Section 1
Cardiology
Section Editor: V K Bahl
Associate Editors: Gurpreet S Wander, Tiny Nair
Kwong JC, Schwartz KL, Campitelli MA, et al. Acute myocardial infarction after laboratory-confirmed influenza infection.
N Engl J Med. 2018;378:345-53.
Abstract*
Background and Methods: Acute myocardial infarction (AMI) has been shown to be triggered by respiratory infections in smaller studies, which were not so well conducted. This association was looked at in a systematic manner in which laboratory-confirmed influenza and other respiratory infections were taken over a period and 7 days following respiratory specimen collection was considered as the risk period and the period 1 year before and after was taken as control.
Results: A total of 364 patients were admitted with AMI, which occurred within 1 year before or after a positive test of influenza. About 20 happened in the risk period and 344 in the control period. Thus, during the risk period, the incidence ratio was 6.05 as compared to control period. Following influenza B, influenza A, respiratory syncytial virus (RSV), and other viruses, the incidence ratios were 10.1, 5.1, 3.5, and 2.7, respectively.
Conclusion: Thus, acute respiratory infections can be precipitating factors for AMI. The risk is highest with influenza, but there are chances of risk involvement with RSV and other viruses causing respiratory infections.
“An ounce of prevention is worth a pound of cure”
―Benjamin Franklin
COMMENT
Infections are known to precipitate acute coronary events. In fact, what causes rupture of a stable atheromatous plaque is a matter of research and curiosity. The known factors are—extreme emotional stress, extreme physical exertion, early morning hours, infections and inflammation. It is known plaques which are having thin fibrous cap and thick lipid core rupture more often than those with thick fibrous cap. In fact, more acute coronary syndromes (ACS) are caused by nonobstructive plaques than by obstructive plaques. However, most ACS events occur without any obvious trigger preceding it. Amongst the known triggers influenza, pneumonia, bronchitis, and other chest infections have all been incriminated. Patients hospitalized for pneumococcal pneumonia have 7–8% risk of ACS. Similar increased risk is known with urinary tract infections and other bacteremias.
This particular study confirms the previously held notion and shows that risk of acute myocardial infarction (AMI) is increased six times during the first week after an episode of influenza as compared to the other periods. Other infections with noninfluenza respiratory viruses also increased the risk of AMI, though to a lesser extent. The mechanism of this increased risk is because of increase in circulating inflammatory cytokines such as interleukins 1, 6, and 8, and tumor necrosis factor-α which activate inflammatory cells in the plaque. In addition, acute infection causes a prothrombotic and a procoagulant state which can increase risk of coronary thrombosis. In addition, tachycardia, hypoxia, and cytokine release associated with the acute inflammation also precipitate AMI. So, we know that influenza can precipitate AMI. Lesson is we should not stop aspirin or statins if the patient is already taking these during an episode of influenza. This highlights the value of vaccination for influenza and pneumococcal vaccine for all those more than 65 years and also younger with coronary artery disease (CAD), especially those with left ventricular dysfunction. Infections not only precipitate acute coronary events but also worsen heart failure and increase the risk of arrhythmias and stroke. So, vaccination for influenza and pneumococci prevents acute complications in these patients. A meta-analysis of five randomized trials showed that cardiovascular events can be reduced by 36% with influenza vaccine and 17% with pneumococcal vaccine amongst adults. Most guidelines today suggest this as an additional secondary prevention method in patients of CAD along with aspirin and statins.