TO THE EDITOR: In their recent study, Eisa et al1 concluded that gastroesophageal reflux disease (GERD) with concomitant metabolic syndrome (MetS) parameters is a risk factor of acute myocardial infarction (AMI) though this risk may be clinically insignificant.
In this regard, there is increasing evidence for association between Helicobacter pylori infection (Hp-I) and insulin resistance (IR) or MetS and related morbidity, including GERD and cardiovascular disease (CVD);2,3 the prevalence of MetS is higher in Hp-positive people;2 Hp-linked MetS is a risk factor of GERD and its eradication exhibits a positive effect against GERD in certain populations;3 AMI, a potentially fatal CVD complication, is closely linked with MetS;2 and Hp is a risk for acute coronary syndrome (ACS) including AMI,2 thus further investigation is warranted to estimate whether Hp eradication affects AMI occurrence.
Specifically, both Hp-I and MetS are highly prevalent worldwide and epidemiological studies as well as meta-analyses have shown that obesity induces inflammation (especially abdominal, visceral obesity) and drives to MetS, thereby being an indirect risk factor for GERD.3 In this respect, the conventional claim that declining Hp prevalence has led to a rise in GERD requires to be better studied since, for instance, the current global prevalence of Hp-I varies from 39.9% to 84.2% whereas the comparable picture for GERD is quite less varying from 2.5% to 51.2%.4 Moreover, several data indicate that Hp may contribute to GERD pathogenesis by several mechanisms and its eradication results in adequate control of GERD symptoms and improves esophagitis.3,5
A recent meta-analysis also indicated that Hp-I increases the risk of CVD adverse events, particularly AMI;6 there is a link between Hp-related CagA cytotoxin and ACS and the odds ratio of AMI is twice as greater in Hp-positive patients. Likewise, MetS is a major risk factor for AMI,7 increases the risk of CVD adverse events more than 2-fold, whereas its recovery significantly decreases the risk for major adverse cardiovascular events including AMI. Moreover, Hp-I is an independent risk factor for atrial fibrillation (AF),8 which remains a frequent arrhythmia in AMI and is closely linked with augmented subsequent cardiovascular mortality; coronary artery disease is a risk factor for AF and coronary embolism due to AF is a cause of AMI; and Hp-related non-alcoholic fatty liver disease, the hepatic component of MetS, is a risk of AF.8 Finally, Hp-I–related MetS may contribute to the pathophysiology of CVD including AMI by several mechanisms,9,10 thereby signifying eradication therapy as AMI prevention strategy.
Footnotes
Financial support: None.
Conflicts of interest: None.
Author contributions: All the authors have helped in the drafting and writing of the manuscript.
References
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