"Mind the Gap": An 85-Year-Old Man with Severe Tricuspid Valve Regurgitation Who Underwent Percutaneous Edge-to-Edge Valve Leaflet Plication Using the New and Advanced MitraClip XTR System.

BACKGROUND Severe tricuspid valve regurgitation (TR) is associated with high cardiovascular mortality. Safe and feasible interventional approaches to treat severe TR are of clinical relevance. The MitraClip is a device that has been approved by the US Food and Drug Administration (FDA) for the repair of mitral valve lesions. Percutaneous femoral venous access with fluoroscopic and echocardiographic guidance is used to deliver a cobalt-chromium clip to secure the mitral valve leaflets. We report on an 85-year-old man with tricuspid valve regurgitation who underwent percutaneous edge-to-edge tricuspid valve leaflet plication with the new, advanced MitraClip XTR System. CASE REPORT An 85-year-old man with severe TR due to annulus dilation of the right ventricle and short septal leaflet presented repeatedly at our hospital with severe right heart failure symptoms. Transesophageal echocardiography revealed severe TR with a large coaptation gap size of 10.6 mm. Percutaneous edge-to-edge valve repair with the new-generation MitraClip System XTR with wider clip arms could overcome the large coaptation gap. We achieved a strong reduction of TR after deploying 2 MitraClips XTR. The patient recovered quickly and has not been admitted to hospital due to heart failure symptoms since the intervention for more than 6 months. CONCLUSIONS Previous studies have shown the safety and effectiveness of the MitraClip device and supported FDA approval for tricuspid valve repair. This report of a patient with complex tricuspid regurgitation demonstrated the feasible use of the new MitraClip XTR System, which improved edge-to-edge tricuspid valve repair due to its increased span and improved grip.

Deep Sedation in a Patient Undergoing Transfemoral Tricuspid Valve Repair Using the PASCAL System.

A 70-year-old man with severe tricuspid regurgitation and large coaptation gap (0.8 cm) was referred to transfemoral valve repair using the PASCAL system. The procedure was successful in reducing tricuspid regurgitation. The PASCAL device facilitated maximum leaflet insertion and to span large coaptation gap in severe tricuspid regurgitation without ventilation maneuvers under general anesthesia. (Level of Difficulty: Intermediate.).

An Unusual Cause of Dyspnea and Thoracic Pressure.

There is a high prevalence of hepatic cysts in the general population. Simple cysts are most of the times asymptomatic and are usually detected incidentally on ultrasonography, computed tomography, or magnetic resonance imaging. Symptoms may range from abdominal discomfort and pain, early satiety, dyspepsia, nausea, and vomiting to jaundice and portal hypertension due to obstruction of adjacent structures. Complications include spontaneous hemorrhage, infection, thrombosis, and atrophy of surrounding hepatic tissue. We present a unique case of a middle-aged patient with acute onset of dyspnea and thoracic pressure due to compression of the right ventricle by a large hepatic cyst.

Thrombogenicity and Antithrombotic Strategies in Structural Heart Interventions and Nonaortic Cardiac Device Therapy-Current Evidence and Practice.

As the number of, and the indications for, structural heart interventions are increasing worldwide, the optimal secondary prevention to reduce device thrombosis is becoming more important. To date, most of the recommendations are empiric. The current review discusses mechanisms behind device-related thrombosis, the available evidence with regard to antithrombotic regimen after cardiac device implantation, as well as providing an algorithm for identification of risk factors for device thrombogenicity and for management of device thrombosis after implantation of patent foramen ovale and left atrial appendage occluders, MitraClips/transcatheter mitral valve replacement, pacemaker leads, and left ventricular assist devices. Of note, the topic of antithrombotic therapy and thrombogenicity of prostheses in aortic position (transcatheter aortic valve replacement, surgical, mechanical, and bioprostheses) is not part of the present article and is discussed in detail in other contemporary focused articles.

Previous TAVR in patients undergoing percutaneous edge-to-edge mitral valve repair (PMVR) affects improvement of MR.

