Case Report: Successful endovascular treatment of acute type A aortic dissection.

Introduction: Open surgical repair remains the current gold standard for the treatment of acute type A aortic dissection. However, especially elderly patients with relevant comorbidities who are deemed unfit for open surgery may benefit from a minimally invasive endovascular approach. Methods: We report a case of an 80-year-old male with retrograde acute type A aortic dissection and peripheral malperfusion after receiving thoracic endovascular aortic repair due to thoracic aortic aneurysm. Our individualized endovascular approach consisted of left carotid-subclavian bypass, proximal extension of thoracic endovascular aortic repair using a covered stent graft and a single covered stent graft for the ascending aorta in combination with an uncovered stent for the aortic arch. Results: Postoperative computed tomographic angiography demonstrated excellent outcome with no signs of endoleak or patent false lumen. Follow-up after 3.5 years showed a stable result with no signs of stent failure or dissection progress. No aortic re-interventions were needed in the further course. Discussion: An individualized endovascular approach may be justified for acute type A aortic dissection in elderly patients with high surgical risk if performed in specialized aortic centers. Additional short-length stent graft devices are needed to address the anatomical challenges of the ascending aorta. For enhanced remodeling of the dissected aorta, the use of an additional uncovered stent may be advisable.

Outcomes and survival following thoracic endovascular repair in patients with aortic aneurysms limited to the descending thoracic aorta.

BACKGROUND: Thoracic endovascular aortic repair (TEVAR) is a well-established therapy for descending aortic aneurysms (DTA). There is a paucity of large series reporting the mid- and long-term outcomes from this era. The main aim of this study was to evaluate the outcomes of TEVAR with regards to the effect of aortic morphology and procedure-related variables on survival, reintervention and freedom from endoleaks. METHODS: In this retrospective single center study, we evaluated the clinical outcomes among 158 consecutive patients with DTA than underwent TEVAR between 2006 and 2019 at our center. The cohort included 51% patients with device landing zones proximal to the subclavian artery and 25.9% patients undergoing an emergent or urgent TEVAR. The primary outcome was survival, and secondary outcomes were reintervention and occurrence of endoleaks. RESULTS: Median follow-up was 33 months [IQR 12 to 70] while 50 patients (30.6%) had longer than 5-year follow-up. With a median patient age of 74 years, post-operative Kaplan Meyer survival estimates were 94.3% (95%CI 90.8-98.0, SE 0.018%) at 30 days, 76.4% (95%CI 70.0-83.3, SE 0.034%) at one year and, 52.9% (95%CI 45.0-62.2, SE 0.043%) at five years. Freedom from reintervention at 30 days, one year, and five years was 92.9% (95%CI 89.0-97.1, SE 0.021%), 80.0% (95%CI 72.6-88.1, SE 0.039%), and 52.8% (95%CI 41.4-67.4, SE 0.065%), respectively. On cox regression analysis greater aneurysm diameter, and the use of device landing zones in aortic regions 0-1 were associated with an increased probability of all-cause mortality, and with reintervention during follow-up. Independent of aneurysm size undergoing urgent or emergent TEVAR was associated with higher mortality risk for the first three years post-operative but not on long-term follow-up. CONCLUSIONS: Larger aneurysms and those requiring stent-graft landing in aortic zones 0 or 1, are associated with higher risk for mortality and reintervention. There remains a need to optimize clinical management and device design for larger proximal aneurysms.

Aortic remodelling and late outcomes following thoracic endovascular repair with a bare-metal stent distal extension among patients with complicated type-B aortic dissection.

