Natural course of the S-T segment and QRS complex in patients with acute anterior myocardial infarction

Natural Course of the S-T Segment and QRS Complex in Patients With Acute Anterior Myocardial Infarction

RONALD W. ZMYSLINSKI, MD* TOSHIO AKIYAMA, MD THEODORE L. BIDDLE, MD, FACC PRAVIN M. SHAH, MD, FACC+ Rochester, New York

From the Cardiology Unit, Deipartment of Medicine, University of Rochester Medical Center and Strong Memorial Hospital, Rochester, New York. This study was supported in part by a Research Fellowship Grant from the Genesee Valley Heart Association, Rochester, New York and by Grant HL 05500 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Manuscript received June 6, 1976; revised manuscript received Aulgust 4, 1976, accepted August 16, 1976. t Present address: Cardiology Division, Wadsworth Veterans Administration Hospital, Los Angeles, California. ’ Present address and addlress for reprints: Ronald W. Zmyslinski, MD, University of South Carolina School of Medicine, Veterans Administration Hospital Enclave, Columbia, South Carolina 29201.

Sums of the S-T segment elevation from the 35 lead precordial electrocardiographic map (ZSTss) and standard 6 lead precordial electrocardiogram (ZST6) were obtained from 20 patlents after acute anterior myocardial infarction and the calculations repeated 2, 4, 12, 24, 46, 72 and 240 hours later. Q and R wave areas were summed (ZQas, ZQs, ZRs5 and ZRrJ. EST35 and ZSTe values decreased significantly in patients without pericarditis 7 to 12 hours after the onset of symptoms (P <0.02), but increased significantly from these reduced values 25 to 46 hours after the onset of symptoms. An increase in L1STs5and ZSTa (P <0.05) occurred 13 to 24 hours after the onset of symptoms in four patients with pericarditis before a pericardial rub was heard. No significant change in ZQas occurred from the initial to the final map study; a decrease in Z:Rs5 (P <0.02) occurred only in a group of patients studied at or before 5 hours after initial symptoms. No correlation was found between the initial level of S-T segment elevation and subsequent change In Q or R wave areas except in two patients whose initial electrocardiographic studies were performed at or within 5 hours of initial symptoms. Good correlation was found between EST& and ZSTs (r = i-0.906, P
Under controlled experimental conditions, the degree of ischemic myocardial damage after acute coronary arterial ligation has been reported to correlate with the sum of S-T segment elevation (ZST) obtained with epicardial and precordial electrocardiographic mapping techniques.1-3 Furthermore, interventions designed to alter the extent of the ischemic myocardial damage seemed to have influenced the S-T segment map even when they were employed as late as 3 to 6 hours after coronary ligation.1-7 Although controversial,s these experimental observations have been extended to man, and it has been suggested that at least directional changes in the degree of myocardial ischemic injury after acute infarction are reflected by changes in the ZST obtained with precordial electrocardiographic maps.g More recent investigations suggest a measurement of the sum of R (ZR) and Q (ZQ) wave voltages from precordial electrocardiographic maps and use of differences in these sums over time as a more direct measure of the amount of myocardial necrosis after acute infarction.2,4J0 QRS and S-T mapping has been proposed as a guide to the effectiveness of therapeutic interventions designed to reduce the ultimate size of myocardial infarction. However, an acute myocardial infarction in man is different from the controlled circumstance created in the experimental animal. Variations in age, sex, chest contour, location of in-

January 1979

The American Journal of CARDIOLOGY

Volume 43

29

S-T AND QRS AFTER MYOCARDIAL INFARCTION-ZMYSLINSKI ET AL.

TABLE I Patient Characteristics CK (Wliter)’ On Admission

Case no.

