Author + information
- Maria-Corina Serban, MD, PhD,
- Paul Muntner, PhD∗ ( and )
- Robert S. Rosenson, MD
- ↵∗Department of Epidemiology, University of Alabama at Birmingham, 1665 University Boulevard, Suite 230J, Birmingham, Alabama 35294
We thank Drs. Mascitelli and Goldstein and Drs. Ennezat and Guerbaai for their interest in our paper on the increased risk for recurrent myocardial infarction (MI) and coronary heart disease (CHD) events among Medicare beneficiaries with statin intolerance.
We agree with Drs. Mascitelli and Goldstein that the goal of prevention is to improve patient survival and quality of life. In a meta-analysis that included 5 trials comparing more versus less intensive statin therapy, each 1-mmol/l (38 mg/dl) reduction in low-density lipoprotein cholesterol was associated with 26%, 34%, and 26% decreases in major CHD events, revascularization, and stroke, respectively (1). Although not associated with all-cause mortality, each 1-mmol/l reduction in low-density lipoprotein cholesterol with more versus less intensive statin treatment was associated with a nonstatistically significant 15% reduction in CHD-related mortality. Medicare does not have information on cause of death, and we were unable to evaluate this outcome. With respect to their hypothesis that more versus less intensive statin therapy may prevent less severe MIs, the proportion of MIs that involve non–ST-segment versus ST-segment elevation in contemporary clinical practice has increased with the use of more sensitive diagnostic assays (2). Both ST-segment elevation and non–ST-segment elevation myocardial infarctions are associated with high mortality (3). Also, previous studies have demonstrated that hospitalization for MI is associated with reduced quality of life (4). From this perspective, more versus less intensive statin treatment is likely to have beneficial effects on quality of life through the prevention of recurrent events.
Drs. Ennezat and Guerbaai highlight the importance of encouraging lifestyle changes after MI. As they correctly point out, cigarette smoking is a strong risk factor for recurrent events and death following MI (5). The absence of information on lifestyle factors, including cigarette smoking, is a limitation of using administrative claims data. In response to the comment on antiplatelet treatment, we conducted an analysis including adjustment for this variable in addition to those in the fully adjusted model from Table 2 in our paper. Results from an analysis including adjustment for antiplatelet use and adherence (i.e., proportions of days covered ≥80%) during the year after hospital discharge for MI were virtually unchanged compared with those presented in the paper. Specifically, the hazard ratios associated with statin intolerance versus high statin adherence were 1.49 (95% confidence interval [CI]: 1.29 to 1.71) for recurrent MI, 1.50 (95% CI: 1.33 to 1.69) for CHD events, and 0.95 (95% CI: 0.86 to 1.05) for all-cause mortality. Finally, this research and Amgen’s support is part of an ongoing collaboration to better understand treatment and outcomes in hyperlipidemia. There are no limitations on publications for the academic authors under the collaboration agreement. All authors met the International Committee of Medical Journal Editors criteria and all conflicts of interest were disclosed.
Please note: Dr. Muntner has received grant support from Amgen, Inc. Dr. Rosenson has received research support from Regeneron and Sanofi; and serves on advisory boards for Amgen, Inc., Regeneron, and Sanofi. Dr. Serban has reported that she has no relationships relevant to the contents of this paper to disclose. P.K. Shah, MD, served as Guest Editor-in-Chief of this paper. Karol Watson, MD, PhD, served as Guest Editor for this paper.
- 2017 American College of Cardiology Foundation
- Dodson J.A.,
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