-1 extraction through the heart. Conclusions In patients with AMI, plasma ET-1 during the acute phase was significantly lower in the CS than in the Ao, suggesting ET-1 extraction across the heart. The transcardiac gradient of plasma ET-1 in the acute phase was correlated with the absolute change in LVEDVI 1 month after onset. Moreover, transcardiac ET-1 extraction in the acute phase affected LVEDVI after 1 month independent of infarct size. These findings suggest that elevated transcardiac ET-1 extraction through the heart plays a significant role in regulating post-infarct LV remodelling in patients with AMI. Acknowledgements This study was partly supported by a Japanese Grant-in-Aid for Scientific Research. We wish to thank Ms Ikuko Sakaguchi for excellent technical assistance. We also express thanks to Mr Daniel Mrozek for assistance in preparing the manuscript. References 1. Yanagisawa M, Kurihara H, Kimura S et al. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 1988;332: Ito H, Hirata Y, Hiroe M et al. Endothelin-1 induces hypertrophy with enhanced expression of muscle-specific genes in cultured neonatal rat cardiomyocytes. Circ Res 1991; 69: Takuwa N, Takuwa Y, Yanagisawa M et al. A novel vasoactive peptide endothelin stimulate mitogenesis through isositol lipid turnover in Swiss 3T3 fibroblasts. J Biol Chem 1989; 264: Guarda E, Katwa LC, Myers PR et al. Effects of endothelin on collagen turnover in cardiac fibroblasts. Cardiovasc Res 1993;27: Han H, Neubauer B, Braeker B et al. Endothelin-1 contributes to ischemia/reperfusion injury in isolated rat heart. Attenuation of ischemic injury by the endothelin-1 antagonists BQ 123 and BQ 610. J Mol Cell Cardiol 1995;27: Sakai S, Miyauchi T, Kobayashi M et al. Inhibition of myocardial endothelin pathway improves long term survival in heart failure. Nature 1996;384: Tonnessen T, Christensen G, Oie E et al. Increased cardiac expression of endothelin-1 mrna in ischemic heart failure in rays. Cardiovasc Res 1997;33: Kobayashi T, Miyauchi T, Sakai S et al. Expression of endothelin-1, ET-A and ET-B receptors, and ECE and distribution of endothelin-1 in failing rat heart. Am J Physiol 1999;276:H Mulder P, Richard V, Derumeaux G et al. Role of endogenous endothelin in chronic heart failure: effect of long-term treatment with an endothelin antagonist on survival, hemodynamics, and cardiac remodeling. Circulation 1997; 96: Tranidis A, Lim S, Hanna RD et al. Combined angiotensin and endothelin receptor blockade attenuates adverse cardiac remodeling post-myocardial infarction in the rat: possible role of tansforming growth factor b1. J Mol Cell Cardiol 2001;33:
10 Transcardiac extraction of endothelin in AMI Omland T, Lie RT, Aakvaag A et al. Plasma endothelin determination as a prognostic indicator of 1-year mortality after acute myocardial infarction. Circulation 1994; 89: Hayashi M, Tsutamoto T, Wada A et al. Intravenous atrial natriuretic peptide prevents left ventricular remodeling in patients with first anterior acute myocardial infarction. J Am Coll Cardiol 2001;37: Suzuki T, Kumazaki T, Mitsui Y. Endothelin-1 is produced and secreted by neonatal rat cardiac myocytes in vitro. Biochem Biophys Res Commun 1993;191: Thomas PB, Liu ECK, Webb ML et al. Evidence of endothelin-1 autocrine loop in cardiac myocytes; relation to contractile function with congestive heart failure. Am J Physiol 1996;40:H Tonnessen T, Giaid A, Saleh GD et al. Increased in vivo expression and production of endothelin-1 by porcine cardiacmyocytes subjected to ischemia. Circ Res 1995; 76: Sakai S, Miyauchi T, Sakurai T et al. Endogenous endothelin-1 participates in the maintenance of cardiac function in rats with congestive heart failure: marked increase in endothelin-1 production in the failing heart. Circulation 1996;93: Tsutamoto T, Wada A, Maeda K et al. Transcardiac extraction of circulating endothelin-1 across the failing heart. Am J Cardiol 2000;86: Azevedo ER, Stewart DJ, Parker JD. Increased extraction of endothelin-1 across the failing human heart. Am J Cardiol 2001;88: Yoshibayashi M, Nishioka K, Nakao K et al. Plasma endothelin concentrations in patients with pulmonary hypertension associated with congestive heart defects: evidence of increased production of endothelin in pulmonary hypertension. Circulation 1991;84: Tsutamoto T, Wada A, Maeda Y et al. Relation between endothelin-1 spillover in the lungs and pulmonary vascular resistance in patients with chronic heart failure. J Am Coll Cardiol 1994;23: Tsutamoto T, Wada A, Maeda K et al. Attenuation of compensation of endogenous cardiac natriuretic peptide system in chronic heart failure: prognostic role of plasma brain natriuretic peptide concentration in patients with chronic symptomatic left ventricular dysfunction. Circulation 1997; 96: Liu J, Chen R, Casley DJ et al. Ischemic and reperfusion increase 125I-labeled endothelin-1 binding in rat cardiac membranes. Am J Physiol 1990;258:H Strasser RH, Krimmer J, Marquetant R. Regulation of a adrenergic receptors: impaired densitization in myocardial ischemia. J Cardiovasc Pharmacol 1988;12:S Hayashi M, Tsutamoto T, Wada A et al. Relationship between transcardiac extraction of aldosterone and left ventricular remodeling in patients with first acute myocardial infarction: extracting aldosterone through the heart promotes ventricular remodeling after acute myocardial infarction. J Am Coll Cardiol 2001;38:
Comparison with plasma angiotensin II and endothelin-1
European Heart Journal (1999) 2, 1799 187 Article No. euhj.1999.1746, available online at http://www.idealibrary.com on Plasma brain natriuretic peptide level as a biochemical marker of morbidity and mortality
More informationJournal of the American College of Cardiology Vol. 33, No. 2, by the American College of Cardiology ISSN /99/$20.
