scholarly journals Cardiac remodeling in the acute period of Q-myocardial infarction, complicated by acute heart failure and hyperglycemia

Pathologia ◽  
2019 ◽  
Vol 0 (1) ◽  
Author(s):  
V. D. Syvolap ◽  
N. I. Kapshytar
PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112359 ◽  
Author(s):  
Trygve Husebye ◽  
Jan Eritsland ◽  
Harald Arnesen ◽  
Reidar Bjørnerheim ◽  
Arild Mangschau ◽  
...  

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Sinkovic ◽  
M Krasevec ◽  
D Suran ◽  
M Marinsek ◽  
A Markota

Abstract Introduction Air pollution, in particular exposure to particulate matter fine particles of less than 2.5 microns in diameter (PM2.5), increases the risk of cardiovascular events. Short-term exposure (hours to few days prior) to increased PM2.5 levels even may help trigger ST-elevation myocardial infarction (STEMI) and heart failure exacerbation in susceptible individuals. The risk of vascular events is increased even in exposures below the current European air quality limit values (mean annual levels for PM2.5 less than 10μg/m3, 24-hour mean level less than 25μg/m3). Purpose To evaluate predictive role of PM2.5 levels ≥20 μg/m3 one day prior to hospital admission for the risk of admission acute heart failure (AAHF) in STEMI patients. Methods In 290 STEMI patients (100 women, 190 men, mean age 65.5±12.9 years), treated by primary percutaneous coronary intervention (PPCI) in 2018, we retrospectively registered the AAHF, defined as classes II-IV by Killip Kimbal classification. Additionally, we registered admission clinical data, potentially contributing to AAHF in STEMI patients such as gender, age ≥65 years, prior resuscitation, admission cTnI ≥5 μg/L (normal levels up to 0.045 μg/L), comorbidities, time to PPCI, and mean daily levels of PM2.5 ≥20 μg/m3 one day before admission. Mean daily, freely available, levels of PM2.5 were measured and registered by Chemical analytic laboratory of Environmental agency of Republic Slovenia. We evaluated the predictive role of admission data for admission AHF in STEMI patients. Results AAHF was observed in 34.5% of STEMI patients with the mean daily PM2.5 level 15.7±10.9 μg/m3 on the day before admission. PPCI was performed in 92.1% of all STEMI patients, in AAHF in 87.1% and in non-AAHF patients in 94.7% (p=0.037). AAHF in comparison to non-AAHF was associated significantly with female gender (50.5% vs 25.9%, p<0.001), age over 65 years (71.3% vs 45%, p<0.001), prior diabetes (33.7% vs 14.8%, p<0.001), left bundle branch block (LBBB) (10.9% vs 0.5%, <0.001), admission cTnI ≥5 μg/L (46.7% vs 25.9%, p<0.001) and mean daily levels of PM2.5 ≥20 μg/m3 one day before admission (31.7% vs 19%, p=0.020), but nonsignificantly with arterial hypertension, prior myocardial infarction, anterior STEMI and time to PPCI. Logistic regression demonstrated that significant independent predictors of AAHF were age over 65 years (OR 3.349, 95% CI 1.787 to 6.277, p<0.001), prior diabetes (OR 2.934, 95% CI 1.478 to 5.821, p=0.002), admission LBBB (OR 10.526, 95% CI 1.181 to 93.787, p=0.03), prior resuscitation (OR 3.221, 95% CI 1.336 to 7.761, p=0.009), admission cTnI ≥5μg/l (OR 2.984, 95% CI 1.618 to 5.502, p<0.001) and mean daily levels of PM2.5 ≥20 μg/m3 (OR 2.096, 95% CI 1.045 to 4.218, p=0.038) one day before admission. Conclusion Mean daily levels of PM2.5 ≥20μg/m3 one day before admission were among significant independent predictors of AAHF in STEMI patients. FUNDunding Acknowledgement Type of funding sources: None.


2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Claire Zhang ◽  
David M Calcagno ◽  
Avinash Toomu ◽  
Kenneth M Huang ◽  
Zhenxing Fu ◽  
...  

Myocardial infarction (MI) elicits a rapid and vigorous reaction from the bone marrow hematopoietic compartment, inducing a massive efflux of myeloid first responders into the bloodstream. These cells traffic to the infarct, where they mediate cardiac remodeling and repair through inflammatory signaling and recruitment of additional immune cells to the injured myocardium. A hyperinflammatory myeloid compartment, as is produced by mutations in epigenetic regulator TET2 associated with clonal hematopoiesis, can thus drive adverse cardiac remodeling after MI and accelerate progression to heart failure. Whether loss of TET2 alters the transcriptional landscape of MI-induced myelopoiesis remains to be investigated in an unbiased fashion. Here, we performed single-cell RNA sequencing of >16,000 bone marrow myeloid cells isolated from wild-type and Tet2 -/- mice after MI to characterize the emergency hematopoietic response in the presence and absence of TET2. Our data capture distinct transitional states of myeloid lineage commitment and maturation, originating from myeloid progenitors and progressing along divergent granulocytic and monocytic differentiation trajectories. Additionally, we delineate a subpopulation of interferon (IFN)-activated myeloid progenitors, monocytes, and neutrophils characterized by the concerted upregulation of various Type I IFN-stimulated genes, and find the fraction of IFN-activated cells, as well as the degree of activation, to be markedly higher in Tet2 -/- mice. We have previously described activation of this pathway after MI in mice, and demonstrated cardioprotective effects of its genetic or pharmacological inhibition. Our findings reveal heightened activation of the antiviral Type I interferon response among bone marrow myeloid cells of Tet2 -/- mice during MI-induced emergency hematopoiesis. This highlights IFN signaling as a potential candidate driver of cardiovascular pathologies (including atherosclerosis, myocardial infarction, and heart failure) associated with TET2-mediated clonal hematopoiesis. Further studies are necessary to investigate whether Tet2 -/- mice exhibit enhanced response to blockade of Type I IFN signaling after MI, and to determine whether myeloid cells of TET2 -mutant humans are similarly activated.


2014 ◽  
Vol 96 (8) ◽  
pp. e26-e27
Author(s):  
NA Ismail ◽  
J Bence ◽  
TJ Spyt

We describe a case of 64-year-old female patient with ventricular tachycardia intractable to medical treatment and acute heart failure following myocardial infarction. Emergency surgical ventricular reconstruction and subendocardial resection was undertaken. We discuss the option of surgical intervention in this difficult and unusual clinical scenario.


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