Endothelial progenitor cells and plaque burden in stented coronary artery segments: an optical coherence tomography study six months after elective PCI.

BACKGROUND: Endothelial progenitor cells (EPC) are involved in neovascularization and endothelial integrity. They might be protective in atherosclerosis. Optical coherence tomography (OCT) is a precise intracoronary imaging modality that allows assessment of subintimal plaque development. We evaluated the influence of EPC on coronary plaque burden in stable disease and implemented a novel computational plaque analysis algorithm using OCT. METHODS: Forty-three patients (69.8% males, 69.6 ± 7.7 years) were investigated by OCT during re-angiography 6 months after elective stent implantation. Different subpopulations of EPCs were identified by flow cytometry according to their co-expression of antigens (CD34+, CD133+, kinase domain receptor, KDR+). An algorithm was applied to calculate the underlying total plaque burden of the stented segments from OCT images. Plaque morphology was assessed according to international consensus in OCT imaging. RESULTS: A cumulative sub-strut plaque volume of 10.87 ± 12.7 mm3 and a sub-stent plaque area of 16.23 ± 17.0 mm2 were found within the stented vessel segments with no significant differences between different stent types. All EPC subpopulations (mean of EPC levels: CD34+/CD133+: 2.66 ± 2.0%; CD34+/KDR+: 7.50 ± 5.0%; CD34+/CD133+/KDR+: 1.12 ± 1.0%) inversely correlated with the identified underlying total plaque volume and plaque area (p ≤ 0.012). CONCLUSIONS: This novel analysis algorithm allows for the first time comprehensive quantification of coronary plaque burden by OCT and illustration as spread out vessel charts. Increased EPC levels are associated with less sub-stent coronary plaque burden which adds to previous findings of their protective role in atherosclerosis.

The transcatheter valve technology pipeline for treatment of adult valvular heart disease.

The transcatheter valve technology pipeline has started as simple balloon valvuloplasty for the treatment of stenotic heart valves and evolved since the year 2000 to either repair or replace heart valves percutaneously with multiple devices. In this review, the present technology and its application are illuminated and a glimpse into the near future is dared from a physician's perspective.

Decrease in circulating plasmacytoid dendritic cells during short-term systemic normobaric hypoxia.

BACKGROUND: During exposure to high altitude, the immune system is altered. During hypoxia, an increase in interleukin (IL)-6 and high sensitivity C-reactive protein (hs-CRP), and an increase in natural killer cells and decrease in T cells in blood was shown. However, the impact of hypoxia on dendritic cells has not been investigated yet. MATERIAL AND METHODS: Twelve healthy volunteers were subjected to a transient normobaric hypoxia for 6·5 h simulating an oxygen concentration at 5500 m. During exposure to hypoxia, blood samples were collected and analysed by flow cytometrical cell sorting (FACS) for circulating myeloid (mDCs) and plasmacytoid (pDCs) DCs. Serum levels of IL-6 and tumour necrosis factor (TNF)-α were analysed. In a cell culture hypoxia chamber, blood samples were subjected to the same hypoxia and analysed regarding DCs. RESULTS: Exposure to normobaric hypoxia induced a significant decrease in circulating pDCs about 45% (P = 0·001) but not of mDC compared to baseline normoxia. Furthermore, we observed a significant increase of TNF-α about 340% (P = 0·03) and of IL-6 about 286% (P = 0·002). In cell culture experiments exposure of blood to hypoxia led to no significant changes in DCs, so that a direct cytotoxic effect was excluded. During hypoxia, we observed a transient increase in stromal-derived factor 1 (SDF-1) which is important for pDC tissue recruitment. CONCLUSIONS: We show a significant decrease in circulating pDCs during hypoxia in parallel to a pro-inflammatory response. Further studies are necessary to evaluate whether the decrease in circulating pDCs might be the result of an enhanced tissue recruitment.

Transcatheter treatment of tricuspid regurgitation by caval valve implantation--experimental evaluation of decellularized tissue valves in central venous position.

