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ST-Segment Elevation in Precordial Leads
selected reports ST-Segment Elevation in Precordial Leads* Anterior or Right Ventricular Myocardial Infarction?
(Fig 1, bottom, c). The right coronary artery had a large RV branch and a small posterior descending artery. Left ventriculography showed minimal inferior wall segment hypokinesia. A right coronary angioplasty was performed with stent implantation. At discharge, the ECG showed T-wave inversion in the inferior leads but no significant abnormality in the precordial leads. Case 2
Damien Logeart, MD; Dominique Himbert, MD; and Alain Cohen-Solal, MD, PhD
Isolated acute right ventricular (RV) infarction is rare, and ECG diagnosis may be difficult. We report two cases of acute myocardial infarction with STsegment elevation in anterior precordial leads caused by such an RV involvement. Potential mechanisms for the relationship are given. (CHEST 2001; 119:290 –292) Key words: ECG; myocardial infarction; right ventricular Abbreviations: LV ⫽ left ventricular; MI ⫽ myocardial infarction; RV ⫽ right ventricular
right ventricular (RV) myocardial infarction (MI) is A cute usually associated with inferior left ventricular (LV) MI and results in a high in-hospital mortality rate.1 Isolated RV MI is rare, and bedside diagnosis may be difficult and misleading because ECG changes are inconsistent. We describe the cases of two patients admitted with ECG changes that were suggestive of acute anterior LV MI but that were subsequently confirmed as being due to RV MI.
Case Reports Case 1 A 39-year-old man was admitted 1 h after the onset of chest pain suggesting acute MI. The admission ECG (Fig 1, top, a) showed a 3- to 5-mm ST-segment elevation in precordial leads V1 to V4 with no decrease in the R wave and no Q wave, and a slight reciprocal change in lead aVL. Thrombolytic treatment was started. Two-dimensional and Doppler echocardiograms showed mild RV enlargement and an abnormal pulmonary regurgitation Doppler pattern, which suggested RV dysfunction (Fig 1, middle, b). Rapid relief of chest pain and resolution of ST-segment abnormalities were achieved about 60 min after the onset of thrombolysis. On day 5, coronary angiography showed a normal left coronary artery and a patent but severely diseased right coronary artery, with a tight stenosis in its proximal portion *From the Department of Cardiology, Beaujon Hospital, Clichy, France. Manuscript received November 9, 1999; revision accepted May 24, 2000. Correspondence to: Damien Logeart, MD, Department of Cardiology, Beaujon Hospital, 100 Blvd General Leclerc, 92110 Clichy, France 290
A 44-year-old man was admitted for unstable angina. Because of the recurrence of chest pain with an ST-segment elevation in leads V1 to V3 on the ECG (Fig 2, top, a), emergent cardiac catheterization was performed, which revealed the complete occlusion of the proximal right coronary artery (Fig 2, bottom, b). The left coronary artery was normal and gave off collaterals to the posterior descending and posterolateral LV branches. After successful recanalization by angioplasty and stent implantation, the chest pain resolved, and an ECG after the angioplasty showed the complete disappearance of the ST-segment elevation and no Q wave. The findings of echocardiography were normal.
