Kacena, personal communication, InterScience Institute, Los Angeles). The generation of ischemic pain is a complex and, as yet, unclear phenomenon that may involve different metabolites15 or mechanical stimuli, or both.’ Our data suggest that activation of myocardial nociceptive receptors, either directly by bradykinin or indirectly through arachidonic acid metabolites, is an unlikely mechanism of angioplasty-induced ischemic pain in human subjects.
1. Malliani A, Pagani M, Lombardi F. Visceral versus somatic mechanisms. In: Wall PD, M&rack R, eds. Textbook of Pain. New York, Churchill Livingstone, 1989:128-140. 2. Lewis T. Pain in muscular ischemia, its relation to angina1 pain. Arch Intern Med 1932;49:113-721. 3. Katz LN, Lindner E, Landt H. On the nature of the substance(s) producing pain in contracting skeletal muscle: its bearing on the problems of angina pectoris and intermittent claudification. J Chin Invest 1935;14:807-821. 4. Raab W. Myocardial metabolism in the pathogen&s and treatment of angina pectoris. Cardiologia 1953;22:291-303. 5. Burch GE, Depasquale NP. Bradykinin. Am Heart J 1963;65:116-123. 6. Sicuteri F, Franchi G, DelBianco PL, Franciullacci M. Peptides and pain. In: Rocha E, Silva M, Rothchild HA, eds. International symposium on vasoactive polypeptides: bradykinin and related kinius. Proc Third Internat Phnrmacol Con-
gress and Sot Brad Pharmacol Ther Exper (SBPTE). Sao Paula, Brazil, 1967:251. 7. Kimura E, Hashimoto K, Furukawa S, Hayakawa H. Changes in bradykinin level in coronary sinus blood after the experimental occlusion of a coronary artery. Am Heart J 1973;85:635-647. 8. Mersey JH, Williams GH, Emanuel R, Biuhy RG, Wong PY, Moore TJ. Plasma bradykinin levels and urinary kallikerin excretion in normal renin essential hypertension. J Clin Endocrinol Metab 1979;48:642-647. 9. Sheubuski RJ, Blood JC, Sellers TS, Fujita T, Storer B, Oh&in EH. Attenuation of the inhibitory effect of prostacyclii on platelet function before and after tissue plasminogen activator or streptokinase infusion in the rabbit. Pibrino~ysis 1989;3:115-123. 10. Baker DG, Coleridge HM, Coleridge JCG, Nerdrum T. Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of a cat. J Physiol 1980;306:519-536. Il. Katori M, Hori Y, Uchida Y, Tanaka K, Harada Y. Different modes of interaction of bradykinin with prostaglandins in pain and acute inflammation. Adv Exp Med Biol 1986:198(part B):393-398. 12. Taiwo YO, Levine JD. Characterization of the arachidonic acid metabolites mediating bradykinin and noradrenaline hyperalgesia. Brain Res 1988;458: 402-406. 13. Hori Y, Katori M, Harada Y, Uchida Y, Tanaka K. Potentiation of bradykinin-induced nociceptive response by arachidonate metabolites in dogs. Eur J Pharmacol 1986;132:47-52. 14. Stebbins CL, Carretero 0, Longhurst JC. Bradykinin release from contracting skeletal muscle of the cat. J Appl Physior 1990;69:1225-1230. 15. Campbell JN, Raja SN, Cohen RH, Manning DC, Khan AA, Meyer RA. Peripheral neural mechanisms of ntiception. In: Wall PD, Melzack R, eds. Textbook of Pain. New York: Churchill Livingstone, 1989:22-45.
Lack of Relation of Coronary Sinus Oxygen Content to Extent of Coronary Artery Disease or Left Ventricular Dysfunction James D. Boehrer,
MD,
Richard A. Lange,
MD,
John E. Willard, MD, and L. David Hillis,
recent study suggests that the prognosis of patients
A with congestive heart failure is related to the oxygen content of coronary sinus blood: the lower the oxygen content at rest, the worse the outlook.’ Although it is hypothesized that the oxygen content of coronary sinus blood decreases as coronary artery disease worsens, no previous study has assessed the relation, if any, between the oxygen content of coronary sinus blood at rest and the extent of (1) atherosclerotic coronary artery disease, or (2) left ventricular systolic dysfunction. This study was performed for this purpose. We reviewed the results of all cardiac catheterizations at Parkland Memorial Hospital, Dallas, Texas from July 1978 to May 1992, and identified the patients in whom the coronary sinus was cannulated and a blood sample obtainedfor measurement of oxygen saturation. In each subject, the catheter’s location was confirmedfluoroscopically with an injection of contrast material. Oxygen saturation was measured with a reJzectance oximeter (American Optical), and the oxygen content (in ml/liter) was calculated by multiplying the saturation, the hemoglobin (g/d& the oxygen-carrying capacity of hemoglobin (ml/g) and 10 (dllliter). The oxygen saturation of systemic arterial blood was measured in most patients, and the transcardiac oxygen content difference was quantitated. In each subject, single plane (30” right anterior oblique) left ventriculography was performed, from From the Department of Internal Medicine (Cardiovascular Division), the University of Texas Southwestern Medical Center, and the Cardiac Catheterization Laboratory, Parkland Memorial Hospital, 5323 Harry Hines Boulevard, Dallas, Texas 75235.