9

77M 56M 48M 45M 79M 62M 73M 74F 59M 78M 52M 44M 49M 63F 49M 35M 56F 49M 55M 71M

A0 i; 70 21 AI 226 28

tlii 46 9”:

2% 76 3:; 200

Highest Value

Site of Infarct A-S A-S A-S A-S A-S A-S A-S

488 386 449 462 745

765 380 161 529 646 2507 3056 a33 2630 2100 1540 3140 1200

A” A-S A-S A-S A-L A-S A-L A-S A-S A-L A-S A-S

Time of First Study+ 11.5 3.0 4.0 9.5 5.0 7.0 17.0 6.0 5.5 10.0 3.0 11.0 5.5 7.0 10.0 4.5 5.0 1.0 6.0 1.5

Killip Class*

Pericarditisg

II I I II II I

48

II

.

..

II I

farction, additional coronary lesions and other factors occur more frequently in man, and variability among patients would be greater than in the experimental animal. A variable degree of spontaneous change in the precordial electrocardiographic map after acute myocardial infarction has been suggested.2F3J1-15 Before S-T segment and QRS complex mapping can be utilized as a reliable clinical research tool, the spontaneous evolution of the S-T segment and QRS complex during the acute phase of myocardial infarction in man needs to be evaluated. In this study we examined the natural history of the precordial electrocardiographic map in patients during the early and subsequent hours after acute myocardial infarction and compared the results of precordial mapping with results obtained from use of the standard six lead precordial electrocardiogram. Methods Patient characteristics: The study population comprised 20 patients from the coronary care unit of the Strong Memorial Hospital who met the following conditions: (1) evidence of acute transmural anterior, anteroseptal or anterolateral myocardial infarction on the basis of history, serial electrocardiograms and serum creatine kinase enzyme and isoenzyme abnormalities, and (2) onset of symptoms less than 24 hours before initial electrocardiographic mapping. Patients with any of the following were excluded from the study: (1) cardiogenic shock; (2) historical or electrocardiographic evidence of prior transmural myocardial infarction; (3) atria1 fibrillation or atria1 flutter; and (4) right bundle branch block, left bundle branch block, hemiblock, paced rhythm or nonspecific widening of the QRS complex to 110 msec or more. If an intraventricular conduction abnormality developed after a patient’s entry into the study, the electrocardiographic records

30

January 1979

The American Journal of CARDIOLOGY

. 3: .. 24

II II Ill I

. .. .

I

Normal values for Patients 1 to 11 = 0 to 70 IUlliter, and for patients 12 to 20 = 3 to 142 It-+/liter for men and 7 to 69 Ill/liter + Time (in hours) from onset of symptoms to time of initial study. + Killip classification ** at time of admission. * Time (hours) from onset of symptoms when pericardial rub was first heard. Abbreviations: A = anterior; A-L = anterolateral; A-S = anteroseptal; CK = serum creatine kinase. l

.

I11 I

for women.

up to that point were analyzed and the remainder excluded. Individual patient characteristics are given in Table I. There were 17 men and 3 women (mean age 58.7 years, range 35 to 79). The first electrocardiographic study was performed a mean of 6.5 hours (range 1 to 17) after the onset of symptoms, and all but one patient underwent the first study before 12 hours had elapsed. Pericarditis, which developed in four patients was diagnosed from the presence of a pericardial friction rub heard by at least two examiners (patient examinations were performed at least twice daily). Patient 5 died 9 hours after the onset of symptoms after left ventricular wall rupture, and Patient 9 died 6 days after admission from noncardiac causes. Only Patient 10 had evidence of infarct extension during the 10 day period of observations; he had recurrent chest pain, electrocardiographic changes and new elevation of creatine kinase enzyme values on day 7. Patients in the study received standard coronary care unit treatment. All were given morphine and oxygen at the time of admission. At some point during the course of electrocardiographic studies, all received either intravenous lidocaine or procainamide. Furosemide and potassium chloride were administered to 14 patients and nitroglycerin for angina to 2 patients 48 and 24 hours, respectively, after the initial study. Five patients received digitalis, three 48 hours after the initial study and two within 36 hours. Sodium nitroprusside infusion was administered to two patients, in one for 48 and in the other for 24 hours after admission. Mild hypokalemia was present on admission in two patients (serum potassium 3.2 and 3.1 mEq/liter, respectively) who required treatment with potassium chloride. Daily records of the patients’ clinical course, serum enzyme values and other laboratory studies were maintained. Electrocardiographic data: Precordial electrocardiographic mapping was performed utilizing 35 leads on the chest surface from lead positions as previously described.3J6 The initial 35 lead electrocardiographic maps as well as standard

Volume 43

S-T AND QRS AFTER MYOCARDIAL INFARCTION-ZMYSLINSKI ET AL.

a

10

5

20

100

50

200

HOURS FROM ONSET OF SYMPTOMS FIGURE 1. Typical course of X:SmTs5 (dashed line) and ZSTs (solid line) over time in two patients with acute anterior myocardial infarction; Patient 17 had no pericarditis and Patient 13 had pericarditis. See text for explanation of XSTs5 and ISTs. Pt = patient.

6 lead precordial electrocardiograms

were performed as soon as possible after admission to the coronary care unit and at 2, 4, 12, 24,48,72 and 240 hours later when conditions permitted. All recordings were made on a Hewlett-Packard 1511 B electrocardiograph at a paper speed of 50 mm/set and sensitivity of 20 mm/mv. A Hewlett-Packard Welsh suction cup electrode (diameter 15 mm) with the electrocardiograph switched to the unipolar precordial position was used for all recordings. Each precordial map and standard six lead precordial electrocardiogram were obtained by manually moving the suction cup electrode from one lead position to the next. The time required to obtain both records was 10 to 15 minutes. The 35 lead positions of the initial precordial map and standard 6 lead precordial electrocardiogram were marked with a skin pencil on the chest surface to ensure consistent lead placement for subsequent recordings.

TABLE

Changes

Electrocardiographic analysis: In all electrocardiographic recordings, a line drawn between two adjacent T-P segments was utilized as the baseline, and subsequent measurements were obtained from an average of at least three QRS-T complexes in each lead. S-T segment elevation in each lead was determined as the vertical distance of the S-T segment deflection above the baseline 40 msec after the end of the QRS complex. The sum of the S-T segment elevations from either the 35 lead electrocardiographic map (ZSTss) or standard 6 lead precordial electrocardiogram (ZSTs) was obtained by adding the S-T segment elevations from each lead Nhose elevation was equal to or greater than 0.10 mv. From ‘each initial and 240 hour 35 lead electrocardiographic map and standard 6 lead precordial electrocardiogram the sums of the Q wave areas (ZQs5 and ZQs, respectively) and sums of the R wave areas (ER35 and ZRg, respectively) were determined. A “QS” deflection was considered a Q wave. The assumption was made that each Q and R wave approximated a triangle (area = l/z height X width) and the result expressed in mvmsec. Each electrocardiogram was analyzed by a single observer, and blinded reproducibility testing using five different patient records showed no significant errors. Statistical analysis: Standard descriptive statistical methods were used for all analyses.17 Paired t tests were used to follow the changes in ZSTs5 and ZSTs, ZQs5 and ZQs, and ZR35 and ZRs over time. The total group of 20 patients was subdivided for S-T segment analysis into groups with and without pericarditis, and for QRS analysis into groups with an initial onset of symptoms more than 5 hours before the first electrocardiographic study and 5 hours or less before the first electrocardiographic study. Initial S-T segment elevation was correlated with changes in the Q and R wave areas from the initial to the final electrocardiographic records 10 days later, and the 35 lead electrocardiographic map was correlated with the standard 6 lead precordial electrocardiogram.

Results Serial S-T segment mapping: The typical course of EST35 and ZSTs over time is represented in Figure 1 by Patient 17 (without pericarditis) and Patient 13 (with pericarditis), and the results of the entire group are shown in Table II. At 7 to 12 hours after the onset of symptoms the mean ZST,, decreased significantly

II

In ZST35* Over Tilme

Time Periods+ l-6 vs 7-1211 7-12 vs 13-24 7-12 vs 25-46 7-12 vs 49-72 7-12 vs 73-96 13-24 vs 25-46 13-24vs49-72 13-24vs73-96 25-48 vs 49-72 25-48 vs 73-96 49-72 vs 73-96 73-96 vs 240

