A link between acute infection and myocardial infarction (MI) has been long suspected; in fact, researchers have been studying the correlation for >30 years.1 Newer research, however, posits that there is a more pronounced relationship than previously thought.
In the 20th century, an increase in deaths because of cardiovascular disease during influenza epidemics was acknowledged, but the specific correlation between influenza and other infections and MI was not completely understood.2
Recent research helps provide more context regarding the connection. Specifically, an elevated risk for having an MI has been associated with:
- acute bronchitis2
- other chest infections2
- urinary tract infections2
In fact, a recent study found an increased risk for MI the week after laboratory-confirmed infection with influenza virus, respiratory syncytial virus, or other respiratory viruses, at a rate 6, 4, and 3 times higher, respectively, than in the year before or after infection.2 Another study found that the influenza virus was associated with a higher rate of MI than all other respiratory viruses combined.3
A Closer Look at the Pneumonia Connection
The risk for MI is more pronounced in chest infections, both viral and bacterial.
- Between 7% and 8% of patients hospitalized for pneumococcal pneumonia had an MI.2
- The risk for MI during the first 15 days after hospitalization for acute bacterial pneumonia was 48 times higher than in any 15-day period during the year before or after the onset of infection.2
- Results of a similar Scottish study found substantially increased MI rates in the week after Streptococcus pneumoniae and influenza virus infection.3
- Cardiovascular complications affected approximately 18% of patients hospitalized for community-acquired pneumonia, with 5% of that population experiencing acute coronary syndrome.3
Researchers have also found that the risk for MI continues beyond the immediate post-infection period. Specifically:2
- The risk for MI in patients with mild respiratory or urinary tract infections returns to baseline levels within a few months after infection.
- In individuals with pneumonia, the risk decreases over time, but still exceeds the baseline risk for ≤10 years after infection.
- The risk after sepsis or bacteremia declines slowly in the years after acute infection.
- In nearly all cases, the more severe the infection, the higher the risk for MI.2
What Is the Reason for the Link?
Because the association between acute infection and MI has been seen in both viral and bacterial cases in a variety of infection sites and tends to be stronger and lasts longer with infection severity, it is likely that the infection and the host’s response to the infection are major factors in the relationship.2
Type 1 MI is ischemia caused by acute coronary obstruction related to atherosclerotic-plaque interference and resulting thrombosis. These plaques contain inflammatory cells, which can be activated by infection elsewhere in the body when inflammatory cytokines are produced. Studies have shown that inflammatory activity in atheromatous plaques increases after infection.2 Further, the prothrombotic, procoagulant condition associated with acute infection can also increase the risk for coronary thrombosis at sites of plaque disruption.2
In type 2 MI, the metabolic demands of the myocardial cells surpass the capacity of the blood to supply oxygen to the cells, called demand ischemia. In addition, inflammation and fever tax the system, increasing the metabolic needs of organs and peripheral tissues. If pneumonia is the source of the infection, blood oxygen levels may fall, further limiting the oxygen supply to the myocardium.2
Although most studies of acute infection do not distinguish between type 1 and type 2 MI, researchers contend that demand ischemia should explain only a small percentage of infection-related MI events that occur in the short-term post-infection period and not beyond that time.2
Animal studies open the door for a third way that infection may adversely affect cardiac function. In these studies, experimentally induced pneumococcal bacteremia caused cardiac lesions marked by vacuolization and loss of myocytes without the accumulation of inflammatory cells. These changes were associated with elevated troponin levels, arrhythmias, and electrocardiogram (EKG) abnormalities.2
In patients with sepsis, an overproduction of immune cells called a cytokine storm can impede oxygen use by mitochondria, which can lead to acute heart failure even in young adults with no other cardiac risk factors or coronary artery abnormalities.2
Implications for Clinical Practice
Studies have shown that glucocorticoids and drugs that block angiotensin lowered the risk for post-pneumonia MI.2 The study researchers assert it is worth investigating whether statins and drugs that inhibit platelet activation offer a benefit in patients with acute infection, including patients who do not have known clinical indications for these interventions.2
Because respiratory viruses for which vaccines are not available have also been shown to trigger cardiac events, antithrombotic strategies during acute respiratory tract infections may be clinically indicated in vulnerable groups.3
An Opposing Viewpoint
Josh Farkas, editor of the clinically focused blog PulmCrit, questions the renewed emphasis on linking acute infection with MIs. He contends that any source of physiologic stress — infection, extreme exertion, surgery, critical illness, emotional stress —increases the risk for MI.4
Mr Farkas questions whether critically ill patients with infection are more likely to have an MI compared with non-infected patients with the same level of physiologic stress, as measured by Sequential Organ Failure Assessment score. The challenge, he says, is that few studies have looked at risk specifically for type 1 vs type 2 MI.
He cautions that clinicians should not change how they manage patients with acute infections solely on the basis of the latest research. “Ultimately, no evidence is presented to indicate that we should treat these patients differently from any other ill patients. Thus, initial evaluation should include an EKG and a thorough history and physical. For patients with evidence of ischemia, further evaluation and treatment should be pursued as per routine. If the EKG and [history and physical] don’t arouse genuine suspicion for ischemia, then just treat their pneumonia,”Mr Farkas stated.
Implications for Vaccination
Because researchers have determined a causal link between MI and several vaccine-preventable diseases, it may be beneficial to expand vaccine outreach in certain populations as a preventive measure.
Studies show that:2,3
- Influenza vaccination reduced the risk for cardiovascular events in adults by 36%.
- Pneumococcal vaccination reduced the risk for cardiovascular events in adults by 17%.
As the world’s population ages and the prevalence of multi-morbidity increases, understanding and preventing interactions between diseases will become more important. Clinicians may be able to reduce the risk for MI in their patients if they remain mindful of the potential affect acute infections can have in this scenario. In addition, increased vaccine vigilance for diseases such as influenza and pneumonia for at-risk populations may further reduce the incidence of post-infection MI.
- Spodick DH. Infection and infarction. Acute viral (and other) infection in the onset, pathogenesis, and mimicry of acute myocardial infarction. Am J Med. 1986;81(4):661-668.
- Musher DM, Abers MS, Corrales-Medina VF. Acute infection and myocardial infarction. N Engl J Med. 2019;380(2):171-176.
- Warren-Gash C, Blackburn R, Whitaker H, McMenamin J, Hayward AC. Laboratory-confirmed respiratory infections as triggers for acute myocardial infarction and stroke: a self-controlled case series analysis of national linked datasets from Scotland. Eur Respir J. 2018;51(3).
- Farkas J. EmCrit Project website. PulmCrit — acute infection & myocardial infarction: How afraid should we be? January 14, 2019. https://emcrit.org/pulmcrit/infection-mi/. Accessed February 6, 2019.
This article originally appeared on The Cardiology Advisor