Robotic Mitral Valve Repair for Degenerative Mitral Valve Regurgitation: Is it for Everyone? [Editorials]Historically, the standard approach for all mitral valve surgery has been the mediasternotomy. Although initially developed for cosmesis, minimally invasive techniques for mitral valve surgery use a limited right anterior thoracotomy with and without endoscopic techniques, which have resulted in outcomes comparable to the traditional mediasternotomy incision1,2.
Advances in robotic technology, including three dimensional visualization and improved dexterity have facilitated the introduction of robotic surgery for mitral valve repairs. In an FDA safety and efficacy trial in 2000 involving 20 patients, Nifong and co-workers used robotic technology to perform a wide spectrum of mitral valve repair procedures3. Although crossclamp and operative times were longer when compared to the conventional mediasternotomy approach, the morbidity and mortality was similar and the mean hospital length of stay (LOS) was only 4 days. A follow-up study involving 112 patients showed a 30-day mortality of 0.7% and no conversions to a mediasternotomy4. The mean hospital LOS was 5 days and the 5-year freedom from reoperation was 90%. More recent series using robotic techniques for mitral valve repairs have duplicated these excellent outcomes5,6. Although crossclamp, cardiopulmonary bypass, and total operative times are significantly longer, there are no differences in morbidity or mortality between robotic and non-robotic repairs. In general, robotic patients spend one less day in the hospital. Follow-up from 1-3 years show that > 90% of patients are free of moderate-to-severe mitral regurgitation (MR) and the need for another mitral valve procedure. However, despite the apparent cost savings of spending one less day in the hospital, Kam and co-workers could not demonstrate any differences in hospital expenses for patients undergoing robotic mitral repairs7. The decreased LOS appears to be offset by increased operation time. Furthermore, the cost of purchasing the robotic equipment, its maintenance and need for upgrades and supplies are usually not factored into most cost analyses. |
| The Ongoing Evolution of Outcomes Analysis for Pediatric and Congenial Cardiac Catheterization [Editorials]Jayaram and colleagues are to be congratulated for their important manuscript in this issue of Circulation.1 The IMPACTTM Registry (IMproving Pediatric and Adult Congenital Treatment) of the National Cardiovascular Data Registry (NCDR) of the American College of Cardiology (ACC) is the largest registry, to date, collecting information on pediatric and adult patients with congenital heart disease undergoing diagnostic or interventional cardiac catheterization. Jayaram and colleagues used the IMPACTTM Registry to develop and internally validate a model to predict the occurrence of a major adverse event following cardiac catheterization, using a cohort of 19,608 cardiac catheterizations that were performed at 58 U.S. centers between January 2011 and March 2013. A major adverse event occurred in 378 (1.9%) of all cases. After multivariable adjustment, eight variables were identified as critical for risk-standardization: patient age, renal insufficiency, single-ventricle physiology, procedure-type risk group, low systemic saturation, low mixed venous saturation, elevated systemic ventricular end diastolic pressure, and elevated main pulmonary artery pressures. The model had good discrimination (C-statistic of 0.70), confirmed by bootstrap validation (validation C-statistic of 0.69). |
Robotic Mitral Valve Repair for Simple and Complex Degenerative Disease: Mid-Term Clinical and Echocardiographic Quality Outcomes [Original Articles]Background—Severe primary (degenerative) mitral valve regurgitation (MR) is repaired with durable results when "simple" single scallop disease is addressed. The mid-term quality outcomes of minimally invasive repair for "complex disease" are unknown however.
Methods and Results—From January 2008 to January 2015, 487 patients (56±11 years, 360 men, ejection fraction 65±6%, 98.8% complete follow-up) underwent robotic mitral valve repair for severe non-ischemic degenerative MR. Simple pathology was addressed in 289/487 (59%) and complex repair (all others) was performed in 198/487 (41%). Four patients died during follow-up with a 5-year survival rate 99.5% (99.4% simple; 99.5% complex, HR=0.48, 95% CI 0.05-4.59); and NYHA functional class I/II was documented in 97.9%(477/487). Eight patients had recurrence of ≥moderate MR, (4 simple, 4 complex), with a 5 year freedom from MR of 94.6% (96.2% simple; 92.7%, complex, p=0.67; HR=1.36, 95% CI 0.34-5.43). Seven patients (2 simple, 5 complex), underwent mitral reoperation, with a 5-year freedom from reoperation of 97.7% (99.2% simple and 95.7% complex, p=0.13; HR=3.35, 95% CI 0.65-17.32).
