Methanol intoxication, when sever enough, causes many electrocardiographic changes. J point elevation and U wave are most frequent (figure 1), While others like QTc more than 500 milli-second tends to be an index of severity (Table 3).
A total number of 356 patients were included in this study, a majority of whom were male. This can be explained by the participants’ cultural background and relevant social stigma of alcohol usage for women in Iran. Compared to previous outbreaks [18, 19], the age distribution of the population was broader as the study included teenagers as well as senior patients who were in their 70’s in some cases. The involvement of the youths may be a matter of concern for social activists in Iran.
In this study, interesting finding were myocardial infarction, AVB and sinus tachycardia, and QT>500, all of which predispose the patients to arrythmia. The mechanism of arrythmia is tightly related to acidosis. Acidosis is an obvious biochemical marker with regard to its several mechanisms. Formic acid makes a pivotal contribution to the PH drop, which causes hyperkalemia when acidosis makes potassium to shift out of cells. Another reason for high potassium level may be oliguria, which prevent potassium loss in urine. Another consequence of acidosis seems to be hypercalcemia caused by a decrease in binding to protein under this condition. The extra amount of both ions contributes to arrhythmia mechanism .
Different mortality rates have been reported for methanol intoxication. The reason may be controversy in definitions. Taiwan nationwide survey showed 40% long-term mortality ; however, a study from UK reported a 11% rate . Another research with the rate of 40% was performed by Sanaei-Zade et al. . The mortality rate in our series was slightly <17%, which seems to be more comparable to a study by Jaff et al. ; however, this is an in-hospital mortality in two referral centers, and the ones related to the outpatient cases were not included. The mortality and ocular and brain damage rates are in agreement with some previous outbreak reports [19, 22-24].
Although the most common finding in a previous report from the UK  was sinus tachycardia, most cases in this study seemed to have normal heart rate; however, the tachycardia proved to be a severity index in the present research. In this regard, the lower prevalence may be due to less severe intoxication in our patients. The heart rate>100 was observed in 25.3% of the sample, which was nearly six times as great as bradycardia (rate<60). In other words, about three quarter of our cases were at a normal range in this regard.
Although there are few case reports on the myocardial infarction in methanol toxicity , our survey was the first study, which could determine the prevalence of this complication. However, the exact pathophysiologic mechanism yet requires further research. We proposed the following hypotheses: (1) This infarction is possible in relatively young patients with no usual risk factors for atherosclerosis ; (2) severe acidosis causes bleeding due to a decrease in fibrinogen level. In-situ thrombosis may sometimes occur with ongoing disseminated intravascular coagulation and possible myocardial infarction ; (3) Possible pathophysiologic mechanism may be endothelial dysfunction, which is a known entity in reduced extracellular PH, however such a dysfunction will end in vasodilation frustratingly ; and (4) Acidosis causes vasodilatation; thus, spasm, as a mechanism of myocardial infarction cannot be blamed . Such hypotheses necessitate further investigation and research.
In our study, J point elevation was the most prevalent finding; therefore, repolarization abnormalities were to be categorized as early repolarization, Brugada phenocopy, and QT prolongation syndrome. According to the literature, arrhythmia can be predicted in accordance with the ECG findings such as QT prolongation, Brugada pattern, negative terminal portion of P wave in V1, inter-atrial block, and so on . Another newly introduced observation on ECG is QRS fragmentation, which is correlated with mortality in myocardial infarction in recent surveys . The only variable which was consistently correlated with the severity of disease was QTc prolongation>500. The QT prolongation was reported in mostly all the previous studies [e.g., 3, 30, 31]. However, its significance could not be emphasized due to the lower volume in older reports. QTc prolongation is the most commonly-used indicator; however, prolongation< 500 msec. may be interpreted doubtfully. Accordingly, we approached the values >500 as an independent marker of severity [32, 33].
We noted two type 1 Brugada ECG pattern in two brain-dead patients as terminal event before their arrest. This finding has been reported in some critical situations with deadly consequences. As an example, similar pattern has observed in some head injured patients before their death in Neurosurgery Intensive care unit. There are also reports of same pattern during Propofol infusion [34, 35].
The best independent ECG indicators of methanol toxicity severity were QTc>500 and heart rate>100. Interestingly, severe poisoning was strongly associated with myocardial infarction and atrioventricular block in our survey (Table 3).
The research design is cross-sectional so that it suffers from lack of long-term perspectives. Our diagnosis on myocardial infarction was based on the ECG finding, evolutionary changes, and enzyme rising in those with chest pain or chest pain equivalents; however, it disregarded coronary angiography and cardiac MRI.