Printer Friendly

Common infections are potent risk factors for stroke.

ORLANDO -- A respiratory or urinary tract infection severe enough to land a patient in the hospital is a novel independent risk factor for subsequent ischemic heart disease and ischemic stroke, according to a "big data" registry study from the United Kingdom.

"Our data show infection was just as much a risk factor or more compared with the traditional atherosclerotic cardiovascular disease risk factors," Paul Carter, MD, said at the annual meeting of the American College of Cardiology.

Dr. Carter of Aston Medical School in Birmingham, England, presented a retrospective analysis from the ACALM (Algorithm for Comorbidities Associated With Length of Stay and Mortality) study of administrative data on all of the more than 1.22 million patients admitted to seven U.K hospitals in 20002013. His analysis included all 34,027 adults aged 40 years or older admitted with a urinary tract infection (UTI) or respiratory infection on their index hospitalization who had no history of ischemic heart disease or ischemic stroke.

These patients, with a mean age of 73 years, 59% of whom were women, were compared with an equal number of age- and gender-matched adults whose index hospitalization was for reasons other than ischemic heart disease, stroke, UTI, or respiratory infection.

Patients with a respiratory infection or UTI had a 9.9% incidence of new-onset ischemic heart disease and a 4.1% rate of ischemic stroke during follow-up starting upon discharge from their index hospitalization, significantly higher than the 5.9% and 1.5% rates in controls. In a multivariate logistic regression analysis adjusted for demographics, standard cardiovascular risk factors, and the top 10 causes of mortality in the United Kingdom, patients with respiratory infection or UTI as their admitting diagnosis had a 1.36fold increased likelihood of developing ischemic heart disease post discharge and a 2.5-fold greater risk of ischemic stroke than matched controls.

Moreover, mortality following diagnosis of ischemic heart disease was 75.2% in patients whose index hospitalization was for infection, compared with 51.1% in controls who developed ischemic heart disease without a history of hospitalization for infection, for an adjusted 2.98fold increased likelihood of death. Similarly, mortality after an ischemic stroke was 59.8% in patients with a prior severe infection, compared with 30.8% in controls, which translated to an adjusted 3.1-fold increased risk of death post stroke in patients with a prior hospitalization for infection.

In the multivariate analysis, hospitalization for infection was a stronger risk factor for subsequent ischemic stroke than was atrial fibrillation, heart failure, type 1 or type 2 diabetes, hypertension, or hyperlipidemia. The risk of ischemic heart disease in patients with an infectious disease hospitalization was similar to the risks associated with most of those recognized risk factors.

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/NEJMoal707914).

"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," he said. "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."

Dr. Carter reported having no relevant financial conflicts.

[email protected]

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

BY BRUCE JANCIN REPORTING FROM ACC 2018

Caption: Dr. Paul Carter said infection is a risk factor for ischemic stroke.

Bruce Jancin/MDedge News

Please Note: Illustration(s) are not available due to copyright restrictions.
COPYRIGHT 2018 International Medical News Group
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2018 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author: Jancin, Bruce
Publication: Internal Medicine News
Geographic Code: 4EUUK
Date: May 1, 2018
Words: 728
Previous Article: Mixed outcomes found in analysis of NSAIDs and IBD.
Next Article: Look for ways to increase PrEP uptake, particularly in blacks, Hispanics.
Topics:

Terms of use | Privacy policy | Copyright © 2024 Farlex, Inc. | Feedback | For webmasters |