Ventricular activation is impaired in aged rat hearts

Area of Science:

• Cardiovascular Physiology
• Cardiac Electrophysiology
• Gerontology

Background:

• Ventricular arrhythmias are common in the elderly due to age-related cardiac changes.
• The precise mechanisms underlying these age-related arrhythmias are not fully understood.
• Identifying age-related structural and electrical changes is crucial for understanding arrhythmogenic substrates.

Purpose of the Study:

• To investigate age-related alterations in ventricular electrophysiological properties.
• To examine age-related changes in myocardial structure.
• To correlate these changes with a potential structural-functional arrhythmogenic substrate in aged hearts.

Main Methods:

• Recorded unipolar electrograms in vivo from control and aged rats during normal sinus rhythm and ventricular pacing.
• Analyzed electrical data alongside morphometric and immunohistochemical parameters of ventricular myocardium.
• Evaluated heart weight, myocyte size, interstitial fibrosis, and connexin expression.

Main Results:

• Aged hearts exhibited significantly delayed total ventricular activation time (QRS duration +69%) but unchanged conduction velocity.
• Abnormal ventricular activation patterns with variable epicardial breakthrough points were observed in aged rats.
• Increased heart weight, myocyte diameter, subendocardial fibrosis, and decreased gap junction connexin expression were noted in aged hearts.

Conclusions:

• Delayed ventricular activation and abnormal patterns in aged hearts are not caused by slowed conduction.
• Impaired impulse propagation through the conduction system leads to uncoordinated myocardial excitation.
• Altered conduction system-myocardium interaction may create a substrate for reentry arrhythmias in the elderly.