BACKGROUND: Caval valve implantation has been suggested for transcatheter treatment of severe tricuspid regurgitation (TR). Combining the interventional technique with the promising surgical experience with decellularized valves, we sought to evaluate the functional and structural outcome of decellularized pericardial tissue valves (dTVs) in the low-pressure venous circulation in a chronic model of TR. METHODS AND RESULTS: Sixteen pericardial tissue valves were heterotopically implanted in the inferior and superior vena cava in a sheep model (54-98 kg; median 74.5 kg, n = 8) of severe TR. The devices were assembled using self-expanding nitinol stents and bovine pericardia decellularized by a detergent-based protocol (group dTV; n = 8). Glutaraldehyde-fixed pericardial tissue valves served as control (GaTV, n = 8). After 6 months, device function and structural maturation were analyzed using echocardiographic, histologic, immunohistologic, and electron microscopic approaches. After implantation, cardiac output increased significantly from 3.7 ± 1.1 l/min to 4.8 ± 1.1 l/min (P < 0.05) and competent valve function was verified by angiography. At 6 months, angiographic and echocardiographic evaluation revealed moderate to severe regurgitation in all GaTV. In contrast, five of the eight dTVs functioned well with only minor regurgitation. In these animals, autopsy revealed preserved valve structure with tender leaflets without signs of thrombosis or calcification. Conversely, GaTV showed severe degeneration with large calcification areas. Microscopic and histologic analysis confirmed endothelial repopulation in both valve types. However, additional interstitial reseeding was observed in decellularized valves. CONCLUSIONS: In the venous circulation in severe TR, decellularized valves show superior functional performance compared to Ga-fixed tissue valves. Macroscopic and microscopic analyses suggest preserved structural integrity and advanced endothelial and interstitial repopulation with evidence of less degradation in dTV. © 2014 Wiley Periodicals, Inc.

Decrease in circulating dendritic cell precursors in patients with peripheral artery disease.

Peripheral artery disease (PAD) is a common manifestation of atherosclerosis. Inflammation is important for initiation and progression of the disease. Dendritic cells (DCs) as antigen-presenting cells play an important role in the immune system. Therefore, we hypothesize that, in patients with PAD, DCPs might be reduced in blood due to their recruitment into the vascular wall and induce a proinflammatory response. The numbers of myeloid DCPs, plasmacytoid DCPs, and total DCPs were analyzed by flow cytometry in blood of patients with PAD (n = 52) compared to controls (n = 60). Femoralis plaques (n = 12) of patients who underwent surgery were immunostained for CD209 and CD83 (mDCs) as well as CD304, CD123 (pDCs), and HLA-DR. In patients with PAD, a significant decrease in mDCPs, pDCPs, and tDCPs was observed. In immunostaining, markers indicative for mDCs (CD209: 16 versus 8 cells/0.1 mm(2), P = 0.02; CD83: 19 versus 5 cells/0.1 mm(2), P = 0.03) were significantly elevated in femoralis plaques compared to control vessels. We show for the first time that mDCPs, pDCPs, and tDCPs are significantly reduced in patients with PAD. Immunohistochemical analysis unraveled that the decrease in DCPs might be due to their recruitment into atherosclerotic plaques.

Increased arginase levels contribute to impaired perfusion after cardiopulmonary resuscitation.