Journal of the American College of Cardiology Vol. 33, No. 2, 1999 1999 by the American College of Cardiology ISSN 0735-1097/99/$20.00 Published by Elsevier Science Inc. PII S0735-1097(98)00573-7 Relationship
More informationLow fractional diastolic pressure in the ascending aorta increased the risk of coronary heart disease
(2002) 16, 837 841 & 2002 Nature Publishing Group All rights reserved 0950-9240/02 $25.00 www.nature.com/jhh ORIGINAL ARTICLE Low fractional diastolic pressure in the ascending aorta increased the risk
More informationOutline. Pathophysiology: Heart Failure. Heart Failure. Heart Failure: Definitions. Etiologies. Etiologies
Outline Pathophysiology: Mat Maurer, MD Irving Assistant Professor of Medicine Definitions and Classifications Epidemiology Muscle and Chamber Function Pathophysiology : Definitions An inability of the
More informationIntraaortic Balloon Counterpulsation- Supportive Data for a Role in Cardiogenic Shock ( Be Still My Friend )
Intraaortic Balloon Counterpulsation- Supportive Data for a Role in Cardiogenic Shock ( Be Still My Friend ) Stephen G. Ellis, MD Section Head, Interventional Cardiology Professor of Medicine Cleveland
More informationPathophysiology: Heart Failure
Pathophysiology: Heart Failure Mat Maurer, MD Irving Assistant Professor of Medicine Outline Definitions and Classifications Epidemiology Muscle and Chamber Function Pathophysiology Heart Failure: Definitions
More informationThe ACC 50 th Annual Scientific Session
Special Report The ACC 50 th Annual Scientific Session Part One From March 18 to 21, 2001, physicians from around the world gathered to learn, to teach and to discuss at the American College of Cardiology
More informationConflict of Interest Slide
Comparison of six- month clinical outcomes, event free survival rates of patients undergoing enhanced external counterpulsation (EECP) for coronary artery disease in the United States and Europe Ozlem
More informationClinical Investigations
Clinical Investigations Deeply Reinverted T Wave at 14 Days After the Onset of First Anterior Acute Myocardial Infarction Predicts Improved Left Ventricular Function at 6 Months Address for correspondence:
More informationIn Vivo Animal Models of Heart Disease. Why Animal Models of Disease? Timothy A Hacker, PhD Department of Medicine University of Wisconsin-Madison
In Vivo Animal Models of Heart Disease Timothy A Hacker, PhD Department of Medicine University of Wisconsin-Madison Why Animal Models of Disease? Heart Failure (HF) Leading cause of morbidity and mortality
More informationCardiogenic Shock. Carlos Cafri,, MD
Cardiogenic Shock Carlos Cafri,, MD SHOCK= Inadequate Tissue Mechanisms: Perfusion Inadequate oxygen delivery Release of inflammatory mediators Further microvascular changes, compromised blood flow and
More informationVentricular Arrhythmias in Acute MI Patients Undergoing Primary PCI
Ventricular Arrhythmias in Acute MI Patients Undergoing Primary PCI Bulent Gorenek MD FACC FESC Eskişehir Osmangazi University Cardiology Department Eskisehir-Turkey I do not have any potential conflict
More informationIschemic Postconditioning During Primary Percutaneous Coronary Intervention Mechanisms and Clinical Application Jian Liu, MD FACC FESC FSCAI Chief Phy
Ischemic Postconditioning During Primary Percutaneous Coronary Intervention Mechanisms and Clinical Application Jian Liu, MD FACC FESC FSCAI Chief Physician, Professor of Medicine Department of Cardiology,
More informationPlasma Brain Natriuretic Peptide as a Noninvasive Marker for Efficacy of Pulmonary Thromboendarterectomy
Plasma Brain Natriuretic Peptide as a Noninvasive Marker for Efficacy of Pulmonary Thromboendarterectomy Noritoshi Nagaya, MD, Motomi Ando, MD, Hideo Oya, MD, Yutaka Ohkita, MD, Shingo Kyotani, MD, Fumio
More informationJournal of the American College of Cardiology Vol. 38, No. 4, by the American College of Cardiology ISSN /01/$20.
