Myocardial Infarction as a Clinical End Point in Research

DeFilippis, Andrew P.; Nasir, Khurram; Blaha, Michael J.

doi:10.1161/circresaha.119.315101

Cited by 21 publications

(15 citation statements)

References 17 publications

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“…It is worth noting that cardiac remodelling and fibrosis are the important outcomes of prolonged myocardial infarction, which are closely related to the occurrence of heart failure 3‐5 . Thus, novel therapeutic approaches against cardiac remodelling and myocardial fibrosis are critical for the long‐term quality of life of patients with myocardial ischaemia 6 …”

Section: Introductionmentioning

confidence: 99%

“…[3][4][5] Thus, novel therapeutic approaches against cardiac remodelling and myocardial fibrosis are critical for the long-term quality of life of patients with myocardial ischaemia. 6 Hydrogen gas (H 2 ) is a colourless and easily combustible gas at normal temperature and pressure. In the past, it was considered to be an inert gas without any biological effect.…”

Section: Introductionmentioning

confidence: 99%

“… 3 , 4 , 5 Thus, novel therapeutic approaches against cardiac remodelling and myocardial fibrosis are critical for the long‐term quality of life of patients with myocardial ischaemia. 6 …”

Section: Introductionmentioning

confidence: 99%

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Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Nie

Zou

Pan

et al. 2021

J Cellular Molecular Medi

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It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective and practical means of either prevention or treatment. Thus, novel therapeutic approaches are critical for the long‐term quality of life of individuals with myocardial ischaemia. Herein, we aimed to explore the protective effect of H2, a novel gas signal molecule with anti‐oxidative stress and anti‐inflammatory effects, on cardiac remodelling and fibrosis in MI rats, and to explore its possible mechanism. First, we successfully established MI model rats, which were then exposed to H2 inhalation with 2% concentration for 28 days (3 hours/day). The results showed that hydrogen gas can significantly improve cardiac function and reduce the area of cardiac fibrosis. In vitro experiments further proved that H2 can reduce the hypoxia‐induced damage to cardiomyocytes and alleviate angiotensin II‐induced migration and activation of cardiac fibroblasts. In conclusion, herein, we illustrated for the first time that inhalation of H2 ameliorates myocardial infarction‐induced cardiac remodelling and fibrosis in MI rats and exert its protective effect mainly through inhibiting NLRP3‐mediated pyroptosis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Nie

Zou

Pan

et al. 2021

J Cellular Molecular Medi

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“…Possible explanations have been attributed to the presence of high levels of angiotensin converting enzyme 2 receptors in pericytes and endothelial cells, determining severe microvascular dysfunction enhanced by the cytokines storm [ 30 ]. Mismatch between oxygen supply and demand was reported to be a second potential mechanism of injury [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

T2-mapping increase is the prevalent imaging biomarker of myocardial involvement in active COVID-19: a Cardiovascular Magnetic Resonance study

Galea

Marchitelli

Pambianchi

et al. 2021

Journal of Cardiovascular Magnetic Resonance

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Background Early detection of myocardial involvement can be relevant in coronavirus disease 2019 (COVID-19) patients to timely target symptomatic treatment and decrease the occurrence of the cardiac sequelae of the infection. The aim of the present study was to assess the clinical value of cardiovascular magnetic resonance (CMR) in characterizing myocardial damage in active COVID-19 patients, through the correlation between qualitative and quantitative imaging biomarkers with clinical and laboratory evidence of myocardial injury. Methods In this retrospective observational cohort study, we enrolled 27 patients with diagnosis of active COVID-19 and suspected cardiac involvement, referred to our institution for CMR between March 2020 and January 2021. Clinical and laboratory characteristics, including high sensitivity troponin T (hs-cTnT), and CMR imaging data were obtained. Relationships between CMR parameters, clinical and laboratory findings were explored. Comparisons were made with age-, sex- and risk factor–matched control group of 27 individuals, including healthy controls and patients without other signs or history of myocardial disease, who underwent CMR examination between January 2020 and January 2021. Results The median (IQR) time interval between COVID-19 diagnosis and CMR examination was 20 (13.5–31.5) days. Hs-cTnT values were collected within 24 h prior to CMR and resulted abnormally increased in 18 patients (66.6%). A total of 20 cases (74%) presented tissue signal abnormalities, including increased myocardial native T1 (n = 11), myocardial T2 (n = 14) and extracellular volume fraction (ECV) (n = 10), late gadolinium enhancement (LGE) (n = 12) or pericardial enhancement (n = 2). A CMR diagnosis of myocarditis was established in 9 (33.3%), pericarditis in 2 (7.4%) and myocardial infarction with non-obstructive coronary arteries in 3 (11.11%) patients. T2 mapping values showed a moderate positive linear correlation with Hs-cTnT (r = 0.58; p = 0.002). A high degree positive linear correlation between ECV and Hs-cTnT was also found (r 0.77; p < 0.001). Conclusions CMR allows in vivo recognition and characterization of myocardial damage in a cohort of selected COVID-19 individuals by means of a multiparametric scanning protocol including conventional imaging and T1–T2 mapping sequences. Abnormal T2 mapping was the most commonly abnormality observed in our cohort and positively correlated with hs-cTnT values, reflecting the predominant edematous changes characterizing the active phase of disease.

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“…Distinguishing between myocardial infarction (especially type 2 myocardial infarction) and other recently redefined causes of myocardial injury [16] is often clinically challenging. However, this distinction is needed for a deeper understanding and better prediction, prevention and management of myocardial injury events [17], which are especially frequent after AP.…”

Section: Introductionmentioning

confidence: 99%

Troponin Elevation in Older Patients with Acute Pneumonia: Frequency and Prognostic Value

Putot

Bouhey

Tetu

et al. 2020

JCM

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Cardiovascular (CV) events are particularly frequent after acute pneumonia (AP) in the elderly. We aimed to assess whether cardiac troponin I, a specific biomarker of myocardial injury, independently predicts CV events and death after AP in older inpatients. Among 214 consecutive patients with AP aged ≥75 years admitted to a university hospital, 171 with a cardiac troponin I sample in the 72 h following diagnosis of AP were included, and 71 (42%) were found to have myocardial injury (troponin > 100 ng/L). Patients with and without myocardial injury were similar in terms of age, gender and comorbidities, but those with myocardial injury had more severe clinical presentation (median (interquartile range) Pneumonia Severity Index: 60 (40–95) vs. 45 (30–70), p = 0.003). Myocardial injury was strongly associated with in-hospital myocardial infarction (25% vs. 0%, p < 0.001), CV mortality (11 vs. 1%, p = 0.003) and all-cause mortality (34 vs. 13%, p = 0.002). After adjustment for confounders, myocardial injury remained a strong predictive factor of in-hospital mortality (odds ratio (95% confidence interval): 3.32 (1.42–7.73), p = 0.005) but not one-year mortality (1.61 (0.77–3.35), p = 0.2). Cardiac troponin I elevation, a specific biomarker of myocardial injury, was found in nearly half of an unselected cohort of older inpatients with AP and was associated with a threefold risk of in-hospital death.

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Myocardial Infarction as a Clinical End Point in Research

Cited by 21 publications

References 17 publications

Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats

T2-mapping increase is the prevalent imaging biomarker of myocardial involvement in active COVID-19: a Cardiovascular Magnetic Resonance study

Troponin Elevation in Older Patients with Acute Pneumonia: Frequency and Prognostic Value

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