J. ELECTROCARDIOLOGY 11 (1), 1978, 97-100
Review
Electrocardiographic Mapping of the Precordium in the Coronary Care Unit BY JOHN E. MADIAS, M.D. AND WILLIAM B. HOOD, JR., M.D.
tions of the QRS complex, used as a parameter of ischemic necrosis.
SUMMARY Precordial electrocardiographic mapping systems comprising a large number of recording sites have been utilized in the Coronary Care Unit for following the natural course of ischemic injury and detecting extension o f a c u t e m y o c a r d i a l infarction in patients. These electrocardiographic techniques have also been found useful in evaluating the effects o f a number of metabolic, hemodynamic and pharmacologic interventions currently proposed as effective m e a n s of reducing the extent of ischemic damage. However, these methods have not been found useful in the study o f patients with inferior transmural or nontransmural myocardial infarctions. Bundle branch blocks and pericarditis complicating acute myocardial infarction invalidate the mapping technique. To assess effectiveness of therapeutic interventions, ST-segment changes taken as an index of ischemic injury are correlated with altera-
Recent animal studies have suggested that a c u t e m y o c a r d i a l i n f a r c t i o n (AMI) is a dynamic process involving gradual necrosis of the involved myocardium, and not a phenomenon completed shortly after coronary arterial perfusion ceases. 1 Clinical autopsy d a t a have also indicated t h a t the area of myocardial d a m a g e in patients dying of a heart attack is comprised of cells at different stages of ischemic involvement, ranging from irreversible necrosis to reversible ischemia. 2 In addition, it has become apparent to the clinician that m a n y patients treated in the Coronary Care Unit succumb to intractable power failure despite close monitoring of their clinical parameters and careful management. Despite the inroads made in the prevention and m a n a g e m e n t of cardiac dysrhythmias, the problem of severe hemodynamic decompensation is as yet unsolved and is the main contributor to the still high mortality of patients with AMI. Prognosis has been found to be directly related to the amount of normally functioning cardiac muscle remaining after both old and fresh myocardial infarctions (MIs). Currently the concept is being developed that the physician ought not be merely a passive observer of the dynamic process of ischemic involvement of a progressively larger number of myocardial cells, but rather a practitioner engaged in the effort of salvaging a portion of the injured myocardial zone. This can be partially accomplished by applying the conventional protocols of managing patients with AMI. 3 In addition, results from smallscale pilot studies show that application to the
From the Cardiology Department of the Thorndike Memorial Laboratory and the Department of Medicine, Boston City Hospital, Boston University School of Medicine, Boston, Massachusetts. Supported in part by USPHS Grants HL-14646, RR-533, HE-07299, Contract HV-53001, and American Heart Association Grant 74-1031 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. w solely to indicate this fact. Reprint requests to: John E. Madias, M.D., Cardiology Department, Boston City Hospital, 818 Harrison Avenue, Boston, MA 02118. 97
98
MADIAS AND HOOD
m a n a g e m e n t of patients of certain concepts derived from studies of experimental MI in the animal laboratory can further assist the physician's efforts to spare as much normally functioning myocardium as possible. 1'4-7 A host of pharmacologic, metabolic and hemod y n a m i c i n t e r v e n t i o n s has been tested in animals with acute t r a n s m u r a l myocardial injury. Most of these maneuvers exert their therapeutic or h a r m f u l effects by altering favorably or unfavorably the delicate regional balance of oxygen supply and demand. In a number of such studies epicardial electrograms from multiple areas of the ischemic canine left ventricle have been used as an index of the magnitude of ischemic damage. Comparisons of epicardial and precordial electrocardiograms (ECGs) obtained simultaneously in the same animals have shown parallel alterations in the two methods as a result of application of various interventions, superimposed upon coronary occlusion, s The technique of electrocardiographic mapping of the precordium has also been utilized in the clinical setting. An increasing number of clinical investigators are using this electrocardiographic m e t h o d , and m a n y p r a c t i c i n g physicians have their patients participating in research projects dealing with protection of the ischemic myocardium in the acute stage of heart attacks. A description of the technique of precordial mapping and an assessment of its usefulness and limitations are therefore timely.
