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Right ventricular infarction mimicking anterior infarction: A case report
Journal of Electrocardiology Vol. 32 No. 4 1999
Right Ventricular Infarction Mimicking Anterior Infarction: A Case Report
M i g u e l A n g e l A m a u V i ves, M D , L u i s A l m e n a r B o n e r , M D , J o a q u i n R u e d a Soriano, MD, Luis A n d r e s L a l a g u n a , MD, A n a O s a Sdez, M D , A d o l f o R i n c 6 n d e A r e l l a n o , M D , M i g u e l P a l e n c i a P~rez, MD
Abstract: Right ventricular infarction usually occurs in association with
inferior infarction, with no remarkable electrocardiographic signs in conventional leads. This report describes a patient with a previous inferior acute myocardial infarction who developed right ventricular infarction with significant anterior lead ST segment elevation (V1-V4) caused by the loss of two large right ventricular branches during a coronary angioplasty of the right coronary artery. The case is discussed and the literature is reviewed. Key w o r d s : right ventricular, infarction, electrocardiography, coronary angioplasty.
Case Report
study was performed. Ventriculography showed severe posterobasal hypokinesia with slightly depressed ventricular function. Coronary angiography demonstrated subtotal occlusion of the middle right coronary artery, distal to the exit of two large right ventricular branches, with a normal left coronary tree (Fig. 1C). It was decided to perform percutaneous transluminal coronary angioplasty (PTCA) on this lesion. When the guide was inserted, a complete retrograde, nonobstructive dissection up to the right coronary artery opening occurred (Fig. 1D). T h e patient reported chest pain, and ST segment elevation showed in the monitoring leads. The pain and ST segment elevation subsided with sublingual nitrates, intracoronary verapamil, and intravenous morphine hydrochloride. The control ECG performed 1 hour later, w h e n the patient was fully asymptomatic, showed a significant ST segment elevation in V1-V4 with minimal or no changes in the inferior aspect compared with baseline ECGs (Fig. 2A). Repeat angiography was performed, and showed a complete occlusion
A 34-year old patient with a history of smoking (40 cigarettes a day) and mild hypertension attending the emergency unit for chest pain. On admission, the physical examination was normal, with a blood pressure of 130/70 m mHg. An electrocardiogram (ECG) showed sinus r hyt hm with normal atrioventricular and intraventricular conduction and inferior lead ST segment elevation with a depressed ST segment in I, aVL, and VI-V 6 (Fig. 1A). Therapy with aspirin, fibrinolysis with rTPA, and intravenous heparin was started. The peak enzyme increase was creatine phosphokinase (CPK) 963 IU/L, with CK-MB 102 IU/L. The ECG progressed to a pattern of Q wave inferior myocardial infarction (Fig. 1B). On day 10, the patient suffered rest angina, and an angiohemodynamic From the Hospital La Fe, Valencia, Spain.
Reprint requests: Miguel Angel Arnau Vives, MD, C/Padre Tomds de Montafiana 22-25, C.Postah 46023, Valencia, Espafia. Copyright © 1999 by Churchill Livingstone ®
0022-0736/99• 3204-0008510.00/0 359
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Journal of Electrocardiology Vol. 32 No. 4 October 1999
!l
v3 i
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~ i! +7 ?~.: . 2 2 , ~ ; : 2 2 k
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B
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Fig. 1. (A) ECG on admission, showing acute inferior infarction with depressed ST segment in all precordial leads, I and aVL. (B) ECG after 8 days of evolution, showing Q wave inferior myocardial infarction. (C) Coronary angiography, showing subtotal lesion in middle right coronary artery distal to right ventricular branches, with normal left coronary tree. (D) Complete retrograde nonobstructive dissection up to the opening of the right coronary artery when the guide was inserted to perform PTCA.
of the p r o x i m a l right c o r o n a r y artery with loss of b o t h ventricular branches. The left c o r o n a r y tree was not involved (Fig. 2D). An e n z y m e increase consistent with myocardial necrosis was s h o w n (CPK, 6,300 IU/L; CK-MB, 204 IU/L). Echocardiography d e m o n s t r a t e d h y p o k i n e sia of the basal and middle segments of the posterior interventricular s e p t u m and inferior wall, with norm a l m o v e m e n t of all other segments, mild ventricular dilation, and left ventricular ejection fraction of 53%. Resolution of the changes in V~-V 4 was associated with n e w ST elevation of the inferior leads (III, aVF) and ST depression in lateral leads (I, aVL) (Fig. 2B). W h e n the acute stage resolved, no QS patterns developed and there was n o loss of voltage/amplitude of r waves c o m p a r e d with the baseline ECG. (Fig. 2C).
