Conference Coverage

Common infections are potent risk factor for MI, stroke

 

Key clinical point: Once patients have been hospitalized for a respiratory infection or UTI, their postdischarge risk of ischemic stroke is 2.5-fold greater than in those without such a history.

Major finding: Patients with a history of hospitalization for UTI or a respiratory infection who later develop ischemic heart disease or stroke have a threefold higher mortality risk than those without such a hospitalization.

Study details: This was a retrospective study of more than 68,000 subjects in the U.K. ACALM registry study.

Disclosures: The study presenter reported having no financial conflicts of interest.

Source: Carter P. ACC 2018, Abstract 1325M-0.


 

REPORTING FROM ACC 2018


Two possible mechanisms by which infection might predispose to subsequent ischemic heart disease and stroke are via a direct effect whereby pathogens such as Chlamydia pneumoniae are taken up into arterial plaques, where they cause a local inflammatory response, or an indirect effect in which systemic inflammation primes the atherosclerotic plaque through distribution of inflammatory cytokines, according to Dr. Carter.

He said the ACALM findings are particularly intriguing when considered in the context of the 2017 results of the landmark CANTOS trial, in which canakinumab (Ilaris), a targeted anti-inflammatory agent that inhibits the interleukin-1 beta innate immunity pathway, reduced recurrent ischemic events in post-MI patients who had high systemic inflammation as evidenced by their elevated C-reactive protein level but a normal-range LDL cholesterol (N Engl J Med. 2017 Aug 27. doi: 10.1056/NEJMoa1707914).

“If atherosclerosis is an inflammatory condition, this begs the question of whether other inflammatory conditions, like infection, which induces a large systemic inflammatory response, might drive atherosclerosis,” Dr. Carter commented.

“It’s now very well understood that inflammatory mediators, cells, and processes are involved in every step from the initial endothelial dysfunction that leads to uptake of LDL, inflammatory cells, and monocytes all the way through to plaque progression and rupture, where Th1 cytokines have been implicated in causing that rupture, and ultimately in patient presentation at the hospital,” he added.

Next Article: