Mitral valve regurgitation aggravates symptoms and prognosis in ischemic cardiomyopathy (1- 2). Secondary mitral regurgitation caused by annular dilation and subvalvular traction in cardiomyopathy can be corrected by surgical annuloplasty and adjunctive leaflet and subvalvular repair (3- 4).

Investigational catheter-based procedures improve valve function in this setting (2). These include devices that shorten or displace the coronary sinus (5- 11), transcameral fixtures (12- 14), endoventricular annular placation (15), subpapillary interstitial polymer injections (16), and direct leaflet stapling (17- 20). Most suffer important limitations compared with surgical repair. Coronary sinus approaches are limited by discordant anatomic planes of the sinus and mitral annulus (21- 23), by devices that shorten only a small arc of annular circumference not necessarily encompassing or in-phase with the mitral commissures, and by compression of entrapped left circumflex coronary arteries (21- 23). Leaflet-stapling procedures constrain leaflet excursion, do not reduce annular dilation, and may exacerbate subvalvular traction (24).

Inspired by epicardial purse-string annuloplasty before the cardiopulmonary bypass era (25), we have developed a novel catheter-based technique to reduce mitral annular circumference. A circumferential “cerclage” suture traverses the coronary sinus and basal septal myocardium, and is secured within the right atrium. Cerclage introduces centripetal force uniformly, irrespective of the rotational orientation of the commissures, to enhance mitral leaflet coaptation.

In this report, we address whether cerclage is feasible in swine, whether entrapped coronary arteries can be protected from extrinsic compression, whether cerclage affects mitral regurgitation and mitral annular dynamics in ischemic cardiomyopathy, and what mechanisms appear to underlie cerclage action.

Animal care and the porcine model of ischemic cardiomyopathy are described in the Online Appendix. For cerclage, 9-F introducer sheaths were placed percutaneously into the right jugular and femoral veins, 6-F introducer sheaths were placed into a femoral artery, and heparin (150 U/kg) was administered. After endpoint assessment, animals were euthanized under general anesthesia.

A guidewire loop is created around the mitral annulus and left ventricular outflow tract, and then exchanged for a suture (Figure 1). The guidewire traverses the coronary sinus and the proximal great cardiac vein into the first septal perforator vein towards the basal interventricular septum. It is then directed across a short segment of myocardium under imaging guidance (Online Appendix) to re-enter a right heart chamber where it is ensnared and exchanged for a suture and tension-fixation device.

To conduct cerclage, a transjugular balloon-tipped guiding catheter (Vueport 8-F, Cardima, Fremont, California) is introduced into the coronary sinus beyond the hemiazygous branch (common in pigs [26]), the occlusion balloon inflated, and a retrograde venogram pressurizes and opacifies the great cardiac vein and septal perforator veins. A 0.014-inch guidewire (MiracleBros 3 or 4.5, or Confianza, Asahi, Abbott Vascular, Abbott Park, Illinois) is steered using a deflectable microcatheter (Venture, St. Jude Medical, St. Paul, Minnesota) into the first basal septal perforator vein. Once the targeted right heart chamber is entered, the guidewire is ensnared and replaced with a braided nonabsorbable suture. To fix the tension, both suture free ends were externalized and tied beyond a short catheter, which was implanted in a subcutaneous pocket.

Circumflex coronary artery branches underlie the coronary sinus in most human (21- 23) and porcine hearts, and are susceptible to compression during coronary sinus annuloplasty. We developed a rigid-arch protection device to displace compressive forces away from an entrapped coronary artery (Figure 2). The device is positioned over the cerclage suture where it crosses the coronary artery, identified by selective coronary arteriography. The suture tension anchors and orients the arch away from the underlying artery. The prototype consists of a length of seamless, annealed, and sinter-polished nitinol alloy hypotube. It has an inner diameter of 1.1 mm, an outer diameter of 1.5 mm, a length of 12 mm, and an arch-to-base height of 4 mm.

Protection efficacy was measured during graded annuloplasty tension, recording simultaneous aortic and distal coronary artery pressure, using a 0.014-inch guidewire pressure transducer (PressureWire, Radi Medical Systems, St. Jude Medical). Cerclage annular tension was measured with a digital force meter (ZPH, IMADA Inc., Northbrook, Illinois).

Magnetic resonance imaging (MRI)-derived roadmap registration, assessment of ventricular function and flow, and of mitral annular dynamics are described in the Online Appendix.

