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European Journal of Echocardiography 2005 6(1):72-74; doi:10.1016/j.euje.2004.07.002
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Copyright © 2005, The European Society of Cardiology

Incomplete myocardial rupture after coronary embolism of an isolated single coronary artery

Javier Pindado, Pedro Marcos-Alberca*, Manuel Rey, Rosa Rábago, Carlos de Diego, Borja Ibáñez, Manuel Córdoba and Jerónimo Farré

Servicio de Cardiología, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain

Received 11 March 2004; received in revised form 22 June 2004; accepted after revision 1 July 2004.

* Corresponding author. Laboratorio de Ecocardiografía, Servicio de Cardiología, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Avenida Reyes Católicos 2, 28040 Madrid, Spain. Tel.: +34 91 550 48 56; fax: +34 91 549 70 33. pmarcos{at}fjd.es


    Abstract
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 Abstract
 Case report
 Discussion
 References
 
An 82-year-old female was admitted to the coronary care unit with an anterior wall myocardial infarction and cardiogenic shock. She was in chronic atrial fibrillation without oral anticoagulation. Coronary angiography showed occlusion of the left main coronary artery which originated together with a normal right coronary artery from the right sinus of Valsalva. The advanced age, the presence of chronic atrial fibrillation not anticoagulated and the normal appearance of the remaining coronary arteries suggested a thromboembolic origin. Transthoracic echocardiography showed an abrupt interruption of the myocardial wall, in the apical portion of the interventricular septum, not communicating with the pericardial sac or right ventricular cavity suggesting the presence of an incomplete contained rupture of the myocardial wall at this location. She died in cardiogenic shock due to the extensive left ventricular damage.

Keywords: Atrial fibrillation; Myocardial infarction; Embolism; Complications


    Case report
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 Abstract
 Case report
 Discussion
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An 82-year-old female was admitted to the coronary care unit because of sudden onset of severe chest pain lasting for 4h. She had a past history of high blood pressure, type II diabetes and a transient ischemic cerebrovascular attack. She had been for at least seven months in atrial fibrillation without receiving oral anticoagulation. On admission, the blood pressure was 65/55mmHg, and the heart rate was 85bpm. Clinical examination showed intense pallor, cold extremities, elevated central venous pressure, a gallop rhythm and bilateral rales occupying more than half of the lungs. The ECG showed atrial fibrillation, ST-segment elevation in leads V2 to V6, I, aVL and ST-segment depression in leads II, III and aVF. With the diagnosis of acute anterior wall myocardial infarction and cardiogenic shock, coronary angiography was performed after hemodynamic stabilisation with dobutamine and dopamine infusion and insertion of an intra-aortic counterpulsation balloon (IACB).

Coronary arteriography showed the main left coronary artery and the right coronary artery originating from a single ostium in the right sinus of Valsalva. There was a complete occlusion of the anomalous left main coronary artery (Fig. 1). After the balloon dilation of the left main coronary artery, the whole left coronary artery appeared free of arteriosclerotic lesions. The right coronary artery was also normal.


Figure 1
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Figure 1 LAO angiographic view showing complete occlusion of the left main coronary artery, which arises from the right sinus of Valsalva and sharing it with a normal right coronary artery. The origin and course of the isolated coronary artery fulfill the criteria of RIIA-type of Yamanaka and Hobbs classification. Arrow shows the occlusion in the left main coronary artery. LMCA: left main coronary artery; RCA: right coronary artery.

 
Transthoracic echocardiography showed extensive akinesis of the anterior wall, apex, anterior interventricular septum, and the middle and apical segments of the lateral and inferior walls. Left ventricular ejection fraction was estimated to be 15%. In addition, there was an abrupt discontinuity, 10mm-wide, localized at the most apical portion of the interventricular septum suggesting myocardial rupture (Figs. 2 and 3Go). The rupture involved the whole thickness of the myocardial wall and was contained by the epicardium and, the thickened pericardium and the right ventricle. Nonetheless, the absence of pericardial effusion or left-to-right shunt in color Doppler examination, led us to diagnose the rupture as contained and incomplete. The maximal CK value was 4034UI/l and its MB fraction 544UI/l, 9h after the onset of symptoms. The patient remained in cardiogenic shock despite the percutaneous coronary intervention and the infusion of high dose intravenous inotropic drugs and the use of intra-aortic balloon counterpulsation.


Figure 2
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Figure 2 Four-chamber apical echocardiographic view. There is an abrupt interruption of the myocardial wall, communicating neither with the pericardial sac nor the right ventricle, suggesting the presence of an incomplete and contained rupture of the myocardial wall at this location. There was no pericardial effusion. LV: left ventricle; LA: left atrium; RV: right ventricle; RA: right atrium.

 


Figure 3
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Figure 3 Modified two-chamber apical echocardiographic view (anterior rotation) that shows an abrupt discontinuity, 10mm-wide, located at the most apical portion of the interventricular septum. The rupture reached the epicardium and comprised the whole myocardial wall, in close contact with the pericardium and the right ventricle. LV: left ventricle.

