Juergen Schreieck

Effects of Mechanical Ventilation on Heart Geometry and Mitral Valve Leaflet Coaptation During Percutaneous Edge-to-Edge Mitral Valve Repair

OBJECTIVES This study sought to evaluate a ventilation maneuver to facilitate percutaneous edge-to-edge mitral valve repair (PMVR) and its effects on heart geometry. BACKGROUND In patients with challenging anatomy, the application of PMVR is limited, potentially resulting in insufficient reduction of mitral regurgitation (MR) or clip detachment. Under general anesthesia, however, ventilation maneuvers can be used to facilitate PMVR. METHODS A total of 50 consecutive patients undergoing PMVR were included. During mechanical ventilation, different levels of positive end-expiratory pressure (PEEP) were applied, and parameters of heart geometry were assessed using transesophageal echocardiography. RESULTS We found that increased PEEP results in elevated central venous pressure. Specifically, central venous pressure increased from 14.0 ± 6.5 mm Hg (PEEP 3 mm Hg) to 19.3 ± 5.9 mm Hg (PEEP 20 mm Hg; p < 0.001). As a consequence, the reduced pre-load resulted in reduction of the left ventricular end-systolic diameter from 43.8 ± 10.7 mm (PEEP 3 mm Hg) to 39.9 ± 11.0 mm (PEEP 20 mm Hg; p < 0.001), mitral valve annulus anterior-posterior diameter from 32.4 ± 4.3 mm (PEEP 3 mm Hg) to 30.5 ± 4.4 mm (PEEP 20 mm Hg; p < 0.001), and the medio-lateral diameter from 35.4 ± 4.2 mm to 34.1 ± 3.9 mm (p = 0.002). In parallel, we observed a significant increase in leaflet coaptation length from 3.0 ± 0.8 mm (PEEP 3 mm Hg) to 5.4 ± 1.1 mm (PEEP 20 mm Hg; p < 0.001). The increase in coaptation length was more pronounced in MR with functional or mixed genesis. Importantly, a coaptation length >4.9 mm at PEEP of 10 mm Hg resulted in a significant reduction of PMVR procedure time (152 ± 49 min to 116 ± 26 min; p = 0.05). CONCLUSIONS In this study, we describe a novel ventilation maneuver improving mitral valve coaptation length during the PMVR procedure, which facilitates clip positioning. Our observations could help to improve PMVR therapy and could make nonsurgical candidates accessible to PMVR therapy, particularly in challenging cases with functional MR.

Percutaneous closure of a periprosthetic leakage after mitral valve reoperation due to recurrent endocarditis

Paravalvular leakage following the atrioventricular valve replacement, though mostly harmless with insignificant morbidity, can result in heart failure and significant hemolysis that requires treatment. Reoperation is still the treatment of choice, but there is a high risk of recurrence, especially in patients with a history of endocarditis and/or those who have already undergone reoperation for paravalvular leakage. Recently, percutaneous closure of perivalvular leaks with occluders or coils have become an alternative to surgery. However, up to now, the collective of patients who benefit from this approach still has to be defined. Here, we present a case of a highly symptomatic 64‐year‐old male with severe hemolysis caused by paravalvular leakages after reoperation of a mechanical mitral valve replacement due to recurrent endocarditis.

Percutaneous Mitral Valve Edge-to-Edge Repair With Simultaneous Biatrial Intracardiac Echocardiography First-in-Human Experience

Recently, we described a percutaneous mitral valve edge-to-edge repair (PMVR) procedure in a patient using both transesophageal echocardiography (TOE) and intracardiac echocardiography (ICE).1 In that patient, however, central steps of PMVR were guided primarily by TOE. Advantages of intracardiac echocardiography are avoidance of TOE and thus general anesthesia. The procedure can be performed in a conscious patient. Accordingly, the need for catecholamines, the risk of hypotension, prolonged periods of weaning from mechanical ventilation, and postinterventional delirium are reduced. Although in theory the use of left atrial ICE is sufficient to guide PMVR, ICE has not been used as the only imaging modality to guide PMVR because of disadvantages such as the lack of 3-dimensional (3D) vision with X-plane views and particularly the lack of experience using ICE for PMVR. Here, we report a PMVR procedure in a patient with functional mitral regurgitation (MR) using ICE because TOE guidance was not possible. A 78-year-old patient presented with decompensated heart failure with MR grade IV (Figure, A and B). He had a history of repeated hospitalizations for heart failure caused by ischemic cardiomyopathy with severely reduced left ventricular function. An internal cardioverter-defibrillator had been implanted because he had repeated ventricular arrhythmias. As a result of severe comorbidities, a decision for PMVR was made by our interdisciplinary heart team. TOE was not possible (even with endoscopic guidance) because …

Percutaneous Edge-to-Edge Mitral Valve Repair Escorted by Left Atrial Intracardiac Echocardiography (ICE)

