Acta Cardiologica
ISSN: 0001-5385 (Print) 0373-7934 (Online) Journal homepage: http://www.tandfonline.com/loi/tacd20
Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review Hannes Vervaeke, Nathalie Becaus, Martin Penicka & Marc Vanderheyden To cite this article: Hannes Vervaeke, Nathalie Becaus, Martin Penicka & Marc Vanderheyden (2014) Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review, Acta Cardiologica, 69:2, 209-212, DOI: 10.1080/AC.69.2.3017307 To link to this article: https://doi.org/10.1080/AC.69.2.3017307
Published online: 23 May 2017.
Submit your article to this journal
Article views: 1
View related articles
View Crossmark data
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=tacd20
Acta Cardiol 2014; 69(2): 209-212
209
doi: 10.2143/AC.69.2.3017307
Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review Hannes VERVAEKE1,2, MD; Nathalie BECAUS1,2, MD; Martin PENICKA1, MD, PhD; Marc VANDERHEYDEN1, MD, PhD 1
Onze-Lieve-Vrouwziekenhuis, Aalst, Belgium; 2Universitair Ziekenhuis Gent, Belgium.
Abstract We report the case of a 62-year-old woman presenting with symptoms and findings of myocardial infarction and a left ventricular free wall rupture. Coronary angiography revealed a critical stenosis in the middle right coronary artery. A contrast left ventriculogram revealed extravasation of contrast through the inferolateral wall of the left ventricle. Left ventricular free wall rupture is a rare complication of acute myocardial infarction, occurring in approximately 2% of cases. It is often fatal because of the development of haemopericardium and tamponade. Some patients, like the one described in this case, may present with small leaks that might close spontaneously by epicardial fibrin deposits, thus selflimiting, without requiring surgical intervention. This patient received only intense medical treatment. Indeed, blood clots at the endocardial and the epicardial site of the rupture have often been identified, suggesting protection for further rupture.
Keywords Left ventricular wall – rupture – self-limiting – myocardial infarction.
CASE REPORT A 62-year-old woman with a history of percutaneous coronary intervention (PCI) of the left anterior descending artery (LAD) presented in the emergency room with recurrent chest pain during the last 10 days. The patient appeared neurologically adequate and was haemodynamically stable at admission. Vital signs included a blood pressure of 137/75 mmHg, heart rate 67/min, normal breathing sounds and no peripheral oedema. No abnormalities on heart auscultation were heard. The cardiac risk factors included hypercholesterolaemia, arterial hypertension and obesity. Electrocardiography showed: (i) sinus rhythm; (ii) negative T-waves;
Address for correspondence: Hannes Vervaeke, De Pintelaan 185, 9000 Gent, Belgium. E-mail: [email protected] Received 20 December 2013; accepted for publication 15 January 2014.
(iii) inferolateral and lateral Q-waves in the inferior leads, suggesting a semi-recent inferior infarction. An echocardiogram performed at the referring hospital revealed hypokinesia in the posterior part but the acoustic window was limited because of obesity. Because of the instable character of the chest pain the patient was transferred to our centre for further evalution. Cardiac biomarkers were as follows: the creatine phosphokinase and high sensitive troponins were 278 U/L (range 10-142 U/L) and 166.6 ng/L (range > 14 ng/L), respectively. Coronary angiography on the day of arrival showed a critical stenosis in de middle right coronary artery (RCA) and diffuse atheromatosis in the other segments. The in situ stent in the LAD was patent. A PCI with “spot” bare metal stenting (Pro-kinetic 3 × 15 mm) in the culprit lesion in the RCA was performed and a loading dose of clopidogrel (600 mg) was administered. A contrast left ventriculogram revealed a restricted aneurysm in the basal inferior part and extravasation of contrast through the inferolateral wall of the left ventricle suggesting left ventricular wall rupture in the
210
H. Vervaeke et al.
Fig. 1a Left ventriculogram (RAO): contrast extravasation.
