JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Karamichali, E. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Karamichali, E. A.
Related Collections
Right arrow Cardiovascular
Right arrow Heart
Right arrow Monitoring (Cardiac)
Anesth Analg 2001;93:56-59
© 2001 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Intracoronary Thrombolysis and Intraaortic Balloon Counterpulsation for the Emergency Treatment of Probable Coronary Embolism After Repair of an Acute Ascending Aortic Dissection

Spyros D. Mentzelopoulos, MD, John N. Kokotsakis, MD*, Constantina N. Romana, MD, and Evangelia A. Karamichali, MD, PHD

Departments of Anesthesiology and *Second Division of Cardiac Surgery, Evangelismos General Hospital, Athens, Greece

Address correspondence and reprint requests to Spyros D. Mentzelopoulos MD, 2A Kypseli Street, GR-11362, Athens, Greece. Address e-mail to sdm{at}hol.gr


   Abstract
Top
 Abstract
Introduction
 Case Report
 Discussion
 References
 

Implications: This report shows that if diffuse coronary thromboembolism is encounteredduring ascending aortic dissection-repair, the option of combiningsingle-bolus, intracoronary thrombolysis with intraaortic ballooncounterpulsation should beconsidered.


   Introduction
Top
 Abstract
 Introduction
Case Report
 Discussion
 References
 
Coronary and cerebral air embolisms are major complications during repair of ascending aortic dissection (1); prophylaxis and treatment are well described in the literature (1–3). We present a case of obstruction of the coronary circulation by clots originating from a dissected aortic root that was successfully treated with selective thrombolysis and intraaortic balloon pump (IABP) counterpulsation.


   Case Report
Top
 Abstract
 Introduction
 Case Report
Discussion
 References
 
A 54-yr-old, 68-Kg, hypertensive woman with no prior coronary artery disease history presented with sudden onset of excruciating chest pain. Arterial blood pressure and heart rate were 190/80 mm Hg and 96 bpm, respectively. On clinical examination, an aortic regurgitation murmur was present and major, peripheral vessel pulses were symmetrically detectable (4). The 12-lead electrocardiogram (ECG) was normal. The laboratory findings (including cardiac troponin-T/creatine phosphokinase-MB-isoenzyme levels) were unremarkable.

DeBakey type I aortic dissection with aortic regurgitation (10–15 mL/beat, quantified by measuring the regurgitant jet/left ventricular outflow tract surface area) (5) was confirmed by magnetic resonance imaging angiography and transthoracic color Doppler echocardiography. Urgent surgery was planned; aortography and coronary angiography were not used (4). Patient consent for transesophageal echocardiography was refused and epiaortic scanning was unavailable.

Intraoperative monitoring (1) included 5-lead ECG, left radial artery pressure, continuous cardiac index display, and mixed venous oxygen saturation. After anesthesia induction, median sternotomy, and heparinization, right atrial and aortic arch cannulation was done. The use of femorofemoral cardiopulmonary bypass (CPB) was precluded by bilateral atherosclerotic femoral artery stenoses.

On aortic cannulation, severe hemodynamic disturbances (Table 1), and diffuse, 1-mm ST segment depression (6) ensued. Hypothermic CPB (nonpulsatile perfusion: 2.0–2.4 L/min/m2, core temperature: 28–30°C, target mean left radial artery pressure: 70–80 mm Hg) was initiated within 3–4 min after cannulation. Deep hypothermic circulatory arrest was not used, because according to the magnetic resonance imaging findings and surgeon’s judgment, involvement of major neck vessels in the dissection process was unlikely. Aprotinin/{varepsilon}-aminocaproic or tranexamic acid (1) were not given because of the surgeon’s anticipation of "brief" CPB-duration (<90 min).


View this table:
[in this window]
[in a new window]
  		Table 1. Values of Monitored Hemodynamic Variables 1 min Before/3 min After the Aortic Arch Cannulation (AAC), and on Discontinuation of Intraaortic Balloon Pump (IABP) Counterpulsation
 
The distal ascending aorta was cross-clamped and retro/antegrade cold blood cardioplegia administered. Several aortic root clots were removed; the coronary ostia were anatomically intact and patent. The aortic valve was resuspended and the ascending aorta replaced by a Dacron tube-graft. Cross-clamp duration was 74 min. After retrograde, warm blood (37°C) coronary perfusion (at 50 mm Hg), and conventional deairing (1,2), the aortic clamp was released. On patient rewarming (1), the ECG displayed normal sinus rhythm.

The first two CPB discontinuation attempts failed because of recurrent ventricular fibrillation that was preceded by ischemic ECG-changes (6). Each time, CPB was resumed and sinus rhythm (with ST-T increase of >2 mm) restored by a 20-J internal defibrillation (1). Before the second weaning attempt, coronary air embolism was suspected; the retrograde perfusion/conventional deairing maneuvers were repeated (during a 3-min graft cross-clamp) and nitroglycerine/dobutamine/aminodarone infusions started, resulting in ST-T segment deviation <2 mm.

Based on the improbability of air embolism because of the ineffectiveness of meticulous deairing (1,2,7) in preventing the ischemic ventricular fibrillations, the pre-CPB hemodynamic lability/ECG ischemia, and the intraoperative findings, we deduced that aortic root emboli had dispersed into the coronary circulation. Acute myocardial "ischemia time" had already exceeded 14 min, so an IABP was introduced through the graft. Furthermore, 300 mL saline containing 20 mg of reverse tissue-type plasminogen activator (rt-PA) (8) were flushed (at 250–300 mm Hg) into the aortic root within a 1-min graft cross-clamp, resulting in resolution of ST-T increase (to <2 mm) and 3–5/min-ventricular premature beats. The subsequent, IABP-assisted (balloon inflation volume 32 mL) attempt at separation from CPB was successful; prethrombolysis right atrial/coronary sinus D-dimer values were 1.3/0.8 µg/mL (respectively).

ECG-normalization occurred within 30 min after CPB; arterial and right atrium D-dimer levels were similar: 2.7–2.8 µg/mL; however, the coronary sinus blood D-dimer concentration exceeded 20 µg/mL. IABP counterpulsation was uneventfully discontinued after another 30 min (Table 1). Intraoperatively, three units of packed red blood cells were transfused (post-CPB "hemoglobin trigger" set at <=8.5 g/dL) (9). After partial reversal of heparin (postprotamine kaolin activated clotting time 216 s) (10), the chest wound was closed.

Significant segmental coronary stenoses (> 25%) and major intracranial bleeding were excluded by urgent postoperative coronary angiography and brain computed tomography, respectively. The postoperative chest tube drainage, transfusion requirements, urine output, hemostasis study results, and cardiac troponin-T values are presented in Table 2. Tracheal extubation occurred 18 h after intensive care unit admission; mental status/neurological examination was unremarkable. The postoperative 12 lead ECGs, seventy-two hour follow-up brain computed tomographic scan, and myocardial 99m Tc-sestamibi single photon emission tomography were normal. Hospital discharge occurred 9 days after admission. Four weeks later magnetic resonance imaging demonstrated clotting of the aortic false lumen without any IABP counterpulsation-related, residual, aneurysmal dilation of the descending thoracic aorta.


View this table:
[in this window]
[in a new window]
  		Table 2. Cumulative Postoperative Chest Tube Drainage (CTD), Blood Product Transfusion Urinary Output and Perioperative Laboratory Data Profile
 

   Discussion
Top
 Abstract
 Introduction
 Case Report
 Discussion
References
 
A thrombus filled, proximal, blind, false lumen pocket is frequently encountered during proximal aortic dissection repair (11). However, the potential for intracoronary migration, fragmentation, and dispersal of thrombus, has not been described. In the present case, the aortic cannulation and cross-clamp are the major likely mechanical causes of retrograde false lumen clot dislodgment and initial intracoronary dispersal; the subsequent antegrade cardioplegia administration should have induced further distal and diffuse clot embolization and coronary branch obstruction. However, on exposure, the coronary ostia seemed patent and intact, and thus, a post-CPB myocardial malperfusion was considered unlikely (11).

The rt-PA single bolus is comparable to the initial 15 mg bolus of a standard 100 mg IV thrombolytic regimen (12). An augmented, initial, lytic effect was expected in the presence of heparin anticoagulation (13) and CPB-associated, intrinsic fibrinolytic system activation (14). However, the risk of thrombolysis-induced, severe/fatal bleeding (12) was reduced by rt-PA’s short plasma half-life (approximately 1 min) (15) and probable binding to intracoronary fibrin (16). Despite the lack of relevant data, we believe that the severe bleeding risk would have been increased if there were no intracoronary clots to induce a "first-pass" rt-PA-capture; in such a case, the arterial blood D-dimer levels might well exceed the values present in our case.

