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Wall motion abnormalities and electrocardiographic changes in acute transmural myocardial infarction: Implications of reciprocal ST segment depression
Wall motion abnormalities and electrocardiographic changes in acute transmural myocardial infarction: Implications reciprocal ST segment depression
of
Left ventricular ejection fraction and regional wall motion were assessed by multigated equilibrium radionuclide ventriculography within 24 hours of onset of first acute transmural myocardial infarction (Ml) in 32 patients. Abnormal left ventricular wall motion was noted in all 16 patients with anterior infarction and in 14 of 16 (87.5%) patients with inferior infarction. Regional wall motion abnormalities frequently included areas adjacent to and remote from those predicted by the ECG location of ST elevation and pathologic 0 waves. Such remote wall motion abnormalities were associated with reciprocal ST segment depression in 17 of 18 (94%) patients, and conversely reciprocal ST segment depressions were associated with remote wall motion abnormalities in 17 of 24 (71%) patients. The left ventricular ejection fraction was lower in patients with a reciprocal ST segment depression compared to those without (anterior MI 0.29 +- 0.07 vs 0.43 f 0.08, p < 0.01; inferior MI 0.45 + 0.11 vs 0.63 ? 0.06, p < 0.001). In addition, the peak MB-CK levels were higher in patients with compared to those without reciprocal ST segment depression (anterior MI 268 f 183 vs 102 + 60, p < 0.05; inferior MI 186 f 120 vs 67 f 20, p < 0.05). Thirteen of 18 (72%) patients with reciprocal ST segment depression compared to 4 of 13 (31%) patients without reciprocal ST segment depression had a complicated clinical course during their hospital stay. These observation suggest that global left ventricular dysfunction in first acute transmural Ml is greater when reciprocal ST segment depression is present on the 12-lead ECG. Such reciprocal changes are frequently associated with enzymatic evidence of larger infarction, regional left ventricular dysfunction extending to segments remote from the ECG predicted site of transmural infarction, and an unfavorable clinical course. (AM HEART J 106:1003, 1983.)
Max Pichler, M.D., Prediman K. Shah, M.D., Thomas Peter, M.D., Bramah Singh, M.D., Ph.D., Daniel Berman, M.D., Frank Shellock, and H. J. C. Swan, M.D., Ph.D. Los Angeles, Calif.
Evolving ST segment elevation and the appearance of new Q waves, the conventional criteria for the diagnosis of acute transmural myocardial infarction, are widely accepted as being indicative of both the location’~ 2 and the extent of acute necrosis.3-5 This view is based, however, on information gathered from contrast ventriculography6-lo or autopsy”-l5 performed after delay of days or months after the From the Division of Cardiology, and the Departments of Medicine and Nuclear Medicine, Cedars-Sinai Medical Center; and the UCLA School of Medicine. Supported by a Max Kade Postdoctoral Research Exchange Grant (Dr. Pichler) from Vienna, Austria. Received for publication Apr. 30, 1982; accepted June 19, 1982. Reprint requests: Prediman K. Shah, M.D., Director, Inpatient Cardiology and Cardiac Care Unit, Room 5314, Cardiology Division, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA 90048.
M.S.,
acute event. For this reason, only limited data are available concerning the relationship between the ECG location of acute infarction and its associated functional correlate, i.e., the regional wall motion abnormality. The recent development of radionuclide ventriculography’6-18 has made it possible to evaluate left ventricular wall motion at the bedside of the acutely ill patient during the early phases of acute myocardial infarction. The purpose of this study was therefore (1) to compare the site, extent, and severity of left ventricular segmental dysfunction to the location and extent of myocardial infarction as gauged by conventional ECG criteria within 24 hours of infarction and (2) to determine the functional significance of “reciprocal” ST segment depression associated with acute myocardial infarction (AMI).
1004
WALL
Pichler
et al.
American
LV SEGMENT
MOTION SCORF
4
Table 1.Assignmentof regional LV wall motion abnormal-
ity
6 z Normal 5 * ny;;*i
0
3
* Akinefi: 2 ~Dyskinetic (Mild) I =Dytkinetic ~SOUd
to
ECG site of infarction
ECG site infarction
‘ H@i&
of
LV wall segment(s) assigned
Anteroseptal ANTERIOR
@I; lwm~;plerol
45’L80
3 6, 1 2 3 4 5 3 8,
Anterolateral
(31; I-tfekapicol
TOTAL WALL
MOTION SCORE=
Sum of score of individual
segments
November, 1983 Heart Journal
Inferior
1. Semiquantitative assessmentof segmental LV wall motion by ggmTcRBC blood pool scintigraphy. The left ventricle is divided into 10 segmentslisted on the right of the figure. Each segment is assigneda score for wall motion listed on the left of the figure. The values are the consensusof two independent and expert observers. Fig.
(anteroapical) 7 (proximal and distal (anterobasal) (anterolateral) (anteroapical) (distal-inferior) (proximal-inferior) (inferoapical) 9 (proximal and distal posterolateral)
septal)
II. ECG site of infarction and regional wall motion abnormality Table METHODS AMI criteria.
The data on 32 consecutive patients (24 males,8 females) admitted to the coronary care unit with a first acute transmural myocardial infarction and evaluated within 24 hours of the onsret of symptoms were reviewed. The mean age was 59 years, ranging from 32 to 82 years. The criteria used for the diagnosis of acute myocardial infarction were the combined presenceof (1) a history of sustained (>30 minutes) substernal chest pain, (2) an unequivocal elevation of serum creatine kinase isoenzyme MB (CK-MB), and (3) typical acute ischemic evolutionary changesin the ECG. Transmural myocardial infarction was diagnosedby ST segmentelevation of ~1 mm, associated with newly evolving Q waves (~0.03 secondduration) in at least two of the 12 leads and was categorized into anteroseptal (leadsV, to V,), anterolateral (leadsV, to V6, I, and aVL), and inferior (leads II, III, and aVr) infarction. Reciprocal ST depression. “Reciprocal” ST segment depressionwasdefined ashorizontal ST depressionof ~1 mm in at least two out of four precordial leadsV, to V, in patients with inferior infarction, and in at least two of the three inferior leads II, III, and aV, in patients with anteroseptal and/or anterolateral myocardial infarction. Patients. None of the patients included in this study had any of the following features: (1) documented previous myocardial infarction, (2) QRS duration >120 msec, (3) atrial fibrillation, (4) ECG evidence of left ventricular hypertrophy, (5) valvular heart diseaseor cardiomyopathy, (6) ECG signsof true posterior infarction,20 and (7) none were on cardioactive medication at the time of initial evaluation. The patients were treated conventionally with oxygen and if necessarywith morphine for pain, and with lidoCaine for ventricular arrhythmias. The patients who demonstrated clear clinical and radiologic evidence of pulmonary congestion and/or objective evidence of peripheral hypoperfusion (according to rigorous clinical criteria previously described from this department?Owere designated as “clinically complicated.” A 12-lead ECG
Anteroseptal and/or anterolateral MI (n = 16) Correspondence between ECG site of MI with the segments of greatest depression of wall motion No. of patients showing severest wall motion abnormality Limited to 1 segment 2 segments 3 or more segments MI = myocardial
Inferior MI (n = 16)
16116
14116
2 9 5
9 4 1
infarction.
wasobtained within 1 hour of radionuclide ventriculography and daily thereafter for 3 days. All tracings were read by one cardiologist (T.P.) not aware of the patient’s clinical diagnosis. Assessment of left ventricular function. Radionuclide ventriculography was performed in all patients within 24 ‘hoursof onset of symptomsusing in vitro technetium-99m labeled autologous red blood ce11s.17,21 Multipleigated equilibrium blood pool imaging was performed using a mobile gamma camera (Ohio Nuclear, Sigma 420) equipped with a low-energy, all-purpose collimator and a mobile computer (Technicare). Left ventricular regionsof interest in end diastole and end systole were assigned using a light pen and a left paraventricular background was selected in end systole. Left ventricular ejection fraction was derived from the quotient of backgroundcorrected stroke counts and end-diastolic counts. For visual assessment of regional left ventricular wall motion, the scintigraphic data were displayed in a flicker-free closed loop movie format and each of 10 left ventricular segmentswas assigneda score according to the format shown in Fig. 1. In those patients, in Whom inferior wall motion could not be properly assessedbecauseof right
Volume Number
106 5, Part 1
Wall motion
and reciprocal
ST depression
in AMI
1005
III. Location of segmentswith the most depressedwall motion in patients with various ECG locations of myocardial infarction*
Table
Segments * Anterobasal 1
ECG Anteroseptal (n = 6)t 14 segments* Anterolateral (n = 4)t 10 segments* Anteroseptal and anterolateral (n = 6)t 17 segments* Inferior (n = 16)t 20 segments* *One
tNo.
or more segments of patients.
may be equally
Anterolateral 2
Apical 3
Septal 6
Inferoapical 7
Distal inferior 4
3
5 3
3 2
4 1
2 1
3 2
5 3
2 7
5 6
2 1
Proximal inferior 5
Posterolateral 8
Distal proximal 9
1
reduced.
ventricular overlap in the anterior view, a 70% left anterior oblique view image was also obtained to clearly determine the pattern of wall motion of inferior segments. All scintigraphic data were analyzed in the division of nuclear cardiology without knowledge of clinical status of the patient. This technique of determination of left ventricular ejection fraction and regional wall motion has been validated before and is described in detail elsewhere.‘?.*I For comparison of regional wall motion abnormalities and the location of the ECG abnormality, the 10 segments of the left ventricle were assignedto corresponding ECG leads, as shown in Table I. Scintigraphic and ECG data were analyzed to separately determine the relationship betweenleft ventricular (LV) regional wall motion and the ECG location of transmural infarction (ST elevation, new Q waves), as well as “reciprocal” ST segment depressions. Statistical analysis. The unpaired t test and chi square test were usedfor comparative statistical analysisto assess differences between groups of non-paired data. A p value ~0.05 was defined as significant. RESULTS
Sixteen patients had anterior myocardial infarction (six anteroseptal, four anterolateral, six both anteroseptal and anterolateral) and 16 patients had inferior infarction. ECG localization and regional and global LV dysfunction. Thirty of 32 patients (94%) had scintigraphic
wail motion abnormalities that corresponded to the ECG location of infarction. The two patients without scintigraphic abnormalities both had ECG evidence of inferior myocardial infarction (Table II). In every case, the scintigraphic region exhibiting the most severe wall motion abnormality corresponded to that predicated from the ECG (Table III). Thus in the six patients with ECG abnormalities of anteroseptal infarction, the greatest depression of wall motion was distributed as tabulated in line 1 of Table III. Both the severity and extent of regional
wall motion abnormality, however, were most severe in anterior myocardial infarction. Thus in anterior infarction severe wall motion abnormality (severe hypokinesis, akinesis, or dyskinesis) were observed in two segments in 9 .of 16 patients and in three or more segments in 5 of 16 patients, whereas only two patients had severe wall motion abnormality limited to a single segment. In contrast, in patients with inferior myocardial infarction, the most severe wall motion abnormality was limited to a single segment in nine patients and involved two segments in four patients and three or more segments in only one patient. Ejection fraction was depressed below the lower limits of normal (<0.54) in all but one patient (94 % ) with anterior myocardial infarction, averaging 0.35 + 0.10, whereas a depressed ejection fraction was observed in only 9 of 16 patients (56%) with inferior infarction, averaging 0.53 +- 0.13. The difference in average ejection fraction between anterior and inferior infarction was highly significant (p < 0.092). Clinical complications of pump failure were more prevalent in patients with anterior myocardial infarction. Twelve of the 16 (75%) patients with anterior infarction demonstrated clear-cut “clinical” signs of heart failure compared to only 5 out of 16 (31%) with inferior infarction (p < 0.02). There was therefore a significant tendency for patients with anterior infarction to demonstrate a greater degree of hemodynamic and functional impairment. The observed depression in regional left ventricular function correlated well with ejection fraction (Fig. 2). Thus the mean ejection fraction in patients without an akinetic or dyskinetic segment was 0.59 ? 0.08, which was significantly (p < 0.001) higher than the corresponding mean value of 0.36 + 0.11 in patients with one or more akinetic or dyskinetic segments.
November,
1006
Pichler et al.
EF (o/o)
American
0
70
50
Heart
1983 Journal
changes (0.45 + 0.11 versus 0.63 f 0.06, p < 0.001) (Table V). Peak MB-CK isoenrymes. The higher peak MB-CK levels in patients with reciprocal ST depression compared to those without reciprocal changes (anterior infarction: 268 + 183 vs 102 + 60 IU/L, p < 0.05; inferior infarction 186 + 120 vs 67 + 20 IU/L, p < 0.05) suggested greater extent of myocardial necrosis in the former. DISCUSSION
Since the classical work of Smith22 and Pardee, the ECG has been the basis of clinical detection and localization of AMI. Our study confirms these observations but adds new information regarding the interrelationship of the location, extent, and severity of segmental wall motion abnormalities and the ECG site of infarction as designated by 12-lead ECG. Specifically, 94% of the patients in this study demonstrated wall motion abnormalities in the area defined by ECG abnormalities.
30
IO WITH
WITHOUT
AKINETIC or DYSKINETIC SEGMENTS Fig. 2. LV ejection fraction in patients with and without one or more akinetic (grade 0) or dyskinetic (grade 1) LV segments. M + SD = mean + 1 standard deviation for each group.
Wall motion its association
abnormality in remote LV segments and with reciprocal ST segment depression.