inferolateral parts presumably covered by fistulization to the coronary sinus (figure 1a, figure 1b). Because of a poor acoustic window a transthoracic echocardiography with contrast was performed. No clear cardiac rupture could be detected and signs of tamponade or haemopericardium were not present. The cardiac surgeon was consulted. Because of the clinically and haemodynamically stable condition of the patient (the symptoms disappeared completely) only intense medical treatment and monitoring were initiated. Finalization of the pseudo-aneurysm with echocardiography and magnetic resonance imaging (MRI) scan were suggested to be performed in a later stage. MRI of the heart revealed slightly depressed left ventricular function with ejection fraction of 55%. On the delayed enhancement images transmural infarction was noted at the inferolateral segments of the mid-ventricle whereas in the inferoseptal regions the delayed enhancement was less than 50%. A small fistula from the left ventricle to the coronary sinus was suggested. Imaging of the MRI is not included due to bad quality due to irregular heart rhythm. To exclude a congenital anomaly we reviewed the ventriculogram performed at het time of PCI in 2006 (figure 2). No fistula and no contrast staining were seen at that time. Interestingly, contrast ventriculography repeated one week after the event showed no extravasation anymore (figure 3). Epicardial fibrin deposits possibly closed the small leaks spontaneously. Indeed, thrombus and haematoma together with the pericardium sealed the rupture of the left ventricle.
Fig. 1b
Fig. 2
Left ventriculogram (LAO): contrast extravasation.
Left ventriculogram (RAO) from 2006.
The patient remained stable during her stay in the hospital. No operation was needed. The patient left the hospital on day 18 without sequelae.
DISCUSSION Rupture of the free wall of an infarcted ventricle is a relatively common finding in patients dying from an acute
Left ventricular wall rupture and myocardial infarction
Fig. 3 Control left ventriculogram (RAO) after one week: no contrast extravasation anymore.
myocardial infarction (MI). Several large studies have found cardiac rupture in 14 to 26% of such patients1. The incidence is much lower when all patients with acute MI are considered. The incidence ranges from 0.93 to 2.7% according to different registries2 but appears to have decreased in patients undergoing primary percutaneous intervention for MI. The clinical manifestations of left ventricular free wall rupture (LVFWR) depend on both the amount and the rate of intrapericardial bleeding. It varies from a catastrophic event, with an acute tear in the infarcted myocardium leading to immediate death – acute rupture –, or slow and incomplete tear leading to a late rupture – subacute rupture – as in this case. An abrupt slit-like tear in the infarcted myocardium characterizes early rupture, with a preference for anterior infarction sites. LVFWR occurs in up to 10% of the inhospital deaths following acute MI (usually between 3 to 6 days)3. There is no difference in incidence between patients treated with conventional and reperfusion therapy. LVFWR is then a devastating event and only a few patients may reach the operating room (OR) alive. Sudden haemodynamic collapse is followed by electromechanical dissociation and death. Subacute free wall rupture counts for 30% of all cases of in-hospital LVFWR and are less frequent in patients
with successful reperfusion. They are usually accompanied with a moderate to severe pericardial effusion without haemodynamic compromise. The cardiac rupture may be clinically undetected and mostly identified on a routine post-infarction echocardiogram4. Incomplete rupture may occur when the thrombus and haematoma together with the pericardium seal the rupture of the left ventricle and may develop into a pseudo-aneurysm5. LVFWR is more common in women and older patients than in patients with hypertension and first lateral or anterior wall acute MI6. The MI causing a free wall rupture is often relatively small. Other reported risk factors are ST-segment elevation or Q wave development on the initial ECG, peak MB-creatine kinase above 150 IU/L, delayed reperfusion, lack of LV hypertrophy, heart failure, prolonged angina and delay of hospitalization4. Steroid use and late thrombolysis do not appear to increase the risk of LVFWR6. Transthoracic echography with Doppler is the noninvasive method of choice for patients with suspected LVFWR5. Echocardiography has a diagnostic sensitivity of 100% and a specificity of 93%6. In this case, the acoustic window was limited, so diagnosis was set by contrast ventriculogram. LVFWR is a life-threatening event and only a few patients may reach the OR. Surgeons then perform the patch and glue method in combination with bypass surgery, often accompanied by insertion of an intraaortic balloon pump7. Based on current literature, pseudoaneurysms are also surgical emergencies and even though the scar tissue may have closed the rupture, the large majority needs to be treated aggressively. However, the postoperative mortality after surgical repair of a pseudoaneurysm ranges from 13% to 29% and may be even higher in many hospitals due to a lack of experience8. In this case, the patient was stable and the symptoms completely disappeared after PCI. Furthermore, there was no haemopericardium or tamponade visible on the emergency transthoracic echocardiography. That is why the cardiac surgery team suggested giving only intense medical treatment. Indeed, blood clots at the endocardial as well as the epicardial site of rupture have often been identified, suggesting protections for further rupture.