OBJECTIVES: The goal of this study was to describe the factors affecting mid and late aortic remodelling following thoracic endovascular aortic repair with the PETTICOAT (Provisional Extension To Induce Complete Attachment) technique among patients with complicated acute or subacute type B aortic dissection. METHODS: A retrospective single-centre study that evaluates clinical and morphological outcomes among 65 consecutive patients. The area and diameter of the true and false lumen, overall aortic diameter and false lumen perfusion were evaluated. RESULTS: Concomitant direct visceral artery stenting was successfully conducted in 32 (49%) patients. There was one (1.5%) postoperative stroke; three (4.6%) patients developed spinal cord ischaemia; two (3%) patients suffered retrograde type A dissection; and two (3%) patients had mesenteric ischaemia, despite successful reperfusion, that required a bowel resection. Median postoperative follow-up was 63.1 (interquartile range, 32.1- 91.8) months. The probability of survival was 96.9% [95% confidence interval (CI) 88.3%-99.2%] at 30 days, 93.9% (95% CI 84.4%-97.6%) at 1 year, 78.0 (95% CI 64.2%-87.0%) at 5 years and 72.8% (95% CI at 57.9%-83.2%) at 10 years postoperatively. There was a statistically significant postoperative increase in true-lumen area, diameter and true-lumen index in all five aortic levels measured. Complete false lumen (FL) thrombosis at the coeliac trunk, renal arteries and aortic bifurcation levels was observed in 47%, 15% and 24% of patients at midterm (6-15 months) and in 29%, 21% and 29% on late (later than 21 months) computed tomography angiograms (CTA). Persistent false lumen (FL) perfusion at the coeliac level on midterm CTA was associated with a larger extent of late aortic growth (P = 0.042) and was, in the majority of cases, caused by iliac re-entries either alone (28.57) or in combination with visceral and lumbar (28.57%) or distal aortic (10.71%) re-entries. A larger abdominal aortic diameter at midterm was associated with an increased probability of distal aortic reinterventions (hazard ratio 7.26, 95% CI 2.41-21.9, P < 0.001). CONCLUSIONS: Persistent FL perfusion of the distal aorta at midterm following TEVAR with the PETTICOAT technique among patients with acute and subacute type B dissection is caused mainly by iliac, visceral, lumber and distal aorta re-entries. Patients with persistent FL perfusion have an increased risk of aortic aneurysmal growth at late follow-up.

A new calcium score to predict paravalvular leak in transcatheter aortic valve implantation.

OBJECTIVES: The present study sought to develop a reliable calcium score (Ca-score) to predict paravalvular leak (PVL) in patients undergoing transcatheter aortic valve (AV) implantation. METHODS: A total of 965 patients were prospectively included from 2012 to 2019. Preprocedural contrast-media-enhanced computed tomography scans were analysed regarding the amount of AV cusp calcification and the presence of upper and lower left ventricular outflow tract calcification. The calcium volume threshold of each AV cusp [non-coronary cusp (NCC); left coronary cusp (LCC); right coronary cusp (RCC)] with optimal PVL prediction was defined using the Youden index value derived from receiver operating characteristic analysis. The final score was developed based on the multivariable regression analysis, while individual variables were weighted based on their corresponding odds ratio. RESULTS: The AV calcium volume threshold with optimal PVL prediction was 733.6, 296.0 and 131.2 mm3 for the NCC, RCC and LCC respectively. Overall, calcification of the upper left ventricular outflow tract was present in 233 (23%), 111 (12%) and 304 (32%) of patients below the NCC, RCC and LCC respectively, while 260 (27%), 44 (5%) and 217 (23%) patients suffered from calcification under the NCC, RCC and LCC, respectively. A total Ca-score of ≥4 was present in 356 (37%) of patients and was independently associated with ≥ mild PVL [odds ratio 3.662; 95% confidence interval (2.740-4.911); P < 0.001]. The area under the curve of the Ca-score was 0.713 [95% confidence interval (0.678-0.748); P < 0.001]. CONCLUSION: The provided Ca-score independently correlates with the development of PVL and improves risk stratification in patients undergoing transcatheter AV implantation.

Transcatheter Aortic Valve Implantation in Nonagenarians.

OBJECTIVE: In this report, we assess the outcome of transcatheter aortic valve implantation (TAVI) in nonagenarians at our institution during a 6-year period. METHODS: Between April 2008 and July 2014, 40 patients with a mean ± SD age of 91.8 ± 2.3 years (range, 90-98 years) underwent TAVI. Thirty-three patients (82.5%) received transapical TAVI, and seven patients (17.5%) received transfemoral TAVI. Baseline characteristics were as follows: mean ± SD EuroSCORE II, 23.9 ± 14.21; mean ± SD Society of Thoracic Surgeons mortality score, 24.2 ± 11.4; mean ± SD SYNTAX score, 7.6 ± 9.3; mean ± SD NYHA class, 3.5 ± 0.5; mean ± SD transvalvular gradient, 46.8 ± 17.8 mm Hg; mean ± SD aortic valve area, 0.7 ± 0.2 cm. RESULTS: Intraoperative mortality was 2.5% and 30-day all-cause mortality was 10%. The actuarial survival rates at 1 and 5 years were 58.6% and 30.4%, respectively. Seven patients (17.5%) underwent simultaneous elective TAVI and percutaneous coronary intervention. Three patients (7.5%) were operated on with the use of cardiopulmonary bypass. No conversion to open surgery occurred. In transesophageal echocardiography assessment, no moderate or severe prosthetic aortic valve regurgitation was observed. Four patients (10%) had postoperative acute renal failure stage 3 and needed new dialysis (P = 0.125). Three patients (7.5%) had a disabling stroke. Periprocedural myocardial infarction occurred in one patient (2.5%). Seven patients (17.5%) needed postoperative pacemaker implantation. Male sex and renal insufficiency were found to be predictors of mortality in univariable analysis. CONCLUSIONS: Transcatheter aortic valve implantation can be performed in nonagenarians despite very high preoperative risk scores and substantial multimorbidity, with acceptable outcomes.

Multislice computed tomography-guided surgical repair of acquired posterior left ventricular aneurysms: demonstration of mitral valve and left ventricular reverse remodelling.

OBJECTIVES: Involvement of the mitral valve (MV) apparatus represents a challenge in surgical ventricular repair (SVR) of posterior left ventricular (LV) aneurysms. This study sought to investigate whether multislice computed tomography (MSCT) assessment can be used to optimize the surgical procedure for posterior LV aneurysms. METHODS: Thirty patients (m : w = 24 : 6, age 38-78, median 66 years; mean New York Heart Association class 2.98) with posterior LV aneurysm were operated upon. MSCT was performed in 24 patients before and after surgery. End-diastolic and end-systolic volumes of LV and aneurysm were indexed to body surface area (LVEDVI/LVESVI, AEDVI/AESVI). The MV apparatus was characterized by coaptation distance (CD), tenting area (TA), MV closure angle (MVCA), MV annulus area (MVAA) and interpapillary muscle distance (IMD). RESULTS: Thirty-day mortality was 10% and 5-year survival rate was 83%. After surgery, LVEDVI decreased from 151.2 ± 84.1 to 85.7 ± 28.3 ml/m(2) (P = 0.001) and LVESVI from 110.6 ± 88.8 to 50.2 ± 22.9 ml/m(2) (P = 0.001). LV ejection fraction increased from 31.5 ± 15.1 to 43.4 ± 9.9% (P = 0.001). Preoperative MSCT showed significantly higher values of MVAA, CD and TA in patients who needed MV repair or replacement. Postoperative reduction of mitral regurgitation in patients without MV surgery corresponded with significant reduction in intercommissural diameter, anteroposterior diameter, MVAA, TA, CD, MVCA and IMD. CONCLUSIONS: MSCT represents an excellent diagnostic tool for the assessment of MV and LV geometry. MSCT-guided SVR of submitral LV aneurysms leads to excellent mid-term results. On the basis of the MSCT assessment, we propose an algorithm for surgical planning in posterior LV aneurysms.

Transcatheter aortic valve implantation combined with elective coronary artery stenting: a simultaneous approach†.

OBJECTIVES: Many patients referred for transcatheter aortic valve implantation (TAVI) also require percutaneous coronary intervention (PCI). The aim of the study was to identify whether combined treatment of patients with aortic stenosis and coronary artery disease (CAD) with TAVI and PCI has comparable results to treatment of patients with no CAD or with CAD with non-significant lesions who receive only TAVI. METHODS: Between April 2008 and August 2013, 730 consecutive patients underwent transapical TAVI at our institution. In our study population of 593 patients, 285 (48.1%) had no CAD and received TAVI only (Group I); 232 (39.1%) presented with CAD but no highly significant coronary artery lesion(s) and also received TAVI only (Group II), and 76 (12.8%) had CAD and highly significant coronary lesion(s) and underwent combined, single-staged TAVI and PCI (Group III). Three transapical TAVI patients who received PCI because of iatrogenic coronary artery obstruction during TAVI and 134 transapical TAVI patients with previous CABG were excluded from this study. RESULTS: Group II showed a calculated mean SYNTAX score of 5.7 ± 7.4. However, Group III showed a statistically significantly higher mean SYNTAX score of 8.0 ± 5.7 than Group II (P < 0.001) before the combined procedure. Combined TAVI and PCI reduced the mean SYNTAX score significantly from 8.0 ± 5.7 to 3.0 ± 4.9 (P < 0.001) in those patients presenting with severe aortic stenosis and highly significant CAD (Group III). The thirty-day all-cause mortality rate was 5.3, 3.9 and 2.6% for Group I, II and III, respectively (P = 0.609). Patients with highly significant CAD undergoing TAVI and PCI had similar survival up to 3 years as patients without CAD undergoing TAVI only. Radiation time and amount of contrast agent were higher during combined treatment in Group III (P < 0.05). However, no difference in acute kidney injury post-procedurally was observed. CONCLUSIONS: Single-stage combined treatment of severe aortic stenosis and highly relevant coronary lesions is a safe and feasible procedure. Early survival and survival up to 3 years are comparable to that observed in patients presenting without CAD who received TAVI only. PCI effectively reduces the complexity of coronary lesions. Although more contrast agent is applied during the combined treatment, the rate of acute kidney injury was not higher.

Transapical aortic valve implantation: predictors of survival up to 5 years in 730 patients. An update†.

OBJECTIVES: A major limitation of transcatheter aortic valve implantation (TAVI) is that its long-term outcomes are still unknown. The purpose of this study was to evaluate survival up to 5 years after implantation and to identify predictors of follow-up mortality in a large cohort of patients who underwent exclusively a transapical TAVI procedure. METHODS: Outcomes in terms of mortality and freedom from structural valve deterioration were evaluated in 730 consecutive patients. The median age was 80 years (range, 29-99 years). Forty patients (5.5%) presented with cardiogenic shock. The mean logistic European System for Cardiac Operative Risk Evaluation (EuroSCORE) was 35.0 ± 21.9%, the mean EuroSCORE II was 16.2 ± 16.2% and the mean Society of Thoracic Surgeons predicted operative mortality score was 14.0 ± 11.8%. According to allocation in EuroSCORE II quartiles, four equal subgroups of different risk profile were defined with low, intermediate, high and very high arithmetic risks. RESULTS: The overall 30-day mortality rate was 4.5% (33/730); 3.9% (27/690) in patients without cardiogenic shock. Survival at 1, 3 and 5 years were 80 ± 2%, 60 ± 2% and 41 ± 4%. Best survival up to 58 ± 7% at 5 years was found in the low and intermediate arithmetic risk quartile (P ≤ 0.001). In multivariable analysis, age (hazard ratio [HR]: 1.04, 95% confidence interval [CI]: 1.03-1.06, P < 0.001), New York Heart Association class IV (HR: 1.69, CI: 1.28-2.23, P < 0.001), cardiogenic shock (HR: 2.80, CI: 1.73-4.54, P < 0.001), serum creatinine level (HR: 1.24, CI: 1.10-1.40, P < 0.001) and atrial fibrillation (HR: 1.66, CI: 1.27-2.16, P < 0.001) were predictive of follow-up mortality, whereas the absence of post-procedural acute kidney injury (HR: 0.50, CI: 0.38-0.67, P < 0.001) was protective against follow-up mortality. The freedom from structural valve deterioration requiring reoperation on the prosthesis was 95.7 ± 1.9% at 5 years. CONCLUSIONS: We identified three main causes of follow-up mortality: non-cardiac comorbidity, advanced stages of heart failure and procedure-related complications. Further improvements of the TAVI technique should concentrate on the complete exclusion of the latter.

Transapical aortic valve implantation: predictors of leakage and impact on survival: an update.

BACKGROUND: In line with our institutional strategy, we do not accept paravalvular leakage after transcatheter aortic valve implantation (TAVI). Apart from data from very limited initial experience, predictors of leakage in large cohorts treated with new types of TAVI prostheses are still lacking. METHODS: From April 2008 to August 2013, 730 patients underwent transapical TAVI at our institution. The study group consisted of all 324 patients who received the new generation of balloon-expandable prostheses (SAPIEN XT; Edwards Lifesciences, LLC, Irvine, CA). Based on the Society of Thoracic Surgeons predicted risk of mortality, the arithmetic risk for surgery in the study cohort was 11% ± 9% (1% to 62%) and 20 (6%) patients were in cardiogenic shock. RESULTS: In study cohort, the overall 30-day mortality rate was 4.0% (3.3% in patients without cardiogenic shock). The postprocedural grade of regurgitation was absent or trace in 269 of 324 patients (83%), mild in 52 of 324 (16%), and moderate in 3 of 324 (< 1%); there was no severe postprocedural regurgitation. Regurgitation occurred less often (p < 0.001) in patients who received the XT-type prosthesis. Patients with more than trace regurgitation presented with less oversizing of the prosthesis in terms of annular area (p < 0.001) and higher calcium scores of the device landing zone (p < 0.001). The presence of calcified plaques in the left ventricular outflow tract was the strongest predictor of leakage (odds ratio 10.23, 95% confidence interval 5.12 to 20.45, p < 0.001). The regurgitation grade was not predictive for follow-up mortality (hazard ratio 1.08, 95% confidence interval 0.61 to 1.90, p = 0.800). CONCLUSIONS: In transapical TAVI, the risk of relevant paravalvular leakage may be eliminated completely. There is no negative impact on survival in patients with lesser, irrelevant grades of regurgitation.