Conclusions—At a large tertiary care referral center, mid-term quality outcomes after robotic correction of degenerative MR are excellent, with very high survival, infrequent complications and a low likelihood of MR recurrence - regardless of mitral valve repair complexity. Awareness of these improvements in outcome is important to inform contemporary decisions regarding high-quality alternatives to conventional and percutaneous mitral repair. |
Adjusting for Risk Associated with Pediatric and Congenital Cardiac Catheterization: A Report from the NCDR(R) IMPACTTM Registry [Original Articles]Background—As US healthcare increasingly focuses upon outcomes as a means for quantifying quality, there is a growing demand for risk models that can account for the variability of patients treated at different hospitals so that equitable comparisons between institutions can be made. We sought to apply aspects of prior risk-standardization methodology in order to begin development of a risk-standardization tool for the NCDR® IMPACTTM (Improving Pediatric and Adult Congenital Treatment) Registry.
Methods and Results—Using IMPACT, all patients undergoing diagnostic or interventional cardiac catheterization between January 2011 and March 2013 were identified. Multivariable hierarchical logistic regression was used to identify patient and procedural characteristics predictive of experiencing a major adverse event following cardiac catheterization. A total of 19,608 cardiac catheterizations were performed between January 2011 and March 2013. Amongst all cases, a major adverse event occurred in 378 (1.9%) of all cases. After multivariable adjustment, eight variables were identified as critical for risk-standardization: patient age, renal insufficiency, single-ventricle physiology, procedure-type risk group, low systemic saturation, low mixed venous saturation, elevated systemic ventricular end diastolic pressure, and elevated main pulmonary artery pressures. The model had good discrimination (C-statistic of 0.70), confirmed by bootstrap validation (validation C-statistic of 0.69).
Conclusions—Using prior risk-standardization efforts as a foundation, we developed and internally validated a model to predict the occurrence of a major adverse event following cardiac catheterization for congenital heart disease. Future efforts should be directed towards further refinement of the model variables within this large, multicenter dataset. |
| Atherothrombosis: Seeing Red? [Editorials]The initiation, progression, and complications of atherosclerosis are mediated by a complex interplay of hematopoietic cells, vascular cells, and the extracellular matrix in response to metabolic (e.g., hyperlipidemia, diabetes mellitus) and environmental (e.g., smoking) injury1. Recruitment and activation of immune cells of hematopoietic origin are key elements in the development of atherosclerosis2. Elegant experimental studies, typically performed in compound mutant mice susceptible to diet-induced atherosclerosis, indicate important roles for monocytes, T-lymphocytes, neutrophils, and mast cells in lesion formation. While Barger and colleagues proposed a role for vasa vasorum, neovascularization, and intra-plaque hemorrhage with extravasation of red blood cells (RBCs) as a mechanism of atherosclerotic lesion progression3, 4, a direct contribution of RBCs in atherogenesis is uncertain. In this issue of Circulation, Bogdanov and coworkers5 report that high-fat diet induces RBC dysfunction, which is capable of promoting atherosclerosis by enhancement of the recruitment of inflammatory monocytes. |
Red Blood Cell Dysfunction Induced by High Fat Diet: Potential Implications for Obesity-Related Atherosclerosis [Original Articles]Background—High fat diet (HFD) promotes endothelial dysfunction and pro-inflammatory monocyte activation, which contribute to atherosclerosis in obesity. We investigated whether HFD also induces dysfunction of red blood cells (RBC), which serve as a reservoir for chemokines via binding to Duffy antigen receptor for chemokines (DARC).