CONFLICT OF INTEREST: none declared.
211
212
H. Vervaeke et al. REFERENCES 1. Ekim H, Tuncer M, Basel H. Repair of ventricle free wall rupture after acute myocardial infarction: a case report. Cases J 2009; 2: 9099. 2. Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J, Dzavik V, Greenberg M, Menegus M, Connery C, Hochman JS. Cardiogenic shock due to cardiac free-wall rupture of tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? J Am Coll Cardiol 2000; 36(3 Suppl A): 1117-22. 3. Bashour T, Kabbani SS, Ellertson DG, Crew J, Hanna ES. Surgical salvage of heart rupture: report of two cases and
review of the literature. Ann Thorac Surg 1983, 36: 209-213. 4. Huang CM, Chen LW, Huang SH, Huang SS, Wang KL, Chiang CE. Acute left ventricular rupture following posterior wall myocardial infarction. Intern Med 2010; 49: 1387-90. 5. Roa-Castro VH, Molina-Bello E, Valenzuela-Suarez H, Rotberg-Jagode T, Espinola-Zavaleta N. Survival after left ventricular free wall rupture in an elderly woman with acute myocardial infarction treated only medically. Case Rep Vasc Med 2012; 2012: 728602. 6. Gosal T, Phillipp, R, Morris AL. Myocardial infarction and left ventricular free wall
rupture in a patient with a prior pericardiectomy. Can J Cardiol 2008; 24: 513-5. 7. Zoffoli G, Battaglia F, Venturini A, Asta A, Terrini A, Zanchettin C, Mangino D. A novel approach to ventricular rupture: clinical needs and surgical technique. Annals Thoracic Surgery 2012; 93: 1002-3. 8. Figueras, J, Cortadellas J, Domingo E, Soler-Soler J. Survival following self-limited left ventricular free wall rupture during myocardial infarction. Management differences between patients with or without pseudoaneurysm formation. Int J Cardiol 2001; 79: 103-111.
ISSN: 0001-5385 (Print) 0373-7934 (Online) Journal homepage: http://www.tandfonline.com/loi/tacd20
Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review Hannes Vervaeke, Nathalie Becaus, Martin Penicka & Marc Vanderheyden To cite this article: Hannes Vervaeke, Nathalie Becaus, Martin Penicka & Marc Vanderheyden (2014) Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review, Acta Cardiologica, 69:2, 209-212, DOI: 10.1080/AC.69.2.3017307 To link to this article: https://doi.org/10.1080/AC.69.2.3017307
Published online: 23 May 2017.
Submit your article to this journal
Article views: 1
View related articles
View Crossmark data
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=tacd20
Acta Cardiol 2014; 69(2): 209-212
209
doi: 10.2143/AC.69.2.3017307
Self-limiting left ventricular wall rupture following myocardial infarction: a case report and literature review Hannes VERVAEKE1,2, MD; Nathalie BECAUS1,2, MD; Martin PENICKA1, MD, PhD; Marc VANDERHEYDEN1, MD, PhD 1
Onze-Lieve-Vrouwziekenhuis, Aalst, Belgium; 2Universitair Ziekenhuis Gent, Belgium.
Abstract We report the case of a 62-year-old woman presenting with symptoms and findings of myocardial infarction and a left ventricular free wall rupture. Coronary angiography revealed a critical stenosis in the middle right coronary artery. A contrast left ventriculogram revealed extravasation of contrast through the inferolateral wall of the left ventricle. Left ventricular free wall rupture is a rare complication of acute myocardial infarction, occurring in approximately 2% of cases. It is often fatal because of the development of haemopericardium and tamponade. Some patients, like the one described in this case, may present with small leaks that might close spontaneously by epicardial fibrin deposits, thus selflimiting, without requiring surgical intervention. This patient received only intense medical treatment. Indeed, blood clots at the endocardial and the epicardial site of the rupture have often been identified, suggesting protection for further rupture.
Keywords Left ventricular wall – rupture – self-limiting – myocardial infarction.