Twenty-four of the 32 patients (75% ) had wall motion abnormalities in LV segments adjacent to or remote from those predicted by the ECG location of infarction (Table IV). Of the 15 patients with anterior infarction and remote wall motion abnormalities, nine had associated reciprocal ST segment depression. Thus in 17 of 24 patients (71%), remote wall motion abnormalities were associated with reciprocal ECG abnormalities. Conversely, 17 out of 18 patients (95%) with reciprocal ECG changes had wall motion abnormalities remote from the area indicated by conventional criteria of infarction. The left ventricular ejection fraction (LVEF) was significantly lower in patients with anterior infarction and concomitant reciprocal ST segment depression than in those without reciprocal ST segment depression (0.29 -+ 0.07 vs 0.43 + 0.08, p < 0.01). Similarly, patients with inferior infarction and reciprocal ST segment depression had a significantly lower ejection fraction than those without reciprocal
Extent reciprocal
and location of wall motion ECG changes. Although
abnormality
and
the location of dysfunction detected by the two techniques corresponded closely, the extent did not. LV wall motion abnormalities clearly involved regions other than those indicated by the ECG in 94% (15 of 16) of patients with anterior and in 56% (9 of 16) of patients with inferior infarction. This discrepancy between ECG extent of infarction and the extent of regional mechanical dysfunction determined by scintigraphy is consistent with animal studies which suggest that the area of AM1 is often surrounded by an even larger dysfunctional ischemic zone. Indeed, Wyatt et a1.24 and Mathes et al.% both found “remote” depression of regional function following acute coronary occlusion in areas served by other patent coronary arteries. In our study, 75% (24 of 32) of all patients exhibited such remote wall motion abnormalities, and 71% (17 of 24) of these had associated ECG ST segment depression. These observations suggest that the interpretation of reciprocal ST segment depression in AM126,27 requires reappraisal. In the absence of such remote regional dysfunction, reciprocal ECG changes were not seen. Since 94% of the patients with reciprocal changes had associated wall motion abnormalities, the concept that reciprocal ST segment depression is purely a vectorial ECG phenomenon and therefore of little clinical relevance must be questioned. On the contrary, our data suggest that the presence of ECG abnormalities in reciprocal ECG leads implies a concomitant depression of regional wall motion in the corresponding LV segments. Similarly, since the
Volume Number
106 5, Part 1
Table
Wall
and
reciprocal
ST
depression
in
AMI
1007
IV. Reciprocal ST segment depressionand remote wall motion abnormalities in 32 patients with AM1 Anteroseptal
and/or
anterolateral
Present
ST depression
= wall
motion
(n = 16)
AM1
No 0 = acute
Absent
9
Yes 6
myocardial
(n = 16)
Present
7
Yes 9 abnormality;
Inferior
Absent
9
Remote WMA WMA
motion
No 1
Yes 8
7 No 1
Yes 1
No 6
infarction.
V. Presenceor absenceof reciprocal ST segmentdepressionand parameters of infarct size, global LV function, and clinical classification Table
Reciprocal ST depression
Anteroseptal
and anterolateral
No. of patients
Yes
Inferior
9
No
7
Yes
9
No
= creatine 2 SD.
peak (IUIL)
Mean+
LVEF
268 (+- 183) 102 (k60) 186 (?I 120)
( * 0.07) 0.43 ( 2 0.08) 0.45
(CO,
0.63 ( zt 0.06)
I
Total CK-MB *Mean
Mean* CK-MB
0.29
No. of patients with complications 8
4 5
(kO.11)
0
32 kinase
isoenzyme
MB;
LVEF
= left ventricular
ejection
location and extent of regional dysfunction are related to the global LV performance, reciprocal ST segment changes are indirectly indicative of lower levels of ejection fraction and consequently of the presence of clinical heart failure. Electrophysiologic correlates of ST segment alterations. The ST segment deviations during acute myo-
cardial ischemia are primarily dependent on the extracellular accumulation of potassium and the consequent transmembrane gradient across the border between ischemic and nonischemic tissue. Both spatial factors (size and shape of ischemic area, electrode position) and nonspatial factors (electrolytes, antiarrhythmic agents, heart rate) alter this gradient. 28 During systole, current flows from the ischemic to the normal tissue and the converse occurs in diastole. Thus ST segment deviations in acute ischemia or infarction depict the sum of ST segment elevation and the ST segment depression, or vice versa. In unipolar precordial recordings, the ST deflections mainly depend upon the interrelationship between the position of the recording electrode and the geometry of the ischemic area and its boundaries. Thus though the ST segment depression seen in right precordial leads in patients with inferior infarction is conventionally regarded as presenting mirror images or reciprocal changes,26p27
fraction
the logic of solid angle theory** suggests that all patients with inferior myocardial infarction should exhibit reciprocal ST segment depressions anteriorly, since the recording electrode will have similar spatial relationship with the site and size of inferior infarction. It could be argued that precordial ST segment depression is a reflection of the wider solid angle as a result of larger ischemic involvement of the inferior epicardial surface area in such patients. This viewpoint is partly supported by a higher peak creatine kinase isoenzyme MB value in patients with reciprocal ST segment depression compared to those without. Further research should be directed to resolve the questions whether higher creatine kinase isoenzyme MB levels reflect large inferior infarct or additional infarction extending into remote LV segments. Technetium-99m pyrophosphate29 and/or thallium-201 scintigraphy30 in the acute phase may be helpful in this regard. Even if one accepts the theory that reciprocal ST segment depressions only indicate large infarcts, the observation that 94% of these patients in our study had remote wall motion abnormalities favors the possibility that the function of the remote segments is indeed compromised from ischemia or infarction or some other as yet unidentified mechanism.
November,
1008
Pichler et al.
Disordered global cardiac performance was more frequent and more severe in anterior myocardial infarction. This observation is consistent with previous hemodynamic studies,31-33 but the data in the present study support the conclusion that a major determinant of the level of LV function in the acute phase of infarction is the extent and magnitude of disordered regional function, rather than the site of infarction itself. This concept is supported by the findings of Miller et a1.,34 who observed no differences in LV wall motion abnormality, regardless of its location. Clinical implications. Previous studies from this laboratory have demonstrated that patients with AM1 may be divided into specific clinica120 and hemodynamic35 subsets which exhibit major differences in their mortality and their response to therapy.36 The data in this study further suggest that scintigraphic analysis of mechanical LV dysfunction provides more precise definition of the magnitude of functional impairment within these subsets and may thereby allow a more rational selection of appropriate therapeutic interventions. Conclusions. Although there is close correlation between the regional ECG and functional manifestation of ischemia, important differences of clinical relevance also exist. Segmental wall motion abnormalities are frequently more extensive than ECG abnormalities suggest, and may occur in areas apparently remote from the putatively infarcted zone.37 The presence of such a remote area of regional dysfunction is suggested by reciprocal ST segment depression. Although the therapeutic significance of these relationships remains to be determined, it is likely that important prognostic and therapeutic subsets may emerge from such investigations. The authors gratefully acknowledge the assistance of Beverly Yoshioka, Lilian Solomon, Joye Nunn, and Lance Laforteza in the preparation of this manuscript. REFERENCES
1. The Criteria Committee of the New York Heart Association: Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. Boston, 1973, Little, Brown & Co, pp 95-123. 2. Working Group on Ischemic Heart Disease Registers, World Health Organization: Report Euro 8201 (5). Copenhagen, 1971, WHO Regional Office for Europe. 3. Madias JE: Use of precordial ST-segment mapping. AM HEART J 95:96, 1978. 4. Savage RM, Wagner GS, Ideker RE, et al: Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction. Circulation 55:279, 1977. 5. Selvester RH, Wagner JO, Rubin HB: Quantitation of myocardial infarct size and location by electrocardiogram and vector cardiogram. In Snellen HA, editor: Boerhave course in
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quantitation in cardiology. Leyden, 1972, Leyden University Press, p 32. Williams RA, Cohn PF, Vokanas PS, et al: Electrocardiographic, arteriographic and ventriculographic correlations in transmural myocardial infarction. Am J Cardiol 31:595, 1973. Hamby RI, Hoffman I, Hilsenrath J, et al: Clinical, hemodynamic and angiographic aspects of inferior and anterior myocardial infarctions in patients with angina pectoris. Am J Cardiol 34:513, 1974. Miller RR, Amsterdam EZ, Bogren HG, et al: Electrocardiographic, and cineangiographic correlations in assessment of the location, nature and extent of abnormal left ventricular segmental contraction in coronary artery disease. Circulation 49~447, 1974. Rios JC, Sinderson TH, Goldberg S: Electrocardiographicangiographic correlations in coronary heart disease. In Rios JC, editor: Clinical electrocardiographic correlations. Cardiovascular Clinics 8/3. Philadelphia, 1977, F. A. Davis Co, p. 111. Helfant RM, Bodenheimer MM, Banka VSL: Asynergy in coronary heart disease. Evolving clinical and pathophysiologic concepts. Ann Intern Med 87:475, 1977. Myers GB, Klein HA, Stofer BE: I. Correlation of electrocardiographic and pathophysiologic findings in anteroseptal infarction. AM HEART J 36:535, 1948. Myers GB, Klein HA, Hiratzka T: II. Correlation of electrocardiographic and pathologic findings in large anteroseptal infarcts. AM HEART J 36:838, 1948. Burch GE, Horan LG, Ziskind J, et al: A correlative study of postmortem, electrocardiographic, and spatial vectorcardiographic data in myocardial infarction. Circulation 18:325, 1958.
14. Horan LG, Flowers NC, Johnson JC: Significance of the diagnostic Q-wave of myocardial infarction. Circulation 43:428, 1971. 15. Gottlieb RS, Duca PR, Kasparian H, et al: Correlation of abnormal Q-waves, coronary pathology, and ventricular contractility. AM HEART J 90:451, 1975. 16. Zaret BL, Strauss HW, Hurley PJ, et al: A noninvasive scintiphotographic method for detecting regional ventricular dysfunction in man. N Engl J Med 284:1165, 1971. 17. Strauss HW, Pitt B: Gated cardiac blood pool scan: Use in patients with coronary heart disease. Prog Cardiovasc Dis 20:207, 1977. 18. Strauss HW, Pitt B: Evaluation of cardiac function and structure with radioactive tracer techniques. Circulation 57:645, 1978. 19. Tullough GA: The electrocardiographic features of high posterolateral infarction. Br Heart J 14:379, 1952. 20. Forrester JS, Diamond GA, Swan HJC: Correlative classification of clinical and hemodynamic function after acute myocardial infarction. Am J Cardiol 39:137, 1977. 21. Maddahi J, Berman DS, Diamond GA, et al: Evaluation of left ventricular ejection fraction and segmental wall motion by multiple gate equilibrium cardiac blood pool scintigraphy. in Cady L, editor: Computer techniques in cardiology. Marcel Dekker, Publisher (In press) 22. Smith FM: The ligation of coronary arteries with electrocardiographic study. Arch Intern Med 22:8, 1918. 23. Pardee HEB: An electrocardiographic sign of coronary artery obstruction. Arch Intern Med 26:244. 1920. 24. Wyatt HL, Forrester JS, da Luz PL, et al: Functional abnormalities in nonoccluded regions of myocardium after experimental coronary artery occlusion. Am J Cardiol37:366, 1976. 25. Mathes P, Sack DW, Romig D, et al: Kontraktilitaet des ueberlebenden Herzmuskels nach experimentellem Infarkt. Z Kardiol 64:503, 1975. 26. Holzmann M: Klinische Elektrokardiographie. StuttgartNew York, 1965, Georz Thieme Verlaa. n 441. 27. Schamroth L: The electrocardiographic diagnosis of acute myocardial infarction. In Meltzer LE, Dunning AJ, editors:
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Textbook of coronary care. Philadelphia, 1972, The Charles Press, pp 61-81. Holland RP, Brooks H: TQ-ST segment mapping: Critical review and analysis of current concepts. Am J Cardiol40:110, 1977. Holman BL, Lesch M, Alpert JS: Myocardial scintigraphy with ‘++“technetium pyrophosphate during the early phase of acute infarction. Am J Cardiol 41:39, 1978. Wackers FJ, Sokole EB, Samson G, et al: Value and limitations of thallium-201 scintigraphy in the acute phase of mvocardial infarction. N Enrrl J Med 295:l. 1976. R&se1 JR, Hunt RO, Rackley CE: Left ventricular hemodynamics in anterior and inferior myocardial infarction. Am J Cardiol 32:8, 1973. Bodenheimer MM, Banka VS, Helfant RH: Q-waves and ventricular asynergy. Predictive value and hemodynamic significance of anatomic location. Am J Cardiol 35:615, 1975. Ratshin RA, Massing GK, James TN: The clinical signifi-
The effect of early exercise infarct scar formation
34.
35.
36.
37.
and reciprocal
ST depression
in AMI
cance of the location of acute myocardial infarction. In Corday E, Swan HJC, editors: Myocardial infarction. Baltimore, 1973, The Williams & Wilkins Co, p 77. Miller RR, Olson HG, Vismara LA, et al: Pump dysfunction after myocardial infarction: Importance of location, extent, and pattern of abnormal left ventricular segmental contraction. Am J Cardiol 37:340, 1976. Forrester JS, Diamond GA, Chatterjee K, et al: Medical therapy of acute myocardial infarction by application of hemodynamic subsets. N Engl J Med 295:1356, and 1404, 1976. Forrester JS, Waters DD: Hospital treatment of congestive heart failure. Management according to hemodynamic profile. Am J Med 65:173, 1978. Shah PK, Pichler M, Berman DS, Maddahi J, Peter T, Singh BN, Swan HJC: Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction. Am J Cardiol 46:915, 1980.
on myocardial
The purpose of this study was to determine if exercise undertaken during the phase of incomplete healing after myocardial infarction influences scar formation. Eighteen ether-anesthetized rats underwent coronary artery occlusion (CAO) and were paired by matching ECG infarct size as assessed by QRS morphology. One member of each pair was randomized to a nonswimming group (NoS) or a graded swimming (S) protocol group (up to 40 minutes of swimming per day) beginning 7 days after CAO. Twenty-one days after CAO, rats were reanesthetized, hearts were excised and examined under magnification, and were then sectioned for histology. Transmural scar thickness (mm) measured on gross pathologic specimens was thinner in the S rats (1.0 + 0.2, p < 0.05) than in the NoS rats (1.4 f 0.3, p < O-05), while noninfarcted septal wall thickness (mm) was similar in the two groups (2.2 f 0.1 versus 2.1 + 0.1, respectively). The thinnest portion of the scar in S rats measured only 0.6 ? 0.2 mm compared to that of NoS rats (1.1 ? 0.3 mm, p < 0.05). In this experiment exercise during the healing phase of acute myocardial infarction (AH) caused thinning of the transmural scar. (AM HEART J 106:1009, 1983.)
Robert
A. Kloner,
M.D., Ph.D., and Judith
A. Kloner,
Over the past decade there has been interest in the determinants of irreversible myocardial cell injury during the early phase of acute myocardial infarction. There is considerably less known about the later phases of infarction, including the determiFrom the Department of Medicine, Harvard Medical School; and Boston Beth Israel Hospital. Supported in part by Heart, Lung and Blood Received accepted Reprint Longwood
for publication Jan. 21, 1983.
Ischemia Institute, Oct.
Brigham
University
and
SCOR grant 26215 Bethesda, Md. 5, 1981;
requests: Robert A. Kloner, Ave., Room 235, Boston,
revision
M.D., Harvard MA 02115.