OBJECTIVES: The postcardiac arrest syndrome occurs after global hypoxia leading to microcirculatory impairment. Nitric oxide (NO) is a key molecule regulating microvascular function. The enzyme arginase has been suggested to modulate microvascular function by regulating NO metabolism. Therefore, we investigated whether arginase increases following global hypoxia and resuscitation and tested whether arginase inhibition influences altered microcirculation in resuscitated patients. METHODS: To determine the effect of global hypoxia on circulating arginase levels, fourteen healthy subjects were exposed to hypoxia in a normobaric hypoxia chamber (FiO² = 9·9%). In addition, 31 resuscitated patients were characterized clinically, and arginase 1 was measured on days 1 and 3. In eight resuscitated patients, a microcirculatory analysis was performed using a sidestream darkfield microcirculation camera. Perfused capillary density (PCD) was recorded before and after sublingual incubation of N-omega-hydroxy-nor-l-arginine (nor-NOHA) alone or together with the NOS inhibitor NG-monomethyl-l-arginine (l-NMMA). RESULTS: Circulating arginase 1 levels increased in healthy volunteers following global hypoxia in the hypoxic chamber (P < 0·01). In addition, arginase 1 levels were higher on day 1 (69·1 ± 83·3 ng/mL) and on day 3 (44·2 ± 65·6 ng/mL) after resuscitation than in control subjects (P < 0·001). Incubation of the sublingual mucosa with nor-NOHA increased microcirculatory perfusion (P < 0·001). This effect was inhibited by co-incubation with K-NMMA. CONCLUSIONS: Circulating arginase 1 levels are increased following exposure to global hypoxia and in patients who have been successfully resuscitated after cardiac arrest. Topical arginase inhibition improves microcirculatory perfusion following resuscitation. This is of potential therapeutic importance for the postcardiac arrest syndrome.

Cryptogenic left main thrombosis: successful mechanical clot retrieval with a self-expanding trapping device.

We present the case of a 52-year-old male with ST-segment elevation myocardial infarction due to a spontaneous large left main thrombosis, without any angiographic evidence for coronary artery disease. After multiple unsuccessful attempts of thrombaspiration the large clot was mechanically retrieved by a flow restoration device that was primarily made for intracranial interventions. Intravascular ultrasound revealed marginal lumen narrowing after the intervention, but the final coronary angiogram showed a patent left main and there was no relevant stenosis remaining.

Valve-in-valve transcatheter aortic valve implantation: the new playground for prosthesis-patient mismatch.

Transcatheter aortic valve implantation (TAVI) has become an established procedure for patients with aortic valve stenosis and significant comorbidities. One option offered by this technique is the implantation of a transcatheter valve inside a surgically implanted bioprosthesis. Many reports address the feasibility but also the pitfalls of these valve-in-valve (VIV) procedures. Review articles provide tables listing which valve sizes are appropriate based on the size of the initially implanted bioprosthesis. However, we previously argued that the hemodynamic performance of a prosthetic tissue valve is in large part a result of the dimensions of the bioprosthesis in relation to the patient's aortic outflow dimensions. Thus, the decision if a VIV TAVI procedure is likely to be associated with a favorable hemodynamic result cannot safely be made by looking at premade sizing tables that do not include patient dimensions and do not inquire about the primary cause for bioprosthetic valve stenosis. Prosthesis-patient mismatch (PPM) may therefore be more frequent than expected after conventional aortic valve replacement. Importantly, it may be masked by a potentially flawed method assessing its relevance. Such PPM may therefore impact significantly on hemodynamic outcome after VIV TAVI. Fifteen percent of currently published VIV procedures show only a minimal reduction of pressure gradients. We will address potential pitfalls in the current determination of PPM, outline the missing links for reliable determination of PPM, and present a simplified algorithm to guide decision making for VIV TAVI.

Increased levels of circulating arginase I in overweight compared to normal weight adolescents.

BACKGROUND AND AIMS: Overweight and the metabolic syndrome have become major problems, especially in children and adolescents. Obesity at a young age increases the risk for cardiovascular diseases and diabetes mellitus later in life. An early event in the development of cardiovascular disease is endothelial dysfunction which is found in obese young individuals. Increased activity of the enzyme arginase has been described as a central mechanism for endothelial dysfunction, especially in patients with diabetes mellitus. The aim of the study was to determine plasma levels of arginase in overweight adolescents. METHODS: Sixty-six male German adolescents (age: 15.2 ± 1.1 years old) were included. Thirty-one of them were overweight (>90th age-specific weight percentile). Plasma arginase I and tumor necrosis factor alpha (TNFα) were determined. In addition, clinical data were recorded and anthropometrical measurements of obesity were performed. RESULTS: Overweight adolescents had a higher systolic blood pressure, lower high-density lipoprotein and increased levels of high-sensitive C-reactive protein (CRP). Circulating arginase I was elevated in overweight adolescents (95.8 ± 68.2 ng/ml) compared to normal weight adolescents (39.3 ± 26.9 ng/ml, p < 0.001) and correlated with markers of obesity. There was no difference between the two groups regarding TNFα. CONCLUSIONS: We demonstrate that arginase I levels are increased in obese adolescents. Knowing the important role for arginase in endothelial dysfunction, elevated levels of arginase I may represent a link between obesity, endothelial dysfunction and related comorbidities.

