Failure to demonstrate myocardial ischaemia in patients with angina and normal coronary arteries. Evaluation by continuous coronary sinus pH monitoring and lactate metabolism.

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.

[1]  D. Tousoulis,et al.  Coronary Vasodilator Reserve, Pain Perception, and Sex in Patients With Syndrome X , 1994, Circulation.

[2]  C. Sylvén,et al.  Lower threshold for adenosine-induced chest pain in patients with angina and normal coronary angiograms , 1992, British heart journal.

[3]  P. Camici.  Myocardial metabolism in patients with chest pain and normal coronary angiograms , 1992 .

[4]  R. Cannon,et al.  Pathophysiological dilemma of syndrome X. , 1992, Circulation.

[5]  P. Poole‐Wilson,et al.  Syndrome X: an hypothesis for cardiac pain without ischaemia. , 1991, Cardiologia.

[6]  E. Ferrannini,et al.  Coronary hemodynamics and myocardial metabolism in patients with syndrome X: response to pacing stress. , 1991, Journal of the American College of Cardiology.

[7]  R. Bonow,et al.  Exercise Testing in Patients With Microvascular Angina , 1991, Circulation.

[8]  F. Crea,et al.  Mechanisms of angina pectoris in syndrome X. , 1991, Journal of the American College of Cardiology.

[9]  A. Quyyumi,et al.  Abnormal cardiac sensitivity in patients with chest pain and normal coronary arteries. , 1990, Journal of the American College of Cardiology.

[10]  B. Sobel,et al.  Increased myocardial perfusion at rest and diminished perfusion reserve in patients with angina and angiographically normal coronary arteries. , 1990, Journal of the American College of Cardiology.

[11]  Timothy G. Fleming,et al.  Frequency of normal coronary arteriograms in three academic medical centers and one community hospital. , 1988, The American journal of cardiology.

[12]  R. Cannon,et al.  "Microvascular angina" as a cause of chest pain with angiographically normal coronary arteries. , 1988, The American journal of cardiology.

[13]  P. Poole‐Wilson,et al.  Is altered cardiac sensation responsible for chest pain in patients with normal coronary arteries? Clinical observation during cardiac catheterisation , 1988, British medical journal.

[14]  P. Poole‐Wilson,et al.  Continuous recording of coronary sinus oxygen saturation during atrial pacing in patients with coronary artery disease or with syndrome X. , 1988, British heart journal.

[15]  M. Turiel,et al.  Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris. , 1987, The American journal of cardiology.

[16]  M. Cohen,et al.  Impaired coronary vasodilator responsiveness as a cause of lactate production during pacing-induced ischemia in patients with angina pectoris and normal coronary arteries. , 1987, Journal of the American College of Cardiology.

[17]  K. Fox,et al.  Diurnal variation in left ventricular function: a study of patients with myocardial ischaemia, syndrome X, and of normal controls. , 1987, British heart journal.

[18]  M. Leon,et al.  Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction. , 1987, Circulation.

[19]  K. Virtanen.  Evidence of myocardial ischaemia in patients with chest pain syndromes and normal coronary angiograms. , 2009, Acta medica Scandinavica. Supplementum.

[20]  Michael V. Green,et al.  Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve. , 1985, Circulation.

[21]  M. Leon,et al.  Chest pain and "normal" coronary arteries--role of small coronary arteries. , 1985, The American journal of cardiology.

[22]  P A Poole-Wilson,et al.  Potassium and the heart. , 1984, Clinics in endocrinology and metabolism.

[23]  R. Cannon,et al.  Angina caused by reduced vasodilator reserve of the small coronary arteries. , 1983, Journal of the American College of Cardiology.

[24]  P. Poole‐Wilson,et al.  Continuous coronary sinus and arterial pH monitoring during pacing-induced ischaemia in coronary artery disease. , 1982, British heart journal.

[25]  S. Cobbe,et al.  Tissue and coronary venous pH in ischemic canine myocardium , 1982, Clinical cardiology.

[26]  W. Kübler,et al.  Reduced Coronary Dilatory Capacity and Ultrastructural Changes of the Myocardium in Patients with Angina Pectoris But Normal Coronary Arteriograms , 1981, Circulation.

[27]  A. Bruschke,et al.  Clinical Course of Patients with Normal or Slightly or Moderately Abnormal Coronary Arteriograms: 10‐year Follow‐up of 521 Patients , 1980, Circulation.

[28]  S M Cobbe,et al.  Catheter tip pH electrodes for continuous intravascular recording. , 1980, Journal of medical engineering & technology.

[29]  J. Parker,et al.  Angina pectoris with normal coronary arteriograms: hemodynamic and metabolic response to atrial pacing. , 1975, American heart journal.