BACKGROUND: Patients after transcatheter aortic valve replacement (TAVR) and persistent severe mitral regurgitation (MR) are increasingly treated with percutaneous edge-to-edge mitral valve repair (PMVR). The impact of a former TAVR on PMVR procedures is not clear. METHODS AND RESULTS: We retrospectively analyzed 332 patients undergoing PMVR using the MitraClip system with respect to procedural and clinical outcome. 21 of these 332 patients underwent TAVR before PMVR. Intra-procedural transthoracic (TTE) and transesophageal echocardiograms (TEE) immediately before and after clip implantation as well as invasive hemodynamic measurements were evaluated. At baseline, we found a significantly smaller mitral valve anterior-posterior diameter in the TAVR cohort (p < 0.001). A reduction of MR by at least three grades was achieved in a smaller fraction in the TAVR cohort as compared to the cohort with a native aortic valve (p = 0.02). Accordingly, we observed a smaller post-procedural cardiac output in the TAVR cohort (p = 0.02). CONCLUSION: PMVR in patients who had a TAVR before, is associated with altered MR anatomy before and a reduced improvement of MR after the procedure. Future larger and prospective studies will have to determine, whether a previous TAVR influences long-term clinical outcome of patients undergoing PMVR.

Improved mitral valve coaptation and reduced mitral valve annular size after percutaneous mitral valve repair (PMVR) using the MitraClip system.

Aims: Improved mitral valve leaflet coaptation with consecutive reduction of mitral regurgitation (MR) is a central goal of percutaneous mitral valve repair (PMVR) with the MitraClip® system. As influences of PMVR on mitral valve geometry have been suggested before, we examined the effect of the procedure on mitral annular size in relation to procedural outcome. Methods and results: Geometry of the mitral valve annulus was evaluated in 183 patients undergoing PMVR using echocardiography before and after the procedure and at follow-up. Mitral valve annular anterior-posterior (ap) diameter decreased from 34.0 ± 4.3 to 31.3 ± 4.9 mm (P < 0.001), and medio-lateral (ml) diameter from 33.2 ± 4.8 to 32.4 ± 4.9 mm (P < 0.001). Accordingly, we observed an increase in MV leaflet coaptation after PMVR. The reduction of mitral valve ap diameter showed a significant inverse correlation with residual MR. Importantly, the reduction of mitral valve ap diameter persisted at follow-up (31.3 ± 4.9 mm post PMVR, 28.4 ± 5.3 mm at follow-up). Conclusion: This study demonstrates mechanical approximation of both mitral valve annulus edges with improved mitral valve annular coaptation by PMVR using the MitraClip® system, which correlates with residual MR in patients with MR.

Comparison of Deep Sedation With General Anesthesia in Patients Undergoing Percutaneous Mitral Valve Repair.

BACKGROUND: Percutaneous edge-to-edge mitral valve repair (PMVR) has become an established treatment option for mitral regurgitation in patients not eligible for surgical repair. Currently, most procedures are performed under general anesthesia (GA). An increasing number of centers, however, are performing the procedure under deep sedation (DS). Here, we compared patients undergoing PMVR with GA or DS. METHODS AND RESULTS: A total of 271 consecutive patients underwent PMVR at our institution between May 2014 and December 2016. Seventy-two procedures were performed under GA and 199 procedures under DS. We observed that in the DS group, doses of propofol (743±228 mg for GA versus 369±230 mg for DS, P<0.001) and norepinephrine (1.1±1.6 mg for GA versus 0.2±0.3 mg for DS, P<0.001) were significantly lower. Procedure time, fluoroscopy time, and dose area product were significantly higher in the GA group. There was no significant difference between GA and DS with respect to overall bleeding complications, postinterventional pneumonia (4% for GA versus 5% for DS), or C-reactive protein levels (361±351 nmol/L for GA versus 278±239 nmol/L for DS). Significantly fewer patients with DS needed a postinterventional stay in the intensive care unit (96% for GA versus 19% for DS, P<0.001). Importantly, there was no significant difference between DS and GA regarding intrahospital or 6-month mortality. CONCLUSIONS: DS for PMVR is safe and feasible. No disadvantages with respect to procedural outcome or complications in comparison to GA were observed. Applying DS may simplify the PMVR procedure.

Sequential Venous Percutaneous Transluminal Angioplasty and Balloon Dilatation of the Interatrial Septum during Percutaneous Edge-to-Edge Mitral Valve Repair.

Percutaneous edge-to-edge mitral valve repair (PMVR) is widely used for selected, high-risk patients with severe mitral valve regurgitation (MR). This report describes a case of 81-year-old woman presenting with severe and highly symptomatic mitral valve regurgitation (MR) caused by a flail of the posterior mitral valve leaflet (PML). PMVR turned out to be challenging in this patient because of a stenosis and tortuosity of both iliac veins as well as sclerosis of the interatrial septum, precluding the vascular and left atrial access by standard methods, respectively. We managed to achieve atrial access by venous percutaneous transluminal angioplasty (PTA) and balloon dilatation of the interatrial septum. Subsequently, we could advance the MitraClip® system to the left atrium, and deployment of the clip in the central segment of the mitral valve leaflets (A2/P2) resulted in a significant reduction of MR.