MD
which ejection fraction was calculated, in accordance with previously described techniques.2 The presence and severity of atherosclerotic coronary artery disease were assessed by selective coronary arteriography. A coronary artery was said to be diseased if its luminal diameter was narrowed 170%. A blood sample was obtainedfrom the coronary sinus for measurement of oxygen saturation in 254 patients (163 men and 91 women, aged 51 f 11 [mean f SD] years). Of these, 241 underwent catheterization for the evaluation of chest pain: 8 to assess the cause of congestive heart failure, and 5 for the evaluation of valvular disease. Systemic arterial oxygen saturation was measured in 213, allowing a calculation of the transcardiac oxygen content difference. The oxygen content of coronary sinus blood was similar among patients with angiographically normal coronary arteries, 59 f 20 ml/liter, n = 68; 1 -vessel coronary artery disease, 68 f 18 ml/liter, n = 71; 2-vessel disease, 63 f 14 ml/liter, n = 49; 3-vessel disease, 66 f I9 ml/liter, n = 60; and left main disease, 63 f 12 ml/liter, n = 6 (p = not significant [NS]) (Figure 1, top panel). The transcardiac oxygen content difference was similar among the 5 groups (no coronary artery disease, 104 f 17 ml/liter, n = 59; 1 -vessel disease, 108 f 18 ml/liter, n = 56; 2-vessel disease, 109 f 18 ml/liter, n = 40; 3vessel disease, 107 f 21 ml/liter, n = 52; left main disease, 97 f 15 ml/liter, n = 6) (p = NS) (Figure 1, bottom panel). There was no relation between left ventricular ejection fraction and (I) the oxygen content of coronary sinus blood (r = 0.04, p = NS) (Figure 2, top panel), or (2) the transcardiac oxygen content difference (r = 0.09, p = NS) (Figure 2, bottom panel). BRIEF REPORTS
1623
Of the 254 subjects, 63 had a left ventricular ejection fraction
1. Malliani A, Pagani M, Lombardi F. Visceral versus somatic mechanisms. In: Wall PD, M&rack R, eds. Textbook of Pain. New York, Churchill Livingstone, 1989:128-140. 2. Lewis T. Pain in muscular ischemia, its relation to angina1 pain. Arch Intern Med 1932;49:113-721. 3. Katz LN, Lindner E, Landt H. On the nature of the substance(s) producing pain in contracting skeletal muscle: its bearing on the problems of angina pectoris and intermittent claudification. J Chin Invest 1935;14:807-821. 4. Raab W. Myocardial metabolism in the pathogen&s and treatment of angina pectoris. Cardiologia 1953;22:291-303. 5. Burch GE, Depasquale NP. Bradykinin. Am Heart J 1963;65:116-123. 6. Sicuteri F, Franchi G, DelBianco PL, Franciullacci M. Peptides and pain. In: Rocha E, Silva M, Rothchild HA, eds. International symposium on vasoactive polypeptides: bradykinin and related kinius. Proc Third Internat Phnrmacol Con-
gress and Sot Brad Pharmacol Ther Exper (SBPTE). Sao Paula, Brazil, 1967:251. 7. Kimura E, Hashimoto K, Furukawa S, Hayakawa H. Changes in bradykinin level in coronary sinus blood after the experimental occlusion of a coronary artery. Am Heart J 1973;85:635-647. 8. Mersey JH, Williams GH, Emanuel R, Biuhy RG, Wong PY, Moore TJ. Plasma bradykinin levels and urinary kallikerin excretion in normal renin essential hypertension. J Clin Endocrinol Metab 1979;48:642-647. 9. Sheubuski RJ, Blood JC, Sellers TS, Fujita T, Storer B, Oh&in EH. Attenuation of the inhibitory effect of prostacyclii on platelet function before and after tissue plasminogen activator or streptokinase infusion in the rabbit. Pibrino~ysis 1989;3:115-123. 10. Baker DG, Coleridge HM, Coleridge JCG, Nerdrum T. Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of a cat. J Physiol 1980;306:519-536. Il. Katori M, Hori Y, Uchida Y, Tanaka K, Harada Y. Different modes of interaction of bradykinin with prostaglandins in pain and acute inflammation. Adv Exp Med Biol 1986:198(part B):393-398. 12. Taiwo YO, Levine JD. Characterization of the arachidonic acid metabolites mediating bradykinin and noradrenaline hyperalgesia. Brain Res 1988;458: 402-406. 13. Hori Y, Katori M, Harada Y, Uchida Y, Tanaka K. Potentiation of bradykinin-induced nociceptive response by arachidonate metabolites in dogs. Eur J Pharmacol 1986;132:47-52. 14. Stebbins CL, Carretero 0, Longhurst JC. Bradykinin release from contracting skeletal muscle of the cat. J Appl Physior 1990;69:1225-1230. 15. Campbell JN, Raja SN, Cohen RH, Manning DC, Khan AA, Meyer RA. Peripheral neural mechanisms of ntiception. In: Wall PD, Melzack R, eds. Textbook of Pain. New York: Churchill Livingstone, 1989:22-45.
