- Email: [email protected]
Single right-sided precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction
Single right-sided precordial lead in the diagnosis of right ventricular involvement in inferior myocardial infarction Leif R. Erhardt Andreas SjSgren Inger Wahlberg Stockholm, Sweden
Acute myocardial infarction (AMI) is mainly a disease of the left ventricle; infarction of the right ventricle is considered rare. Isolated right ventricular infarction (RVI) has been found in 2.5 per cent 1 and in 4.6 per cent ~ in autopsy studies of myocardial infarction, whereas RVI as an extension from left ventricular infarction (LVI) occurs more commonly2, 3 RVI is probably more common than previously thought, however, as evidenced by a recent autopsy study in which transverse heart slicing and enzyme staining were employed, revealing RVI in 43 per cent of the patients2 In the literature, small attention has been paid to the clinical aspects of RVI, and it is mostly during later years t h a t papers have appeared concerning its diagnosis, hemodynamics, implications, and treatment. ~-11 Some authors have considered hemodynamic evaluation a mainstay for the diagnosis, ~~ ~1whereas others have studied the ECG but not found it useful in this respect, which may have hampered further studies2 T M In addition to conventionally used precordial CR ECG leads, a right-sided chest lead, CR~R, has been recorded routinely in our hospital. CR leads have been used because these have been routinely employed in preference to V leads in this hospital in recent years. In the autopsy study by Erhardt, ~ ST-segment elevation in Lead CR~R From the Dept. of Medicine, Karolinska Institutet at Serafimerlasarettet, Stockholm, Sweden. This study was supported by a grant from the Swedish National Association Against Heart and Chest Diseases. Received for publication April 9, 1975. Reprint requests: Dr. Inger Wahlberg, Department of Medicine, Karolinska Institutet at Serafimerlasarettet, Stockholm 112 83, Sweden (Box 12700).
May, 1976, Vol. 91, No. 5, pp. 571-576
was a common finding in patients with RVI a s a n extension from inferior LVI, but was a rare and unspecific finding in anterior LVI with extension to the anterior right ventricular wall. The purpose of the present investigation was to evaluate the diagnostic significance and clinical consequences of ST-segment elevation in Lead CR4R in patients with inferior LVI in a larger patient group. Patients and methods
All patients were treated in the CCU of Serafimerlasarettet from July, 1972, through March, 1974. A total of 98 patients with acute transmural inferior myocardial infarction were investigated. Six patients were excluded: two on account of complete right bundle branch block, two on account of complete heart block, and two because of differing ECG interpretations among the authors, thus leaving a study group of 92 patients. There were 22 women and 70 men, of whom 18 died {mean age, 71 years) and 74 survived (mean age, 61 years). The electrocardiographic (ECG) criteria of acute transmural inferior myocardial infarction were the appearance of a pathological Q wave and the appearance of a local ST elevation followed by T inversion in Leads II, III, and aVF. Admission criteria, serum enzyme diagnostics, and policy of treatment have been published previously.4, ~5 Twelve-lead ECG's (I, II, III, aVR, aVL, aVF, CR4R, CR1, 2, ,, 5, 7) were routinely recorded on admission and every subsequent morning for 3 days, and additionally if indicated clinically. The CR4R electrode was placed in the fifth intercostal space in the right midclavicular line and ST elevations of more than 1 mm. in this lead in any
American Heart Journal
571
Erhardt, Sjbgren, and Wahlberg
h e a r t failure was considered p r e s e n t when t h e r e were distended neck veins a b o v e the level of the clavicle with the p a t i e n t sitting at a 45 degree angle, or if the central v e n o u s pressure (CVP) exceeded 12 cm. H~0. Left h e a r t failure was considered present w h e n b a s a l r~les were h e a r d on the lungs with or w i t h o u t a third h e a r t sound, or when chest x-ray showed c e n t r a l or p e r i p h e r a l vascular enlargement, a n d / o r confluent areas compatible with p u l m o n a r y edema. At a u t o p s y the h e a r t was e x a m i n e d b y a serial transverse-slice m e t h o d TM a n d the slices were stained with nitro-BT. 17 T h e size of the i n f a r c t i o n was e s t i m a t e d by a p o i n t - c o u n t i n g t e c h n i q u e TM and expressed in per cent of the left a n d right ventricular m y o c a r d i u m , respectively. T h e stained and n o n s t a i n e d areas were counted, giving the proportion of infarcted to n o n i n f a r c t e d m y o c a r dial area. After weighing e a c h slice the m a s s of infarcted m y o c a r d i u m could also be e s t i m a t e d . W h e n the area of i n f a r c t e d m y o c a r d i u m differed m a r k e d l y on each side of a slice, b o t h sides were counted and the m e a n v a l u e was used. All autopsies were p e r f o r m e d b y one of the a u t h o r s (L. R. E.) a n d for f u r t h e r details see E r h a r d t . 4 M a j o r infarction of the right v e n t r i c u l a r free wall was defined as an extension of the i n f a r c t i o n in at least one transverse h e a r t slice to or b e y o n d the lateral margin, whereas R V I with less extension was defined as m i n o r (see Fig. 1). For the evaluation of the results, c o n v e n t i o n a l statistical m e t h o d s were used. Results
Fig. 1. Pictorial classification of transverse heart slice showing infarction (black area). Upper: Inferior LV infarction without RV involvement. Middle: Inferior LV infarction with minor RV involvement. Lower: Inferior LV infarction with major RV involVement.