Technique of Precordial Electrocardiographic Mapping. A variety of methods of electrocardiographic mapping has been applied to patients with AMI, comprising different arrays of recording sites on the precordium. We have employed a method consisting of recording the ECG from 49 sites on the anterior chest-wall2 Recording sites are marked on the chest with skin pencil to assure accurate repositioning of the ~V" lead of a conventional electrocardiograph when serial studies are undertaken. Standardization is 1 mV = 1.0 cm and the paper speed is 25 mm/sec. The 49 positions on the anterior chest form a grid consisting of seven transverse rows, each consisting of seven recording positions. The first row is placed at the level of the second intercostal space and the last row 6 to 8 cm below the xiphisternum. Distance between the seven transverse rows equals the distance between the first two rows. The first recording point of each row is located at the right sternal border, the second at the left sternal border and the fifth, sixth and seventh points at the anterior, mid and posterior axillary lines respectively. The third and fourth points are placed equidistant between the second and fifth points (Fig. 1).
Fig. 1. Torso showing the location of the 49 recording sites arranged in seven transverse rows, each consisting of seven points (filled small circles). The position of the six standard precordial leads (open circles) is also depicted. Reproduced with permission of Circulation2
The sum of ST elevations of all recording sites (~ST) is taken as an index of ischemic injury, and the number of sites showing an ST elevation ~> 0.1 mV is used as a parameter of the extent of the ischemic damage. Measurem e n t s of ST e l e v a t i o n s a r e m a d e to t h e nearest 0.5 mm, 0.06 sec following the nadir of the S waves, or in the absence of an S wave, 0.06 sec after the peak of the R waves, taking the TP segment as the isoelectric line, except in cases of tachycardia, when the PR is used instead. Serial maps of the precordium are clone and the rate of disappearance of ST elevation is analyzed. Lately another approach has developed in the s t u d y of electrocardiographic changes seen during the first week following the onset of a heart attack. This consists of correlation of ST elevations (an index of ischemic injury) with pathologic Q waves and reduction of R wave voltages (an index of necrosis) appearing later. The n u m b e r of sites on the precordium at which ST elevation exceeds a certain magnitude (NST) is monitored for development of Q waves. Also the initial total voltage of all R waves in m m ( ~ R) is measured on admission and its course over the span of the initial 48 hours is followed. Appearance of pathologic Q waves and reduction of ~ R taking place in an area which previJ. ELECTROCARDIOLOGY, VOL. 11, NO. 1, 1978
MAPPING IN THE CCU
ously had displayed ST elevation is t a k e n as evidence t h a t an area of ischemic injury has progressed to a stage of necrosis. 1~ Usefulness of the Technique of Precordial Electrocardiographic Mapping. Chest wall electrocardiographic mapping has been applied in the Coronary Care Unit for following patients with acute anterior, lateral, anterolateral, high anterior, true posterior, and inferior t r a n s m u r a l myocardial infarctions. ~'9 Both ~ST and NST have been computed from serial electrocardiographic maps and utilized in monitoring of ischemic injury, along with other conventional clinical parameters. In uncomplicated acute anterior t r a n s m u r a l MI, a mean reduction of ST by one-third of the initial values has been observed within the first 24 hours. 1,9 Extension of MI can be detected by the re-elevation of ST segments along with a new enzyme rise and exacerbation of, or new, chest pain. 9 Occasionally the diagnosis of an extension of the original ischemic damage can be made only by the electrocardiographic map, in the presence of a n unchanged standard 12-lead ECG. 9 Precordial maps are also useful in the detection of ischemic electrocardiographic changes in the high anterior regions of the chest, which reflect high anterior basal ischemic injury, i~ Precordial mapping has been found useful in the diagnosis of t r a n s m u r a l MI which did not produce changes in conventional ECGs in one p a t i e n t . 