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Left ventricular function in patients with the anginal syndrome and normal coronary arteriograms
EDITORIALS
Left Ventricular Function in Patients with the Anginal Syndrome and Normal Coronary Arteriograms HARVEY G. KEMP, Jr., MD, FACC
New York, New York
The existence of the anginal syndrome in patients with normal or near-normal coronary anatomy as visualized by arteriography remains an enigma. Although initially some argued that most if not all of these patients had problems of primary psychiatric origin, the demonstration of electrocardiographic and metabolic abnormalities consistent with ischemia was a strong argument against the pure psychosomatic theory. On the other hand, long-term followup studies of this group have shown the prognosis to be relatively benign, at least as regards mortality. 1 In the current issue of the Journal, Arbogast and Bourassa 2 present data suggesting that, although these patients have electrocardiographic and metabolic abnormalities, they do not experience changes in left ventricular function during stress induced by atrial pacing. The writers go on to deduce that ischemia is therefore unlikely. Their study, although carefully performed, is not without weakness. The number of patients in both the group with coronary artery disease and the group with anginal pain and normal coronary arteriograms (group X) is small. Data on the extent and severity of atherosclerosis in the former group are not given. On the other hand, the two groups appear to have a comparable resting hemodynamic status, and they show quite comparable metabolic evidence of ischemia during stress. In addition, ischemic electrocardiographic S T - T segment changes were present during pacing stress in all patients of both groups. It has been previously pointed out that interpretation of S T - T segment depression is hazardous during atrial pacing. Artifactual S T - T segment depression may result from the prolonged P - R interval which, at rapid rates, superimposes QRS and P wave pacing artifact complexes. 3 Ischemic changes can best be determined by intermittent interruption of pacing, since pacinginduced artifacts disappear within a beat or two of cessation of pacing, whereas truly ischemic changes persist as after exercise. Although these considerFrom the Division of Cardiology, Medical Service, St. Luke's Hospital Center and the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, N. Y. Address for reprints: Harvey G. Kemp, Jr., MD, St. Luke's Hospital Center, Amsterdam Ave. at 114th St., New York, N. Y. 10025.
ations allow a potential criticism of the electrocardiographic portion of the present study, the demonstration of production of lactate by the myocardium or significant reduction of extraction is difficult to explain without evoking an ischemic mechanism. Prior investigations have failed to show consistent alteration of left ventricular performance in subjects with coronary artery disease during pacing-induced tachycardia. Helfant and co-workers 4 were unable to show a significant change in left ventricular end-diastolic pressure during atrial pacing in subjects with coronary artery disease whether or not angina was precipitated. However, a small but significant fall in cardiac index was observed in the group experiencing angina. Dwyer 5 found an increase in left ventricular end-diastolic pressure in only 4 of 10 subjects with coronary artery disease, and in all but 1 of these left ventricular end-diastolic volume was reduced, thus suggesting decreased compliance. Pasternac et al. B were unable to find any significant change in left ventricular end-diastolic pressure or volume after pacing in subjects with coronary artery disease, and were only able to detect diminished left ventricular function angiographically by showing inducement of asynergy and reduced ejection fraction. 6 These studies suggest that despite gross regional abnormalities of contraction, left ventricular end-diastolic volume and pressure may remain unchanged and can therefore be relatively insensitive indicators of a transient reduction of left ventricular performance. The significant reduction in left ventricular end-diastolic pressure and slight rise in cardiac index in subjects in group X is nevertheless most compatible with the response to pacing of subjects with a normal heart. By the same token, the absence of a clear-cut reduction in left ventricular end-diastolic volume and pressure in the group with coronary artery disease is reasonably convincing evidence of impaired left ventricular function. Subjects without left ventricular dysfunction uniformly show a striking reduction of both pressure and volume and a return to normal levels with cessation of tachycardia.7 Therefore, it seems reasonable to conclude, as did Arbogast and Bourassa, that despite evidence of ischemia in both groups, group X showed a normal response to atrial pacing in terms of left ventricular
September 7, 1973
The American Journal of CARDIOLOGY
Volume 32
375
EDITORIALS
hemodynamics, and the group with coronary artery disease s.howed evidence of impaired left ventricular function during stress. Because of the disparity of hemodynamic results obtained during pacing in the subjects with coronary artery disease cited, it would seem desirable to pursue these studies but, if the findings are confirmed, they add yet another paradox to an already paradoxical syndrome. Arbogast and Bourassa go on to conclude that ischemia is not present in group X despite the electrocardiographic and metabolic evidence. An alternative explanation seems possible. It may be that the extent or distribution of ischemia in group X is such as to account for the lack of hemodynamic change. This sort of explanation is more appealing than an attempt to explain lactate production occurring simultaneously with segmental S T - T depression in the absence of ischemia. Finally, a major problem of all studies of syndrome X is the assumption of homogeneity of cause in all subjects. It seems unlikely that a syndrome defined
by the presence of chest pain and the absence of coronary artery disease would have a unique etiology. More likely, all the factors that have been suggested may at one time or another be the causative factor in a given individual. If 5 of the 10 subjects with syndrome X in this study (that is, those not demonstrating lactate abnormality) are, in fact, victims of esophagitis, the effect of this dilution of the group with subjects who have a normal cardiovascular system is apparent. Having come to realize that patients can have the anginal syndrome yet have normal coronary arteries, and that other patients can even sustain transmural myocardial infarction in the absence of demonstrable coronary artery disease, we now must digest the fact that they can also show what we believe to be clearcut evidence of ischemia without a measurable effect on left ventricular function. These observations, like the clues in the first half of an Agatha Christie novel, may not be readily understandable, but we can be certain they are important.