of the E C G ' s recorded during t h e first 3 d a y s were classified as a b n o r m a l , the recordings being checked b y the a u t h o r s s e p a r a t e l y . H y p o t e n s i o n was defined as a systolic blood pressure of 90 m m . H g or less and oliguria as a urine flow of less t h a n 20 ml. per hour. R i g h t
572
A b n o r m a l S T - s e g m e n t elevations in L e a d CR4R were found in 16 of t h e 74 survivors a n d in nine of the 18 deceased p a t i e n t s (p < 0.025). T h e validity of an a b n o r m a l S T : s e g m e n t elevation in Lead CR~R as a sign of right v e n t r i c u l a r involvem e n t in a c u t e inferior i n f a r c t i o n is given in T a b l e I, in which the a u t o p s y results are presented. T h e patients were divided into t h r e e groups: m a j o r , minor, or absence of R V I a n d t h e y did n o t differ concerning left v e n t r i c u l a r infarction size. No patient with purely left inferior v e n t r i c u l a r engagement showed an S T - s e g m e n t elevation in Lead CR~R in c o n t r a s t to all with m a j o r R V I (p < 0.01). T h e p a t i e n t s w i t h m i n o r R V I h a d this elevation in 33 per cent. All p a t i e n t s h a d some degree of posterior s e p t u m i n f a r c t i o n which was not related to the size of R V I . In p a t i e n t s with R V I a fresh t h r o m b u s was present in the right
May, 1976, Vol. 91, No. 5
Diagnosis of right ventricular i n v o l v e m e n t
Table I. R e l a t i o n b e t w e e n S T - s e g m e n t elevation
Hypotension
in L e a d C R , R a n d right v e n t r i c u l a r infarction found at a u t o p s y in 18 p a t i e n t s with a c u t e inferior left v e n t r i c u l a r m y o c a r d i a l i n f a r c t i o n
n=9
No R V involvement (n = 5)
ST-segment elevation No ST-segment elevation % ST-segment elevation
Minor R V involvement (n = 6)
0liguria n=3
Major R V involvement (n = 7)
0 5
2 4
7 0
0
33
100
Table II.
S T - s e g m e n t elevation in L e a d CR~R and R V I size in p a t i e n t s with m i n o r R V I
Pt.
1 2 3 4 5 6
Abnormal I RV ST-segment involvement elevation infarction in Lead CR,R size (%)
+ + --
25 48 10 30 23 15
Survival time (days)
10 2 1 1 9 5
c o r o n a r y a r t e r y in 85 per cent as c o m p a r e d to 17 per cent in p a t i e n t s w i t h o u t R V I (p < 0.05). In major RVI, the mass of infarcted right v e n t r i c u l a r m y o c a r d i u m r a n g e d f r o m 25 to 90 per cent (mean, 46 per cent) a n d survival t i m e r a n g e d from 1 to 21 days (mean, 8 days}. C o r r e s p o n d i n g results for minor R V I are s h o w n in T a b l e II. I n the l a t t e r group the t i m e f r o m onset of s y m p t o m s to the first E C G was less t h a n 12 h o u r s with t h e exception of P a t i e n t 4, in w h o m the s e r u m e n z y m e changes a n d clinical s y m p t o m s suggested t h a t the A M I d a t e d b a c k a couple of days. In the 16 survivors with S T - s e g m e n t elevation in Lead CR~R this was present on admission in 13 and was m o s t p r o n o u n c e d on the first day. T h e S T - s e g m e n t rise h a d usually vanished a f t e r 3 days, remaining in only one patient. T h e remaining three p a t i e n t s h a d long-lasting chest pains and presented with S T - s e g m e n t elevation on the second day. All nine p a t i e n t s with S T segment elevation who died h a d this on admission. Clinical characteristics in relation to S T -
American Heart Journal
Right heart failure n =11 Fig. 2. Interrelation between hypotension, oliguria, and right heart failm~e in 16 survivors with ST-segment elevation in Lead CR4R.
s e g m e n t elevation in L e a d CR4R in t h e survivors and in the deceased are s h o w n in T a b l e s I I I a n d IV. H y p o t e n s i o n a n d r i g h t a n d left Ventricular failure were significantly m o r e c o m m o n a m o n g the survivors with this E C G p a t t e r n , w h e r e a s no such significances were f o u n d when the deceased were compared. If survivors a n d deceased patients are considered together, those with a n S T segment rise in CR~R as c o m p a r e d to those without h a d a significantly higher incidence of right (76 per cent as c o m p a r e d to 27 per cent, p < 0.001) a n d left (96 per cent as c o m p a r e d to 63 per cent, p < 0,01) h e a r t failure, h y p o t e n s i o n (68 per cent as c o m p a r e d to 25 per cent, p < 0.001) as well as oliguria (36 per cent as c o m p a r e d to 9 per cent, p < 0.01.) T h e interrelation b e t w e e n h y p o tension, oliguria, a n d right h e a r t failure is s h o w n in Fig. 2. S e r u m e n z y m e d e t e r m i n a t i o n s p e r m i t t i n g the e s t i m a t i o n of p e a k levels were available for all the 74 survivors. T h e survivors with the described S T segment elevation in L e a d Cr, R h a d significantly higher p e a k levels of S G O T (fn=258), S G P T
573
Erhardt, Sjbgren, and Wahlberg
Table III. Clinical characteristics in relation to
Table IV. Clinical characteristics in relation to
abnormal ST-segment elevation in Lead CR~R among the survivors (n = 74)
abnormal ST-segment elevation in Lead CR4R among the deceased (n = 18) Abnormal CR~R ST-segment elevation
Abnormal CR~R ST-segment elevation Clinical characteristic
Hypotension Oliguria Right heart failure Left heart failure
Clinical characteristic
Present [ Not present
50 19 63 94
19 5 21 57
< 0.05 N.S. < 0.01 < 0.05
(ff1=85) and LDHt (if:= 1,230) t ha n those without this elevation (ffl= 170, 41, and 750, respectively) (p < 0.05). Discussion