CASE REPORT A 62-year-old woman with a history of percutaneous coronary intervention (PCI) of the left anterior descending artery (LAD) presented in the emergency room with recurrent chest pain during the last 10 days. The patient appeared neurologically adequate and was haemodynamically stable at admission. Vital signs included a blood pressure of 137/75 mmHg, heart rate 67/min, normal breathing sounds and no peripheral oedema. No abnormalities on heart auscultation were heard. The cardiac risk factors included hypercholesterolaemia, arterial hypertension and obesity. Electrocardiography showed: (i) sinus rhythm; (ii) negative T-waves;
Address for correspondence: Hannes Vervaeke, De Pintelaan 185, 9000 Gent, Belgium. E-mail: [email protected] Received 20 December 2013; accepted for publication 15 January 2014.
(iii) inferolateral and lateral Q-waves in the inferior leads, suggesting a semi-recent inferior infarction. An echocardiogram performed at the referring hospital revealed hypokinesia in the posterior part but the acoustic window was limited because of obesity. Because of the instable character of the chest pain the patient was transferred to our centre for further evalution. Cardiac biomarkers were as follows: the creatine phosphokinase and high sensitive troponins were 278 U/L (range 10-142 U/L) and 166.6 ng/L (range > 14 ng/L), respectively. Coronary angiography on the day of arrival showed a critical stenosis in de middle right coronary artery (RCA) and diffuse atheromatosis in the other segments. The in situ stent in the LAD was patent. A PCI with “spot” bare metal stenting (Pro-kinetic 3 × 15 mm) in the culprit lesion in the RCA was performed and a loading dose of clopidogrel (600 mg) was administered. A contrast left ventriculogram revealed a restricted aneurysm in the basal inferior part and extravasation of contrast through the inferolateral wall of the left ventricle suggesting left ventricular wall rupture in the
210
H. Vervaeke et al.
Fig. 1a Left ventriculogram (RAO): contrast extravasation.
inferolateral parts presumably covered by fistulization to the coronary sinus (figure 1a, figure 1b). Because of a poor acoustic window a transthoracic echocardiography with contrast was performed. No clear cardiac rupture could be detected and signs of tamponade or haemopericardium were not present. The cardiac surgeon was consulted. Because of the clinically and haemodynamically stable condition of the patient (the symptoms disappeared completely) only intense medical treatment and monitoring were initiated. Finalization of the pseudo-aneurysm with echocardiography and magnetic resonance imaging (MRI) scan were suggested to be performed in a later stage. MRI of the heart revealed slightly depressed left ventricular function with ejection fraction of 55%. On the delayed enhancement images transmural infarction was noted at the inferolateral segments of the mid-ventricle whereas in the inferoseptal regions the delayed enhancement was less than 50%. A small fistula from the left ventricle to the coronary sinus was suggested. Imaging of the MRI is not included due to bad quality due to irregular heart rhythm. To exclude a congenital anomaly we reviewed the ventriculogram performed at het time of PCI in 2006 (figure 2). No fistula and no contrast staining were seen at that time. Interestingly, contrast ventriculography repeated one week after the event showed no extravasation anymore (figure 3). Epicardial fibrin deposits possibly closed the small leaks spontaneously. Indeed, thrombus and haematoma together with the pericardium sealed the rupture of the left ventricle.
Fig. 1b
Fig. 2
Left ventriculogram (LAO): contrast extravasation.
Left ventriculogram (RAO) from 2006.
The patient remained stable during her stay in the hospital. No operation was needed. The patient left the hospital on day 18 without sequelae.
DISCUSSION Rupture of the free wall of an infarcted ventricle is a relatively common finding in patients dying from an acute
Left ventricular wall rupture and myocardial infarction
Fig. 3 Control left ventriculogram (RAO) after one week: no contrast extravasation anymore.
