Transcatheter Structural Heart Interventions for the Treatment of Chronic Heart Failure
2015; Lippincott Williams & Wilkins; Volume: 8; Issue: 7 Linguagem: Inglês
10.1161/circinterventions.114.001943
ISSN1941-7632
AutoresMaría Del Trigo, Josep Rodés‐Cabau,
Tópico(s)Cardiovascular Function and Risk Factors
ResumoHomeCirculation: Cardiovascular InterventionsVol. 8, No. 7Transcatheter Structural Heart Interventions for the Treatment of Chronic Heart Failure Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBTranscatheter Structural Heart Interventions for the Treatment of Chronic Heart Failure Maria Del Trigo, MD and Josep Rodés-Cabau, MD Maria Del TrigoMaria Del Trigo From the Quebec Heart & Lung Institute, Quebec City, Quebec, Canada. and Josep Rodés-CabauJosep Rodés-Cabau From the Quebec Heart & Lung Institute, Quebec City, Quebec, Canada. Originally published22 Jun 2015https://doi.org/10.1161/CIRCINTERVENTIONS.114.001943Circulation: Cardiovascular Interventions. 2015;8IntroductionHeart failure (HF) is a major cause of mortality and morbidity in developed countries.1 In the past 2 decades, improvements in drug therapy and the widespread use of implantable cardioverter-defibrillators and cardiac resynchronization therapy devices has improved the prognosis of HF patients.2 However, morbidity and mortality rates remain high, with an estimated 5-year mortality rate exceeding 50% coupled with significant rehospitalization rates. Several transcatheter implantable devices have recently emerged in an attempt to improve the prognosis and quality of life of such patients.We reviewed the current literature on interventional chronic HF. The review focus on the description of the devices and main procedural characteristics, patient eligibility, procedural results, and clinical outcomes associated with such devices. This article will focus only on mechanical transcatheter structural heart interventions for treating chronic HF. Devices used for percutaneously delivering biological therapies and interventions for acute HF fall beyond the scope of this article.Left Ventricular Restoration DevicesSeveral surgical and device-based therapies have emerged in an attempt to reverse LV remodeling by restoring normal LV architecture and reducing LV volumes and wall stress. Among these surgical therapies, the most commonly used is the endoventricular circular patch plasty or Dor procedure, which consists of excluding the akinetic septal and apical ventricular regions by performing aneurysm resection with the insertion of a circular pericardial patch. Although this procedure showed promising results in multicenter registries,3 the only randomized trial—Surgical Treatment for Ischemic Heart Failure (STICH)—failed to demonstrate differences in the composite end point of death and rehospitalization for cardiac causes between surgical ventricular restoration+coronary artery bypass graft versus coronary artery bypass graft alone.4 However, some subgroups, experienced significant benefits with surgical ventricular restoration.5,6In this regard, the parachute device (Cardiokinetix, Inc, Menlo Park, CA) emerged as a percutaneous device with the purpose of excluding the dysfunctional area of the LV, leading to a geometric reconfiguration and corresponding reductions in LV volumes.7 It consists of a ventricular partitioning device composed of a self-expanding nitinol frame, an expanded polytetrafluoroethylene occlusive membrane, and a distal atraumatic (pebax polymer) foot (Figure 1). The nitinol frame is shaped like an umbrella with 16 struts. The tip of each strut ends in a 2-mm anchor. The device is available in expanded nominal diameters of 65, 75, 85, and 95 mm.Download figureDownload PowerPointFigure 1. The parachute device. A, The parachute device is composed of an expanded polytetrafluoroethylene (ePTFE) occlusive membrane (a), a self-expanding nitinol frame (b), and a distal radio-opaque atraumatic foot (c). B–D, Fluoroscopic/angiographic images of parachute device implantation. B, Device placement in the left ventricular (LV) apex. C, Device expanded but still attached to the delivery system. D, Final left ventriculography after release of the device. E–H, Transthoracic echocardiography images of the LV pre and post (2 years) parachute device implantation. E, LV in diastole at baseline. F, LV in diastole at 2-year follow-up. G, LV in systole at baseline. H, LV in systole at 2-year follow-up. (Courtesy of Cardiokinetix Inc, Menlo Park, CA.)The device is self-expandable and is deployed by retracting the delivery catheter. Full expansion of the