On day 4 postcatheterization, cardiac scintigrap h y was p e r f o r m e d with Tc 9 9 m p y r o p h o s p h a t e , w h i c h ruled out anterior acute myocardial infarction (AMI) and c o n f i r m e d the presence of right ventricular necrosis.
Discussion C h o u et al. (1) w e r e the first to report that right ventricular infarction could be evidenced as ST s e g m e n t elevation on the anterior side. They studied 11 cases of inferior AMI with necropsy (n = 5) and h e m o d y n a m i c (n = 6) data suggesting right ventricle i n v o l v e m e n t . In 8 of the 11 cases, t h e y f o u n d ST s e g m e n t elevations in precordial leads (6 in V~, 1 in V~-V 3, 1 in V~-V4), in addition to the
Right Ventricular Infarction
A
B
C
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Arnau Vives et al.
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D
Fig. 2. (A) ECG after dissection, showing significant anterior lead ST segment elevation (Vx-V4), with no significant changes in the inferior side. (B) ECG 6 hours later, showing the trend to correction of the anterior lesion associated with a new ST segment elevation in the inferior side with a mirror image in the upper lateral region (I, aVL). (C) ECG on discharge, showing resolution of repolarization changes, with no development of QS patterns and/or loss or reduction in r waves compared with baseline ECG (Fig. 1B). (D) The electrocardiographic findings resulted from the loss of the right ventricular branches, after a stump in the proximal right coronary artery was evidenced on coronary angiography. The left coronary tree was spared.
inferior aspect, w h i c h were considered to suggest coexistent right ventricular infarction "in the absence of other explanations." Geft et al. (2) studied 69 patients with ST segment elevation in V~-V 5 (not necessarily in all). In five (7%), such electrocardiographic expression suggested right ventricular infarction, w h i c h was confirmed by echocardiography, coronary angiography, Tc 99m pyrophosphate, thallium 201, and isotopic ventriculography. In two cases, ST elevation occurred in V1-V 5, and in the other three cases in Vx-V 3. Four cases had a m i n i m u m ST segment elevation at the inferior side; the other h a d a i - m m depression. All of t h e m s h o w e d occlusion of the right c o r o n a r y artery, proximal to the exit of ventricular branches, with no significant lesions in the
left coronary tree (3 cases, normal; 1 case, 20% lesion in the anterior descending artery; 1 case, lesion < 5 0 % in the anterior descending artery). Bellamy and Hollman (3) later reported the case of a patient w h o developed isolated right ventricular infarction after a major right ventricular b r a n c h was lost during coronary angioplasty. The left coro n a r y artery s h o w e d minimal irregularities. The ECG s h o w e d ST segment elevation at the inferior side and VI-V 3. Echocardiography and scintigraphy with Tc 99m p y r o p h o s p h a t e evidenced right ventricular infarction with n o r m a l m o v e m e n t and no uptake at the left ventricle. Halkett et al. (4) reported two cases of inferior AMI with elevated ST segment in the anterior side (VI-V 3 and V1-V5). Right ventricular infarction was
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demonstrated by echocardiography and radioisotopes, both showing occlusion of the proximal right coronary artery with normal left coronary tree. M a r c h e n a et al. (5) reported the case of a patient with residual inferior AMI (coronary angiography showed 99% lesion of the right coronary artery distal to a ventricular branch, minimal abnormalities in the left coronary artery) which, 2 years after this angiography, evidenced enzymatically docum e n t e d AMI with ST segment elevation in V~-V 3 and 1 m m ST depression in the inferior side. Repeat coronary angiography found occlusion of the proximal right coronary artery with loss of the right ventricular branch and no significant changes in the left 'coronary artery. The electric signs of right ventricular infarction were not masked by those usually prevailing in the posteroinferior wall, due to residual necrosis in that area. Bolt et al. (6) reviewed their database of 10,000 patients w h o u n d e r w e n t coronary angioplasty and found 9 cases of PTCA to proximal or middle right coronary artery in which a major ventricular branch was lost during the procedure. Six patients had d o c u m e n t