Case Presentation:
We present a 76-year-old male (1,78 m, 72,5 kg, BSA 1,89
m2, BMI 22,8) stage D congestive heart failure status
and HeartWare HVAD (Medtronic Heart-Ware International, Framingham, MA)
ventricular assist device implantation as destination therapy three
years prior. The patient had a cardioverter-defibrillator device (ICD)
implantation five years earlier. His medical history was pertinent for
type II heparin-induced thrombocytopenia, forefoot amputation secondary
to chronic peripheral artery disease, and chronic kidney disease.
The patient experienced inappropriate shocks from his ICD. Consequently,
he presented to our institution. The ECG in the emergency department
showed sinus tachycardia. ICD Interrogation revealed evidence of a lead
fracture. Admission to the hospital was recommended for definitive
correction of his problem. Under local anesthetic, he was posted for ICD
lead replacement. During the procedure, the patient constantly developed
LVAD low flow alarm. Instantly echocardiography was performed, which
showed insufficient unloading of the left ventricle. After successful
implantation of a new right ventricle lead and closing of the wound, a
prompt computed tomography angiography was undertaken, which was
negative for pulmonary embolism and showed LV dilatation with no
definitive outflow cannula thrombosis or significant stenosis.
HVAD interrogation showed a reduced average flow of 1,98 L/min and power
of 3,1Watts at the speed of 2700 Rpm.
The diagnosis of an occlusive thrombus of the inflow cannula was made
based on an acute decrease in power consumption and the calculated blood
flow without changes in the acoustic signal, and there was no evidence
of hemolysis.
The bedside transthoracic echocardiography showed the LV to be enlarged
and ejecting. Thrombolysis therapy in our patient carried a very high
risk because of the fresh wound and the possibility of developing a
massive pectoral subcutaneous hematoma. The decision was made to perform
a retrograde thrombus washout maneuver with the patient awake and
spontaneously breathing. A neuroprotective device was omitted due to the
emergency situation with low cardiac output syndrome and raised serum
lactate levels. The mean blood pressure was increased to 100 mmHg with
vasopressors, and with the intravenous administrated adrenaline, the
ventricle contractility was enhanced. After manually compressing both
carotid arteries in Trendelenburg’s position to avoid thromboembolism to
the brain, the pump was stopped for ten seconds. After restarting the
pump, the parameters returned to normal values with a flow of 4,2 L/min
and power of 4,1 Watts at the speed of 2700 Rpm.
LV becomes unloaded again in the bedside transthoracic echocardiogram.
The patient showed no perfusion or neurological deficits after the
procedure, and he was then transferred to the normal ward after
withdrawal of the catecholamine.
LVAD pump exchange was deferred because of the multiple co-morbidities
of the patient (e.g., peripheral vascular disease and prior sternotomy)
as well as the abolition of the HeartWare pump from the market, which
increased the burden of that procedure. The patient was then discharged
home with normal HVAD parameters.