parachute device is facilitated by inflating a low-pressure contrast-filled 6-mL balloon with a nominal diameter of 24 mm until the anchors are fully expanded and in contact with the LV wall (Figure 1). The procedure is performed under local anesthesia and is guided angiographically and via transthoracic echocardiography.Patients selected for device implantation had a history of anterior myocardial infarction, resulting in antero-apical akinesia or dyskinesia, left ventricular ejection fraction (LVEF) <40%, and chronic HF (New York Heart Association [NYHA] class II–IV), despite optimal medical therapy. Although transthoracic echocardiography remains the initial imaging tool, the importance of multimodality image techniques, including cardiac computed tomography has become relevant for patient selection.8The first-in-man experience with the parachute device included 39 patients.7 The primary end point was successful device delivery and deployment without the occurrence of device-related major adverse cardiovascular events at 6 months, and this was observed in 74% of the patients. There were no cases of ventricular perforation or stroke. At 12-month follow-up, patients improved their NYHA class (from 2.5±0.6 at baseline to 1.3±0.6 at 12 months P<0.001) and there was a significant reduction in left ventricular end-systolic and left ventricular end-diastolic volumes (from 93.6±4.1 mL to 79.5±3.6 mL and from 127.2±4.2 mL to 110.4±4.6 mL, all P<0.001). However, changes in 6-minute walk test (6MWT) were not statistically significant (from 359±20 m to 375±26 m, P=0.19). Costa et al9 recently reported the 3-year follow-up of this initial cohort of patients. NYHA class improved in 52% of patients, did not change in 33%, and worsened in 15%. The combined 3-year incidence of death or HF hospitalization was 38.7%. Improvements in LV volume indices were sustained through the 3-year follow-up.After this initial experience, cardiac computed tomography exams were added to the preprocedural workup to improve patient selection. The Parachute III postmarket European study, including 100 patients, showed a procedural success rate of 97% (Abraham W. HFSA meeting 2014). Procedural or device-related events at 1-year follow-up (primary safety end point) occurred in 7% of the patients, and all of these were related to vascular access complications (partially related to the use of 14 or 16F delivery catheters). At 1-year follow-up, 65% of the patients were classified as NYHA I or II, echocardiography data showed significant reductions in left ventricular end-diastolic and left ventricular end-systolic volumes (P<0.0001), and there was a significant increase in exercise capacity as evaluated by 6MWT (P 300 days before.11 Although no adverse events were associated with the device fracture, these findings led to modifications of the composite material to improve durability.In summary, available data supports the feasibility and safety of the parachute device as a novel concept of minimally invasive ventricular restoration therapy. Definitive device efficacy will be determined by the ongoing Parachute IV trial12 (clinicaltrials.gov≠NCT01614652). This trial will randomly (1:1) assign 478 patients with NYHA class III-IV ischemic HF, akinetic or dyskinetic LV wall abnormality, and LVEF between 15% and 35% to optimal medical therapy (control) versus parachute device implantation.Left-to-Right Interatrial Shunt DevicesRegardless of the underlying precipitant, elevated left atrial (LA) filling pressure leading to pulmonary congestion is the common final pathway in decompensated HF.13 This provides the basis for the proposition of creating a left-to-right shunt as a novel treatment concept in chronic HF for reducing LA pressures, improving functional class, and reducing rehospitalizations.Interatrial Septal Device SystemThe interatrial septal device (DC Devices Inc, Tewksbury, MA) system consists of a nitinol device (outer diameter 19 mm) inserted percutanously in the interatrial septum to produce a permanent 8 mm atrial septal communication (Figure 3). The device was designed after testing its potential hemodynamic effects using a previously validated computed model of HF.15Download figureDownload PowerPointFigure 3. Left-to-right interatrial shunt devices. A, The interatrial septal device. B, The V-Wave device. C, Transoesophageal echocardiography image of the interatrial shunt device showing left to right shunt. D, Transoesophageal echocardiography image of the V-Wave device at 30-day follow-up showing left-to-right shunt. A and C, Courtesy of DC Devices Inc, Tewksbury, MA; B and D, adapted from Amat-Santos et al14 with permission of the author. Copyright ©2014, Europa Digital & Publishing. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.The initial experience with this device included a total of 11 patients with chronic HF, NYHA class >II, preserved LVEF (LVEF≥45%), and pulmonary capillary wedge pressure ≥15 mm Hg at rest or ≥25 mm Hg during exercise.16 The device was successfully implanted in all patients without complications. At 30 days, echocardiography showed no device displacement and device permeability with left-to-right shunt in 10 patients. In the remaining patient, flow direction could not be determined. Significant improvements in pulmonary wedge pressure (P=0.005), quality of life (P=0.005), and 6MWT results (P=0.025) were observed at 30-day follow-up (Table 1).Table 1. Atrial Shunt Devices: Baseline and Short-Term Clinical and Hemodynamic DataIASD Device (n=11)V-WAVE Device (n=6)Baseline30d. FUP ValueBaseline90d. FUP ValueNYHA III-IV, % patients100%45%N/A100%0%N/ALVEF, %57±9*N/AN/A32 [20–35]33 [20–35]NS6-MWD, m338 [52–540]387 [104–522]0.025274 [186–358]314 [205–480]0.006NT-proBNP, pg/mL1254 [186–3907]1356 [68–3119]NS2909 [698–7033]1519 [431–5637]NSQoL: MLWHF56 [17–78]30 [9–68]0.005N/AN/AN/AQoL: KCCQN/AN/AN/A40 [39–41]70 [47–75]0.009mPCWP, mm Hg19 [6–25]13 [9–18]0.00520 [18–22]14 [11–14]0.018mPAP, mm Hg31 [19–39]26 [19–39]NS25 [20–30]25 [17–26]NSCI, L/(min/m2)2.3 [1.6–3.3]N/AN/A2.2 [2.2–2.4]2.5 [2.4–2.6]NSQp/QsN/AN/AN/A1.0 [0.9–1.0]1.1 [1.1–1.2]0.04Values are presented as median [range] or mean±SD. 6MWT indicates 6-minute walk test; CI, cardiac index; FU, follow-up; IASD, interatrial septal device; KCCQ, Kansas City Cardiomyopathy Questionnaire; LVEF, left ventricular ejection fraction; MLWHF, Minnesota living with heart failure; mPAP, mean pulmonary artery pressure; mPCWP, mean pulmonary capillary wedge pressure; N/A, not available; NS, not significant; NT-proBNP, N-terminal prohormone of brain natriuretic peptide; NYHA, New York Heart Association functional class; and QoL, quality of life.V-Wave DeviceThe V-Wave atrial–septal shunt device (V-Wave Ltd, Or Akiva, Israel) consists of an hourglass-shaped nitinol frame with expanded polytetrafluoroethylene encapsulation that is implanted at the level of the interatrial septum and contains a trileaflet porcine pericardium tissue valve sutured inside, allowing a unidirectional left-to-right atrial flow. The minimal lumen size of the device is 5 mm (Figure 3).14The V-Wave device was evaluated in an ovine model of ischemic HF, including a total of 21 sheeps (14 received the device, 7 controls). The device implantation was associated with a persistent decrease in LA pressure, improved LVEF, and lower mortality, with no changes in right atrial or pulmonary artery pressure. Patent left–to-right shunt was documented in all devices over the entire duration of the study (12 weeks).17The first patient was treated in October 2013, and data from the first 6 patients treated with this device have been recently reported.18 All patients had chronic systolic HF (LVEF <40%), were in NYHA class ≥III despite optimal medical treatment, and had a pulmonary capillary wedge pressure ≥15 mm Hg. The V-Wave device was successfully implanted in all patients with no complications. At hospital discharge, patients were treated with aspirin and oral anticoagulation (for a period of 3 months in those patients with no other indications for anticoagulant therapy). No device-related adverse events occurred. One patient experienced gastrointestinal bleeding related to warfarin at 2 months postprocedure, and another patient with LVEF of 15% and a history of ventricular arrhythmias had several episodes of symptomatic ventricular tachycardia requiring hospitalization and ablation therapy 5 weeks postprocedure. This patient continued to deteriorate in the ensuing weeks after hospitalization and finally died of terminal HF.At 1-month follow-up, transesophageal echocardiography showed patent left-to-right atrial shunt in all patients. No thrombus or device migrations were documented. At 3-month follow-up, there were significant improvements in PWCP, quality of life, and 6MWT (P<0.05 for all; Table 1). There were no significant changes between baseline and 3 months in LVEF, telediastolic LV diameter, left atrial volume, prohormone of brain natriuretic peptide values, mitral regurgitation (MR) grade, or right arterial pressure (Table 1).Data from the first patient with HF and preserved LVEF treated with the V-Wave device were recently presented (Rodés-Cabau J, TCT 2014). The procedure was performed successfully with no complications, and the patient had significant improvements in NYHA class, quality of life, 6MWT distance, and prohormone of brain natriuretic peptide values at 3-month follow-up.Therefore, data from these 2 first-in-man experiences showed that the creation of a left-to-righ shunt with the implantation of the interatrial septal device or v-wave systems is safe, feasible, and seems to be associated with good short-term clinical and hemodynamic outcomes. Larger trials are required to confirm these early findings.Renal DenervationCatheter-based radiofrequency renal artery denervation has been developed as a new potential treatment for resistant hypertension.19 However, the only blinded, sham-controlled, appropriately powered study of renal denervation conducted to date, the SYMPLICITY HTN-3 study, failed to show differences in the primary and secondary efficacy end points (change in office systolic blood pressure at 6 months and change in ambulatory blood pressure at 6 months, respectively).20 Despite these controversial results, renal denervation's effects are not limited to pressure-lowering applications. Thus, renal denervation is thought to be beneficial in several diseases influenced by sympathetic overactivity, including HF, chronic kidney disease, sympathetically driven arrhythmias, obstructive sleep apnea, and polycystic ovarian syndrome.21 Although evidence is still lacking, renal denervation is thought to be useful in HF patients with low and preserved LVEF because of its inhibitory effects on the renin–angiotensin system.In a randomized study including 64 patients (46 treated with bilateral renal denervation and 18 controls, all of them with resistant hypertension), renal denervation with the Symplicity or Flex ablation catheters (Ardian [now Medtronic], Palo Alto, CA) significantly reduced interventricular septal thickness and LV mass index. LV filling pressures and LVEF significantly improved in the treatment group.22 Schirmer et al23 showed that in patients undergoing renal denervation, the improvement in LV structure and function may be independent of changes in blood pressure and heart rate. This study enrolled 66 patients with resistant hypertension. LV hypertrophy and diastolic function improved 6 months after renal denervation, without significant relation to blood pressure or heart rate reductions. In a first-in-man experience, including 7 nonhypertensive patients with chronic systolic HF (Renal Artery Denervation in Chronic Heart Failure [REACH] Pilot study), renal denervation was performed without complication, and it was associated with significant improvements in symptoms and distance walked at the 6MWT (P=0.03) and reduction in loop diuretic doses (P=0.046) at 6-month follow-up. Interestingly, no significant changes in blood pressure, heart rate of renal function were observed (Figure 4).24Download figureDownload PowerPointFigure 4. The REACH-Pilot study (n=7).24 Changes from baseline to 6 months after renal denervation in systemic (systolic and diastolic) pressures (A), 6-minute walk test (B), and loop diuretic doses (C and D).Preliminary data suggest a potential benefit of renal denervation for treating patients with chronic HF, irrespective of the presence of hypertension. After this initial experience, several trials using renal denervation in HF are currently ongoing.25 The Renal Sympathetic Denervation for patients with Chronic Heart Failure (RSD4CHF) trial (clinicaltrials.gov≠NCT01790906) is expected to include 200 symptomatic patients (100 treated with renal denervation and 100 controls) with NYHA II-IV and severe systolic dysfunction (LVEF≤35%). The primary end point will be all-cause mortality and cardiovascular events at 24-month follow-up.Implantable Hemodynamic MonitoringSeveral strategies for measuring intrathoracic impedance26 or RV pressure have been proposed to reduce HF readmissions by detecting early evidence of HF decompensation. However, no randomized clinical trials have shown a reduction in HF hospitalizations with these approaches.27,28 In an attempt to more accurately assess the hemodynamic status of HF patients, several implantable hemodynamic monitoring devices have been developed.Pulmonary Artery Pressure MonitorsThe pulmonary artery pressure monitoring system (CardioMEMS, St Jude Medical, Minnessota, MN) consists of an implantable HF sensor, a delivery catheter, an electronic monitoring unit with a barometer, and a database in a secure website (Figure 5). The sensor is a coil and a pressure-sensitive capacitor encased in a hermetically sealed silica capsule covered by silicone, which is implanted in the distal pulmonary artery. It is powered by an external antenna containing no batteries or internal power source. A wired loop made from PTFE-coated nitinol wire is attached to each end to prevent sensor distal embolization. Pressure changes from inside the pulmonary artery are transmitted wirelessly by using an external antenna. This external electronic unit is held against the patient's side or back in the area of the sensor, allowing device calibration and daily waveform recording. The data are finally transmitted by telephone line to a website.30Download figureDownload PowerPointFigure 5. The pulmonary artery pressure monitoring system. A, The implantable heart failure (HF) sensor consists of a pressure-sensitive capacitor (a), an inductor coil (b), and a fused silica housing with silicone coating (c). B, The sensor is implanted into a distal branch of the pulmonary artery. C and D, CHAMPION trial results. C, Kaplan–Meier cumulative of HF-related hospitalizations during entire period of randomized single-blind follow-up. D, Kaplan–Meier freedom from first HF-related hospitalization or mortality during the entire period of randomized follow-up. (Adapted from Abraham et al29 with permission of the publisher. Copyright ©2011, Elsevier Ltd. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.)After first-in-man and feasibility studies,31 the prospective randomized CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in NYHA Class III Heart Failure Patients (CHAMPION) trial evaluated the efficacy of this device in 550 patients with chronic HF.29 All patients received the CardioMEMS HF sensor and were randomized before discharge to receive HF management guided by hemodynamic information from the sensor (treatment group n=270) or traditional HF standard of care (control group n=280). Antithrombotic treatment consisted of anticoagulation therapy in the presence of AF or dual antiplatelet therapy in the absence of AF.Sensor implantation was attempted in 575 patients and achieved in 550 (95.7%). Fifteen serious adverse events were registered, 8 device-related or system-related complications (1%), and 7 procedure-related adverse events. No pressure-sensor failures were registered.The primary efficacy end point of HF-related hospitalizations within 6 months follow up occurred in 84 patients in the treatment group and in 120 in the control group (hazard ratio =0.72, 95% confidence interval [CI] 0.60–0.85, P=0.0002). During a mean follow up of 15 months, a 37% relative risk reduction in HF-related hospitalization was observed in the treatment group (158 versus 254, hazard ratio =0.63, 95% CI 0.52–0.77; P<0.0001). No differences were found regarding survival rates (94% versus 93%, hazard ratio =0.77, 95% CI 0.40–1.51; P=0.45; Figure 5).The results of a prespecified subgroup analysis of CHAMPION focusing on patients with preserved LVEF (n=119, mean LVEF=51%) also showed a significant reduction in HF hospitalizations at 6-month follow up, representing a 46% reduction compared with the control group (incidence rate ratio 0.54, 95% CI 0.38–0.70; P 50% of patients with LVEF 20 000 patients have been treated with the MitraClip system worldwide. The FDA has recently approved the device for the treatment of degenerative MR, but increasing experience exists on the treatment of functional MR in patients with chronic HF.Treatment of Functional MR With the MitraClip System: Observational StudiesSeveral observational studies have focused on the evaluation of the use of the MitraClip device for the treatment of functional MR, and their main results are summarized in Table 2. Overall, a total of 553 patients have been included in these studies, Hospital/30-day mortality was 3.6%, and a successful result (MR≤2+ at discharge) was obtained in 89% of the patients (from 80% to 96%). After a follow-up ranging from 7 to 14 months, all cause mortality rate was 19%, (ranging from 13% to 22%), most (80%) patients were in functional class I or II, and MR remained <2+ in 85% of the patients at risk.Table 2. MitraClip Experience for the Treatment of Functional Mitral Regurgitation: Nonrandomized TrialsStudyNo of PatientsAge, YearsLVEF, %Risk Score, %, Logistic EuroScoreProcedural Success, %Need for ≥2 Devices, %Residual MR ≤2+ at Discharge, %Mortality at 30 Days/in Hospital,* %Mean/Median† FU, MonthsNYHA I-II at FU, %LVEF at FU, %Residual MR ≤2+ at FU, %All Cause Mortality/CV Death‡ at FU, %PERMIT-CARE405170±92
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