Journal of the American College of Cardiology Vol. 38, No. 4, 2001 2001 by the American College of Cardiology ISSN 0735-1097/01/$20.00 Published by Elsevier Science Inc. PII S0735-1097(01)01477-2 Diabetes
More informationValve Disease in Patients With Heart Failure TAVI or Surgery? Miguel Sousa Uva Hospital Cruz Vermelha Lisbon, Portugal
Valve Disease in Patients With Heart Failure TAVI or Surgery? Miguel Sousa Uva Hospital Cruz Vermelha Lisbon, Portugal I have nothing to disclose. Wide Spectrum Stable vs Decompensated NYHA II IV? Ejection
More informationRelationship between body mass index, coronary disease extension and clinical outcomes in patients with acute coronary syndrome
Relationship between body mass index, coronary disease extension and clinical outcomes in patients with acute coronary syndrome Helder Dores, Luís Bronze Carvalho, Ingrid Rosário, Sílvio Leal, Maria João
More informationPreoperative Parameters Predicting the Postoperative Course of Endoventricular Circular Patch Plasty
Original Article Preoperative Parameters Predicting the Postoperative Course of Endoventricular Circular Patch Plasty Keiichiro Kondo, MD, Yoshihide Sawada, MD, and Shinjiro Sasaki, MD, PhD It is necessary
More informationCHRONIC HEART FAILURE : WHAT ELSE COULD WE OFFER TO OUR PATIENTS? Cardiac Rehabilitation Society of Thailand
CHRONIC HEART FAILURE : WHAT ELSE COULD WE OFFER TO OUR PATIENTS? Cardiac Rehabilitation Society of Thailand ENHANCED EXTERNAL COUNTER PULSATION Piyanuj Ruckpanich, MD. Cardiac Rehabilitation Center Perfect
More informationDr. Khairy Abdel Dayem. Professor of Cardiology Ain-Shams University
Dr. Khairy Abdel Dayem Professor of Cardiology Ain-Shams University RALES Randomized Aldactone Evaluation Study 1. NEJM 1999 2. Bertram Pitt 3. 1660 Class III and IV HF patients 4. EF 35% 5. 841 placebo
More informationCardiovascular Disorders Lecture 3 Coronar Artery Diseases
Cardiovascular Disorders Lecture 3 Coronar Artery Diseases By Prof. El Sayed Abdel Fattah Eid Lecturer of Internal Medicine Delta University Coronary Heart Diseases It is the leading cause of death in
More informationHFpEF. April 26, 2018
HFpEF April 26, 2018 (J Am Coll Cardiol 2017;70:2476 86) HFpEF 50% or more (40-71%) of patients with CHF have preserved LV systolic function. HFpEF is an increasingly frequent hospital discharge. Outcomes
More informationCommon Codes for ICD-10
Common Codes for ICD-10 Specialty: Cardiology *Always utilize more specific codes first. ABNORMALITIES OF HEART RHYTHM ICD-9-CM Codes: 427.81, 427.89, 785.0, 785.1, 785.3 R00.0 Tachycardia, unspecified
More informationSUPPLEMENTAL MATERIAL
SUPPLEMENTAL MATERIAL Clinical perspective It was recently discovered that small RNAs, called micrornas, circulate freely and stably in human plasma. This finding has sparked interest in the potential
More informationVentricular tachycardia and ischemia. Martin Jan Schalij Department of Cardiology Leiden University Medical Center
Ventricular tachycardia and ischemia Martin Jan Schalij Department of Cardiology Leiden University Medical Center Disclosure: Research grants from: Boston Scientific Medtronic Biotronik Sudden Cardiac
More informationInfluence of Paroxysmal Atrial Fibrillation Attack on Brain Natriuretic Peptide Secretion
Influence of Paroxysmal Atrial Fibrillation Attack on Brain Natriuretic Peptide Secretion Keizo Kazuhiko TSUCHIDA,MD TANABE, MD Abstract Objectives. Plasma brain natriuretic peptide BNP concentration is
More informationExternal Counterpulsation
External Counterpulsation Presented by Dr Rakesh Mohanlall 2011 14 September ASPECTS Overview of ECP The Place of ECP in the Medical Arena Economic Impact of ECP & Cost Benefits Academic Impact of ECP
More informationCronicon CARDIOLOGY. N Laredj*, HM Ali Lahmar and L Hammou. Abstract
Cronicon OPEN ACCESS CARDIOLOGY Research Article Persistent Ischemia in Recovery Predicts Mortality after Myocardial Infarction in Patients Undergoing Dobutamine N Laredj*, HM Ali Lahmar and L Hammou Department
More informationRecovering Hearts. Saving Lives.