Microembolization and myonecrosis during elective percutaneous coronary interventions in diabetic patients: an intracoronary Doppler ultrasound study with 2-year clinical follow-up.

Elevation of cardiac troponin I (cTnI) is a well-known complication after percutaneous coronary interventions (PCI). The aims of this study were to quantify the extent of coronary microembolization during elective PCI, to identify predisposing anatomical and procedural factors, and to evaluate its impact on long-term outcome in diabetic patients with a high cardiovascular risk. 48 patients (pts, median 66.7 years) with type 2 diabetes and coronary artery disease underwent elective PCI with stenting to treat single-vessel lesions. Real-time microembolization during PCI ("HITS") was detected by an intracoronary Doppler guide wire. Peak levels of cTnI were measured within 24 h after PCI. Pts were followed for 2 years to record major cardiac events (MACE: death, myocardial infarction, revascularization of target and non-target vessels). In 47 patients microemboli were detected during PCI. Nineteen patients showed pathologic cTnI elevation (0.13-28.9, median 0.39 µg/l). The amount of HITS correlated with cTnI levels (r = 0.43, p = 0.003), but not with other clinical or angiographic data. Within 2 years MACE were detected in 9 patients, who had significantly more microemboli (15.4 ± 11.8 vs. 28.2 ± 16.0 HITS; p = 0.009, OR 1.07; 95 % CI 1.011-1.13) during PCI. HITS >23, but not cTnI elevation, predicted later MACE (ROC analysis, p = 0.025). A high amount of microembolization during elective PCI in diabetic patients appears to be an indicator of greater atherosclerotic burden and accelerated coronary artery disease progression, associated with acute biomarker elevation and adverse long-term outcomes.

Testosterone deficiency in male heart failure patients and its effect on endothelial progenitor cells.

BACKGROUND: Endothelial progenitor cells (EPCs) are thought to contribute to reendothelialization and neoangiogenesis. Since it is known that EPCs express a testosterone receptor, we wanted to assess the prevalence of testosterone deficiency in patients with CHF and its impact on circulating EPCs. METHODS: 137 male patients with chronic heart failure (CHF) were included (age 61 ± 13 years; BMI 29 ± 5 kg/m(2); New York Heart Association classification (NYHA) I: n = 47, NYHA II: n = 51, NYHA III: n = 39). Numbers of different populations of circulating EPCs were quantified using flow cytometry. Levels of free testosterone and EPC-regulating cytokines were determined using ELISA. RESULTS: The prevalence of testosterone deficiency in our University CHF clinic was 39%. However, there was no difference between patients with and without testosterone deficiency regarding their levels of EPCs. Testosterone levels were inversely correlated with age (R(2) = -0.32, p = 0.001) and NYHA status (R(2) = 0.28, p = 0.001) and correlated with cardiorespiratory capacity (R(2) = 0.26, p = 0.03). CONCLUSION: Testosterone deficiency is frequent in male patients with CHF but does not appear to impact the regenerative EPCs.

Optimization of the atrioventricular delay during cardiac resynchronization therapy using a device for non-invasive measurement of cardiac index at rest and during exercise.

