There is a Significant Link Between Salmonellosis and Myocardial Infarction
Introduction
Food poisoning — clinically referred to as gastroenteritis — affects millions worldwide, and is caused by a variety of pathogens, including bacteria such as Salmonella. While gastroenteritis primarily presents with gastrointestinal symptoms like diarrhea, vomiting, fever, and abdominal cramps, an important question in clinical research is whether such infections can contribute to cardiovascular events, specifically myocardial infarctions (MI). A myocardial infarction, commonly known as a heart attack, occurs when blood flow to the heart muscle is blocked, often by a blood clot that formed on ruptured plaque (which is essentially cholesterol/fat buildup) in a coronary artery. This in turn results in the heart not getting the oxygen it needs, causing the tissue to die. Traditional risk factors (e.g., hypertension, hyperlipidemia, smoking) explain most MI cases, but infection-associated inflammation and systemic physiologic stress may also act as triggers, particularly in vulnerable individuals.
The linkage between systemic infectious illnesses and MIs have been observed in respiratory infections (e.g., influenza) and is hypothesized for other infections. This paper critically evaluates evidence regarding gastroenteritis from bacterial pathogens—especially Salmonella—and the risk of myocardial infarction, focusing on epidemiological associations, biological mechanisms, rare cardiovascular complications, and clinical implications.
Epidemiological Evidence: Gastroenteritis and Acute Myocardial Infarction
Systematic epidemiological investigations provide foundational insights into whether infectious gastroenteritis correlates with MI risk.
A nested case-control study using a large healthcare database in Taiwan found that individuals who experienced gastroenteritis shortly (within ~2 weeks) before MI had significantly higher odds of acute myocardial infarction compared with matched controls. Gastroenteritis was significantly associated with subsequent AMI, with an adjusted odds ratio of 1.68 (95% CI: 1.54–1.83), and the association was stronger for hospitalized gastroenteritis cases (adjusted OR 2.50). Importantly, patients with preceding gastroenteritis also had worse post-AMI outcomes including increased in-hospital mortality and longer stays. The authors suggest that gastroenteritis may act as a trigger for MI, possibly due to systemic inflammation and procoagulant changes resulting from the diarrheal illness.
Another analysis of hospital discharge data showed that ≈1.3% of AMI hospitalizations were temporally linked with a prior episode of gastroenteritis. These cases were also characterized by longer stays and higher mortality, suggesting that gastroenteritis might have contributed to a pathophysiologic environment favouring myocardial ischemia and infarction.
Taken together, these broad population-based data support an epidemiological link between gastroenteritis and MI, even though they do not implicate specific pathogens such as Salmonella in all cases. They highlight that severe gastroenteritis, especially when associated with dehydration and systemic stress, appears to elevate MI risk.
Biological Mechanisms: How Could Gastroenteritis Trigger MI?
Understanding mechanisms is essential to interpreting whether gastroenteritis can plausibly trigger MI. Several biological pathways have been proposed:
1. Systemic Inflammation and Hypercoagulability
Gastroenteritis induces inflammatory signaling and immune activation beyond the gut. Inflammatory cytokines (e.g., C-reactive protein, interferon-gamma) become elevated and can alter coagulation pathways, increasing expression of tissue factor and prothrombotic factors. Systemic inflammation also activates platelets and destabilizes vulnerable atherosclerotic plaques, predisposing them to rupture and thrombosis, key steps in MI pathogenesis.
2. Dehydration, Hemoconcentration, and Viscosity Changes
Diarrhea and vomiting — hallmarks of gastroenteritis — can cause dehydration and hemoconcentration, leading to elevated blood viscosity. Hemoconcentration increases thrombosis risk, impairs microvascular perfusion, and can stimulate clotting pathways (and subsequently decrease perfusion). Severe dehydration may thereby contribute to conditions favourable for myocardial ischemia or infarction.
3. Electrolyte Imbalances and Clotting Factor Dysregulation
4. Cardiac Stress from Systemic Physiological Perturbations
Severe gastroenteritis places stress on cardiovascular homeostasis, increasing cardiac metabolic demand and systemic vascular resistance variability. These changes can compromise myocardial oxygen balance, particularly in patients with preexisting coronary disease or limited cardiac reserve.
Evidence from observational studies and mechanistic models thus provides biological plausibility that the systemic effects of gastroenteritis can create a milieu conducive to MI, especially as a trigger rather than a primary cause.
Specific Arguments Regarding Salmonella Infections
While many gastroenteritis cases are self-limited and caused by various bacteria and viruses, Salmonella species — especially non-typhoidal Salmonella (NTS) — are among the most common bacterial causes of food poisoning. Salmonella infections provide a useful model for examining potential cardiovascular complications and rare direct links to cardiac injury.