Changet -1.13 to.13 $0.68 t 0.32 to.51 to.13 -0.02 t 0.02 -0.15 -0.88 to.06 - 1.92

f f f f

l

f f f f f f f

Patients Without Pericarditis no.5

0.38 0.36 0.39 0.43 0.51 0.36 0.33 0.52 0.37 0.63 0.25 0.64

9 :; 11 7 :; a

13 : 7

P Value <0.02 <0.70 <0.05 <0.50 <0.40 co.80 <0.90 <0.90 =0.70 <0.25 x0.80 <0.025

Patients With Pericarditis Change* no.5 tl.0k.i +2.00 +3.13 +2.72 +0.98

0.32 f 1.13 f 0.37 f 0.71 f 0.31

t7.88 t1.53 +0.78 +0.77 -0.08 -4.62

f f f f f f

0.13 0.36 0.38 0.32 0.03 1.07

P Value hi05 <0.20 <0.02
See text for explanation. t Time (hours) after initial onl;et of symptoms. t Mean change in %Ts5 and standard error with + = increase and - = decrease. 5 Number of patients compared in a given time period. 11 The last value of XSTs5 in the first time period compared with the last value in the second time period. This method is used for all subsequent comparisons. P = probability. l

January 1979

The American Journal of CARDIOLOGY

Volume 43

31

S-T AND QRS AFTER MYOCARDIAL INFARCTION-ZMYSLINSKI ET AL.

TABLE III Mean %T~s* at Various Time Periods In Patients With and Without Pericarditis (in mv) Time Period+ l-6 7-12 13-24 25-48 49-72 73-96 240

With Pericarditis

Without Pericarditis no.5

XSTs5$ 4.72 3.23 3.26 3.22 2.64 3.26 1.23

f f f 4 f f f

0.78 0.64 0.57 0.61 0.52 0.72 0.32

18 22 18 14 13 1:

ZSTssz 6.70 5.55 5.43 7.43 7.66 6.43

f f f f f

0.70 0.69 0.40 0.78 0.32 3.80 f 0.81

no.5

7 : 3 4

P value11 <0.50
See text for explanation. t Time (hours) from initial onset of symptoms. f Mean value of XSTs5 f standard error from all recordings obtained during the time period. 5 Number of records of ZSTss obtained during the time period (some ‘ents were studied more than once in a given time period). Patr Probability value obtained from results of unpaired t tests comparing patients with and without pericarditis. l

onset of symptoms, but still did not reach statistical significance. Initial S-T versus change in Q and R wave areas: No significant correlation between initial ZZSTas and change in ZQss or 8Rs5 over time was found regardless of the time of entry into the study after onset of symptoms. In only two patients did the initial S-T segment measurements correlate with the subsequent changes in Q wave areas from corresponding leads (r = 0.862, P
in patients without pericarditis, but increased significantly from this value at 13 to 24 hours. Between 7 to 12 hours and 13 to 24 hours and between 25 to 48 hours and 72 to 96 hours the XSTas remained stable in patients without pericarditis. At all time periods after 12 hours the mean ZSTs5 was significantly higher in patients with than in those without pericarditis (Table III). Between 73 to 96 hours and 10 days, YZSTssdecreased significantly in both groups of patients, although the mean values of patients with pericarditis remained significantly higher than those of patients without this complication. ZSTss increased significantly in the group with pericarditis at 13 to 24 hours before a pericardial friction rub was heard (24 to 72 hours). Changes in ZQ35and ZRas over time: For the entire group, between the initial and final recordings, ZQss tended to increase, although not significantly (P <0.20), whereas ERa5 decreased significantly (Table IV). When the patients were separated into those whose first electrocardiographic study was performed at or within 5 hours of initial symptoms and those whose first study was performed after 5 hours, one difference was noted. The decrease in ZRas over time remained significant only in patients studied at or within 5 hours after initial symptoms. The increase in ZQas was more prominent in the patients studied at or before 5 hours after the

