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Isolated Right Ventricular Infarct Presenting as Ventricular Fibrillation Arrest and Confirmed by Delayed-Enhancement Cardiac MRI
CLINICAL SPOTLIGHT
Clinical Spotlight
Isolated Right Ventricular Infarct Presenting as Ventricular Fibrillation Arrest and Confirmed by Delayed-Enhancement Cardiac MRI João L. Cavalcante, MD ∗ , Mouaz Al-Mallah, MD, MS, FACC and Michael Hudson, MD, MPH, FACC Henry Ford Hospital, Heart and Vascular Institute, 2799 West Grand Blvd, K-14, Detroit, MI 48202, United States
Malignant ventricular arrhythmias resulting from isolated right ventricular myocardial infarction (RVMI) without left ventricular myocardial ischaemia or infarction occur rarely. We present a case of a 61 year-old male with acute onset of chest pain and ventricular fibrillation cardiac arrest requiring prompt defibrillation. Subsequent 15-lead EKG, showed ST-segment elevation in the anterior and right precordial leads without ST-segment elevation in the inferior leads. Angiography documented occlusion of a large RV marginal branch. Delayed enhancement cardiac magnetic resonance imaging (DE-CMR) with gadolinium performed two days post-infarct showed isolated RVMI. Patient remained symptom free and haemodynamically stable throughout his hospital stay. The clinical presentation of isolated RV infarct can be misleading and diagnosis difficult. EKG findings can resemble acute anterior wall myocardial infarction, while its course can be accompanied by life-threatening ventricular arrhythmias. This case uniquely combines this rare clinical sequence with DE-CMR images using gadolinium to confirm isolated RVMI. A brief review of RVMI presentation and associated EKG patterns is also discussed. (Heart, Lung and Circulation 2010;19:620–623) Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Keywords. Right ventricle infarct; Ventricular fibrillation; Cardiac magnetic resonance; Anterior ST segment elevation
Case Report
A
61 year-old male with previous history of cigarette smoking, non-insulin-dependent diabetes mellitus and family history of premature coronary artery disease presented to ED with one hour history of substernal chest pain, nausea and diaphoresis. During ED physician assessment, the patient collapsed with ventricular fibrillation cardiac arrest for which he was promptly defibrillated. Subsequent 15-lead EKG, showed ST-segment elevation in the anterior and right precordial leads without ST-segment elevation in the inferior leads (Fig. 1). Electrolytes were unremarkable. Cardiac catheterisation showed nonobstructive coronary artery disease of left main, left anterior descending, dominant left circumflex coronary arteries and their branches with TIMI 3 flow. The RCA was a nondominant vessel with a 50% stenosis in the mid segment along with a significant 80% proximal stenosis and occlusion (TIMI grade 1 flow) in a right ventricle (RV) marginal branch. No PCI was performed as RCA was nondominant and RV
Received 10 June 2009; received in revised form 22 February 2010; accepted 20 May 2010 ∗ Corresponding author. Tel.: +1 313 916 2871; fax: +1 313 916 4513. E-mail address: [email protected] (J.L. Cavalcante).
marginal branch moderate sized (Fig. 2). Ventriculography and 2D echocardiography revealed normal left ventricular function and patient had peak cardiac troponin I of 18.1 ng/mL. Patient remained symptom free and haemodynamically stable throughout his hospital stay. Delayed enhancement cardiac magnetic resonance imaging (DECMR) with gadolinium performed two days later showed isolated RV myocardial infarction (RVMI) without LV oedema or delayed enhancement (Fig. 3). Approximately 16 hours after presentation, patient had one episode of monomorphic nonsustained ventricular tachycardia. He was later discharged following negative programmed stimulation electrophysiology study. Eighteen months following RVMI, the patient has experienced no recurrent angina, cardiac arrhythmia or congestive heart failure.
Discussion The prevalence of isolated RVMI is quite low ranging from 0.4 to 2.5% in autopsy series [1]. Concomitant RVMI occurs in 30–50% of cases of patients with acute inferior myocardial infarction [1,2]. The diagnosis can be challenging. Wellens et al. have proposed that lead V4 R should always be obtained in patients presenting with acute inferior ST elevation myocardial infarction, to assess whether RV involvement is
Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.
