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Isolated right ventricular dysfunction without myocardial infarction
International Journal of Cardiology 124 (2008) e1 – e3 www.elsevier.com/locate/ijcard
Letter to the Editor
Isolated right ventricular dysfunction without myocardial infarction Yoritaka Otsuka a,⁎, Atsushi Kawamura a , Shunichi Miyazaki a,b a
b
Division of Cardiology, National Cardiovascular Center, Osaka, Japan Division of Cardiology, Kinki University School of Medicine, Osaka, Japan Received 14 December 2006; accepted 3 January 2007 Available online 16 April 2007
Abstract Right ventricular (RV) infarction or dysfunction is commonly complicated with acute inferior myocardial infarction. In this report, we describe a patient with unstable angina pectoris who showed a temporary isolated RV dysfunction. The patient had total occlusion of proximal right coronary artery, including RV branch, with good collateral circulation from left coronary artery. Recanalization was obtained by percutaneous coronary intervention (PCI). Echocardiography at admission showed RV dilatation and severe hypokinesis of RV free wall but no left ventricular wall motion abnormalities. Hemodynamic examination showed high right atrial pressure with a non-compliant pattern and low cardiac output immediately after PCI. Cardiac enzymes were not elevated even after PCI. RV asynergy and hemodynamics were improved at 2 days after PCI. The 99 m technetium-pyrophosphate and 201 thallium dual single-photon emission computed tomography showed uptake of 99 m technetium-pyrophosphate in only the RV free wall, but in the left ventricle no uptake of 99 m technetiumpyrophosphate and no perfusion defect of 201 thallium. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Right ventricular dysfunction; Unstable angina; Percutaneous coronary intervention
1. Introduction Right ventricular (RV) infarction or dysfunction is commonly complicated with acute inferior myocardial infarction [1]. Isolated RV infarction or dysfunction is very rare. It has been known that isolated RV infarction or dysfunction could occur under the following two situations, occlusion of nondominant right coronary artery (RCA) and isolated occlusion of RV branch. In this report, we describe a patient with unstable angina pectoris who had isolated RV dysfunction without previous situations. 2. Case report A 74-year-old man with a history of smoking was admitted to the coronary care unit in our hospital due to ⁎ Corresponding author. Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Fujishirodai 5-7-1, Suita, Osaka, 565-8565, Japan. Tel.: +81 6 6833 5012; fax: +81 6 6872 7486. E-mail address: [email protected] (Y. Otsuka). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.01.095
frequent chest pain of short duration at rest and on exersion. A 12-lead electrocardiogram at admission showed a transient complete atrio-ventricular block at a heart rate of 40 beats per minute and ST depression in leads II aVF V4–V6, while he had no chest pain at admission. Plasma creatine kinase and MB fraction levels were within normal range, but cardiac troponin T level was ≧ 0.1 ng/mL at admission. Echocardiography at admission showed RV dilatation and severe hypokinesis of RV free wall, but left ventricular wall motion was normal. Emergency coronary angiography revealed total occlusion of proximal RCA with thrombus (Fig. 1a) and good collateral vessels from left coronary artery to distal RCA (Fig. 1b). Percutaneous coronary intervention (PCI) with stent implantation after thrombus aspiration was performed. Recanalization and TIMI 3 flow was achieved (Fig. 1c). Left ventriography showed no asynergy, indicating no left ventricular damage (Fig. 1d and e). Plasma cardiac enzyme levels were not elevated even after PCI. However, hemodynamic examination using Swan–Ganz catheter showed high right atrial pressure with a non-compliant pattern and low cardiac output with absence of pulmonary hypertension immediately
e2
Y. Otsuka et al. / International Journal of Cardiology 124 (2008) e1–e3
Fig. 1. a. A total occlusion of the proximal right coronary artery with thrombus. b. Good collaterals from the left coronary artery to the right coronary artery. c. After stent implantation, normal coronary flow was achieved. d. A left ventricle showed normal function without segmental asynergy.
after PCI (Fig. 2). Because of persistent decreased urine volume and cardiac output which was not corrected by volume loading, dobutamine infusion was started. Hemody-
namic examination showed immediate improvement by dobutamine infusion resulting in urine volume increase. On the third hospital day, non-compliant pattern of right atrial pressure wave form (Fig. 2) and RV segmental asynergy disappeared without dobutamine infusion. The 99 m technetium-pyrophosphate and 201 thallium dual single-photon emission computed tomography showed isolated uptake of 99 m technetium-pyrophosphate in the RV free wall, but no uptake of 99 m technetium-pyrophosphate and no perfusion defect of 201 thallium in the left ventricle. In addition, magnetic resonance imaging also showed no delayed hyperenhancement of left and right ventricles, indicating no myocardial infarction of both ventricles. Therefore, this case was diagnosed as unstable angina pectoris accompanied by isolated RV dysfunction. 3. Discussion
Fig. 2. Hemodynamics examination and right atrial pressure waves at admission and at 2 days after PCI. The right atrial wave on admission showed non-complainant pattern. Right atrial pressure was high and cardiac output was low on admission. They were improved at 2 days after treatment. HR = heart rate; Ao = aortic pressure; PA = pulmonary artery pressure; mRA: mean right atrial pressure; mPCW = mean pulmonary capillary wedge pressure; CI = cardiac index.