In RVI clinical and ECG diagnostics have previously not been considered sensitive enough for the diagnosis, 1~ 11 whereas others have suggested t h a t RVI may be visualized by changes in precordial leads reflecting the right ventricle, i.e., V: to V3.'4, :9, 2o According to our findings a major RVI can be recognized by an abnormal STsegment elevation in Lead CR4R in patients with acute transmural inferior left ventricular myocardial infarction. It must be stressed t h a t this finding is valid only in the absence of anteroseptal infarction which may interfere with the ECG interpretation concerning RVI (see Fig. 3). Earlier autopsy studies ~....... have mostly reported involvement of the posterior right ventricular free wall accompanying inferior LVI with ECG signs typical for diaphragmatic wall infarction. As the right ventricle and the inferior left ventricle wall are usually both supplied by the right coronary artery, this is to be expected. Myers and associates :4 suggested that great difficulty could be anticipated in the ECG differentiation between septal and right ventricular infarction, since ~he former may also be manifested by changes in the precordial leads over the right ventricle. In the present study, however, the STsegment elevation in Lead CR~R was not seen in any of the five patients with posterior septal infarction without right ventricular engagement. Although our present finding of ST-segment elevation in Lead CR4R in RVI could be influ-
574
Hypotension Oliguria Right heart failure Left heart failure
Present ~)
Not present ~)
100 67 100 100
67 33 67 100
N.S. N.S. N.S. N.S.
enced by the position of the heart in the chest as well as by the transient nat ure of ST-rises in AMI, all patients with major right ventricular involvement showed this pattern. Thus, bo th extension and mass of the RVI seem to be of great importance for the ECG diagnosis. Furthermore, all but one of the d e c e a s e d p a t i e n t s with more than 25 per cent of the right ventricular mass engaged showed ST-segment rise in Lead CR4R. The exception was a patient with onset of symptoms 2 days before admission, in whom the absence of this rise may be explained by the transient nature of the ST-segment elevation, ~1as this had vanished after 2 to 3 days in our study. Extension of the infarction from the inferior wall beyond the lateral margin of the right ventricle was found in seven of the nine deceased with STsegment elevation in Lead CR~R which could mean that not only mass but also location of the infarction is of importance for the ECG changes. Our present study does not allow conclusions as to possible ECG changes caused by isolated RVI involving the lateral margin. Furthermore, it cannot be excluded t hat right-sided precordial leads other than CR~R are more revealing in the diagnosis of RVI. However, preliminary results from a study presently performed in our CCU with a further four right-sided chest leads, i.e., CR~R, CR7R, and two leads placed one intercostal space above and below CR4R, respectively, do not suggest t hat much is to be gained by additional leads. Correlation between infarction size and peak enzyme levels, usually SGOT and LDHt, has previously been described ~ and in the present study ST-segment rises in Lead CR4R were corre-
May, 1976, Vol. 91, No. 5
Diagnosis of right ventricular involvement
Fig. 3. Representative ECG showing ST-segment elevation in Lead CR~R in a patient with acute inferior infarction. V leads have been added for comparison. This patient had the following hemodynamic data: RV pressures 24/12 and pulmonary artery 20/10 mm. Hg on the first day, with a subsequent further increase in rightsided filling pressures. There was hypotension and there were long periods of oliguria requh'ing furosemide doses exceeding 500 mg. daily. Paper speed 50 mm. per second.
lated to higher S G O T and L D H t peak values, which suggests greater infarction sizes, perhaps in part due to the additional damage of the right ventricular myocardium. Cohn and associates 1~ suggested t h a t a u n i q u e clinical and h e m o d y n a m i c s y n d r o m e arises when LVI is accompanied by RVI. T h e i r six p a t i e n t s presented clinically with engorged neck veins, hypotension, and h e a r t block, and h e m o d y n a m i c measurements disclosed t h a t the right v e n t r i c u l a r filling pressure equalled or exceeded left ventricular end-diastolic pressures. Others 6-', 1~have also shown this h e m o d y n a m i c p a t t e r n . T h e findings in the present s t u d y of an association between this ST-segment elevation in Lead CR~R and hypotension and right and left h e a r t failure are in accordance with these studies (Table III). Several of the patients with these E C G findings, however, failed to show clinical signs of this h e m o d y n a m i c pattern. This m a y have been due to diuretic t h e r a p y in some cases, yet it needs pointing o u t t h a t little is known of the h e m o d y n a m i c consequences of infarction of the free right v e n t r i c u l a r wall per se. Septal and right v e n t r i c u l a r papillary muscle infarction which o f t e n accompanies R V I ~ m a y also be of m a j o r i m p o r t a n c e , and t h e added
American Heart Journal
afterload due to c o n c o m i t a n t left h e a r t failure may also affect right h e a r t performance. According to our results, S T - s e g m e n t elevation in Lead CR4R implies poor prognosis as to shortterm survival, and early recognition of R V I could be vital. This is compatible with the low incidence of old RVI previously r e p o r t e d at a u t o p s y 4, 12 In conclusion, our findings lend support to the following: 1. An ST-segment elevation of more t h a n 1 mm. in Lead CR~R indicates right ventricular involvement in patients with t r a n s m u r a l acute inferior myocardial infarction. 2. This ST-segment elevation indicates right ventricular myocardial d a m a g e exceeding 25 per cent or reaching the lateral margin of right ventricular free wall. 3. Patients with the above S T - s e g m e n t elevation often develop hypotension, oliguria and right and left h e a r t failure, and h a v e poor prognosis as to short-term survival.