1443-9506/04/$36.00 doi:10.1016/j.hlc.2010.05.010
Figure 1. 15 lead EKG post defibrillation showing ST-segment elevation in the anterior leads (V1–V5) and ST-segment elevation seen in the right precordial leads (V4 r only). Note that: (a) no concomitant inferior ST-segment elevation; (b) the ST-segment elevation decreases from V1 through V5, with absence of anterior Q waves.
also present [1]. ST-segment elevation in lead V4 R greater than 1.0 mm has been shown not only to be a reliable marker of RVMI but also an independent predictor of inhospital mortality [3]. Anterior ST segment elevation in the setting of isolate RVMI has been previously reported [4–7]. The mechanism is related to the: (a) anterior location of the RV in the chest wall, (b) mean ST-vector of the RV injury current directed inferiorly, to the right, and anteriorly. A few criteria have been proposed to differentiate between LAD vs RCA culprit lesions causing RVMI. With RCA occlusion, ST-segment elevation is restricted to leads V1, V2, V3, and even to V4, with ST-segment elevation decreasing from V1 through V4, without Q-wave formation or decrease in the R-wave. In contrast, in cases of LAD occlusion, the ST-segment elevation is usually lowest in lead V1 and increases towards the V5 lead [8,9]. Despite limited extent of vulnerable or infarcted myocardium, RVMI can precipitate malignant ventricu-
Cavalcante et al. RVMI Presenting as Ventricular Fibrillation Arrest
621
lar arrhythmias [10–12]. In a recent case series by Ricci et al. of 48 patients presenting with acute RVMI, malignant ventricular arrhythmias occurred in up to 38% of patients and tended to be associated with larger infarct size (measured by peak CPK). Despite the arrhythmic burden, there was no significant impact in the length of stay and/or mortality in these patients who received reperfusion, although the study was not powered to assess these differences [12]. DE-CMR with gadolinium has emerged as an important clinical tool in the diagnosis and management of patients with myocardial infarction [13,14]. A seminal paper by Kumar et al. demonstrated that DE-CMR more sensitively identifies RVMI in patients presenting with acute inferior myocardial infarction than any other current standard diagnostic techniques such as ECG, physical exam or echocardiography [15]. For his analysis, a short-axis stack covering the RV completely or with three short-axes (apex, mid, basal) was obtained 10 minutes after IV injection of 0.2 mmol/kg Gadolinium-DTPA. RVMI was defined to be present if DE extended from the inferior LV myocardium or the inferior interventricular septum into the RV free wall in any one or more DE-CMR images. DE was seen in 36 out of 37 patients (97%) with 21 of these patients have RVMI involvement (59%). Contrary to the findings of Ricci et al. [12], time to reperfusion, maximum creatine kinase elevation, and LV ejection fraction did not differ significantly between the RVMI positive and RVMI negative groups. DE-CMR also diagnosed RVMI in five patients in whom other diagnostic techniques failed to initially identify but who later developed clinically overt RV failure symptoms. Since the authors included patients presenting with acute inferior myocardial infarction, evaluation of isolated RVMI by DE-CMR has been rarely reported in the medical literature [16,17]. Cardiology providers are reminded that RCA or RV branch occlusions may cause isolated RVMI with anterior ST segment elevation and that serious arrhythmia complications may occur despite absence of LV necrosis or dysfunction. In our case, DE-CMR provided clear evidence of isolated
Figure 2. Coronary angiogram of non-dominant RCA showing a significant 90% stenosis (arrow) and distal occlusion of RV marginal branch (arrow-heads).
CLINICAL SPOTLIGHT
Heart, Lung and Circulation 2010;19:620–623
622
Cavalcante et al. RVMI Presenting as Ventricular Fibrillation Arrest
Heart, Lung and Circulation 2010;19:620–623
CLINICAL SPOTLIGHT
Figure 3. (A) Cardiac MR SSFP sequence of LV/RV short-axis demonstrating in the end-systolic frame clear dyskinesis of RV free wall (arrow heads). (B) and (C) Cardiac MR short-axis with gadolinium showing delayed enhancement of the RV free wall (in between arrows) compatible with isolated RV infarction. Also note that there is no delayed enhancement involving the left ventricle. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of the article.)