Recovering Hearts. Saving Lives ṬM The Door to Unload (DTU) STEMI Safety & Feasibility Pilot Trial November 218 Recovering Hearts. Saving Lives. LEGAL DISCLAIMERS This presentation includes select slides
More informationScreening for Cardiac Dysfunction in Asymptomatic Patients by Measuring B-type Natriuretic Peptide Levels
Screening for Cardiac Dysfunction in Asymptomatic Patients by Measuring B-type Natriuretic Peptide Levels Toru SUZUKI, MD, Kazuhide YAMAOKI,MD,OsamuNAKAJIMA, 1 MD, Tsutomu YAMAZAKI, MD, Yoshiharu YAMADA,
More informationHeart Failure with Preserved Ejection Fraction: Mechanisms and Management
Heart Failure with Preserved Ejection Fraction: Mechanisms and Management Jay N. Cohn, M.D. Professor of Medicine Director, Rasmussen Center for Cardiovascular Disease Prevention University of Minnesota
More informationCardiac Drugs: Chapter 9 Worksheet Cardiac Agents. 1. drugs affect the rate of the heart and can either increase its rate or decrease its rate.
Complete the following. 1. drugs affect the rate of the heart and can either increase its rate or decrease its rate. 2. drugs affect the force of contraction and can be either positive or negative. 3.
More informationHospital and 1-year outcome after acute myocardial infarction in patients with diabetes mellitus and hypertension
(2003) 17, 665 670 & 2003 Nature Publishing Group All rights reserved 0950-9240/03 $25.00 www.nature.com/jhh ORIGINAL ARTICLE Hospital and 1-year outcome after acute myocardial infarction in patients with
More informationThe Who, How and When of Advanced Heart Failure Therapies. Disclosures. What is Advanced Heart Failure?
The Who, How and When of Advanced Heart Failure Therapies 9 th Annual Dartmouth Conference on Advances in Heart Failure Therapies Dartmouth-Hitchcock Medical Center Lebanon, NH May 20, 2013 Joseph G. Rogers,
More informationPathophysiology: Heart Failure. Objectives
Pathophysiology: Heart Failure Mat Maurer, MD Irving Assistant Professor of Clinical Medicine Objectives At the conclusion of this seminar, learner will be able to: 1. Define heart failure as a clinical
More informationCover Page. The handle holds various files of this Leiden University dissertation
Cover Page The handle http://hdl.handle.net/1887/21543 holds various files of this Leiden University dissertation Author: Dharma, Surya Title: Perspectives in the treatment of cardiovascular disease :
More informationChapter 10. Learning Objectives. Learning Objectives 9/11/2012. Congestive Heart Failure
Chapter 10 Congestive Heart Failure Learning Objectives Explain concept of polypharmacy in treatment of congestive heart failure Explain function of diuretics Learning Objectives Discuss drugs used for
More informationPrediction of Mortality by High-Sensitivity C-Reactive Protein and Brain Natriuretic Peptide in Patients With Dilated Cardiomyopathy
Circ J 6; 7: 87 863 Prediction of Mortality by High-Sensitivity C-Reactive Protein and Brain Natriuretic Peptide in Patients With Dilated Cardiomyopathy Chitose Ishikawa, MD; Takayoshi Tsutamoto, MD; Masanori
More informationTopic Page: congestive heart failure
Topic Page: congestive heart failure Definition: congestive heart f ailure from Merriam-Webster's Collegiate(R) Dictionary (1930) : heart failure in which the heart is unable to maintain an adequate circulation
More informationDIASTOLIC HEART FAILURE
DIASTOLIC HEART FAILURE M Mohsen Ibrahim, MD Alexandria, Proposed Criteria for Diastolic Heart Failure ESC Working Group (EHJ 1998) CHF signs/symptoms EF 45% Hemodynamic or echo evidence of diastolic dysfunction
More informationAssessing Cardiac Risk in Noncardiac Surgery. Murali Sivarajan, M.D. Professor University of Washington Seattle, Washington
Assessing Cardiac Risk in Noncardiac Surgery Murali Sivarajan, M.D. Professor University of Washington Seattle, Washington Disclosure None. I have no conflicts of interest, financial or otherwise. CME
More informationValue of echocardiography in chronic dyspnea
Value of echocardiography in chronic dyspnea Jahrestagung Schweizerische Gesellschaft für /Schweizerische Gesellschaft für Pneumologie B. Kaufmann 16.06.2016 Chronic dyspnea Shortness of breath lasting
More informationAcute Myocardial Infarction
Acute Myocardial Infarction Hafeza Shaikh, DO, FACC, RPVI Lourdes Cardiology Services Asst.Program Director, Cardiology Fellowship Associate Professor, ROWAN-SOM Acute Myocardial Infarction Definition:
More informationDefinition of Congestive Heart Failure
Heart Failure Definition of Congestive Heart Failure A clinical syndrome of signs & symptoms resulting from the heart s inability to supply adequate tissue perfusion. CHF Epidemiology Affects 4.7 million
More informationIn the name of GOD. Animal models of cardiovascular diseases: myocardial infarction & hypertension
In the name of GOD Animal models of cardiovascular diseases: myocardial infarction & hypertension 44 Presentation outline: Cardiovascular diseases Acute myocardial infarction Animal models for myocardial
More informationAcute Changes in Circulating Natriuretic Peptide Levels in Relation to Myocardial Ischemia
Journal of the American College of Cardiology Vol. 44, No. 10, 2004 2004 by the American College of Cardiology Foundation ISSN 0735-1097/04/$30.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2004.07.057
More informationWHI Form Report of Cardiovascular Outcome Ver (For items 1-11, each question specifies mark one or mark all that apply.