AIMS: It is not clear whether cardiac resynchronization therapy (CRT) should only be optimized at rest or whether it is necessary to perform CRT optimization during exercise. Our study aims to answer this question by using an inert gas rebreathing method (Innocor®). METHODS AND RESULTS: Twenty-seven patients with congestive heart failure and implanted CRT devices were included in the study. The aetiology of the heart failure was ischaemic in nine (33%) patients. Patients had low left ventricular ejection fraction (29 ± 8%) and enlarged LV end-diastolic diameters (63 ± 7 mm). Atrioventricular delay (AVD) was optimized at rest according to cardiac index (CI), measured by inert gas rebreathing (Innocor®). Thereafter, patients performed standardized, steady-state bicycle exercise at 30 W in sitting body position. Three AVDs were tested during exercise in a random sequence: optimized resting AVD (AVD(opt)) according to baseline measurement; AVD(opt) - 30 ms; and AVD(opt) + 30 ms. Cardiac index was measured in each AVD by inert gas rebreathing. Cardiac index increased significantly during exercise. However, neither AVD(opt) shortening nor prolongation during exercise had significant effect on CI (shortening of AVD(opt) - 30 ms was accompanied by a reduction of CI of 4.8%, prolongation of AVD(opt) + 30 ms was accompanied by a reduction of CI of 7.7%). CONCLUSION: Shortening or lengthening of the AVD during exercise has no impact on CI in CRT patients. On the basis of our results, we conclude that in CRT patients the AVD should be programmed, fixed even during exercise.

Left atrial endocarditis as a rare complication of mitral valve endocarditis: a clinical case.

BACKGROUND: Infective Endocarditis (IE) is considered as a multifaceted problem in every aspect from etiology and presentation to diagnosis and management. Early recognition of this disease and especially its complications, remain a critical task for the cardiologist. Atrial endocarditis is a rare and sometimes unrecognized complication of mitral valve endocarditis. CASE PRESENTATION: We present a 48 year-old male patient who was admitted to our clinic because of recent onset of malaise, fever, jaundice and peripheral edema. Important physical findings were peripheral stigmata of IE in addition to holosystolic murmur over the left sternal border. Transthoracic and transesophageal echocardiophy revealed a severe eccentric MR due to a flailed posterior mitral valve caused by IE. The presence of atrial septal endocarditis caused by jet streaming was also observed. Blood culture was positive for streptococcus oralis and antibiotic therapy was immediately initiated. Considering the large burden of infective tissue, the patient was planned for an early surgical intervention. A minimally invasive resection of the atrial mass, direct closure of the defect, resection of the diseased portions of mitral leaflets and implantation of a biological mitral valve prosthesis was performed. Intra-operative and histological findings confirmed provisional diagnosis by echocardiography. CONCLUSIONS: Together with comprehensive echocardiographic evaluation, attention should be placed on mural vegetations and excluded among all cases of mitral valve endocarditis, particularly those with severe eccentric regurgitant jets.

Blood pressure variability as sign of autonomic imbalance in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: The problem of identifying idiopathic dilated cardiomyopathy (IDC) patients who are at risk of sudden death is still unsolved. The presence of autonomic imbalance in patients with IDC might predict sudden death and tachyarrhythmic events. The aim of this study was to analyze the suitability of blood pressure variability (BPV) compared to heart rate variability (HRV) for noninvasive risk stratification in IDC patients. METHODS: Continuous noninvasive blood pressure and high-resolution electrocardiogram were recorded from 91 IDC patients for 30 minutes. During a median follow-up period of 28 months (range: [17-38] months), 14 patients died due to sudden death or necessary resuscitation due to a life-threatening arrhythmia. HRV and BPV analyses were performed in time domain, frequency domain, and nonlinear dynamics. Using the Mann-Whitney U test and Cox regression, we estimated the accuracy of clinical and nonclinical parameters in discriminating high-risk from low-risk patients. RESULTS: Dynamics of blood pressure regulation was significantly changed in high-risk patients, indicating an increased BPV. BPV indexes from nonlinear symbolic dynamics revealed significant univariate (sensitivity: 85.7%; specificity 77.9%; area under receiver-operator characteristics [ROC] curve: 87.8%) differences. In an optimum multivariate set consisting of two clinical indexes (left ventricular end-diastolic diameter, New York Heart Association) and one nonlinear index (symbolic dynamics), highly significant differences between low- and high-risk IDC groups were estimated (sensitivity of 92.9%, specificity of 86.5%, and area under ROC curve of 95.3%). CONCLUSION: Diastolic BPV indexes, especially those from symbolic dynamics, appear to be useful for risk stratification of sudden death in patients with IDC.