RVMI as the cause of the patient’s chest pain and ventricular arrhythmia.
Disclosures Dr. João L. Cavalcante and Dr. Mouaz Al-Mallah: None. Dr. Michael Hudson has received research grant support from Scios/Johnson & Johnson, Schering-Plough, GlaxoSmithKline, BRAHMS AG, Nanopshere, and Ikaria.
References [1] Wellens HJ. Right ventricular infarction. N Engl J Med 1993;328(14):1036–8. [2] Moye S, Carney MF, Holstege C, Mattu A, Brady WJ. The electrocardiogram in right ventricular myocardial infarction. Am J Emerg Med 2005;23(6):793–9. [3] Zehender M, Kasper W, Kauder E, Schonthaler M, Geibel A, Olschewski M, Just H. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328(14):981–8. [4] Hilliard AA, Nkomo VT, Mathew V, Prasad A. Isolated right ventricular infarction—an uncommon cause of acute anterior ST segment elevation. Int J Cardiol 2009;132(2):e51–3. [5] Muhammad KI, Kapadia SR. Anterior ST-segment elevation with right coronary artery occlusion: a unique case of isolated right ventricular infarction. Angiology 2008;59(5):622–4. [6] Vavuranakis M, Drakopoulou M, Toutouzas K, Polychronis D, Stefanadis C. Right ventricular infarction mimicking anterior infarction. Ann Noninvasive Electrocardiol 2006;11(2):194–7.
[7] Collins N, Elliott V, Seidelin P. True isolated right ventricular infarction with tombstone anterior ST elevation. Heart 2007;93(3):374. [8] Eskola MJ, Kosonen P, Sclarovsky S, Vikman S, Nikus KC. The ECG pattern of isolated right ventricular infarction during percutaneous coronary intervention. Ann Noninvasive Electrocardiol 2007;12(1):83–7. [9] Geft IL, Shah PK, Rodriguez L, Hulse S, Maddahi J, Berman DS, Ganz W. ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53(8):991–6. [10] Chang KY, Ebrahimi R, Bersohn MM. Ventricular fibrillation resulting from acute right ventricular infarction from isolated occlusion of a right ventricular branch artery. J Cardiovasc Pharmacol Ther 2003;8(1):5–8. [11] Cordoba Tejada M, Olivares A, Gonzalez-Hermosillo JA, Hurtado Buen Abad L, Virgos A, Cardenas Loaeza M. [Arrhythmia in acute myocardial infarction with involvement of the right ventricle]. Arch Inst Cardiol Mex 1989;59(2):113–9. [12] Ricci JM, Dukkipati SR, Pica MC, Haines DE, Goldstein JA. Malignant ventricular arrhythmias in patients with acute right ventricular infarction undergoing mechanical reperfusion. Am J Cardiol 2009;104(12):1678–83. [13] Al-Mallah M, Kwong RY. Clinical application of cardiac CMR. Rev Cardiovasc Med 2009;10(3):134–41. [14] Kim HW, Farzaneh-Far A, Kim RJ. Cardiovascular magnetic resonance in patients with myocardial infarction: current and emerging applications. J Am Coll Cardiol 2009;55(1): 1–16. [15] Kumar A, Abdel-Aty H, Kriedemann I, Schulz-Menger J, Gross CM, Dietz R, Friedrich MG. Contrast-enhanced car-
diovascular magnetic resonance imaging of right ventricular infarction. J Am Coll Cardiol 2006;48(10):1969–76. [16] Younger J, Plein S, Greenwood JP. Isolated right ventricular infarct demonstrated by cardiac MRI. Int J Cardiol 2006;113(2):e62–3.
Cavalcante et al. RVMI Presenting as Ventricular Fibrillation Arrest
623
[17] Saremi F, Gurudevan SV, Harrison AT. Isolated right ventricular infarction owing to anomalous origin of right coronary artery: role of MR and CT in diagnosis. J Thorac Imaging 2009;24(1):34–7.