WHI Form - Report of Cardiovascular Outcome Ver. 6. COMMENTS To be completed by Physician Adjudicator Date Completed: - - (M/D/Y) Adjudicator Code: OMB# 095-044 Exp: 4/06 -Affix label here- Clinical Center/ID:
More informationIndications of Coronary Angiography Dr. Shaheer K. George, M.D Faculty of Medicine, Mansoura University 2014
Indications of Coronary Angiography Dr. Shaheer K. George, M.D Faculty of Medicine, Mansoura University 2014 Indications for cardiac catheterization Before a decision to perform an invasive procedure such
More informationHeart Failure. Subjective SOB (shortness of breath) Peripheral edema. Orthopnea (2-3 pillows) PND (paroxysmal nocturnal dyspnea)
Pharmacology I. Definitions A. Heart Failure (HF) Heart Failure Ezra Levy, Pharm.D. HF Results when one or both ventricles are unable to pump sufficient blood to meet the body s needs There are 2 types
More informationInfluence of Treatment Delay on Infarct Size and Clinical Outcome in Patients With Acute Myocardial Infarction Treated With Primary Angioplasty
629 Influence of Treatment Delay on Infarct Size and Clinical Outcome in Patients With Acute Myocardial Infarction Treated With Primary Angioplasty AYLEE L. LIEM, MD, ARNOUD W.J. VAN T HOF, MD, JAN C.A.
More informationOnline Appendix (JACC )
Beta blockers in Heart Failure Collaborative Group Online Appendix (JACC013117-0413) Heart rate, heart rhythm and prognostic effect of beta-blockers in heart failure: individual-patient data meta-analysis
More informationW e1 CARDIOVASCULAR MEDICINE
573 CARDIOVASCULAR MEDICINE Serial changes in plasma brain natriuretic peptide concentration at the infarct and non-infarct sites in patients with left ventricular remodelling after myocardial infarction
More informationMedical Management of Acute Coronary Syndrome: The roles of a noncardiologist. Norbert Lingling D. Uy, MD Professor of Medicine UERMMMCI
Medical Management of Acute Coronary Syndrome: The roles of a noncardiologist physician Norbert Lingling D. Uy, MD Professor of Medicine UERMMMCI Outcome objectives of the discussion: At the end of the
More informationPeripheral and Cardiology Coder 2018
Peripheral and Cardiology Coder 2018 Cardiovascular Services and Procedures Prepared and Published By: MedLearn Publishing A Division of MedLearn Media, Inc. 445 Minnesota Street, Suite 514 St. Paul, MN
More informationPathophysiology of Coronary Microvascular Dysfunction
Pathophysiology of Coronary Microvascular Dysfunction Cheol Woong Yu, MD, PhD Cardiology Department Division of Internal Medicine Korea University Anam Hospital. Etiologies of Chest Pain without obstructive
More informationNo-reflow Phenomenon in Patients with Acute Myocardial Infarction: Its Pathophysiology and Clinical Implications
No-reflow Phenomenon in Patients with Acute Myocardial Infarction: Its Pathophysiology and Clinical Implications * 164 Ito Acta Med. Okayama Vol. 63, No. 4 Normal case Anterior MI Fig. 3 Myocardial contrast
More informationHon-Kan Yip, MD; Chiung-Jen Wu, MD; Morgan Fu, MD; Kuo-Ho Yeh, MD; Teng-Hung Yu, MD; Wei-Chin Hung, MD; and Mien-Cheng Chen, MD
Clinical Features and Outcome of Patients With Direct Percutaneous Coronary Intervention for Acute Myocardial Infarction Resulting From Left Circumflex Artery Occlusion* Hon-Kan Yip, MD; Chiung-Jen Wu,
More informationThe Author(s) This article is published with open access by ASEAN Federation of Cardiology
DOI 10.7603/s40602-014-0011-3 ASEAN Heart Journal http://www.aseanheartjournal.org/ Vol. 22, no. 1, 60 65 (2014) ISSN: 2315-4551 Erratum Erratum to: Impact Of Sex On Clinical Characteristics And In-Hospital
