Transcatheter Aortic Valve-in-Valve-in-Valve Replacement in a Young Woman With Transcatheter Structural Valve Deterioration Within a Degenerated Aortic Root Homograft.

Transcatheter aortic valve replacement is a well-established procedure for older patients with symptomatic, severe aortic stenosis. However, data are lacking on its durability and long-term complications, particularly in young patients and patients treated for aortic valve regurgitation. This article describes the case of a 27-year-old woman with complex congenital cardiovascular disease who, after 4 previous aortic valve replacement procedures, presented with structural deterioration of her most recent replacement valve, which had been placed by transcatheter aortic valve replacement inside a failed aortic root homograft 6 years earlier. After the patient had undergone this transcatheter aortic valve replacement procedure to treat aortic valve regurgitation related to her degenerated aortic root homograft, she became pregnant and successfully carried her high-risk pregnancy to term. However, the replacement valve deteriorated during the late stages of pregnancy, resulting in substantial hemodynamic changes between the first trimester and the postpartum period. To avoid repeat sternotomy, a redo transcatheter valve-in-valve replacement procedure procedure was performed through the right carotid artery. Because the patient wanted to have more children and therefore avoid anticoagulation, a SAPIEN 3 transcatheter valve (Edwards Lifesciences) was placed as a bridge to a future, more-durable aortic root replacement. The result in this case suggests that in patients with complex adult congenital pathology, transcatheter aortic valve replacement can be used as a temporizing bridge to subsequent, definitive aortic valve repair.

Use of a self-expanding transcatheter valve for a degenerated INTUITY valve.

Valve-in-valve transcatheter aortic valve replacement for degenerated surgical bioprosthesis is becoming a more common therapeutic option. Rapid-deployment valves are novel, have distinct structural differences from standard surgical valves, and are increasingly used in minimal-access surgery. We report the case of a 61-year-old man who developed severe stenosis of an Edwards INTUITY Elite rapid-deployment valve and who subsequently underwent successful valve-in-valve placement of a self-expanding transcatheter valve. To our knowledge, this is the first description of the technical aspects of and considerations for using the self-expanding transcatheter platform in the Edwards INTUITY Elite valve.

Hemodynamic outcomes after valve-in-valve transcatheter aortic valve replacement: a single-center experience.

BACKGROUND: Valve-in-valve transcatheter aortic valve replacement (ViV-TAVR) has emerged as a safe, effective alternative to redo aortic valve surgery in high-risk patients with degenerated surgical bioprosthetic valves. However, ViV-TAVR has been associated high postprocedural valvular gradients, compared with TAVR for native-valve aortic stenosis. METHODS: We performed a retrospective study of all patients who underwent ViV-TAVR for a degenerated aortic valve bioprosthesis between January 1, 2013 and March 31, 2019 at our center. The primary outcome was postprocedural mean aortic valve gradient. Outcomes were compared across surgical valve type (stented versus stentless), surgical valve internal diameter (≤19 versus >19 mm), and transcatheter aortic valve type (self-expanding vs. balloon-expandable). RESULTS: Overall, 89 patients underwent ViV-TAVR. Mean age was 69.0±12.6 years, 61% were male, and median Society of Thoracic Surgeons Predicted Risk of Mortality score was 5.4 [interquartile range, 3.2-8.5]. Bioprosthesis mode of failure was stenotic (58% of patients), regurgitant (24%), or mixed (18%). The surgical valve was stented in 75% of patients and stentless in 25%. The surgical valve's internal diameter was ≤19 mm in 45% of cases. A balloon-expandable transcatheter valve was used in 53% of procedures. Baseline aortic valve area and mean gradients were 0.87±0.31 cm2 and 36±18 mmHg, respectively. These improved after ViV-TAVR to 1.38±0.55 cm2 and 18±11 mmHg at a median outpatient follow-up of 331 [67-394] days. Higher postprocedural mean gradients were associated with surgical valves having an internal diameter ≤19 mm (24±13 versus 16±8, P=0.002) and with stented surgical valves (22±11 versus 12±6, P<0.001). CONCLUSIONS: ViV-TAVR is an effective option for treating degenerated surgical aortic bioprostheses, with acceptable hemodynamic outcomes. Small surgical valves and stented surgical valves are associated with higher postprocedural gradients.

Transcatheter valve-in-valve implantation for degenerated stentless aortic bioroots.

