Ischemic Cardiomyopathy

Ischemic Cardiomyopathy

Introduction

Patients with end-stage heart failure secondary to either ischemic or idiopathic cardiomyopathy frequently demonstrate worsening renal function prior to initiating mechanical circulatory support. Extended cardiopulmonary bypass times and large post-operative transfusion requirements contribute to the development of third space fluid retention often seen in this population. Additionally, diuretic response can be extremely variable in the early post-operative period in these patients. This report describes the use of our system in the early post-operative period in a patient receiving an LVAD as a bridge to transplantation.

Patient History

A 61 year old male with ischemic cardiomyopathy listed as status lb on our transplant waiting list presented with decompensated congestive heart failure despite chronic Milrinone infusion. The patient had insertion of a Swan-Ganz catheter and augmentation of his inotropic support with the addition of Dobutamine. Attempts to diurese the patient with loop diuretics initially were effective with some decrease in the patient’s pulmonary artery wedge pressure. However, after 72 hours he became refractory to diuretics and demonstrated continued decompensation with reduced cardiac output and serum sodium levels as well as a rising serum creatinine level.

At this point, the decision was made to implant an LVAD as a bridge to transplantation. The patient had a cardiopulmonary bypass time of 225 minutes. Multiple rounds of platelets and fresh frozen plasma were transfused in the early post-operative period to control bleeding and correct his coagulopathy. On post-operative day number one, the patient was found to be 9 Kg over his preoperative weight. Additionally, he was demonstrating moderate to severe right ventricular dysfunction with central venous pressures running in the range of 20 to 24 mmHg. Diuresis was attempted for 24 hour using a continuous infusion of loop diuretics without significant response.

On postoperative day number two , our system was begun through a subclavian vein central line. Initial volume removal goals were an average of 150 to 200 cc of fluid removal every hour. Treatment lasted approximately 24 hours with nearly 6 liters of fluid removed. The patients’ central venous pressures decreased to 12 to 15 mmHg and inotropic support was able to be weaned. The patient tolerated our system well with stable hemodynamics and LVAD flow rates in the range of 5 to 5.5 liters per minute.

This patient was ultimately successfully transplanted and currently maintains normal renal function.

Discussion

Decompensated congestive heart failure is typically characterized by a constellation of findings including reduced cardiac output, volume overload, decreased systemic perfusion, and worsening renal function. Reduced renal perfusion leads to activation of the Renin-Angiotensin-Aldosterone System (RAAS), which in turn causes salt and water retention, expansion of intravascular volume and exacerbation of CHF.

While, diuretic therapy has been a mainstay in the treatment of end stage congestive heart failure, many patients become resistant to diuretic therapy with prolonged exposure. Additionally, loop diuretics have been shown to decrease glomerular filtration rate in patients with heart failure making adequate fluid removal in the face of decompensation difficult [1].

Patients requiring LVAD placement for bridge to transplantation are characterized by continued hemodynamic deterioration and organ function despite maximal medical therapy [2]. Given time, ventricular support can reverse the end organ ischemic insult seen in these patients. However, in the early post-operative period these patients still have profound RAAS activation in addition to elevated levels of neurohormones that in combination can make diuretic responsiveness unpredictable [3].

We have found that our system to be a safe and effective technique for volume reduction in the early post-operative period in these patients. This technique is well tolerated hemodynamically, and does not appear to affect the performance of the LVAD in regards to cardiac output or stroke volume.

Case history courtesy of:

Cardiothoracic and Transplant surgeon

Texas

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