12 However, the s e n s i t i v i t y of the mapping systems in diagnosing MI in patients with normal 12-lead ECGs has not been studied as yet. Magnitude and extent of ST-segment elevations, rate of appearance of Q waves, and extent of reduction of R wave voltage can all be u t i l i z e d in concert in t h e a s s e s s m e n t of therapeutic interventions directed at decreasing the severity of myocardial ischemic damage. i~ By studying patients before and after a therapeutic maneuver s'7 or by comparing a treated group of patients with a control cohort of patients 4'5'1~effectiveness of an intervention can be judged. Pilot studies have been completed showing the benefit of fl-blockade, 6 i n t r a - a o r t i c b a l l o o n c o u n t e r p u l s a t i o n , i3 hyaluronidase, a'i~ nitroglycerin~ and inhalation of high oxygen concentrations von the magnitude of ischemic damage. While large-scale studies are being designed to prove or disprove beyond any doubt t h a t these therapeutic maneuvers are as beneficial in the clinical s e t t i n g as t h e y h a v e been in t h e a n i m a l l a b o r a t o r y , the i m p o r t a n c e of c o r r e l a t i n g changes in the chest wall maps with alterations in blood pressure, h e a r t rate, symptomatology of the patients 7 and changes in long-term parameters of morbidity, and finally mortality cannot be over-emphasized. J. ELECTROCARDIOLOGY, VOL. 11, NO. 1, 1978
99
Limitations of the Technique of Precordial Electrocardiographic Mapping. Precordial ST-segment mapping is not a suitable method for m o n i t o r i n g p a t i e n t s w i t h a c u t e nont r a n s m u r a l myocardial infarction2 It has also been found useless for the study of patients with inferior t r a n s m u r a l MI. 9 Since bundle branch blocks alter the ST segments of the electrocardiographic curves markedly, the presence of these conduction abnormalities render mapping meaningless, and detection of changes in ischemic damage is impossible. 9 Chest pain other t h a n t h a t accompanying extension of MI can elevate the ST segments in such a manner t h a t diagnosis of an extension is suspected, b u t is not s u b s t a n t i a t e d by enzyme re-elevation. Such difficulties can be avoided by performing mapping during painfree periods, except for the initial recordings. 14 Ventricular fibrillation can also alter the map s u b s t a n t i a l l y , but the changes suggestive of exacerbation of ischemic injury following such an electrical derangement are transient. T M Pericarditis can render the map invalid for following patients with AMI, since patients with this complication m a i n t a i n elev a t e d ~ S T a n d NST, while clinical and biochemical parameters show improvement2 Serially monitoring changes in the rate of development of Q waves and reduction of R wave voltages as myocardial necrosis ensues will provide a useful parameter to follow patients, while interventions to contain the ischemic damage are applied, lo This additional m e t h o d will n o t e x c l u d e p a t i e n t s w i t h pericarditis from inclusion in the group suitable for analysis even if results of ST segment elevation mapping might be uninterpretable. Despite these limitations, the technique of chest wall electrocardiographic mapping, in conjunction with conventional and other new techniques such as serial enzyme analysis 15 and cardiac radionuclide-imaging methods i6 will be useful in assessing the usefulness and p r a c t i c a l i t y of some c u r r e n t l y proposed therapeutic concepts for patients with acute heart attacks.
1.
2.
3. 4.
REFERENCES MAROKO,P R, LIBBY,P, COVELL,J W, SOBEL, B E, Ross, J, Jr AND BRAUNWALD,E: An atraumatic method for assessing alterations in the extent of myocardial ischemic injury. The effects of pharmacologic and hemodynamic interventions. Am J Cardiol 29:223, 1972 PAGE, D L, CAUFIELD, J B, KASTOR,J A AND DESANCTIS, R W: Myocardial changes associated with cardiogenic shock. N Engl J Med 285:133, 1971 FRIEDBERG, C K: Symposium myocardial infarction 1972 (Part 1). Introduction. Circulation 45:179, 1972 MAROKO, P R, DAVIDSON, D M, LIBBY, P,
100
5.
6.
7.
8.
9.
10.
MADIAS AND HOOD
HAGAN, A D AND BRAUNWALD, E: Effects of hyaluronidase administration on myocardial ischemic injury in acute infarction. Ann Intera Med 82:516, 1975 FLAHERTY, J T, REID, P R, KELLY, D T, TAYLOR,D R, WEISFELDT,M L AND PITT, B: Intravenous nitroglycerin in acute myocardial infarction. Circulation 51:132, 1975 PELIDES,L J, REID, D S, THOMAS,M AND SHILLINGFORD, J P: Inhibition by fi-blockade of the ST segment elevation after acute myocardial infarction in man. Cardiovasc Res 6:295, 1972 MADIAS,J E, MADIAS, N E AND HOOD, W B, Jr: Precordial ST-segment mapping. 2. Effects of oxygen inhalation on ischemic injury in patients with acute myocardial infarction. Circulation 53:411, 1976 MULLER,J E, MAROKO, P R AND BRAUNWALD, E: E v a l u a t i o n of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury. Circulation 52:16, 1975 MADIAS, J E, VENKATARAMAN, K AND HOOD, W B, Jr: Precordial ST-segment mapping. 1. Clinical studies in the coronary care unit. Circulation 52:799, 1975 MAROKO, P R, HILLIS, L D, MULLER, J E, TAVAZZI, L, HEYNDRICKS, G R , RAY, M, CHIARIELLO, M, DISTANTE, A, ASKENAZI, J, SALERNO,J, CARPENTIER,J, RESHETNAYA,N J,
11.