Discussion As shown by these two cases, ST-segment elevation in leads V1 to V4 during acute MI may be caused by isolated ischemic injury of the RV wall rather than the LV anterior wall and septum. ST-segment elevation in the right-sided precordial leads, especially in V4R, is observed in 60 to 90% of patients with acute RV MI but is often transient.1 ST-segment elevation suggesting anterior infarction and involving leads V1 to V3 also has been reported in a few cases of RV involvement.2–5 ST elevation in these precordial leads is usually observed with a specific pattern (ie, ST elevation restricted to leads V1, V2, V3, and even to V4, and ST elevation decreasing from V1 through V4, without Q-wave formation). It is difficult to determine whether ST-segment elevation in leads V1 to V3 or V4 is caused by RV involvement or damage to the septum. In the two cases we describe, the left anterior descending artery and its septal branches were normal. Twodimensional echocardiograms also showed no evidence of septum involvement and no obvious LV wall motion abnormality in both cases. In contrast, echocardiograms showed direct evidence for RV ischemic involvement in case 1, in which the most obvious criteria were assessed using Doppler pulmonary regurgitant flow analysis.6 The RV was more difficult to examine in case 2, which is often experienced in the clinical setting underlining the frequent difficulty in directly establishing the diagnosis of RV infarction during the acute phase. Using an experimental infarction model, Geft et al4 found evidence that the ST segment in the left precordial leads was dependent on the coexisting electrical forces ratio between the ischemic RV free wall and the LV inferior wall. Isolated RV MI yielded an ST-segment elevation in the precordial leads, whereas its combination Selected Reports
Figure 1. Top, a: 12-lead ECG recorded on admission (case 1) shows ST-segment elevation in leads V1 to V4, with no Q wave, and with reciprocal changes in lead aVL. Middle, b: continuous-wave Doppler echocardiographic tracing of physiologic pulmonary regurgitation (case 1) characterized by an abrupt deceleration of the jet velocity in mid-diastole. Bottom, c: right coronary angiogram (case 1) on day 5 shows a patent but severely diseased right coronary artery, with tight stenosis in the proximal portion. The right coronary artery also has a large RV branch and a small posterior descending artery.
with inferior LV MI suppressed this ST-segment elevation in the precordial leads and yielded an ST-segment elevation in leads DII, DIII, and aVF. On the other hand, van der Bolt et al5 observed that isolated acute occlusion of the RV branch after angioplasty could be followed by STsegment elevations in leads V1 to V3. In the clinical setting, RV coronary perfusion is usually compromised by the occlusion of a rudimentary or nondominant right coronary artery (as in our case 1) or by proximal right coronary artery occlusion with or without partial left to right collateral circulation (as in our case 2). In summary, a diagnosis of RV MI has to be considered when such an ECG pattern is observed, especially regarding the specific in-hospital complications, high in-hospital mortality rates, and therapeutic consequences that are associated with RV MI.1
References 1 Kinch J, Ryan TJ. Right ventricular infarction. N Engl J Med 1994; 330:1211–1217 2 Khan ZU, Chou T-C. Right ventricular infarction mimicking acute anteroseptal left ventricular infarction. Am Heart J 1996; 132:1089 –1093 3 Lopez-Sendon J, Coma-Canella I, Alcasena S, et al. Electrocardiographic findings in acute RV infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2 and V3. J Am Coll Cardiol 1985; 6:1273–1279 4 Geft IL, Shah PK, Rodriguez L. ST elevation in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984; 53:991–996 5 van der Bolt CL, Vermeersch PH, Plokker HW. Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty: the CHEST / 119 / 1 / JANUARY, 2001
291
Figure 2. Top, a: 12-lead ECG recorded while the patient was experiencing chest pain (case 2) shows ST-segment elevation in leads V1, V2, and V3, and a slight depression and T-wave inversion in leads DII, DIII, and aVF. Bottom, b: right coronary angiogram shows the complete occlusion of the proximal right coronary artery.