e d previous inferior AMI. In all cases in which V3R-VsR were recorded (n = 6) there was ST segment elevation in those leads, and only in one patient a m i n i m u m ST segment elevation was d o c u m e n t e d in the inferior aspect. ST segment was elevated in V1-V 3 in 6 cases, in V~-V 4 in 2 cases, and in V~-V 5 in the other. The authors concluded that the pattern of ST segment elevation in V3R-VsR and V~-V 3 could be specific of isolated right ventricle AMI related to PTCA and secondary to the occlusion of a ventricular branch perfusing the anterior wall of the right ventricle. In 1996, Klan and Chou (7) d o c u m e n t e d four cases of inferior AMI associated to with right ventricular infarction. In all cases, a complete occlusion of the proximal right coronary artery was found, in three cases the left coronary artery was normal, and in the other a 60% lesion was s h o w n at the circumflex artery. The four patients had ST segment elevation in V4R, and three of t h e m in V1-V 3. Initial and evolutive electrocardiographic patterns to guide the differential diagnosis b e t w e e n right ventricular infarction and anterior AMI have been investigated. The fact that the magnitude of ST segment elevation in V~-V 5 decreases from right to left and that the progressive regression of ST changes occurs with no development of Q waves suggests right ventricular infarction (1,2). In eight patients from the series of Chou et al. (1) and five patients from that of Geft et al. (2) with anterior ST elevation, there was no progression to a QS pattern after the acute stage was resolved. However, these
findings do not seem to be pathognomonic, since the two patients reported by Halkett (4) developed anterior QS pattern (Vx-V3 and V~-Vs) and showed normal m o t i o n of the left ventricle by echocardiography, these patterns being attributed to right ventricular dilation with clockwise rotation. Of the four patients of Klan and Chou (7), the three showing ST segment elevation in V~-V 3 progressed to a QS pattern in those leads, and the remaining patient had embryonic r waves in V~-V 4. In all cases, a normal motility of the anterior aspect and anterior septum of the left ventricle and the permeability of the anterior descending artery were s h o w n by echocardiography. Therefore, there are no consistent evolutive patterns, and the appearance of ST, while usually m a x i m u m in Vl-V 2 and decreasing to the left, m a y be capricious and progress to n o r m a l without dev e l o p m e n t of Q waves or loss of r waves, or lead to QS patterns (sometimes extensive in Vx-Vs) without this causing left heart disease. An electrocardiographic criterion established by Ldpez-Senddn and Coma-Canella (8) in the differential diagnosis of right ventricular infarction and anteroseptal AMI is the relationship b e t w e e n ST segment upsloping in V4R-V3. In most patients with right ventricular infarction, ST segment elevation in V4R is higher t h a n that f o u n d in V~-V3, leads in which there m a y or m a y not be electrocardiographic changes. By contrast, in infarctions of the anterior side or interventricular septum, ST segm e n t elevation in V4R, if any, is always lower than that f o u n d in V~-V 3. Kim et al. (9) have described the association of several electrocardiographic patterns in acute anterior myocardial infarction with the culprit lesion site in left anterior descending coronary artery, making an algorithm based on a VL and VI-V 3. M o r e o v e r Correale et al. (10) compared ECG patterns in acute inferior myocardial infarction with and without right ventricular involvement, and discovered h o w extension to the right ventricle could affect or mask the ECG signs of posterior wall. Thus, the presence of an acute right ventricular infarction in the context of a previous posteroinferior myocardial infarction could m a k e that the vector of the ST segment will point forward, causing anterior lead ST segment elevation (V1-V4). In our patient, after dissection of the right coronary artery and the loss of right ventricular marginal arteries, significant ST segment elevation occurred in V~-V 4, which was m a x i m u m in V2, with minimal changes in the inferior side. This reflected a prevailing lesion in the right ventricle, which in this case masked the electric forces of the postero-
Right Ventricular Infarction