BACKGROUND: Open surgical repair of a failed valve-sparing aortic root replacement (VSARR) or stentless bioroot aortic root replacement (bio-ARR) entails significant operative risks. Whether valve-in-valve transcatheter aortic valve replacement (ViV-TAVR) is feasible in patients with a previous VSARR or stentless bio-ARR remains unclear, given lingering concerns about the ill-defined aortic annulus in these patients and the potential for coronary obstruction. We present our experience with patients who had a previous VSARR or stentless bio-ARR and underwent ViV-TAVR to repair a degenerated aortic valve with combined valvular disease, aortic insufficiency and aortic stenosis. METHODS: In this retrospective data review, we identified and analyzed consecutive patients with a previous VSARR or stentless bio-ARR who underwent ViV-TAVR between December 1, 2014 and August 31, 2019. RESULTS: ViV-TAVR was performed in twelve high-risk patients with previous VSARR or bio-ARR during the study period. Of these, seven received Medtronic Freestyle porcine stentless bioprosthetic aortic roots, three received homograft aortic roots, one underwent a Ross procedure and one underwent VSARR. ViV-TAVR restored satisfactory valve function in all patients, and technical success was 100%. No patient had more than mild regurgitation after implantation. No thirty-day mortality was seen. One patient had major bleeding after transapical access, one patient had a transient ischemic stroke, and one patient needed permanent pacemaker implantation. At a median last follow-up of 21.5 months (interquartile range, 9.0-69.0 months), all patients remained alive and had satisfactory valve function. CONCLUSIONS: In this study, ViV-TAVR was a clinically effective option for treating patients with a failed stentless bio-ARR or previous VSARR. Short-term and intermediate-term results after these procedures were favorable. These findings may have important implications for treating high-risk patients with structural aortic root deterioration and call for better transcatheter heart valves that are suitable for treating aortic insufficiency.

Transcatheter Aortic Valve-in-Valve Replacement Instead of a 4th Sternotomy in a 21-Year-Old Woman with Aortic Homograft Failure.

Transcatheter aortic valve replacement (TAVR) is a well-established method for replacing native aortic valves; however, it was conceived for elderly patients with aortic valve stenosis, and the lack of data on long-term durability has led practitioners to restrict the use of TAVR to patients who have short life expectancies. Here, we describe the case of a 21-year-old woman who had undergone 3 previous open aortic valve replacements and who presented with symptoms of recurrent valvular failure. Transthoracic echocardiograms and computed tomographic angiograms revealed a degenerating aortic root homograft with substantial calcification, moderate-to-severe aortic valve stenosis, and severe aortic valve regurgitation. Open surgical valve replacement posed substantial risk to our patient, so we decided to perform valve-in-valve TAVR with use of the Edwards Sapien XT Transcatheter Heart Valve. The patient's pulmonary artery pressure, valvular regurgitation, and symptoms improved substantially thereafter. We found that valve-in-valve TAVR into a failing aortic root homograft was less invasive than repeat surgical valve replacement in this young patient who had congenital vascular anomalies and a complex surgical history.

Evaluation of bivalirudin hyper- and hypo-ACT responses in the setting of percutaneous coronary intervention.

BACKGROUND: Bivalirudin has emerged as a suitable alternative anticoagulant to unfractionated heparin and low-molecular-weight heparins during percutaneous coronary intervention (PCI) procedures in the management of coronary artery disease and acute coronary syndromes (ACS). In clinical trials, bivalirudin dosing was standardized, and activated clotting time (ACT) did not influence dosing adjustments. The role of ACT monitoring of bivalirudin in PCI is not defined based on current practice guidelines. HYPOTHESIS: The hypothesis of this study is that hyper- and hypo-ACT responses to bivalirudin in PCI may be associated with excessive bleeding or thrombotic complications. METHODS: The planned protocol screened all patients who received bivalirudin therapy and ACT monitoring during PCI in a single center's cardiac catheterization laboratory from July 2009 to June 2010. The first ACT monitored 5 to 60 minutes after bivalirudin initiation was screened for inclusion. Values above 800 seconds and below 300 seconds were included as hyper- and hypo-ACT responses, respectively. Outcomes assessed include thrombotic and bleeding complications. RESULTS: There were 32 patients identified as hyper-responders and 20 patients identified as hypo-responders. There were no significant thrombotic or bleeding complications in the hyper-responder group. There was 1 case (1/20, 5%) of angiographically confirmed acute stent thrombosis immediately following the placement of 5 adjoining bare-metal stents in the right coronary artery of a hypo-responder. CONCLUSIONS: Hyper-ACT responses to bivalirudin therapy in PCI were not associated with additional bleeding risk. Bivalirudin may not adequately protect hypo-ACT responders against thrombotic complications during PCI.

Differentiating ST-elevation myocardial infarction from nonischemic ST-elevation in patients with chest pain.