Impact of diabetes mellitus on quality of life in patients with congestive heart failure.

OBJECTIVES: Congestive heart failure (CHF) and diabetes mellitus (DM) are increasing in prevalence. There are conflicting data regarding the crosstalk of DM and CHF with respect to the prognostic impact for the patients. Health-related quality of life (Hr-QoL) has been reported to be useful for risk stratification. The purpose of this study was to investigate the impact of DM on Hr-QoL in a CHF population. METHODS: 325 consecutive patients with CHF were retrospectively analyzed (age 49 ± 12 years, 74.2% male, 18% had diabetes). After a median follow-up time of 7.4 years, we compared Hr-QoL of patients with and without DM. Hr-QoL was assessed using the Minnesota Living with Heart Failure Questionnaire (MLHFQ). Kaplan-Meier curves were used to compare survival. RESULTS: The presence of DM reduced Hr-QoL in patients with CHF, indicated by a higher overall MLHFQ score (43.5 vs. 21, P = 0.013). Kaplan-Meier survival curves showed a significant survival difference (P = 0.024). Survival rates of both groups differed significantly after 3 (P = 0.031), 5 (P = 0.006), and 10 years (P = 0.047) favoring the group without DM. CONCLUSIONS: In patients with CHF, the coexistence of DM is associated with a reduced Hr-QoL and a particularly poor long-term survival. Our results indicate that CHF patients with DM are at increased risk.

Detection of coronary microembolization by Doppler ultrasound in patients with stable angina pectoris during percutaneous coronary interventions under an adjunctive antithrombotic therapy with abciximab: design and rationale of the High Intensity Transient Signals ReoPro (HITS-RP) study.

BACKGROUND: Embolization of atherosclerotic debris from the rupture of a vulnerable atherosclerotic plaque occurs iatrogenically during percutaneous coronary interventions (PCI) and can induce myocardial necrosis. These microembolizations are detected as high intensity transient signals (HITS) using intracoronary Doppler technology. PRESENTATION OF THE HYPOTHESIS: In the presented study we will test if abciximab (ReoPro®) infusion reduces high intensity transient signals in patients with stable angina pectoris undergoing PCI in comparison to standard therapy alone. TESTING THE HYPOTHESIS: The High Intensity Transient Signals ReoPro® (HITS-RP) study will enroll 60 patients. It is a prospective, single center, randomized, double-blinded, controlled trial. The study is designed to compare the efficacy of intravenous abciximab administration for reduction of microembolization during elective PCI. Patients will be randomized in a 1:1 fashion to abciximab or placebo infusion. The primary end point of the HITS-RP-Study is the number of HITS during PCI measured by intracoronary Doppler wire. Secondary endpoints are bleeding complications, elevation of cardiac biomarkers or ECG changes after percutaneous coronary interventions, changes in coronary flow velocity reserve, hs-CRP elevation, any major adverse cardio-vascular event during one month follow-up. IMPLICATIONS OF THE HYPOTHESIS: The HITS-RP-Study addresses important questions regarding the efficacy of intravenous abciximab administration in reducing microembolization and periprocedural complications in stable angina pectoris patients undergoing PCI. TRIAL REGISTRATION: The trial is registered under http://www.drks-neu.uniklinik-freiburg.de/drks_web/:DRKS00000603.

Immunomodulatory effects of cardiotrophin-1 on in vitro cytokine production of monocytes & CD4 + T-lymphocytes.

