Abstract
A 52-year-old woman presented with malignant ventricular
arrthythmogenesis intraoperatively during kyphoplasty for an
osteoporotic fracture of a lumbar vertebra. No previous cardiovascular
condition was known. Causes of arrhythmogenesis associated with the
procedure were excluded. Due to her positive family history for dilated
cardiomyopathy, upcoming thoughts were made for unmasking a previous
asymptomatic cardiomyopathy. Nevertheless, an intracardiac cement
embolism was diagnosed and, finally, the patient underwent an open heart
surgery with successful removal of the cardiac cement while no new
arrhythmogenic episode was recorded during follow up.
Introduction:
Percutaneous balloon kyphoplasty (KP) is a minimally invasive technique
performed for painful osteoporotic or neoplastic vertebral compression
fractures refractory to maximum applied conservative
measures1. A frequently reported complication of KP
concerns cement leakage, which can occur locally in the intervertebral
disc space and into paravertebral soft tissues, but also at more distant
sites through the paravertebral veins (up to 24%). Once bone cement
inserts the veins, it migrates through the valveless venous plexus to
the azygos venous system, reaching the superior vena cava. The embolus
may further migrate into the right heart chambers and the pulmonary
arterial system ultimately causing cardiopulmonary embolism, also known
as cement embolism2.
Case Report
A cardiology consult was sought for a 52‐year‐old female from
Neurosurgery Department when recurrent episodes of polymorphic
non-sustained ventricular tachycardia (NSVT) were recorded
intraoperatively. The patient was referred for kyphoplasty (KP), due to
a recent fracture of an osteoporotic lumbar vertebra that was refractory
to conventional analgesics. Her preoperative examination was
unremarkable except for back sensitivity. The procedure was completed
uneventfully and the patient was transferred to the Cardiology
Department for further evaluation.
A transthoracic echocardiogram (TTE) performed at first evaluation
demonstrated a normal sized left ventricle (left ventricular
end-diastolic diameter, LVEDD=52mm) with a normal ejection fraction (EF)
of 55%.
A subsequent 24-hour ambulatory electrocardiogram (ECG) revealed
intermittent ventricular arrhythmogenesis (single premature ventricular
contractions 688/24h, nsVT, 22 episodes/24h). Common reversible causes
of arrhythmogenesis associated with the procedure were excluded (e.g.
intraoperative hypoxia, hypotension, or electrolyte imbalance). Other
causes of arrhythmogenesis, such as myocardial ischemia or inflammatory
processes, inherited or acquired cardiac channel dysfunctions were of
low suspicion given the normal serial 12-lead ECG and blood test
findings.
The patient was free of cardiovascular disease and denied any episodes
of chest pain, dizziness, palpitations or syncope in the past. She
smoked tobacco, but she did not drink alcohol, or use illicit drugs. Her
brother had received a cardioverter-defibrillator after being diagnosed
with dilated cardiomyopathy (DCM) and had subsequently died at the age
of 60. Her father had died suddenly at the age of 62.
The patient’s clinical presentation raised suspicion of an inherited
cardiomyopathy due to her family history of DCM and the documented VTs.
In some cases, a preclinical phase without cardiac expression
subsequently progresses towards mild cardiac abnormalities, such as
isolated LV dilatation, or arrhythmogenic features with life-threatening
ventricular arrhythmias (2%) or with frequent ventricular arrhythmias
(30%), which are unrelated to the severity of LV dysfunction. These
clinical manifestations are described otherwise as arrhythmogenic
DCM.3
The next diagnostic step included a scheduled coronary angiography in
order to exclude coronary artery disease. Of surprise, fluoroscopy
imaging depicted a mobile radiopaque material projected right upon the
cardiac silhouette, moving simultaneously with the cardiac contractions,
postulating an intracardiac position (Video). The catheterization was
interrupted until further evaluation.
The Neurosurgery Department was contacted and after reviewing the
procedural protocol, the case of an inserted and abandoned guidewire,
needle or suture was rejected. However, as cement material had been
injected into the vertebra intraprocedurally to stabilize the fracture,
an intravenous cement leak could have occurred that had been entrapped
and solidified inside the cardiac cavities.
The patient underwent a dedicated TTE focusing on the right ventricle
(RV) demonstrating a linear structure constituting of two parts, that
were parallel to the elongated axis of the RV and rebounded at the
inferior basal segment of the latter; the free ends were directing
towards the RV free wall (Figure 1). A chest computed tomography (CT)
was also performed that confirmed the above findings and also excluded
coronary heart disease (Figure 2).
Anticoagulation was initiated and the patient was transferred to the
Cardiac Surgery Unit. The patient underwent an open heart surgery with
successful removal of the foreign body (Figure 3), confirming that the
material was composed of cement related to her recent spinal procedure.
The successful surgical removal of the cement material led to the cease
of the patient’s arrhythmogenesis.
The patient recovered from the spinal cord procedure uneventfully and
regained full mobility. Serial TTEs and ambulatory ECGs reported normal
finding during follow-up.
Discussion
Most cases of cement embolism are asymptomatic, with only 1% presenting
with dyspnea, which usually resolves with conservative management (i.e.,
oxygen therapy, anticoagulants), so the incidental finding of cement
emboli in an asymptomatic patient does not definitely necessitate
medical treatment or removal.4 This is because the
cement emboli are generally small and scatter in the peripheral areas of
the lung arteries.
However, in patients with central emboli (cardiac chambers, main
pulmonary artery branches), the anticoagulants cannot dissolve the
cement or relieve the right ventricular overload; furthermore, when the
cement is localized into the heart, it can cause cardiac rupture and/or
cardiac tamponade, thus surgical extraction might be
warranted.5 Symptomatic patients with cement material
into the right atrium are usually managed via percutaneous retrieval,
whilst those with RV involvement or perforation are managed
surgically.6
High level of suspicion is required when in patient’s history is
referred that material such as cement has been injected during a KP
procedure. To the best of our knowledge this is the first reported case
of ventricular arrhythmogenic presentation of a cardiac cement embolus
after a KP procedure.