We sought evidence from 2 clinical datasets that humans have septal perforator veins suitable for cerclage. In the first, we reviewed 10 anonymized and delinked coronary venograms obtained during left ventricular pacemaker lead implantation for congestive heart failure (courtesy of M.S. Lee and R.R. Makkar, Cedars-Sinai Medical Center, Los Angeles, California). In the second, we analyzed 24 sequential anonymized coronary computed tomography (CT) datasets (64 × 0.625-mm detector rows [Brilliance, Philips Healthcare, Andover, Massachusetts]) from electrocardiogram (ECG)-gated breath-held acquisitions (courtesy of D.E. Bush and E.P. Shapiro, Johns Hopkins Bayview Medical Center, Baltimore, Maryland). These do not constitute human subject research under US 45CFR§46.102(f).

Continuous parameters were compared using a Student t test (paired when appropriate) and their correlation measured using a Pearson product-moment correlation coefficient r. Regurgitation grades were compared using a Wilcoxon signed rank test. Parameters are reported as mean ± SD. Right atrial and ventricular cerclage success were compared using a Fisher exact test. A p value <0.05 is considered significant.

We identified 2 suitable cerclage guidewire trajectories ((Figure 1)A and Figure 1B). A “simple,” or right ventricular, cerclage traverses a short distance of myocardium into the nearby right ventricular outflow tract. The wire re-enters the right atrium along the septal tricuspid valve commissure. A “right atrial” cerclage trajectory extends from the septal vein further inside the basal septal myocardium into the right atrium near the coronary sinus ostium. Upon re-entry, the guidewire moves freely, as it does after successful recanalization of arterial occlusion. To avoid trabecular entrapment, the guidewire is directed into the pulmonary artery, ensnared, externalized, and then replaced with a suture. Graded cerclage tension can be applied to both ends of the cerclage suture, interactively during MRI until further tension does not further abate regurgitation. Finally, a fixation device secures the tension near the origin of the coronary sinus.

(Figure 1)C through (Figure 1)E illustrate X-ray fused with magnetic resonance imaging (XFM)-guided trajectory planning for myocardial guidewire traversal.

The first 12 consecutive cerclage attempts failed. In the next 13 consecutive technical development experiments, cerclage was successful in 8 (62%) naive swine. Of these, one suffered coronary sinus thrombosis attributed to prolonged guiding-catheter manipulation, another suffered tricuspid chordal transection by an entrapped cerclage guidewire, and another suffered intraventricular conduction delay.

In the third phase in 16 consecutive swine with ischemic cardiomyopathy, cerclage was successful in 14 (88%). Both failures were nonfatal exit (perforation) into the pericardium, once from the right ventricular free wall, and another from the left ventricular septum. These are attributed to inadequate use of imaging guidance to distinguish the septum and free wall. There were two major complications, including one pericardial tamponade during jugular vein access, and high-degree atrioventricular block after right atrial cerclage. One animal developed reversible tricuspid valve regurgitation after right ventricular cerclage tension entrapped a variant septal tricuspid valve leaflet.

Combining naive and myopathic animals, right ventricular cerclage succeeded in 15 of 16 animals (94%) compared with right atrial cerclage (7 of 10 animals, 70% success, p = 0.26). Right ventricular cerclage required less fluoroscopy time (55 ± 20 min vs. 144 ± 84 min, p = 0.02).

Necropsy examination confirmed the predicted guidewire trajectory for right ventricular (Figure 1G) and right atrial (Figure 1H) cerclage. In right ventricular cerclage, the suture traversed a 28 ± 4.8-mm intraseptal path measured from the epicardium including approximately 15 mm of septal vein, passed near tricuspid chordae, and re-entered the right atrium along the septal tricuspid commissure.

A minority of animals had unsuitable coronary venous anatomy by coronary venography. A great cardiac vein was not contiguous with the coronary sinus in 4 of 45 animals, which were excluded from analysis. One animal had an absent basal septal perforating vein but underwent successful right ventricular cerclage using an enhanced-stiffness guidewire (a transected Confianza [Asahi]).

Major circumflex coronary artery branches were entrapped by the cerclage suture in all animals. Cerclage with 400 g tension induced subtotal angiographic occlusion (Figure 2E) and halved resting distal coronary pressure without a protection device in place (Figure 2G).

With the coronary artery protection device deployed, cerclage tension caused no angiographic stenosis (Figure 2F) or relative reduction in distal coronary pressure, even at supratherapeutic (800 g) tension that impaired transmitral filling and lowered systemic blood pressure (Figure 2H). The protection device remained in deployed position in all animals assessed at necropsy, and remained effective in 1 animal that survived for 6 weeks.

Graded tension progressively reduced the septal-lateral dimension of the mitral annulus but not significantly the commissural width ((Figure 3)A,Table 1). Compared with baseline, 600 g of tension reduced septal-lateral dimension approximately 20% in both systole and diastole. The septal-lateral diameter fell in linear proportion to cerclage diameter as tension was applied (Figure 3B), r² = 0.54.

Ventricular volumes declined nonsignificantly when tension was applied (Table 1), and left ventricular ejection fraction fell in these animals with ischemic cardiomyopathy and mitral regurgitation.

Progressive tension did not reduce conductance catheter-based measures of global myocardial performance. End-systolic elastance (Ees), the slope of end-systolic pressure–volume relationship as preload changes, was 2.2 ± 1.3 mm Hg/ml at baseline and 2.6 ± 1.5 mm Hg/ml during tension, p < 0.01 (Figure 4).

MRI regional wall motion appeared unaffected by cerclage (wall motion score index 1.54 ± 0.12 before vs. 1.56 ± 0.16 after cerclage, p = 0.76). No new late gadolinium enhancement was evident to suggest cerclage-induced myocardial infarction.

One of 16 animals with ischemic cardiomyopathy suffered high-degree atrioventricular block associated with pericardial tamponade. In the others, cerclage tension induced no ECG depolarization or repolarization abnormalities.

Two-thirds of animals surviving with ischemic cardiomyopathy (ejection fraction 39.2 ± 7.6) developed significant mitral regurgitation (n = 10). Successful cerclage reduced mitral valve regurgitation. (Figure 5) and Online Video 1 depict a representative animal with severe ischemic cardiomyopathy before and after application of cerclage tension. Black jets of dephased spins are seen regurgitating from the left ventricle (arrows). After applying 400 g of cerclage tension (Figure 5B), the septal-lateral annular dimension (between arrowheads 1 and 2) is reduced, as is the cerclage diameter (between arrowheads 3 and 4). Regurgitant jets are no longer evident. Discordant cerclage and annular planes are evident, and the coronary sinus (arrowhead 4) does not overlap the posterior annulus (arrowhead 2).

Velocity-encoded MRI was available for 5 animals. In these, the regurgitant fraction was reduced from 22.8 ± 12.7% to 7.2 ± 4.4% (p = 0.04) when cerclage tension was applied ((Figure 6),Table 2). Results are similar using radiocontrast ventriculography (n = 10).

In preliminary experiments, 3 animals survived for 3 weeks or more after cerclage without recurrent mitral regurgitation or evident myocardial erosion.

(Figure 5)C and (Figure 5)D and Online Video 2 show simultaneous tagged and color-flow MRI in an animal with mitral regurgitation that is reduced by cerclage tension. Posterobasal myocardial thinning, late enhancement, and severe hypokinesis also are evident, as expected in this ischemic cardiomyopathy model.

Mitral valve tenting area, a measure of annular dilation and subvalvular traction, was reduced after application of cerclage tension (Table 2). The degree of tenting was reduced in proportion to the reduction in cerclage diameter (Figure 3C). By virtue of reducing septal-lateral distance, the posterior displacement of the line of coaptation was reduced by cerclage.

Cerclage tension did not significantly change 2-dimensional measures of mitral leaflet curvature and angulation with regard to the annulus (Table 3), which reflect leaflet traction.

Variable coronary sinus anatomy contributes to discordant cerclage and mitral annular planes (Figure 1F). In our pig model, the average maximum distance of the coronary sinus to the mitral annulus was 6.6 ± 2.0 mm, and the angle of the 2 planes was 21.8 ± 6.4°. These did not vary significantly throughout the cardiac cycle or during application of tension.

Because the posterior coronary sinus may pass along the atrial aspect of the mitral valve annulus, the vector difference of these discordant planes contributes an apical displacement force to the cerclage annuloplasty.

Cerclage induced conformational changes in the mitral valve annulus (Table 3). Mitral annular area (measured as a 3-dimensional surface) fell with application of tension. Mitral annular geometry varied throughout the cardiac cycle (Figure 7). This cyclical annular contraction is preserved despite application of cerclage tension, which nevertheless reduced circumference and septal-lateral width. Annular height to commissure width ratio is increased by cerclage, which alters the annular saddle morphology. Tension acted to displace the posterior annulus caudally, towards the posterior papillary muscle ((Figure 7)E and (Figure 7)F, Online Videos 3 and 4).

Cerclage annuloplasty encircles both the mitral annulus and the left ventricular outflow tract ((Figure 8),Table 4). We observed reciprocal constraint of these 2 structures during the cardiac cycle when cerclage tension was applied. Whereas the cerclage diameter remains fixed throughout the cardiac cycle, the left ventricular outflow tract diameter enlarges during systole and contracts during diastole. Conversely, the constrained septal-lateral dimension of the mitral annulus is reduced by the left ventricular outflow tract during systole but not constrained during diastole. There was no gradient induced across the left ventricular outflow tract using conventional fluid-filled catheters, nor was aortic regurgitation induced.

We reviewed pressurized coronary venous angiograms in 10 patients with congestive heart failure undergoing cardiac resynchronization therapy. Eight had evident proximal septal coronary veins arising from the great cardiac vein that appear suitable for cerclage (Figure 9). The other 2 had inadequate angulation to view septal perforator veins.

We also reviewed 29 sequential CT angiograms in a coronary teaching file. The mean age was 53.2 ± 12.3 years, 79% were male. Of these, 24 (83%) had proximal septal perforator veins that appear suitable for cerclage.

We have developed a novel procedure for catheter-based mitral cerclage annuloplasty. We have shown that circumferential tension can be introduced near the mitral annulus plane via basal septal perforator veins in swine, that attainable tension reduces annular circumference and septal-lateral diameter, that annuloplasty does not appear to alter measures of global myocardial performance, that a simple device protects entrapped coronary artery branches even during supratherapeutic annuloplasty tension, and in a preliminary review, that humans appear to have comparable coronary septal perforator vein anatomy.

We have also shown that cerclage annuloplasty immediately attenuates functional mitral valve regurgitation in a clinically relevant animal model of ischemic cardiomyopathy characterized by left ventricular dysfunction, mitral annular dilation, and posterior papillary muscle traction. Qualitative and quantitative measures of mitral regurgitation are reduced immediately after cerclage. Magnetic resonance imaging has provided insight into the mechanism of cerclage action. First, flexible cerclage reduces annular size while preserving annular motion. Second, in this model, the cerclage suture folds the annulus and displaces the posterior annulus caudally, apparently to accommodate posterior papillary traction. Third, cerclage introduces reciprocal constraint to the left ventricular outflow tract and mitral annulus such that systolic ejection enhances anterior mitral leaflet coaptation.

Anatomic and geometric factors appear to limit innovative approaches to transcatheter coronary sinus-based annuloplasty reported previously. First, the coronary sinus is often found along the left atrial wall, far from the mitral annular plane. Second, the coronary sinus usually entraps underlying major coronary artery branches, so annular compression can induce myocardial ischemia. Third, noncircumferential coronary sinus annuloplasty devices may limit annular shortening to only a small arc of annular circumference.

Cerclage annuloplasty addresses these shortcomings. The crossing planes of the mitral annulus and the cerclage trajectory (Figure 1F) permit effective reduction of the septal-lateral dimension even though the coronary sinus plane does not parallel the annulus. Our protection device averts coronary artery compression, and may have value in other coronary sinus-based annuloplasty approaches. Circumferential cerclage constrains the annulus, including the fibrous trigones, unlike other coronary sinus-based devices.

Functional mitral regurgitation is a manifestation of severe myocardial dysfunction (1) associated with worse symptoms and prognosis. Global and regional myocardial dysfunction and remodeling contribute to functional mitral regurgitation through annular dilation, traction by displaced and elongated chordal-papillary apparatus (usually posterior), regional left ventricular dyssynchrony, and deleterious compensatory loading conditions. Nonsurgical treatment may include cardiac resynchronization therapy, beta-adrenergic blockade, and angiotensin-converting enzyme inhibitors. Surgical repair for organic mitral regurgitation has been extended to patients with cardiomyopathy and normal mitral leaflets. Bolling et al. (27) advocate “undersized” annuloplasty. Additional surgical options include papillary-chordal repair, reinforcement, relocation, ligation, or bowtie constraint of the leaflets (28- 29). Myocardial reduction procedures or constraining devices also are under development (2,4).

