ST-segment elevation: are we cautious enough?

6 We read the case report of Sharma et al [1] with great interest and 7 would like to share some more information. Although myocardial 8 infarctionhas tobe consideredas thefirst and foremostwith ST-segment 9 elevation froman electrocardiogramfor optimalmanagement, however, 10 there are various noncardiac fatal conditions present as ST-segment 11 changes in electrocardiogram [2]. Furthermore, targets for reperfusion 12 have drastically altered the assessment of patientswith chest pain. Gu et 13 al [3] reported analternative diagnosis in 2.3%of patientswith suspected 14 ST-segment elevation myocardial infarction (STEMI) referred for 15 primary percutaneous coronary intervention, although it varies between 16 1.4% and 13% in literature [4]. We have previously reported a case series 17 of ST-segment abnormalities in spontaneous pneumothorax along with 18 mechanisms for these changes [5]. 19 Interestingly, Sampson et al [6] hypothesized that hypoxic 20 vasoconstriction of the pulmonary vessels of the collapsed left lung 21 with resultant diversion of cardiac output to right lung might have 22 increased the pressure in the pulmonary vasculature causing sudden 23 pressure load on right ventricle leading to focal or global myocardial 24 ischemia, which might have triggered epicardial or microvascular 25 coronary vasospasm resulting in ST elevation. Severe hypoxemia 26 induces a catecholamine surge, which increases myocardial workload 27 and results in ischemia. In addition, change in intrapleural pressure 28 influences the venous return and stroke volume. Tachycardia as seen 29 in the patient reported might have increased the oxygen demand and 30 shortened diastolic perfusion, which have led to ischemia of 31 myocardium. Hypoxia also generates super oxide, which abolishes 32 the vasodilatory effect of nitrous oxide and thereby aggravates 33 coronary vasospasm [7]. Thus, a combination of multiple mechanisms 34 might have played a role for the ST elevation. 35 Hence, chest pain with ST-segment changes is not always 36 synonymous with acute coronary syndrome, and there is no 37 skepticism that early coronary reperfusion is beneficial in STEMI. 38 Nevertheless, maintaining a high index of clinical suspicion of 39 conditions mimicking STEMI is crucial as the advantages of timely 40 intervention in patients with STEMI should be weighed against the 41 possible risks caused by thrombolysis and by a delay in the 42 treatment of the underlying diseases that mimics STEMI. Therefore 43 noncardiac conditions causing STEMI have to be reinforced in regular 44 teaching and training programs and remembered by emergency