Effects of estrogen, an ERα agonist and raloxifene on pressure overload induced cardiac hypertrophy.

The aim of this study was to investigate the effects of 17ß-estradiol (E2), the selective ERα agonist 16α-LE2, and the selective estrogen receptor modulator (SERM) raloxifene on remodeling processes during the development of myocardial hypertrophy (MH) in a mouse model of pressure overload. Myocardial hypertrophy in ovariectomized female C57Bl/6J mice was induced by transverse aortic constriction (TAC). Two weeks after TAC, placebo treated mice developed left ventricular hypertrophy and mild systolic dysfunction. Estrogen treatment, but not 16α-LE2 or raloxifene reduced TAC induced MH compared to placebo. E2, 16α-LE2 and raloxifene supported maintenance of cardiac function in comparison with placebo. Nine weeks after induction of pressure overload, MH was present in all TAC groups, most pronounced in the raloxifene treated group. Ejection fraction (EF) was decreased in all animals. However, 16α-LE2 treated animals showed a smaller reduction of EF than animals treated with placebo. E2 and 16α-LE2, but not raloxifene diminished the development of fibrosis and reduced the TGFß and CTGF gene expression. Treatment with E2 or 16α-LE2 but not with raloxifene reduced survival rate after TAC significantly in comparison with placebo treatment. In conclusion, E2 and 16α-LE2 slowed down the progression of MH and reduced systolic dysfunction after nine weeks of pressure overload. Raloxifene did not reduce MH but improved cardiac function two weeks after TAC. However, raloxifene was not able to maintain EF in the long term period.

Female sex and estrogen receptor-beta attenuate cardiac remodeling and apoptosis in pressure overload.

We investigated sex differences and the role of estrogen receptor-beta (ERbeta) on myocardial hypertrophy in a mouse model of pressure overload. We performed transverse aortic constriction (TAC) or sham surgery in male and female wild-type (WT) and ERbeta knockout (ERbeta(-/-)) mice. All mice were characterized by echocardiography and hemodynamic measurements and were killed 9 wk after surgery. Left ventricular (LV) samples were analyzed by microarray profiling, real-time RT-PCR, and histology. After 9 wk, WT males showed more hypertrophy and heart failure signs than WT females. Notably, WT females developed a concentric form of hypertrophy, while males developed eccentric hypertrophy. ERbeta deletion augmented the TAC-induced increase in cardiomyocyte diameter in both sexes. Gene expression profiling revealed that WT male hearts had a stronger induction of matrix-related genes and a stronger repression of mitochondrial genes than WT female hearts. ERbeta(-/-) mice exhibited a different transcriptional response. ERbeta(-/-)/TAC mice of both sexes exhibited induction of proapoptotic genes with a stronger expression in ERbeta(-/-) males. Cardiac fibrosis was more pronounced in male WT/TAC than in female mice. This difference was abolished in ERbeta(-/-) mice. The number of apoptotic nuclei was increased in both sexes of ERbeta(-/-)/TAC mice, most prominent in males. Female sex offers protection against ventricular chamber dilation in the TAC model. Both female sex and ERbeta attenuate the development of fibrosis and apoptosis, thus slowing the progression to heart failure.

Sex-specific pathways in early cardiac response to pressure overload in mice.

Pressure overload (PO) first causes cardiac hypertrophy and then heart failure (HF), which are associated with sex differences in cardiac morphology and function. We aimed to identify genes that may cause HF-related sex differences. We used a transverse aortic constriction (TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks, but with sex differences in hypertrophy 6 and 9 weeks after TAC. Cardiac gene expression was analyzed 2 weeks after surgery. Deregulated genes were classified into functional gene ontology (GO) categories and used for pathway analysis. Classical marker genes of hypertrophy were similarly upregulated in both sexes (alpha-actin, ANP, BNP, CTGF). Thirty-five genes controlling mitochondrial function (PGC-1, cytochrome oxidase, carnitine palmitoyl transferase, acyl-CoA dehydrogenase, pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC. Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males (collagen 3, matrix metalloproteinase 2, TIMP2, and TGFbeta2, all about twofold) after TAC. We confirmed 87% of the gene expression by real-time polymerase chain reaction. By GO classification, female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis. Promoter studies confirmed the upregulation of PGC-1 by E2. Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO. These differences could contribute to subsequent sex differences in cardiac function and HF.