CLINICAL SPOTLIGHT
Heart, Lung and Circulation 2010;19:620–623
Clinical Spotlight
Isolated Right Ventricular Infarct Presenting as Ventricular Fibrillation Arrest and Confirmed by Delayed-Enhancement Cardiac MRI João L. Cavalcante, MD ∗ , Mouaz Al-Mallah, MD, MS, FACC and Michael Hudson, MD, MPH, FACC Henry Ford Hospital, Heart and Vascular Institute, 2799 West Grand Blvd, K-14, Detroit, MI 48202, United States
Malignant ventricular arrhythmias resulting from isolated right ventricular myocardial infarction (RVMI) without left ventricular myocardial ischaemia or infarction occur rarely. We present a case of a 61 year-old male with acute onset of chest pain and ventricular fibrillation cardiac arrest requiring prompt defibrillation. Subsequent 15-lead EKG, showed ST-segment elevation in the anterior and right precordial leads without ST-segment elevation in the inferior leads. Angiography documented occlusion of a large RV marginal branch. Delayed enhancement cardiac magnetic resonance imaging (DE-CMR) with gadolinium performed two days post-infarct showed isolated RVMI. Patient remained symptom free and haemodynamically stable throughout his hospital stay. The clinical presentation of isolated RV infarct can be misleading and diagnosis difficult. EKG findings can resemble acute anterior wall myocardial infarction, while its course can be accompanied by life-threatening ventricular arrhythmias. This case uniquely combines this rare clinical sequence with DE-CMR images using gadolinium to confirm isolated RVMI. A brief review of RVMI presentation and associated EKG patterns is also discussed. (Heart, Lung and Circulation 2010;19:620–623) Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Keywords. Right ventricle infarct; Ventricular fibrillation; Cardiac magnetic resonance; Anterior ST segment elevation
Case Report
A
61 year-old male with previous history of cigarette smoking, non-insulin-dependent diabetes mellitus and family history of premature coronary artery disease presented to ED with one hour history of substernal chest pain, nausea and diaphoresis. During ED physician assessment, the patient collapsed with ventricular fibrillation cardiac arrest for which he was promptly defibrillated. Subsequent 15-lead EKG, showed ST-segment elevation in the anterior and right precordial leads without ST-segment elevation in the inferior leads (Fig. 1). Electrolytes were unremarkable. Cardiac catheterisation showed nonobstructive coronary artery disease of left main, left anterior descending, dominant left circumflex coronary arteries and their branches with TIMI 3 flow. The RCA was a nondominant vessel with a 50% stenosis in the mid segment along with a significant 80% proximal stenosis and occlusion (TIMI grade 1 flow) in a right ventricle (RV) marginal branch. No PCI was performed as RCA was nondominant and RV
Received 10 June 2009; received in revised form 22 February 2010; accepted 20 May 2010 ∗ Corresponding author. Tel.: +1 313 916 2871; fax: +1 313 916 4513. E-mail address: [email protected] (J.L. Cavalcante).
marginal branch moderate sized (Fig. 2). Ventriculography and 2D echocardiography revealed normal left ventricular function and patient had peak cardiac troponin I of 18.1 ng/mL. Patient remained symptom free and haemodynamically stable throughout his hospital stay. Delayed enhancement cardiac magnetic resonance imaging (DECMR) with gadolinium performed two days later showed isolated RV myocardial infarction (RVMI) without LV oedema or delayed enhancement (Fig. 3). Approximately 16 hours after presentation, patient had one episode of monomorphic nonsustained ventricular tachycardia. He was later discharged following negative programmed stimulation electrophysiology study. Eighteen months following RVMI, the patient has experienced no recurrent angina, cardiac arrhythmia or congestive heart failure.
Discussion The prevalence of isolated RVMI is quite low ranging from 0.4 to 2.5% in autopsy series [1]. Concomitant RVMI occurs in 30–50% of cases of patients with acute inferior myocardial infarction [1,2]. The diagnosis can be challenging. Wellens et al. have proposed that lead V4 R should always be obtained in patients presenting with acute inferior ST elevation myocardial infarction, to assess whether RV involvement is
Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.