Salmonella Gastroenteritis and Rare Cardiac Events
Although most gastroenteritis cases do not result in cardiovascular complications, Salmonella can rarely invade beyond the gut and cause bacteremia. When Salmonella enters the bloodstream, a constellation of serious cardiovascular manifestations has been documented:
- Myocarditis and myopericarditis linked to Gastrointestinal Distress: Several case reports describe patients with preceding Salmonella gastroenteritis who developed acute myocarditis, a direct inflammatory involvement of the heart muscle. Myocarditis can mimic MI clinically, often with elevated cardiac biomarkers and ECG changes, though without obstructive coronary artery disease.
- Endocarditis and infected atheroma: Though exceptionally rare, Salmonella bacteremia can lead to infection of heart valves (endocarditis) or infected atheromatous plaques, conditions that may precipitate thrombotic cardiovascular events.
- Case reports with STEMI-like presentations: Isolated case descriptions report Salmonella-associated myocarditis presenting with ST-elevation, a classic finding in myocardial infarction.
These documented cardiac complications illustrate that direct Salmonella involvement of the heart (via bacteremia) is possible but extremely uncommon. Most Salmonella gastroenteritis remains confined to the gastrointestinal tract without spreading.
Bacteremia-Mediated Mechanisms
When Salmonella breaches gut barriers and enters the bloodstream, it can adhere to damaged endothelium and may invade vascular structures. This can result in inflammation of cardiovascular tissue (myocardium, endocardium) leading to functional impairment. However, such complications are rare and typically reported in case studies rather than large cohorts, limiting inference about population-level risk.
Even in severe Salmonella bacteremia, direct occlusive coronary thrombosis due to the organism itself is atypical. Instead, cardiovascular involvement generally reflects systemic inflammatory or immune-mediated injury rather than classic plaque rupture. Still, these cases underscore that microbial invasion beyond the GI tract may lead to serious cardiac consequences in select instances.
Comparison With Other Infection-Related Cardiac Risk
The potential link between infections and MI is not unique to gastroenteritis. Respiratory infections (e.g., influenza, pneumonia) have a documented association with elevated MI risk through systemic inflammation and clotting activation. Thus, the hypothesis that acute infection of any type can transiently increase MI risk is consistent with broader cardiology literature. Gastroenteritis — particularly severe or systemic cases — fits within this paradigm, though the degree of risk varies by pathogen, host health status, and severity of illness.
Importantly, viral gastroenteritis (e.g., norovirus) does not typically cause bacteremia, and direct cardiovascular involvement is less documented compared with bacterial pathogens; however, general systemic stress and dehydration may still contribute to transient cardiac risk.
Clinical Implications
Given the association between gastroenteritis (especially severe cases) and transient MI risk, there are important clinical considerations:
1. Vigilance for Cardiac Symptoms in High-Risk Patients
Patients with significant risk factors for coronary disease (e.g., older age, hypertension, diabetes) who develop severe gastroenteritis with dehydration should be monitored for chest pain and other cardiac symptoms, as systemic stress may unmask coronary vulnerability.
2. Optimal Management of Gastroenteritis
Prompt and adequate rehydration, correction of electrolyte imbalances, and careful observation may mitigate systemic stress responses that contribute to cardiovascular strain. In scenarios where gastroenteritis results in bacteremia or systemic sepsis, broad clinical vigilance is warranted.
3. Consideration of Rare but Serious Complications
While rare, clinicians should consider serious cardiovascular complications — such as myocarditis, pericarditis, and endocarditis — when patients with confirmed Salmonella infection exhibit persistent chest pain or ECG abnormalities, and pursue appropriate imaging and laboratory evaluation.
Limitations and Gaps in Knowledge
While population studies suggest a correlation between gastroenteritis and MI risk, several limitations warrant mention:
- Causality: Observational data cannot definitively establish causation; associations may be confounded by unmeasured factors such as preexisting subclinical cardiovascular disease.
- Pathogen specificity: Most large cohort analyses do not differentiate by pathogen (e.g., Salmonella versus other causes), limiting conclusions about Salmonella-specific effects.
- Severity bias: Severe gastroenteritis cases requiring hospitalization may inherently represent sicker patients with higher baseline MI risk.
- Rare complications: Case reports of Salmonella-associated myocarditis and other cardiac conditions are anecdotal and do not provide population risk estimates.
Future research, including prospective cohort studies with precise microbiological characterization and mechanistic studies, is needed to refine understanding of infection-linked cardiac risk.
Conclusion
In summary, broad evidence supports the concept that gastroenteritis, especially when severe and systemic, can act as a trigger for myocardial infarction, likely through mechanisms related to systemic inflammation, dehydration-induced hemoconcentration, and procoagulant changes. Salmonella gastroenteritis in particular can rarely lead to bacteremia and direct cardiovascular complications, including myocarditis and endocarditis, though such outcomes are outliers rather than common sequelae.
While direct causation remains complex and multifactorial, clinicians should recognize that severe gastrointestinal infection may transiently elevate cardiovascular stress and MI risk, particularly in high-risk individuals. Further research is needed to clarify pathogen-specific effects and optimal prevention strategies.