Summary T h e S T segment in a single right-sided chest lead, CR~R, has been studied in 92 consecutive patients with acute inferior t r a n s m u r a l ' l e f t ven-
575
Erhardt, Sjbgren, and Wahlberg
tricular myocardial infarction. A transient STs e g m e n t r i s e o f m o r e t h a n 1 m m . w a s r e c o r d e d in 25 p a t i e n t s , a n d s t r o n g l y i n d i c a t e d a s i g n i f i c a n t extension of the infarction to the posterior free right ventricular wall according to autopsy findings. T h i s E C G p a t t e r n w a s f u r t h e r m o r e associated with right-sided heart failure, hypotension and oliguria. Left heart failure was also common. The short-term prognosis of patients with STsegment elevation in CR4R was poor.
10. 11. 12. 13. 14.
REFERENCES
1. Wartman, W. B., and Hellerstein, H. K.: The incidence of heart disease in 2000 consecutive autopsies, Ann. Intern. Med. 28:41, 1948. 2. Yater, W. M., Traum, A. H., Springs, S., Brown, W. G., Fitzgerald, R. P., Geisler, M. A , and Wilcox, B. B.: Coronary artery disease in men 18 to 39 years of age. Report of 866 cases, 450 with necropsy examination, AM. HEART J. 36:683, 1948. 3. Lisa, J. R., and Ring, A.: Myocardial infarction or gross fibrosis. Analysis of 100 necropsies, Arch. Intern. Med. 50:131, 1932. 4. Erhardt, L. R.: Clinical and pathological observations in different types of acute myocardial infarction, Acta Med. Scand. SuppL 560, 1974. 5. Lassers, B. W,, George, M., Anderton, J. L., Higgins, M. R., and Philip, T.: Left ventricular failure in acute myocardial infarction, AM. HEART J. 25:511, 1970. 6. Fluck, D. C., Valentine, P. A., Treister, B., Higgs, B., Reid, D. N., Steiner, R. E., and Monsey, J. P. D.: Right heart pressures in acute myocardial infarction, Br. Heart J. 29:748, 1967. 7. Rigo, P., Taylor, D . , Weisfeldt, M., Kelly, D., and Strauss, H. W.: Right ventricular dysfunction in patients with inferior myocardial infarction (abst.), Circulation, 47-48(Suppl. IV):207, 1973. 8. Guiha, N. H., Limas, C. J., Broder, M. I., and Cohn, J. N.: Predominant right ventricular failure in clinical and experimental right ventricular infarction (abst.), Clin. Res. 20:375, 1972. 9. A1-Sadir, J., Falicov, R., Zahavi, I., Brooks, H,, and Resnekov, L.: Right ventricular dysfunction in acute
576
15.
16.
17. 18. 19. 20. 21.
22.
inferior myocardial infarction (abst.), Circulation Suppl. IV:59, 1973. Cohn, J. N., Guiha, N. H., Broder, M.I., and Limas, C. J.: Right ventricular infarction, AM. HEART J. 33:209, 1974. Rotman, M., Ratliff, N. B., and Hawley, J: Right ventricular infarction: A hemodynamic diagnosis, Br. Heart J. 36:941, 1974. Wade, W. G.: The pathogenesis of infarction of the right ventricle, Br. Heart J. 21:545. 1959. Wells, D. E., and Befeler, B.: Dysfunction of the right ventricle in coronary artery disease, Chest 66:230. 1974. Myers, G. B., Klein, H. A., and Hiratzka, T.: IV. Correlation of electrocardiographic and pathologic findings in infarction of the interventricular septum and right ventricle, AM. HEART J. 37:720, 1949. Hofvendahl, S.: Influence of treatment in a coronary care unit on prognosis in acute myocardial infarction A controlled study in 271 cases. Acta Med. Scand. Suppl. 519, 1971. Sayen, J. J.. and Sheldon, W. F.: The heart muscle and the electrocardiogram in coronary disease. II. Difficulties of description and illustration of ventricular muscle lesions with a method for their graphic representation m a myocardial map, AM. HEART J. 38:688. 1949. Nachlas, M. M.. and Schnitka, T. K.: Macroscopic identification of early myocardial infarcts by alterations in dehydrogenase activity, Am. J. Pathol. 42:379, 1963. Harnarayan, C.. Bennett, M A., Pentecost. B. L., and Brewer. D. B.: Quantitative study of infarcted myocardium in cardiogenic shock, Br. Heart J. 32:728, 1970. Hfibner, A.: fiber den Rechsherzinfarkt, Deutsch. Gesundheitsw, 23:7074, 1968. Levy, L.. and Hyman, A. L.: Difficulties in the electrocardiographic diagnoses of myocardial infarction, AM. HEART J. 39:243, 1950. Bayley, R. H., LaDue, J. S.. and York. D. J.: Electrocardiographic changes (local ventricular ischemia and injury) produced in the dog by temporary occlusion of a coronary artery, showing a new stage in the evolution of a myocardial infarction, AM. HEART J. 27:164, 1944. Nachlas, M. M., Friedman. M. M., and Cohen. S. P.: A method for the quantification of myocardial infarcts and the relation of serum enzyme levels to infarct size, Surgery 55:700, 1964.
