Heart failure after myocardial infarction: incidence and predictors

Jenča, Dominik; Melenovský, Vojtěch; Stehlik, Josef; Staněk, Vladimír; Kettner, Jiří; Kautzner, Josef; Adámková, Věra; Wohlfahrt, Peter

doi:10.1002/ehf2.13144

Cited by 324 publications

(248 citation statements)

References 164 publications

(288 reference statements)

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“…Thus, it is clear that some monocytes infiltrate the heart after injury, differentiate into macrophages, and persist in the heart for a long period [ 10 , 17 , 26 ]. However, it is unclear if these macrophages adopt the same phenotype and functions of cardiac-resident macrophages present before injury, or if they contribute to ischemic heart failure development and progression [ 85 ]. There is also a lack of studies that track cardiac-resident macrophage abundance and impact beyond 1 month after MI.…”

Section: Role Of Cardiac Macrophages Following Adult Cardiac Injurymentioning

confidence: 99%

The Evolving Roles of Cardiac Macrophages in Homeostasis, Regeneration, and Repair

Alvarez‐Argote

O’Meara

2021

IJMS

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Macrophages were first described as phagocytic immune cells responsible for maintaining tissue homeostasis by the removal of pathogens that disturb normal function. Historically, macrophages have been viewed as terminally differentiated monocyte-derived cells that originated through hematopoiesis and infiltrated multiple tissues in the presence of inflammation or during turnover in normal homeostasis. However, improved cell detection and fate-mapping strategies have elucidated the various lineages of tissue-resident macrophages, which can derive from embryonic origins independent of hematopoiesis and monocyte infiltration. The role of resident macrophages in organs such as the skin, liver, and the lungs have been well characterized, revealing functions well beyond a pure phagocytic and immunological role. In the heart, recent research has begun to decipher the functional roles of various tissue-resident macrophage populations through fate mapping and genetic depletion studies. Several of these studies have elucidated the novel and unexpected roles of cardiac-resident macrophages in homeostasis, including maintaining mitochondrial function, facilitating cardiac conduction, coronary development, and lymphangiogenesis, among others. Additionally, following cardiac injury, cardiac-resident macrophages adopt diverse functions such as the clearance of necrotic and apoptotic cells and debris, a reduction in the inflammatory monocyte infiltration, promotion of angiogenesis, amelioration of inflammation, and hypertrophy in the remaining myocardium, overall limiting damage extension. The present review discusses the origin, development, characterization, and function of cardiac macrophages in homeostasis, cardiac regeneration, and after cardiac injury or stress.

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Section: Role Of Cardiac Macrophages Following Adult Cardiac Injurymentioning

confidence: 99%

The Evolving Roles of Cardiac Macrophages in Homeostasis, Regeneration, and Repair

Alvarez‐Argote

O’Meara

2021

IJMS

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“…The follow-up considered only total mortality. Neither the classification of mortality modes nor data on other follow-up events such as stroke [ 26 , 27 ], re-infarctions [ 28 ], or heart-failure worsening [ 29 ] were available.…”

Section: Discussionmentioning

confidence: 99%

In Comparison to Pathological Q Waves, Selvester Score Is a Superior Diagnostic Indicator of Increased Long-Term Mortality Risk in ST Elevation Myocardial Infarction Patients Treated with Primary Coronary Intervention

et al. 2021

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The development of pathological Q waves has long been correlated with worsened outcome in patients with ST elevation myocardial infarction (STEMI). In this study, we investigated long-term mortality of STEMI patients treated by primary percutaneous coronary intervention (PPCI) and compared predictive values of Q waves and of Selvester score for infarct volume estimation. Data of 283 consecutive STEMI patients (103 females) treated by PPCI were analysed. The presence of pathological Q wave was evaluated in pre-discharge electrocardiograms (ECGs) recorded ≥72 h after the chest pain onset (72 h Q). The Selvester score was evaluated in acute ECGs (acute Selvester score) and in the pre-discharge ECGs (72 h Selvester score). The results were related to total mortality and to clinical and laboratory variables. A 72 h Q presence and 72 h Selvester score ≥6 was observed in 184 (65.02%) and 143 (50.53%) patients, respectively. During a follow-up of 5.69 ± 0.66 years, 36 (12.7%) patients died. Multivariably, 72 h Selvester score ≥6 was a strong independent predictor of death, while a predictive value of the 72 h Q wave was absent. In high-risk subpopulations defined by clinical and laboratory variables, the differences in total mortality were highly significant (p < 0.01 for all subgroups) when stratified by 72 h Selvester score ≥6. On the contrary, the additional risk-prediction by 72 h Q presence was either absent or only borderline. In contemporarily treated STEMI patients, Selvester score is a strong independent predictor of long-term all-cause mortality. On the contrary, the prognostic value of Q-wave presence appears limited in contemporarily treated STEMI patients.

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“…MI defines cardiomyocyte necrosis in a clinical situation consistent with acute myocardial ischemia, which causes ventricular remodeling and HF (89,90). Myocardial iron is a risk factor for adverse left ventricular (LV) remodeling after MI.…”

Section: Ferroptosis and Myocardial Infarctionmentioning

confidence: 99%

The Link Between Ferroptosis and Cardiovascular Diseases: A Novel Target for Treatment

Chen

Jing

et al. 2021

Front. Cardiovasc. Med.

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Ferroptosis is an iron-dependent cell death, which is characterized by iron overload and lipid peroxidation. Ferroptosis is distinct from apoptosis, necroptosis, autophagy, and other types of cell death in morphology and function. Ferroptosis is regulated by a variety of factors and controlled by several mechanisms, including mitochondrial activity and metabolism of iron, lipid, and amino acids. Accumulating evidence shows that ferroptosis is closely related to a majority of cardiovascular diseases (CVDs), including cardiomyopathy, myocardial infarction, ischemia/reperfusion injury, heart failure, and atherosclerosis. This review summarizes the current status of ferroptosis and discusses ferroptosis as a potential therapeutic target for CVDs.

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Heart failure after myocardial infarction: incidence and predictors

Cited by 324 publications

References 164 publications

The Evolving Roles of Cardiac Macrophages in Homeostasis, Regeneration, and Repair

The Evolving Roles of Cardiac Macrophages in Homeostasis, Regeneration, and Repair

In Comparison to Pathological Q Waves, Selvester Score Is a Superior Diagnostic Indicator of Increased Long-Term Mortality Risk in ST Elevation Myocardial Infarction Patients Treated with Primary Coronary Intervention

The Link Between Ferroptosis and Cardiovascular Diseases: A Novel Target for Treatment

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