ORCID Profile
0000-0003-4766-0922
Current Organisations
Karolinska University Hospital
,
Karolinska Institutet
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Publisher: Elsevier BV
Date: 05-2020
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-11-2021
DOI: 10.1161/CIRCULATIONAHA.121.057042
Abstract: Observational and small, randomized studies suggest that influenza vaccine may reduce future cardiovascular events in patients with cardiovascular disease. We conducted an investigator-initiated, randomized, double-blind trial to compare inactivated influenza vaccine with saline placebo administered shortly after myocardial infarction (MI 99.7% of patients) or high-risk stable coronary heart disease (0.3%). The primary end point was the composite of all-cause death, MI, or stent thrombosis at 12 months. A hierarchical testing strategy was used for the key secondary end points: all-cause death, cardiovascular death, MI, and stent thrombosis. Because of the COVID-19 pandemic, the data safety and monitoring board recommended to halt the trial before attaining the prespecified s le size. Between October 1, 2016, and March 1, 2020, 2571 participants were randomized at 30 centers across 8 countries. Participants assigned to influenza vaccine totaled 1290 and in iduals assigned to placebo equaled 1281 of these, 2532 received the study treatment (1272 influenza vaccine and 1260 placebo) and were included in the modified intention to treat analysis. Over the 12-month follow-up, the primary outcome occurred in 67 participants (5.3%) assigned influenza vaccine and 91 participants (7.2%) assigned placebo (hazard ratio, 0.72 [95% CI, 0.52–0.99] P =0.040). Rates of all-cause death were 2.9% and 4.9% (hazard ratio, 0.59 [95% CI, 0.39–0.89] P =0.010), rates of cardiovascular death were 2.7% and 4.5%, (hazard ratio, 0.59 [95% CI, 0.39–0.90] P =0.014), and rates of MI were 2.0% and 2.4% (hazard ratio, 0.86 [95% CI, 0.50–1.46] P =0.57) in the influenza vaccine and placebo groups, respectively. Influenza vaccination early after an MI or in high-risk coronary heart disease resulted in a lower risk of a composite of all-cause death, MI, or stent thrombosis, and a lower risk of all-cause death and cardiovascular death, as well, at 12 months compared with placebo. URL: www.clinicaltrials.gov Unique identifier: NCT02831608.
Publisher: Oxford University Press (OUP)
Date: 24-12-2018
DOI: 10.1093/CVR/CVY314
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 26-10-2012
DOI: 10.1161/CIRCRESAHA.111.262477
Abstract: At the onset of ST-elevation acute myocardial infarction (STEMI), patients can present with very high circulating interleukin-6 (IL-6 + ) levels or very low-IL-6 – levels. We compared these 2 groups of patients to understand whether it is possible to define specific STEMI phenotypes associated with outcome based on the cytokine response. We compared 109 patients with STEMI in the top IL-6 level (median, 15.6 pg/mL IL-6 + STEMI) with 96 in the bottom IL-6 level (median, 1.7 pg/mL IL-6 − STEMI) and 103 matched controls extracted from the multiethnic First Acute Myocardial Infarction study. We found minimal clinical differences between IL-6 + STEMI and IL-6 − STEMI. We assessed the inflammatory profiles of the 2 STEMI groups and the controls by measuring 18 cytokines in blood s les. We exploited clustering analysis algorithms to infer the functional modules of interacting cytokines. IL-6 + STEMI patients were characterized by the activation of 2 modules of interacting signals comprising IL-10, IL-8, macrophage inflammatory protein-1α, and C-reactive protein, and monocyte chemoattractant protein-1, macrophage inflammatory protein-1β, and monokine induced by interferon-γ. IL-10 was increased both in IL-6 + STEMI and IL-6 − STEMI patients compared with controls. IL-6 + IL-10 + STEMI patients had an increased risk of systolic dysfunction at discharge and an increased risk of death at 6 months in comparison with IL-6 − IL-10 + STEMI patients. We combined IL-10 and monokine induced by interferon-γ (derived from the 2 identified cytokine modules) with IL-6 in a formula yielding a risk index that outperformed any single cytokine in the prediction of systolic dysfunction and death. We have identified a characteristic circulating inflammatory cytokine pattern in STEMI patients, which is not related to the extent of myocardial damage. The simultaneous elevation of IL-6 and IL-10 levels distinguishes STEMI patients with worse clinical outcomes from other STEMI patients. These observations could have potential implications for risk-oriented patient stratification and immune-modulating therapies.
Publisher: Springer Science and Business Media LLC
Date: 13-09-2021
DOI: 10.1007/S00395-021-00893-5
Abstract: Acute myocardial infarction (AMI) and the heart failure (HF) which may follow are among the leading causes of death and disability worldwide. As such, new therapeutic interventions are still needed to protect the heart against acute ischemia/reperfusion injury to reduce myocardial infarct size and prevent the onset of HF in patients presenting with AMI. However, the clinical translation of cardioprotective interventions that have proven to be beneficial in preclinical animal studies, has been challenging. One likely major reason for this failure to translate cardioprotection into patient benefit is the lack of rigorous and systematic in vivo preclinical assessment of the efficacy of promising cardioprotective interventions prior to their clinical evaluation. To address this, we propose an in vivo set of step-by-step criteria for IM proving P reclinical A ssessment of C ardioprotective T herapies (‘IMPACT’), for investigators to consider adopting before embarking on clinical studies, the aim of which is to improve the likelihood of translating novel cardioprotective interventions into the clinical setting for patient benefit.
No related grants have been discovered for John Pernow.