Methods and Results—60% HFD for 12 weeks, which produced only minor changes in lipid profile in C57/BL6 mice, markedly augmented the levels of MCP-1 bound to RBC, which in turn stimulated macrophage migration through an endothelial monolayer. Levels of RBC bound KC were also increased by HFD. These effects of HFD were abolished in DARC -/- mice. In RBC from HFD-fed wild-type and DARC -/- mice, levels of membrane cholesterol and phosphatidylserine externalization were increased, fostering RBC-macrophage inflammatory interactions and promoting macrophage phagocytosis in vitro. When labeled ex vivo and injected into control mice, RBC from HFD-fed mice exhibited ~3 fold increase in splenic uptake. Finally, RBC from HFD-fed mice induced increased macrophage adhesion to the endothelium when they were incubated with isolated aortic segments, indicating endothelial activation.
Conclusions—RBC dysfunction, analogous to endothelial dysfunction, occurs early during diet-induced obesity and may serve as a mediator of atherosclerosis. These findings may have implications for the pathogenesis of atherosclerosis in obesity, a worldwide epidemic. |
Characteristics and Survival of Malignant Cardiac Tumors: A 40-Year Analysis of Over 500 Patients [Original Articles]Background—To investigate the incidence, histopathology, demographics and survival associated with primary malignant cardiac tumors (PMCTs).
Methods and Results—We queried the Surveillance, Epidemiology and End-Results (SEER) 18-registry from National Cancer Institute for all PMCTs diagnosed from 1973 to 2011. We describe PMCT histopathology and incidence, comparing characteristics and survival of these patients, to those with extra-cardiac malignancies of similar histopathology. From a total of 7,384,580 cases of cancer registered in SEER, we identified 551 (0.008%) PMCTs. The incidence of PMCT diagnosis is 34 cases per 100 million persons and has increased over time: 25.1 (1973-1989), 30.2 (1990-1999) and 46.6 (2000-2011). Most patients are female (54.1%), white (78.6%), with median age at diagnosis of 50 years. The most common PMCTs are sarcomas (n=357, 64.8%), followed by lymphomas (n=150, 27%), and mesotheliomas (n=44, 8%). Most patients are diagnosed with tissue sample (96.8%). Although use of chemotherapy is not documented in SEER, 19% of patients received radiation and 44% had surgery. After a median follow-up of 80 months, 413 patients had died. The 1, 3, and 5- year survival was 46%, 22%, and 17% and has improved over the eras with (1-, 3-, 5-year) of 32%, 17%, 14% (1973-1989) to 50%, 24%, 19% (2000-2011) (p=0.009). Cardiac sarcomas and mesotheliomas are the most lethal PMCTs, with 1-, 3-, 5- year survival of 47%, 16%, and 11%, and 51%, 26%, and 23%, respectively, compared with lymphoma 59%, 41%, and 34%, respectively (log rank test p<0.001). Patients with cardiac lymphomas and sarcomas are younger and have worse survival than patients with extra-cardiac disease of similar histopathology (p<0.001).
Conclusions—PMCTs are extremely rare and continue to be associated with poor prognosis. Over the past five decades, the incidence and survival of patients diagnosed with PMCT appears to have increased. Compared to those with extra-cardiac cancers of similar histopathology, patients with PMCTs are often younger and have worse survival. |
Direct Evidence for Microdomain-Specific Localization and Remodeling of Functional L-Type Calcium Channels in Rat and Human Atrial Myocytes [Original Articles]Background—Distinct subpopulations of L-type calcium channels (LTCCs) with different functional properties exist in cardiomyocytes. Disruption of cellular structure may affect LTCC in a microdomain-specific manner and contribute to the pathophysiology of cardiac diseases, especially in cells lacking organized T-tubules such as atrial myocytes (AMs).