12. 13.
14.
15. 16.
RADVANY, P, LIBBY, P, RAABE, D S, CHAZOV, E I, BOBBA, P AND BRAUNWALD,E: Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction. N Engl J Med 296:898, 1977 MADIAS,J E AND HOOD, W B, Jr: Diagnosis of high anterolateral and true posterior myocardial infarction by chest wall ECG-mapping. J Electrocardiol 9:375, 1976 REID, D S, PELIDES, L J AND SHILLINGFORD, J P: Surface mapping of RS-T segment in acute myocardial infarction. Br Heart J 33:370, 1971 MAROKO, P R, BERNSTEIN, E F, LIBBY, P, DELARIA, G A, COVELL, J W, ROSS, J, Jr AND BRAUNWALD,E: The effects of intra-aortic balloon c o u n t e r p u l s a t i o n on the severity of myocardial ischemic injury following acute coronary occlusion. Counterpulsation and myocardial injury. Circulation 45: 1150, 1972 MADIAS, J E AND HOOD, W B, Jr: Precordial ST-segment mapping. 3. Stability of maps in the early phase of acute myocardial infarction. Am Heart J 93:603, 1977 SHELL, W E AND SOBEL, B E: Biochemical m a r k e r s of ischemic injury. C i r c u l a t i o n 53:Suppl 1-98, 1976 HOLMAN, B E: Radionuclide methods in the evaluation of myocardial ischemia and infarction. Circulation 53:Suppl 1-112, 1976
J. ELECTROCARDIOLOGY, VOL. 11, NO. 1, 1978
Review
Electrocardiographic Mapping of the Precordium in the Coronary Care Unit BY JOHN E. MADIAS, M.D. AND WILLIAM B. HOOD, JR., M.D.
tions of the QRS complex, used as a parameter of ischemic necrosis.
SUMMARY Precordial electrocardiographic mapping systems comprising a large number of recording sites have been utilized in the Coronary Care Unit for following the natural course of ischemic injury and detecting extension o f a c u t e m y o c a r d i a l infarction in patients. These electrocardiographic techniques have also been found useful in evaluating the effects o f a number of metabolic, hemodynamic and pharmacologic interventions currently proposed as effective m e a n s of reducing the extent of ischemic damage. However, these methods have not been found useful in the study o f patients with inferior transmural or nontransmural myocardial infarctions. Bundle branch blocks and pericarditis complicating acute myocardial infarction invalidate the mapping technique. To assess effectiveness of therapeutic interventions, ST-segment changes taken as an index of ischemic injury are correlated with altera-
Recent animal studies have suggested that a c u t e m y o c a r d i a l i n f a r c t i o n (AMI) is a dynamic process involving gradual necrosis of the involved myocardium, and not a phenomenon completed shortly after coronary arterial perfusion ceases. 1 Clinical autopsy d a t a have also indicated t h a t the area of myocardial d a m a g e in patients dying of a heart attack is comprised of cells at different stages of ischemic involvement, ranging from irreversible necrosis to reversible ischemia. 2 In addition, it has become apparent to the clinician that m a n y patients treated in the Coronary Care Unit succumb to intractable power failure despite close monitoring of their clinical parameters and careful management. Despite the inroads made in the prevention and m a n a g e m e n t of cardiac dysrhythmias, the problem of severe hemodynamic decompensation is as yet unsolved and is the main contributor to the still high mortality of patients with AMI. Prognosis has been found to be directly related to the amount of normally functioning cardiac muscle remaining after both old and fresh myocardial infarctions (MIs). Currently the concept is being developed that the physician ought not be merely a passive observer of the dynamic process of ischemic involvement of a progressively larger number of myocardial cells, but rather a practitioner engaged in the effort of salvaging a portion of the injured myocardial zone. This can be partially accomplished by applying the conventional protocols of managing patients with AMI. 3 In addition, results from smallscale pilot studies show that application to the
From the Cardiology Department of the Thorndike Memorial Laboratory and the Department of Medicine, Boston City Hospital, Boston University School of Medicine, Boston, Massachusetts. Supported in part by USPHS Grants HL-14646, RR-533, HE-07299, Contract HV-53001, and American Heart Association Grant 74-1031 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. w solely to indicate this fact. Reprint requests to: John E. Madias, M.D., Cardiology Department, Boston City Hospital, 818 Harrison Avenue, Boston, MA 02118. 97
98
MADIAS AND HOOD
m a n a g e m e n t of patients of certain concepts derived from studies of experimental MI in the animal laboratory can further assist the physician's efforts to spare as much normally functioning myocardium as possible. 1'4-7 A host of pharmacologic, metabolic and hemod y n a m i c i n t e r v e n t i o n s has been tested in animals with acute t r a n s m u r a l myocardial injury. Most of these maneuvers exert their therapeutic or h a r m f u l effects by altering favorably or unfavorably the delicate regional balance of oxygen supply and demand. In a number of such studies epicardial electrograms from multiple areas of the ischemic canine left ventricle have been used as an index of the magnitude of ischemic damage. Comparisons of epicardial and precordial electrocardiograms (ECGs) obtained simultaneously in the same animals have shown parallel alterations in the two methods as a result of application of various interventions, superimposed upon coronary occlusion, s The technique of electrocardiographic mapping of the precordium has also been utilized in the clinical setting. An increasing number of clinical investigators are using this electrocardiographic m e t h o d , and m a n y p r a c t i c i n g physicians have their patients participating in research projects dealing with protection of the ischemic myocardium in the acute stage of heart attacks. A description of the technique of precordial mapping and an assessment of its usefulness and limitations are therefore timely.
Technique of Precordial Electrocardiographic Mapping. A variety of methods of electrocardiographic mapping has been applied to patients with AMI, comprising different arrays of recording sites on the precordium. We have employed a method consisting of recording the ECG from 49 sites on the anterior chest-wall2 Recording sites are marked on the chest with skin pencil to assure accurate repositioning of the ~V" lead of a conventional electrocardiograph when serial studies are undertaken. Standardization is 1 mV = 1.0 cm and the paper speed is 25 mm/sec. The 49 positions on the anterior chest form a grid consisting of seven transverse rows, each consisting of seven recording positions. The first row is placed at the level of the second intercostal space and the last row 6 to 8 cm below the xiphisternum. Distance between the seven transverse rows equals the distance between the first two rows. The first recording point of each row is located at the right sternal border, the second at the left sternal border and the fifth, sixth and seventh points at the anterior, mid and posterior axillary lines respectively. The third and fourth points are placed equidistant between the second and fifth points (Fig. 1).
Fig. 1. Torso showing the location of the 49 recording sites arranged in seven transverse rows, each consisting of seven points (filled small circles). The position of the six standard precordial leads (open circles) is also depicted. Reproduced with permission of Circulation2
The sum of ST elevations of all recording sites (~ST) is taken as an index of ischemic injury, and the number of sites showing an ST elevation ~> 0.1 mV is used as a parameter of the extent of the ischemic damage. Measurem e n t s of ST e l e v a t i o n s a r e m a d e to t h e nearest 0.5 mm, 0.06 sec following the nadir of the S waves, or in the absence of an S wave, 0.06 sec after the peak of the R waves, taking the TP segment as the isoelectric line, except in cases of tachycardia, when the PR is used instead. Serial maps of the precordium are clone and the rate of disappearance of ST elevation is analyzed. Lately another approach has developed in the s t u d y of electrocardiographic changes seen during the first week following the onset of a heart attack. This consists of correlation of ST elevations (an index of ischemic injury) with pathologic Q waves and reduction of R wave voltages (an index of necrosis) appearing later. The n u m b e r of sites on the precordium at which ST elevation exceeds a certain magnitude (NST) is monitored for development of Q waves. Also the initial total voltage of all R waves in m m ( ~ R) is measured on admission and its course over the span of the initial 48 hours is followed. Appearance of pathologic Q waves and reduction of ~ R taking place in an area which previJ. ELECTROCARDIOLOGY, VOL. 11, NO. 1, 1978
MAPPING IN THE CCU