In this report, we described a case of unstable angina complicated with isolated RV dysfunction without acute myocardial infarction, occurred in different situations from that of previously reported. RV infarction or dysfunction is commonly complicated with acute inferior myocardial infarction [1]. It is known that isolated RV infarction or dysfunction occur under the following two situations though it is very rare. One is occlusion of a nondominant RCA with the posterior descending coronary artery arising from circumflex coronary artery. Second is isolated occlusion of one of the RV branches of RCA without collateral vessels. To
Y. Otsuka et al. / International Journal of Cardiology 124 (2008) e1–e3
the best of my knowledge, there is no prior report of isolated occlusion of a dominant RCA resulting in significant RV dysfunction and hemodynamic compromise. This case showed proximal occlusion of a dominant RCA including RV branch with good collateral flow from left coronary artery, indicating salvage for the myocardium perfused by collateral vessels. In fact, there was no myocardial damage of left ventricle confirmed by left ventriography, serial measurement of cardiac enzyme and 99 m technetiumpyrophosphate scintigraphy. On the other hand, we have demonstrated RV dilatation and severe hypokinesis by echocardiography, hemodynamic compromise, and uptake of 99 m technetium-pyrophosphate only in the RV free wall. In addition, by contrast-enhanced magnetic resonance imaging we described no myocardial infarction of both ventricles. Okuda et al. reported that uptake of 99 m technetium-pyrophosphate is not only an indicator of myocardial infarction but also temporary myocardial injury by ischemia [2]. It has been reported that abnormal phospholipid metabolism during ischemia causes a Ca++ permeability change resulting in increased intracellular Ca++ and subsequent accumulation of 99 m technetium-pyrophosphate [2]. It has been recently reported that contrast-enhanced magnetic resonance imaging is useful for detection of isolated RV infarction [3]. Thus, frequent severe myocardial ischemia possibly caused by occlusion of dominant RCA may induce temporary isolated RV dysfunction through the mechanism of stunned myocardium of RV free wall. Also this indicates that there are the dramatic differences in oxygen supply-demand between both ventricles, which allow the RV to withstand severe ischemia and recover despite prolonged RCA occlusion [4,5]. In present case, we demonstrated the non-compliant pattern of high right atrial pressure wave form with depressed A-wave and blunted Y descent immediately after PCI. It has been known that right atrial waveform shows augmented A-wave and blunted Y descent representing RV
e3
dysfunction when mid-RCA occlusions [6]. Conversely, proximal RCA occlusions compromising the atrial as well as the RV branches result in ischemic depression of atrial function, manifesting as more severely elevated right atrial pressure with depressed A-wave and blunted Y descent [6]. Therefore, we suggest this case also had ischemic depression of right atrial function along together with RV dysfunction due to proximal RCA occlusion. It is important to consider the possibility of RV dysfunction when abnormal hemodynamics in patients with occlusion of dominant RCA, because therapeutic management should be different and acute RV ischemic dysfunction contributes to early morbidity and mortality [6]. However, clinically diagnosed isolated RV dysfunction without acute inferior myocardial infarction is rare and may be misdiagnosed in clinical setting. As shown in this report, occlusion of dominant RCA without acute inferior myocardial infarction could cause isolated RV dysfunction. References [1] Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 1994;330:1211–7. [2] Okuda K, Nohara R, Fujita M, Tamaki N, Konishi J, Sasayama S. Technetium-99 m-pyrophosphate uptake as an indicator of myocardial injury without infarct. J Nucl Med 1994;35:1366–70. [3] Ibrahim T, Schwaiger M, Schomig A. Assessment of isolated right ventricular myocardial infarction by magnetic resonance imaging. Circulation 2006;113:e78–9. [4] Bowers TR, O'Neill WW, Grines C, Pica MC, Safian RD, Goldstein JA. Effect of reperfusion on biventricular function and survival after right ventricular infarction. N Engl J Med 1998;338:933–40. [5] Laster SB, Shelton TJ, Barzilai B, Goldstein JA. Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion. Circulation 1993;88:696–708. [6] Goldstein JA. Pathophysiology and management of right heart ischemia. J Am Coll Cardiol 2002;40:841–53.