The patient’s gradual, favorable response and coronary D-dimer level changes showed that our combined, ultimate interventions were effective and complementary to each other. In our opinion, the high pressure intracoronary flushing of the rt-PA containing solution facilitated rt-PA penetration of obstructing-clot, and resulted in the initiation of both mechanical and enzymatic clot lysis. The subsequent augmentation of diastolic perfusion by IABP counterpulsation (17) should have effectively maintained the mechanical fragmentation of the partially digested clots. In contrast, the preceding retrograde perfusion proved ineffective, probably because of its low pressure (as opposed to flushing of the antegrade thrombolytic solution) and short duration, and the concomitant absence of rapid, plasmin mediated clot lysis.

Previously published criteria and data (18,19) suggest that postoperative blood loss and transfusion requirements were moderately increased in the present case. Causative factors (20,21) could include CPB hemodilution, CPB surgical trauma related hemostatic activation, release of elastase from polymorphonuclear leukocytes, use of heparin anticoagulation per se, and most importantly, partial post-CPB heparin reversal and excessive plasmin activity. However, the postoperative mild hypofibrinogenemia (1), and prothrombin times and D-dimer level fluctuations were not suggestive of moderate to severe systemic fibrinolysis (18,22). Heparin- and/or plasmin-induced platelet dysfunction (20,21) seemed more likely.

The post-CPB administration of antifibrinolytic drugs was not considered, because antagonism of the intracoronary plasmin activity in the potential presence of embolism reperfusion-induced endothelial trauma (23) might increase the risk of thrombus formation. Furthermore, heparin was only partially reversed, mainly to reduce the risk of acute, post-rt-PA coronary reocclusion (24).

The postoperative ECGs, cardiac troponin-T levels (25), follow-up imaging, and patient mental/neurological status were confirmative of timely/global myocardial salvage without any concomitant irreversible complications. Thus, in this particular patient, the risk-to-benefit analysis of our acute, pharmacomechanical intervention leaned markedly toward the effective prevention of cardiac death and/or sustained myocardial infarction.


   Acknowledgments
 
We wish to acknowledge the excellent performance of the perfusionist Mrs. M. Tzima in this emergency situation.


