Wow. I did not realize this was a negative trial!! 🤯. And your review of the US carvedilol study series showed that those results were underwhelming with soft endpoints also.
Hopefully there will be no nasty surprises when you review MERIT-HF and CIBIS 1 and 2. Otherwise I will really have to wonder what basis we’ve had for doing what we do for HFREF all these years wrt beta blocker usage.
We will be discussing MERIT-HF, CIBIS 1 and 2 in the heart failure section. The results of CAPRICORN and COMMIT don't apply to the chronic heart failure population as they are different populations with different pathophysiology. We have referred to your question and answered it in more detail in our podcast (Summary and discussion of CAPRICORN and COMMIT) which will be available on Feb 12 at 5:30 am EST
What was their theory for the efficacy (physiology) of Beta-blocker for these patients? Why was carvedilol not efficacious? Did it (in tandem with ACE) lower BP and cardiac output too much? Or was their no measurable difference in clinical measures when added to ACE?
Good question! We have responded to your question during our podcast (Summary and discussion of CAPRICORN and COMMIT) which will be available on Feb 12 at 5:30 am EST. Beta-blockers have acute and chronic effects on the heart. Acutely, it can worsen hemodynamics in the vulnerable population as seen in COMMIT trial. In chronic heart failure, it antagonizes catecholamines and upregulates myocardial B-receptors.
Wow. I did not realize this was a negative trial!! 🤯. And your review of the US carvedilol study series showed that those results were underwhelming with soft endpoints also.
Hopefully there will be no nasty surprises when you review MERIT-HF and CIBIS 1 and 2. Otherwise I will really have to wonder what basis we’ve had for doing what we do for HFREF all these years wrt beta blocker usage.
We will be discussing MERIT-HF, CIBIS 1 and 2 in the heart failure section. The results of CAPRICORN and COMMIT don't apply to the chronic heart failure population as they are different populations with different pathophysiology. We have referred to your question and answered it in more detail in our podcast (Summary and discussion of CAPRICORN and COMMIT) which will be available on Feb 12 at 5:30 am EST
What was their theory for the efficacy (physiology) of Beta-blocker for these patients? Why was carvedilol not efficacious? Did it (in tandem with ACE) lower BP and cardiac output too much? Or was their no measurable difference in clinical measures when added to ACE?
Good question! We have responded to your question during our podcast (Summary and discussion of CAPRICORN and COMMIT) which will be available on Feb 12 at 5:30 am EST. Beta-blockers have acute and chronic effects on the heart. Acutely, it can worsen hemodynamics in the vulnerable population as seen in COMMIT trial. In chronic heart failure, it antagonizes catecholamines and upregulates myocardial B-receptors.