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An Unusual Complication After Coronary Catheterization

Dominique Grisoli, MD1, Vlad Gariboldi, MD1, Jacques Quilici, MD2

Dominique Grisoli, MD1, Vlad Gariboldi, MD1, Jacques Quilici, MD2

ABSTRACT: Valvular complications after coronary catheterization are extremely rare and are seldom reported in the literature. We report a patient who experienced acute traumatic aortic regurgitation after repeated coronary transcatheter procedures. Despite clinical stabilization under medical treatment, his clinical course led to an aortic-valve replacement.

J INVASIVE CARDIOL 2012;24(2):E22-E23

Key words: percutaneous coronary intervention, aortic valve, replacement, echocardiography

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Case Report

A 69-year-old man with a smoking history, hypertension, and peripheral arterial disease was admitted as an emergency to a community hospital for inferior acute myocardial infarction (MI). Upon admission, a transthoracic echocardiography was performed bedside to evaluate left-ventricle (LV) function and to rule out any associated valvular disease. LV and valve functions were found to be normal. The patient underwent emergent percutaneous transluminal coronary angioplasty (PTCA) and drug-eluting stents (DES) were implanted for the culprit lesion in the right coronary artery (RCA). After recovering for 4 days, he underwent PTCA and DES implantations in the left anterior descending (LAD) and circumflex coronary arteries.

During recovery, he rapidly developed a new onset of shortness of breath during exertion. His physician noticed increased differential arterial blood pressure and ordered a transthoracic echocardiography, which showed a severe aortic regurgitation. The patient was then sent to our university hospital for further evaluation.

Upon admission, the patient presented with NYHA 2 shortness of breath, but with no physical signs of heart failure. Transthoracic and transesophageal echocardiography confirmed severe high-velocity aortic insufficiency (PISA: 10 mm), which developed towards the anterior mitral valve. It also found a dilated left ventricle (LVEDD: 62 mm), a normal LV ejection fraction, and some destruction of the non-coronary cusp free edge (Figure 1).

Despite the absence of fever and blood test having normal inflammatory biological indicators, we made 2 hypotheses concerning the etiology of this aortic insufficiency:

  1. An aortic endocarditis
  2. A mechanical coronary catheterization complication.

All the endocarditis check-ups remained negative.

Symptoms were well controlled with low-dose diuretics, and the patient could return home to await surgery. He was readmitted 3 months after the initial STEMI for aortic valve replacement.

Intraoperative findings confirmed mechanical deterioration of the non-coronary cusp’s free edge, near the commissure between the non-coronary and left-coronary cusp, with no evidence of infection (Figure 2). We performed a standard aortic valve replacement with a size 27 bioprosthesis, and the patient underwent an uneventful postoperative course.

All explorations performed on the resected native aortic valve were found to be negative; therefore, we attributed the acute aortic regurgitation and leaflet injury to the repeated transluminal coronary catheterization.

Discussion

PTCA changed the immediate prognosis of acute MI with success rates reaching 97% in experienced centers, and this process has demonstrated superiority over fibrinolysis  in terms of reinfarction, intracranial hemorrhage, and mortality.1 Furthermore, primary PCI demonstrated its superiority over fibrinolysis in the long-term with maintained benefit in terms of reinfarction and mortality at 8 years.2,3

Despite this high success rate, unfavorable events can occur in the catheterization laboratory. Minor events are common but life-threatening complications such as acute vessel closure, cardiogenic shock, or death, are infrequent (ie <10%).4

Temporary acute aortic regurgitation in relation to stiff catheters, brought too low in the aortic root, is quite common and can result in a sudden cardiogenic shock. Removing catheters from the aortic valve leaflets can easily restore hemodynamic conditions.5

However, irreversible aortic valve deterioration in relation to coronary catheterization is seldom reported in the literature. In most reports, aortic valve lesions are caused by a right coronary stent inappropriately protruding into the aortic lumen.6,7 A case of torn old aortic bioprosthesis that caused acute aortic regurgitation was recently reported.8

Conclusion

In this case, severe aortic insufficiency developed immediately after repeated coronary catheterization in a patient with a normal preoperative native aortic valve. Although stents were implanted into the 3 main coronary vessels, none of these were implanted close to the coronary ostia. Within 1 week after PTCA, the patient developed signs of heart failure. After diagnosis of aortic insufficiency, transesophageal echocardiography provided an accurate identification of the aortic regurgitation mechanism, which correlated perfectly with the intraoperative findings.

References

  1. Grines CL, Browne KF, Marco J, et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group. N Engl J Med. 1993 Mar;328(10):673-679.
  2. Nielsen PH, Maeng M, Busk M, et al; for the DANAMI-2 Investigators. Primary angioplasty versus fibrinolysis in acute myocardial infarction: long-term follow-up in the Danish acute myocardial infarction 2 trial. Circulation. 2010 Apr;121(13):1484-1491. 
  3. Andersen HR, Nielsen TT, Rasmussen K, et al; for the DANAMI-2 Investigators. A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med. 2003 Aug;349(8):733-742.
  4. Kahn JK, Rutherford BD, McConahay DR, et al. Catheterization laboratory events and hospital outcome with direct angioplasty for acute myocardial infarction. Circulation. 1990 Dec;82(6):1910-1915.
  5. Javeed N, Shaikh J, Patel M, Rezai F, Wong P. Catheter-induced acute aortic insufficiency with hemodynamic collapse during PTCA: an unreported complication. Cathet Cardiovasc Diagn. 1997 Nov;42(3):305-307.
  6. Kotoulas C, Bigeon JY, Patris K, Hasan R. Aortic valve as a victim of percutaneous coronary angioplasty and stenting. Ann Thorac Surg. 2007 Nov;84(5):1765.
  7. Quintana E, Mestres CA, Congiu S, Josa M, Cartañá R. Delayed aortic regurgitation caused by a right coronary stent protruding into the aorta. J Heart Valve Dis. 2009 Nov;18(6):717-719.
  8. Michelena HI, Enriquez-Sarano M, Sundt TM 3rd. A torn 15-year-old aortic bioprosthesis in the setting of percutaneous coronary intervention: echocardiographic diagnosis and pathologic correlation. A case report. J Heart Valve Dis. 2009 Mar;18(2):228-231.

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From the 1Department of Cardiac Surgery and 2Department of Cardiology, Hôpital de la Timone, Université de la Méditerranée, Marseilles, France.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted April 29, 2011, provisional acceptance given June 3, 2011, final version accepted June 27, 2011.
Address for correspondence: Dr. Dominique Grisoli, Service de Chirurgie Cardiaque Adulte, Hôpital de la Timone Adulte, 264 rue Saint Pierre, 13005 Marseille, France. E-mail: dominique.grisoli@ap-hm.fr