1443-9506/04/$36.00 doi:10.1016/j.hlc.2010.05.010
Figure 1. 15 lead EKG post defibrillation showing ST-segment elevation in the anterior leads (V1–V5) and ST-segment elevation seen in the right precordial leads (V4 r only). Note that: (a) no concomitant inferior ST-segment elevation; (b) the ST-segment elevation decreases from V1 through V5, with absence of anterior Q waves.
also present [1]. ST-segment elevation in lead V4 R greater than 1.0 mm has been shown not only to be a reliable marker of RVMI but also an independent predictor of inhospital mortality [3]. Anterior ST segment elevation in the setting of isolate RVMI has been previously reported [4–7]. The mechanism is related to the: (a) anterior location of the RV in the chest wall, (b) mean ST-vector of the RV injury current directed inferiorly, to the right, and anteriorly. A few criteria have been proposed to differentiate between LAD vs RCA culprit lesions causing RVMI. With RCA occlusion, ST-segment elevation is restricted to leads V1, V2, V3, and even to V4, with ST-segment elevation decreasing from V1 through V4, without Q-wave formation or decrease in the R-wave. In contrast, in cases of LAD occlusion, the ST-segment elevation is usually lowest in lead V1 and increases towards the V5 lead [8,9]. Despite limited extent of vulnerable or infarcted myocardium, RVMI can precipitate malignant ventricu-
Cavalcante et al. RVMI Presenting as Ventricular Fibrillation Arrest
621
lar arrhythmias [10–12]. In a recent case series by Ricci et al. of 48 patients presenting with acute RVMI, malignant ventricular arrhythmias occurred in up to 38% of patients and tended to be associated with larger infarct size (measured by peak CPK). Despite the arrhythmic burden, there was no significant impact in the length of stay and/or mortality in these patients who received reperfusion, although the study was not powered to assess these differences [12]. DE-CMR with gadolinium has emerged as an important clinical tool in the diagnosis and management of patients with myocardial infarction [13,14]. A seminal paper by Kumar et al. demonstrated that DE-CMR more sensitively identifies RVMI in patients presenting with acute inferior myocardial infarction than any other current standard diagnostic techniques such as ECG, physical exam or echocardiography [15]. For his analysis, a short-axis stack covering the RV completely or with three short-axes (apex, mid, basal) was obtained 10 minutes after IV injection of 0.2 mmol/kg Gadolinium-DTPA. RVMI was defined to be present if DE extended from the inferior LV myocardium or the inferior interventricular septum into the RV free wall in any one or more DE-CMR images. DE was seen in 36 out of 37 patients (97%) with 21 of these patients have RVMI involvement (59%). Contrary to the findings of Ricci et al. [12], time to reperfusion, maximum creatine kinase elevation, and LV ejection fraction did not differ significantly between the RVMI positive and RVMI negative groups. DE-CMR also diagnosed RVMI in five patients in whom other diagnostic techniques failed to initially identify but who later developed clinically overt RV failure symptoms. Since the authors included patients presenting with acute inferior myocardial infarction, evaluation of isolated RVMI by DE-CMR has been rarely reported in the medical literature [16,17]. Cardiology providers are reminded that RCA or RV branch occlusions may cause isolated RVMI with anterior ST segment elevation and that serious arrhythmia complications may occur despite absence of LV necrosis or dysfunction. In our case, DE-CMR provided clear evidence of isolated
Figure 2. Coronary angiogram of non-dominant RCA showing a significant 90% stenosis (arrow) and distal occlusion of RV marginal branch (arrow-heads).
CLINICAL SPOTLIGHT
Heart, Lung and Circulation 2010;19:620–623
622
Cavalcante et al. RVMI Presenting as Ventricular Fibrillation Arrest
Heart, Lung and Circulation 2010;19:620–623
CLINICAL SPOTLIGHT
Figure 3. (A) Cardiac MR SSFP sequence of LV/RV short-axis demonstrating in the end-systolic frame clear dyskinesis of RV free wall (arrow heads). (B) and (C) Cardiac MR short-axis with gadolinium showing delayed enhancement of the RV free wall (in between arrows) compatible with isolated RV infarction. Also note that there is no delayed enhancement involving the left ventricle. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of the article.)