Immediate increase of cardiac output after percutaneous mitral valve repair (PMVR) determined by echocardiographic and invasive parameters: Patzelt: Increase of cardiac output after PMVR.

BACKGROUND: Successful percutaneous mitral valve repair (PMVR) in patients with severe mitral regurgitation (MR) causes changes in hemodynamics. Echocardiographic calculation of cardiac output (CO) has not been evaluated in the setting of PMVR, so far. Here we evaluated hemodynamics before and after PMVR with the MitraClip system using pulmonary artery catheterization, transthoracic (TTE) and transesophageal (TEE) echocardiography. METHODS: 101 patients with severe MR not eligible for conventional surgery underwent PMVR. Hemodynamic parameters were determined during and after the intervention. We evaluated changes in CO and pulmonary artery systolic pressure before and after PMVR. CO was determined with invasive parameters using the Fick method (COi) and by a combination of TTE and TEE (COe). RESULTS: All patients had successful clip implantation, which was associated with increased COi (from 4.6±1.4l/min to 5.4±1.6l/min, p<0.001). Furthermore, pulmonary artery systolic pressure (PASP) showed a significant decrease after PMVR (47.6±16.1 before, 44.7±15.5mmHg after, p=0.01). In accordance with invasive measurements, COe increased significantly (COe from 4.3±1.7l/min to 4.8±1.7l/min, p=0.003). Comparing both methods to calculate CO, we observed good agreement between COi and COe using Bland Altman plots. CONCLUSIONS: CO increased significantly after PMVR as determined by echocardiography based and invasive calculation of hemodynamics during PMVR. COe shows good agreement with COi before and after the intervention and, thus, represents a potential non-invasive method to determine CO in patients with MR not accessible by conventional surgery.

Clinical outcome and paravalvular leakage of the new balloon-expandable Edwards Sapien 3 valve in comparison to its predecessor model (Edwards Sapien XT) in patients undergoing transfemoral aortic valve replacement.

OBJECTIVES: The aim of this study was to compare the 30-day procedural, clinical and echocardiographic outcome of the new balloon-expandable Edwards Sapien 3 (ES3) valve with the Edwards Sapien XT (ESXT). BACKGROUND: Post-implant paravalvular leaks (PVL) after transfemoral aortic valve replacement (TAVR) resulting in residual aortic regurgitation (AR) are a major limitation for long term outcome. New TAVR-devices have to eliminate this problem. METHODS: Transfemoral TAVR was performed in 209 consecutive intermediate-high-risk surgical patients (pts) with symptomatic aortic stenosis (ESXT n = 102, ES3 n = 107). Transthoracic echocardiography (TTE) and 3-dimensional computed tomography were used for valve size selection. Primary endpoint of the study was none/trace AR derived by TTE 30-days after TAVR. RESULTS: All pts underwent successfully TAVR with a combined device success of 100/102 (99%) in ESXT and 107/107 (100%) in ES3 pts. Fluoroscopy time (ESXT 11.8 ± 0.5 min vs. ES3 10.0 ± 0.5 min, P = 0.003) and contrast (ESXT 188.9 ± 5.6 mL vs. ES3 170.4 ± 4.7 mL, P = 0.04) were significantly lower in ES3 patients. 30-day clinical events did not differ. Transvalvular mean pressure gradients were significantly reduced to 7.4 ± 0.8 mmHg after ESXT and to 10.1± 0.4 mmHg after ES3 implantation. After 30 days none/trace AR was found in 34.3% (n = 35) of all ESXT pts in contrast to 89.7% (n = 96) of all ES3 patients. Moderate-to-severe AR was found rarely (ESXT 2.9% vs. ES3 0%, P = 0.073). CONCLUSIONS: Although there was no significant difference in 30 day mortality, the newer ES3 valve reduced significantly residual paravalvular leakage. © 2016 Wiley Periodicals, Inc.

Platelet activation is less enhanced in the new balloon expandable Edwards Sapien 3 valve compared to its predecessor model (Edwards Sapien XT).