ously had displayed ST elevation is t a k e n as evidence t h a t an area of ischemic injury has progressed to a stage of necrosis. 1~ Usefulness of the Technique of Precordial Electrocardiographic Mapping. Chest wall electrocardiographic mapping has been applied in the Coronary Care Unit for following patients with acute anterior, lateral, anterolateral, high anterior, true posterior, and inferior t r a n s m u r a l myocardial infarctions. ~'9 Both ~ST and NST have been computed from serial electrocardiographic maps and utilized in monitoring of ischemic injury, along with other conventional clinical parameters. In uncomplicated acute anterior t r a n s m u r a l MI, a mean reduction of ST by one-third of the initial values has been observed within the first 24 hours. 1,9 Extension of MI can be detected by the re-elevation of ST segments along with a new enzyme rise and exacerbation of, or new, chest pain. 9 Occasionally the diagnosis of an extension of the original ischemic damage can be made only by the electrocardiographic map, in the presence of a n unchanged standard 12-lead ECG. 9 Precordial maps are also useful in the detection of ischemic electrocardiographic changes in the high anterior regions of the chest, which reflect high anterior basal ischemic injury, i~ Precordial mapping has been found useful in the diagnosis of t r a n s m u r a l MI which did not produce changes in conventional ECGs in one p a t i e n t . 12 However, the s e n s i t i v i t y of the mapping systems in diagnosing MI in patients with normal 12-lead ECGs has not been studied as yet. Magnitude and extent of ST-segment elevations, rate of appearance of Q waves, and extent of reduction of R wave voltage can all be u t i l i z e d in concert in t h e a s s e s s m e n t of therapeutic interventions directed at decreasing the severity of myocardial ischemic damage. i~ By studying patients before and after a therapeutic maneuver s'7 or by comparing a treated group of patients with a control cohort of patients 4'5'1~effectiveness of an intervention can be judged. Pilot studies have been completed showing the benefit of fl-blockade, 6 i n t r a - a o r t i c b a l l o o n c o u n t e r p u l s a t i o n , i3 hyaluronidase, a'i~ nitroglycerin~ and inhalation of high oxygen concentrations von the magnitude of ischemic damage. While large-scale studies are being designed to prove or disprove beyond any doubt t h a t these therapeutic maneuvers are as beneficial in the clinical s e t t i n g as t h e y h a v e been in t h e a n i m a l l a b o r a t o r y , the i m p o r t a n c e of c o r r e l a t i n g changes in the chest wall maps with alterations in blood pressure, h e a r t rate, symptomatology of the patients 7 and changes in long-term parameters of morbidity, and finally mortality cannot be over-emphasized. J. ELECTROCARDIOLOGY, VOL. 11, NO. 1, 1978
99
Limitations of the Technique of Precordial Electrocardiographic Mapping. Precordial ST-segment mapping is not a suitable method for m o n i t o r i n g p a t i e n t s w i t h a c u t e nont r a n s m u r a l myocardial infarction2 It has also been found useless for the study of patients with inferior t r a n s m u r a l MI. 9 Since bundle branch blocks alter the ST segments of the electrocardiographic curves markedly, the presence of these conduction abnormalities render mapping meaningless, and detection of changes in ischemic damage is impossible. 9 Chest pain other t h a n t h a t accompanying extension of MI can elevate the ST segments in such a manner t h a t diagnosis of an extension is suspected, b u t is not s u b s t a n t i a t e d by enzyme re-elevation. Such difficulties can be avoided by performing mapping during painfree periods, except for the initial recordings. 14 Ventricular fibrillation can also alter the map s u b s t a n t i a l l y , but the changes suggestive of exacerbation of ischemic injury following such an electrical derangement are transient. T M Pericarditis can render the map invalid for following patients with AMI, since patients with this complication m a i n t a i n elev a t e d ~ S T a n d NST, while clinical and biochemical parameters show improvement2 Serially monitoring changes in the rate of development of Q waves and reduction of R wave voltages as myocardial necrosis ensues will provide a useful parameter to follow patients, while interventions to contain the ischemic damage are applied, lo This additional m e t h o d will n o t e x c l u d e p a t i e n t s w i t h pericarditis from inclusion in the group suitable for analysis even if results of ST segment elevation mapping might be uninterpretable. Despite these limitations, the technique of chest wall electrocardiographic mapping, in conjunction with conventional and other new techniques such as serial enzyme analysis 15 and cardiac radionuclide-imaging methods i6 will be useful in assessing the usefulness and p r a c t i c a l i t y of some c u r r e n t l y proposed therapeutic concepts for patients with acute heart attacks.