May, 1976, Vol. 91, No. 5
Acute myocardial infarction (AMI) is mainly a disease of the left ventricle; infarction of the right ventricle is considered rare. Isolated right ventricular infarction (RVI) has been found in 2.5 per cent 1 and in 4.6 per cent ~ in autopsy studies of myocardial infarction, whereas RVI as an extension from left ventricular infarction (LVI) occurs more commonly2, 3 RVI is probably more common than previously thought, however, as evidenced by a recent autopsy study in which transverse heart slicing and enzyme staining were employed, revealing RVI in 43 per cent of the patients2 In the literature, small attention has been paid to the clinical aspects of RVI, and it is mostly during later years t h a t papers have appeared concerning its diagnosis, hemodynamics, implications, and treatment. ~-11 Some authors have considered hemodynamic evaluation a mainstay for the diagnosis, ~~ ~1whereas others have studied the ECG but not found it useful in this respect, which may have hampered further studies2 T M In addition to conventionally used precordial CR ECG leads, a right-sided chest lead, CR~R, has been recorded routinely in our hospital. CR leads have been used because these have been routinely employed in preference to V leads in this hospital in recent years. In the autopsy study by Erhardt, ~ ST-segment elevation in Lead CR~R From the Dept. of Medicine, Karolinska Institutet at Serafimerlasarettet, Stockholm, Sweden. This study was supported by a grant from the Swedish National Association Against Heart and Chest Diseases. Received for publication April 9, 1975. Reprint requests: Dr. Inger Wahlberg, Department of Medicine, Karolinska Institutet at Serafimerlasarettet, Stockholm 112 83, Sweden (Box 12700).
May, 1976, Vol. 91, No. 5, pp. 571-576
was a common finding in patients with RVI a s a n extension from inferior LVI, but was a rare and unspecific finding in anterior LVI with extension to the anterior right ventricular wall. The purpose of the present investigation was to evaluate the diagnostic significance and clinical consequences of ST-segment elevation in Lead CR4R in patients with inferior LVI in a larger patient group. Patients and methods
All patients were treated in the CCU of Serafimerlasarettet from July, 1972, through March, 1974. A total of 98 patients with acute transmural inferior myocardial infarction were investigated. Six patients were excluded: two on account of complete right bundle branch block, two on account of complete heart block, and two because of differing ECG interpretations among the authors, thus leaving a study group of 92 patients. There were 22 women and 70 men, of whom 18 died {mean age, 71 years) and 74 survived (mean age, 61 years). The electrocardiographic (ECG) criteria of acute transmural inferior myocardial infarction were the appearance of a pathological Q wave and the appearance of a local ST elevation followed by T inversion in Leads II, III, and aVF. Admission criteria, serum enzyme diagnostics, and policy of treatment have been published previously.4, ~5 Twelve-lead ECG's (I, II, III, aVR, aVL, aVF, CR4R, CR1, 2, ,, 5, 7) were routinely recorded on admission and every subsequent morning for 3 days, and additionally if indicated clinically. The CR4R electrode was placed in the fifth intercostal space in the right midclavicular line and ST elevations of more than 1 mm. in this lead in any
American Heart Journal
571
Erhardt, Sjbgren, and Wahlberg
h e a r t failure was considered p r e s e n t when t h e r e were distended neck veins a b o v e the level of the clavicle with the p a t i e n t sitting at a 45 degree angle, or if the central v e n o u s pressure (CVP) exceeded 12 cm. H~0. Left h e a r t failure was considered present w h e n b a s a l r~les were h e a r d on the lungs with or w i t h o u t a third h e a r t sound, or when chest x-ray showed c e n t r a l or p e r i p h e r a l vascular enlargement, a n d / o r confluent areas compatible with p u l m o n a r y edema. At a u t o p s y the h e a r t was e x a m i n e d b y a serial transverse-slice m e t h o d TM a n d the slices were stained with nitro-BT. 17 T h e size of the i n f a r c t i o n was e s t i m a t e d by a p o i n t - c o u n t i n g t e c h n i q u e TM and expressed in per cent of the left a n d right ventricular m y o c a r d i u m , respectively. T h e stained and n o n s t a i n e d areas were counted, giving the proportion of infarcted to n o n i n f a r c t e d m y o c a r dial area. After weighing e a c h slice the m a s s of infarcted m y o c a r d i u m could also be e s t i m a t e d . W h e n the area of i n f a r c t e d m y o c a r d i u m differed m a r k e d l y on each side of a slice, b o t h sides were counted and the m e a n v a l u e was used. All autopsies were p e r f o r m e d b y one of the a u t h o r s (L. R. E.) a n d for f u r t h e r details see E r h a r d t . 4 M a j o r infarction of the right v e n t r i c u l a r free wall was defined as an extension of the i n f a r c t i o n in at least one transverse h e a r t slice to or b e y o n d the lateral margin, whereas R V I with less extension was defined as m i n o r (see Fig. 1). For the evaluation of the results, c o n v e n t i o n a l statistical m e t h o d s were used. Results
Fig. 1. Pictorial classification of transverse heart slice showing infarction (black area). Upper: Inferior LV infarction without RV involvement. Middle: Inferior LV infarction with minor RV involvement. Lower: Inferior LV infarction with major RV involVement.
of the E C G ' s recorded during t h e first 3 d a y s were classified as a b n o r m a l , the recordings being checked b y the a u t h o r s s e p a r a t e l y . H y p o t e n s i o n was defined as a systolic blood pressure of 90 m m . H g or less and oliguria as a urine flow of less t h a n 20 ml. per hour. R i g h t
572
A b n o r m a l S T - s e g m e n t elevations in L e a d CR4R were found in 16 of t h e 74 survivors a n d in nine of the 18 deceased p a t i e n t s (p < 0.025). T h e validity of an a b n o r m a l S T : s e g m e n t elevation in Lead CR~R as a sign of right v e n t r i c u l a r involvem e n t in a c u t e inferior i n f a r c t i o n is given in T a b l e I, in which the a u t o p s y results are presented. T h e patients were divided into t h r e e groups: m a j o r , minor, or absence of R V I a n d t h e y did n o t differ concerning left v e n t r i c u l a r infarction size. No patient with purely left inferior v e n t r i c u l a r engagement showed an S T - s e g m e n t elevation in Lead CR~R in c o n t r a s t to all with m a j o r R V I (p < 0.01). T h e p a t i e n t s w i t h m i n o r R V I h a d this elevation in 33 per cent. All p a t i e n t s h a d some degree of posterior s e p t u m i n f a r c t i o n which was not related to the size of R V I . In p a t i e n t s with R V I a fresh t h r o m b u s was present in the right
May, 1976, Vol. 91, No. 5
Diagnosis of right ventricular i n v o l v e m e n t
Table I. R e l a t i o n b e t w e e n S T - s e g m e n t elevation
Hypotension
in L e a d C R , R a n d right v e n t r i c u l a r infarction found at a u t o p s y in 18 p a t i e n t s with a c u t e inferior left v e n t r i c u l a r m y o c a r d i a l i n f a r c t i o n
n=9
No R V involvement (n = 5)
ST-segment elevation No ST-segment elevation % ST-segment elevation
Minor R V involvement (n = 6)
0liguria n=3
Major R V involvement (n = 7)
0 5
2 4
7 0
0
33
100
Table II.
S T - s e g m e n t elevation in L e a d CR~R and R V I size in p a t i e n t s with m i n o r R V I
Pt.
1 2 3 4 5 6
Abnormal I RV ST-segment involvement elevation infarction in Lead CR,R size (%)
+ + --
25 48 10 30 23 15
Survival time (days)
10 2 1 1 9 5
c o r o n a r y a r t e r y in 85 per cent as c o m p a r e d to 17 per cent in p a t i e n t s w i t h o u t R V I (p < 0.05). In major RVI, the mass of infarcted right v e n t r i c u l a r m y o c a r d i u m r a n g e d f r o m 25 to 90 per cent (mean, 46 per cent) a n d survival t i m e r a n g e d from 1 to 21 days (mean, 8 days}. C o r r e s p o n d i n g results for minor R V I are s h o w n in T a b l e II. I n the l a t t e r group the t i m e f r o m onset of s y m p t o m s to the first E C G was less t h a n 12 h o u r s with t h e exception of P a t i e n t 4, in w h o m the s e r u m e n z y m e changes a n d clinical s y m p t o m s suggested t h a t the A M I d a t e d b a c k a couple of days. In the 16 survivors with S T - s e g m e n t elevation in Lead CR~R this was present on admission in 13 and was m o s t p r o n o u n c e d on the first day. T h e S T - s e g m e n t rise h a d usually vanished a f t e r 3 days, remaining in only one patient. T h e remaining three p a t i e n t s h a d long-lasting chest pains and presented with S T - s e g m e n t elevation on the second day. All nine p a t i e n t s with S T segment elevation who died h a d this on admission. Clinical characteristics in relation to S T -
American Heart Journal
Right heart failure n =11 Fig. 2. Interrelation between hypotension, oliguria, and right heart failm~e in 16 survivors with ST-segment elevation in Lead CR4R.
s e g m e n t elevation in L e a d CR4R in t h e survivors and in the deceased are s h o w n in T a b l e s I I I a n d IV. H y p o t e n s i o n a n d r i g h t a n d left Ventricular failure were significantly m o r e c o m m o n a m o n g the survivors with this E C G p a t t e r n , w h e r e a s no such significances were f o u n d when the deceased were compared. If survivors a n d deceased patients are considered together, those with a n S T segment rise in CR~R as c o m p a r e d to those without h a d a significantly higher incidence of right (76 per cent as c o m p a r e d to 27 per cent, p < 0.001) a n d left (96 per cent as c o m p a r e d to 63 per cent, p < 0,01) h e a r t failure, h y p o t e n s i o n (68 per cent as c o m p a r e d to 25 per cent, p < 0.001) as well as oliguria (36 per cent as c o m p a r e d to 9 per cent, p < 0.01.) T h e interrelation b e t w e e n h y p o tension, oliguria, a n d right h e a r t failure is s h o w n in Fig. 2. S e r u m e n z y m e d e t e r m i n a t i o n s p e r m i t t i n g the e s t i m a t i o n of p e a k levels were available for all the 74 survivors. T h e survivors with the described S T segment elevation in L e a d Cr, R h a d significantly higher p e a k levels of S G O T (fn=258), S G P T
573
Erhardt, Sjbgren, and Wahlberg
Table III. Clinical characteristics in relation to
Table IV. Clinical characteristics in relation to
abnormal ST-segment elevation in Lead CR~R among the survivors (n = 74)
abnormal ST-segment elevation in Lead CR4R among the deceased (n = 18) Abnormal CR~R ST-segment elevation
Abnormal CR~R ST-segment elevation Clinical characteristic
Hypotension Oliguria Right heart failure Left heart failure
Clinical characteristic
Present [ Not present
50 19 63 94
19 5 21 57
< 0.05 N.S. < 0.01 < 0.05
(ff1=85) and LDHt (if:= 1,230) t ha n those without this elevation (ffl= 170, 41, and 750, respectively) (p < 0.05). Discussion
