INFECTIONS TRIGGER CARDIOVASCULAR DISEASE
When someone has an infection their risk of having a heart attack or stroke rises abruptly before returning to pre-infection levels over the next few weeks.1 The increase in risk is particularly high for respiratory infections like influenza and pneumonia. There are biologically plausible mechanisms by which infections could cause cardiovascular disease (CVD). Respiratory infections could trigger CVD by functional changes, like tachycardia, blood pressure instability, and hypercoagulable states. Increased cardiac demand can be enough to cause myocardial ischaemia downstream of stenosed vessels, even if the obstruction is stable.2 Infection might worsen or trigger existing CVD. Atheroma is thought to result from inappropriate inflammation. Infection could accelerate this inflammatory process, and destabilise plaques, much as chronic inflammatory conditions worsen coronary disease. Infections are also triggers for arrhythmias, which can in turn cause myocardial infarction and stroke. But even if the association between infections and CVD is only a marker of risk and not causative, it could still be useful clinically. There are precedents for short-term interventions: for example, temporary dual antiplatelet therapy after transient ischaemic attacks (TIAs). The benefit of prevention is proportional to the risk of CVD events, so treatments can be beneficial during periods of higher risk, when the balance of risks to benefits favours intervention.
A typical question GPs ask is: ‘Why has this person got this disease at this time?’ Often we focus on the diagnosis and cause but forget the temporal element, or at least don’t take it into account in our practice. At one time, even death was assumed to strike people at random. During the plague, London …
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