Myocardial ischaemia and cardiac pain – a mysterious relationship

Abstract

Pain related to cardiac disease has been recognised for centuries. However, the precise mechanisms of angina pectoris remain bafflingly obscure. Conventional cardiological angina management concentrates on methods to improve oxygen delivery to cardiac myocytes as our understanding of cardiac muscle cells' response to hypoxia increases. In common with other chronic visceral pain syndromes, little is understood about how pain signals are generated and propagated by visceral nerves. Improved imaging and other physiological assessments have demonstrated important central nervous system (CNS) responses to myocardial ischaemia, including activation of CNS areas known to be 'key players' in chronic pain syndromes. Patients with stable angina usually have an excellent prognosis, especially if left ventricular function is preserved. Educating patients about their condition, teaching simple techniques known to help chronic pain patients and introducing targeted pain treatments specific to angina can be extremely helpful adjuncts to conventional cardiological treatments and will often bring about significant improvements in quality of life.

Energetic metabolism in cardiomyocytes: molecular basis of heart ischemia and arrhythmogenesis

“…Myocardial metabolism has been historically described as the "lost child of cardiology" [131] , as clinicians have rather focused on arrhythmia remain unclear, yet various alternatives have been proposed [111] . During an infarction, numerous events develop in parallel, with some of the earliest being precordial pain and increased sympathetic activity [112] . Although a moderate increase in catecholamines may aid in maintaining cardiac contractility in the face of oxygen depletion, excessive signaling can augment the energetic demands of the myocardium, impairing functionality [113] .…”

Guillain–Barré syndrome presenting with an ‘angina’ mimic and posterior reversible encephalopathy syndrome

“…These also mix with afferent fibres from the tracheo-bronchial tree, lungs, oesophagus and stomach accounting for the extensive area of referred pain over the upper body in angina. 10 Interestingly, our case is the first patient to present with severe crushing chest pain and PRES. The 'anginal' character led to a flurry of investigations to Takotsubo cardiomyopathy.…”

The Beriberi Heart

“…Serial lactate measurements, red blood cell transketolase and activity with the thiamin pyrophosphate response test were concordant with a thiamin deficiency state (6). Improved imaging and other physiological assessments have demonstrated important central nervous system responses to myocardial ischemia, including activation of CNS areas known to be "key players" in chronic pain syndromes, including cardiac pain (7). A review considered how ischemia at the tissue level triggers activation of afferent nociceptive pain fibers involving the projections of sympathetic and vagal afferent fibers (8).…”