 
Serial echocardiographic examinations showed persistence of severe systolic ventricular dysfunction. The rupture did not progress to an interventricular communication or a ventricular pseudoaneurysm. Surgery was excluded due to the cardiogenic shock and the absence of improvement of the left ventricular systolic function after reperfusion. Finally, the patient died.


    Discussion
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 Abstract
 Case report
 Discussion
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Incomplete rupture of the free myocardial wall is a rare mechanical complication after an acute myocardial infarction.1 The event was most likely caused by an embolic occlusion of the main left coronary artery with an anomalous origin and a common orifice with the right coronary artery.

In patients with an acute myocardial infarction treated with percutaneous coronary interventions, the incidence of free-wall myocardial rupture is 1.8% compared to 3.3% in patients treated with thrombolysis.2 Post-myocardial infarction rupture has a 70% mortality during hospitalisation.1 There are several forms of post-myocardial infarction free-wall rupture. For the diagnosis, two-dimensional echocardiography is the technique of choice, with high sensitivity and specificity.3 Incomplete rupture is relatively uncommon and occurs in 16.6% of the total free-wall ruptures. Cardiogenic shock is present in 58% of the patients with an incomplete myocardial rupture, most likely due to the extensive anterior wall infarction and severe pump failure.4

On the other hand, a single coronary artery is a very rare anatomic anomaly, present in 0.06% of non-selected, consecutive diagnostic coronary arteriograms.5 There are several types of single coronary arteries, defined by the point of origin of the left and right coronary arteries, the distribution over the ventricular surface and their relationship with the great vessels (aorta and pulmonary trunk). Our case belongs to the so-called RIIA-type of the Yamanaka and Hobbs classification, modified from Lipton.5,6 In this classification, according to the site of origin of single coronary artery in the right or the left sinus of Valsalva, the R or the L letter is assigned. Thereafter, the Latin number I, II or III depends on the relationship between the three main epicardial vessels. Thus, in group I they emerge separately, following the normal anatomical course of either a right or a left coronary artery; in group II, they originate from the proximal part of the normally located coronary artery and, in group III, the left anterior descending artery and the circumflex coronary artery arise separately from the proximal part of the normal right coronary artery, without a common left main coronary artery. Finally, the last capital letter designates the relationship of the anomalous coronary arteries with the great vessel: whether they have a course anterior letter A, posterior letter P, between the great vessels letter B and combined letter C. The presented RIIA-type accounts for 12% of the isolated coronary arteries.7 Reports of acute myocardial infarctions related with a single coronary artery are very uncommon, and even more when the left main coronary artery originates from the right sinus of Valsalva.8

Thromboembolism is the most probable cause of a coronary occlusion when it is associated with chronic atrial fibrillation without anticoagulation and the coronary angiogram does not show signs of arteriosclerotic lesions in the coronary tree.9


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 Abstract
 Case report
 Discussion
 References
 

  1. Slater J., Brown R.J., Antonelli T.A., Menon V., Boland J., Col J., et al. Cardiogenic shock due to cardiac free-wall rupture or 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) 36:1117–1122.[Abstract/Free Full Text]
  2. Moreno R., Lopez-Sendon J., Garcia E., Perez de Isla L., Lopez de Sa E., Ortega A., et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction. J Am Coll Cardiol (2002) 39:598–603.[Abstract/Free Full Text]
  3. Lopez-Sendon J., Gonzalez A., Lopez de Sa E., Coma-Canella I., Roldan I., Dominguez F., et al. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol (1992) 19:1145–1153.[Abstract]
  4. Perdigao C., Andrade A., Ribeiro C. Cardiac rupture in acute myocardial infarction. Various clinico-anatomical types in 42 recent cases observed over a period of 30 months. Arch Mal Coeur Vaiss (1987) 80:336–344.[Web of Science][Medline]
  5. Lipton M.J., Barry W.H., Obrez I., Silverman J.F., Wexler L. Isolated single coronary artery: diagnosis, angiographic classification, and clinical significance. Radiology (1979) 130:39–47.[Abstract]
  6. Yamanaka O., Hobbs R.E. Coronary artery anomalies in 126,595 patients undergoing coronary arteriography. Catheter Cardiovasc Diagn (1990) 21:28–40.[Web of Science][Medline]
  7. Desmet W., Vanhaecke J., Vrolix M., Van de Werf F., Piessens J., Willems J., et al. Isolated single coronary artery: a review of 50,000 consecutive coronary angiographies. Eur Heart J (1992) 13:1637–1640.[Abstract/Free Full Text]
  8. Lanzieri M., Khabbaz K., Salomon R.N., Kimmelstiel C. Primary angioplasty of an anomalous left main coronary artery: diagnostic and technical considerations. Catheter Cardiovasc Interv (2003) 58:185–188.[CrossRef][Web of Science][Medline]
  9. Prizel K.R., Hutchins G.M., Bulkley B.H. Coronary artery embolism and myocardial infarction. Ann Intern Med (1978) 88:155–161.[Abstract/Free Full Text]

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