Letter to the Editor
Isolated right ventricular dysfunction without myocardial infarction Yoritaka Otsuka a,⁎, Atsushi Kawamura a , Shunichi Miyazaki a,b a
b
Division of Cardiology, National Cardiovascular Center, Osaka, Japan Division of Cardiology, Kinki University School of Medicine, Osaka, Japan Received 14 December 2006; accepted 3 January 2007 Available online 16 April 2007
Abstract Right ventricular (RV) infarction or dysfunction is commonly complicated with acute inferior myocardial infarction. In this report, we describe a patient with unstable angina pectoris who showed a temporary isolated RV dysfunction. The patient had total occlusion of proximal right coronary artery, including RV branch, with good collateral circulation from left coronary artery. Recanalization was obtained by percutaneous coronary intervention (PCI). Echocardiography at admission showed RV dilatation and severe hypokinesis of RV free wall but no left ventricular wall motion abnormalities. Hemodynamic examination showed high right atrial pressure with a non-compliant pattern and low cardiac output immediately after PCI. Cardiac enzymes were not elevated even after PCI. RV asynergy and hemodynamics were improved at 2 days after PCI. The 99 m technetium-pyrophosphate and 201 thallium dual single-photon emission computed tomography showed uptake of 99 m technetium-pyrophosphate in only the RV free wall, but in the left ventricle no uptake of 99 m technetiumpyrophosphate and no perfusion defect of 201 thallium. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Right ventricular dysfunction; Unstable angina; Percutaneous coronary intervention
1. Introduction Right ventricular (RV) infarction or dysfunction is commonly complicated with acute inferior myocardial infarction [1]. Isolated RV infarction or dysfunction is very rare. It has been known that isolated RV infarction or dysfunction could occur under the following two situations, occlusion of nondominant right coronary artery (RCA) and isolated occlusion of RV branch. In this report, we describe a patient with unstable angina pectoris who had isolated RV dysfunction without previous situations. 2. Case report A 74-year-old man with a history of smoking was admitted to the coronary care unit in our hospital due to ⁎ Corresponding author. Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Fujishirodai 5-7-1, Suita, Osaka, 565-8565, Japan. Tel.: +81 6 6833 5012; fax: +81 6 6872 7486. E-mail address: [email protected] (Y. Otsuka). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.01.095
frequent chest pain of short duration at rest and on exersion. A 12-lead electrocardiogram at admission showed a transient complete atrio-ventricular block at a heart rate of 40 beats per minute and ST depression in leads II aVF V4–V6, while he had no chest pain at admission. Plasma creatine kinase and MB fraction levels were within normal range, but cardiac troponin T level was ≧ 0.1 ng/mL at admission. Echocardiography at admission showed RV dilatation and severe hypokinesis of RV free wall, but left ventricular wall motion was normal. Emergency coronary angiography revealed total occlusion of proximal RCA with thrombus (Fig. 1a) and good collateral vessels from left coronary artery to distal RCA (Fig. 1b). Percutaneous coronary intervention (PCI) with stent implantation after thrombus aspiration was performed. Recanalization and TIMI 3 flow was achieved (Fig. 1c). Left ventriography showed no asynergy, indicating no left ventricular damage (Fig. 1d and e). Plasma cardiac enzyme levels were not elevated even after PCI. However, hemodynamic examination using Swan–Ganz catheter showed high right atrial pressure with a non-compliant pattern and low cardiac output with absence of pulmonary hypertension immediately
e2
Y. Otsuka et al. / International Journal of Cardiology 124 (2008) e1–e3
Fig. 1. a. A total occlusion of the proximal right coronary artery with thrombus. b. Good collaterals from the left coronary artery to the right coronary artery. c. After stent implantation, normal coronary flow was achieved. d. A left ventricle showed normal function without segmental asynergy.
after PCI (Fig. 2). Because of persistent decreased urine volume and cardiac output which was not corrected by volume loading, dobutamine infusion was started. Hemody-
namic examination showed immediate improvement by dobutamine infusion resulting in urine volume increase. On the third hospital day, non-compliant pattern of right atrial pressure wave form (Fig. 2) and RV segmental asynergy disappeared without dobutamine infusion. The 99 m technetium-pyrophosphate and 201 thallium dual single-photon emission computed tomography showed isolated uptake of 99 m technetium-pyrophosphate in the RV free wall, but no uptake of 99 m technetium-pyrophosphate and no perfusion defect of 201 thallium in the left ventricle. In addition, magnetic resonance imaging also showed no delayed hyperenhancement of left and right ventricles, indicating no myocardial infarction of both ventricles. Therefore, this case was diagnosed as unstable angina pectoris accompanied by isolated RV dysfunction. 3. Discussion
Fig. 2. Hemodynamics examination and right atrial pressure waves at admission and at 2 days after PCI. The right atrial wave on admission showed non-complainant pattern. Right atrial pressure was high and cardiac output was low on admission. They were improved at 2 days after treatment. HR = heart rate; Ao = aortic pressure; PA = pulmonary artery pressure; mRA: mean right atrial pressure; mPCW = mean pulmonary capillary wedge pressure; CI = cardiac index.