More informationPre-discussion questions
Amanda Bartlett, PA-C Dustin Bartlett, PA-C Andrea Applegate, PA-C Leslie Yearta Brown, NP CHF Round Table Discussion Objectives ANDREA- Discuss the definition and different categories of CHF DUSTIN- Define
More informationA-type (atrial) and B-type (brain) natriuretic peptides (ANP and
Secretion of A-type and B-type natriuretic peptides into the bloodstream and pericardial space in children with congenital heart disease Yoshio Ootaki, MD, PhD Masahiro Yamaguchi, MD, PhD Naoki Yoshimura,
More informationPhysiologically Assessed Coronary Collateral Flow and Adverse Cardiac Ischemic Events: A Follow-Up Study in 403 Patients With Coronary Artery Disease
Journal of the American College of Cardiology Vol. 40, No. 9, 2002 2002 by the American College of Cardiology Foundation ISSN 0735-1097/02/$22.00 Published by Elsevier Science Inc. PII S0735-1097(02)02378-1
More informationCardiovascular Nursing Practice: A Comprehensive Resource Manual and Study Guide for Clinical Nurses 2 nd Edition
Cardiovascular Nursing Practice: A Comprehensive Resource Manual and Study Guide for Clinical Nurses 2 nd Edition Table of Contents Volume 1 Chapter 1: Cardiovascular Anatomy and Physiology Basic Cardiac
More informationObjectives. Acute Coronary Syndromes; The Nuts and Bolts. Overview. Quick quiz.. How dose the plaque start?
Objectives Acute Coronary Syndromes; The Nuts and Bolts Michael P. Gulseth, Pharm. D., BCPS Pharmacotherapy II Spring 2006 Compare and contrast pathophysiology of unstable angina (UA), non-st segment elevation
More informationLack of Effect of Beta-blocker Therapy in Patients with ST-elevation Acute Myocardial Infarction in PCI Era
Lack of Effect of Beta-blocker Therapy in Patients with ST-elevation Acute Myocardial Infarction in PCI Era B. Bao 1, N. Ozasa 1, T. Morimoto 2, Y. Furukawa 3, M. Shirotani 4, H. Ogawa 5, C. Tei 6, H.
More informationAcute Myocardial Infarction. Willis E. Godin D.O., FACC
Acute Myocardial Infarction Willis E. Godin D.O., FACC Acute Myocardial Infarction Definition: Decreased delivery of oxygen and nutrients to the myocardium Myocardial tissue necrosis causing irreparable
More informationFFR-guided Complete vs. Culprit Only Revascularization in AMI Patients Ki Hong Choi, MD On Behalf of FRAME-AMI Investigators
FFR-guided Complete vs. Culprit Only Revascularization in AMI Patients Ki Hong Choi, MD On Behalf of FRAME-AMI Investigators Heart Vascular Stroke Institute, Samsung Medical Center, Seoul, Republic of
More informationRationale for Prophylactic Support During Percutaneous Coronary Intervention
Rationale for Prophylactic Support During Percutaneous Coronary Intervention Navin K. Kapur, MD, FACC, FSCAI Assistant Director, Interventional Cardiology Director, Interventional Research Laboratories
More informationSTEMI Stents What next? Arshad Khan - HNE Clinical Research Fellow. Supervisors: Prof Boyle and Attia.
STEMI Stents What next? Arshad Khan - HNE Clinical Research Fellow. Supervisors: Prof Boyle and Attia. PART 1 Systems of care for STEMI. STEMI Management Coronary angiogram +/- stenting. Prehospital thrombolysis
More informationDiastolic Heart Failure. Edwin Tulloch-Reid MBBS FACC Consultant Cardiologist Heart Institute of the Caribbean December 2012
Diastolic Heart Failure Edwin Tulloch-Reid MBBS FACC Consultant Cardiologist Heart Institute of the Caribbean December 2012 Disclosures Have spoken for Merck, Sharpe and Dohme Sat on a physician advisory
More informationJournal of the American College of Cardiology Vol. 35, No. 4, by the American College of Cardiology ISSN /00/$20.
