Key result
Ouabain produces a ~52% weaker maximum inotropic effect in RV versus LV failing human myocardium.
Why the study?
Does the inotropic effect of ouabain vary according to the heart chamber or aetiology of heart failure in failing human myocardium?
Does the inotropic effect of ouabain vary according to the heart chamber or aetiology of heart failure in failing human myocardium?
Absolute Event Rate: 121% vs 250%
The inotropic effect of ouabain in failing human myocardium varies by heart failure aetiology and ventricle, with lower maximum efficacy in the right ventricle and a higher threshold concentration in ischaemic cardiomyopathy.
Variation in ouabain responsiveness by ventricle and aetiology in failing myocardium; leaves open chamber-specific digitalis effects for clinical validation.
AIMS: To investigate whether the inotropic effect of ouabain in failing human myocardium varies according to the heart chamber tested (right or left ventricle) or the aetiology of the heart disease, i.e. ischaemic or idiopathic. METHODS: The inotropic effect of ouabain was measured, as the percentage change in baseline tension, in myocardial strips isolated from right (RV; n=21) and left ventricles (LV; n=21) of hearts explanted from patients with idiopathic (IDC; n=11) and ischaemic cardiomyopathy (CAD; n=10). Concentration-effect curves obtained with ouabain (0.05-1.6 micromol l-1 ) were analysed using the Emax sigmoidal model, and the following parameters were calculated: Emax, EC50, n and EC10 (threshold concentration). The influence of ventricular chamber and heart failure aetiology on these parameters was evaluated by means of a two-way anova. RESULTS: Age and baseline haemodynamic parameters did not differ between IDC and CAD patients. Baseline strip contractility was highly variable (range: 0.48-10.0 mN), but neither ventricular chamber nor aetiology could explain such variability. A two-way anova showed that EC10 was greater in CAD than in IDC preparations (0.097+/-0.013 micromol l-1 vs 0.059+/-0. 009 micromol l-1; 95% C.I. for difference 0.043, 0.071) and Emax was lower in RV than in LV (121+/-21% vs 250+/-38%; 95% C.I. -221, -36), while EC50 and n were not significantly different between groups. CONCLUSIONS: The inotropic effect of ouabain in human myocardium may vary according to aetiology of heart failure and the ventricle being tested. Although our results do not support the hypothesis of increased sensitivity to cardiac glycosides in CAD patients, they may explain the diminished effect observed in patients with RV failure.
No takes yet. Share an insight, caveat, or question.
Padrini et al. (1999) studied Heart failure (idiopathic and ischaemic cardiomyopathy) (n=21). Ouabain vs. Left ventricle (vs Right ventricle) and Idiopathic (vs Ischaemic) cardiomyopathy was evaluated on Emax (maximum percentage change in baseline tension) (95% CI -221 to -36). The maximum inotropic effect of ouabain was significantly lower in right ventricular compared to left ventricular failing human myocardium (121% vs 250%; 95% CI for difference -221 to -36).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: