As the myokardium itself is not or hardly innervated by afferent nerves, I wonder how the pain in a heart attack is generated? Is it mediated by visceral innervation of the coronary vessels or by afferent nerves of the perikard?
Immunohistochemical evidence has been provided for the presence of a large population of the sensory afferent nerve fibers innervating the heart that contain the TRPV1 receptor (Szallasi and Blumberg, 1999, Ma, 2002 and Zahner et al., 2003). These include cardiac ischemic-sensitive afferent neurons (CISAN) that contain both C- and Aδ-afferent fibers. CISAN have cell bodies in dorsal root ganglia (DRG) of spinal segments cervical 8–thoracic 9 (C8–T9). The primary central input from these CISAN occurs into spinal cord laminae I–V, VII and X. Nociceptor C-fibers expressing Substance P and TRPV1 were found to terminate in laminae I and II (Ustinova et al., 1995), while the Aδ fibers expressing TRPV1 terminate in laminae I, II/III border and V (Ma, 2002). Activation of CISAN by occlusion of the left anterior descending coronary artery (CoAO) causes an increase in c-Fos expression in the thoracic spinal cord (Hua et al., 2004b) and release of substance P. In the spinothalamic tract (STT), which is a major spinal cord pathway that carries information about noxious stimuli to the brain, binding of Substance P to its neurokinin-1 receptor can ultimately excite areas in higher centers where pain is perceived (Boscan et al., 2002, Gauriau and Bernard, 2002 and Sylven, 2004).
Immunohistochemical evidence has been provided for the presence of a large population of the sensory afferent nerve fibers innervating the heart that contain the TRPV1 receptor (Szallasi and Blumberg, 1999, Ma, 2002 and Zahner et al., 2003). These include cardiac ischemic-sensitive afferent neurons (CISAN) that contain both C- and Aδ-afferent fibers. CISAN have cell bodies in dorsal root ganglia (DRG) of spinal segments cervical 8–thoracic 9 (C8–T9). The primary central input from these CISAN occurs into spinal cord laminae I–V, VII and X. Nociceptor C-fibers expressing Substance P and TRPV1 were found to terminate in laminae I and II (Ustinova et al., 1995), while the Aδ fibers expressing TRPV1 terminate in laminae I, II/III border and V (Ma, 2002). Activation of CISAN by occlusion of the left anterior descending coronary artery (CoAO) causes an increase in c-Fos expression in the thoracic spinal cord (Hua et al., 2004b) and release of substance P. In the spinothalamic tract (STT), which is a major spinal cord pathway that carries information about noxious stimuli to the brain, binding of Substance P to its neurokinin-1 receptor can ultimately excite areas in higher centers where pain is perceived (Boscan et al., 2002, Gauriau and Bernard, 2002 and Sylven, 2004).
A simple version is that the heart is hooked to the brain through nerve pathways that developed when we survived the dinosaurs. Their primitive and don't localize very well. That's why people with heart attacks often say, it wasn't pain or, it wasn't in my chest. The nerve pathways hooked to the brain just tell you that something is badly wrong. They just don't always tell you where. that's why every ER doc everywhere will ask for an ECG for any adult who looks sick. The above description is nice and correct but the short version is protopathic pain, c fibers and thalamic transmission.
The risk of a heart attack is 8.5 times higher in the two hours following a burst of intense anger, researchers have found after investigating the link between acute emotional triggers and high risk of severe cardiac episodes. High levels of anxiety were associated with a 9.5 fold increased risk of triggering a heart attack in the two hours after an anxiety episode.
http://www.sciencedaily.com/releases/2015/02/150224083819.htm
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