Key result
Incremental atrial pacing in patients with angina and normal coronary arteries resulted in a significantly smaller fall in coronary sinus pH compared to CAD patients (-0.02 vs -0.11 pH units; P<0.01).
Why the study?
Does incremental atrial pacing induce metabolic evidence of myocardial ischemia in patients with angina and normal coronary arteries compared to patients with coronary artery disease?
Observational (n=23)
Does incremental atrial pacing induce metabolic evidence of myocardial ischemia in patients with angina and normal coronary arteries compared to patients with coronary artery disease?
Despite experiencing severe chest pain and having reduced coronary flow reserve, most patients with angina and normal coronary arteriograms do not exhibit metabolic evidence of myocardial ischemia during atrial pacing.
BACKGROUND: Whether myocardial ischaemia is the mechanism underlying chest pain in patients with angina and normal coronary arteriograms is controversial. We sought to detect the presence of transient myocardial ischaemia using continuous monitoring of coronary sinus blood pH during atrial pacing. METHODS AND RESULTS: We studied 14 patients (eight women, six men, mean age 51 +/- 3 years) with typical exertional angina and normal coronary arteriograms and nine patients with coronary artery disease (two men, seven women, mean age 61 +/- 7 years). Of the 14 patients with normal coronary arteries, eight had a reduced coronary blood flow reserve (< 2.5-fold increase), 11 had an ischaemic-appearing response to exercise testing, six had reversible perfusion detects on exercise thallium scans and one had resting left bundle branch block. All patients underwent continuous pH monitoring of coronary sinus blood at rest and during incremental atrial pacing (up to 160 bpm). Coronary sinus oxygen saturation and myocardial lactate extraction ratio were also evaluated at rest and at peak pacing. Eleven patients with angina and normal coronary arteries and eight with coronary artery disease had angina during pacing. Both patients with angina and normal coronary arteries (n = 13) and patients with coronary artery disease (n = 9) showed a fall in coronary sinus pH (-0.02 +/- 0.02 vs -0.11 +/- 0.03 pH units, respectively, P < 0.01). Coronary sinus oxygen saturation expressed as a percentage dropped by 19 +/- 6% in patients with coronary artery disease and by 6 +/- 2% in patients with angina and normal coronary arteriograms (P < 0.05). Myocardial lactate extraction ratio decreased from 33 +/- 6% to -1.4 +/- 4% in patients with coronary artery disease and from 23 +/- 8% to 20 +/- 8% in those with angina and normal coronary arteriograms. Three patients with angina and normal coronary arteries had a drop in coronary sinus pH > 0.02 pH units (-0.043 +/- 0.006 pH units) and in coronary sinus oxygen saturation > 8% (16 +/- 3%) consistent with myocardial ischaemia. CONCLUSION: Despite severe chest pain and reduced coronary flow reserve after pacing, most patients with angina and normal coronary arteriograms do not show metabolic evidence of myocardial ischaemia.
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Rosano et al. (1996) conducted an observational in Angina with normal coronary arteries (n=23). Incremental atrial pacing vs. Patients with coronary artery disease was evaluated on Fall in coronary sinus pH (p=< 0.01). Incremental atrial pacing in patients with angina and normal coronary arteries resulted in a significantly smaller fall in coronary sinus pH compared to CAD patients (-0.02 vs -0.11 pH units; P<0.01).
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