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Vitamin C improves acetylcholine-stimulated vasodilation in post-ischemic dilated cardiomyopathy.
AJH-APRIL 1999-VOL. 12, NO. 4, PART 2
POSTERS: Heart Failure
FO05
F006
VITAMIN C IMPROVES A C E T Y L C H O L I N E - S T I M U L A T E D VASODILATION IN POST-ISCHEMIC DILATED CARDIOMYOPATHY. F Perticone, R Ceravolo, C Cos¢o, C CIoro, S lacopino, M Candigliota, PL MattiolL Dpt of Medicina Sperimentale e Clinica "G Salvatore", University of Catanzaro, Italy. Heart failure is associated with endothelial dysfunction, probably due to accelerated degradation of nitric oxide by radicals. Actually, no evidences are present about endothelium-dependent vasodllation in patients with secondary dilated cardiomyopathy (DCM). The aim of our study was to test the effect of antioxidant vitamin C on endothelium-dependent vasodilation in a group of 12 patients with post-ischemic DCM (8M/4W, age = 56.7_+4.9 yrs) and in 12 healthy volunteers ~a~ w=rmc ~ (SM/4W, age = 55.6+5.1
HISTORY OF HYPERTENSION AND HEART FAILURE DURING ACUTE MYOCARDIAL INFARCTION. G. Barton, R. Palmieri, R Cordiano, G.L. Guamieri, V. Pagliara, S. Pianca, P. Zampieri, S. Mbaso, A. Javemaro, and Paolo Palatini*. Conegliano, Adria and Basssno City Hospitals, Clinica Medica la University of Padova, Italy. The aim of this study was to assess the relationship between history of hypertension (HH) and heart failure (HF) in 385 consecutive patients admitted to 3 coronary care units for acute myocardial infarction (AMI). Patients with HH were 177 (46%) (mean duration 11.4+8.9 years). Heart failure was evaluated according to Killip classification on the 1=, 3ru and 7th day after admission. Patients who died or were discharged before 7t" day were excluded from the study. Among the normotensives (NT), 71(34%) had Killip class score>l on the 1= day of hospital stay. Among those with HH, 75(42%) had Killip class score>l (ns). 53 (25%) NT and 42 (24%) HH patients showed an improvement of their score on the 3 rd and/or 7th day after admission as compared to I st day score (ns). 8 patients (4%) among the NT and 16 (9%) among the HH patients worsened their score after I st day (X==4.2, p=0.03). None of the NT with Killip class>l on the 1't day worsened their score in the following days, while 5 patients with HH (8%) did. Furthermore, in a multivariate regression model including Killip class (1 to 4) as dependent variable and HH and other 9 clinical variables (including thrombolytic therapy) as independent ones, HH resulted as an independent predictor of Killip class on the 7th day (p=0.O4). Conclusion. Our data show that patients with HH have no increased incidence of HF when admitted to intensive care unit for AMI, but tend to have a worae behavior in the subsequent days than NT. Furthermore, HH seems to be independently related to degree of HF 1 week after admission to intensive care unit.
strain-gauge plethysmography, forearm blood ;~ ~ ~ o flOW (FBF) modification ~zo induced by intrabrechial ~t acetylcholine (ACh) (7.5, 15,30 p.g/min/5min) and sodium nitroprusside 7.5 15 30 7.5 15 30 7.5 ~5 30 Acetyfcholine(~m/n) (SNP) (0.8,1.6,3.2 ~,g/ min/5min) in baseline and during co-infusion of vitamin C at constant dose of 24 mg/min and indomethacin (500 p.g/min). The andotheliumdependent vasodilation was significantly lower in DCM than in controls (figure). In DCM group, but not in controls, vitamin C and indomethacin significantly (p<0.0001) enhanced the impaired ACh-stimulated vaaodilation, whereas the response to SNP was unaffected. In conclusion, in patients with postiechemic DCM is present an endothelial dysfunction due to oxidative stress as confirmed by FBF modifications during coinfusion of vitamin C and indomethacin. "
Key Words:
c=~ *ec~
Cardiomyopathy, endothelium, vitamin C.
