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Heart Failure II: Pathophysiology01:29

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine
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Stroke-induced chronic systolic dysfunction driven by sympathetic overactivity.

Michael Bieber1,2, Rudolf A Werner2,3,4, Edit Tanai2,5

  • 1Department of Neurology, University Hospital Würzburg, Würzburg, Germany.

Annals of Neurology
|October 13, 2017
PubMed
Summary
This summary is machine-generated.

Ischemic stroke can cause long-term heart dysfunction due to increased sympathetic activity. Metoprolol treatment in mice prevented this chronic cardiac dysfunction, suggesting potential therapeutic implications for stroke patients.

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Area of Science:

  • Neuroscience
  • Cardiology
  • Pathophysiology

Background:

  • Cardiac diseases are known risk factors for ischemic stroke.
  • Emerging evidence suggests brain ischemia can precipitate cardiac dysfunction, a phenomenon termed neurogenic heart disease.
  • The delayed cardiovascular effects following ischemic stroke remain poorly understood.

Purpose of the Study:

  • To investigate the long-term cardiac consequences of focal cerebral ischemia.
  • To elucidate the underlying mechanisms of neurogenic heart disease post-stroke.
  • To evaluate metoprolol as a potential therapeutic intervention for preventing heart failure after ischemic stroke.

Main Methods:

  • Mice underwent transient middle cerebral artery occlusion (tMCAO) to induce focal cerebral ischemia.
  • Cardiac function was assessed using serial transthoracic echocardiography and hemodynamic measurements up to 8 weeks post-surgery.
  • Animals received metoprolol treatment to evaluate its efficacy in preventing heart failure.

Main Results:

  • Focal cerebral ischemia resulted in chronic cardiac dysfunction, characterized by reduced left ventricular ejection fraction and increased left ventricular volumes.
  • This dysfunction was correlated with elevated peripheral sympathetic activity.
  • Metoprolol administration successfully prevented chronic cardiac dysfunction by mitigating extracellular cardiac remodeling and inhibiting sympathetic signaling.

Conclusions:

  • Focal cerebral ischemia in mice induces chronic systolic dysfunction mediated by heightened sympathetic activity.
  • These findings suggest a need for clinical vigilance regarding heart failure signs in post-stroke patients.
  • Successful beta-blockade with metoprolol in this model indicates potential future therapeutic applications for stroke-induced cardiac complications.