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Computer simulation of myocardium depolarization: Application to ventricular fibrillation
J Mol
Cell
Cardiol
22 (Supplement
IV)
(1990)
LOW ANGIOTENSINOGEN LEVELS AS AN INDEX OF SEVERITY AND OF LIVER DYSFUNCTlDN IN CONGESTIVE HEART FAILURE: IMPLICATIONS FOR RENIN MEASUREMENTS. Jean-Franpois ARNAL, Paulette CUDEK. Pierre-Franqois PLOUIN. Thahn-Tam GUYENNE, Jean-Baptiste MICHEL, Pierre CORVOL. Paris, France. The status of the renin system in congestive heart failure (CHF) was assessed by measuring the plasma renin substrate (AG) concentration, plasma renin activity (PRA), and plasma concentrations of active renin in 37 patients with mild to severe CHF. Natremia and plasma levels of atrial natriuretic factor were determined as biological indexes of the severity of CHF, and concentrations of prealbumin and retinol binding protein were used as indexes of liver dysfunction. The PRA and the concentrations of active renin and atrial natriuretic factor were markedly higher in patients with NYHA grade IV CHF than in patients with grade ll-lll CHF, while natremia and the concentrations of AG, prealbumin and retinol binding protein were markedly lower in the grade IV patients than in the grade ll-lll patients. Plasma AG concentration was negatively correlated with active renin concentration (n=37, r=-0.45, p=O.OOS), and positively related to natremia (r=0.56, pcO.O005), prealbumin (r=0.54, pcO.001) and retinol binding protein (r=0.60, pcO.0001) concentrations. In patients with grade IV CHF, low levels of AG led to a marked underestimation of active renin concentration from the measurement of PRA. Thus, low levels of plasma AG provide a new index of severity in CHF and reflect both the high levels of the circulating active enzyme and the decrease in hepatic protein output.
CORONARY FLOW IN RYPERTROPRIC CARDIOMYOPATHY : EVIDENCE FOR A VASCULAR TONE IMPAIm. P. Aubry, P. Assayag, X. H. Du Fretay, A. Haddad, A. Akesbi, E. Brochet, P. Beyne, P.E. Valere. HBpital Beaujon, Clichy, France. Coronary flow (CF) troubles have been described in left ventricle hypertrophy but.are unclear in hypertrophic cardiomyopathy withoui (LVH) due to pressure overload, obstruction (HCM). We compared CF and reserve in HCM (n=6), hypertensive LVH (n =7) and control (n=7) groups. CF (ml/mn.lOOg.mass) was measured by coronary sinus thermodilution at rest (B) and after dipyridamole (D) as well as coronary resistance (CR ; mmHg/ml.mn).All patients had normal coronary angiograms. HCM LVH Results : CTL 50
+
22*
62 157
.98
+ +
69+ .35
.79
+
.25
.53
+
.34*
.30
&
.lO
C.Flow
(B)
73
+
12*
C.Flow
(D)
254
37*+
111
.17 .05*
C.Resistance
(B)
.75
-+ -+
C.Resistance
(D)
.22
+
c.05 - + p<.oa1 HCM, besides an inadequate severe vasodilation impairment, smaller CR fall after dipyridamole.
-+ 14 -+ 59*
(*p
coronary with low
vascular bed like in (total and mass-indexed)
LVH,
seems maximal
to have CF, and
a
COMPUTER SIMULATION OF MYOCARDIUM DEPOLARIZATION : APPLICATION TO VENTRICULAR FIBRILLATION. P. Augerl, M. Chesnais2, A. Coulombe2, MC Covaere3, L. Rochette4, J-P Schreiberl, 0. Von Euws, A. Bardou3. I Lab. de Biophysique, FacuW de Pharmacie, Dijon, France ; 2 Lab. d’&ctrophysiologie, Orsay. France ; 3 I.N.S.E.R.M. U256, Paris, France ; 4 Lab. de Pharmacodynamie, Facula de Pharmacie, Dijon, France. We present a physiological application of computer simulations of an activation wave propagation through the ventricular wall based on the Huygens’constructlon method. Effects of severe ischemia are simulated, considering both a progressive inactivation of sodium channels leading to a decrease in conduction velocity and an irregularity in action potential duratlon resultlng in a refractory perlod dlsperslon. The slmulatlons show that a decrease In the conduction velocity in a ratio one to three provoke a distortion of activation wave and has an effect on the myocardial contraction without triggering reentries. On the contrary, a dispersion in refractory periods even with a narrow gaussian distribution (17% for the ratio mean refractory period / standard deviation) is able to induce reentries by a percolation phenomenon leading to a chaotic process which can be related to ventricular fibrillation. To conclude, considering that during ischemia, both decrease in conduction velocity and a dispersion in refractory periods are observed, these results suggest that dispersion in refractory perlods is the most dangerous parameter in ventricular flbrlllation Induction. s.2