Key words: myocardial hypertension.
infarction,
heart failure,
history of
Key Words:
FO07
F008
BETA BLOCKING THERAPY IN CHF: AN OUT-
EFFECT OF BENAZEPRIL ON MYOCARDIAL APOPTOSIS IN CHRONIC HEART FAILURE FROM RATS. SJ Zhu*. HX Hu, ZM Zhu#,YJ Yang, GH Chen, and FG Liu. Division of Cardiology, Xinqian Hospital, and #Hypertension Center, Third Military Medical University, Chongqing, P.R.China. Myocardial apoptosis may contribute to cardiac dysfunction. This work studies whether benazepril, an angiotensin converting enzyme inhibitor (ACE inhibitor), can affect myocardial apoptosis that was produced by chronic heart failure (CHF) from rats. Male Wistar rats were divided into three groups (20 rats/each group). CHF was induced by left coronary ligation and control group was performed by sham operation. Partial CHF rats were given with hanazepril (8 mg/kg/day) for one month. Cardiac function was evaluated by polygraph system and myocardial apoptosis was examined using terminal transferase-mediated dUTP-biotin nick end-labeling (TUNEL). The expression of apoptosis-related proteins (bcl-2 and bax) was observed by immunohistochemistry. Compared with control group, left ventricular systolic pressure (LVSP) and +dp/dt was significantly decreased (p<0.05) in CHF groups with and without benazepril. Lef~ ventdcular diastolic pressure CLVDP) was markedly increased in CHF compared with CHF with henazepril and control groups. Increasing volumes and thinner wall of LV were observed in CHF and CHF with benazepril groups. Myocardial TUNEL-positive cells and expression of bax protein were observed in CHF and mainly located around the infarct area, while only slight positive expression of bax was seen in CHF with benazepril, however positive staining of bax protein was rarely detected in control group. In contrast, the expression of bcl-2 protein showed no significant difference among three groups. The ratio of bcl-2 protein to bax protein is negatively correlated with the number of myocardial apoptosis and damage of myocardium. It concluded that myocardial apoptosis may be involved in the development of heart failure and ACE inhibitor may delay the process of heart failure by inhibition of myocardial apoptosis. (Supported by NSFC grants 39725013 and 39770314)
H O S P I T A L R E G I S T R Y . A.Vado. A.Deorsola, U.Uilanese, E.Uslenghi. Cardiology Dept. Ospedale S.Cmce. Cuneo. ITALY Bac,kgmund: to evaluate feasibility, tolerability, efficiency of beta blocking therapy in CHF in a patient registry from a single outhospital canter. Methods: patients with CHF of any etiology were enrolled in an out-hospital beta biocking therapy and survey program. All subjects without overt contraindication to beta blockers (severe asthma, peripheral artery disease, uncontrolled insulin dependent diabetes) were followed up to 2 years. Beta blocker carvedilol was tittered starting from 3.125mg to 25 mg a day if tolerated. Pnmary end point was cardiac death; secondary end point was Beta blocking withdrawal Results: 78 (74.8%) out of 105 patients referred started carvedilol. Age was 62+11 years. NHYA class was 1 in 26, 2 in 43, 3 in 30 and 4 in NHYA 4. CHF etiology was CAD in 28.2%, idiopathic in 33.3%, hypertension in 19.2% and other causes in 19.2%. Atrial fibrillation was present in 19.2%. 92.3% of patients was on ACE-inhibitors. Mean ejection fraction was 29~9.7. There were 16 deaths (20.5) during a mean follow-up of 14 months. Beta blocking withdrawal was due in 7/78 patients (7.7%). In patients that tolerated carvedilol mortality rate was 16.7%, whereas in patients who did not it was 66.7% (7.2 8.42, 1>=.003). Multivariate logistic regression analysis showed an overall accuracy to primary end point of 82.5%: the independent factors predicting death were: Beta blocking withdrawal (p=.01) and ejection fraction (p=.05) Conclusions: out-hospital CHF patients showed low Beta blocking withdrawal rate. Death rate was higher in patients who did not tolerate beta Mocking therapy. Beta blocking withdrawal and ejection fraction are independent predictors of cardiac death.
