ABC | Volume 111, Nº5, November 2018

Original Article Soeiro et al ACS in Men vs. women Arq Bras Cardiol. 2018; 111(5):648-653 Table 1 – Baseline clinical characteristics of male vs. female patients Characteristic Male (n = 2,437) Female (n = 1,308) p-value Age 60.3 ± 11.6 64.7 ± 10.4 < 0.0001* BMI 26.1 ± 6.5 24.3 ± 6.1 < 0.0001 † Diabetes Mellitus 1,041 (42.7) 627 (47.9) 0.011 ‡ SAH 1,652 (67,8) 968 (72.9) 0.001 ‡ Smoking 819 (33.6) 332 (25.4) < 0.0001 ‡ FH positive for CAD 361 (14.8) 171 (12.9) 0.113 ‡ Dyslipidemia 1,136 (46.6) 666 (50.9) 0.011 ‡ Heart failure 214 (8.8) 133 (10) 0.778 ‡ Previous iCVA 124 (5.1) 67 (5.1) 0.925 ‡ Previous AMI 819 (33.6) 378 (28.9) 0.004 ‡ Previous CABG 356 (14.6) 140 (10.7) 0.001 ‡ Previous CA 522 (21.4) 234 (17.9) 0.011 ‡ Hemoglobin, mg/dL 14.6 ± 1.9 13.2 ± 1.7 < 0.001* Peak troponin, ng/dL 11.8 ± 5.9 8.0 ± 7.2 < 0.001* Creatinine, mg/dL 1.3 ± 0.5 1.5 ± 0.4 < 0.0001* SBP, mmHg 134.2 ± 29.4 133.0 ± 27.2 0.104 † LVEF,% 52.3 ± 19.9 51.8 ± 18.7 0.09 † Killip ≥ 2 212 (8.7) 99 (7.6) 0.259 ‡ ASA 2,383 (97.8) 1,267 (96.9) 0.081 ‡ Beta-blocker 2,149 (88.2) 1,105 (84.5) 0.002 ‡ GPI IIb/IIIa 202 (8.3) 114 (8.7) 0.292 ‡ Enoxaparin 1,859 (76.3) 981 (75) 0.405 ‡ Fondaparinux 258 (10.6) 128 (9.8) 0.46 ‡ Clopidogrel 1,772 (72.7) 920 (70.3) 0.132 ‡ Statins 1,228 (50.4) 647 (49.5) 0.768 ‡ ACE inhibitor 1.694 (69.5) 870 (66.5) 0.065 ‡ Results are expressed as mean ± standard deviation, median ± standard deviation or n (%). *Unpaired t test; † Mann-Whitney U test; ‡ chi-square test. BMI: body mass index; SAH: systemic arterial hypertension; FH: family history; CAD: coronary artery disease; iCVA: ischemic cerebrovascular accident; AMI: acute myocardial infarction; CABG: coronary artery bypass grafting; CA: coronary angioplasty; SBP: systolic blood pressure; LVEF: left ventricular ejection fraction; ASA: acetylsalicylic acid; GPI: glycoprotein inhibitor; ACE inhibitor: angiotensin-converting enzyme inhibitor. 360,000 women submitted to Percutaneous Coronary Intervention (PCI) only in 2007. 5 The number of women with ACS (34.9%) found in this study is proportionally lower than the data published in most international studies. One of the hypotheses for this fact is that there is still a reasonable index of diagnostic error regarding ACS in women, perhaps more pronounced in Brazil, due to the difficulty of access to health care services. Some studies make it clear that the clinical manifestations of coronary disease in women are sometimes non-specific and/or underrated, and a large number of female patients are discharged without a correct diagnosis. 2 Another interesting finding of this study was the fact that the group of women, in addition to being older, also had a higher number of comorbidities, such as diabetes mellitus, hypertension and dyslipidemia. Women, in most instances, are older when they exhibit their first manifestation of ACS, at a mean age of 71.8 years, compared to 65 years for men. 2,5-10 The older age of onset in women, when compared to men, is probably due to the protective role of estrogen circulation in the vascular endothelium. This hypothesis derives mainly from the observation that the incidence of AMI increases substantially in postmenopausal women. The effects of estrogen on the vascular system include increased nitric oxide release, which leads to vasodilation, prostaglandin production regulation, and smooth muscle proliferation inhibition. 2 Corroborating these data, a retrospective study in patients with STE-ACS showed that women were significantly older (70.9 years vs. 63 years, p < 0.001) and more often had diabetes mellitus (36.2% vs. 21.0%, p < 0.001) and hypertension (82.3% vs. 73.7%, p = 0.006). 6 As for the ACS presentation, due perhaps to the greater number of comorbidities and the older age at presentation, women classically had a higher proportion of NSTE‑ACS when compared to men. 2,5,7-9,11,12 In a retrospective 650