(Circulation. 1995;91:291-297.)
© 1995 American Heart Association, Inc.
Articles |
From Divisione di Cardiologia and Fondazione Cardiologica "M.Z. Sacco," Ospedale G.B. Morgagni, Forlì, Italy.
Correspondence to Filippo Ottani, MD, Fondazione Cardiologica "M.Z. Sacco," P.le Solieri 1, 47100 Forlì, Italy.
Background In the experimental setting, it has been demonstrated that preconditioning myocardium before prolonged occlusion with brief ischemic episodes affords substantial protection to the cells by delaying lethal injury, thereby limiting infarct size. Whether the same occurs in humans remains unknown.
Methods and Results This study was undertaken to determine
whether new-onset prodromal angina, defined as chest pain episodes
limited to the 24 hours before myocardial infarction, is the clinical
correlate of the ischemic preconditioning phenomenon. Twenty-five
patients with their first anterior myocardial infarction treated with
thrombolysis (recombinant tissue plasminogen activator [r-TPA], 100
mg/3 hours) were retrospectively included in the study because they met
the following criteria: (1) <120 minutes from onset of symptoms to
reperfusion therapy, (2) <90 minutes from the beginning of
thrombolytic therapy to reperfusion (defined as rapid ST elevation
reduction >50%), (3) a patent infarct-related coronary artery with
TIMI 3 flow and complete absence of collateral circulation to the
infarct related artery (assessed at 24±5 days), and (4) the presence
of new-onset prodromal angina, ie, typical chest pain episodes
occurring at rest within 24 hours or, alternatively, a complete absence
of symptoms before onset of infarction. Therefore, on the basis of
their clinical status before infarction, the patients were divided into
two groups: group 1, 13 patients without prodromal angina, and group 2,
12 patients with prodromal angina. Despite no difference in time to
treatment (81±19 versus 75±21 minutes in group 1 and group 2,
respectively; P=NS) and time to reperfusion (58±34
versus
46±24 minutes; P=NS), the peak of CKMB release was
markedly
lower in group 2 (86.3±66 versus 192.3±108.3 IU/L;
P<.01). In addition, although both groups were comparable
in terms of area at risk (amount of myocardium beyond the
infarct-related stenosis; 15.1±4.6 versus 13.7±4.6 hypokinetic
segments in group 1 and group 2, respectively, P=NS), the
final infarct size (11±7.5 versus 5.6±4 hypokinetic segments,
P<.04) was smaller in group 2. Thus, the limitation of the
infarct size was significantly greater in group 2 (69% versus 36%;
P<.05), and this represents an additional 33%
reduction (95% confidence intervals, 7.1% to 58.9%;
P=.01) in the group of patients with prodromal angina. Also,
the third index, that is, the ECG, showed a favorable trend toward a
lesser number of Q waves and a higher
R waves, although the values
did not reach statistical significance.
Conclusions Despite a similar area at risk, patients with new-onset prodromal angina showed a significantly smaller infarct size compared with patients without prodromal symptoms. Since the two groups had similar times to reperfusion and no evidence of collateral circulation to the infarct related artery, the protection afforded by angina in group 2 patients might be explained by the occurrence of ischemic preconditioning.
Key Words: ischemia preconditioning myocardial infarction myocardium
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