Current guidelines state that patients with compatible symptoms and ST-segment elevation (STE) in ≥2 contiguous electrocardiographic leads should undergo immediate reperfusion therapy. Aggressive attempts at decreasing door-to-balloon times have led to more frequent activation of primary percutaneous coronary intervention (pPCI) protocols. However, it remains crucial to correctly differentiate STE myocardial infarction (STEMI) from nonischemic STE (NISTE). We assessed the ability of experienced interventional cardiologists in determining whether STE represents acute STEMI or NISTE. Seven readers studied electrocardiograms of consecutive patients showing STE. Patients with left bundle branch block or ventricular rhythms were excluded. Readers decided if, based on electrocardiographic results, they would have activated the pPCI protocol. If NISTE was chosen, readers selected from 12 possible explanations as to why STE was present. Of 84 patients, 40 (48%) had adjudicated STEMI. The percentage for which readers recommended pPCI varied (33% to 75%). Readers' sensitivity and specificity ranged from 55% to 83% (average 71%) and 32% to 86% (average 63%), respectively. Positive and negative predictive values ranged from 52% to 79% (average 66%) and 67% to 79% (average 71%), respectively. Broad inconsistencies existed among readers as to the chosen reasons for NISTE classification. In conclusion, we found wide variations in experienced interventional cardiologists in differentiating STEMI with a need for pPCI from NISTE.

Ticagrelor: the evidence for its clinical potential as an oral antiplatelet treatment for the reduction of major adverse cardiac events in patients with acute coronary syndromes.

INTRODUCTION: Ticagrelor, the first direct-acting, reversibly binding oral P2Y12 receptor antagonist, appears to have a favorable efficacy and safety profile. AIMS: To update the evidence and provide an overview of the available data on ticagrelor. EVIDENCE REVIEW: Peer reviewed articles published and listed under Medline Search, and published updated guidelines for pharmacotherapies in acute coronary syndromes were reviewed. PLACE IN THERAPY: Clinical evidence is increasing to support the use of new thienopyridines and the direct-acting P2Y12 receptor in the setting of acute coronary syndromes. CONCLUSION: The options for drugs to inhibit the platelet P2Y12 receptor for adenosine diphosphate are rapidly expanding. Ticagrelor has shown benefits in clinical trials. Its rapid onset of platelet inhibition and short half-life make it an attractive alternative to thienopyridines, especially when rapid inhibition of platelet aggregation or its quick reversal are required.

Incidencia de trombosis de stents coronarios en el ®mundo real¼ / Incidence of coronary stent thrombosis in the ®real world¼

ANTECEDENTES: la evidencia disponible de stents liberadores de medicamento proviene de estudios controlados con estrictos criterios de inclusión, limitando sus conclusiones y haciendo difícil la aplicación de sus resultados en el mundo real. OBJETIVO: determinar la incidencia de trombosis de stents liberadores y no liberadores de medicamento en pacientes del ®mundo real¼. METODOLOGÍA: estudio de incidencia para determinar el número de casos de trombosis de stents implantados, mediante información obtenida a partir de historias clínicas, bases de datos y seguimiento clínico, y con base en características demográficas, factores de riesgo, consumo de clopidogrel y casos de trombosis del stent con un seguimiento de cero días a un año. RESULTADOS: 640 stents implantados (69,2% no medicados, 30,8% medicados de los cuales 18,9% eran medicados con placlitaxel y 11,9% medicados con sirolimus). Se identificaron doce eventos de trombosis (siete stents medicados y cinco no medicados). La incidencia de trombosis con cualquier tipo de stent fue de 1,88% (IC 95% 0,97-3,28). La incidencia de trombosis con stent medicado fue 3,55% (IC 95% 1,43-7,32), y con stent no medicado 1,13% (IC 95% 0,37-2,64) p=0,000. El riesgo relativo de trombosis con stent medicado es de 3,14 (IC 95% 1,01-9,78) p=0,037. El riesgo relativo de presentar trombosis con stent medicado en infarto agudo del miocardio es 8,11 (IC 95% 2,32-28,31) p=0,001. CONCLUSIONES: la incidencia de trombosis del stent aumenta en el mundo real, y existe mayor riesgo de trombosis de stents medicados especialmente cuando son implantados en el contexto de un infarto agudo del miocardio. Es necesario realizar estudios futuros que involucren una población de pacientes más amplia y con seguimiento a largo plazo.