References 1. Kemp HG, Vokonas PS, Cohn PF, et ah The anginal syndrome associated with normal coronary angiograms. Report of a 6 year experience. Amer J Med 54: 735-742, 1973 2. Arbogast R, Bourassa MG: Myocardial function during atrial pacing in patients with angina pectoris and normal coronary arteriograms. Comparison with patients having significant coronary artery disease. Amer J Cardiol 32:257-263, 1973 3. Parker JO, Chiong MA, West RO, et ah Sequential alterations in myocardial lactate metabolism, ST segments, and left ventricular function during angina induced by atrial pacing. Circulation 40:113-131, 1969 4. Helfant RH, Forrester JS, Hampton JR, et ah Coronary heart
disease: differential hemodynamic, metabolic, and electrocardiographic effects in subjects with and without angina pectoris during atrial pacing. Circulation 42:601-610, 1970 5. Dwyer EM Jr" Left ventricular pressure-volume alterations and regional disorders of contraction during myocardial ischemia induced by atrial pacing. Circulation 42:1111-1122, 1970 6. Pasternac A, Gorlin R, Sonnenblick EH, et ah Abnormalities of ventricular motion induced by atrial pacing in coronary artery disease. Circulation 45:1195-1205, 1972 7. Ross J Jr, Unhart JW, Braunwald E: Effects of changing heart rate in man by electrical stimulation of the right atrium. Circulation 32:549-558, 1965
376
Volume 32
September 7, 1973
The American Journal of C A R D I O L O G Y
Left Ventricular Function in Patients with the Anginal Syndrome and Normal Coronary Arteriograms HARVEY G. KEMP, Jr., MD, FACC
New York, New York
The existence of the anginal syndrome in patients with normal or near-normal coronary anatomy as visualized by arteriography remains an enigma. Although initially some argued that most if not all of these patients had problems of primary psychiatric origin, the demonstration of electrocardiographic and metabolic abnormalities consistent with ischemia was a strong argument against the pure psychosomatic theory. On the other hand, long-term followup studies of this group have shown the prognosis to be relatively benign, at least as regards mortality. 1 In the current issue of the Journal, Arbogast and Bourassa 2 present data suggesting that, although these patients have electrocardiographic and metabolic abnormalities, they do not experience changes in left ventricular function during stress induced by atrial pacing. The writers go on to deduce that ischemia is therefore unlikely. Their study, although carefully performed, is not without weakness. The number of patients in both the group with coronary artery disease and the group with anginal pain and normal coronary arteriograms (group X) is small. Data on the extent and severity of atherosclerosis in the former group are not given. On the other hand, the two groups appear to have a comparable resting hemodynamic status, and they show quite comparable metabolic evidence of ischemia during stress. In addition, ischemic electrocardiographic S T - T segment changes were present during pacing stress in all patients of both groups. It has been previously pointed out that interpretation of S T - T segment depression is hazardous during atrial pacing. Artifactual S T - T segment depression may result from the prolonged P - R interval which, at rapid rates, superimposes QRS and P wave pacing artifact complexes. 3 Ischemic changes can best be determined by intermittent interruption of pacing, since pacinginduced artifacts disappear within a beat or two of cessation of pacing, whereas truly ischemic changes persist as after exercise. Although these considerFrom the Division of Cardiology, Medical Service, St. Luke's Hospital Center and the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, N. Y. Address for reprints: Harvey G. Kemp, Jr., MD, St. Luke's Hospital Center, Amsterdam Ave. at 114th St., New York, N. Y. 10025.