In this report, we described a case of unstable angina complicated with isolated RV dysfunction without acute myocardial infarction, occurred in different situations from that of previously reported. RV infarction or dysfunction is commonly complicated with acute inferior myocardial infarction [1]. It is known that isolated RV infarction or dysfunction occur under the following two situations though it is very rare. One is occlusion of a nondominant RCA with the posterior descending coronary artery arising from circumflex coronary artery. Second is isolated occlusion of one of the RV branches of RCA without collateral vessels. To
Y. Otsuka et al. / International Journal of Cardiology 124 (2008) e1–e3
the best of my knowledge, there is no prior report of isolated occlusion of a dominant RCA resulting in significant RV dysfunction and hemodynamic compromise. This case showed proximal occlusion of a dominant RCA including RV branch with good collateral flow from left coronary artery, indicating salvage for the myocardium perfused by collateral vessels. In fact, there was no myocardial damage of left ventricle confirmed by left ventriography, serial measurement of cardiac enzyme and 99 m technetiumpyrophosphate scintigraphy. On the other hand, we have demonstrated RV dilatation and severe hypokinesis by echocardiography, hemodynamic compromise, and uptake of 99 m technetium-pyrophosphate only in the RV free wall. In addition, by contrast-enhanced magnetic resonance imaging we described no myocardial infarction of both ventricles. Okuda et al. reported that uptake of 99 m technetium-pyrophosphate is not only an indicator of myocardial infarction but also temporary myocardial injury by ischemia [2]. It has been reported that abnormal phospholipid metabolism during ischemia causes a Ca++ permeability change resulting in increased intracellular Ca++ and subsequent accumulation of 99 m technetium-pyrophosphate [2]. It has been recently reported that contrast-enhanced magnetic resonance imaging is useful for detection of isolated RV infarction [3]. Thus, frequent severe myocardial ischemia possibly caused by occlusion of dominant RCA may induce temporary isolated RV dysfunction through the mechanism of stunned myocardium of RV free wall. Also this indicates that there are the dramatic differences in oxygen supply-demand between both ventricles, which allow the RV to withstand severe ischemia and recover despite prolonged RCA occlusion [4,5]. In present case, we demonstrated the non-compliant pattern of high right atrial pressure wave form with depressed A-wave and blunted Y descent immediately after PCI. It has been known that right atrial waveform shows augmented A-wave and blunted Y descent representing RV
e3
dysfunction when mid-RCA occlusions [6]. Conversely, proximal RCA occlusions compromising the atrial as well as the RV branches result in ischemic depression of atrial function, manifesting as more severely elevated right atrial pressure with depressed A-wave and blunted Y descent [6]. Therefore, we suggest this case also had ischemic depression of right atrial function along together with RV dysfunction due to proximal RCA occlusion. It is important to consider the possibility of RV dysfunction when abnormal hemodynamics in patients with occlusion of dominant RCA, because therapeutic management should be different and acute RV ischemic dysfunction contributes to early morbidity and mortality [6]. However, clinically diagnosed isolated RV dysfunction without acute inferior myocardial infarction is rare and may be misdiagnosed in clinical setting. As shown in this report, occlusion of dominant RCA without acute inferior myocardial infarction could cause isolated RV dysfunction. References [1] Kinch JW, Ryan TJ. Right ventricular infarction. N Engl J Med 1994;330:1211–7. [2] Okuda K, Nohara R, Fujita M, Tamaki N, Konishi J, Sasayama S. Technetium-99 m-pyrophosphate uptake as an indicator of myocardial injury without infarct. J Nucl Med 1994;35:1366–70. [3] Ibrahim T, Schwaiger M, Schomig A. Assessment of isolated right ventricular myocardial infarction by magnetic resonance imaging. Circulation 2006;113:e78–9. [4] Bowers TR, O'Neill WW, Grines C, Pica MC, Safian RD, Goldstein JA. Effect of reperfusion on biventricular function and survival after right ventricular infarction. N Engl J Med 1998;338:933–40. [5] Laster SB, Shelton TJ, Barzilai B, Goldstein JA. Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion. Circulation 1993;88:696–708. [6] Goldstein JA. Pathophysiology and management of right heart ischemia. J Am Coll Cardiol 2002;40:841–53.