IJCS | Volume 32, Nº2, May/June 2019

265 Table 5 - Association of smoking (year-pack) with severity of injuries and with ventricular function. Assessment using the independent sample t-test and the Mann-Whitney test Variables Smoking - mean ± standard deviation Yes No p-value SYNTAX score 13.10 ± 10.02 12.97 ± 9.89 0.924 LVRF* 50.54 ± 13.61 50.16 ± 14.67 0.882 TIMI frame count † 20 (12.5 - 34) 28 (16 - 36) 0.123 *Left ventricle ejection fraction; †Median (interquartile amplitude). Source: Author’s elaboration, 2017. Table 6 - Correlation between alcohol consumption and severity of coronary injuries and ventricular function. Assessment using Kendall’s correlation coefficients Variables SYNTAX score r (p) LVEF* r (p) TIMI frame count r (p) Amount of alcohol consumed (g) 0.019 (0.728) -0.026 (0.683) 0.072 (0.404) Amount of wine consumed (g) 0.056 (0.325) -0.095 (0.159) 0.030 (0.745) Amount of alcohol consumed per week (g) 0.007 (0.896) -0.007 (0.912) 0.049 (0.562) Amount of wine consumed per week (g) 0.027 (0.632) -0.097 (0.154) 0.033 (0.725) *Left ventricle ejection fraction; †Median (interquartile amplitude). Source: Author’s elaboration, 2017. Table 7 - Correlation between smoking and severity of coronary injuries and ventricular function. Assessment using Kendall’s correlation coefficients Variables SYNTAX score r (p) LVEF* r (p) TIMI frame count r (p) Years of smoking 0.010 (0.855) -0.015 (0.806) 0.019 (0.823) Pack-year -0.025 (0.635) 0.019 (0.763) -0.174 (0.041) Cigarettes per day -0.029 (0.593) 0.017 (0.788) -0.192 (0.027) *Left ventricle ejection fraction. Source: Author’s elaboration, 2017. Albuquerque et al. Association smoking and alcohol consumption AMI Int J Cardiovasc Sci. 2019;32(3)261-268 Original Article Several data in the literature have found results compatible with the so-called Smoker’s Paradox, according to which there is fewer mortality among smoker patients who suffered AMI, in addition to an apparent better coronary perfusion after the use of the thrombolytic therapy or PCI. 17,18 Such reduction in mortality is attributable to the difference in the profile of patients who suffer an AMI and are smokers: in their vast majority they are younger, since AMI tends to occur up to elevenyears earlier among smokers, with fewer associated morbidities – such as DM and SAH – and usually in the inferior wall – associated with lower mortality than anterior wall MI. 19,20 However, even after adjusting these clinical differences, such paradox persisted, which could be explained by differences in the coronary anatomy and flow patterns in smokers and non-smokers. 20-22 Angeja et al., 19 confirmed that smokers demonstrated better epicardial flow than non-smokers, but when they studied microvascular flow measurements, they could not note any differences between these two groups. 19 A possible explanation for these better results seem to lie in the physiopathological differences between smokers and non-smokers with AMI – due to increased thrombus in smokers – which would induce a greater effectiveness of thrombolytic therapy and a better response to anti- plaquetary therapy. 23-26 However, the literature still lacks studies that quantitatively compare the TFC with the number of cigarettes smoked per day and the number of pack-years of smoking. This finding could thus be explained by the paradoxical effect of smoking on CAD and its association with a better response to post-AMI reperfusion procedures, assuming that smokers may have better myocardial vascularization, in addition to changes at the biochemical physiopathological levels and, therefore, present better TIMI frame count values. We cannot still rule out that this result may also be attributed to chance, given the small proportion of the sample, together with a weak correlation effect. Despite