Women’s
Hospital,
School of Nursing from
received Medical
the July
and
National 13, 1982;
School,
180
R.N., MS. Boston, Muss.
nants of myocardial infarct scar formation. Specifically, it is unknown whether early exercise following myocardial infarction can affect the formation and topographic configuration of the infarct scar. The purpose of this study was to determine if exercise undertaken during the period of incomplete healing post myocardial infarction influences scar formation. A rat model of experimental myocardial infarction was used, since the healing phase ,of infarction has been well characterized in this mode11v2 and qualitatively the rat model has many similarities to man. It is known that in this model healing and scar formation is complete by 3 weeks after coronary artery occlusion (CAO).lm3 1009
of
Left ventricular ejection fraction and regional wall motion were assessed by multigated equilibrium radionuclide ventriculography within 24 hours of onset of first acute transmural myocardial infarction (Ml) in 32 patients. Abnormal left ventricular wall motion was noted in all 16 patients with anterior infarction and in 14 of 16 (87.5%) patients with inferior infarction. Regional wall motion abnormalities frequently included areas adjacent to and remote from those predicted by the ECG location of ST elevation and pathologic 0 waves. Such remote wall motion abnormalities were associated with reciprocal ST segment depression in 17 of 18 (94%) patients, and conversely reciprocal ST segment depressions were associated with remote wall motion abnormalities in 17 of 24 (71%) patients. The left ventricular ejection fraction was lower in patients with a reciprocal ST segment depression compared to those without (anterior MI 0.29 +- 0.07 vs 0.43 f 0.08, p < 0.01; inferior MI 0.45 + 0.11 vs 0.63 ? 0.06, p < 0.001). In addition, the peak MB-CK levels were higher in patients with compared to those without reciprocal ST segment depression (anterior MI 268 f 183 vs 102 + 60, p < 0.05; inferior MI 186 f 120 vs 67 f 20, p < 0.05). Thirteen of 18 (72%) patients with reciprocal ST segment depression compared to 4 of 13 (31%) patients without reciprocal ST segment depression had a complicated clinical course during their hospital stay. These observation suggest that global left ventricular dysfunction in first acute transmural Ml is greater when reciprocal ST segment depression is present on the 12-lead ECG. Such reciprocal changes are frequently associated with enzymatic evidence of larger infarction, regional left ventricular dysfunction extending to segments remote from the ECG predicted site of transmural infarction, and an unfavorable clinical course. (AM HEART J 106:1003, 1983.)
Max Pichler, M.D., Prediman K. Shah, M.D., Thomas Peter, M.D., Bramah Singh, M.D., Ph.D., Daniel Berman, M.D., Frank Shellock, and H. J. C. Swan, M.D., Ph.D. Los Angeles, Calif.
Evolving ST segment elevation and the appearance of new Q waves, the conventional criteria for the diagnosis of acute transmural myocardial infarction, are widely accepted as being indicative of both the location’~ 2 and the extent of acute necrosis.3-5 This view is based, however, on information gathered from contrast ventriculography6-lo or autopsy”-l5 performed after delay of days or months after the From the Division of Cardiology, and the Departments of Medicine and Nuclear Medicine, Cedars-Sinai Medical Center; and the UCLA School of Medicine. Supported by a Max Kade Postdoctoral Research Exchange Grant (Dr. Pichler) from Vienna, Austria. Received for publication Apr. 30, 1982; accepted June 19, 1982. Reprint requests: Prediman K. Shah, M.D., Director, Inpatient Cardiology and Cardiac Care Unit, Room 5314, Cardiology Division, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA 90048.
M.S.,
acute event. For this reason, only limited data are available concerning the relationship between the ECG location of acute infarction and its associated functional correlate, i.e., the regional wall motion abnormality. The recent development of radionuclide ventriculography’6-18 has made it possible to evaluate left ventricular wall motion at the bedside of the acutely ill patient during the early phases of acute myocardial infarction. The purpose of this study was therefore (1) to compare the site, extent, and severity of left ventricular segmental dysfunction to the location and extent of myocardial infarction as gauged by conventional ECG criteria within 24 hours of infarction and (2) to determine the functional significance of “reciprocal” ST segment depression associated with acute myocardial infarction (AMI).
1004
WALL
Pichler
et al.
American
LV SEGMENT
MOTION SCORF
4
Table 1.Assignmentof regional LV wall motion abnormal-
ity
6 z Normal 5 * ny;;*i
0
3
* Akinefi: 2 ~Dyskinetic (Mild) I =Dytkinetic ~SOUd
to
ECG site of infarction
ECG site infarction
‘ H@i&
of
LV wall segment(s) assigned
Anteroseptal ANTERIOR
@I; lwm~;plerol
45’L80
3 6, 1 2 3 4 5 3 8,
Anterolateral
(31; I-tfekapicol
TOTAL WALL
MOTION SCORE=
Sum of score of individual
segments
November, 1983 Heart Journal
Inferior
1. Semiquantitative assessmentof segmental LV wall motion by ggmTcRBC blood pool scintigraphy. The left ventricle is divided into 10 segmentslisted on the right of the figure. Each segment is assigneda score for wall motion listed on the left of the figure. The values are the consensusof two independent and expert observers. Fig.
(anteroapical) 7 (proximal and distal (anterobasal) (anterolateral) (anteroapical) (distal-inferior) (proximal-inferior) (inferoapical) 9 (proximal and distal posterolateral)
septal)
II. ECG site of infarction and regional wall motion abnormality Table METHODS AMI criteria.
The data on 32 consecutive patients (24 males,8 females) admitted to the coronary care unit with a first acute transmural myocardial infarction and evaluated within 24 hours of the onsret of symptoms were reviewed. The mean age was 59 years, ranging from 32 to 82 years. The criteria used for the diagnosis of acute myocardial infarction were the combined presenceof (1) a history of sustained (>30 minutes) substernal chest pain, (2) an unequivocal elevation of serum creatine kinase isoenzyme MB (CK-MB), and (3) typical acute ischemic evolutionary changesin the ECG. Transmural myocardial infarction was diagnosedby ST segmentelevation of ~1 mm, associated with newly evolving Q waves (~0.03 secondduration) in at least two of the 12 leads and was categorized into anteroseptal (leadsV, to V,), anterolateral (leadsV, to V6, I, and aVL), and inferior (leads II, III, and aVr) infarction. Reciprocal ST depression. “Reciprocal” ST segment depressionwasdefined ashorizontal ST depressionof ~1 mm in at least two out of four precordial leadsV, to V, in patients with inferior infarction, and in at least two of the three inferior leads II, III, and aV, in patients with anteroseptal and/or anterolateral myocardial infarction. Patients. None of the patients included in this study had any of the following features: (1) documented previous myocardial infarction, (2) QRS duration >120 msec, (3) atrial fibrillation, (4) ECG evidence of left ventricular hypertrophy, (5) valvular heart diseaseor cardiomyopathy, (6) ECG signsof true posterior infarction,20 and (7) none were on cardioactive medication at the time of initial evaluation. The patients were treated conventionally with oxygen and if necessarywith morphine for pain, and with lidoCaine for ventricular arrhythmias. The patients who demonstrated clear clinical and radiologic evidence of pulmonary congestion and/or objective evidence of peripheral hypoperfusion (according to rigorous clinical criteria previously described from this department?Owere designated as “clinically complicated.” A 12-lead ECG
Anteroseptal and/or anterolateral MI (n = 16) Correspondence between ECG site of MI with the segments of greatest depression of wall motion No. of patients showing severest wall motion abnormality Limited to 1 segment 2 segments 3 or more segments MI = myocardial
Inferior MI (n = 16)
16116
14116
2 9 5
9 4 1
infarction.
