Role of Heart Rate Reduction in the Management of Myocarditis

2018 ◽  
Vol 24 (3) ◽  
pp. 365-378 ◽  
Author(s):  
Chen Guang-Yi ◽  
Ge Li-Sha ◽  
Li Yue-Chun

The morbidity of myocarditis demonstrates an upward tendency by years, is commonly defined as the inflammation of myocytes and is caused by multiple factors. With the development of the molecular biological technique, great breakthroughs in the diagnosis and understanding of pathophysiological mechanisms of myocarditis have recently been achieved. Several questions remain unresolved, however, including standard treatment approaches to myocarditis, which remain controversial and ambiguous. Heart rate, as an independent risk factor, has been shown to be related to cardiac disease. Recent studies also show that the autonomic nervous system is involved in immunomodulatory myocarditis processes. Heart rate reduction treatment is recommended in myocarditis based on a number of animal experiments and clinical trials. It is possible that heart rate-lowering treatments can help to attenuate the inflammatory response and myocyte injury and reverse ventricular remodeling. However, how to execute the protective effects of heart rate reduction on myocarditis is still not clear. In this review, we discuss the pathogenesis and pathophysiological process of viral myocarditis and propose heart rate lowering as a therapeutic target for myocarditis, especially in light of the third-generation β-blockade carvedilol and funny channel blocker ivabradine. We also highlight some additional beneficial effects of such heart rate reduction agents, including anti-inflammatory, antioxidation, anti-nitrosative stress, anti-fibrosis and antiapoptosis properties.

2004 ◽  
Vol 286 (4) ◽  
pp. H1281-H1288 ◽  
Author(s):  
Kai Hu ◽  
Anne Naumann ◽  
Daniela Fraccarollo ◽  
Peter Gaudron ◽  
Jens J. Kaden ◽  
...  

The importance of heart rate for left ventricular remodeling and prognosis after myocardial infarction is not known. We examined the contribution of heart rate reduction by zatebradine, a direct sinus node inhibitor without negative inotropic effects on left ventricular function and dilatation, on mortality, energy metabolism, and neurohormonal changes in rats with experimental myocardial infarction (MI). Thirty minutes after left coronary artery ligation or sham operation, the rats were randomized to receive either placebo or zatebradine (100 mg·kg–1·day–1 per gavage) continued for 8 wk. Mortality during 8 wk was 33.3% in the placebo and 23.0% in the zatebradine group ( P < 0.05); MI size was 36 ± 2% and 30 ± 1% (means ± SE, P < 0.05), respectively. Zatebradine improved stroke volume index in all treated rats but increased left ventricular volume in rats with small MI (2.43 ± 0.10 vs. 1.81 ± 0.10 ml/kg, P < 0.05) but not in rats with large MI (2.34 ± 0.09 vs. 2.35 ± 0.11 ml/kg, not significant). Zatebradine reduced left and right ventricular norepinephrine and increased left and right ventricular 3,4-dihydroxyphenyl ethylene glycol-to-norepinephrine ratio suggesting aggravation of cardiac sympathetic activation by zatebradine after MI. Creatine kinase and lactate dehydrogenase isoenzymes in rats with MI remained unchanged by zatebradine. Lowering heart rate per se reduces mortality and MI size in this model but induces adverse effects on left ventricular remodeling in rats with small MI.


2021 ◽  
Vol 40 (4) ◽  
pp. S122
Author(s):  
R. Adorisio ◽  
E. Mencarelli ◽  
N. Cantarutti ◽  
L. Amato ◽  
M. Ciabattini ◽  
...  

2007 ◽  
Vol 7 (2) ◽  
pp. 208-213 ◽  
Author(s):  
A BUCCHI ◽  
A BARBUTI ◽  
M BARUSCOTTI ◽  
D DIFRANCESCO

2015 ◽  
Vol 70 (5) ◽  
pp. 565-572
Author(s):  
Frederik H. Verbrugge ◽  
Jeroen Vrijsen ◽  
Jan Vercammen ◽  
Lars Grieten ◽  
Matthias Dupont ◽  
...  

1998 ◽  
Vol 46 (02) ◽  
pp. 63-69 ◽  
Author(s):  
A. Granetzny ◽  
U. Schwanke ◽  
C. Schmitz ◽  
G. Arnold ◽  
D. Schäfer ◽  
...  

2012 ◽  
Vol 36 (2) ◽  
pp. 68-73 ◽  
Author(s):  
Baskar Sekar ◽  
William R. Critchley ◽  
Simon G. Williams ◽  
Steven M. Shaw

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