only ’true’ model to study ECG changes in acute, isolated right ventricular infarction. Eur Heart J 1996; 17:247–250 6 Cohen A, Logeart D, Costagliola D, et al. Usefulness of pulmonary regurgitation Doppler tracings in predicting inhospital and long-term outcome in patients with inferior wall acute myocardial infarction. Am J Cardiol 1998; 81:276 –281
Dieulafoy’s Disease of the Bronchus in Association With a Paravertebral Neurilemoma* Enrique Stoopen, MD; Javier Baquera-Heredia, MD; Diana Cortes; and Leon Green, MD, FCCP
Dieulafoy’s disease is a vascular anomaly characterized by the presence of a dysplastic artery that is related to an epithelial ulcer. While it is most frequently a GI condition, occurrence in the bronchus has been reported previously in six cases. We present the case of a 51-yearold man with severe hemoptysis and epistaxis. Chest radiographs showed diffuse density in the right base and a mass in the pedicle of T4. The results of bronchoscopy corroborated an active arterial bleeding point in the bronchus of the right middle lobe. A middle and lower lobectomy was performed with resection of the paravertebral mass. The final diagnoses were bronchial Dieulafoy’s disease and paravertebral neurilemoma. (CHEST 2001; 119:292–294) 292
Key words: bronchial vascular lesion; Dieulafoy’s disease; hemoptysis
disease was first described in 1898 by the D ieulafoy’s French surgeon Georges Dieulafoy. The gastric lesion is defined as a vascular malformation characterized by a dysplastic artery contiguous to the superficial epithelium of the mucosa.1 The lesion is uncommon, but it is seen in 1 to 2% of patients presenting with massive upper GI hemorrhaging.2 It has been reported in the esophagus, stomach, duodenum, gall bladder, jejunum, colon, rectum, and bronchus.1,3,4 This malformation originates from a tortuous dysplastic artery in the submucosa, from which vascular branches derive that can be located in the mucosa.3 The low levels of inflammatory infiltrate and fibrin deposition suggest that the thrombosis and not the epithelial ulcer was the condition that preceded the disruption. A congenital origin for the lesion has been suggested, but the regulating mechanisms of the dysplastic alteration are unknown.3,4 Alcohol, gastritis, thrombotic phenomena, and trauma have been proposed as causes of GI hemorrhage, but none have been described for bronchial bleeding. *From the Departments of Surgery (Drs. Stoopen and Green) and Pathology (Drs. Baquera-Heredia and Cortes), The ABC Medical Center, Mexico City, Mexico. Manuscript received July 21, 1999; revision accepted June 20, 2000. Correspondence to: Enrique Stoopen, MD, The ABC Medical Center, Sur 136 No. 116, Col. Las Americas, CP 01120, D.F., Mexico; e-mail: [email protected] Selected Reports
(Fig 1, bottom, c). The right coronary artery had a large RV branch and a small posterior descending artery. Left ventriculography showed minimal inferior wall segment hypokinesia. A right coronary angioplasty was performed with stent implantation. At discharge, the ECG showed T-wave inversion in the inferior leads but no significant abnormality in the precordial leads. Case 2
Damien Logeart, MD; Dominique Himbert, MD; and Alain Cohen-Solal, MD, PhD
Isolated acute right ventricular (RV) infarction is rare, and ECG diagnosis may be difficult. We report two cases of acute myocardial infarction with STsegment elevation in anterior precordial leads caused by such an RV involvement. Potential mechanisms for the relationship are given. (CHEST 2001; 119:290 –292) Key words: ECG; myocardial infarction; right ventricular Abbreviations: LV ⫽ left ventricular; MI ⫽ myocardial infarction; RV ⫽ right ventricular
right ventricular (RV) myocardial infarction (MI) is A cute usually associated with inferior left ventricular (LV) MI and results in a high in-hospital mortality rate.1 Isolated RV MI is rare, and bedside diagnosis may be difficult and misleading because ECG changes are inconsistent. We describe the cases of two patients admitted with ECG changes that were suggestive of acute anterior LV MI but that were subsequently confirmed as being due to RV MI.