Cell
Cardiol
22 (Supplement
IV)
(1990)
LOW ANGIOTENSINOGEN LEVELS AS AN INDEX OF SEVERITY AND OF LIVER DYSFUNCTlDN IN CONGESTIVE HEART FAILURE: IMPLICATIONS FOR RENIN MEASUREMENTS. Jean-Franpois ARNAL, Paulette CUDEK. Pierre-Franqois PLOUIN. Thahn-Tam GUYENNE, Jean-Baptiste MICHEL, Pierre CORVOL. Paris, France. The status of the renin system in congestive heart failure (CHF) was assessed by measuring the plasma renin substrate (AG) concentration, plasma renin activity (PRA), and plasma concentrations of active renin in 37 patients with mild to severe CHF. Natremia and plasma levels of atrial natriuretic factor were determined as biological indexes of the severity of CHF, and concentrations of prealbumin and retinol binding protein were used as indexes of liver dysfunction. The PRA and the concentrations of active renin and atrial natriuretic factor were markedly higher in patients with NYHA grade IV CHF than in patients with grade ll-lll CHF, while natremia and the concentrations of AG, prealbumin and retinol binding protein were markedly lower in the grade IV patients than in the grade ll-lll patients. Plasma AG concentration was negatively correlated with active renin concentration (n=37, r=-0.45, p=O.OOS), and positively related to natremia (r=0.56, pcO.O005), prealbumin (r=0.54, pcO.001) and retinol binding protein (r=0.60, pcO.0001) concentrations. In patients with grade IV CHF, low levels of AG led to a marked underestimation of active renin concentration from the measurement of PRA. Thus, low levels of plasma AG provide a new index of severity in CHF and reflect both the high levels of the circulating active enzyme and the decrease in hepatic protein output.
CORONARY FLOW IN RYPERTROPRIC CARDIOMYOPATHY : EVIDENCE FOR A VASCULAR TONE IMPAIm. P. Aubry, P. Assayag, X. H. Du Fretay, A. Haddad, A. Akesbi, E. Brochet, P. Beyne, P.E. Valere. HBpital Beaujon, Clichy, France. Coronary flow (CF) troubles have been described in left ventricle hypertrophy but.are unclear in hypertrophic cardiomyopathy withoui (LVH) due to pressure overload, obstruction (HCM). We compared CF and reserve in HCM (n=6), hypertensive LVH (n =7) and control (n=7) groups. CF (ml/mn.lOOg.mass) was measured by coronary sinus thermodilution at rest (B) and after dipyridamole (D) as well as coronary resistance (CR ; mmHg/ml.mn).All patients had normal coronary angiograms. HCM LVH Results : CTL 50
+
22*
62 157
.98
+ +
69+ .35
.79
+
.25
.53
+
.34*
.30
&
.lO
C.Flow
(B)
73
+
12*
C.Flow
(D)
254
37*+
111
.17 .05*
C.Resistance
(B)
.75
-+ -+
C.Resistance
(D)
.22
+
c.05 - + p<.oa1 HCM, besides an inadequate severe vasodilation impairment, smaller CR fall after dipyridamole.
-+ 14 -+ 59*
(*p
coronary with low
vascular bed like in (total and mass-indexed)
LVH,
seems maximal
to have CF, and
a
COMPUTER SIMULATION OF MYOCARDIUM DEPOLARIZATION : APPLICATION TO VENTRICULAR FIBRILLATION. P. Augerl, M. Chesnais2, A. Coulombe2, MC Covaere3, L. Rochette4, J-P Schreiberl, 0. Von Euws, A. Bardou3. I Lab. de Biophysique, FacuW de Pharmacie, Dijon, France ; 2 Lab. d’&ctrophysiologie, Orsay. France ; 3 I.N.S.E.R.M. U256, Paris, France ; 4 Lab. de Pharmacodynamie, Facula de Pharmacie, Dijon, France. We present a physiological application of computer simulations of an activation wave propagation through the ventricular wall based on the Huygens’constructlon method. Effects of severe ischemia are simulated, considering both a progressive inactivation of sodium channels leading to a decrease in conduction velocity and an irregularity in action potential duratlon resultlng in a refractory perlod dlsperslon. The slmulatlons show that a decrease In the conduction velocity in a ratio one to three provoke a distortion of activation wave and has an effect on the myocardial contraction without triggering reentries. On the contrary, a dispersion in refractory periods even with a narrow gaussian distribution (17% for the ratio mean refractory period / standard deviation) is able to induce reentries by a percolation phenomenon leading to a chaotic process which can be related to ventricular fibrillation. To conclude, considering that during ischemia, both decrease in conduction velocity and a dispersion in refractory periods are observed, these results suggest that dispersion in refractory perlods is the most dangerous parameter in ventricular flbrlllation Induction. s.2