i n f e r i o r wall, r e d u c e d b y t h e e x i s t e n c e of p r e v i o u s n e c r o s i s i n t h a t a r e a . W h e n t h e ECG r e s o l v e d , a n e w ST s e g m e n t e l e v a t i o n w a s e v i d e n c e d in III a n d a VF w i t h a m i r r o r i m a g e i n I a n d aVL, w h i c h w a s l i k e l y to b e p r e s e n t i n i t i a l l y b u t w a s " m a s k e d " b y the dominant, transient anterior right lesion. F i n a l l y , e l e v a t i o n s i n ST s e g m e n t at t h e a n t e r i o r side r e s o l v e d , i n o u r case w i t h o u t d e v e l o p m e n t of a QS p a t t e r n or loss or r e d u c t i o n of r w a v e s f r o m b a s e l i n e ECGs. In conclusion, isolated right ventricular infarction o r i n f a r c t i o n p r e v a i l i n g in t h e r i g h t v e n t r i c l e c a n c a u s e ST s e g m e n t e l e v a t i o n i n t h e a n t e r i o r leads. T h e c o n d i t i o n s u s u a l l y l e a d i n g to it a r e t h o s e in which the right ventricular lesion prevails over p o s t e r o i n f e r i o r a c u t e i s c h e m i a , w h i c h c a n o c c u r in a c u t e o c c l u s i o n s of small, n o n d o m i n a n t r i g h t c o r o n a r y arteries, o c c l u s i o n s of p r o x i m a l r i g h t c o r o n a r y b e f o r e t h e o u t l e t of v e n t r i c u l a r b r a n c h e s , p a r t i c u l a r l y in p a t i e n t s w i t h p r e v i o u s i n f e r i o r A M I a n d / o r w i t h left d o m i n a n c e o r c o d o m i n a n c e . It also o c c u r s w i t h t h e loss of v e n t r i c u l a r b r a n c h e s d u r i n g a n g i o p l a s t y of t h e p r o x i m a l o r m i d d l e r i g h t c o r o n a r y a r t e r y a n d in p a t i e n t s w i t h s e v e r e l e s i o n s a s s o c i a t e d with the right coronary artery preventing collateral circulation.
References 1. Chou T, Bel-Kahn JV, Alien J e t al: Electrocardiographic diagnosis of right ventricular infarction. Am J Med 70:1175, 1981
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2. Geft IL, Shah PK, Rodriguez L e t al: ST elevations in leads V1 to V5 m a y be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 53:991, 1984 3. Bellamy GR, Hollman J: Isolated right ventricular infarction following percutaneous translmninal coronary angioplasty. Am Heart J 111:168, 1986 4. Halkett JA, Commerford PJ, Scott R: Right ventricular infarction mimicking extensive anterior infarction. Chest 90:617, I986 5. Marchena E J, Palomo AR, Trohman RG et al: Anglographically demonstrated isolated acute right ventricular infarction presenting as ST elevation in leads V1 to V3. Am Heart J 113:391, 1987 6. Bolt CL, Vermeersch PH, Plokker HW: Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary ballon angioplasty. Eur Heart J I7:247, 1996 7. Klan ZU, Chou T: Right ventricular infarction mimicking acute anteroseptal left ventricular infarction. Am Heart J 132:1089, 1996 8. L6pez-Send6n J, Coma-Canella J: Diagndstico electrocardiogr~fico del infarto de ventrfculo derecho, p. 283. In Formaci6n continuada en Cardiologia. Avances en electrocardiologfa. Doyma SA, Barcelona, 1992 9. Kim T, Alturk N, Shaikh N, et al: An electrocardiographic algorithm for the prediction of the culprit lesion site in acute anterior myocardial infarction. Clin Cardiol 22:77, 1999 10. Correale F, Battista R, Martone A, et al: Electrocardiographic patterns in acute inferior myocardial infarction with and without right ventricular involvement: Classification, diagnostic and prognostic value, masking effect. Clin Cardiol 22:37, 1999
Right Ventricular Infarction Mimicking Anterior Infarction: A Case Report
M i g u e l A n g e l A m a u V i ves, M D , L u i s A l m e n a r B o n e r , M D , J o a q u i n R u e d a Soriano, MD, Luis A n d r e s L a l a g u n a , MD, A n a O s a Sdez, M D , A d o l f o R i n c 6 n d e A r e l l a n o , M D , M i g u e l P a l e n c i a P~rez, MD
Abstract: Right ventricular infarction usually occurs in association with
inferior infarction, with no remarkable electrocardiographic signs in conventional leads. This report describes a patient with a previous inferior acute myocardial infarction who developed right ventricular infarction with significant anterior lead ST segment elevation (V1-V4) caused by the loss of two large right ventricular branches during a coronary angioplasty of the right coronary artery. The case is discussed and the literature is reviewed. Key w o r d s : right ventricular, infarction, electrocardiography, coronary angioplasty.
Case Report
study was performed. Ventriculography showed severe posterobasal hypokinesia with slightly depressed ventricular function. Coronary angiography demonstrated subtotal occlusion of the middle right coronary artery, distal to the exit of two large right ventricular branches, with a normal left coronary tree (Fig. 1C). It was decided to perform percutaneous transluminal coronary angioplasty (PTCA) on this lesion. When the guide was inserted, a complete retrograde, nonobstructive dissection up to the right coronary artery opening occurred (Fig. 1D). T h e patient reported chest pain, and ST segment elevation showed in the monitoring leads. The pain and ST segment elevation subsided with sublingual nitrates, intracoronary verapamil, and intravenous morphine hydrochloride. The control ECG performed 1 hour later, w h e n the patient was fully asymptomatic, showed a significant ST segment elevation in V1-V4 with minimal or no changes in the inferior aspect compared with baseline ECGs (Fig. 2A). Repeat angiography was performed, and showed a complete occlusion
A 34-year old patient with a history of smoking (40 cigarettes a day) and mild hypertension attending the emergency unit for chest pain. On admission, the physical examination was normal, with a blood pressure of 130/70 m mHg. An electrocardiogram (ECG) showed sinus r hyt hm with normal atrioventricular and intraventricular conduction and inferior lead ST segment elevation with a depressed ST segment in I, aVL, and VI-V 6 (Fig. 1A). Therapy with aspirin, fibrinolysis with rTPA, and intravenous heparin was started. The peak enzyme increase was creatine phosphokinase (CPK) 963 IU/L, with CK-MB 102 IU/L. The ECG progressed to a pattern of Q wave inferior myocardial infarction (Fig. 1B). On day 10, the patient suffered rest angina, and an angiohemodynamic From the Hospital La Fe, Valencia, Spain.
Reprint requests: Miguel Angel Arnau Vives, MD, C/Padre Tomds de Montafiana 22-25, C.Postah 46023, Valencia, Espafia. Copyright © 1999 by Churchill Livingstone ®
0022-0736/99• 3204-0008510.00/0 359
360
Journal of Electrocardiology Vol. 32 No. 4 October 1999
!l
v3 i
AVL
~ i! +7 ?~.: . 2 2 , ~ ; : 2 2 k
AVF
If6 1 A
B
C
D
Fig. 1. (A) ECG on admission, showing acute inferior infarction with depressed ST segment in all precordial leads, I and aVL. (B) ECG after 8 days of evolution, showing Q wave inferior myocardial infarction. (C) Coronary angiography, showing subtotal lesion in middle right coronary artery distal to right ventricular branches, with normal left coronary tree. (D) Complete retrograde nonobstructive dissection up to the opening of the right coronary artery when the guide was inserted to perform PTCA.
of the p r o x i m a l right c o r o n a r y artery with loss of b o t h ventricular branches. The left c o r o n a r y tree was not involved (Fig. 2D). An e n z y m e increase consistent with myocardial necrosis was s h o w n (CPK, 6,300 IU/L; CK-MB, 204 IU/L). Echocardiography d e m o n s t r a t e d h y p o k i n e sia of the basal and middle segments of the posterior interventricular s e p t u m and inferior wall, with norm a l m o v e m e n t of all other segments, mild ventricular dilation, and left ventricular ejection fraction of 53%. Resolution of the changes in V~-V 4 was associated with n e w ST elevation of the inferior leads (III, aVF) and ST depression in lateral leads (I, aVL) (Fig. 2B). W h e n the acute stage resolved, no QS patterns developed and there was n o loss of voltage/amplitude of r waves c o m p a r e d with the baseline ECG. (Fig. 2C).
On day 4 postcatheterization, cardiac scintigrap h y was p e r f o r m e d with Tc 9 9 m p y r o p h o s p h a t e , w h i c h ruled out anterior acute myocardial infarction (AMI) and c o n f i r m e d the presence of right ventricular necrosis.
Discussion C h o u et al. (1) w e r e the first to report that right ventricular infarction could be evidenced as ST s e g m e n t elevation on the anterior side. They studied 11 cases of inferior AMI with necropsy (n = 5) and h e m o d y n a m i c (n = 6) data suggesting right ventricle i n v o l v e m e n t . In 8 of the 11 cases, t h e y f o u n d ST s e g m e n t elevations in precordial leads (6 in V~, 1 in V~-V 3, 1 in V~-V4), in addition to the
Right Ventricular Infarction
A
B
C
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Arnau Vives et al.
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D
Fig. 2. (A) ECG after dissection, showing significant anterior lead ST segment elevation (Vx-V4), with no significant changes in the inferior side. (B) ECG 6 hours later, showing the trend to correction of the anterior lesion associated with a new ST segment elevation in the inferior side with a mirror image in the upper lateral region (I, aVL). (C) ECG on discharge, showing resolution of repolarization changes, with no development of QS patterns and/or loss or reduction in r waves compared with baseline ECG (Fig. 1B). (D) The electrocardiographic findings resulted from the loss of the right ventricular branches, after a stump in the proximal right coronary artery was evidenced on coronary angiography. The left coronary tree was spared.
inferior aspect, w h i c h were considered to suggest coexistent right ventricular infarction "in the absence of other explanations." Geft et al. (2) studied 69 patients with ST segment elevation in V~-V 5 (not necessarily in all). In five (7%), such electrocardiographic expression suggested right ventricular infarction, w h i c h was confirmed by echocardiography, coronary angiography, Tc 99m pyrophosphate, thallium 201, and isotopic ventriculography. In two cases, ST elevation occurred in V1-V 5, and in the other three cases in Vx-V 3. Four cases had a m i n i m u m ST segment elevation at the inferior side; the other h a d a i - m m depression. All of t h e m s h o w e d occlusion of the right c o r o n a r y artery, proximal to the exit of ventricular branches, with no significant lesions in the
left coronary tree (3 cases, normal; 1 case, 20% lesion in the anterior descending artery; 1 case, lesion < 5 0 % in the anterior descending artery). Bellamy and Hollman (3) later reported the case of a patient w h o developed isolated right ventricular infarction after a major right ventricular b r a n c h was lost during coronary angioplasty. The left coro n a r y artery s h o w e d minimal irregularities. The ECG s h o w e d ST segment elevation at the inferior side and VI-V 3. Echocardiography and scintigraphy with Tc 99m p y r o p h o s p h a t e evidenced right ventricular infarction with n o r m a l m o v e m e n t and no uptake at the left ventricle. Halkett et al. (4) reported two cases of inferior AMI with elevated ST segment in the anterior side (VI-V 3 and V1-V5). Right ventricular infarction was
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demonstrated by echocardiography and radioisotopes, both showing occlusion of the proximal right coronary artery with normal left coronary tree. M a r c h e n a et al. (5) reported the case of a patient with residual inferior AMI (coronary angiography showed 99% lesion of the right coronary artery distal to a ventricular branch, minimal abnormalities in the left coronary artery) which, 2 years after this angiography, evidenced enzymatically docum e n t e d AMI with ST segment elevation in V~-V 3 and 1 m m ST depression in the inferior side. Repeat coronary angiography found occlusion of the proximal right coronary artery with loss of the right ventricular branch and no significant changes in the left 'coronary artery. The electric signs of right ventricular infarction were not masked by those usually prevailing in the posteroinferior