Lack of Relation of Coronary Sinus Oxygen Content to Extent of Coronary Artery Disease or Left Ventricular Dysfunction James D. Boehrer,
MD,
Richard A. Lange,
MD,
John E. Willard, MD, and L. David Hillis,
recent study suggests that the prognosis of patients
A with congestive heart failure is related to the oxygen content of coronary sinus blood: the lower the oxygen content at rest, the worse the outlook.’ Although it is hypothesized that the oxygen content of coronary sinus blood decreases as coronary artery disease worsens, no previous study has assessed the relation, if any, between the oxygen content of coronary sinus blood at rest and the extent of (1) atherosclerotic coronary artery disease, or (2) left ventricular systolic dysfunction. This study was performed for this purpose. We reviewed the results of all cardiac catheterizations at Parkland Memorial Hospital, Dallas, Texas from July 1978 to May 1992, and identified the patients in whom the coronary sinus was cannulated and a blood sample obtainedfor measurement of oxygen saturation. In each subject, the catheter’s location was confirmedfluoroscopically with an injection of contrast material. Oxygen saturation was measured with a reJzectance oximeter (American Optical), and the oxygen content (in ml/liter) was calculated by multiplying the saturation, the hemoglobin (g/d& the oxygen-carrying capacity of hemoglobin (ml/g) and 10 (dllliter). The oxygen saturation of systemic arterial blood was measured in most patients, and the transcardiac oxygen content difference was quantitated. In each subject, single plane (30” right anterior oblique) left ventriculography was performed, from From the Department of Internal Medicine (Cardiovascular Division), the University of Texas Southwestern Medical Center, and the Cardiac Catheterization Laboratory, Parkland Memorial Hospital, 5323 Harry Hines Boulevard, Dallas, Texas 75235.
MD
which ejection fraction was calculated, in accordance with previously described techniques.2 The presence and severity of atherosclerotic coronary artery disease were assessed by selective coronary arteriography. A coronary artery was said to be diseased if its luminal diameter was narrowed 170%. A blood sample was obtainedfrom the coronary sinus for measurement of oxygen saturation in 254 patients (163 men and 91 women, aged 51 f 11 [mean f SD] years). Of these, 241 underwent catheterization for the evaluation of chest pain: 8 to assess the cause of congestive heart failure, and 5 for the evaluation of valvular disease. Systemic arterial oxygen saturation was measured in 213, allowing a calculation of the transcardiac oxygen content difference. The oxygen content of coronary sinus blood was similar among patients with angiographically normal coronary arteries, 59 f 20 ml/liter, n = 68; 1 -vessel coronary artery disease, 68 f 18 ml/liter, n = 71; 2-vessel disease, 63 f 14 ml/liter, n = 49; 3-vessel disease, 66 f I9 ml/liter, n = 60; and left main disease, 63 f 12 ml/liter, n = 6 (p = not significant [NS]) (Figure 1, top panel). The transcardiac oxygen content difference was similar among the 5 groups (no coronary artery disease, 104 f 17 ml/liter, n = 59; 1 -vessel disease, 108 f 18 ml/liter, n = 56; 2-vessel disease, 109 f 18 ml/liter, n = 40; 3vessel disease, 107 f 21 ml/liter, n = 52; left main disease, 97 f 15 ml/liter, n = 6) (p = NS) (Figure 1, bottom panel). There was no relation between left ventricular ejection fraction and (I) the oxygen content of coronary sinus blood (r = 0.04, p = NS) (Figure 2, top panel), or (2) the transcardiac oxygen content difference (r = 0.09, p = NS) (Figure 2, bottom panel). BRIEF REPORTS
1623
Of the 254 subjects, 63 had a left ventricular ejection fraction