BACKGROUND & OBJECTIVES: In congestive heart failure (CHF), increased concentrations of several cytokines including cardiotrophin-1 (CT-1) and immunactivation are found. This study was performed to evaluate whether CT-1 can induce in vitro cytokines in monocytes and CD4 + T-lymphocytes of healthy volunteers. METHODS: The study was performed in vitro to see whether CT-1 can modulate monocyte or CD4 + T-lymphocyte interleukin (IL)-1ß, -2, -4, -5, -10, interferon γ (IFNγ), and tumour necrosis factor α (TNFα) expression by flow cytometry following stimulation with CT-1 alone or together with lipopolysaccharide (LPS) or phorbol myristate acetate (PMA)/ionomycine (iono). RESULTS: CT-1 increased the number of TNFα and IL-1ß positive monocytes. LPS induced IL-10, TNFα, and IL-1ß in monocytes but only IL-2 in CD4+ T-lymphocytes, whereas PMA/iono induced all cytokines besides IL-5 in monocytes and IL-1ß in CD4+ T-lymphocytes. In LPS activated monocytes, CT-1 induced a concentration-dependent reduction in the number of TNFα positive monocytes. After LPS activation, CT-1 decreased the number of CD4+ lymphocytes positive for IL-2, IL-4, and IL-5. In addition, following PMA/iono stimulation, CT-1 initiated a concentration-dependent decrease of CD4 + T-lymphocytes positive for TNFα, IL-4, IL-5, and IL-10. INTERPRETATION & CONCLUSIONS: The present data show that in vitro CT-1 can activate monocytes and modulate cytokine production of activated CD4 + T-lymphocytes. We speculate that CT-1 may at least be partly responsible for immunactivation in CHF.

Cardiac magnetic resonance imaging as a tool to link cardiac conduction disease to myocarditis with minimal left ventricular impairment.

Myocarditis is an injury of the myocardium caused by a variety of agents. Conduction disturbances such as complete atrioventricular block (AV block) may occur as an infrequent but serious complication of myocarditis. Early detection and accurate diagnosis of myocarditis are still unresolved challenges. We present 2 cases of otherwise mild myocarditis complicated by high-degree AV block in combination with isolated delayed uptake of contrast at the septal regions in the cardiac magnetic resonance imaging. Because the AV block was persistent in both cases, permanent pacemaker implantation was necessary. Delayed enhancement in the septal area in myocarditis might be predictive of infra-Hisian AV block.

Heterotopic transcatheter tricuspid valve implantation: first-in-man application of a novel approach to tricuspid regurgitation.

AIMS: Transcatheter treatment of heart valve disease is well established today. However, for the treatment of tricuspid regurgitation (TR), no effective catheter-based approach is available. Herein, we report the first human case description of transcatheter treatment of severe TR in a 79-year-old patient with venous congestion and associated non-cardiac diseases. In this patient, surgical treatment had been declined and pharmacological therapy had been ineffective. After ex vivo and animal studies, the treatment of TR was performed by percutaneous caval valve implantation. METHODS AND RESULTS: In a transcatheter approach through the right femoral vein, a custom-made self-expanding heart valve was implanted into the inferior vena cava (IVC). The device was anchored in the IVC at the cavoatrial junction with the level of the valve aligned immediately above the hepatic inflow and protruding into the right atrium. After deployment, excellent valve function was observed resulting in a marked reduction in caval pressure and an abolition of the ventricular wave in the IVC. Sequential echocardiographic exams over a follow-up period of 8 weeks confirmed continuous device function without paravalvular leakage or remaining venous regurgitation. The patient experienced improved physical capacity and was able to resume off-bed activities. There was no recurrence of right heart failure during follow-up and a partial reduction of ascites. The patient was discharged from hospital into a rehabilitation programme. CONCLUSION: Transcatheter treatment of severe TR by caval valve implantation is feasible resulting in an immediate abolition of IVC regurgitation and mid-term clinical improvement. Thus, in selected non-surgical patients, caval valve implantation may become a therapeutic option to treat venous regurgitation and improve associated non-cardiac diseases. Further confirmatory experience with longer follow-up is required to evaluate the long-term clinical benefit of the procedure as well as potential deleterious effects.