Cardiovascular complications following pneumonia

Bartlett, Benjamin; Ludewick, Herbert P.; Lee, Silvia; Dwivedi, Girish

doi:10.1097/hco.0000000000000604

Cited by 17 publications

(14 citation statements)

References 55 publications

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“…Hence, our model is relevant to the study of the changes that could occur following an episode of pneumonia on subclinical atherosclerosis and future cardiovascular events. The suggested underlying mechanism for plaque rupture and adverse events in patients with pneumonia is persistent inflammation from the respiratory infection(1,3,45), (46). Our study suggests that a delayed and robust pro-inflammatory response to S. pneumoniae has the potential to contribute to the increased risk of cardiovascular complications that is seen among pneumonia survivors(35, 47).…”

Section: Discussionmentioning

confidence: 99%

A multiple comorbidities mouse model to assess atherosclerosis progression following lung infection in ApoE deficient mice

Bartlett

Lee

Ludewick

et al. 2022

Preprint

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Background: Inflammation is a risk factor for atherosclerosis progression. Hospitalisation for pneumonia is associated with increased risk of cardiovascular disease. Herein, we describe a multiple comorbidities murine model to study the impact of bacterial pneumonia on atherosclerosis. Methods: Firstly, a minimal infectious dose of Streptococcus pneumoniae (TIGR4 strain) to produce clinical pneumonia with a low mortality rate (20%) was established. C57Bl/6 ApoE-/- mice were fed a high-fat diet prior to administering intranasally 105 colony forming units of TIGR4 or phosphate buffered saline (PBS). At days 2, 7 and 28 post inoculation (PI), the lungs of mice were imaged by MRI and PET. Mice were euthanised and investigated for changes in systemic inflammation and changes in lung morphology using ELISA, Luminex assay and real-time PCR. Results: TIGR4 inoculated mice presented with varying degrees of lung infiltrate, pleural effusion and consolidation on MRI at all timepoints up to 28 days PI. Moreover, PET scans identified significantly higher FDG uptake in the lungs of TIGR4 inoculated mice up to 28 days PI. Majority (90%) TIGR4-inoculated mice developed pneumococcal-specific IgG antibody response at 28 days PI. Consistent with these observations, TIGR4 inoculated mice displayed significantly increased inflammatory gene expression (IL-1β & IL6) in the lungs and significantly increased levels of circulating inflammatory protein (CCL3) at 7- and 28- days PI respectively. Conclusions: Our mouse model presents a discovery tool to understand the link between acute infections, including pneumonia, and increased cardiovascular disease risk in humans with inflammation as the mechanistic catalyst.

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Section: Discussionmentioning

confidence: 99%

A multiple comorbidities mouse model to assess atherosclerosis progression following lung infection in ApoE deficient mice

Bartlett

Lee

Ludewick

et al. 2022

Preprint

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“…Several other recent studies have shown that (CVEs) occur relatively frequently in patients with pneumococcal CAP, which is the cause of CAP that is best studied with regard to pathogenic mechanisms (13,28,29). This contention is underscored by the findings of a recent secondary analysis of data from an international, multicenter, observational, cohort study involving 18 hospitals in 7 countries, encompassing 2,088 patients, 921 (44%) of whom had bacteremic pneumococcal pneumonia and 1,167 (55.9%) non-bacteremic pneumococcal pneumonia (30).…”

Section: Cardiac Complications In Pneumococcal Capmentioning

confidence: 99%

Platelets and Their Role in the Pathogenesis of Cardiovascular Events in Patients With Community-Acquired Pneumonia

Feldman

Anderson

2020

Front. Immunol.