Stroke and thromboembolic events after transfemoral aortic valve replacement (TAVR) continue to be a problem. The aim of our study was to compare platelet aggregation (Agg) and platelet activation (PA) observed with two different catheter valves, the ESV-XT and the newer ESV-3 valve in patients (pts) undergoing TAVR on dual antiplatelet therapy (DAPT). A total of 174 patients with severe aortic stenosis and high surgical risk successfully underwent TAVR (60 ESV-XT; 114 ESV-3). Platelet Agg and PA (CD62P expression) were evaluated before and the following three days after TAVR under DAPT. Platelet Agg was inhibited to the same extent in both valve types and there was no significant difference in platelet drop between both valve types between day 0 and day 3 [ESV-XT vs ESV-3: median (25th-75th percentile): platelet count (x1000): 55 (42-74) vs 61(42-93), p=0.280]. However, there was an enhanced CD62P expression directly after TAVR with the ESV-XT compared to the ESV-3 [CD62P (MIF): 7.4 (6.8-8.6) vs 6.6 (6-7.9), p=0.014]. Surface expression of platelet CD62P was associated with the occurrence of residual aortic regurgitation (AR) and was significantly higher in patients with residual AR [CD62P (mild AR) vs CD 62P (no or trace AR): 7.9 (7.3-9.1) vs 7.1 (6.4-8.0), p < 0.001)]. PA was significantly enhanced in patients with the ESV-XT compared to the ESV-3 valve and was associated with the amount of residual AR which was significantly reduced by ESV-3. This may have implications for thromboembolic events following TAVR procedure.

Expression of platelet-bound stromal-cell derived factor-1 (SDF-1) and number of CD34(+) progenitor cells in patients with congestive heart failure.

Platelet-bound stromal cell-derived factor-1 (SDF-1) plays a crucial role in attachment of circulating CD34(+) progenitor cells to the vascular wall, facilitating tissue healing after injury. However there is no evidence about expression of platelet-bound SDF-1 in patients with congestive heart failure (CHF). The aim of our study was to evaluate expression of platelet-bound SDF-1 and number of CD34(+) progenitor cells in patients with CHF. Forty-eight patients with idiopathic dilated cardiomyopathy (DCM) and 61 patients with ischaemic cardiomyopathy (ICM) were consecutively enrolled into the study. Blood taken from 109 consecutive patients was studied for surface expression of platelet-bound SDF-1 and number of CD34(+) progenitor cells by flow cytometry. The highest expression of platelet-bound SDF-1 was observed in patients with severe impairment of left ventricular systolic function compared with patients with mild or moderate impairment of left ventricular systolic function (mild vs. moderate vs. severe impairment of left ventricular systolic function: MFI ± SD: 35.6 ± 34 vs. 101.45 ± 73 vs. 124.86 ± 86.7, Kruskal-Wallis p < 0.001). Similar to platelet-bound SDF-1 number of CD34(+) progenitor cells was the highest in severe impairment of left ventricular systolic function (mild vs. moderate vs. severe impairment of left ventricular systolic function: mean ± SD: 260.4 ± 177.5 vs. 580.7 ± 340.5 vs. 640.82 ± 370.6, Kruskal-Wallis p < 0.001). Platelet-bound SDF-1 expression was associated with number of circulating CD34(+) progenitor cells (r = 0.454, p < 0.001) in patients with CHF. Expression of platelet-bound SDF-1 and number of CD34(+) cells were higher in patients with DCM compared with patients with ICM (p < 0.001 for both) and inversely correlated with age and aspirin therapy. Platelet-bound SDF-1 and CD34(+) progenitor cells are especially increased in patients with severe impairment of left ventricular systolic function in CHF.

Gremlin-1 identifies fibrosis and predicts adverse outcome in patients with heart failure undergoing endomyocardial biopsy.

BACKGROUND: Gremlin-1 (Grem1), an antagonist of bone morphogenetic proteins, is involved in fibrotic tissue formation in kidney and lung. The impact of myocardial Grem1 expression is unknown. We investigated the prognostic value of Grem1 expression in 214 consecutive patients with nonischemic heart failure (HF) undergoing endomyocardial biopsy. METHODS: In all patients, the following risk factors were assessed: Grem1 expression (semiquantitative score scheme ranging from 1 to 4), presence of inflammatory markers, detection of viral genome, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), New York Heart Association functional class (NYHA), troponin I, and B-type natriuretic peptide. Degree of myocardial fibrosis was defined as an index. Study end point was a combination of all-cause death and HF-related rehospitalization within 3 years of follow-up. RESULTS: Grem1 expression significantly correlated with the degree of myocardial fibrosis (correlation coefficient r = 0.619; P < .0001). Patients with the highest Grem1 expression (score 4) showed the most severely impaired LVEF and highest LVEDD (P < .0001 and P = .030, respectively, for comparison of semiquantitative scores). During follow-up, 33 patients (15.4%) reached the study end point. Grem1 expression and NYHA ≥II were independent predictors of the end point (Grem1: hazard ratio [HR] 7.5, 95% confidence interval [CI] 1.8-32.2; P = .006; NYHA ≥II: HR 2.0, 95% CI 1.0-4.1; P = .048). CONCLUSIONS: Grem1 correlates with the degree of myocardial fibrosis and left ventricular dysfunction and is an independent predictor of adverse outcome in patients with nonischemic HF.

