Pharmacogenetic interactions between angiotensin-converting enzyme inhibitor therapy and the angiotensin-converting enzyme deletion polymorphism in patients with congestive heart failure
Dennis M. McNamara, MD*,*,
Richard Holubkov, PhD ,
Lisa Postava, MBA*,
Karen Janosko, MSN*,
Guy A. MacGowan, MD*,
Michael Mathier, MD*,
Srinivas Murali, MD*,
Arthur M. Feldman, MD, PhD and
Barry London, MD, PhD*
* Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Department of Family and Preventive Medicine, School of Medicine, University of Utah, Salt Lake City, Utah
Department of Medicine, Thomas Jefferson Medical Center, Philadelphia, Pennsylvania

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Figure 1 (A) Overall transplant-free survival by angiotensin-converting enzyme (ACE) genotype (n = 479, p = 0.026). (B) Transplant-free survival by ACE genotype with no beta-blocker therapy (n = 277, p = 0.004). (C) Transplant-free survival by ACE genotype with beta-blocker therapy (n = 202, p = 0.97).
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Figure 2 (A) Transplant-free survival by angiotensin-converting enzyme (ACE) genotype: low-dose ACE inhibitor (n = 227, p = 0.032).(B) Transplant-free survival by ACE genotype: high-dose ACE inhibitor (n = 201, p = 0.64).
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Figure 3 (A) Transplant-free survival by angiotensin-converting enzyme (ACE) genotype: low-dose ACE inhibitor therapy with no beta-blockers (n = 130, p = 0.005). (B) Transplant-free survival by ACE genotype: high-dose ACE inhibitor therapy with no beta-blockers (n = 117, p = 0.47).
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Figure 4 (A) Transplant-free survival by treatment strategy, DD genotype only (n = 128, p = 0.001). (B) Transplant-free survival by treatment strategy, ID and II genotypes combined (n = 300, p = 0.38). ACE = angiotensin-converting enzyme; Beta = beta-blockers.
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