wasobtained within 1 hour of radionuclide ventriculography and daily thereafter for 3 days. All tracings were read by one cardiologist (T.P.) not aware of the patient’s clinical diagnosis. Assessment of left ventricular function. Radionuclide ventriculography was performed in all patients within 24 ‘hoursof onset of symptomsusing in vitro technetium-99m labeled autologous red blood ce11s.17,21 Multipleigated equilibrium blood pool imaging was performed using a mobile gamma camera (Ohio Nuclear, Sigma 420) equipped with a low-energy, all-purpose collimator and a mobile computer (Technicare). Left ventricular regionsof interest in end diastole and end systole were assigned using a light pen and a left paraventricular background was selected in end systole. Left ventricular ejection fraction was derived from the quotient of backgroundcorrected stroke counts and end-diastolic counts. For visual assessment of regional left ventricular wall motion, the scintigraphic data were displayed in a flicker-free closed loop movie format and each of 10 left ventricular segmentswas assigneda score according to the format shown in Fig. 1. In those patients, in Whom inferior wall motion could not be properly assessedbecauseof right
Volume Number
106 5, Part 1
Wall motion
and reciprocal
ST depression
in AMI
1005
III. Location of segmentswith the most depressedwall motion in patients with various ECG locations of myocardial infarction*
Table
Segments * Anterobasal 1
ECG Anteroseptal (n = 6)t 14 segments* Anterolateral (n = 4)t 10 segments* Anteroseptal and anterolateral (n = 6)t 17 segments* Inferior (n = 16)t 20 segments* *One
tNo.
or more segments of patients.
may be equally
Anterolateral 2
Apical 3
Septal 6
Inferoapical 7
Distal inferior 4
3
5 3
3 2
4 1
2 1
3 2
5 3
2 7
5 6
2 1
Proximal inferior 5
Posterolateral 8
Distal proximal 9
1
reduced.
ventricular overlap in the anterior view, a 70% left anterior oblique view image was also obtained to clearly determine the pattern of wall motion of inferior segments. All scintigraphic data were analyzed in the division of nuclear cardiology without knowledge of clinical status of the patient. This technique of determination of left ventricular ejection fraction and regional wall motion has been validated before and is described in detail elsewhere.‘?.*I For comparison of regional wall motion abnormalities and the location of the ECG abnormality, the 10 segments of the left ventricle were assignedto corresponding ECG leads, as shown in Table I. Scintigraphic and ECG data were analyzed to separately determine the relationship betweenleft ventricular (LV) regional wall motion and the ECG location of transmural infarction (ST elevation, new Q waves), as well as “reciprocal” ST segment depressions. Statistical analysis. The unpaired t test and chi square test were usedfor comparative statistical analysisto assess differences between groups of non-paired data. A p value ~0.05 was defined as significant. RESULTS
Sixteen patients had anterior myocardial infarction (six anteroseptal, four anterolateral, six both anteroseptal and anterolateral) and 16 patients had inferior infarction. ECG localization and regional and global LV dysfunction. Thirty of 32 patients (94%) had scintigraphic
wail motion abnormalities that corresponded to the ECG location of infarction. The two patients without scintigraphic abnormalities both had ECG evidence of inferior myocardial infarction (Table II). In every case, the scintigraphic region exhibiting the most severe wall motion abnormality corresponded to that predicated from the ECG (Table III). Thus in the six patients with ECG abnormalities of anteroseptal infarction, the greatest depression of wall motion was distributed as tabulated in line 1 of Table III. Both the severity and extent of regional
wall motion abnormality, however, were most severe in anterior myocardial infarction. Thus in anterior infarction severe wall motion abnormality (severe hypokinesis, akinesis, or dyskinesis) were observed in two segments in 9 .of 16 patients and in three or more segments in 5 of 16 patients, whereas only two patients had severe wall motion abnormality limited to a single segment. In contrast, in patients with inferior myocardial infarction, the most severe wall motion abnormality was limited to a single segment in nine patients and involved two segments in four patients and three or more segments in only one patient. Ejection fraction was depressed below the lower limits of normal (<0.54) in all but one patient (94 % ) with anterior myocardial infarction, averaging 0.35 + 0.10, whereas a depressed ejection fraction was observed in only 9 of 16 patients (56%) with inferior infarction, averaging 0.53 +- 0.13. The difference in average ejection fraction between anterior and inferior infarction was highly significant (p < 0.092). Clinical complications of pump failure were more prevalent in patients with anterior myocardial infarction. Twelve of the 16 (75%) patients with anterior infarction demonstrated clear-cut “clinical” signs of heart failure compared to only 5 out of 16 (31%) with inferior infarction (p < 0.02). There was therefore a significant tendency for patients with anterior infarction to demonstrate a greater degree of hemodynamic and functional impairment. The observed depression in regional left ventricular function correlated well with ejection fraction (Fig. 2). Thus the mean ejection fraction in patients without an akinetic or dyskinetic segment was 0.59 ? 0.08, which was significantly (p < 0.001) higher than the corresponding mean value of 0.36 + 0.11 in patients with one or more akinetic or dyskinetic segments.
November,
1006
Pichler et al.
EF (o/o)
American
0
70
50
Heart
1983 Journal
changes (0.45 + 0.11 versus 0.63 f 0.06, p < 0.001) (Table V). Peak MB-CK isoenrymes. The higher peak MB-CK levels in patients with reciprocal ST depression compared to those without reciprocal changes (anterior infarction: 268 + 183 vs 102 + 60 IU/L, p < 0.05; inferior infarction 186 + 120 vs 67 + 20 IU/L, p < 0.05) suggested greater extent of myocardial necrosis in the former. DISCUSSION
Since the classical work of Smith22 and Pardee, the ECG has been the basis of clinical detection and localization of AMI. Our study confirms these observations but adds new information regarding the interrelationship of the location, extent, and severity of segmental wall motion abnormalities and the ECG site of infarction as designated by 12-lead ECG. Specifically, 94% of the patients in this study demonstrated wall motion abnormalities in the area defined by ECG abnormalities.
30
IO WITH
WITHOUT
AKINETIC or DYSKINETIC SEGMENTS Fig. 2. LV ejection fraction in patients with and without one or more akinetic (grade 0) or dyskinetic (grade 1) LV segments. M + SD = mean + 1 standard deviation for each group.
Wall motion its association
abnormality in remote LV segments and with reciprocal ST segment depression.
Twenty-four of the 32 patients (75% ) had wall motion abnormalities in LV segments adjacent to or remote from those predicted by the ECG location of infarction (Table IV). Of the 15 patients with anterior infarction and remote wall motion abnormalities, nine had associated reciprocal ST segment depression. Thus in 17 of 24 patients (71%), remote wall motion abnormalities were associated with reciprocal ECG abnormalities. Conversely, 17 out of 18 patients (95%) with reciprocal ECG changes had wall motion abnormalities remote from the area indicated by conventional criteria of infarction. The left ventricular ejection fraction (LVEF) was significantly lower in patients with anterior infarction and concomitant reciprocal ST segment depression than in those without reciprocal ST segment depression (0.29 -+ 0.07 vs 0.43 + 0.08, p < 0.01). Similarly, patients with inferior infarction and reciprocal ST segment depression had a significantly lower ejection fraction than those without reciprocal
Extent reciprocal
and location of wall motion ECG changes. Although
abnormality
and
the location of dysfunction detected by the two techniques corresponded closely, the extent did not. LV wall motion abnormalities clearly involved regions other than those indicated by the ECG in 94% (15 of 16) of patients with anterior and in 56% (9 of 16) of patients with inferior infarction. This discrepancy between ECG extent of infarction and the extent of regional mechanical dysfunction determined by scintigraphy is consistent with animal studies which suggest that the area of AM1 is often surrounded by an even larger dysfunctional ischemic zone. Indeed, Wyatt et a1.24 and Mathes et al.% both found “remote” depression of regional function following acute coronary occlusion in areas served by other patent coronary arteries. In our study, 75% (24 of 32) of all patients exhibited such remote wall motion abnormalities, and 71% (17 of 24) of these had associated ECG ST segment depression. These observations suggest that the interpretation of reciprocal ST segment depression in AM126,27 requires reappraisal. In the absence of such remote regional dysfunction, reciprocal ECG changes were not seen. Since 94% of the patients with reciprocal changes had associated wall motion abnormalities, the concept that reciprocal ST segment depression is purely a vectorial ECG phenomenon and therefore of little clinical relevance must be questioned. On the contrary, our data suggest that the presence of ECG abnormalities in reciprocal ECG leads implies a concomitant depression of regional wall motion in the corresponding LV segments. Similarly, since the
Volume Number
106 5, Part 1
Table
Wall
and
reciprocal
ST
depression
in
AMI
1007
IV. Reciprocal ST segment depressionand remote wall motion abnormalities in 32 patients with AM1 Anteroseptal
and/or
anterolateral
Present
ST depression
= wall
motion
(n = 16)
AM1
No 0 = acute
Absent
9
Yes 6
myocardial
(n = 16)
Present
7
Yes 9 abnormality;
Inferior
Absent
9
Remote WMA WMA
motion
No 1
Yes 8
7 No 1
Yes 1
No 6
infarction.