Case Reports Case 1 A 39-year-old man was admitted 1 h after the onset of chest pain suggesting acute MI. The admission ECG (Fig 1, top, a) showed a 3- to 5-mm ST-segment elevation in precordial leads V1 to V4 with no decrease in the R wave and no Q wave, and a slight reciprocal change in lead aVL. Thrombolytic treatment was started. Two-dimensional and Doppler echocardiograms showed mild RV enlargement and an abnormal pulmonary regurgitation Doppler pattern, which suggested RV dysfunction (Fig 1, middle, b). Rapid relief of chest pain and resolution of ST-segment abnormalities were achieved about 60 min after the onset of thrombolysis. On day 5, coronary angiography showed a normal left coronary artery and a patent but severely diseased right coronary artery, with a tight stenosis in its proximal portion *From the Department of Cardiology, Beaujon Hospital, Clichy, France. Manuscript received November 9, 1999; revision accepted May 24, 2000. Correspondence to: Damien Logeart, MD, Department of Cardiology, Beaujon Hospital, 100 Blvd General Leclerc, 92110 Clichy, France 290
A 44-year-old man was admitted for unstable angina. Because of the recurrence of chest pain with an ST-segment elevation in leads V1 to V3 on the ECG (Fig 2, top, a), emergent cardiac catheterization was performed, which revealed the complete occlusion of the proximal right coronary artery (Fig 2, bottom, b). The left coronary artery was normal and gave off collaterals to the posterior descending and posterolateral LV branches. After successful recanalization by angioplasty and stent implantation, the chest pain resolved, and an ECG after the angioplasty showed the complete disappearance of the ST-segment elevation and no Q wave. The findings of echocardiography were normal.
Discussion As shown by these two cases, ST-segment elevation in leads V1 to V4 during acute MI may be caused by isolated ischemic injury of the RV wall rather than the LV anterior wall and septum. ST-segment elevation in the right-sided precordial leads, especially in V4R, is observed in 60 to 90% of patients with acute RV MI but is often transient.1 ST-segment elevation suggesting anterior infarction and involving leads V1 to V3 also has been reported in a few cases of RV involvement.2–5 ST elevation in these precordial leads is usually observed with a specific pattern (ie, ST elevation restricted to leads V1, V2, V3, and even to V4, and ST elevation decreasing from V1 through V4, without Q-wave formation). It is difficult to determine whether ST-segment elevation in leads V1 to V3 or V4 is caused by RV involvement or damage to the septum. In the two cases we describe, the left anterior descending artery and its septal branches were normal. Twodimensional echocardiograms also showed no evidence of septum involvement and no obvious LV wall motion abnormality in both cases. In contrast, echocardiograms showed direct evidence for RV ischemic involvement in case 1, in which the most obvious criteria were assessed using Doppler pulmonary regurgitant flow analysis.6 The RV was more difficult to examine in case 2, which is often experienced in the clinical setting underlining the frequent difficulty in directly establishing the diagnosis of RV infarction during the acute phase. Using an experimental infarction model, Geft et al4 found evidence that the ST segment in the left precordial leads was dependent on the coexisting electrical forces ratio between the ischemic RV free wall and the LV inferior wall. Isolated RV MI yielded an ST-segment elevation in the precordial leads, whereas its combination Selected Reports
Figure 1. Top, a: 12-lead ECG recorded on admission (case 1) shows ST-segment elevation in leads V1 to V4, with no Q wave, and with reciprocal changes in lead aVL. Middle, b: continuous-wave Doppler echocardiographic tracing of physiologic pulmonary regurgitation (case 1) characterized by an abrupt deceleration of the jet velocity in mid-diastole. Bottom, c: right coronary angiogram (case 1) on day 5 shows a patent but severely diseased right coronary artery, with tight stenosis in the proximal portion. The right coronary artery also has a large RV branch and a small posterior descending artery.
