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Published on: March 8, 2013
[Tolerance of beta blockader treatment in dilated cardiomyopathy]
A V Mattioli1, G Bettelli, G Mattioli
1Cattedra di Malattie dell'Apparato Cardiovascolare, Università degli Studi, Modena.
Insights
High neurohumoral activation, indicated by elevated norepinephrine and renin activity, may predict poor tolerance to beta-blocker therapy in heart failure patients with dilatative cardiomyopathy.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Dilatative cardiomyopathy is a common cause of heart failure.
- Beta-blockers are a cornerstone therapy for heart failure, but patient tolerance varies.
- Identifying predictors of beta-blocker intolerance is crucial for optimizing treatment.
Purpose of the Study:
- To evaluate hemodynamic and neurohumoral parameters for predicting beta-blocker tolerance in heart failure patients.
- To identify specific markers associated with intolerance to atenolol therapy.
Main Methods:
- Seventy-eight patients with dilatative cardiomyopathy and heart failure were assessed.
- Hemodynamic parameters (e.g., MPAP, cardiac output) and neurohumoral markers (NE, PRA) were measured.
- Patients received escalating doses of atenolol, and tolerance was assessed.
Main Results:
- Forty-one out of 78 patients did not tolerate beta-blocker therapy.
- Intolerant patients exhibited significantly higher mean pulmonary arterial pressure (MPAP), plasma norepinephrine (NE), and plasma renin activity (PRA) at baseline.
- MPAP (p=0.02), NE (p=0.01), and PRA (p=0.02) were significantly different between tolerant and intolerant groups.
Conclusions:
- Elevated baseline neurohumoral activation (NE, PRA) and MPAP may indicate poor tolerance to beta-blockers in heart failure patients.
- These parameters could serve as potential biomarkers to guide beta-blocker therapy selection.
Abstract:
We studied 78 consecutive patients with dilatative cardiomyopathy who were in our hospital because of heart failure. We wanted to evaluate which parameters could be useful in identifying patients who could be treated with betablockers. All patients were hemodynamically well balanced. They were treated with effective dosage of digoxin and diuretics. We evaluated the following hemodynamic parameters: heart rate, mean arterial pressure, mean pulmonary arterial pressure (MPAP), right atrial pressure, pulmonary wedge pressure, cardiac output, cardiac index, systemic vascular resistance, pulmonary vascular resistance, and also the neurohumoral parameters: VO2, max exercise duration, plasmatic norepinephrine levels (NE) and plasmatic renin activity (PRA). Then all patients were treated with atenolol 25 mg/die followed by 50 mg/die. In the overall population, 37 patients well tolerated the therapy with betablocker (Group A); 41 patients did not tolerate the therapy (Group B). Between the 2 groups we only found a significant difference in MPAP 31 +/- 20 vs 51 +/- 31 mmHg (p = 0.02), NE 781 +/- 467 vs 1551 +/- 1249 pg/ml (p = 0.01), PRA 1.8 +/- 2.9 vs 5.6 +/- 4.5 ng/ml/h (p = 0.02). On the basis of our results we hypothesize that patients with high neurohumoral activation do not tolerate betablocker treatment.
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