Journal of the American College of Cardiology Vol. 35, No. 4, 2000 2000 by the American College of Cardiology ISSN 0735-1097/00/$20.00 Published by Elsevier Science Inc. PII S0735-1097(99)00643-9 Early
More informationInnovation therapy in Heart Failure
Innovation therapy in Heart Failure P. Laothavorn September 2015 Topics of discussion Basic Knowledge about heart failure Standard therapy New emerging therapy References: standard Therapy in Heart Failure
More informationProtocol Identifier Subject Identifier Visit Description. [Y] Yes [N] No. [Y] Yes [N] N. If Yes, admission date and time: Day Month Year
PAST MEDICAL HISTORY Has the subject had a prior episode of heart failure? o Does the subject have a prior history of exposure to cardiotoxins, such as anthracyclines? URGENT HEART FAILURE VISIT Did heart
More informationAPPENDIX F: CASE REPORT FORM
APPENDIX F: CASE REPORT FORM Instruction: Complete this form to notify all ACS admissions at your centre to National Cardiovascular Disease Registry. Where check boxes are provided, check ( ) one or more
More informationIschemic Heart Disease Interventional Treatment
Ischemic Heart Disease Interventional Treatment Cardiac Catheterization Laboratory Procedures (N = 11,61) is a regional and national referral center for percutaneous coronary intervention (PCI). A total
More informationBeta-blockers in Patients with Mid-range Left Ventricular Ejection Fraction after AMI Improved Clinical Outcomes
Beta-blockers in Patients with Mid-range Left Ventricular Ejection Fraction after AMI Improved Clinical Outcomes Seung-Jae Joo and other KAMIR-NIH investigators Department of Cardiology, Jeju National
More informationDiagnosis & Management of Heart Failure. Abena A. Osei-Wusu, M.D. Medical Fiesta
Diagnosis & Management of Heart Failure Abena A. Osei-Wusu, M.D. Medical Fiesta Learning Objectives: 1) Become familiar with pathogenesis of congestive heart failure. 2) Discuss clinical manifestations
More informationCounterpulsation. John N. Nanas, MD, PhD. Professor and Head, 3 rd Cardiology Dept, University of Athens, Athens, Greece
John N. Nanas, MD, PhD Professor and Head, 3 rd Cardiology Dept, University of Athens, Athens, Greece History of counterpulsation 1952 Augmentation of CBF Adrian and Arthur Kantrowitz, Surgery 1952;14:678-87
More informationInvited Experts' Case Presentation and 5-Slides Focus Review
Invited Experts' Case Presentation and 5-Slides Focus Review FFR and IVUS in Myocardial Bridging Haegeun, Song. M.D. Heart Institute, Asan Medical Center, Seoul, Korea Myocardial Bridging Common congenital
More informationLeft atrial function. Aliakbar Arvandi MD
In the clinic Left atrial function Abstract The left atrium (LA) is a left posterior cardiac chamber which is located adjacent to the esophagus. It is separated from the right atrium by the inter-atrial
More informationHeart Failure (HF) Treatment
Heart Failure (HF) Treatment Heart Failure (HF) Complex, progressive disorder. The heart is unable to pump sufficient blood to meet the needs of the body. Its cardinal symptoms are dyspnea, fatigue, and
More informationDOWNLOAD PDF MYOCARDIAL CONTRAST TWO DIMENSIONAL ECHOCARDIOGRAPHY (DEVELOPMENTS IN CARDIOVASCULAR MEDICINE)
Chapter 1 : Imaging Cardiovascular Medicine Stanford Medicine contrast two-dimensional echocardiography (MC-2DE), a new and exciting diagnostic methodology for assessment of myocardial perfusion, which
More informationCirculation. Blood Pressure and Antihypertensive Medications. Venous Return. Arterial flow. Regulation of Cardiac Output.
