Uncontrolled blood pressure as an independent risk factor of early impaired left ventricular systolic function in treated hypertension

2016 ◽  
Vol 33 (10) ◽  
pp. 1488-1494 ◽  
Author(s):  
Xiao-Jing Chen ◽  
Xiao-Lin Sun ◽  
Qing Zhang ◽  
Xi-Lian Gao ◽  
Yu-Jia Liang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Risk Factor ◽  
Independent Risk Factor ◽  
Systolic Function ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Ventricular Systolic Function ◽  
Uncontrolled Blood Pressure

scholarly journals Tissue Doppler indexes of left ventricular systolic function in relation to the pulsatile and steady components of blood pressure in a general population

2012 ◽  
Vol 30 (2) ◽  
pp. 403-410 ◽  
Author(s):  
Wojciech Sakiewicz ◽  
Tatiana Kuznetsova ◽  
Malgorzata Kloch-Badelek ◽  
Jan D’hooge ◽  
Andrew Ryabikov ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Population ◽  
Systolic Function ◽  
Left Ventricular Systolic Function ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Ventricular Systolic Function

scholarly journals Heart Rate Control during Experimental Sepsis in Mice

2020 ◽  
Vol 132 (2) ◽  
pp. 321-329
Author(s):  
Alexandre Bedet ◽  
Guillaume Voiriot ◽  
Julien Ternacle ◽  
Elisabeth Marcos ◽  
Serge Adnot ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Rate Control ◽  
Transthoracic Echocardiography ◽  
Systolic Function ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Heart Rate Control ◽  
Ventricular Systolic Function

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Tachycardia is a hallmark of sepsis. An elevated heart rate could impair ventricular filling and increase myocardial oxygen demand. β-Blockers and ivabradine (a selective inhibitor of If channels in the sinoatrial node) are both able to control sinus tachycardia, with the latter drug being devoid of negative inotropic effect. This work aimed at assessing the hemodynamic effects of ivabradine as compared with a β-blocker (atenolol) during murine peritonitis. Methods Ivabradine (3 μg/g), atenolol (3 μg/g), or placebo was administered intraperitoneally 2 h after induction of peritonitis (cecal ligation and puncture) in male C57BL6 mice. The authors used invasive (left ventricular catheterization) and noninvasive (transthoracic echocardiography) monitoring to assess hemodynamics 20 h after surgery, including heart rate, blood pressure, left ventricular systolic, and diastolic function (n = 10 mice/group). The authors also assessed overall mortality 30 and 60 h after surgery in a distinct subset of animals (n = 20 mice/group). Descriptive data are presented as median (25th to 75th percentile). Results As compared with placebo (601 beats/min [547 to 612]), ivabradine (447 beats/min [430 to 496]) and atenolol (482 beats/min [412 to 505]) blunted sepsis-induced tachycardia assessed by transthoracic echocardiography in awake animals (P < 0.001 and P = 0.004, respectively). Unlike ivabradine, atenolol reduced cardiac output, systolic blood pressure, and left ventricular systolic function (as assessed by ejection fraction, maximal left ventricular pressure rise, and anterior wall strain rate) as compared with septic mice receiving placebo. There was no difference in survival 60 h after sepsis induction with ivabradine (6 of 20, 30%) or atenolol (7 of 20, 35%), as compared with placebo (5 of 20, 25%; P = 0.224). Conclusions Heart rate control could be similarly achieved by ivabradine or atenolol, with preservation of blood pressure, cardiac output, and left ventricular systolic function with the former drug.

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