Key Words:
Key Words: Heart Failure, Carvedilol, beta-blocker
Heart failure Apoptosis Angiotensin converting enzyme inhibitor
195A
POSTERS: Heart Failure
FO05
F006
VITAMIN C IMPROVES A C E T Y L C H O L I N E - S T I M U L A T E D VASODILATION IN POST-ISCHEMIC DILATED CARDIOMYOPATHY. F Perticone, R Ceravolo, C Cos¢o, C CIoro, S lacopino, M Candigliota, PL MattiolL Dpt of Medicina Sperimentale e Clinica "G Salvatore", University of Catanzaro, Italy. Heart failure is associated with endothelial dysfunction, probably due to accelerated degradation of nitric oxide by radicals. Actually, no evidences are present about endothelium-dependent vasodllation in patients with secondary dilated cardiomyopathy (DCM). The aim of our study was to test the effect of antioxidant vitamin C on endothelium-dependent vasodilation in a group of 12 patients with post-ischemic DCM (8M/4W, age = 56.7_+4.9 yrs) and in 12 healthy volunteers ~a~ w=rmc ~ (SM/4W, age = 55.6+5.1
HISTORY OF HYPERTENSION AND HEART FAILURE DURING ACUTE MYOCARDIAL INFARCTION. G. Barton, R. Palmieri, R Cordiano, G.L. Guamieri, V. Pagliara, S. Pianca, P. Zampieri, S. Mbaso, A. Javemaro, and Paolo Palatini*. Conegliano, Adria and Basssno City Hospitals, Clinica Medica la University of Padova, Italy. The aim of this study was to assess the relationship between history of hypertension (HH) and heart failure (HF) in 385 consecutive patients admitted to 3 coronary care units for acute myocardial infarction (AMI). Patients with HH were 177 (46%) (mean duration 11.4+8.9 years). Heart failure was evaluated according to Killip classification on the 1=, 3ru and 7th day after admission. Patients who died or were discharged before 7t" day were excluded from the study. Among the normotensives (NT), 71(34%) had Killip class score>l on the 1= day of hospital stay. Among those with HH, 75(42%) had Killip class score>l (ns). 53 (25%) NT and 42 (24%) HH patients showed an improvement of their score on the 3 rd and/or 7th day after admission as compared to I st day score (ns). 8 patients (4%) among the NT and 16 (9%) among the HH patients worsened their score after I st day (X==4.2, p=0.03). None of the NT with Killip class>l on the 1't day worsened their score in the following days, while 5 patients with HH (8%) did. Furthermore, in a multivariate regression model including Killip class (1 to 4) as dependent variable and HH and other 9 clinical variables (including thrombolytic therapy) as independent ones, HH resulted as an independent predictor of Killip class on the 7th day (p=0.O4). Conclusion. Our data show that patients with HH have no increased incidence of HF when admitted to intensive care unit for AMI, but tend to have a worae behavior in the subsequent days than NT. Furthermore, HH seems to be independently related to degree of HF 1 week after admission to intensive care unit.
strain-gauge plethysmography, forearm blood ;~ ~ ~ o flOW (FBF) modification ~zo induced by intrabrechial ~t acetylcholine (ACh) (7.5, 15,30 p.g/min/5min) and sodium nitroprusside 7.5 15 30 7.5 15 30 7.5 ~5 30 Acetyfcholine(~m/n) (SNP) (0.8,1.6,3.2 ~,g/ min/5min) in baseline and during co-infusion of vitamin C at constant dose of 24 mg/min and indomethacin (500 p.g/min). The andotheliumdependent vasodilation was significantly lower in DCM than in controls (figure). In DCM group, but not in controls, vitamin C and indomethacin significantly (p<0.0001) enhanced the impaired ACh-stimulated vaaodilation, whereas the response to SNP was unaffected. In conclusion, in patients with postiechemic DCM is present an endothelial dysfunction due to oxidative stress as confirmed by FBF modifications during coinfusion of vitamin C and indomethacin. "
Key Words:
c=~ *ec~
Cardiomyopathy, endothelium, vitamin C.
