Related Experiment Video

Updated: Jul 13, 2026

Surgical Porcine Model of Chronic Myocardial Ischemia Treated by Exosome-laden Collagen Patch and Off-pump Coronary Artery Bypass Graft
05:25

Surgical Porcine Model of Chronic Myocardial Ischemia Treated by Exosome-laden Collagen Patch and Off-pump Coronary Artery Bypass Graft

Published on: September 15, 2023

Comparison of muscle sympathetic activity in ischemic and nonischemic heart failure

Catherine F Notarius1, Jonas Spaak, Beverley L Morris

  • 1Toronto General Research Institute, Toronto, Ontario, Canada.

Journal of Cardiac Failure
|August 7, 2007
PubMed

Insights

Patients with ischemic cardiomyopathy (ICM) exhibit higher muscle sympathetic nerve activity (MSNA) and reduced exercise capacity compared to non-ischemic dilated cardiomyopathy (DCM). This suggests an ischemic stimulus contributes to sympathetic activation in heart failure.

Area of Science:

  • Cardiology
  • Neuroscience
  • Physiology

Background:

  • Sympathetic activation in chronic heart failure is generally considered cause-independent.
  • Previous studies indicated a higher sympathetic component in heart rate variability (HRV) for patients with ischemic cardiomyopathy (ICM).

Purpose of the Study:

  • To test the hypothesis that patients with ICM have higher resting muscle sympathetic nerve activity (MSNA) than those with non-ischemic dilated cardiomyopathy (DCM).

Main Methods:

  • Assessed resting MSNA via microneurography and HRV using coarse-graining spectral analysis in 30 heart failure patients (12 ICM, 18 DCM) and 23 controls.
  • Measured peak oxygen uptake during graded maximal cycling exercise.

Main Results:

  • Significantly higher MSNA in ICM (60±3 bursts/min) and DCM (47±3 bursts/min) compared to controls (35±3 bursts/min).
  • Lower total and high-frequency HRV power in both ICM and DCM groups versus controls.
  • Lower fractal and low-frequency HRV power observed exclusively in the ICM group.
  • Peak oxygen uptake was significantly lower in ICM compared to DCM and controls.

Conclusions:

  • Findings suggest an additional ischemic stimulus contributes to sympathetic activation in heart failure.
  • This heightened sympathetic drive may reflexively impair exercise capacity in patients with ICM.
Abstract

More Related Videos

Skeletal Muscle Neurovascular Coupling, Oxidative Capacity, and Microvascular Function with 'One Stop Shop' Near-infrared Spectroscopy09:04

Skeletal Muscle Neurovascular Coupling, Oxidative Capacity, and Microvascular Function with 'One Stop Shop' Near-infrared Spectroscopy

Published on: February 20, 2018

Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Pathophysiology of Cardiac Performance01:29

Pathophysiology of Cardiac Performance

Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...