ations allow a potential criticism of the electrocardiographic portion of the present study, the demonstration of production of lactate by the myocardium or significant reduction of extraction is difficult to explain without evoking an ischemic mechanism. Prior investigations have failed to show consistent alteration of left ventricular performance in subjects with coronary artery disease during pacing-induced tachycardia. Helfant and co-workers 4 were unable to show a significant change in left ventricular end-diastolic pressure during atrial pacing in subjects with coronary artery disease whether or not angina was precipitated. However, a small but significant fall in cardiac index was observed in the group experiencing angina. Dwyer 5 found an increase in left ventricular end-diastolic pressure in only 4 of 10 subjects with coronary artery disease, and in all but 1 of these left ventricular end-diastolic volume was reduced, thus suggesting decreased compliance. Pasternac et al. B were unable to find any significant change in left ventricular end-diastolic pressure or volume after pacing in subjects with coronary artery disease, and were only able to detect diminished left ventricular function angiographically by showing inducement of asynergy and reduced ejection fraction. 6 These studies suggest that despite gross regional abnormalities of contraction, left ventricular end-diastolic volume and pressure may remain unchanged and can therefore be relatively insensitive indicators of a transient reduction of left ventricular performance. The significant reduction in left ventricular end-diastolic pressure and slight rise in cardiac index in subjects in group X is nevertheless most compatible with the response to pacing of subjects with a normal heart. By the same token, the absence of a clear-cut reduction in left ventricular end-diastolic volume and pressure in the group with coronary artery disease is reasonably convincing evidence of impaired left ventricular function. Subjects without left ventricular dysfunction uniformly show a striking reduction of both pressure and volume and a return to normal levels with cessation of tachycardia.7 Therefore, it seems reasonable to conclude, as did Arbogast and Bourassa, that despite evidence of ischemia in both groups, group X showed a normal response to atrial pacing in terms of left ventricular
September 7, 1973
The American Journal of CARDIOLOGY
Volume 32
375
EDITORIALS
hemodynamics, and the group with coronary artery disease s.howed evidence of impaired left ventricular function during stress. Because of the disparity of hemodynamic results obtained during pacing in the subjects with coronary artery disease cited, it would seem desirable to pursue these studies but, if the findings are confirmed, they add yet another paradox to an already paradoxical syndrome. Arbogast and Bourassa go on to conclude that ischemia is not present in group X despite the electrocardiographic and metabolic evidence. An alternative explanation seems possible. It may be that the extent or distribution of ischemia in group X is such as to account for the lack of hemodynamic change. This sort of explanation is more appealing than an attempt to explain lactate production occurring simultaneously with segmental S T - T depression in the absence of ischemia. Finally, a major problem of all studies of syndrome X is the assumption of homogeneity of cause in all subjects. It seems unlikely that a syndrome defined
by the presence of chest pain and the absence of coronary artery disease would have a unique etiology. More likely, all the factors that have been suggested may at one time or another be the causative factor in a given individual. If 5 of the 10 subjects with syndrome X in this study (that is, those not demonstrating lactate abnormality) are, in fact, victims of esophagitis, the effect of this dilution of the group with subjects who have a normal cardiovascular system is apparent. Having come to realize that patients can have the anginal syndrome yet have normal coronary arteries, and that other patients can even sustain transmural myocardial infarction in the absence of demonstrable coronary artery disease, we now must digest the fact that they can also show what we believe to be clearcut evidence of ischemia without a measurable effect on left ventricular function. These observations, like the clues in the first half of an Agatha Christie novel, may not be readily understandable, but we can be certain they are important.
References 1. Kemp HG, Vokonas PS, Cohn PF, et ah The anginal syndrome associated with normal coronary angiograms. Report of a 6 year experience. Amer J Med 54: 735-742, 1973 2. Arbogast R, Bourassa MG: Myocardial function during atrial pacing in patients with angina pectoris and normal coronary arteriograms. Comparison with patients having significant coronary artery disease. Amer J Cardiol 32:257-263, 1973 3. Parker JO, Chiong MA, West RO, et ah Sequential alterations in myocardial lactate metabolism, ST segments, and left ventricular function during angina induced by atrial pacing. Circulation 40:113-131, 1969 4. Helfant RH, Forrester JS, Hampton JR, et ah Coronary heart
disease: differential hemodynamic, metabolic, and electrocardiographic effects in subjects with and without angina pectoris during atrial pacing. Circulation 42:601-610, 1970 5. Dwyer EM Jr" Left ventricular pressure-volume alterations and regional disorders of contraction during myocardial ischemia induced by atrial pacing. Circulation 42:1111-1122, 1970 6. Pasternac A, Gorlin R, Sonnenblick EH, et ah Abnormalities of ventricular motion induced by atrial pacing in coronary artery disease. Circulation 45:1195-1205, 1972 7. Ross J Jr, Unhart JW, Braunwald E: Effects of changing heart rate in man by electrical stimulation of the right atrium. Circulation 32:549-558, 1965
376
Volume 32
September 7, 1973
The American Journal of C A R D I O L O G Y