Heart failure (HF) is one of the major unsolved problems in cardiology and one of the leading causes of death. In the majority of cases, the clinical syndrome of HF results from left ventricular systolic dysfunction (LVSD). Obstructive coronary artery disease is the major cause of LVSD, responsible for almost 70% of cases.1

Post-myocardial infarction (MI) HF is more common in patients with an anterior infarction. The anteroapical region is a particularly vulnerable region of the LV for dilatation because of its thinner structure and greater curvature. When this region undergoes expansion and thinning, even small segmental elongation can greatly increase the radius of curvature, resulting in a large increase in wall stress. The associated LV remodeling leads to increased myocardial oxygen consumption secondary to increased wall stress, increased neurohormone and cytokine levels, afterload mismatch, and subendocardial hypoperfusion. This results in an inefficient, dilated and failing LV, leading to HF symptoms. LV remodeling is a progressive and self-perpetuating process, and has long been recognized as a strong predictor of mortality and morbidity after MI.2

There are a number of treatment options available to minimize symptoms and to slow disease progression. A combination of lifestyle changes and drug therapy – the foundation of almost all HF treatment regimens – can improve both survival rates and quality of life. However, these regimens have certain limitations, especially when LV anteroapical wall motion abnormality is present. Currently, the medical community recognizes that pharmacologic therapy has been optimized virtually as far as possible, and morbidity and mortality in post-MI HF patients continue to be excessive despite advances in medical treatment. Patients with advanced heart failure may become candidates for other interventions, including surgery and implantable devices.

Several surgical approaches have been advocated for LV volume reduction, including surgical ventricular remodeling (Dor procedure) and partial left ventriculectomy (Batista procedure). Data from surgical trials indicate that the described procedures significantly reduce LV volumes,3,4 but with mixed effects on functional capacity and quality of life. Favorable outcomes have only been reported in selected patients.5

Against this background, a novel percutaneous implantable device has been developed – the Parachute LV partitioning device (CardioKinetix, Inc, Menlo Park, CA) – which is deployed in the LV of patients with anteroapical regional wall motion abnormalities (akinesia or dyskinesia) following an anterior MI. The purpose of the Parachute device is to partition the LV and isolate the dysfunctional anteroapical region, reduce both systolic and diastolic volumes, decrease myocardial wall stress, and thereby improve LV hemodynamics.

Pre-clinical studies in an animal model of MI were performed before implantation of the Parachute device in humans, and indicated that the device has beneficial acute and medium-term effects on LV function, as measured by a decrease in LV volumes and end-diastolic pressure, increased cardiac output, and improvement in left ventricular ejection fraction (LVEF).6

Data from the first-in-human clinical trial (a single-arm, prospective, nonrandomized, multicenter trial – the Percutaneous Ventricular Restoration in Chronic Heart Failure (PARACHUTE) trial – showed that the Parachute implant was safe and feasible and improved LV hemodynamics, functional class and exercise capacity in the 12 months following the procedure.7 Recently, data from the 24-month follow-up have been released. The benefits achieved at 12 months were maintained at 24 months, associated with a relatively low rate of adverse events.

A dual-arm (Parachute vs. optimal medical therapy), open-label, multicenter registry designed to evaluate the Parachute implant in ischemic heart failure patients in 14 centers across Europe is ongoing – the Percutaneous Ventricular Restoration in Chronic Heart Failure (PARACHUTE, Cohort B) trial. The primary endpoint of the trial is the assessment of safety, defined as the successful delivery and deployment of the Parachute implant through 6-month follow-up without the occurrence of major adverse cardiac events (MACE) related to the investigational device. Other key endpoints include changes in LV volume indices (LV end-systolic and end-diastolic volumes, measured by transthoracic echocardiography) and in exercise tolerance (assessed by the six-minute walk test).

We aim to describe the initial experience of our center with the Parachute implant and its short-term safety, defined as the successful delivery and deployment of the device.

Baseline demographic, echocardiographic, functional capacity and laboratory data of the patients included in the study are shown in Tables 1–4.

A 16-Fr catheter was used in four patients; in the other patient a 14-Fr catheter was used due to peripheral arterial disease. A 95mm implant was used in three patients, an 85mm device in one, and a 75mm device in the other patient. An optimal apical position of the implant was achieved in all patients but one. In this patient, the Parachute device was positioned in a more posterolateral location due to difficulty in accessing the LV apex. No catheter or device malfunctions were noted. Procedure time averaged 62±18min, with a mean fluoroscopy time of 15±4min. A mean of 178±41ml of contrast agent was used per patient. No complications ensued during the procedure. In all patients, vascular access site closure was performed using percutaneous suture.

Regarding in-hospital outcome, only one event was noted, consisting of minor bleeding of the vascular access site. Serum creatinine and blood urea nitrogen showed no significant changes at 24 hours following the procedure or at discharge. CK, CK-MB, and troponin T were consistently within reference ranges, indicating that no myocardial damage had occurred during implantation.

Data on echocardiographic characteristics after Parachute implantation are shown in Table 5. There was a significant reduction in end-diastolic LV volumes, and LV ejection fraction improved slightly after Parachute implantation compared to baseline values. On discharge, there was no leakage between the static and dynamic LV chamber in four patients, while in one patient a mild leakage was noted.

The most direct approach to revert the remodeling itself is a mechanical intervention to decrease LV volume or to constrain the ventricle from further enlargement. Several surgical approaches have been advocated in patients with a dilated LV, including partial left ventriculectomy (Batista procedure) and surgical ventricular remodeling (Dor procedure). Of these procedures, only surgical ventricular remodeling has acceptable short- and long-term effects on mortality and morbidity. Even so, perioperative mortality is more than 5%, and overall 5-year survival is less than 70%.5 By contrast, LV volume reduction with the Parachute device provides a clinical advantage over the currently used mechanical interventions as it is implanted percutaneously, thus avoiding the early mortality and morbidity associated with surgical intervention.

In our patients, Parachute implantation was safe and feasible, with acceptable procedure and fluoroscopy times. There was a significant reduction in end-diastolic volume after implantation. Our patients had very large left ventricles, and hence there was considerable LV volume reduction after implantation. The fact that no device migration occurred during implantation suggests that the Parachute was implanted in a region where anchor penetration in the myocardium was sufficient to provide device stability.

Although current data indicates that the Parachute implant is safe and feasible and improves LV hemodynamics, functional class and exercise capacity in the 24 months following the procedure, longer follow-up is needed to put the Parachute into an appropriate clinical perspective.

The authors have no conflicts of interest to declare.