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Over time, in the minds of clinicians and laypeople alike, cardiogenic pain is intimately associated with angina pectoris, the characteristic syndrome which accompanies myocardial ischaemia. However, in conditions such as myocarditis or cardiac sarcoidosis, both notorious for their silent clinical presentation, tissue damage is caused by inflammation, not ischaemia. One might wonder why there is no pain or angina-like syndrome accompanying these conditions. Recent insights into the molecular mechanisms underlying cardiac pain may provide an explanation.
Ischaemic or inflammatory damage of any tissue, including the myocardium, is accompanied by a series of metabolic changes and the release of a multitude of signal molecules from the affected cells. The end result is a change in the composition of the interstitial fluid, which can be detected by chemosensitive nerve endings.1 ,2
Specifically, in the case of ischaemia, once myocardial perfusion is reduced, aerobic glycolysis and lipolysis cease almost immediately, while anaerobic glycolysis is transiently stimulated. Thus lactate concentration increases and pH is lowered. If perfusion is not restored, cellular ATP stores are depleted and extracellular adenosine concentrations rise dramatically. Contractility is abolished and K+ accumulates extracellularly, as Na-K ATPase activity is reduced.2
Among the immediate metabolic consequences of ischaemia, none is more intimately involved in the genesis of cardiac pain than the rise of interstitial adenosine concentrations. Its activity is most likely mediated by adenosine receptors located on the endings of unmyelinated C fibres.3 As adenosine is typically released when nucleotide triphosphates are depleted, the notion that it is the most significant mediator of …
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