   References
Top
 Abstract
 Introduction
 Case Report
 Discussion
 References
 

  1. Shanewise JS, Hug CC Jr. Anesthesia for adult cardiac surgery. In: Miller RD, ed. Anesthesia. 5th ed. New York: Churchill Livingstone, 2000: 1753–805.
  2. Gundry SR. Facile left ventricular deairing by administration of cardioplegia into the left ventricular vent. Ann Thorac Surg 1998; 66: 2117–8.[Abstract/Free Full Text]
  3. Chaudburi N, Hickey MSTJ. A simple method of treating coronary air embolism after cardiopulmonary bypass. Ann Thorac Surg 1999; 68: 1867–8.[Abstract/Free Full Text]
  4. Borst HG, Heinemann MK, Stone CD. Clinical presentation, diagnosis, indications. In: Borst HG, Heinemann MK, Stone CD, eds. Surgical treatment of aortic dissection. 1st ed. New York: Churchill Livingstone, 1996: 55–109.
  5. Ekery DL, Davidoff R. Aortic regurgitation: quantitative methods by echocardiography. Echocardiography 2000; 17: 293–302.[Web of Science][Medline]
  6. Hillel Z, Thys DM. Electrocardiography. In: Miller RD, ed. Anesthesia. 5th ed. New York: Churchill Livingstone, 2000: 1231–55.
  7. Sandthu AA, Spotnitz HM, Dickstein ML, et al. Retrograde cardioplegia preserves myocardial function after induced coronary air embolism. J Thorac Cardiovasc Surg 1997; 113: 917–22.[Abstract/Free Full Text]
  8. Intracoronary t-PA Registry Investigators. Clinical experience with intracoronary tissue plasminogen activator: results of a multicenter registry. Cathet Cardiovasc Diagn 1995; 34: 196–201.[Web of Science][Medline]
  9. Practice guidelines for blood component therapy: a report by the American Society of Anesthesiologists Task Force on blood component therapy. Anesthesiology 1996; 84: 732–47.[Web of Science][Medline]
  10. Dougherty KG, Gaos CM, Bush HS, et al. Activated clotting times and activated partial thromboplastin times in patients undergoing coronary angioplasty who receive bolus doses of heparin. Cathet Cardiovasc Diagn 1992; 26: 260–3.[Web of Science][Medline]
  11. Borst HG, Heinemann MK, Stone CD. Surgical tactics and techniques. In: Borst HG, Heinemann MK, Stone CD, eds. Surgical treatment of aortic dissection. 1st ed. New York: Churchill Livingstone, 1996: 109–297.
  12. Hockins BEF, Donovan KD. Acute myocardial infarction. In: Oh TE, ed. Intensive care manual. 4th ed. Oxford: Butterworth-Heinemann, 1997: 43–59.
  13. Liang JF, Li Y, Yang VC. The potential mechanism for the effect of heparin on tissue plasminogen activator-mediated plasminogen activation. Thromb Res 2000; 97: 349–58.[Web of Science][Medline]
  14. Despotis GJ, Gravlee G, Filos K, Levy J. Anticoagulation monitoring during cardiac surgery: a review of current and emerging techniques. Anesthesiology 1999; 91: 1122–51.[Web of Science][Medline]
  15. Narita M, Bu G, Herz J, Schwartz AL. Two receptor systems are involved in the plasma clearance of tissue-type plasminogen activator (t-PA) in vivo. J Clin Invest 1995; 96: 1164–8.
  16. Lazos SA, Wong SS. Mechanism of potentiation of tissue-type plasminogen activator. Biochem Mol Int 1995; 37: 1071–7.
  17. Gurbel PA, Anderson D, MacCord CS, et al. Arterial diastolic pressure augmentation by intra-aortic balloon counterpulsation enhances the onset of coronary artery reperfusion by thrombolytic therapy. Circulation 1994; 89: 361–5.[Abstract/Free Full Text]
  18. Despotis GJ, Filos KS, Zoys TN, et al. Factors associated with excessive postoperative blood loss and hemostatic transfusion requirements: a multivariate analysis in cardiac surgical patients. Anesth Analg 1996; 82: 13–21.[Abstract]
  19. Despotis GJ, Vladimir L, Filos KS, et al. Evaluation of a new point-of-care test that measures PAF-mediated acceleration of coagulation in cardiac surgical patients. Anesthesiology 1996; 85: 1311–23.[Web of Science][Medline]
  20. Despotis GJ, Joist H, Goodnough LT. Monitoring of hemostasis in cardiac surgical patients: impact of point-of-care testing on blood loss and transfusion outcomes. Clin Chem 1997; 43: 1684–96.[Abstract/Free Full Text]
  21. Muriithi EW, Belcher PR, Day PS, et al. Heparin-induced platelet dysfunction and cardiopulmonary bypass. Ann Thorac Surg 2000; 69: 1827–32.[Abstract/Free Full Text]
  22. Whitten CW, Greilich PE, Ivy R, et al. D-dimer formation during cardiac and noncardiac thoracic surgery. Anesth Analg 1999; 88: 1226–31.[Abstract/Free Full Text]
  23. Becker RC. Seminars in thrombosis, thrombolysis and vascular biology. 1. The vascular endothelium. Cardiology 1991; 78: 13–22.[Web of Science][Medline]
  24. Golino P, Ashton JH, Glas-Greenwalt P, et al. Mediation of reocclusion by thromboxane A2 and serotonin after thrombolysis with tissue-type plasminogen activator in a canine preparation of coronary thrombosis. Circulation 1988; 77: 678–84.[Abstract/Free Full Text]
  25. Carrier M, Pellerin P, Perrault LP, et al. Troponin levels in patients with myocardial infarction after coronary artery bypass grafting. Ann Thorac Surg 2000; 69: 435–40.[Abstract/Free Full Text]
Accepted for publication February 28, 2001.





This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Karamichali, E. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mentzelopoulos, S. D.
Right arrow Articles by Karamichali, E. A.
Related Collections
Right arrow Cardiovascular
Right arrow Heart
Right arrow Monitoring (Cardiac)

Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2001 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press