Coronary and cerebral air embolisms are major complications during repair of ascending aortic dissection
; prophylaxis and treatment are well described in the literature (1) . 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. (1–3) Case Report
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
. The 12-lead electrocardiogram (ECG) was normal. The laboratory findings (including cardiac troponin-T/creatine phosphokinase-MB-isoenzyme levels) were unremarkable. (4)
DeBakey type I aortic dissection with aortic regurgitation (10–15 mL/beat, quantified by measuring the regurgitant jet/left ventricular outflow tract surface area)
was confirmed by magnetic resonance imaging angiography and transthoracic color Doppler echocardiography. Urgent surgery was planned; aortography and coronary angiography were not used (5) . Patient consent for transesophageal echocardiography was refused and epiaortic scanning was unavailable. (4)
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. (1)
On aortic cannulation, severe hemodynamic disturbances (
Table 1), and diffuse, 1-mm ST segment depression ensued. Hypothermic CPB (nonpulsatile perfusion: 2.0–2.4 L/min/m (6) 2, 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/ε-aminocaproic or tranexamic acid were not given because of the surgeon’s anticipation of “brief” CPB-duration (<90 min). (1) 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
, the aortic clamp was released. On patient rewarming (1,2) , the ECG displayed normal sinus rhythm. (1)
The first two CPB discontinuation attempts failed because of recurrent ventricular fibrillation that was preceded by ischemic ECG-changes
. Each time, CPB was resumed and sinus rhythm (with ST-T increase of >2 mm) restored by a 20-J internal defibrillation (6) . 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. (1)
Based on the improbability of air embolism because of the ineffectiveness of meticulous deairing
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) (1,2,7) 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). (8)
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) . After partial reversal of heparin (postprotamine kaolin activated clotting time 216 s) (9) , the chest wound was closed. (10)
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. Table 2:
Cumulative Postoperative Chest Tube Drainage (CTD), Blood Product Transfusion Urinary Output and Perioperative Laboratory Data Profile
A thrombus filled, proximal, blind, false lumen pocket is frequently encountered during proximal aortic dissection repair
. 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) . (11)
The rt-PA single bolus is comparable to the initial 15 mg bolus of a standard 100 mg IV thrombolytic regimen
. An augmented, initial, lytic effect was expected in the presence of heparin anticoagulation (12) and CPB-associated, intrinsic fibrinolytic system activation (13) . However, the risk of thrombolysis-induced, severe/fatal bleeding (14) was reduced by rt-PA’s short plasma half-life (approximately 1 min) (12) and probable binding to intracoronary fibrin (15) . 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. (16)
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
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. (17)
Previously published criteria and data
suggest that postoperative blood loss and transfusion requirements were moderately increased in the present case. Causative factors (18,19) could include CPB hemodilution, CPB surgical trauma related hemostatic activation, release of elastase from polymorphonuclear leukocytes, use of heparin anticoagulation (20,21) per se, and most importantly, partial post-CPB heparin reversal and excessive plasmin activity. However, the postoperative mild hypofibrinogenemia , and prothrombin times and d-dimer level fluctuations were not suggestive of moderate to severe systemic fibrinolysis (1) . Heparin- and/or plasmin-induced platelet dysfunction (18,22) seemed more likely. (20,21)
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
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 (23) . (24)
The postoperative ECGs, cardiac troponin-T levels
, 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. (25)
We wish to acknowledge the excellent performance of the perfusionist Mrs. M. Tzima in this emergency situation.
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