BACKGROUND: The existing evidence of drug-eluting stents comes from controlled studies done with strict inclusion criteria, limiting their conclusions and making difficult to apply their findings in the real world.Objectives: determine the incidence of thrombosis between bare metal stents versus drug-eluting stents in patients in the ®real world¼. METHODS: incidence study to determine the number of cases of thrombosis in implanted stents through information gathered from clinical records, data bases and clinical follow-up, based on demographic characteristics, risk factors, clopidogrel treatment and events of stent thrombosis with a 0 days to 1 year follow-up. RESULTS: 640 stents were implanted. 69.2% were bare metal stents and 30.8% drug-eluting stents, from which 18.9% were with placlitaxel and 11.9% with sirolimus. 12 thrombosis events were identified (7 with drug-eluting stents and 5 with bare metal stents). The incidence of thrombosis with any kind of stent was 1.88 %( CI 95% 0.97-3.28). The incidence of thrombosis with drug-eluting stents was 3.55% (CI 95%1.43-7.32), and with bare metal stents 1.13% (CI 95% 0.37-2.64) p=0.000. The relative risk of thrombosis with drug eluting stents is 3.14 (CI 95%1.01-9.78) p=0.037. The relative risk of thrombosis with drug eluting stents and acute myocardial infarction is 8.11 (CI 95%2.32-28.31) p=0,001. CONCLUSIONS: there is an increased incidence of thrombosis of coronary stents in the real world and a greater risk of thrombosis with drug eluting stents, especially when implanted in the context of an acute myocardial infarction. It is necessary to conduct further studies that may involve a higher sample of patients population and long-term follow-up.

Practical strategies for the management of anticoagulation therapy: unsolved issues in the cardiac catheterization laboratory.

PURPOSE: Percutaneous coronary intervention (PCI) is the preferred reperfusion strategy in the management of patients with ST-elevation myocardial infarction (STEMI) and higher-risk patients with unstable angina/non-STEMI (UA/NSTEMI). Recent updates have been issued for guidelines from the American College of Cardiology and American Heart Association delineating the appropriate use of anticoagulants as ancillary therapies to PCI. This manuscript reviews the recent clinical trial data supporting the updated guidelines and highlights remaining areas of uncertainty. METHODS: SCOPUS and Pubmed were searched for relevant English-language reports of clinical trials, registries, articles and case reports. Search terms included but were not limited to: PCI, anticoagulation, ancillary, STEMI, NSTEMI, angina, acute coronary syndrome. The reference lists of identified articles were searched for additional relevant publications. RESULTS: Unfractionated heparin (UFH), the historical standard of care for anticoagulation in STEMI and NSTEMI patients undergoing PCI, is sub-optimal and the list of anticoagulants recommended for alternatives in the current guidelines has expanded to include superior anticoagulants, including the low-molecular-weight heparin enoxaparin and the direct thrombin inhibitor bivalirudin. Additionally, fondaparinux is recommended if supplemented during PCI by an additional agent with anti-IIa activity. However, uncertainties in the guidelines remain. Clinical discretion is still required when deciding which anticoagulant to use, ensuring seamless transitions throughout the care pathway, and how to correctly identify the risk status of a patient and modify anticoagulant regimens accordingly, such as in special patient populations. CONCLUSIONS: The published evidence supports the updates to the guidelines. Updated guidelines still have knowledge gaps which require the application of clinical discretion by the cardiologist.

Balancing myocardial ischemic and bleeding risks in patients with non-ST-segment elevation myocardial infarction.

Achieving an appropriate balance of anti-ischemic efficacy versus bleeding risk with antiplatelet and anticoagulant agents demands an accurate estimation of risks. Although traditional risk stratification is available to decrease complications, and various methods of stratifying these risks have been proposed and validated, the stratification of bleeding risk is in its infancy. However, no model currently available permits the simultaneous estimation of these risks. Ischemic risk may be determined using 1 of several validated models, followed by the estimation of bleeding risk according to known risk factors. After selecting appropriate pharmacotherapy on the basis of the stratification of these risks, attention must be paid to proper dosing according to individual risk factors and patient, clinical, and technical variables. The aim of this study was to examine risk stratification models for these parameters to determine clinical characteristics common to ischemia and bleeding that can be used to minimize risks. A "bleeding risk subscale" is proposed, with factors extrapolated from current ischemic risk models, to integrate ischemic mortality and bleeding risk in patients with non-ST-segment elevation acute coronary syndromes. In conclusion, a validated tool to simultaneously evaluate ischemic and bleeding risk will help determine the most well-balanced pharmacotherapy for patients with non-ST-segment elevation acute coronary syndromes.

Safety of enoxaparin versus unfractionated heparin during percutaneous coronary intervention.