V. Presenceor absenceof reciprocal ST segmentdepressionand parameters of infarct size, global LV function, and clinical classification Table
Reciprocal ST depression
Anteroseptal
and anterolateral
No. of patients
Yes
Inferior
9
No
7
Yes
9
No
= creatine 2 SD.
peak (IUIL)
Mean+
LVEF
268 (+- 183) 102 (k60) 186 (?I 120)
( * 0.07) 0.43 ( 2 0.08) 0.45
(CO,
0.63 ( zt 0.06)
I
Total CK-MB *Mean
Mean* CK-MB
0.29
No. of patients with complications 8
4 5
(kO.11)
0
32 kinase
isoenzyme
MB;
LVEF
= left ventricular
ejection
location and extent of regional dysfunction are related to the global LV performance, reciprocal ST segment changes are indirectly indicative of lower levels of ejection fraction and consequently of the presence of clinical heart failure. Electrophysiologic correlates of ST segment alterations. The ST segment deviations during acute myo-
cardial ischemia are primarily dependent on the extracellular accumulation of potassium and the consequent transmembrane gradient across the border between ischemic and nonischemic tissue. Both spatial factors (size and shape of ischemic area, electrode position) and nonspatial factors (electrolytes, antiarrhythmic agents, heart rate) alter this gradient. 28 During systole, current flows from the ischemic to the normal tissue and the converse occurs in diastole. Thus ST segment deviations in acute ischemia or infarction depict the sum of ST segment elevation and the ST segment depression, or vice versa. In unipolar precordial recordings, the ST deflections mainly depend upon the interrelationship between the position of the recording electrode and the geometry of the ischemic area and its boundaries. Thus though the ST segment depression seen in right precordial leads in patients with inferior infarction is conventionally regarded as presenting mirror images or reciprocal changes,26p27
fraction
the logic of solid angle theory** suggests that all patients with inferior myocardial infarction should exhibit reciprocal ST segment depressions anteriorly, since the recording electrode will have similar spatial relationship with the site and size of inferior infarction. It could be argued that precordial ST segment depression is a reflection of the wider solid angle as a result of larger ischemic involvement of the inferior epicardial surface area in such patients. This viewpoint is partly supported by a higher peak creatine kinase isoenzyme MB value in patients with reciprocal ST segment depression compared to those without. Further research should be directed to resolve the questions whether higher creatine kinase isoenzyme MB levels reflect large inferior infarct or additional infarction extending into remote LV segments. Technetium-99m pyrophosphate29 and/or thallium-201 scintigraphy30 in the acute phase may be helpful in this regard. Even if one accepts the theory that reciprocal ST segment depressions only indicate large infarcts, the observation that 94% of these patients in our study had remote wall motion abnormalities favors the possibility that the function of the remote segments is indeed compromised from ischemia or infarction or some other as yet unidentified mechanism.
November,
1008
Pichler et al.
Disordered global cardiac performance was more frequent and more severe in anterior myocardial infarction. This observation is consistent with previous hemodynamic studies,31-33 but the data in the present study support the conclusion that a major determinant of the level of LV function in the acute phase of infarction is the extent and magnitude of disordered regional function, rather than the site of infarction itself. This concept is supported by the findings of Miller et a1.,34 who observed no differences in LV wall motion abnormality, regardless of its location. Clinical implications. Previous studies from this laboratory have demonstrated that patients with AM1 may be divided into specific clinica120 and hemodynamic35 subsets which exhibit major differences in their mortality and their response to therapy.36 The data in this study further suggest that scintigraphic analysis of mechanical LV dysfunction provides more precise definition of the magnitude of functional impairment within these subsets and may thereby allow a more rational selection of appropriate therapeutic interventions. Conclusions. Although there is close correlation between the regional ECG and functional manifestation of ischemia, important differences of clinical relevance also exist. Segmental wall motion abnormalities are frequently more extensive than ECG abnormalities suggest, and may occur in areas apparently remote from the putatively infarcted zone.37 The presence of such a remote area of regional dysfunction is suggested by reciprocal ST segment depression. Although the therapeutic significance of these relationships remains to be determined, it is likely that important prognostic and therapeutic subsets may emerge from such investigations. The authors gratefully acknowledge the assistance of Beverly Yoshioka, Lilian Solomon, Joye Nunn, and Lance Laforteza in the preparation of this manuscript. REFERENCES
1. The Criteria Committee of the New York Heart Association: Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. Boston, 1973, Little, Brown & Co, pp 95-123. 2. Working Group on Ischemic Heart Disease Registers, World Health Organization: Report Euro 8201 (5). Copenhagen, 1971, WHO Regional Office for Europe. 3. Madias JE: Use of precordial ST-segment mapping. AM HEART J 95:96, 1978. 4. Savage RM, Wagner GS, Ideker RE, et al: Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction. Circulation 55:279, 1977. 5. Selvester RH, Wagner JO, Rubin HB: Quantitation of myocardial infarct size and location by electrocardiogram and vector cardiogram. In Snellen HA, editor: Boerhave course in
American
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7.
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13.
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quantitation in cardiology. Leyden, 1972, Leyden University Press, p 32. Williams RA, Cohn PF, Vokanas PS, et al: Electrocardiographic, arteriographic and ventriculographic correlations in transmural myocardial infarction. Am J Cardiol 31:595, 1973. Hamby RI, Hoffman I, Hilsenrath J, et al: Clinical, hemodynamic and angiographic aspects of inferior and anterior myocardial infarctions in patients with angina pectoris. Am J Cardiol 34:513, 1974. Miller RR, Amsterdam EZ, Bogren HG, et al: Electrocardiographic, and cineangiographic correlations in assessment of the location, nature and extent of abnormal left ventricular segmental contraction in coronary artery disease. Circulation 49~447, 1974. Rios JC, Sinderson TH, Goldberg S: Electrocardiographicangiographic correlations in coronary heart disease. In Rios JC, editor: Clinical electrocardiographic correlations. Cardiovascular Clinics 8/3. Philadelphia, 1977, F. A. Davis Co, p. 111. Helfant RM, Bodenheimer MM, Banka VSL: Asynergy in coronary heart disease. Evolving clinical and pathophysiologic concepts. Ann Intern Med 87:475, 1977. Myers GB, Klein HA, Stofer BE: I. Correlation of electrocardiographic and pathophysiologic findings in anteroseptal infarction. AM HEART J 36:535, 1948. Myers GB, Klein HA, Hiratzka T: II. Correlation of electrocardiographic and pathologic findings in large anteroseptal infarcts. AM HEART J 36:838, 1948. Burch GE, Horan LG, Ziskind J, et al: A correlative study of postmortem, electrocardiographic, and spatial vectorcardiographic data in myocardial infarction. Circulation 18:325, 1958.
