HeartWare HVAD: Postoperative issues in our first patient
Sarvesh Pal Singh1, Sandeep Seth2, Manoj Kumar Sahu1, Balram Airan1 1 Department of Cardiothoracic and Vascular Surgery, Cardio-Thoracic Sciences Center, All India Institute of Medical Sciences, New Delhi, India 2 Department of Cardiology, Cardio-Thoracic Sciences Center, All India Institute of Medical Sciences, New Delhi, India
Date of Web Publication
Correspondence Address: Sarvesh Pal Singh Department of Cardiothoracic and Vascular Surgery, C N Center, All India Institute of Medical Sciences, New Delhi - 110 029 India
Source of Support: None, Conflict of Interest: None
Ventricular assist devices (VADs) serve as a bridge to heart transplant or destination therapy in end stage heart failure. HeartWare HVAD is a second generation, non pulsatile, magnetically levitated centrifugal pump, which is preload dependent and afterload sensitive. It has an inlet that is cored into the left ventricular wall and an outflow that is attached to a graft which is sutured into the ascending aorta. The Registry to Evaluate the HeartWare Left Ventricular Assist System (ReVOLVE) registry has reported a 2 year survival of 76% and 5 year survival of 59%. We present our experience of the first HeartWare 2 HVAD implanted at our institute.
Keywords: HeartWare HVAD, issues, postoperative
How to cite this article: Singh SP, Seth S, Sahu MK, Airan B. HeartWare HVAD: Postoperative issues in our first patient. J Pract Cardiovasc Sci 2017;3:63-6
How to cite this URL: Singh SP, Seth S, Sahu MK, Airan B. HeartWare HVAD: Postoperative issues in our first patient. J Pract Cardiovasc Sci [serial online] 2017 [cited 2022 Jan 19];3:63-6. Available from: https://www.j-pcs.org/text.asp?2017/3/1/63/210867
Cardiovascular diseases are the most common cause of death worldwide. Heart transplant is the only definitive treatment for patients with end-stage heart failure. However, due to shortage of donor hearts, the patients are on waiting list for a long time. Ventricular assist devices (VADs) serve as a bridge to heart transplant in these patients. HeartWare HVAD is a second-generation, nonpulsatile, magnetically levitated centrifugal pump, which is preload dependent and afterload sensitive. It has an inlet that is cored into the left ventricular wall and an outflow that is attached to a graft which is sutured into the ascending aorta. The Registry to Evaluate the HeartWare Left Ventricular Assist System Registry has reported a 2-year survival of 76% and 5-year survival of 59%. Here, we discuss our experience of the first HeartWare 2 HVAD implanted at our institute.
A 35-year-old male (body surface area 1.65 m2) suffering from dilated cardiomyopathy, New York Heart Association (NYHA) IV, underwent left ventricular assist device (LVAD) implantation at our institute. After implantation, the patient was weaned off cardiopulmonary bypass (CPB) slowly and the LVAD flows were increased slowly by increasing rotations per minute (rpm) from 1800 to 2400. The patient was maintained on 20 ppm nitric oxide (NO) as a prophylaxis against right ventricular (RV) dysfunction. The patient was shifted to Intensive Care Unit (ICU) on intravenous infusions of dobutamine and nitroglycerine and inhalational NO at 20 ppm. Being a centrifugal pump, the HVAD pump is preload dependent and afterload sensitive. Therefore, the right atrial pressure was maintained between 10 and 12 mmHg, and the mean arterial pressure (MAP) was maintained between 75 and 90 mmHg. The adequacy of flows was judged on the basis of urine output, temperature change, lactate levels, oxygen extraction ratio, Doppler assessment of peripheral pulses, and visualization of aortic valve opening on transthoracic echocardiography. The patient was successfully extubated after 20 h of mechanical ventilation. Since both the pleura were intact during surgery, no intercostal chest tubes were in place. On the 2nd postoperative day, the patient developed hematuria along with high lactate dehydrogenase (LDH) and free plasma hemoglobin levels, indicating a device-induced intravascular hemolysis. During the 1st postoperative week, he had features of acute kidney injury (AKI) which improved with conservative management. The patient developed bilateral pleural effusion repeatedly in the first 2–10 days, for which repeated pleural taps were done. Later, he underwent mediastinal exploration on day 11 and intercostals chest tube drains were put in both the pleurae. Because of repeated inflammation (due to pleural effusion), the compliance of both lungs decreased significantly leading to a restrictive lung disease pattern on pulmonary function testing. Antibiotics were continued for a month to prevent any infection. After 1st month of surgery, the patients' international normalized ratio (INR) values decreased in spite of increasing the warfarin dose. This was attributed to interaction of warfarin and macrolides and the high warfarin doses were given for 3 days, after which the INR increased to more than 2.0. Due to the prolonged stay in the cardiac surgical ICU and attachment of a machine to the body continuously, the patient developed depression. He underwent counseling and meditation, following which he became normal. He was discharged after a hospital stay of 45 days.