The extent (if any) to which standard drug therapy altered the electrocardiograms of our patients is difficult to determine because all patients received morphine and oxygen before entry into the study and no patient was studied at the exact time treatment with a given drug (lidocaine, procainamide, furosemide, for example) was started. The presence of mild hypokalemia and the administration of potassium chloride to two patients on admission may have affected the initial electrocardiograms. To withhold all drug therapy both before and during the period of study was not feasible. However, it is doubtful that digitalis, nitrates or propranolol had any effect on our data because these drugs were administered to a small group of patients relatively late in the study when electrocardiographic variables had already begun to stabilize. Time course of S-T elevation: Only two previous studies reported serial changes in the S-T segment map during the first 24 hours after acute anterior myocardial infarction in a manner similar to ours.i5J8 Maroko et all5 reported only minor changes in the EST during the first 24 hours after myocardial infarction in 11 patients contrasted to the significant decrease of ZSTss noted in our 20 patients within 12 hours after initial onset of symptoms. Kronenberg et al.l* reported stability of the S-T

TABLE IV Change in 2X&*

and Z%&* From Initial Recording to 10 Days Later (in mv- msec)

Patient Group Total Symptoms < 5 hours+ Symptoms > 5 hours

Change in ZC& +134.1 f +287.5 f +57.3 f

92.2 136.3 111.8

no.9

P value

15

<0.20 <0.20 <0.70

1:

See text for explanation. + Refers to hours after initial onset of symptoms. t Mean differences f standard error from initial to final electrocardiographic 5 Number by paired t tests of patients observed. l

32

January 1979

The American Journal of CARDIOLOGY Volume 43

map.

Change in Z&t -79.0 -38.15 -49.4

f 35.1 f 18.2 f 50.1

no.9

P Value

15

<0.05 <0.02 <0.40

1;

S-T AND QRS AFTER MYOCARDIAL INFARCTION-ZMYSLINSKI ET AL.

segment vector during the early phases of acute myocardial infarction, but a gradual decrease was noted in a subgroup of patients without complications. Our results differ probably because of the earlier time of entry into our study, more frequent measurements and fewer patients with complications. Madiasl”Jg and Flaherty20 and their co-workers reported that S-T segment elevation remains stable during the early hours after myocardial infarction. However, early S-T segment maps were obtained only twice in each patient in the former study, and S-T segment elevation was followed up for only 2 hours in the latter. Gold et a1.21also reported stability of the 1%T segment during the initial 4 hours after myocardial infarction, but excluded from study those patients whose S-T segments decreased spontaneously by more than 10 percent during the 1st hour of study. Norris et a1.12reported marked variability in S-T segment elevation in 5 of 12 patients studied acutely on two occasions 1 hour apart. Role of pericarditis: The relative rise in ZSTss noted between 7 to 12 and 25 to 48 hours in our 16 patients without clinical evidence of pericarditis is unexplained. Clinically undetectable pericarditis is one possibility. In this case, reservations regarding the usefulness of S-T segment mapping as a tool for measuring myocardial ischemic injury need to be made. No clinical evidence of infarct extension occurred in these 16 patients, although recurrent ischemic injury, not clinically recognizable, could explain this phenomenon. Reelevation of the XSTs~ occurred in the four patients with pericarditis 13 to 24 hours after the onset of myocardial infarction, although pericardial friction rubs were not heard until 24 to 72 hours despite a minimum of 2 daily patient examinations by two or more observers. Earlier pericardial friction rubs may have been missed in these four patients, but it must be emphasized that early development of increasing S-T segment elevation does not necessarily indicate extension of myocardial injury. R wave and Q wave voltage-correlation with S-T segment: A significant decrease in ZRs5 from the initial to the final study 10 days later was noted only in those patients whose first precordial map was per-

