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Aim of this retrospective, multicenter study was to evaluate early and mid-term clinical and hemodynamic results of patients who underwent surgical aortic valve replacement (SAVR) with Intuity rapid-deployment bioprostheses (RDB) (Edwards Lifesciences, Irvine, CA). We analyzed data from the Italian Registry of Intuity Valve (INTU-ITA registry) that is a national, real-world and independent from the industry registry. Preoperative variables were defined according to EuroSCORE and postoperative outcomes according to Valve Academic Research Consortium (VARC). Survival distribution was evaluated using the Kaplan-Meier approach. A Cox-Proportional Hazard Model was employed to assess the effect of the covariates on patients’ survival. The registry included 1687 patients from 23 centers (June 2012-September 2019). Aortic cross clamp time for isolated SAVR was 55 minutes (IQR: 45–70 minute). Postoperative pace-maker rate was 6.3%. At discharge transaortic peak and mean gradients were: 18 mm Hg (IQR: 14–23 mm Hg) and 10 mmHg (IQR: 8–13 mm Hg), respectively. Indexed effective orifice area was 1.10 cm2/m2 (IQR: 0.91–1.31 cm2/m2) and the incidence of severe patient-prosthesis mismatch was 0.6%. Hemodynamic data for all valve sizes remained stable during follow-up. Thirty-day overall mortality was 1.8% (30 patients), and at follow-up it was 5.3% (89 patients). Kaplan-Meier overall survival was 95.5% (94.3–96.7%); 90.7% (88.3–93.1%); 86.4% (82.6–90.4%) at 1, 3, and 5 years, respectively. Serum creatinine (HR: 1.36; 95%CI: 1.04–1.81; p = 0.0397) and cross-clamp time (HR: 1.01; 95%CI: 1.002–1.017; p = 0.0077) were identified as independent predictors of mortality. According to our data from the INTU-ITA registry, SAVR with RDB provides good early clinical and hemodynamic results that are confirmed at follow-up.

Background: The association of celiac disease (CD) with premature atherosclerosis, including increased carotid artery intima-media thickness and cardiovascular disease (CVD), is controversial. The aim of this study was to investigate this relationship. Methods: Clinical records of patients from Northern Sardinia referred to the Gastroenterology section of the Department of Medicine, University of Sassari, Italy, were analyzed. Unadjusted and adjusted odds ratios (ORs) for CVD with their 95% confidence intervals (CIs) were calculated according to established risk factors, including age, sex, diabetes, dyslipidemia, overweight/obesity, blood hypertension, and cigarette smoking, as well as a possible risk factor such as H. pylori infection. Results: In a total of 8495 patients (mean age 52.1 ± 17.3 years; 64.7% females), 2504 reported a diagnosis of CVD and 632 of CD. Logistic regression analysis showed a significantly reduced risk of CVD among patients with CD (OR 0.30, 95% CI 0.22–0.41). Moreover, the long duration of the gluten-free diet (GFD) was able to lower the risk of CVD in celiac patients. Finally, CD significantly decreased the frequency of carotid plaques (11.8% vs. 40.1%, p < 0.001). Conclusions. Our retrospective study demonstrated that CD reduces the risk of CVD in general and more specifically of carotid lesions after adjusting for potential confounders, especially in those on GFD for a long time.

Arch pathology represents one of the last frontiers in aortic aneurysms endovascular management. Several companies recently developed dedicated branched and fenestrated endografts specifically designed for the aortic arch, aiming to overcome some of the issues associated with standard thoracic endograft and supra-aortic vessels extra-anatomical debranching. This study aimed to evaluate early outcomes obtained with a custom-made fenestrated endograft approved for thoracic aortic aneurysms exclusion.All consecutive patients treated with the Najuta endograft (Kawasumi Laboratories, Inc, Tokyo, Japan) in Italy were prospectively enrolled and included in the study population. Anatomical characteristics and perioperative data were retrospectively analyzed. Study endpoints were technical success, 30-day clinical success, overall survival, supra-aortic vessel patency, endoleak and need for reintervention or surgical conversion.During the period 2018-2022, seventy-six patients received a Najuta endograft in Italy and were enrolled in the study. Median age was 72 (IQR 69-76) years and 80.3% were male. Most of the patients received treatment for atherosclerotic aneurysms (80.3%) while the others for post-dissection aneurysms (7.9%), penetrating aortic ulcer (9.2%), or type I endoleak correction after previous thoracic endovascular repair (2.6%). Overall, 161 supra-aortic vessels were preserved through a dedicated fenestration. Technical success was achieved in 74/76 (97.4%) of procedures; both failures were associated with endoleak detection at final angiography (one type I and one type III endoleak). Two distal migrations occurred during the implanting procedure. Clinical success at 30 days was 94.7%. Two early reinterventions were needed within 30 days after index procedure: in one case an aortic false lumen coils embolization was performed, since distal re-entry caused enlargement of the post dissection thoracic aneurysm. The other procedure consisted of a femoral pseudoaneurysm repair. Median follow-up was 7 (IQR 3-15) months; no supra-aortic vessel occlusions occurred and no patients needed surgical conversion.Early results suggest that in selected patients with aortic arch pathology needing a proximal landing, an endovascular approach with the Najuta system is safe and effective, especially for those at high surgical risk. A strict follow-up with high-quality computed tomography angiography images and eventual long-term complications evaluation is needed to confirm these initial experience findings.

Aim: Recent studies suggest that glucose-6-phosphate dehydrogenase (G6PD) deficiency, a genetically inherited condition causing hemolytic anemia, may be a risk factor for cardiovascular disease (CVD). We aimed to perform a retrospective case–control study in Sardinia taking advantage from clinical records of patients undergoing upper digestive endoscopy and screened for H. pylori infection. Methods: A total of 9,604 patients with a known G6PD status and a complete clinical history, encompassing CVD, and leading CVD risk factors, including H. pylori infection, undergoing upper endoscopy between 2002 and 2017 were enrolled in this study. Results: Multivariate logistic regression analysis confirmed an increased CVD risk in subjects with G6PD deficiency [odd ratio (OR), 3.24; 95% confidence interval (CI) 2.44–4.30] after adjusting for potential confounders and effect modifiers, including H. pylori infection. Cardiovascular risk was similar in subjects with and without G6PD deficiency before age 60 (OR, 1.26; 95% CI 0.78–2.04, P =0.562), whereas it increased after age 60 in the former group (OR, 3.05; 95% CI 2.22–4.19, P ