Effects of Cigarette Smoking & Vaping on Heart Attack

The effects of cigarette products on heart attack (HA) size and microvascular (small blood vessel) obstruction that occurs after the large obstructed coronary artery has been reopened (no-reflow, NR) and heart function restored following heart attack are controversial. Because the magnitude of HA, NR and cardiac function are important independent predictors of long-term clinical outcome after HA, it is essential to determine whether prior exposure to cigarette smoke or electronic-cigarette vapor, with or without nicotine, has a detrimental effect on these parameters. There is a perception that e-cigarette vapors are safer than standard cigarette smoke, but there are no head-to-head comparisons in experimental HA models. Experimental studies examining the effect of standard cigarette products on HA size are controversial. However, initial recent pilot studies from our group showed that prior nicotine exposure increases the extent of NR. An increase in NR in both experimental and clinical studies is a poor prognosticator, associated with dilated and poorly functioning left ventricles, heart failure and death. Our pilot data also showed that after only 3 days of inhalation exposure to e-cigarette vapors that both systolic and diastolic blood pressure increased in an animal model, which could have a major impact on outcome during a HA. Well-established animal models of inhalation exposure and standard analyses of rodent HA and NR will be used. We will test exposure (8 weeks) to standard cigarette smoke or e-cigarette vapor, with and without nicotine, and control (air) in protocols of HA. Our objectives are to determine whether subjects exposed to e-cigarette vapors have exacerbated heart muscle cell damage, worsened microvascular injury, and/or worsened heart function in the setting of HA and to establish whether e-cigarette vapors (with and without nicotine) are safer than standard cigarette smoke.