To the Editor,
We would first like to thank Burillo-Putze et al for their letter. In response to their suggestions concerning the inclusion of cocaine consumption as a cardiovascular risk factor, we are in complete agreement regarding the prothrombotic role of cocaine. We are aware that several mechanisms involve cocaine in the pathogenesis of acute coronary syndromes, such as platelet hyperreactivity, probably as a consequence of the endothelial dysfunction that can be triggered by it.1-4 On the other hand, in addition to cocaine consumption, the prothrombotic role of a high number of "non-classic" cardiovascular risk factors should be considered, such as homocystinemia, hyperfibrinogenemia, some genetic deficiencies (antithrombin III, protein C, and protein S), catecholamine release, and stress, among others, that are involved in the pathogenesis of acute coronary syndromes.5
Our review article is basically devoted to the role of classic cardiovascular risk factors in blood thrombogenicity and, thus, although there is evidence that cocaine seems to trigger an atherothrombotic process, it has not been included as a classic risk factor, given our understanding that cocaine consumers represent a minority in society. Unfortunately, it cannot be ruled out that in the future, due to increased use, cocaine consumption may have to be tacitly included as a classic factor; however, this is not yet the case. This does not imply that any patient less than 45 years old admitted for acute coronary syndrome should not be questioned concerning consumption or those in whom there is no clear risk factor that can be associated with the presentation of a coronary event.