wall, due to residual necrosis in that area. Bolt et al. (6) reviewed their database of 10,000 patients w h o u n d e r w e n t coronary angioplasty and found 9 cases of PTCA to proximal or middle right coronary artery in which a major ventricular branch was lost during the procedure. Six patients had d o c u m e n t e d previous inferior AMI. In all cases in which V3R-VsR were recorded (n = 6) there was ST segment elevation in those leads, and only in one patient a m i n i m u m ST segment elevation was d o c u m e n t e d in the inferior aspect. ST segment was elevated in V1-V 3 in 6 cases, in V~-V 4 in 2 cases, and in V~-V 5 in the other. The authors concluded that the pattern of ST segment elevation in V3R-VsR and V~-V 3 could be specific of isolated right ventricle AMI related to PTCA and secondary to the occlusion of a ventricular branch perfusing the anterior wall of the right ventricle. In 1996, Klan and Chou (7) d o c u m e n t e d four cases of inferior AMI associated to with right ventricular infarction. In all cases, a complete occlusion of the proximal right coronary artery was found, in three cases the left coronary artery was normal, and in the other a 60% lesion was s h o w n at the circumflex artery. The four patients had ST segment elevation in V4R, and three of t h e m in V1-V 3. Initial and evolutive electrocardiographic patterns to guide the differential diagnosis b e t w e e n right ventricular infarction and anterior AMI have been investigated. The fact that the magnitude of ST segment elevation in V~-V 5 decreases from right to left and that the progressive regression of ST changes occurs with no development of Q waves suggests right ventricular infarction (1,2). In eight patients from the series of Chou et al. (1) and five patients from that of Geft et al. (2) with anterior ST elevation, there was no progression to a QS pattern after the acute stage was resolved. However, these
findings do not seem to be pathognomonic, since the two patients reported by Halkett (4) developed anterior QS pattern (Vx-V3 and V~-Vs) and showed normal m o t i o n of the left ventricle by echocardiography, these patterns being attributed to right ventricular dilation with clockwise rotation. Of the four patients of Klan and Chou (7), the three showing ST segment elevation in V~-V 3 progressed to a QS pattern in those leads, and the remaining patient had embryonic r waves in V~-V 4. In all cases, a normal motility of the anterior aspect and anterior septum of the left ventricle and the permeability of the anterior descending artery were s h o w n by echocardiography. Therefore, there are no consistent evolutive patterns, and the appearance of ST, while usually m a x i m u m in Vl-V 2 and decreasing to the left, m a y be capricious and progress to n o r m a l without dev e l o p m e n t of Q waves or loss of r waves, or lead to QS patterns (sometimes extensive in Vx-Vs) without this causing left heart disease. An electrocardiographic criterion established by Ldpez-Senddn and Coma-Canella (8) in the differential diagnosis of right ventricular infarction and anteroseptal AMI is the relationship b e t w e e n ST segment upsloping in V4R-V3. In most patients with right ventricular infarction, ST segment elevation in V4R is higher t h a n that f o u n d in V~-V3, leads in which there m a y or m a y not be electrocardiographic changes. By contrast, in infarctions of the anterior side or interventricular septum, ST segm e n t elevation in V4R, if any, is always lower than that f o u n d in V~-V 3. Kim et al. (9) have described the association of several electrocardiographic patterns in acute anterior myocardial infarction with the culprit lesion site in left anterior descending coronary artery, making an algorithm based on a VL and VI-V 3. M o r e o v e r Correale et al. (10) compared ECG patterns in acute inferior myocardial infarction with and without right ventricular involvement, and discovered h o w extension to the right ventricle could affect or mask the ECG signs of posterior wall. Thus, the presence of an acute right ventricular infarction in the context of a previous posteroinferior myocardial infarction could m a k e that the vector of the ST segment will point forward, causing anterior lead ST segment elevation (V1-V4). In our patient, after dissection of the right coronary artery and the loss of right ventricular marginal arteries, significant ST segment elevation occurred in V~-V 4, which was m a x i m u m in V2, with minimal changes in the inferior side. This reflected a prevailing lesion in the right ventricle, which in this case masked the electric forces of the postero-
