This study aimed to explore the relation between opium consumption and CAE. We selected patients with CAE and without any co-existing CAD as our cases because about 50% of CAE is attributed to concomitant CAD in adult patients with CAE (22). Moreover, we employed PSM to consider the possible confounding effects of traditional cardiovascular risk factors as indicators of atherosclerosis. After taking these considerations into account, we found that the frequency of opium consumption was not significantly different between patients with pure CAE and patients with normal CAG.
In a preprint manuscript, Masoumi reported that opium is an important risk factor for CAE. In this cross-sectional study, they enrolled 46 patients with CAE, 30 patients with CAD, and 42 cases without CAE and CAD. This study revealed that opium consumption was significantly greater in patients with CAE and CAD compared to controls. The number of participants in their study was much less than ours and it can be one of the considerations to explain the different results. Moreover, in that study, they did not adjust other CVD risk factors including age, sex, DM, hypertension, hyperlipidemia, family history of CAD, and cigarette smoking between cases and controls while we used PSM to control the effect of any confounders and it could be another reason to explain the difference (23).
The role of opium consumption in the pathogenesis of CVD and mechanisms involved in increasing the risk of CVD are not yet fully defined. Some studies suggested that inflammation caused by opium may play the main role in developing the CVD especially atherosclerosis but whether this factor can cause CAE without any co-existing stenosis by itself has not yet been considered (4, 8). In this study, we found that opium consumers were more likely to be male and smoke cigarette, and had lower plasma levels of HDL cholesterol that make them more susceptible to CVD; nevertheless, they were younger, had lower plasma levels of total cholesterol, and were less likely to have hypertension or hyperlipidemia which are cardioprotective. We may hypothesize that these contradictive factors eventually resulted in no significant association between opium consumption and CAE. It is noteworthy that due to using PSM to match pure CAE and normal CAG groups, these results are not representative of our database and they can only describe the characteristics of patients included in this study.
Hyperlipidemia is another possible mechanism that can be induced by opium to develop CVD. Some studies have shown that opium may affect the level of HDL, LDL, total cholesterol, and triglyceride and with these effects, it may play a role in developing CVD (24). In addition, the association between CAE and traditional cardiovascular risk factors is still controversial but some studies reported that CAE appears to be associated with these risk factors including hyperlipidemia (25). Although we used PSM to match baseline characteristics regarding hyperlipidemia, the levels of LDL, triglyceride, and total cholesterol were lower among CAE patients in comparison to normal CAGs (Table 1). Although these statistical differences have been observed, there may not be a clinically significant difference. It should be noted that the lower levels of these three in patients with CAE could impact the relationship between opium and CAE in our study.
To the best of our knowledge, this is one of the first studies dedicated to evaluating the association between opium use and CAE. We tried to conduct it as methodologically decent as we could; nevertheless, it has several limitations. First, it is an observational study that bears some inherent biases and falls short in establishing the causal relationship. Second, the missing data on opium consumption might result in bias in our findings. Future prospective cohort studies with larger sample sizes will address these limitations.