myocardial infarction (MI). Several large studies have found cardiac rupture in 14 to 26% of such patients1. The incidence is much lower when all patients with acute MI are considered. The incidence ranges from 0.93 to 2.7% according to different registries2 but appears to have decreased in patients undergoing primary percutaneous intervention for MI. The clinical manifestations of left ventricular free wall rupture (LVFWR) depend on both the amount and the rate of intrapericardial bleeding. It varies from a catastrophic event, with an acute tear in the infarcted myocardium leading to immediate death – acute rupture –, or slow and incomplete tear leading to a late rupture – subacute rupture – as in this case. An abrupt slit-like tear in the infarcted myocardium characterizes early rupture, with a preference for anterior infarction sites. LVFWR occurs in up to 10% of the inhospital deaths following acute MI (usually between 3 to 6 days)3. There is no difference in incidence between patients treated with conventional and reperfusion therapy. LVFWR is then a devastating event and only a few patients may reach the operating room (OR) alive. Sudden haemodynamic collapse is followed by electromechanical dissociation and death. Subacute free wall rupture counts for 30% of all cases of in-hospital LVFWR and are less frequent in patients
with successful reperfusion. They are usually accompanied with a moderate to severe pericardial effusion without haemodynamic compromise. The cardiac rupture may be clinically undetected and mostly identified on a routine post-infarction echocardiogram4. Incomplete rupture may occur when the thrombus and haematoma together with the pericardium seal the rupture of the left ventricle and may develop into a pseudo-aneurysm5. LVFWR is more common in women and older patients than in patients with hypertension and first lateral or anterior wall acute MI6. The MI causing a free wall rupture is often relatively small. Other reported risk factors are ST-segment elevation or Q wave development on the initial ECG, peak MB-creatine kinase above 150 IU/L, delayed reperfusion, lack of LV hypertrophy, heart failure, prolonged angina and delay of hospitalization4. Steroid use and late thrombolysis do not appear to increase the risk of LVFWR6. Transthoracic echography with Doppler is the noninvasive method of choice for patients with suspected LVFWR5. Echocardiography has a diagnostic sensitivity of 100% and a specificity of 93%6. In this case, the acoustic window was limited, so diagnosis was set by contrast ventriculogram. LVFWR is a life-threatening event and only a few patients may reach the OR. Surgeons then perform the patch and glue method in combination with bypass surgery, often accompanied by insertion of an intraaortic balloon pump7. Based on current literature, pseudoaneurysms are also surgical emergencies and even though the scar tissue may have closed the rupture, the large majority needs to be treated aggressively. However, the postoperative mortality after surgical repair of a pseudoaneurysm ranges from 13% to 29% and may be even higher in many hospitals due to a lack of experience8. In this case, the patient was stable and the symptoms completely disappeared after PCI. Furthermore, there was no haemopericardium or tamponade visible on the emergency transthoracic echocardiography. That is why the cardiac surgery team suggested giving only intense medical treatment. Indeed, blood clots at the endocardial as well as the epicardial site of rupture have often been identified, suggesting protections for further rupture.
CONFLICT OF INTEREST: none declared.
211
212
H. Vervaeke et al. REFERENCES 1. Ekim H, Tuncer M, Basel H. Repair of ventricle free wall rupture after acute myocardial infarction: a case report. Cases J 2009; 2: 9099. 2. Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J, Dzavik V, Greenberg M, Menegus M, Connery C, Hochman JS. Cardiogenic shock due to cardiac free-wall rupture of tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? J Am Coll Cardiol 2000; 36(3 Suppl A): 1117-22. 3. Bashour T, Kabbani SS, Ellertson DG, Crew J, Hanna ES. Surgical salvage of heart rupture: report of two cases and
review of the literature. Ann Thorac Surg 1983, 36: 209-213. 4. Huang CM, Chen LW, Huang SH, Huang SS, Wang KL, Chiang CE. Acute left ventricular rupture following posterior wall myocardial infarction. Intern Med 2010; 49: 1387-90. 5. Roa-Castro VH, Molina-Bello E, Valenzuela-Suarez H, Rotberg-Jagode T, Espinola-Zavaleta N. Survival after left ventricular free wall rupture in an elderly woman with acute myocardial infarction treated only medically. Case Rep Vasc Med 2012; 2012: 728602. 6. Gosal T, Phillipp, R, Morris AL. Myocardial infarction and left ventricular free wall
rupture in a patient with a prior pericardiectomy. Can J Cardiol 2008; 24: 513-5. 7. Zoffoli G, Battaglia F, Venturini A, Asta A, Terrini A, Zanchettin C, Mangino D. A novel approach to ventricular rupture: clinical needs and surgical technique. Annals Thoracic Surgery 2012; 93: 1002-3. 8. Figueras, J, Cortadellas J, Domingo E, Soler-Soler J. Survival following self-limited left ventricular free wall rupture during myocardial infarction. Management differences between patients with or without pseudoaneurysm formation. Int J Cardiol 2001; 79: 103-111.
