|
Angina
pectoris and myocardial ischemia
Perhaps surprisingly,
it was only about a century ago that angina pectoris was linked
to myocardial ischemia (Keefer
and Resnic, 1928).
In a normal
heart, the oxygen supply to the myocardium can be increased six-to-eightfold
through an autoregulatory response to meet the increased metabolic
demand for a high workload, such as occurs in exercise (Maseri,
1995).
However, patients
with a critical atherosclerotic stenosis (i.e. > 75% narrowing)
in one or more coronary arteries are not able to sufficiently
increase the oxygen supply to meet the increased metabolic demand
of cardiac myocytes during exercise. The subsequent myocardial
ischemia produces a metabolic imbalance between glucose oxidation
and glycolysis and is responsible for alteration in excitation-contraction
coupling with evolving (regional) contraction failure.
In the ischemic
heart, both in stable circumstances and predominantly during physical
exercise, the "anginal warning signal" is transmitted
to the central nervous system through sensory neural pathways
(Rosen
et al., 1994).
A number of
substances, such as potassium, lactate, adenosine, bradykinin,
and prostaglandins, are released from the ischemic regions of
the heart (Sylven,
1989). These substances sensitize and excite the sensory nerve
endings in the heart (Malliani,
1988; Nerdrum
et al., 1986).
The provoked
visceral nociception is characterized by its vaguely located "emotionally
charged" distribution and by the influence of emotions on
the experience of the anginal pain. In this respect, it is worth
noting that mental stress appears to produce similar myocardial
ischemic alterations as does physical exercise (Deanfield
et al., 1984).
|