Percutaneous mitral valve repair (PMVR) using the MitraClip system is an innovative method allowing treatment of mitral regurgitation (MR) for a patient that is not accessible by conventional operation.1 Consequently, novel pitfalls and obstacles become apparent. PMVR is generally performed under transesophageal echocardiographic guidance. However, in some patients, visualization of structures by transesophageal echocardiography (TOE) is not sufficient. Furthermore, as a consequence of continuous TOE during PMVR, general anesthesia and or tracheal intubation are required and represent a major weaknesses of the procedure, bringing about drops in blood pressure, potential aspiration, or neurological disorders to these frail patients. Intracardiac echocardiography (ICE) from the right atrium has been shown to be a safe imaging method during procedures such as atrial septal defect or complex PFO closure.2 Here, we report visualization of a PMVR procedure via left atrial ICE. A 76-year-old man with a grade-IV functional mitral valve regurgitation (Figure, A) and severely impaired left ventricular (LV) function (LV ejection fraction, 30%) resulting from dilated cardiomyopathy was admitted to our intensive care unit with recurrent left ventricular decompensation. He had recently had multiple implantable cardioverter defibrillator shocks as a …

Inhibition of the renin-angiotensin system: effects on tachycardia-induced early electrical remodelling in rabbit atrium

Introduction. Tachycardia-induced atrial remodelling (as an equivalent to atrial fibrillation) can be influenced by the renin-angiotensin system. Effects of a seven-day enalapril pre-treatment (EPT, 0.16 mg/kg body weight subcutaneously every 24 h) on ionic currents underlying tachycardia-induced early electrical remodelling after 24 h rapid atrial pacing (RAP, 600 beats/min) in rabbit atrium were studied. Materials and methods. Animals were divided into four groups (n=4 each): control; paced only; enalapril only; and enalapril and paced, respectively. Using patch-clamp technique in whole-cell mode, current densities were measured in isolated atrial myocytes. Results. EPT nearly doubled L-type calcium current (ICa,L, −7.7±0.6 pA/pF [control] vs. f −12.3±1.2 pA/pF [enalapril only]). RAP reduced ICa,L to −3.6±0.7 pA/pF (paced only). Also after EPT, RAP led to a significant downregulation of ICa,L by 39% (−7.5±1.3 pA/pF [paced and enalapril]). RAP decreased transient outward potassium current (Ito, −45%, 51.5±3.9 pA/pF [control] vs. 28.5±4.5 pA/pF [paced only]). EPT did not alter Ito (44.2±8.1 pA/pF [enalapril only]). However, RAP did not affect Ito in enalapril-treated animals and averaged 50.4±9.8 pA/pF (paced and enalapril). Conclusions. In summary, EPT has several effects on ion channels in rabbit atrium: 1) EPT increases ICa,L current density, but cannot prevent its downregulation due to RAP; 2) EPT has no influence on Ito current density, but can prevent its downregulation due to RAP. Although changes of single ion channels must be interpreted in context of the complex atrial electrophysiology as a whole, our results provide a possible explanation of the in vivo observation that angiotensin-converting enzyme inhibition is mainly beneficial on the early electrical remodelling due to the atrial fibrillation-equivalent RAP.

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.

Comparison of Ventricular Inducibility with Late Gadolinium Enhancement and Myocardial Inflammation in Endomyocardial Biopsy in Patients with Dilated Cardiomyopathy.

Background Risk stratification of patients with non-ischemic dilated cardiomyopathy remains a matter of debate in the era of device implantation. Objective We investigated associations between histopathological findings, contrast-enhanced cardiac MRI and the inducibility of ventricular tachycardia (VT) or fibrillation (VF) in programmed ventricular stimulation. Methods 56 patients with impaired left ventricular ejection fraction (LVEF≤50%, mean 36.6±10.5%) due to non-ischemic dilated cardiomyopathy underwent cardiac MRI, programmed ventricular stimulation, and endomyocardial biopsy and were retrospectively investigated. Inducibility was defined as sustained mono- or polymorphic VT or unstable VT/VF requiring cardioversion/defibrillation. Primary study endpoint was defined as the occurrence of hemodynamically relevant VT/VF and/or adequate ICD-therapy during follow-up. Results Endomyocardial biopsy detected cardiac fibrosis in 18 (32.1%) patients. Cardiac MRI revealed 35 (62.5%) patients with positive late gadolinium enhancement. VT/VF was induced in ten (17.9%) patients during programmed ventricular stimulation. Monomorphic VT was inducible in 70%, while 20% of patients showed polymorphic VT. One patient (10%) presented with VF. Inducibility correlated significantly with the presence of positive late gadolinium enhancement in cardiac MRI (p<0.01). We could not find a significant association between inducibility and the degree of cardiac inflammation and fibrosis in non-site directed routine right ventricular endomyocardial biopsy. During a mean follow-up of 2.6 years, nine (16.1%) patients reached the primary endpoint. Monomorphic VTs were found in 66.7% patients and were terminated by antitachycardia pacing therapy. One patient with polymorphic VT and two patients with VF received adequate therapy by an ICD-shock. However, inducibility did not correlate with the occurrence of endpoints. Conclusion Inducibilty during programmed ventricular stimulation is associated with positive late gadolinium enhancement in cardiac MRI of patients with non-ischemic dilated cardiomyopathy. The presence of myocardial fibrosis or inflammation in undirected endomyocardial biopsy does not seem to be sufficient to predict future ventricular arrhythmias.