The choice of rigid or flexible annuloplasty devices remains controversial. Normal hearts exhibit cyclic contraction of the mitral valve annulus that may enhance leaflet coaptation (30- 31). Preserved annular contraction is associated with a smaller effective regurgitant orifice (30,32). Rigid annuloplasty rings impede mitral annular contraction and tilting. Partial bands, flexible rings, or open suture annuloplasty (33) preserve annular dynamics and have been advocated as a more “physiologic” annuloplasty associated with lower transvalvular gradients. However, flexible annuloplasty rings may contribute to late recurrence of mitral regurgitation compared with rigid rings (34).

In some reports (35), rigid annuloplasty exacerbates leaflet tethering by displacing the posterior annulus farther away from the papillary muscles. Rigid rings have been developed to compensate for the P2-P3 leaflet tethering by enforcing an apical “dip” in the posterior annulus (36), much like we observe after cerclage. The saddle morphology of the normal mitral annulus may confer a mechanical advantage of reduced leaflet stress (37- 38) that may be reduced by annular flattening in functional mitral regurgitation (39- 40). Similar to flexible annuloplasty and suture annuloplasty (33), cerclage preserves annular dynamics and restores annular height. Like newer rigid annuloplasty devices, cerclage serendipitously redistributes the posterior segment to accommodate apical tethering. However, cerclage appears to induce a more complex shape than the natural annular hyperbolic paraboloid.

Our measures of leaflet configuration and leaflet traction are similar to those reported in patients undergoing surgical repair of ischemic mitral valve regurgitation (35). In that report, persistent posterior leaflet traction (wide α2) corresponded with failed surgical repair. After cerclage, we found the angular relation of the posterior leaflet with the annulus to be comparably narrow. In our experiments, the length of the coaptation line increased nonsignificantly.

Initially, we were concerned that entrapment of the left ventricular outflow tract, inevitable with a transseptal venous cerclage trajectory, might induce dynamic left ventricular outflow tract obstruction. On the contrary, we found reciprocal enlargement of the entrained left ventricular outflow tract and reduction of septal-lateral distance by cerclage during systole. This interaction improved mitral leaflet coaptation during systole and relaxed the mitral orifice during diastolic filling. Similar aorto-mitral interaction has been reported in healthy sheep (41), but was not evident in our experiments until cerclage tension was applied.

Mild-to-moderate mitral regurgitation is hard to measure, especially using magnetic resonance imaging (42), which for clinically relevant examinations tends to have inferior time resolution and leaflet visualization. The severity of mitral regurgitation varies with loading conditions (43), further confounding measurement. Echocardiography in swine has proven unsuitable in our laboratories because of inadequate imaging windows. We therefore used velocity-encoded MRI with slice tracking to measure through-plane regurgitation across the moving mitral valve plane (44).

Because neither conventional X-ray nor ultrasound alone satisfactorily depicts myocardial structures and devices during cerclage, we used fusion image guidance. We superimposed MRI-derived roadmaps onto live X-ray, using a system that compensates automatically for changes in table position or gantry orientation (45).

This is an early experience with a new procedure using largely off-the-shelf catheter tools. We considered several potential failure modes.

Cerclage suture applies nonphysiological centripetal force to multiple structures and may risk chronic erosion. Erosion does not appear limiting after other tangential myocardial sutures including “Fontan” endoventricular pursestring and Paneth-Burr mitral annuloplasty. In general, erosion is related to suture tension and tissue friability, and inversely related to suture diameter and time to scar formation. To mitigate the local force and erosion risk, we selected a cerclage suture significantly larger (0.8 mm vs. 0.3 mm) than 2-0 suture commonly used in myocardial applications with or without pledgets. No erosion was evident in a small number of animals that survived after cerclage. These considerations must be further tested in survival experiments. Guidewire-based cerclage traversal of the interventricular septum is a “blunt dissection” that has not evidently entered or interrupted visible septal perforator arteries to date. Right ventricular cerclage re-enters the coronary sinus ostium across the tricuspid commissure and may encroach on the Koch triangle, but generally not its apex, where the compact atrioventricular nodal is located.