1.
2.
3. 4.
REFERENCES MAROKO,P R, LIBBY,P, COVELL,J W, SOBEL, B E, Ross, J, Jr AND BRAUNWALD,E: An atraumatic method for assessing alterations in the extent of myocardial ischemic injury. The effects of pharmacologic and hemodynamic interventions. Am J Cardiol 29:223, 1972 PAGE, D L, CAUFIELD, J B, KASTOR,J A AND DESANCTIS, R W: Myocardial changes associated with cardiogenic shock. N Engl J Med 285:133, 1971 FRIEDBERG, C K: Symposium myocardial infarction 1972 (Part 1). Introduction. Circulation 45:179, 1972 MAROKO, P R, DAVIDSON, D M, LIBBY, P,
100
5.
6.
7.
8.
9.
10.
MADIAS AND HOOD
HAGAN, A D AND BRAUNWALD, E: Effects of hyaluronidase administration on myocardial ischemic injury in acute infarction. Ann Intera Med 82:516, 1975 FLAHERTY, J T, REID, P R, KELLY, D T, TAYLOR,D R, WEISFELDT,M L AND PITT, B: Intravenous nitroglycerin in acute myocardial infarction. Circulation 51:132, 1975 PELIDES,L J, REID, D S, THOMAS,M AND SHILLINGFORD, J P: Inhibition by fi-blockade of the ST segment elevation after acute myocardial infarction in man. Cardiovasc Res 6:295, 1972 MADIAS,J E, MADIAS, N E AND HOOD, W B, Jr: Precordial ST-segment mapping. 2. Effects of oxygen inhalation on ischemic injury in patients with acute myocardial infarction. Circulation 53:411, 1976 MULLER,J E, MAROKO, P R AND BRAUNWALD, E: E v a l u a t i o n of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury. Circulation 52:16, 1975 MADIAS, J E, VENKATARAMAN, K AND HOOD, W B, Jr: Precordial ST-segment mapping. 1. Clinical studies in the coronary care unit. Circulation 52:799, 1975 MAROKO, P R, HILLIS, L D, MULLER, J E, TAVAZZI, L, HEYNDRICKS, G R , RAY, M, CHIARIELLO, M, DISTANTE, A, ASKENAZI, J, SALERNO,J, CARPENTIER,J, RESHETNAYA,N J,
11.
12. 13.
14.
15. 16.
RADVANY, P, LIBBY, P, RAABE, D S, CHAZOV, E I, BOBBA, P AND BRAUNWALD,E: Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction. N Engl J Med 296:898, 1977 MADIAS,J E AND HOOD, W B, Jr: Diagnosis of high anterolateral and true posterior myocardial infarction by chest wall ECG-mapping. J Electrocardiol 9:375, 1976 REID, D S, PELIDES, L J AND SHILLINGFORD, J P: Surface mapping of RS-T segment in acute myocardial infarction. Br Heart J 33:370, 1971 MAROKO, P R, BERNSTEIN, E F, LIBBY, P, DELARIA, G A, COVELL, J W, ROSS, J, Jr AND BRAUNWALD,E: The effects of intra-aortic balloon c o u n t e r p u l s a t i o n on the severity of myocardial ischemic injury following acute coronary occlusion. Counterpulsation and myocardial injury. Circulation 45: 1150, 1972 MADIAS, J E AND HOOD, W B, Jr: Precordial ST-segment mapping. 3. Stability of maps in the early phase of acute myocardial infarction. Am Heart J 93:603, 1977 SHELL, W E AND SOBEL, B E: Biochemical m a r k e r s of ischemic injury. C i r c u l a t i o n 53:Suppl 1-98, 1976 HOLMAN, B E: Radionuclide methods in the evaluation of myocardial ischemia and infarction. Circulation 53:Suppl 1-112, 1976
J. ELECTROCARDIOLOGY, VOL. 11, NO. 1, 1978
