Author + information
- Jay N. Cohn, MD⁎ ()
- ↵⁎University of Minnesota, Department of Medicine–Cardiology, MMC 508, 420 Delaware Street SE, Minneapolis, Minnesota 55455-0374
To criticize previously identified so-called disease markers (premature ventricular complexes, cardiac output, symptom relief, plasma norepinephrine) because they do not track with disease progression is misdirected, because we all agree these are not fundamental to the disease process. As I have stressed, and Granger and McMurray seem to agree, structural markers are far more discriminating. To suggest that not all therapies that slow disease progression improve outcome is equally disingenuous; that is why I have stressed that safety as well as efficacy must be addressed.
Granger and McMurray avoid the real issue. Our treatments are aimed at slowing or aborting a disease process, but they are administered to individuals whose well-being is also dependent on other factors. Granger and McMurray seem interested only in the net effect. I am interested in separating efficacy from safety. They defend against such attempts, stating that “using measures of disease progression … [should be] rigorously resisted.”
Rather than hiding behind their self-proclaimed inability to “understand the disease” or “the exact mechanism of benefit,” Granger and McMurray would better serve the cardiovascular community by advocating that mechanisms be carefully addressed in future clinical trials so as to gain such understanding. Documentation of the benefit of therapies for early stages of disease requires assessment of disease progression, and strategies for management of advanced disease may require separate and perhaps individualized optimization of efficacy and safety. It is time to accelerate the learning process, not to retreat into the past comfort of simple mortality/morbid events trials.
- American College of Cardiology Foundation