scholarly journals Role of β-Adrenergic Receptors and Estrogen in Cardiac Repair after Myocardial Infarction: An Overview

2021 ◽  
Vol 22 (16) ◽  
pp. 8957
Author(s):  
Paola Matarrese ◽  
Sonia Maccari ◽  
Rosa Vona ◽  
Lucrezia Gambardella ◽  
Tonino Stati ◽  
...  

Acute myocardial infarction (MI) is associated with an intense inflammatory response that is critical for cardiac repair but is also involved in the pathogenesis of adverse cardiac remodeling, i.e., the set of size, geometry, and structure changes that represent the structural substrate for the development of post-MI heart failure. Deciphering the pathophysiological mechanisms underlying cardiac repair after MI is, therefore, critical to favorably regulate cardiac wound repair and to prevent development of heart failure. Catecholamines and estrogen play an active role in regulating the inflammatory response in the infarcted area. For example, stress-induced catecholamines alter recruitment and trafficking of leukocytes to the heart. Additionally, estrogen affects rate of cardiac rupture during the acute phase of MI, as well as infarct size and survival in animal models of MI. In this review, we will summarize the role of β-adrenergic receptors and estrogen in cardiac repair after infarction in preclinical studies.

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.


1999 ◽  
Vol 5 (3) ◽  
pp. 79
Author(s):  
Shintaro Kinugawa ◽  
Hiroyuki Tsutsui ◽  
Tomomi Ide ◽  
Hideo Ustumi ◽  
Nobuhiro Suematsu ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Heng-Jie Cheng ◽  
Tiankai Li ◽  
Che Ping Cheng

Background: Sildenafil (SIL), a selective inhibitor of PDE5 has been shown to exert profound beneficial effects in heart failure (HF). Recently we further found that SIL caused regression of cardiac dysfunction in a rat model with isoproterenol (ISO)-induced progressive HF. However, the molecular basis is unclear. We hypothesized that reversal of HF-induced detrimental alterations on the expressions of cardiac SR Ca 2+ -ATPase (SERCA2a), β-adrenergic receptors (AR) and nitric oxide synthase (NOS) isoforms by SIL may play a key role for its salutary role in HF. Methods: Left ventricular (LV) and myocyte function and the protein levels of myocyte β 1 - and β 3 - AR, SERCA2a, phospholamban (PLB) and three NOS were simultaneously evaluated in 3 groups of male rats (6/group): HF , 3 months (M) after receiving ISO (170 mg/kg sq for 2 days); HF/SIL , 2 M after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and Controls (C). Results: Compared with controls, ISO-treated rats progressed to severe HF at 3 M after ISO followed by significantly decreased LV contractility (E ES , HF: 0.7 vs C: 1.2 mmHg/μl) and slowed LV relaxation, reductions in the peak velocity of myocyte shortening (77 vs 136 μm/sec), relengthening (62 vs 104 μm/sec) and [Ca 2+ ] iT (0.15 vs 0.24) accompanied by a diminished myocyte inotropic response to β-AR agonist, ISO (10 -8 M). These abnormalities were associated with concomitant significant decreases in myocyte protein levels of β 1 -AR (0.23 vs 0.64), SERCA2a (0.46 vs 0.80), PLB Ser16 /PLB ratio (0.24 vs 0.40) and eNOS (0.28 vs 0.46), but significantly increases in protein levels of β 3 -AR (0.29 vs 0.10) and iNOS (0.18 vs 0.08) with relatively unchanged nNOS. Chronic SIL prevented the HF-induced decreases in LV and myocyte contraction, relaxation, peak [Ca 2+ ] iT , and restored normal myocyte contractile response to ISO stimulation. With SIL, protein levels of myocyte β 1 - and β 3 -AR, SERCA2a were restored close to control values, but eNOS was significantly elevated than controls (0.77). Conclusions: Chronic SIL prevents HF-caused downregulation of cardiac β 1 -AR and reverse contrast changes between iNOS and β 3 -AR with SERCA 2a and eNOS expression, leading to the preservation of LV and myocyte function, [Ca 2+ ] iT , and β-adrenergic reserve.


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.


2021 ◽  
Vol 23 (6) ◽  
pp. 491-497
Author(s):  
Igor V. Zhirov ◽  
◽  
Igor V. Zhirov ◽  

In the article is outlined the main concepts use of the mineralocorticoids receptors antagonists in the treatment of congestive heart failure and systolic dysfunction after acute myocardial infarction. Claimed the pivotal role of eplerenone in the long-term treatment strategy due to decrease of mortality and improving the clinical outcomes.


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