Author + information
- Gilbert Zoghbi, MD, FACC⁎ ( and )
- Ami E. Iskandrian, MD, FACC, FAHA, FASNC
- ↵⁎University of Alabama at Birmingham, LHRB 306, 1530 3rd Avenue South, Birmingham, Alabama 35294
We thank Dr. Bangalore and colleagues for their interest in our work (1). We agree that the caffeine content of 1 cup of coffee and its absorption and pharmacokinetics are variable and not easily predictable. We used 1 cup of 8-oz brewed coffee with an estimated content of 100 mg of caffeine. Based on previous studies, the peak caffeine levels after 100 mg of oral caffeine ranged from 0.5 to 3.0 mg/l and were achieved within 15 to 120 min after consumption (2–4). In our study, the mean caffeine level was 3.1 ± 1.6 mg/l (range 1 to 7 mg/l) with 60% of patients achieving levels from 1 to 3 mg/l (see Fig. 1 from our study) (1). There was no dose-response effect of caffeine concentration on perfusion defects as depicted in our Figure 4, although we are aware of the limitations of the sample size and the small number of patients who had caffeine levels >3 mg/l. We did not measure the blood pressure before and after caffeine consumption, although we reported the hemodynamic responses of adenosine in the absence and presence of caffeine in our Table 3 (1). However, the generation of perfusion defects with adenosine stress is not solely dependent on its hemodynamic effects.
Finally, we agree with Dr. Bangolare et al. that our study should be described as hypothesis generating, and a larger study is needed to determine whether a caffeine level cut-off point can be defined that would attenuate the effects of adenosine on perfusion results.
- American College of Cardiology Foundation