RVMI as the cause of the patient’s chest pain and ventricular arrhythmia.
Disclosures Dr. João L. Cavalcante and Dr. Mouaz Al-Mallah: None. Dr. Michael Hudson has received research grant support from Scios/Johnson & Johnson, Schering-Plough, GlaxoSmithKline, BRAHMS AG, Nanopshere, and Ikaria.
References [1] Wellens HJ. Right ventricular infarction. N Engl J Med 1993;328(14):1036–8. [2] Moye S, Carney MF, Holstege C, Mattu A, Brady WJ. The electrocardiogram in right ventricular myocardial infarction. Am J Emerg Med 2005;23(6):793–9. [3] Zehender M, Kasper W, Kauder E, Schonthaler M, Geibel A, Olschewski M, Just H. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993;328(14):981–8. [4] Hilliard AA, Nkomo VT, Mathew V, Prasad A. Isolated right ventricular infarction—an uncommon cause of acute anterior ST segment elevation. Int J Cardiol 2009;132(2):e51–3. [5] Muhammad KI, Kapadia SR. Anterior ST-segment elevation with right coronary artery occlusion: a unique case of isolated right ventricular infarction. Angiology 2008;59(5):622–4. [6] Vavuranakis M, Drakopoulou M, Toutouzas K, Polychronis D, Stefanadis C. Right ventricular infarction mimicking anterior infarction. Ann Noninvasive Electrocardiol 2006;11(2):194–7.
[7] Collins N, Elliott V, Seidelin P. True isolated right ventricular infarction with tombstone anterior ST elevation. Heart 2007;93(3):374. [8] Eskola MJ, Kosonen P, Sclarovsky S, Vikman S, Nikus KC. The ECG pattern of isolated right ventricular infarction during percutaneous coronary intervention. Ann Noninvasive Electrocardiol 2007;12(1):83–7. [9] Geft IL, Shah PK, Rodriguez L, Hulse S, Maddahi J, Berman DS, Ganz W. ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53(8):991–6. [10] Chang KY, Ebrahimi R, Bersohn MM. Ventricular fibrillation resulting from acute right ventricular infarction from isolated occlusion of a right ventricular branch artery. J Cardiovasc Pharmacol Ther 2003;8(1):5–8. [11] Cordoba Tejada M, Olivares A, Gonzalez-Hermosillo JA, Hurtado Buen Abad L, Virgos A, Cardenas Loaeza M. [Arrhythmia in acute myocardial infarction with involvement of the right ventricle]. Arch Inst Cardiol Mex 1989;59(2):113–9. [12] Ricci JM, Dukkipati SR, Pica MC, Haines DE, Goldstein JA. Malignant ventricular arrhythmias in patients with acute right ventricular infarction undergoing mechanical reperfusion. Am J Cardiol 2009;104(12):1678–83. [13] Al-Mallah M, Kwong RY. Clinical application of cardiac CMR. Rev Cardiovasc Med 2009;10(3):134–41. [14] Kim HW, Farzaneh-Far A, Kim RJ. Cardiovascular magnetic resonance in patients with myocardial infarction: current and emerging applications. J Am Coll Cardiol 2009;55(1): 1–16. [15] Kumar A, Abdel-Aty H, Kriedemann I, Schulz-Menger J, Gross CM, Dietz R, Friedrich MG. Contrast-enhanced car-
diovascular magnetic resonance imaging of right ventricular infarction. J Am Coll Cardiol 2006;48(10):1969–76. [16] Younger J, Plein S, Greenwood JP. Isolated right ventricular infarct demonstrated by cardiac MRI. Int J Cardiol 2006;113(2):e62–3.
Cavalcante et al. RVMI Presenting as Ventricular Fibrillation Arrest
623
[17] Saremi F, Gurudevan SV, Harrison AT. Isolated right ventricular infarction owing to anomalous origin of right coronary artery: role of MR and CT in diagnosis. J Thorac Imaging 2009;24(1):34–7.
CLINICAL SPOTLIGHT
Heart, Lung and Circulation 2010;19:620–623