In RVI clinical and ECG diagnostics have previously not been considered sensitive enough for the diagnosis, 1~ 11 whereas others have suggested t h a t RVI may be visualized by changes in precordial leads reflecting the right ventricle, i.e., V: to V3.'4, :9, 2o According to our findings a major RVI can be recognized by an abnormal STsegment elevation in Lead CR4R in patients with acute transmural inferior left ventricular myocardial infarction. It must be stressed t h a t this finding is valid only in the absence of anteroseptal infarction which may interfere with the ECG interpretation concerning RVI (see Fig. 3). Earlier autopsy studies ~....... have mostly reported involvement of the posterior right ventricular free wall accompanying inferior LVI with ECG signs typical for diaphragmatic wall infarction. As the right ventricle and the inferior left ventricle wall are usually both supplied by the right coronary artery, this is to be expected. Myers and associates :4 suggested that great difficulty could be anticipated in the ECG differentiation between septal and right ventricular infarction, since ~he former may also be manifested by changes in the precordial leads over the right ventricle. In the present study, however, the STsegment elevation in Lead CR~R was not seen in any of the five patients with posterior septal infarction without right ventricular engagement. Although our present finding of ST-segment elevation in Lead CR4R in RVI could be influ-
574
Hypotension Oliguria Right heart failure Left heart failure
Present ~)
Not present ~)
100 67 100 100
67 33 67 100
N.S. N.S. N.S. N.S.
enced by the position of the heart in the chest as well as by the transient nat ure of ST-rises in AMI, all patients with major right ventricular involvement showed this pattern. Thus, bo th extension and mass of the RVI seem to be of great importance for the ECG diagnosis. Furthermore, all but one of the d e c e a s e d p a t i e n t s with more than 25 per cent of the right ventricular mass engaged showed ST-segment rise in Lead CR4R. The exception was a patient with onset of symptoms 2 days before admission, in whom the absence of this rise may be explained by the transient nature of the ST-segment elevation, ~1as this had vanished after 2 to 3 days in our study. Extension of the infarction from the inferior wall beyond the lateral margin of the right ventricle was found in seven of the nine deceased with STsegment elevation in Lead CR~R which could mean that not only mass but also location of the infarction is of importance for the ECG changes. Our present study does not allow conclusions as to possible ECG changes caused by isolated RVI involving the lateral margin. Furthermore, it cannot be excluded t hat right-sided precordial leads other than CR~R are more revealing in the diagnosis of RVI. However, preliminary results from a study presently performed in our CCU with a further four right-sided chest leads, i.e., CR~R, CR7R, and two leads placed one intercostal space above and below CR4R, respectively, do not suggest t hat much is to be gained by additional leads. Correlation between infarction size and peak enzyme levels, usually SGOT and LDHt, has previously been described ~ and in the present study ST-segment rises in Lead CR4R were corre-
May, 1976, Vol. 91, No. 5
Diagnosis of right ventricular involvement
Fig. 3. Representative ECG showing ST-segment elevation in Lead CR~R in a patient with acute inferior infarction. V leads have been added for comparison. This patient had the following hemodynamic data: RV pressures 24/12 and pulmonary artery 20/10 mm. Hg on the first day, with a subsequent further increase in rightsided filling pressures. There was hypotension and there were long periods of oliguria requh'ing furosemide doses exceeding 500 mg. daily. Paper speed 50 mm. per second.
lated to higher S G O T and L D H t peak values, which suggests greater infarction sizes, perhaps in part due to the additional damage of the right ventricular myocardium. Cohn and associates 1~ suggested t h a t a u n i q u e clinical and h e m o d y n a m i c s y n d r o m e arises when LVI is accompanied by RVI. T h e i r six p a t i e n t s presented clinically with engorged neck veins, hypotension, and h e a r t block, and h e m o d y n a m i c measurements disclosed t h a t the right v e n t r i c u l a r filling pressure equalled or exceeded left ventricular end-diastolic pressures. Others 6-', 1~have also shown this h e m o d y n a m i c p a t t e r n . T h e findings in the present s t u d y of an association between this ST-segment elevation in Lead CR~R and hypotension and right and left h e a r t failure are in accordance with these studies (Table III). Several of the patients with these E C G findings, however, failed to show clinical signs of this h e m o d y n a m i c pattern. This m a y have been due to diuretic t h e r a p y in some cases, yet it needs pointing o u t t h a t little is known of the h e m o d y n a m i c consequences of infarction of the free right v e n t r i c u l a r wall per se. Septal and right v e n t r i c u l a r papillary muscle infarction which o f t e n accompanies R V I ~ m a y also be of m a j o r i m p o r t a n c e , and t h e added
American Heart Journal
afterload due to c o n c o m i t a n t left h e a r t failure may also affect right h e a r t performance. According to our results, S T - s e g m e n t elevation in Lead CR4R implies poor prognosis as to shortterm survival, and early recognition of R V I could be vital. This is compatible with the low incidence of old RVI previously r e p o r t e d at a u t o p s y 4, 12 In conclusion, our findings lend support to the following: 1. An ST-segment elevation of more t h a n 1 mm. in Lead CR~R indicates right ventricular involvement in patients with t r a n s m u r a l acute inferior myocardial infarction. 2. This ST-segment elevation indicates right ventricular myocardial d a m a g e exceeding 25 per cent or reaching the lateral margin of right ventricular free wall. 3. Patients with the above S T - s e g m e n t elevation often develop hypotension, oliguria and right and left h e a r t failure, and h a v e poor prognosis as to short-term survival.
