Coronary Artery Calcium and Cardiovascular Events in Patients With Familial Hypercholesterolemia Receiving Standard Lipid-Lowering Therapy

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Citações na Scopus
105
Tipo de produção
article
Data de publicação
2019
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ISSN da Revista
Título do Volume
Editora
ELSEVIER SCIENCE INC
Citação
JACC-CARDIOVASCULAR IMAGING, v.12, n.9, p.1797-1804, 2019
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Unidades Organizacionais
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Resumo
OBJECTIVES The aim of this study was to evaluate the role of coronary artery calcium (CAC) as a predictor of atherosclerotic cardiovascular disease (ASCVD) (fatal or not myocardial infarction, stroke, unstable angina requiring revascularization, and elective myocardial revascularization) events in asymptomatic primary prevention molecularly proven heterozygous familial hypercholesterolemia (FH) subjects receiving standard lipid-lowering therapy. BACKGROUND FH is associated with premature ASCVD. However, the clinical course of ASCVD in subjects with FH is heterogeneous. CAC score, a marker of subclinical atherosclerosis burden, may optimize ASCVD risk stratification in FH. METHODS Subjects with FH underwent CAC measurement and were followed prospectively. The association of CAC with ASCVD was evaluated using multivariate analysis. RESULTS A total of 206 subjects (mean age 45 +/- 14 years, 36.4% men, baseline and on-treatment low-density lipoprotein cholesterol 269 +/- 70 mg/dl and 150 +/- 56 mg/dl, respectively) were followed for a median of 3.7 years (interquartile range: 2.7 to 6.8 years). CAC was present in 105 (51%), and 15 ASCVD events (7.2%) were documented. Almost one-half of events were hard outcomes, and the others were elective myocardial revascularizations. The annualized rates of events per 1,000 patients for CAC scores of 0 (n = 101 [49%]), 1 to 100 (n = 62 [30%]) and >100 (n = 43 [21%]) were, respectively, 0, 26.4 (95% confidence interval: 12.9 to 51.8), and 44.1 (95% confidence interval, 26.0 to 104.1). In multivariate Cox regression analysis, log(CAC score 1) was independently associated with incident ASCVD events (hazard ratio: 3.33; 95% CI: 1.635 to 6.790; p = 0.001). CONCLUSIONS CAC was independently associated with ASCVD events in patients with FH receiving standard lipid-lowering therapy. This may help further stratify near-term risk in patients who might be candidates for further treatment with newer therapies. (C) 2019 by the American College of Cardiology Foundation.
Palavras-chave
atherosclerosis, computed tomography, coronary calcification, familial hypercholesterolemia, PCSK9, risk factors, statins
Referências
  1. Benn M, 2012, J CLIN ENDOCR METAB, V97, P3956, DOI 10.1210/jc.2012-1563
  2. Besseling J, 2016, J AM COLL CARDIOL, V68, P252, DOI 10.1016/j.jacc.2016.04.054
  3. Blaha MJ, 2016, CIRCULATION, V133, P849, DOI 10.1161/CIRCULATIONAHA.115.018524
  4. Blaha MJ, 2011, LANCET, V378, P684, DOI 10.1016/S0140-6736(11)60784-8
  5. Braunwald E, 2000, J AM COLL CARDIOL, V36, P970, DOI 10.1016/S0735-1097(00)00889-5
  6. Gidding SS, 2015, CIRCULATION, V132, P2167, DOI 10.1161/CIR.0000000000000297
  7. Hlatky MA, 2017, J AM COLL CARDIOL, V70, P2677, DOI 10.1016/j.jacc.2017.10.001
  8. Humphries SE, 2018, ATHEROSCLEROSIS, V274, P41, DOI 10.1016/j.atherosclerosis.2018.04.040
  9. Jannes CE, 2015, ATHEROSCLEROSIS, V238, P101, DOI 10.1016/j.atherosclerosis.2014.11.009
  10. Jansen ACM, 2004, J INTERN MED, V256, P482, DOI 10.1111/j.1365-2796.2004.01405.x
  11. Kramer CK, 2013, BMJ-BRIT MED J, V346, DOI 10.1136/bmj.f1654
  12. Mangili LC, 2017, ATHEROSCLEROSIS, V263, P393, DOI 10.1016/j.atherosclerosis.2017.04.025
  13. Martinez LRC, 2008, ATHEROSCLEROSIS, V200, P83, DOI 10.1016/j.atherosclerosis.2007.12.014
  14. Miname MH, 2010, ATHEROSCLEROSIS, V213, P486, DOI 10.1016/j.atherosclerosis.2010.10.001
  15. Mortensen MB, 2018, JACC-CARDIOVASC IMAG, V11, P221, DOI 10.1016/j.jcmg.2017.01.029
  16. Mundal L, 2016, EUR J PREV CARDIOL, V23, P1962, DOI 10.1177/2047487316666371
  17. Nasir K, 2015, J AM COLL CARDIOL, V66, P1657, DOI 10.1016/j.jacc.2015.07.066
  18. Neefjes LA, 2011, ATHEROSCLEROSIS, V219, P721, DOI 10.1016/j.atherosclerosis.2011.09.052
  19. Nordestgaard BG, 2013, EUR HEART J, V34, P3478, DOI 10.1093/eurheartj/eht273
  20. Nozue T, 2006, J ATHEROSCLER THROMB, V13, P323, DOI 10.5551/jat.13.323
  21. Orringer CE, 2017, J CLIN LIPIDOL, V11, P880, DOI [10.1016/j.jacl.2017.05.001, 10.1016/j.jac1.2017.05.001]
  22. de Isla LP, 2018, J CLIN LIPIDOL, V12, P948, DOI 10.1016/j.jacl.2018.04.003
  23. de Isla LP, 2017, CIRCULATION, V135, P2133, DOI 10.1161/CIRCULATIONAHA.116.024541
  24. de Isla LP, 2016, J AM COLL CARDIOL, V67, P1278, DOI 10.1016/j.jacc.2016.01.008
  25. Ridker PM, 2018, J CLIN LIPIDOL, V12, P958, DOI 10.1016/j.jacl.2018.03.088
  26. Roffi M, 2016, EUR HEART J, V37, P267, DOI 10.1093/eurheartj/ehv320
  27. Sabatine MS, 2017, NEW ENGL J MED, V376, P1713, DOI 10.1056/NEJMoa1615664
  28. Santos RD, 2016, LANCET DIABETES ENDO, V4, P850, DOI 10.1016/S2213-8587(16)30041-9
  29. Santos RD, 2015, LANCET, V385, P307, DOI 10.1016/S0140-6736(14)61702-5
  30. Santos RD, 2004, HEART, V90, P92, DOI 10.1136/heart.90.1.92
  31. Silverman MG, 2014, EUR HEART J, V35, P2232, DOI 10.1093/eurheartj/eht508
  32. Medel DV, 2013, AM J CARDIOL, V111, P955, DOI 10.1016/j.amjcard.2012.12.012