During the 1st year, postdischarge, the patient was followed up every month. On every visit, the patient had a detailed clinical examination and assessment of electrocardiogram. The arterial blood pressure was measured using a Doppler and invasive arterial line. A detailed echocardiographic examination was done to evaluate for adequate decompression of the left ventricle, biventricular function, aortic valve opening, inflow cannula flow, outflow cannula flow, and inferior vena cava diameter. Oral losartan was titrated to maintain a MAP <85 mmHg.
In first 3 months, postdischarge, there were repeated episodes of superficial infection at driveline site. These episodes were treated with oral amoxicillin + clavulanic acid 625 mg three times a day. Then, the cleaning of driveline was switched over to chlorhexidine-based disinfectant [Figure 1]. Six months after implantation, he developed hepatomegaly with worsening RV dysfunction (deterioration on function from mild to severe) [Video 1]. Oral sildenafil 100 mg/day in two divided doses was added to his treatment. Eight months after surgery, he complained of exercise intolerance and breathlessness. An echocardiography revealed increase in left ventricular dimension; therefore, the rpm were increased gradually from 2400 to 2440. He reported symptomatic relief following increase in rpm. One month later, he complained of low flow alarms consecutively for 3 days in the early morning around 3–4 am. Holter monitoring was done for 24 h which showed nonsustained ventricular tachycardia (NSVT) runs in the morning [Figure 2]. The rpm were further increased to 2500 to decompress the left ventricle and the arrhythmias subsided. One year postimplantation, he is in NYHA Class I, pulmonary artery systolic pressure of 26 mmHg, left ventricular ejection fraction 10%, severe RV dysfunction, mild aortic regurgitation, ventricular assist device (VAD) flows of 3.0–5.0 L/min, power 2.8–3.5 watts, and rpm 2500 [Figure 3].
Figure 1: Driveline site of the patient, repeated infections has led to formation of granulation tissue.
In end-stage heart failure patients, the physiology of body adapts itself to a persistent low cardiac output. An LVAD implantation alters this homeostasis and new physiological perturbations begin to occur. As soon as the pump is initiated, the normal pulsatile blood flow becomes minimally pulsatile. With the increase in flows to achieve cardiac output in normal range, the RV which is acclimatized to low preload is now suddenly exposed to higher venous return and is at risk of failure. Therefore, while coming off CPB, we used NO and intravenous nitroglycerine in our patient to decrease the RV afterload and improve forward stroke volume. The new implantation of a mechanical device in the pericardial cavity with a large heart distorts the topographic position of the heart in the thorax. This abnormal position may cause distortion of the interventricular septum and the RV. The heart is also stunned due to coring into the muscle. Thus, inotropes are required in the immediate postoperative period. It has been shown that patients with preoperative RV dysfunction are at increased risk for gastrointestinal bleeding.
The surgical incisions and coring of left ventricle may cause significant bleeding in the postoperative period. Our patient had to undergo a reexploration for postoperative bleeding on day 11. Although the pump is magnetically levitated, still the blood passes through narrow orifices at extremely high velocities. This leads to hemolysis and hematuria. Our patient developed hematuria and AKI at the same time but responded with conservative management. A raised LDH and plasma-free hemoglobin levels indicated device-induced hemolysis. The incidence of AKI is high as 10%–28% in the initial postoperative period after VAD implantation. The continuous flow VADs increase the MAP and thus improve perfusion of kidneys. The glomerular filtration rate increases in the initial 1–6 months and then by 1 year approaches the preimplantation values. The preoperative serum creatinine (serum creatinine >1.9 mg/dl) is an independent risk factor for temporary renal support and 30-day mortality.
Pleural effusions occur in most of the patients; the incidence with earlier devices is up to 100%. The causes of pleural effusion are increasing RV dysfunction, hypoproteinemia, systemic inflammation (repeated blood transfusions), AKI, and hemothorax. In our patient, repeated bilateral serosanguineous effusion leads to increased morbidity and stay in the ICU.
The driveline-site infection is one of the common complications after discharge. This also occurred repeatedly in our patient but subsided with oral antibiotics and local cleaning with chlorhexidine-based disinfectant. A recent report by Hilker et al. mentions the use of cold atmospheric plasma with kinPen MED jet device (Neoplas Tools, Germany) for the treatment of driveline infection.
The recommended INR for HVAD is 2–3 and an INR >3.0 is associated with higher incidence of hemorrhagic stroke. The MAP of more than 90 mmHg is the strongest predictor for hemorrhagic stroke.
The occurrence of new-onset arrhythmias is an indicator of inadequately decompressed heart. Medical therapy in form of beta-blockers helps reduce the incidence of ventricular arrhythmias. Implantable cardioverter defibrillators can be used safely with HVAD. In our patient with onset of NSVTs, we increased the dose of losartan, added oral sildenafil, and increased the rpm from 2400 to 2500. With this management, his arrhythmias subsided. In cases of progressive RV failure, the patient may be considered for heart transplant or a right VAD.
The development of more than mild aortic valve incompetence following HVAD implantation has been associated with closed aortic valve. In our patient, we did find mild aortic regurgitation at the end of 1 year.
The early recognition and treatment of common complications following HVAD implantation decreases morbidity of the patients.
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