Case presentation

A 57-year-old woman, 7 years status post orthotopic heart transplantation for nonischemic cardiomyopathy, presents for her annual right and left heart catheterization, coronary angiogram, and endomyocardial biopsy. Her last routine coronary angiogram, performed 1 year earlier, demonstrated normal coronary arteries. She has been asymptomatic and feeling well.

Cardiac catheterization

The operator first measured right heart pressures; these were found to be normal with a right atrial pressure of 3 mmHg and preserved cardiac output. The right coronary artery was engaged with a right Judkins 4.0 catheter and appeared angiographically normal (Figure 32-1 and Video 32-1). Using a left Judkins 4.0 catheter, the operator engaged and imaged the left coronary artery; this also appeared angiographically normal (Figure 32-2). At this point, the patient remained symptom-free. Endomyocardial biopsy was performed from the right femoral vein using a 7 French, 98 cm, 40-degree curved sheath positioned into the right ventricle. Three samples were obtained, and while the operator was attempting a fourth sample, the patient developed hypotension and sinus bradycardia. Marked inferior ST-segment elevation appeared on the monitor screen.

FIGURE 32-1 This is the patient’s initial right coronary angiogram, revealing a normal artery 7 years after heart transplantation.

FIGURE 32-2 This is the patient’s left coronary angiogram, revealing a normal artery 7 years after heart transplantation.

The operator engaged a 6 French right Judkins 4.0 guide catheter into the right coronary artery. Angiography demonstrated occlusion of the right coronary artery in the midportion of the vessel (Figure 32-3 and Video 32-2). Another angiogram performed a few minutes later clearly showed air bubbles within the coronary (Figure 32-4 and Video 32-3). She was placed on nasal oxygen at 6 L/min, and heparin (70 U/kg) was administered by intravenous bolus. The operator placed a 0.014 inch floppy-tipped guidewire into the distal artery and aspirated the air bubbles using an aspiration catheter, with resolution of ST-segment elevation and restoration of TIMI-3 flow (Video 32-4). The left coronary was reimaged and showed no abnormalities; similarly, left ventriculography revealed normal ventricular function. The patient was transferred to the coronary care unit for further management.

FIGURE 32-3 The angiogram obtained after performance of the right ventricular biopsy, with occlusion of the vessel. There is a vague cutoff of the vessel noted (arrow).

FIGURE 32-4 Air bubbles are seen in the coronary artery, confirming the diagnosis of air embolism (arrow).

Postprocedural course

Upon arrival in the coronary care unit, she remained hemodynamically stable and without chest pain and her admission electrocardiogram showed no evidence of ST-segment elevation. She reported no other symptoms and her physical examination, including a neurologic exam, was normal. Peak troponin I at 8 hours after the event was 2.65 ng/mL. She was discharged the following morning and was well at follow-up 6 weeks later.

Discussion

Air embolism into the coronary artery is a rare, but potentially serious, iatrogenic complication of cardiac catheterization and coronary intervention. During coronary angiography, coronary air embolism is most commonly due to operator error from failure to aspirate air after connecting the catheter to the manifold. During coronary interventional procedures, this problem may arise from catheter exchanges when the balloon catheter is removed and the hemostatic valve is left open, causing air to enter the guide into the potential space left by the balloon catheter. If the operator fails to purge the air from the guide catheter, coronary air embolism may result during subsequent coronary injections.

In the case presented here, coronary angiography proceeded without complication and thus it is unlikely that coronary air embolism originated from the coronary catheters. The abrupt onset of bradycardia and ST-segment elevation began only after the fourth endomyocardial biopsy. It is likely that given the patient’s very low right atrial pressure, air was introduced into the venous sheath during removal of the bioptome. Since the biopsy sheath was in the right ventricle, it was postulated that the cause of air embolism in this case was due to a small perforation of the septum created by the bioptome, allowing the tip of the biopsy sheath to enter the left ventricle. Air present within the sheath entered the left ventricle and migrated to the aorta, thus causing coronary air embolism.

The diagnosis of coronary air embolism is usually made angiographically. As exemplified by this case, air embolism may occlude the coronary, but the occluded site often appears vaguely defined rather than as the discrete vessel cutoff typically seen when occlusion is caused by a thrombus. The diagnosis is easily made when discrete bubbles are seen in the coronary artery. Air embolism may also result in the angiographic appearance of “no-reflow” or “slow flow.”

Operators can prevent most cases by carefully aspirating catheters when performing exchanges and when connecting to the manifold. In the event that this complication occurs, several treatment options can be considered.¹ Small amounts of air may be tolerated without symptoms or adverse sequelae and usually dissipate spontaneously by dissolving into the blood, requiring no further therapy. Large amounts of air causing adverse clinical consequences require treatment. In addition to aspiration with a simple catheter, as performed in this case, the administration of high concentration oxygen helps dissipate the air bubbles.