Circulation Blood Pressure and Antihypertensive Medications Two systems Pulmonary (low pressure) Systemic (high pressure) Aorta 120 mmhg Large arteries 110 mmhg Arterioles 40 mmhg Arteriolar capillaries
More informationValue of Index of Microvascular Resistance (IMR) in Microvascular Integrity
Value of Index of Microvascular Resistance (IMR) in Microvascular Integrity Seung-Woon Rha, Korea University Guro Hospital, Myeong-Ho Yoon, Ajou University Hospital Imaging & Physiology Summit 2009 Nov
More information12 Lead EKG Chapter 4 Worksheet
Match the following using the word bank. 1. A form of arteriosclerosis in which the thickening and hardening of the vessels walls are caused by an accumulation of fatty deposits in the innermost lining
More informationThe MAIN-COMPARE Study
Long-Term Outcomes of Coronary Stent Implantation versus Bypass Surgery for the Treatment of Unprotected Left Main Coronary Artery Disease Revascularization for Unprotected Left MAIN Coronary Artery Stenosis:
More informationAustralian Journal of Basic and Applied Sciences, 9(36) December 2015, Pages: ISSN: Journal home page:
ISSN:1991-8178 Australian Journal of Basic and Applied Sciences Journal home page: www.ajbasweb.com Role of Biochemical Tests Artery Disease (ANP, BNP) in the Evaluation of Patients with Coronary 1 Saad
More informationCORONARY CHRONIC TOTAL OCCLUSIONS IN THE SETTING OF ACUTE MYOCARDIAL INFARCTION
CORONARY CHRONIC TOTAL OCCLUSIONS IN THE SETTING OF ACUTE MYOCARDIAL INFARCTION *Bimmer Claessen, Loes Hoebers, José Henriques Department of Cardiology, Academic Medical Center, University of Amsterdam,
More informationMy Patient Needs a Stress Test
My Patient Needs a Stress Test Amy S. Burhanna,, MD, FACC Coastal Cardiology Cape May Court House, New Jersey Absolute and relative contraindications to exercise testing Absolute Acute myocardial infarction
More informationIn acute myocardial infarction (AMI), early restoration of
Impact of Microvascular Dysfunction on Left Ventricular Remodeling and Long-Term Clinical Outcome After Primary Coronary Angioplasty for Acute Myocardial Infarction Leonardo Bolognese, MD, FESC; Nazario
More informationMedical Management of Acute Heart Failure
Critical Care Medicine and Trauma Medical Management of Acute Heart Failure Mary O. Gray, MD, FAHA Associate Professor of Medicine University of California, San Francisco Staff Cardiologist and Training
More informationManagement of Heart Failure in Adult with Congenital Heart Disease
Management of Heart Failure in Adult with Congenital Heart Disease Ahmed Krimly Interventional and ACHD consultant King Faisal Cardiac Center National Guard Jeddah Background 0.4% of adults have some form
More informationECHO HAWAII. Role of Stress Echo in Valvular Heart Disease. Not only ischemia! Cardiomyopathy. Prosthetic Valve. Diastolic Dysfunction
Role of Stress Echo in Valvular Heart Disease ECHO HAWAII January 15 19, 2018 Kenya Kusunose, MD, PhD, FASE Tokushima University Hospital Japan Not only ischemia! Cardiomyopathy Prosthetic Valve Diastolic
More informationEffect of Intravascular Ultrasound- Guided vs. Angiography-Guided Everolimus-Eluting Stent Implantation: the IVUS-XPL Randomized Clinical Trial
Effect of Intravascular Ultrasound- Guided vs. Angiography-Guided Everolimus-Eluting Stent Implantation: the IVUS-XPL Randomized Clinical Trial Myeong-Ki Hong, MD. PhD on behalf of the IVUS-XPL trial investigators
More informationCardiovascular Health Practice Guideline Outpatient Management of Coronary Artery Disease 2003
Authorized By: Medical Management Guideline Committee Approval Date: 12/13/01 Revision Date: 12/11/03 Beta-Blockers Nitrates Calcium Channel Blockers MEDICATIONS Indicated in post-mi, unstable angina,
More informationCatheter Interventions for Kawasaki Disease: Current Concepts and Future Directions
REVIEW DOI 10.4070/kcj.2011.41.2.53 Print ISSN 1738-5520 / On-line ISSN 1738-5555 Copyright 2011 The Korean Society of Cardiology Open Access Catheter Interventions for Kawasaki Disease: Current Concepts
More informationAldosterone Antagonism in Heart Failure: Now for all Patients?
Aldosterone Antagonism in Heart Failure: Now for all Patients? Inder Anand, MD, FRCP, D Phil (Oxon.) Professor of Medicine, University of Minnesota, Director Heart Failure Program, VA Medical Center 111C
More informationAortic Stenosis: UPDATE Anjan Sinha, MD Krannert Institute of Cardiology
Aortic Stenosis: UPDATE 2010 Anjan Sinha, MD Krannert Institute of Cardiology None Disclosures 67-Year-Old Male Dyspnea and angina Class III heart failure No PND or orthopnea 3/6 late peak SEM Diminished
More informationSevere left ventricular dysfunction and valvular heart disease: should we operate?
Severe left ventricular dysfunction and valvular heart disease: should we operate? Laurie SOULAT DUFOUR Hôpital Saint Antoine Service de cardiologie Pr A. COHEN JESFC 16 janvier 2016 Disclosure : No conflict
More informationThe development of cardiogenic shock portends an extremely poor prognosis. Cardiogenic Shock: A Lethal Complication of Acute Myocardial Infarction
TREATMENT UPDATE Cardiogenic Shock: A Lethal Complication of Acute Myocardial Infarction David R. Holmes, Jr, MD Mayo Graduate School of Medicine, Mayo Clinic, Rochester, MN Cardiogenic shock is a serious
More informationJournal of the American College of Cardiology Vol. 43, No. 4, by the American College of Cardiology Foundation ISSN /04/$30.
Journal of the American College of Cardiology Vol. 43, No. 4, 2004 2004 by the American College of Cardiology Foundation ISSN 0735-1097/04/$30.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2003.08.055
More information