Key words: myocardial hypertension.
infarction,
heart failure,
history of
Key Words:
FO07
F008
BETA BLOCKING THERAPY IN CHF: AN OUT-
EFFECT OF BENAZEPRIL ON MYOCARDIAL APOPTOSIS IN CHRONIC HEART FAILURE FROM RATS. SJ Zhu*. HX Hu, ZM Zhu#,YJ Yang, GH Chen, and FG Liu. Division of Cardiology, Xinqian Hospital, and #Hypertension Center, Third Military Medical University, Chongqing, P.R.China. Myocardial apoptosis may contribute to cardiac dysfunction. This work studies whether benazepril, an angiotensin converting enzyme inhibitor (ACE inhibitor), can affect myocardial apoptosis that was produced by chronic heart failure (CHF) from rats. Male Wistar rats were divided into three groups (20 rats/each group). CHF was induced by left coronary ligation and control group was performed by sham operation. Partial CHF rats were given with hanazepril (8 mg/kg/day) for one month. Cardiac function was evaluated by polygraph system and myocardial apoptosis was examined using terminal transferase-mediated dUTP-biotin nick end-labeling (TUNEL). The expression of apoptosis-related proteins (bcl-2 and bax) was observed by immunohistochemistry. Compared with control group, left ventricular systolic pressure (LVSP) and +dp/dt was significantly decreased (p<0.05) in CHF groups with and without benazepril. Lef~ ventdcular diastolic pressure CLVDP) was markedly increased in CHF compared with CHF with henazepril and control groups. Increasing volumes and thinner wall of LV were observed in CHF and CHF with benazepril groups. Myocardial TUNEL-positive cells and expression of bax protein were observed in CHF and mainly located around the infarct area, while only slight positive expression of bax was seen in CHF with benazepril, however positive staining of bax protein was rarely detected in control group. In contrast, the expression of bcl-2 protein showed no significant difference among three groups. The ratio of bcl-2 protein to bax protein is negatively correlated with the number of myocardial apoptosis and damage of myocardium. It concluded that myocardial apoptosis may be involved in the development of heart failure and ACE inhibitor may delay the process of heart failure by inhibition of myocardial apoptosis. (Supported by NSFC grants 39725013 and 39770314)
H O S P I T A L R E G I S T R Y . A.Vado. A.Deorsola, U.Uilanese, E.Uslenghi. Cardiology Dept. Ospedale S.Cmce. Cuneo. ITALY Bac,kgmund: to evaluate feasibility, tolerability, efficiency of beta blocking therapy in CHF in a patient registry from a single outhospital canter. Methods: patients with CHF of any etiology were enrolled in an out-hospital beta biocking therapy and survey program. All subjects without overt contraindication to beta blockers (severe asthma, peripheral artery disease, uncontrolled insulin dependent diabetes) were followed up to 2 years. Beta blocker carvedilol was tittered starting from 3.125mg to 25 mg a day if tolerated. Pnmary end point was cardiac death; secondary end point was Beta blocking withdrawal Results: 78 (74.8%) out of 105 patients referred started carvedilol. Age was 62+11 years. NHYA class was 1 in 26, 2 in 43, 3 in 30 and 4 in NHYA 4. CHF etiology was CAD in 28.2%, idiopathic in 33.3%, hypertension in 19.2% and other causes in 19.2%. Atrial fibrillation was present in 19.2%. 92.3% of patients was on ACE-inhibitors. Mean ejection fraction was 29~9.7. There were 16 deaths (20.5) during a mean follow-up of 14 months. Beta blocking withdrawal was due in 7/78 patients (7.7%). In patients that tolerated carvedilol mortality rate was 16.7%, whereas in patients who did not it was 66.7% (7.2 8.42, 1>=.003). Multivariate logistic regression analysis showed an overall accuracy to primary end point of 82.5%: the independent factors predicting death were: Beta blocking withdrawal (p=.01) and ejection fraction (p=.05) Conclusions: out-hospital CHF patients showed low Beta blocking withdrawal rate. Death rate was higher in patients who did not tolerate beta Mocking therapy. Beta blocking withdrawal and ejection fraction are independent predictors of cardiac death.
Key Words:
Key Words: Heart Failure, Carvedilol, beta-blocker
Heart failure Apoptosis Angiotensin converting enzyme inhibitor
195A