In their recent study, Fuller et al investigated the incidence of nausea and vomiting in 180 patients with ST-segment elevation acute myocardial infarctions (STEMIs) or acute myocardial infarctions (AMIs) associated with left bundle branch block. In total, 60% of their patients had inferior and 40% had anterior AMIs. Nausea was present in nearly 2/3 and vomiting in nearly 1/3 of patients, with nonsignificant trends toward greater occurrence of these symptoms with inferior compared to anterior AMI. Several issues regarding their report should be further discussed.

In the investigators’ Table 4, there are some misinterpretations regarding the study published by our group in 2001 in the International Journal of Cardiology but also regarding other cited studies. We included not only patients with STEMIs but all patients with first AMIs, regardless of ST-segment elevation, if the infarct location had been determined. The differences in symptom frequency stated in the investigators’ Table 4 were clearly significant, which can be seen from the odds ratios and confidence intervals provided in the table. In explaining our results and discussing the issue, it is important to note that we distinguished isolated lateral from anterior and inferior AMIs and treated them all as separate groups, which provided a more accurate comparison of the occurrence of nausea and vomiting between the 3 more specific AMI locations. In association with the fact that our study had a far greatest population size, this might have provided both power and sensitivity that could not be achieved in the other studies. In addition, Fuller et al did not include or discuss 2 additional studies reporting a closer relation between gastrointestinal symptoms, such as nausea, vomiting, and hiccups, with inferior AMI.

Although in Fuller et al’s Table 4, 2 studies were presented as investigating Q-wave AMIs, in the text, they were discussed as STEMIs. Although this is the case in most patients, a strict analogy between a STEMI on acute-phase electrocardiography and the later development of a Q-wave AMI cannot be established. Our group has also shown that in comparison to non-Q-wave AMIs, Q-wave AMIs are more often associated with nausea and vomiting. However, those differences observed in the raw data disappeared after adjusting for the increase in cardiac enzyme levels. This suggests that the presence of these 2 symptoms significantly depends on the size of myocardial damage, which is in accordance with other results. The same was observed for sweating, weakness, and hiccups. Fuller et al included only patients with STEMIs and left bundle block, which could be expected to be more extensive infarctions. Although apparent, the differences were not statistically significant, probably at least in part because of the small sample size.

Our group has additionally shown that the occurrence of many symptoms associated with AMI, including vomiting and nausea, also depends on gender, age, and the presence of cardiovascular risk factors such as smoking, hypertension, diabetes, and hypercholesterolemia. Nausea tended to be a significantly more frequent AMI symptom in women, patients with diabetes, those with hypercholesterolemia, and those without hypertension, whereas vomiting more often followed AMIs in smokers than in nonsmokers. After adjustments for age, gender, cardiac enzyme levels, and remaining risk factors, the higher levels of creatine kinase-MB fraction, diabetes, and hypercholesterolemia were independent predictors of nonpain symptoms in general.

Fuller et al mentioned the speculation that a stimulus responsible for nausea and vomiting could be placed in the epicardial rather than in the subendocardial portion of the left ventricle. Another possible mechanism is excitation of the vagal nerve afferents, preferentially located in the inferoposterior cardiac wall. Accordingly, probably vagally referred epigastric, neck, and jaw pain is also more often associated with inferior AMI. None of the published studies has separated patients with preexisting gastrointestinal or dyspeptic disorder and compared them to those without such problems. For example, a large meal and an episode of emotional stress may be involved in triggering an acute coronary event, but at the same time, they may cause exacerbation of the symptoms of a coexisting gastrointestinal disorder.

The actual clinical presentation of AMI is likely multifactorial. Probably the most accurate conclusion is that nausea and vomiting somewhat more often follow more extensive AMIs, as well as AMIs of the inferior wall, compared to other locations. Although some differences in clinical presentation according to AMI size and location likely do exist, they are relative and cannot be used as a reliable diagnostic or prognostic tool.