We sought to determine the safety and efficacy of enoxaparin versus unfractionated heparin during percutaneous coronary intervention (PCI). Four hundred ninety-three consecutive patients undergoing elective or emergency PCI received unfractionated heparin (70 U/kg, intravenously) or enoxaparin (1 mg/kg, intravenously). Patients who had received subcutaneous enoxaparin in the emergency department were given a supplementary 0.3-mg/kg intravenous dose. There was no crossover of therapies. All patients received oral antiplatelet therapy and eptifibatide. Primary safety outcomes were bleeding and a postprocedural hemoglobin decrease of >or=3 g/dL. Troponin I levels were considered a marker for myocardial injury.Two hundred twenty-two patients received enoxaparin, and 271 received unfractionated heparin. There were no thrombotic events or in-hospital deaths. Multivariate logistic regression analysis showed that, compared with unfractionated heparin, enoxaparin yielded a lower risk of bleeding (odds ratio [OR]=0.47; 95% confidence interval [CI], 0.21-1.05) and significantly fewer >3-g/dL decreases in hemoglobin (OR=0.45; 95% CI, 0.22-0.94). Enoxaparin also produced less of a decrease in mean platelet count (41 +/- 34 vs 55 +/- 63 x10(9)/L; P = 0.02) and in platelets >30% from baseline (OR=0.56; 95% CI, 0.31-0.99). After elective PCI, fewer enoxaparin patients had troponin I levels >or=3 times the upper limit of normal (OR=0.40; 95% CI, 0.028-0.66).Compared with unfractionated heparin, enoxaparin entailed less bleeding during both elective and emergent PCI and less cardiac enzyme elevation in patients undergoing elective PCI. Therefore, we believe that intravenous enoxaparin is a safe alternative to unfractionated heparin in both settings.

Practical issues on the use of enoxaparin in elective and emergent percutaneous coronary intervention.

Unfractionated heparin (UFH) has been the standard choice of adjunctive antithrombotic therapy during elective percutaneous coronary intervention (PCI). Evidence is emerging that intravenous (IV) enoxaparin may offer similar benefits to UFH in terms of ischemic events or death, but with the benefit of reduced major bleeding risk. In addition, enoxaparin has pharmacological and practical advantages that can simplify patient management. This review considers the current evidence for IV enoxaparin in the management of patients requiring elective PCI, as well as practical aspects of patient management.

Rosiglitazone reduces serum homocysteine levels, smooth muscle proliferation, and intimal hyperplasia in Sprague-Dawley rats fed a high methionine diet.

Homocysteine (Hcy) is a metabolite of the essential amino acid methionine. Hyperhomocysteinemia is associated with vascular disease, particularly carotid stenosis. Rosiglitazone, a ligand of the peroxisome proliferator-activated receptor gamma , attenuates balloon catheter-induced carotid intimal hyperplasia in type 2 diabetic rats. We studied 4 groups (n = 7 per group) of adult female Sprague-Dawley rats fed (a) powdered laboratory chow (control), (b) control diet with rosiglitazone (3.0 mg/kg/d), (c) diet containing 1.0% l -methionine, and (d) diet containing methionine and rosiglitazone. After 1 week on high methionine diet, the rats were administered an aqueous preparation of rosiglitazone by oral gavage. One week after initiation of rosiglitazone, balloon catheter injury of the carotid artery was carried out using established methods, and the animals continued on their respective dietary and drug regimens for another 21 days. At the end of the experimental period, blood samples were collected, and carotid arteries and liver were harvested. Serum Hcy increased significantly on methionine diet compared with controls (28.9 +/- 3.2 vs 6.3 +/- 0.04 micromol/L). Development of intimal hyperplasia was 4-fold higher in methionine-fed rats; this augmentation was significantly reduced ( P < .018) in rosiglitazone-treated animals. Rosiglitazone treatment significantly ( P < .001) suppressed Hcy levels and increased the activity of the Hcy metabolizing enzyme, cystathionine-beta-synthase in the liver samples. Hcy (100 micromol/L) produced a 3-fold increase in proliferation of rat aortic vascular smooth muscle cells; this augmentation was inhibited by incorporating rosiglitazone (10 micromol/L). After balloon catheter injury to the carotid artery of animals on a high methionine diet, there was an increase in the rate of development of intimal hyperplasia consistent with the known effects of Hcy. It is demonstrated for the first time that the peroxisome proliferator-activated receptor gamma agonist rosiglitazone can attenuate the Hcy-stimulated increase in the rate of development of intimal hyperplasia indirectly by increasing the rate of catabolism of Hcy by cystathionine-beta-synthase and directly by inhibiting vascular smooth muscle cell proliferation. These findings may have important implications for the prevention of cardiovascular disease and events in patients with hyperhomocysteinemia (HHcy).