Summary T h e S T segment in a single right-sided chest lead, CR~R, has been studied in 92 consecutive patients with acute inferior t r a n s m u r a l ' l e f t ven-
575
Erhardt, Sjbgren, and Wahlberg
tricular myocardial infarction. A transient STs e g m e n t r i s e o f m o r e t h a n 1 m m . w a s r e c o r d e d in 25 p a t i e n t s , a n d s t r o n g l y i n d i c a t e d a s i g n i f i c a n t extension of the infarction to the posterior free right ventricular wall according to autopsy findings. T h i s E C G p a t t e r n w a s f u r t h e r m o r e associated with right-sided heart failure, hypotension and oliguria. Left heart failure was also common. The short-term prognosis of patients with STsegment elevation in CR4R was poor.
10. 11. 12. 13. 14.
REFERENCES
1. Wartman, W. B., and Hellerstein, H. K.: The incidence of heart disease in 2000 consecutive autopsies, Ann. Intern. Med. 28:41, 1948. 2. Yater, W. M., Traum, A. H., Springs, S., Brown, W. G., Fitzgerald, R. P., Geisler, M. A , and Wilcox, B. B.: Coronary artery disease in men 18 to 39 years of age. Report of 866 cases, 450 with necropsy examination, AM. HEART J. 36:683, 1948. 3. Lisa, J. R., and Ring, A.: Myocardial infarction or gross fibrosis. Analysis of 100 necropsies, Arch. Intern. Med. 50:131, 1932. 4. Erhardt, L. R.: Clinical and pathological observations in different types of acute myocardial infarction, Acta Med. Scand. SuppL 560, 1974. 5. Lassers, B. W,, George, M., Anderton, J. L., Higgins, M. R., and Philip, T.: Left ventricular failure in acute myocardial infarction, AM. HEART J. 25:511, 1970. 6. Fluck, D. C., Valentine, P. A., Treister, B., Higgs, B., Reid, D. N., Steiner, R. E., and Monsey, J. P. D.: Right heart pressures in acute myocardial infarction, Br. Heart J. 29:748, 1967. 7. Rigo, P., Taylor, D . , Weisfeldt, M., Kelly, D., and Strauss, H. W.: Right ventricular dysfunction in patients with inferior myocardial infarction (abst.), Circulation, 47-48(Suppl. IV):207, 1973. 8. Guiha, N. H., Limas, C. J., Broder, M. I., and Cohn, J. N.: Predominant right ventricular failure in clinical and experimental right ventricular infarction (abst.), Clin. Res. 20:375, 1972. 9. A1-Sadir, J., Falicov, R., Zahavi, I., Brooks, H,, and Resnekov, L.: Right ventricular dysfunction in acute
576
15.
16.
17. 18. 19. 20. 21.
22.
inferior myocardial infarction (abst.), Circulation Suppl. IV:59, 1973. Cohn, J. N., Guiha, N. H., Broder, M.I., and Limas, C. J.: Right ventricular infarction, AM. HEART J. 33:209, 1974. Rotman, M., Ratliff, N. B., and Hawley, J: Right ventricular infarction: A hemodynamic diagnosis, Br. Heart J. 36:941, 1974. Wade, W. G.: The pathogenesis of infarction of the right ventricle, Br. Heart J. 21:545. 1959. Wells, D. E., and Befeler, B.: Dysfunction of the right ventricle in coronary artery disease, Chest 66:230. 1974. Myers, G. B., Klein, H. A., and Hiratzka, T.: IV. Correlation of electrocardiographic and pathologic findings in infarction of the interventricular septum and right ventricle, AM. HEART J. 37:720, 1949. Hofvendahl, S.: Influence of treatment in a coronary care unit on prognosis in acute myocardial infarction A controlled study in 271 cases. Acta Med. Scand. Suppl. 519, 1971. Sayen, J. J.. and Sheldon, W. F.: The heart muscle and the electrocardiogram in coronary disease. II. Difficulties of description and illustration of ventricular muscle lesions with a method for their graphic representation m a myocardial map, AM. HEART J. 38:688. 1949. Nachlas, M. M.. and Schnitka, T. K.: Macroscopic identification of early myocardial infarcts by alterations in dehydrogenase activity, Am. J. Pathol. 42:379, 1963. Harnarayan, C.. Bennett, M A., Pentecost. B. L., and Brewer. D. B.: Quantitative study of infarcted myocardium in cardiogenic shock, Br. Heart J. 32:728, 1970. Hfibner, A.: fiber den Rechsherzinfarkt, Deutsch. Gesundheitsw, 23:7074, 1968. Levy, L.. and Hyman, A. L.: Difficulties in the electrocardiographic diagnoses of myocardial infarction, AM. HEART J. 39:243, 1950. Bayley, R. H., LaDue, J. S.. and York. D. J.: Electrocardiographic changes (local ventricular ischemia and injury) produced in the dog by temporary occlusion of a coronary artery, showing a new stage in the evolution of a myocardial infarction, AM. HEART J. 27:164, 1944. Nachlas, M. M., Friedman. M. M., and Cohen. S. P.: A method for the quantification of myocardial infarcts and the relation of serum enzyme levels to infarct size, Surgery 55:700, 1964.
May, 1976, Vol. 91, No. 5