with inferior LV MI suppressed this ST-segment elevation in the precordial leads and yielded an ST-segment elevation in leads DII, DIII, and aVF. On the other hand, van der Bolt et al5 observed that isolated acute occlusion of the RV branch after angioplasty could be followed by STsegment elevations in leads V1 to V3. In the clinical setting, RV coronary perfusion is usually compromised by the occlusion of a rudimentary or nondominant right coronary artery (as in our case 1) or by proximal right coronary artery occlusion with or without partial left to right collateral circulation (as in our case 2). In summary, a diagnosis of RV MI has to be considered when such an ECG pattern is observed, especially regarding the specific in-hospital complications, high in-hospital mortality rates, and therapeutic consequences that are associated with RV MI.1
References 1 Kinch J, Ryan TJ. Right ventricular infarction. N Engl J Med 1994; 330:1211–1217 2 Khan ZU, Chou T-C. Right ventricular infarction mimicking acute anteroseptal left ventricular infarction. Am Heart J 1996; 132:1089 –1093 3 Lopez-Sendon J, Coma-Canella I, Alcasena S, et al. Electrocardiographic findings in acute RV infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2 and V3. J Am Coll Cardiol 1985; 6:1273–1279 4 Geft IL, Shah PK, Rodriguez L. ST elevation in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984; 53:991–996 5 van der Bolt CL, Vermeersch PH, Plokker HW. Isolated acute occlusion of a large right ventricular branch of the right coronary artery following coronary balloon angioplasty: the CHEST / 119 / 1 / JANUARY, 2001
291
Figure 2. Top, a: 12-lead ECG recorded while the patient was experiencing chest pain (case 2) shows ST-segment elevation in leads V1, V2, and V3, and a slight depression and T-wave inversion in leads DII, DIII, and aVF. Bottom, b: right coronary angiogram shows the complete occlusion of the proximal right coronary artery.
only ’true’ model to study ECG changes in acute, isolated right ventricular infarction. Eur Heart J 1996; 17:247–250 6 Cohen A, Logeart D, Costagliola D, et al. Usefulness of pulmonary regurgitation Doppler tracings in predicting inhospital and long-term outcome in patients with inferior wall acute myocardial infarction. Am J Cardiol 1998; 81:276 –281
Dieulafoy’s Disease of the Bronchus in Association With a Paravertebral Neurilemoma* Enrique Stoopen, MD; Javier Baquera-Heredia, MD; Diana Cortes; and Leon Green, MD, FCCP
Dieulafoy’s disease is a vascular anomaly characterized by the presence of a dysplastic artery that is related to an epithelial ulcer. While it is most frequently a GI condition, occurrence in the bronchus has been reported previously in six cases. We present the case of a 51-yearold man with severe hemoptysis and epistaxis. Chest radiographs showed diffuse density in the right base and a mass in the pedicle of T4. The results of bronchoscopy corroborated an active arterial bleeding point in the bronchus of the right middle lobe. A middle and lower lobectomy was performed with resection of the paravertebral mass. The final diagnoses were bronchial Dieulafoy’s disease and paravertebral neurilemoma. (CHEST 2001; 119:292–294) 292
Key words: bronchial vascular lesion; Dieulafoy’s disease; hemoptysis
disease was first described in 1898 by the D ieulafoy’s French surgeon Georges Dieulafoy. The gastric lesion is defined as a vascular malformation characterized by a dysplastic artery contiguous to the superficial epithelium of the mucosa.1 The lesion is uncommon, but it is seen in 1 to 2% of patients presenting with massive upper GI hemorrhaging.2 It has been reported in the esophagus, stomach, duodenum, gall bladder, jejunum, colon, rectum, and bronchus.1,3,4 This malformation originates from a tortuous dysplastic artery in the submucosa, from which vascular branches derive that can be located in the mucosa.3 The low levels of inflammatory infiltrate and fibrin deposition suggest that the thrombosis and not the epithelial ulcer was the condition that preceded the disruption. A congenital origin for the lesion has been suggested, but the regulating mechanisms of the dysplastic alteration are unknown.3,4 Alcohol, gastritis, thrombotic phenomena, and trauma have been proposed as causes of GI hemorrhage, but none have been described for bronchial bleeding. *From the Departments of Surgery (Drs. Stoopen and Green) and Pathology (Drs. Baquera-Heredia and Cortes), The ABC Medical Center, Mexico City, Mexico. Manuscript received July 21, 1999; revision accepted June 20, 2000. Correspondence to: Enrique Stoopen, MD, The ABC Medical Center, Sur 136 No. 116, Col. Las Americas, CP 01120, D.F., Mexico; e-mail: [email protected] Selected Reports