C. Rajkumar et al., Postprandial silent ischaemia following a fatty meal in patients with recently diagnosed coronary artery disease, J HUM HYPER, 14(6), 2000, pp. 391-394
Silent myocardial ischaemia (SI) is recognised as an important prognostic f
actor in patients with coronary artery disease (CAD). Postprandial angina i
s related to severity of CAD. The effect of postprandial metabolic changes
in the pathogenesis of SI is unclear. We studied the postprandial changes i
n glucose, insulin and triglyceride, and non-esterified fatty acids (NEFA)
in relation to postprandial SI and exercise capacity, in patients with CAD.
Forty elderly volunteers (63 +/- 1 years) mean age +/- s.e.m,, with a hist
ory of angina were selected on the basis of a Rose questionnaire and a posi
tive exercise stress test (modified Bruce protocol). The test meal containe
d 45% fat, The meal was consumed at 9.00 am and hourly blood samples were t
aken for glucose, insulin, triglyceride and NEFA. Continuous Holter monitor
ing for SI was conducted using a Spacelabs 2000 monitor. Twenty-five percen
t of the subjects had episodes of silent ischaemia. Postprandial glucose, i
nsulin, triglyceride, and NEFA were not significantly different in the pati
ents with SI (group 1, n = 10) compared with those without SI (group 2, n =
30). The mean exercise time was 6.1 +/- 0.8 min in group 1 compared with 6
.8 +/- 0.5 minutes in group 2 (P = 0.48). The time to onset of ST depressio
n during exercise test was also not significantly different in the two grou
ps. The occurrence of postprandial SI cannot be related to changes in plasm
a levels of glucose, triglyceride, insulin, and NEFA. The explanation is no
t apparent from this study but may relate to a haemodynamic changes such as
mesenteric steal.