formed at or before 5 hours after the onset of symptoms. No significant change in XQss could be shown, although the Q wave tended to increase over this time period. The initial S-T segment measurements correlate with the subsequent changes in Q wave areas from corresponding leads only in two patients whose initial electrocardiographic studies were performed at or within 5 hours after the onset of initial symptoms. We do not reject the well established observation that Q waves follow transmural myocardial infarction. Our data simply suggests that significant Q wave development occurred before the initial S-T and QRS map was performed. The suggestion of very early and rapid development of Q waves after myocardial infarction is supported by the experimental data of Hillis et a1.4 In general we were unable to show any meaningful correlation between initial S-T segment measurements and subsequent changes in Q and R wave areas. Rapid decline of S-T segment elevation during the early hours of myocardial infarction as well as rapid changes in Q and R wave areas may explain this lack of relation. Our patients were initially studied a mean of 6.5 hours after the onset of symptoms whereas most experimental studies measure initial S-T segment elevation within minutes to 1 hour after coronary occlusion. Comparison of 35 lead electrocardiographic mapping with standard 6 lead precordial electrocardiogram: Our correlations between XSTa5 and ZSTs, ZQs5 and ZQs, and ZRs5 and ZRa suggest that the standard 6 lead precordial electrocardiogram may be a suitable alternative to the more laborious 35 lead electrocardiographic map for the study of patients with acute anterior myocardial infarction. This investigation reveals that the sum of precordial S-T segment elevations after acute anterior myocardial infarction in man undergoes significant natural change dependent on the time measurement is taken after onset of symptoms. Significant changes in Q and R wave areas may occur very early after the onset of symptoms, perhaps before 5 hours have elapsed. Changes in the 35 lead precordial electrocardiographic map may be accurately reflected in the less laborious 6 lead precordial electrocardiogram in patients with acute anterior myocardial infarction.

References 1. Maroko PR, Kjekshus JK, Sobel BE, Watanabe T, Cove8 JW, Ross J Jr, Braunwald E: Factors influencing infarct size following experimental coronary artery occlusions. Circulation 4367-82, 1971 2. Muller JE, Maroko PR, Braunwald E: Evaluation of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury. Circulation 52:16-27, 1975 3. Maroko PR, Libby P, Covell JW, Sobel BE, Ross J Jr, Braunwald E: Precordial S-T segment elevation mapping: an atraumatic method for assessing alterations in the extent of myocardial ischemic injury. Am J Cardiol 29:223-230, 1972 4. Hillis LD, Askenazi J, Braunwald E, Radvany P, Muller JE, Fishbein MC, Maroko PR: tlse of changes in the epicardial QRS complex to assess interventions which modify the extent of myocardial necrosis following coronary artery occlusion. Circulation 54591-598, 1976 5. Maroko PR, Bernstein EF’, Libby P, DeLaria GA, Covell JW, Ross

6.

7.

8. 9. 10.

January 1979

J Jr, Braunwald E: Effects of intraaortic balloon counterpulsation on the severity of myocardial ischemic injury following acute coronary occlusion. Circulation 451150-l 159, 1972 Libby P, Mar&o PR, Bloor CM, Sobel BE, Braunwald E: Reduction of experimental myocardial infarct size by corticosteroid administration. J Clin Invest 52599-607, 1973 Maroko PR, Libby P, Sobel BE, Bloor CM, Sybers HD, Shell WE, Covell JW, Braunwald E: Effect of glucose-insulin-potassium infusion on myocardial infarction following experimental coronary artery occlusion. Circulation 451160-l 175, 1972 Fozzard HA, DasGupta DS: ST-segment potentials and mapping. Theory and experiments. Circulation 54:533-537, 1976 Braunwald E, Maroko PR: ST-segment mapping. Realistic and unrealistic expectations. Circulation 54529-532, 1976 Maroko PR, Hillis LD, Muller JE, Tavazzi L, Heyndrlckx GR, Ray M, Chlariello M, Distante A, Askenazi J, Salerno J, Carpentier J, Reshetnaya NI, Radvany P, Libby P, Raabe DS, Chazov El,

The American Journal of CARDIOLOGY

Volume 43

33

S-T

AND

QRS

AFTER

MYOCARDIAL

INFARCTION-ZMYSLINSKI

Bobba P, Braunwald E: Favorable

ET AL.