Methods and Results—Isolated rat and human AMs were characterized by scanning ion conductance, confocal, and electron microscopy. Half of AMs possessed T-tubules and structured topography, proportional to cell width. Bigger proportion of myocytes in the left atrium had organized T-tubules and topography than in the right atrium. Super-resolution scanning patch-clamp showed LTCCs distribute equally in T-tubules (T-LTCCs) and crest areas of the sarcolemma (C-LTCCs), whereas in ventricular myocytes (VMs) LTCCs primarily cluster in T-tubules. Rat, but not human, T-LTCCs had open probability similar to C-LTCCs, but exhibited ~40% greater current. Optical mapping of Ca2+ transients revealed that rat AMs presented ~3-fold as many spontaneous Ca2+ release events as VMs. Occurrence of C-LTCCs and spontaneous Ca2+ transients were eliminated by either a caveolae-targeted LTCC antagonist or disrupting caveolae with methyl-β-cyclodextrin, with an associated ~30% whole-cell ICa,L reduction. Heart failure (HF, 16-weeks post-MI) in rats resulted in a T-tubule degradation (by ~40%) and significant elevation of spontaneous Ca2+ release events. While not affecting LTCC occurrence, HF led to ~25% decrease in T-LTCC amplitude.
Conclusions—We provide the first direct evidence for the existence of two distinct subpopulations of functional LTCCs in rat and human AMs, with their biophysical properties modulated in HF in a microdomain-specific manner. |
| Drug Coated Balloons as the New Standard of Care for Femoropopliteal In-Stent Restenosis: FAIR Assumption? [Editorials]The femoropopliteal (FP) segment is increasingly treated via an endovascular-first approach for both lifestyle limiting claudication and critical limb ischemia. Nitinol stents have been shown to be superior to percutaneous transluminal angioplasty (PTA) and have become one of the primary modalities for the treatment of FP obstructive atherosclerotic disease due to improved structural integrity and conformability of newer devices1-3. Current nitinol stents have low rates of stent fracture and excellent clinical patency out to three years2,4. Despite these advances, FP in-stent restenosis (FP-ISR) remains an important clinical problem, occurring in up to 19-37% of cases following stenting of moderate length (up to 150mm) lesions and more frequently following treatment of longer lesions.1,2,5 |
Drug-Coated Balloon Versus Standard Balloon for Superficial Femoral Artery In-Stent Restenosis: The Randomized Femoral Artery In-Stent Restenosis (FAIR) Trial [Original Articles]Background—Drug-coated balloon angioplasty (DCBA) was shown to be superior to standard balloon angioplasty (POBA) with regard to restenosis prevention for de-novo superficial femoral artery (SFA) disease. For in-stent restenosis (ISR), the benefit of DCBA over POBA remains uncertain.
Methods and Results—One-hundred-nineteen patients with SFA ISR and chronic limb ischemia were recruited over 34 months at 5 German clinical sites and prospectively randomized to either DCBA (n = 62) or POBA (n = 57). Mean lesion length was 82.2 ± 68.4 mm. Thirty four (28.6%) lesions were totally occluded, 30 (25.2%) were moderately or heavily calcified. Clinical and duplex ultrasound follow-up was conducted at 6 and 12 months. The primary endpoint of recurrent ISR assessed by ultrasound at 6 months was 15.4% (8/52) in the DCBA and 44.7% (21/47) in the POBA group (P = 0.002). Freedom from target lesion revascularization (TLR) was 96.4 % vs. 81.0% (P = 0.0117) at 6 months and 90.8% vs. 52.6% (P < 0.0001) at 12 months, respectively. At 12 months, clinical improvement by ≥ 1 Rutherford category without the need of TLR was observed in 35/45 DCBA patients (77.8%) and 23/44 POBA patients (52.3%, P = 0.015). No major amputation was needed. Two patients in the DCBA and 3 patients in the POBA group died. No death was procedure-related.
Conclusions—DCBA for SFA ISR is associated with less recurrent restenosis and a better clinical outcome than POBA, without an apparent difference in safety.
Clinical Trial Registration Information—www.clinicaltrials.gov. Identifier: NCT01305070. |
When a Thrombus Is Life-Saving [Images in Cardiovascular Medicine] |
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