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Community-acquired pneumonia (CAP) remains an important cause of morbidity and mortality throughout the world with much recent and ongoing research focused on the occurrence of cardiovascular events (CVEs) during the infection, which are associated with adverse short-term and long-term survival. Much of the research directed at unraveling the pathogenesis of these events has been undertaken in the settings of experimental and clinical CAP caused by the dangerous, bacterial respiratory pathogen, Streptococcus pneumoniae (pneumococcus), which remains the most common bacterial cause of CAP. Studies of this type have revealed that although platelets play an important role in host defense against infection, there is also increasing recognition that hyperactivation of these cells contributes to a pro-inflammatory, prothrombotic systemic milieu that contributes to the etiology of CVEs. In the case of the pneumococcus, platelet-driven myocardial damage and dysfunction is exacerbated by the direct cardiotoxic actions of pneumolysin, a major pore-forming toxin of this pathogen, which also acts as potent activator of platelets. This review is focused on the role of platelets in host defense against infection, including pneumococcal infection in particular, and reviews the current literature describing the potential mechanisms by which platelet activation contributes to cardiovascular complications in CAP. This is preceded by an evaluation of the burden of pneumococcal infection in CAP, the clinical features and putative pathogenic mechanisms of the CVE, and concludes with an evaluation of the potential utility of the anti-platelet activity of macrolides and various adjunctive therapies.

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“…There is now a large volume of data demonstrating that CAP is associated with both a high rate of acute cardiac complications including myocardial infarction and arrhythmia, 42–44 as well as there being a substantially increased risk in survivors of myocardial infarction, stroke and heart failure for some years after the acute event. 45 At present there are no confirmed therapies to prevent either the acute or long-term adverse cardiovascular impacts of pneumonia. A small randomized controlled trial of 100 mg of aspirin in patients with CAP did not reduce the cardiovascular event rate; 42 however, an even smaller study of 300 mg of aspirin did significantly reduce the incidence of myocardial infarction.…”

Section: Advances In Treatment: Antimicrobials For Pneumoniamentioning

confidence: 99%

“…78,79 The mechanism(s) driving this excess of cardiovascular and cardiac disease has not been definitively determined, but accelerated atherosclerosis and direct cardiac damage during acute pneumonia are both strong hypotheses. 45 Prospective observational studies have also demonstrated a greater burden of long-term cognitive impairment, functional impairment, and depressive symptoms after pneumonia or sepsis. 80–82 The mechanism of this burden is also unclear and probably has many factors, but one hypothesis includes a similar pathway of endovascular inflammation.…”

Section: Advances In Treatment: Antimicrobials For Pneumoniamentioning

confidence: 99%

Advances in community-acquired pneumonia

Jones

Waterer

2020

Therapeutic Advances in Infection

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Community-acquired pneumonia is one of the commonest and deadliest of the infectious diseases, yet our understanding of it remains relatively poor. The recently published American Thoracic Society and Infectious Diseases Society of America Community-acquired pneumonia guidelines acknowledged that most of what we accept as standard of care is supported only by low quality evidence, highlighting persistent uncertainty and deficiencies in our knowledge. However, progress in diagnostics, translational research, and epidemiology has changed our concept of pneumonia, contributing to a gradual improvement in prevention, diagnosis, treatment, and outcomes for our patients. The emergence of considerable evidence about adverse long-term health outcomes in pneumonia survivors has also challenged our concept of pneumonia as an acute disease and what treatment end points are important. This review focuses on advances in the research and care of community-acquired pneumonia in the past two decades. We summarize the evidence around our understanding of pathogenesis and diagnosis, discuss key contentious management issues including the role of procalcitonin and the use or non-use of corticosteroids, and explore the relationships between pneumonia and long-term outcomes including cardiovascular and cognitive health.

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Cardiovascular complications following pneumonia

Cited by 17 publications

References 55 publications

A multiple comorbidities mouse model to assess atherosclerosis progression following lung infection in ApoE deficient mice

A multiple comorbidities mouse model to assess atherosclerosis progression following lung infection in ApoE deficient mice

Platelets and Their Role in the Pathogenesis of Cardiovascular Events in Patients With Community-Acquired Pneumonia

Advances in community-acquired pneumonia

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