[Renal failure and recurrent episodes of flash pulmonary edema in a 70-year-old patient]. / Nierenversagen und wiederholte Episoden eines blitzartig auftretenden Lungenödems bei einer 70-jährigen Patientin.

HISTORY AND ADMISSION FINDINGS: We report on a patient presenting with renal failure who developed mutliple episodes of flash pulmonary edema. INVESTIGATIONS: Volume retention due to ischemic nephropathy was found to be the cause. DIAGNOSIS, TREATMENT AND COURSE: She was diagnosed to have a high grade renal artery stenosis in a functional solitary kidney and underwent percutaneous angioplasty. After being anuric and dialysis-dependent, she regained her kidney function leading to resolution of the volume retention and could be weaned from dialysis. CONCLUSIONS: Ischemic nephropathy is often accompanied by recurrent episodes of flash pulmonary edema and responds well to an interventional treatment.

Macrophage migration inhibitory factor is enhanced in acute coronary syndromes and is associated with the inflammatory response.

BACKGROUND: Chronic inflammation promotes atherosclerosis in cardiovascular disease and is a major prognostic factor for patients undergoing percutaneous coronary intervention (PCI). Macrophage migration inhibitory factor (MIF) is involved in the progress of atherosclerosis and plaque destabilization and plays a pivotal role in the development of acute coronary syndromes (ACS). Little is known to date about the clinical impact of MIF in patients with symptomatic coronary artery disease (CAD). METHODS AND RESULTS: In a pilot study, 286 patients with symptomatic CAD (n = 119 ACS, n = 167 stable CAD) undergoing PCI were consecutively evaluated. 25 healthy volunteers served as control. Expression of MIF was consecutively measured in patients at the time of PCI. Baseline levels of interleukin 6 (IL-6), "regulated upon activation, normal T-cell expressed, and secreted" (RANTES) and monocyte chemoattractant protein-1 (MCP-1) were measured by Bio-Plex Cytokine assay. C-reactive protein (CRP) was determined by Immunoassay. Patients with ACS showed higher plasma levels of MIF compared to patients with stable CAD and control subjects (median 2.85 ng/mL, interquartile range (IQR) 3.52 versus median 1.22 ng/mL, IQR 2.99, versus median 0.1, IQR 0.09, p<0.001). Increased MIF levels were associated with CRP and IL-6 levels and correlated with troponin I (TnI) release (spearman rank coefficient: 0.31, p<0.001). Patients with ACS due to plaque rupture showed significantly higher plasma levels of MIF than patients with flow limiting stenotic lesions (p = 0.002). CONCLUSION: To our knowledge this is the first study, demonstrating enhanced expression of MIF in ACS. It is associated with established inflammatory markers, correlates with the extent of cardiac necrosis marker release after PCI and is significantly increased in ACS patients with "culprit" lesions. Further attempts should be undertaken to characterize the role of MIF for risk assessment in the setting of ACS.

Plasma levels of stromal cell-derived factor-1 in patients with coronary artery disease: effect of clinical presentation and cardiovascular risk factors.

OBJECTIVE: To investigate the possible association of plasma levels of stromal cell-derived factor-1 (SDF-1; CXCL12) with clinical presentation of symptomatic coronary artery disease (CAD) and with cardiovascular risk factors. METHODS: A cath lab cohort of 492 consecutive patients with symptomatic CAD were recruited. Blood for plasma-SDF-1 determination was taken at the time of heart catheterization before percutaneous coronary intervention. RESULTS: Plasma-SDF-1 was significantly decreased in ST-elevation myocardial infarction (STEMI) compared to stable angina pectoris (SAP) or to non-ST-elevation myocardial infarction (NSTEMI) (SAP vs. NSTEMI vs. STEMI: [pg/ml]: mean ± SD: 2110 ± 562 vs. 2127 ± 467 vs. 1834 ± 377; P < 0.001) independent of cardiovascular therapy. A weak correlation was observed between cholesterol levels and plasma SDF-1 in the whole study population. Left ventricular function and diabetes mellitus associated with plasma SDF-1 levels in patients with NSTEMI, while among STEMI patients, those with hyperlipidemia presented with even further decreased SDF-1 levels. CONCLUSION: Plasma SDF-1 is significantly decreased in patients with STEMI, a fact which may reflect the importance of SDF-1 regulation in patients with acute myocardial infarction.