Rebecca Crosier1, Peter C Austin2, Dennis T Ko3, Patrick R Lawler4, Therese A Stukel2, Michael E Farkouh5, Xuesong Wang6, John A Spertus7, Heather J Ross4, Douglas S Lee8. 1. Department of Medicine, University of Toronto, Toronto, Ontario. 2. ICES, Toronto, Ontario; Institute for Health Policy, Management and Evaluation Toronto, Ontario. 3. Department of Medicine, University of Toronto, Toronto, Ontario; ICES, Toronto, Ontario; Institute for Health Policy, Management and Evaluation Toronto, Ontario; Sunnybrook Health Sciences Centre, Toronto, Ontario. 4. Department of Medicine, University of Toronto, Toronto, Ontario; Peter Munk Cardiac Centre of University Health Network, Toronto, Ontario; Ted Rogers Centre for Heart Research, Toronto, Ontario. 5. Department of Medicine, University of Toronto, Toronto, Ontario; Peter Munk Cardiac Centre of University Health Network, Toronto, Ontario. 6. ICES, Toronto, Ontario. 7. Saint Luke's Mid America Heart Institute/UMKC, Kansas City, Missouri. 8. Department of Medicine, University of Toronto, Toronto, Ontario; ICES, Toronto, Ontario; Institute for Health Policy, Management and Evaluation Toronto, Ontario; Peter Munk Cardiac Centre of University Health Network, Toronto, Ontario; Ted Rogers Centre for Heart Research, Toronto, Ontario. Electronic address: dlee@ices.on.ca.
Abstract
PURPOSE: The impact of guideline-directed medical therapy for coronary heart disease in those hospitalized with acute heart failure is unknown. METHODS: We studied guideline-directed medical therapies for coronary disease: angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs), beta-adrenoreceptor antagonists, antiplatelet agents or anticoagulants, and statins. Using inverse probability of treatment weighting the propensity score, we examined associations of guideline-directed medical therapy intensity (categorized as low [0-1], high [2-3], or very high [4] number of drugs) with mortality in 1873 patients with angina, troponin elevation, or prior myocardial infarction. RESULTS: At discharge, 0-1, 2-3, and 4 medications were prescribed in 467 (25%), 705 (38%), and 701 (37%) patients, respectively. Relative to those prescribed 0-1 drugs (reference), all-cause mortality was lower with 2-3 (hazard ratio [HR] 0.48, 95% confidence interval [CI] 0.28-0.84, P = 0.009) or all 4 drug classes (HR 0.56, 95% CI 0.33-0.96, P = 0.034) over 181-365 days, with similar reductions present from 0-180 days. In those with heart failure with preserved ejection fraction, mortality trended lower with 2-3 drug classes (HR 0.43, 95% CI 0.18-1.02, P = 0.054) and was significantly reduced with 4 drugs (HR 0.32, 95%CI 0.12-0.84, P = 0.021) during 0-180 day follow-up. In heart failure with reduced ejection fraction, all-cause mortality was reduced during both 0-180 and 181-365 days when discharged on 2-3 (HR 0.30 for 181-365 days, 95%CI 0.14-0.64, P = 0.002) or all 4 drug classes (HR 0.43, 95%CI 0.19-0.95, P = 0.038). CONCLUSIONS: Increasing guideline-directed medical therapy intensity for coronary heart disease resulted in lower mortality in patients with acute ischemic heart failure with both preserved and reduced ejection fractions.
PURPOSE: The impact of guideline-directed medical therapy for coronary heart disease in those hospitalized with acute heart failure is unknown. METHODS: We studied guideline-directed medical therapies for coronary disease: angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs), beta-adrenoreceptor antagonists, antiplatelet agents or anticoagulants, and statins. Using inverse probability of treatment weighting the propensity score, we examined associations of guideline-directed medical therapy intensity (categorized as low [0-1], high [2-3], or very high [4] number of drugs) with mortality in 1873 patients with angina, troponin elevation, or prior myocardial infarction. RESULTS: At discharge, 0-1, 2-3, and 4 medications were prescribed in 467 (25%), 705 (38%), and 701 (37%) patients, respectively. Relative to those prescribed 0-1 drugs (reference), all-cause mortality was lower with 2-3 (hazard ratio [HR] 0.48, 95% confidence interval [CI] 0.28-0.84, P = 0.009) or all 4 drug classes (HR 0.56, 95% CI 0.33-0.96, P = 0.034) over 181-365 days, with similar reductions present from 0-180 days. In those with heart failure with preserved ejection fraction, mortality trended lower with 2-3 drug classes (HR 0.43, 95% CI 0.18-1.02, P = 0.054) and was significantly reduced with 4 drugs (HR 0.32, 95%CI 0.12-0.84, P = 0.021) during 0-180 day follow-up. In heart failure with reduced ejection fraction, all-cause mortality was reduced during both 0-180 and 181-365 days when discharged on 2-3 (HR 0.30 for 181-365 days, 95%CI 0.14-0.64, P = 0.002) or all 4 drug classes (HR 0.43, 95%CI 0.19-0.95, P = 0.038). CONCLUSIONS: Increasing guideline-directed medical therapy intensity for coronary heart disease resulted in lower mortality in patients with acute ischemic heart failure with both preserved and reduced ejection fractions.