Early expressed circulating long noncoding RNA CHAST is associated with cardiac contractile function in patients with acute myocardial infarction

Aim. To assess myocardial contractile function in dogs after clinical death following acute myocardial infarction and to determine its role in the development of hemodynamic derangements after cardiopulmonary resuscitation. Methods. 180 dogs included in the experiment received pentobarbital anesthesia to assess contractile function and systemic hemodynamics after a 5-min clinical death caused by myocardial infarction. Results Dogs had phase changes in the myocardial contractile function with its initial increase, subsequent depression and normalization in the early postresuscitation period after myocardial infarction. Depressed cardiac contractile function was accompanied by a decrease in the myocardial functional reserve. A similar tendency was found in the restoration of systemic hemocirculation. Conclusion. Similar phase alterations in the myocardial contractile function and systemic hemodynamics developed in the postresuscitation period of acute myocardial infarction. Immediately after recovery, the parameters of systemic hemoperfusion increased due to the activation of the cardiac contractile function. The subsequent initial (3 – 60 min) decrease in the volumetric perfusion parameters was mainly caused by the depressed cardiac contractile function. Rhythm disturbances affected on-going circulatory insufficiency 4 - 5 hours after the recovery. The subsequent progressive decrease in the volumetric perfusion was caused by the extracardiac factors.

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The German–Austrian S3 Guideline “Cardiogenic Shock Due to Myocardial Infarction: Diagnosis, Monitoring, and Treatment”

The Thoracic and Cardiovascular Surgeon ◽

10.1055/s-0040-1719155 ◽

2020 ◽

Author(s):

Kevin Pilarczyk ◽

Karl Werdan ◽

Martin Russ ◽

Holger Thiele ◽

Guido Michels ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Cardiogenic Shock ◽

Contractile Function ◽

German Society ◽

Evidence Based ◽

Cardiac Contractile Function ◽

Intensive Care Unit Treatment ◽

S3 Guideline ◽

Cardiac Contractile

AbstractDespite advances in the treatment of acute myocardial infarction with subsequent mortality reduction, which are mainly caused by the early timing of revascularization, cardiogenic shock still remains the leading cause of death with mortality rates still approaching 40 to 50%. Cardiogenic shock is characterized by a multiorgan dysfunction syndrome, often complicated by a systemic inflammatory response syndrome that affects the outcome more than the reduction of the cardiac contractile function. However, both European and American guidelines on myocardial infarction focus on interventional or surgical aspects only. Therefore, experts from eight German and Austrian specialty societies including the German Society for Thoracic and Cardiovascular Surgery published the German–Austrian S3 guideline “cardiogenic shock due to myocardial infarction: diagnosis, monitoring, and treatment” to provide evidence-based recommendations for the diagnosis and treatment of infarction-related cardiogenic shock in 2010 covering the topics of early revascularization, revascularization techniques, intensive care unit treatment including ventilation, transfusion regimens, adjunctive medical therapy, and mechanical support devices. Within the last 3 years, this guideline was updated as some major recommendations were outdated, or new evidence had been found. This review will therefore outline the management of patients with cardiogenic shock complicating acute myocardial infarction according to the updated guideline with a major focus on evidence-based recommendations which have been found relevant for cardiac surgery.

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Comparison of early pet metabolic imaging with recovery of cardiac contractile function after acute myocardial infarction

Journal of the American College of Cardiology ◽

10.1016/0735-1097(91)92484-4 ◽

1991 ◽

Vol 17 (2) ◽

pp. A380

Author(s):

Rodney J. Hicks ◽

Victor Kalff ◽

Ronald J. Dick ◽

Eric Topol ◽

Markus Schwaiger

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Contractile Function ◽

Metabolic Imaging ◽

Cardiac Contractile Function ◽

Cardiac Contractile

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Long noncoding RNA ANRIL protects cardiomyocytes against hypoxia/reoxygenation injury by sponging miR-195-5p and upregulating Bcl-2

RSC Advances ◽

10.1039/c9ra04898g ◽

2019 ◽

Vol 9 (61) ◽

pp. 35624-35635 ◽

Cited By ~ 1

Author(s):

Hui Zhao ◽

Li Meng ◽

Chengyang Xu ◽

Bin Lin ◽

Xiangming Zheng ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Noncoding Rnas ◽

Long Noncoding Rnas ◽

Reoxygenation Injury ◽

Hypoxia Reoxygenation

Long noncoding RNAs have been widely accepted to play important roles in acute myocardial infarction (AMI).

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A preliminary course of transauricular electrostimulation mitigates impairment of cardiac contractile function in rats with myocardial infarction

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf02445566 ◽

1995 ◽

Vol 120 (6) ◽

pp. 1186-1189

Author(s):

L. M. Belkina ◽

O. P. Budanova ◽

N. B. Korchazhkina ◽

S. A. Radzievskii ◽

F. Z. Meerson

Keyword(s):

Myocardial Infarction ◽

Contractile Function ◽

Cardiac Contractile Function ◽

Cardiac Contractile

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Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes

Journal of Applied Physiology ◽

10.1152/jappl.1998.84.2.544 ◽

1998 ◽

Vol 84 (2) ◽

pp. 544-552 ◽

Cited By ~ 30

Author(s):

Xue-Qian Zhang ◽

Yuk-Chow Ng ◽

Timothy I. Musch ◽

Russell L. Moore ◽

R. Zelis ◽

...

Keyword(s):

Myocardial Infarction ◽

Citrate Synthase ◽

Contractile Function ◽

Sprint Training ◽

Cardiac Contractile Function ◽

Myocyte Hypertrophy ◽

Cellular Hypertrophy ◽

Cardiac Contractile ◽

Rat Hearts ◽

Exercise Activity

Zhang, Xue-Qian, Yuk-Chow Ng, Timothy I. Musch, Russell L. Moore, R. Zelis, and Joseph Y. Cheung. Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes. J. Appl. Physiol. 84(2): 544–552, 1998.—Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na+/Ca2+exchange currents ( I Na/Ca; 3 Na+ out:1 Ca2+ in) and sarcoplasmic reticulum (SR)-releasable Ca2+contents. These defects in Ca2+regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac α-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively; P ≤ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 ± 4 vs. 130 ± 5 μm in MI-HIST vs. MI-Sed, respectively; P ≤ 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively; P ≤ 0.015). Reverse I Na/Ca was significantly lower ( P ≤ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I Na/Ca( P ≤ 0.05) without affecting the amount of Na+/Ca2+exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca2+ content, as estimated by integrating forward I Na/Ca during caffeine-induced SR Ca2+ release, was also significantly increased ( P ≤ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.

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