The cardiac consequences of stroke

Area of Science:

• Neurocardiology
• Stroke Medicine
• Autonomic Nervous System Research

Background:

• Stroke, encompassing ischemic and hemorrhagic types, is known to cause cardiac damage.
• This cardiac damage occurs via nonischemic mechanisms, suggesting a central nervous system influence.
• Previous evidence includes autopsy findings, ECG abnormalities, cardiac enzyme elevations, and altered plasma catecholamines post-stroke.

Purpose of the Study:

• To investigate the mechanisms underlying nonischemic cardiac damage following stroke.
• To identify the specific brain regions responsible for stroke-induced cardiac dysfunction.
• To elucidate the role of the autonomic nervous system in mediating these effects.

Main Methods:

• Review of autopsy studies.
• Analysis of electrocardiogram (ECG) changes after stroke.
• Measurement of cardiac enzyme levels in plasma.
• Assessment of plasma catecholamine concentrations.
• Examination of recent experimental evidence, particularly focusing on cortical involvement.

Main Results:

• Stroke induces cardiac damage through nonischemic pathways.
• Elevated sympathoadrenal tone is identified as a probable cause of this cardiac damage.
• Damage to specific cortical areas controlling cardiac and autonomic functions is implicated.
• Experimental data highlights the principal role of the insular cortex in stroke-related cardiac damage.

Conclusions:

• Nonischemic cardiac damage is a significant consequence of stroke.
• Increased sympathoadrenal activity, driven by central nervous system injury, is the likely mechanism.
• The insular cortex is a critical brain region involved in the pathogenesis of stroke-related cardiac damage.