Right ventricular cerclage requires care to avoid tricuspid valve injury. Chordal entrapment can be avoided by deflecting the guidewire immediately into the pulmonary artery upon right ventricular re-entry. Leaflet entrapment was observed in 1 animal with variant septal leaflet anatomy and ventricular septal defect. There was no leaflet entrapment when cerclage suture crossed “normal” septal tricuspid commissures, which should be identifiable on cardiac CT or MRI. There is precedent for chronic implantation of pacemaker and defibrillator leads across the tricuspid valve, albeit not under intentional tension. Tricuspid valve function does not appear affected by right ventricular cerclage (data not shown) with tension across the septal tricuspid commissure.

By contrast, right atrial cerclage avoids the tricuspid valve entirely. Right atrial cerclage is more technically demanding, and was associated with conduction block in 1 animal. Further data are necessary to understand the interaction of right atrial cerclage, and normal and pathologic conduction tissue (46).

Although cerclage does not appear possible if the great cardiac vein is not connected to the coronary sinus, in 1 case, we were able to complete cerclage even without an evident basal septal perforator vein. Incorrect guidewire traversal of, for example, a right ventricular free wall, likely can be avoided with procedure experience and enhanced image guidance.

We have shown that compression of entrapped circumflex coronary artery branches can be averted by implanting a simple protection device along the cerclage suture. We are developing a more sophisticated low-profile tension-fixation device.

We are not able to generate severe functional mitral regurgitation in our porcine model of ischemic cardiomyopathy. Regurgitation severity may have been reduced by our use of isoflurane anesthesia (47).

The durability of our short-term findings is not known. The coronary sinus is typically connected to the mitral annulus by nonfibrous atrial myocardium (48). Chronic remodeling of this sino-annular tissue might contribute to late failure of cerclage annuloplasty. Conversely, intertrigonal remodeling may be less likely after circumferential cerclage, compared with flexible annuloplasty bands, which are attached to the trigones only.

Mitral valve repair may not benefit patients with cardiomyopathy (49- 52), even though the perioperative mortality may be low in experienced hands. Surgical repair is usually performed with concomitant myocardial revascularization. Whether primary mitral valve repair improves symptoms or outcome remains to be tested (53). Moreover, we cannot predict where cerclage annuloplasty, if it proves technically successful in humans, would fit into a therapeutic armamentarium against heart failure with mitral regurgitation. Conceivably, it could be combined with effective pharmacologic and cardiac resynchronization treatments, and it would not likely interfere with subsequent surgical valve or myocardial procedures. Cerclage might be used as an adjunct to catheter-based Alfieri-type bowtie repair, which, without annuloplasty, may generate excessive stitch and leaflet tension (54). Early repair of ischemic mitral regurgitation may reverse deleterious remodeling in some animal models (55), but not others (56).

Transcatheter cerclage annuloplasty delivers circumferential annular tension around the mitral annulus and left ventricular outflow tract. Cerclage shrinks the mitral annulus and immediately abates mitral regurgitation in an animal model of chronic ischemic cardiomyopathy. MRI of annular configuration and dynamics suggests cerclage acts by more than reducing annular size. Cyclical annular motion is preserved and height restored. The posterior annulus is displaced toward the posterior papillary apparatus. Reciprocal constraint of the mitral annulus and the left ventricular outflow tract appears to contribute to mitral leaflet coaptation. Entrapped coronary arteries can be protected from extrinsic compression using a simple arch-like device implanted over the cerclage suture. Other potential failure modes appear nonlimiting. A preliminary review of human venograms and CT angiograms suggests a majority have suitable venous anatomy. Further experiments will test the longer-term impact of this approach.

The authors are grateful to Katherine Lucas and Joni Taylor for animal experiments, to David Bush and Edward Shapiro of Johns Hopkins Bayview for anonymized CT images, to Michael Lee and Raj Makkar of Cedars-Sinai for anonymized coronary venograms, and to Lydia Kibiuk of the National Institutes of Health Medical Arts for illustrations. Siemens Corporate Research supported and Christine Lorenz mentored 2 graduate students (M.S. and Akin Yucetas) who contributed to MRI–X-ray registration and investigational velocity-encoded MRI techniques.

For an expanded Methods section, a supplementary figure, and supplementary Videos 1, 2, 3, and 4 and their accompanying legends, please see the online version of this article.

Mitral Cerclage Annuloplasty, a Novel Transcatheter Treatment for Secondary Mitral Valve Regurgitation: Initial Results in Swine