14. Horan LG, Flowers NC, Johnson JC: Significance of the diagnostic Q-wave of myocardial infarction. Circulation 43:428, 1971. 15. Gottlieb RS, Duca PR, Kasparian H, et al: Correlation of abnormal Q-waves, coronary pathology, and ventricular contractility. AM HEART J 90:451, 1975. 16. Zaret BL, Strauss HW, Hurley PJ, et al: A noninvasive scintiphotographic method for detecting regional ventricular dysfunction in man. N Engl J Med 284:1165, 1971. 17. Strauss HW, Pitt B: Gated cardiac blood pool scan: Use in patients with coronary heart disease. Prog Cardiovasc Dis 20:207, 1977. 18. Strauss HW, Pitt B: Evaluation of cardiac function and structure with radioactive tracer techniques. Circulation 57:645, 1978. 19. Tullough GA: The electrocardiographic features of high posterolateral infarction. Br Heart J 14:379, 1952. 20. Forrester JS, Diamond GA, Swan HJC: Correlative classification of clinical and hemodynamic function after acute myocardial infarction. Am J Cardiol 39:137, 1977. 21. Maddahi J, Berman DS, Diamond GA, et al: Evaluation of left ventricular ejection fraction and segmental wall motion by multiple gate equilibrium cardiac blood pool scintigraphy. in Cady L, editor: Computer techniques in cardiology. Marcel Dekker, Publisher (In press) 22. Smith FM: The ligation of coronary arteries with electrocardiographic study. Arch Intern Med 22:8, 1918. 23. Pardee HEB: An electrocardiographic sign of coronary artery obstruction. Arch Intern Med 26:244. 1920. 24. Wyatt HL, Forrester JS, da Luz PL, et al: Functional abnormalities in nonoccluded regions of myocardium after experimental coronary artery occlusion. Am J Cardiol37:366, 1976. 25. Mathes P, Sack DW, Romig D, et al: Kontraktilitaet des ueberlebenden Herzmuskels nach experimentellem Infarkt. Z Kardiol 64:503, 1975. 26. Holzmann M: Klinische Elektrokardiographie. StuttgartNew York, 1965, Georz Thieme Verlaa. n 441. 27. Schamroth L: The electrocardiographic diagnosis of acute myocardial infarction. In Meltzer LE, Dunning AJ, editors:
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28.
29.
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31.
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33.
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Textbook of coronary care. Philadelphia, 1972, The Charles Press, pp 61-81. Holland RP, Brooks H: TQ-ST segment mapping: Critical review and analysis of current concepts. Am J Cardiol40:110, 1977. Holman BL, Lesch M, Alpert JS: Myocardial scintigraphy with ‘++“technetium pyrophosphate during the early phase of acute infarction. Am J Cardiol 41:39, 1978. Wackers FJ, Sokole EB, Samson G, et al: Value and limitations of thallium-201 scintigraphy in the acute phase of mvocardial infarction. N Enrrl J Med 295:l. 1976. R&se1 JR, Hunt RO, Rackley CE: Left ventricular hemodynamics in anterior and inferior myocardial infarction. Am J Cardiol 32:8, 1973. Bodenheimer MM, Banka VS, Helfant RH: Q-waves and ventricular asynergy. Predictive value and hemodynamic significance of anatomic location. Am J Cardiol 35:615, 1975. Ratshin RA, Massing GK, James TN: The clinical signifi-
The effect of early exercise infarct scar formation
34.
35.
36.
37.
and reciprocal
ST depression
in AMI
cance of the location of acute myocardial infarction. In Corday E, Swan HJC, editors: Myocardial infarction. Baltimore, 1973, The Williams & Wilkins Co, p 77. Miller RR, Olson HG, Vismara LA, et al: Pump dysfunction after myocardial infarction: Importance of location, extent, and pattern of abnormal left ventricular segmental contraction. Am J Cardiol 37:340, 1976. Forrester JS, Diamond GA, Chatterjee K, et al: Medical therapy of acute myocardial infarction by application of hemodynamic subsets. N Engl J Med 295:1356, and 1404, 1976. Forrester JS, Waters DD: Hospital treatment of congestive heart failure. Management according to hemodynamic profile. Am J Med 65:173, 1978. Shah PK, Pichler M, Berman DS, Maddahi J, Peter T, Singh BN, Swan HJC: Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction. Am J Cardiol 46:915, 1980.
on myocardial
The purpose of this study was to determine if exercise undertaken during the phase of incomplete healing after myocardial infarction influences scar formation. Eighteen ether-anesthetized rats underwent coronary artery occlusion (CAO) and were paired by matching ECG infarct size as assessed by QRS morphology. One member of each pair was randomized to a nonswimming group (NoS) or a graded swimming (S) protocol group (up to 40 minutes of swimming per day) beginning 7 days after CAO. Twenty-one days after CAO, rats were reanesthetized, hearts were excised and examined under magnification, and were then sectioned for histology. Transmural scar thickness (mm) measured on gross pathologic specimens was thinner in the S rats (1.0 + 0.2, p < 0.05) than in the NoS rats (1.4 f 0.3, p < O-05), while noninfarcted septal wall thickness (mm) was similar in the two groups (2.2 f 0.1 versus 2.1 + 0.1, respectively). The thinnest portion of the scar in S rats measured only 0.6 ? 0.2 mm compared to that of NoS rats (1.1 ? 0.3 mm, p < 0.05). In this experiment exercise during the healing phase of acute myocardial infarction (AH) caused thinning of the transmural scar. (AM HEART J 106:1009, 1983.)
Robert
A. Kloner,
M.D., Ph.D., and Judith
A. Kloner,
Over the past decade there has been interest in the determinants of irreversible myocardial cell injury during the early phase of acute myocardial infarction. There is considerably less known about the later phases of infarction, including the determiFrom the Department of Medicine, Harvard Medical School; and Boston Beth Israel Hospital. Supported in part by Heart, Lung and Blood Received accepted Reprint Longwood
for publication Jan. 21, 1983.
Ischemia Institute, Oct.
Brigham
University
and
SCOR grant 26215 Bethesda, Md. 5, 1981;
requests: Robert A. Kloner, Ave., Room 235, Boston,
revision
M.D., Harvard MA 02115.
Women’s
Hospital,
School of Nursing from
received Medical
the July
and
National 13, 1982;
School,
180
R.N., MS. Boston, Muss.
nants of myocardial infarct scar formation. Specifically, it is unknown whether early exercise following myocardial infarction can affect the formation and topographic configuration of the infarct scar. The purpose of this study was to determine if exercise undertaken during the period of incomplete healing post myocardial infarction influences scar formation. A rat model of experimental myocardial infarction was used, since the healing phase ,of infarction has been well characterized in this mode11v2 and qualitatively the rat model has many similarities to man. It is known that in this model healing and scar formation is complete by 3 weeks after coronary artery occlusion (CAO).lm3 1009