Mechanism for perceiving heart pain in T1-4 dermatomes
Mechanism for perceiving heart pain in T1–T4 dermatomes
Cardiac pain is perceived in the T1–T4 dermatomes because of shared neural pathways between the heart and the upper thoracic spinal cord segments. The heart is innervated primarily by sympathetic afferent fibers that travel alongside sympathetic efferents. These visceral afferents originate from nociceptors in the myocardium, pericardium, and coronary vessels, which respond to ischemia, chemical mediators, and mechanical stretching.
The pain signals travel through the cardiac plexus and ascend via sympathetic cardiac nerves to reach the dorsal root ganglia of spinal segments T1–T4. These same segments also receive somatic sensory input from the skin and musculature of the upper chest, medial arm, and shoulder region. Within the dorsal horn, visceral and somatic afferent fibers converge on the same second-order neurons, a phenomenon known as convergence–projection.
Because the brain is more accustomed to interpreting somatic rather than visceral pain, it “projects” the pain to the somatic region served by the same spinal segments. This misinterpretation results in referred pain felt in the anterior chest wall, inner aspect of the left arm and forearm, axilla, upper back, and sometimes neck and jaw. Additionally, the involvement of the left arm is influenced by asymmetric dominance of left-sided sympathetic afferents in many individuals.
Central sensitization further amplifies the sensation. Persistent myocardial ischemia increases dorsal horn neuron excitability in T1–T4 segments, lowering the threshold for pain perception and widening the referral zone. Higher centers such as the thalamus and insular cortex integrate these inputs, producing the characteristic diffuse, poorly localized nature of anginal pain.
Thus, the overlap of cardiac visceral afferents with somatic afferents in spinal segments T1–T4 forms the anatomical and physiological basis for referred heart pain into these dermatomes.

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