Right Ventricular Infarction
i n f e r i o r wall, r e d u c e d b y t h e e x i s t e n c e of p r e v i o u s n e c r o s i s i n t h a t a r e a . W h e n t h e ECG r e s o l v e d , a n e w ST s e g m e n t e l e v a t i o n w a s e v i d e n c e d in III a n d a VF w i t h a m i r r o r i m a g e i n I a n d aVL, w h i c h w a s l i k e l y to b e p r e s e n t i n i t i a l l y b u t w a s " m a s k e d " b y the dominant, transient anterior right lesion. F i n a l l y , e l e v a t i o n s i n ST s e g m e n t at t h e a n t e r i o r side r e s o l v e d , i n o u r case w i t h o u t d e v e l o p m e n t of a QS p a t t e r n or loss or r e d u c t i o n of r w a v e s f r o m b a s e l i n e ECGs. In conclusion, isolated right ventricular infarction o r i n f a r c t i o n p r e v a i l i n g in t h e r i g h t v e n t r i c l e c a n c a u s e ST s e g m e n t e l e v a t i o n i n t h e a n t e r i o r leads. T h e c o n d i t i o n s u s u a l l y l e a d i n g to it a r e t h o s e in which the right ventricular lesion prevails over p o s t e r o i n f e r i o r a c u t e i s c h e m i a , w h i c h c a n o c c u r in a c u t e o c c l u s i o n s of small, n o n d o m i n a n t r i g h t c o r o n a r y arteries, o c c l u s i o n s of p r o x i m a l r i g h t c o r o n a r y b e f o r e t h e o u t l e t of v e n t r i c u l a r b r a n c h e s , p a r t i c u l a r l y in p a t i e n t s w i t h p r e v i o u s i n f e r i o r A M I a n d / o r w i t h left d o m i n a n c e o r c o d o m i n a n c e . It also o c c u r s w i t h t h e loss of v e n t r i c u l a r b r a n c h e s d u r i n g a n g i o p l a s t y of t h e p r o x i m a l o r m i d d l e r i g h t c o r o n a r y a r t e r y a n d in p a t i e n t s w i t h s e v e r e l e s i o n s a s s o c i a t e d with the right coronary artery preventing collateral circulation.
References 1. Chou T, Bel-Kahn JV, Alien J e t al: Electrocardiographic diagnosis of right ventricular infarction. Am J Med 70:1175, 1981
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2. Geft IL, Shah PK, Rodriguez L e t al: ST elevations in leads V1 to V5 m a y be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 53:991, 1984 3. Bellamy GR, Hollman J: Isolated right ventricular infarction following percutaneous translmninal coronary angioplasty. Am Heart J 111:168, 1986 4. Halkett JA, Commerford PJ, Scott R: Right ventricular infarction mimicking extensive anterior infarction. Chest 90:617, I986 5. Marchena E J, Palomo AR, Trohman RG et al: Anglographically demonstrated isolated acute right ventricular infarction presenting as ST elevation in leads V1 to V3. Am Heart J 113:391, 1987 6. Bolt CL, Vermeersch PH, Plokker HW: Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary ballon angioplasty. Eur Heart J I7:247, 1996 7. Klan ZU, Chou T: Right ventricular infarction mimicking acute anteroseptal left ventricular infarction. Am Heart J 132:1089, 1996 8. L6pez-Send6n J, Coma-Canella J: Diagndstico electrocardiogr~fico del infarto de ventrfculo derecho, p. 283. In Formaci6n continuada en Cardiologia. Avances en electrocardiologfa. Doyma SA, Barcelona, 1992 9. Kim T, Alturk N, Shaikh N, et al: An electrocardiographic algorithm for the prediction of the culprit lesion site in acute anterior myocardial infarction. Clin Cardiol 22:77, 1999 10. Correale F, Battista R, Martone A, et al: Electrocardiographic patterns in acute inferior myocardial infarction with and without right ventricular involvement: Classification, diagnostic and prognostic value, masking effect. Clin Cardiol 22:37, 1999