Influence of dexamethasone on atrial ion currents and their early ionic tachycardia-induced electrical remodeling in rabbits.

Background: Certain evidence points to a role of inflammation in AF pathophysiology. Thus, antiinflammatory treatment of AF is discussed. Effects of a dexamethasone treatment (7 days) on atrial ion currents (ICa,L, Ito, Isus) and their tachycardia-induced remodeling were studied in a rabbit model. Methods: 6 groups of 4 animals each were built. Rapid atrial pacing (600 min) was performed for 24 and 120 hours with/ without dexamethasone treatment. Ion currents were measured using whole cell patch clamp method. Results: Rapid atrial pacing reduced (ICa,L, Ito was decreased after 24 hours but almost returned to control values after 120 hours. When dexamethasone-treated animals also underwent atrial tachypacing, pacing-induced reduction of ICa,L was still observed after 24 hours and was even augmented after 120 hours compared to untreated but tachypaced animals. Ito was not influenced by dexamethasone alone. In dexamethasone-treated animals, reduction of Ito was not observed after 24 hours but occurred after 120 hours of atrial tachypacing. Isus was neither influenced by rapid atrial pacing nor by dexamethasone. Biophysical properties of all currents were affected neither by rapid atrial pacing nor by dexamethasone. Conclusion: Dexamethasone influenced tachycardia-induced alterations of atrial Ito. Our experiments give evidence that - amongst other anti-inflammatory action – impact of dexamethasone on ion currents and their tachycardia-induced alterations might also play a role in treatment/prevention of AF with steroids.

Genetic Polymorphisms as Risk Stratification Tool in Primary Preventive ICD Therapy

More and more implantable cardioverter-defibrillators (ICDs) are implanted as primary prevention of sudden cardiac death (SCD). However, major problem in practice is to identify high-risk patients for SCD. Different methods for noninvasive risk stratification do not have a sufficient positive or negative predictive value. Since current approaches lead to implantation of ICDs in a large number of patients who will never suffer an arrhythmic event and simultaneously patients still die of SCD who currently did not seem eligible for primary preventive ICD implantation, there is a need for additional tools for risk stratification. Epidemiological studies point to a hereditary risk of SCD. Different susceptibility of each person concerning arrhythmogenic events might be explained by genetic polymorphisms. By obtaining an individual “pattern” of polymorphisms of genes encoding for proteins which are important in arrhythmogenesis in one patient, risk stratification in primary prevention of SCD might by improved.

First Experience with the MitraClip XTR® Compared to the MitraClip NTR® System in a Patient with Severe Mitral Regurgitation and Complex Mitral Valve Anatomy

Percutaneous edge-to-edge mitral valve repair (PMVR) is a successful treatment option in patients with severe mitral regurgitation (MR) not eligible for conventional open surgery. There are two new MitraClip® systems available (Abbott Vascular, Wetzlar, Germany), the MitraClip XTR® and the MitraClip NTR®. While the latter has the same clip geometry as the contemporary MitraClip NT® system, the XTR® system has longer clip-arms (extended 3 mm of length for each arm) and improved grippers with two additional rows of frictional elements. Here, we report the case of a patient with complex mitral valve anatomy and severe MR. While grasping with the NTR® system was difficult, we experienced a straightforward implantation using the XTR® system instead. The patient presented with a history of repeated hospitalization due to decompensated heart failure. Echocardiography showed a good systolic left ventricular (LV) function with severe primary MR with a prolapse of the anterior mitral valve (MV) leaflet (AML) in segment 2 with an eccentric posterior-directed jet (Figure 1A,B). Furthermore, calcifications were present with a restrictive posterior MV leaflet (PML) (Figure 1C). 3D EROA (effective regurgitant orifice area) was measured as 1.46 cm (Figure 1D). A decision for PMVR was made by our interdisciplinary heart team due to severe comorbidities. Although in difficult mitral valve anatomies mechanical ventilation with elevated positive endexpiratory pressure may facilitate PMVR, we chose to carry out the intervention in conscious sedation considering the frailty of our patient. First, a MitraClip NTR® was advanced and positioned underneath the mitral valve plane. However, due to the prolapse of the AML and the restrictive PML, no sufficient grasp of both leaflets could be promptly achieved. Thus, the MitraClip NTR® was removed and a MitraClip XTR® was introduced, instead. In our experience, the location of the transseptal puncture does not differ between the NTR® and the XTR® clip. Due to its extended arms, sufficient leaflet material could be loaded rather easily on both arms of the device (Figure 1E). 3D view of the mitral valve confirmed optimal orientation of the opened clip device (Figure 1F) and implantation of the clip resulted in good coaptation and a clear reduction of MR. Subsequently, a second MitraClip XTR® (Figure 1G) further improved the result with only mild residual MR (Figure 1H). 3D EROA showed two small residual regurgitant orifices with a total area of 0.26 cm (Figure 1I).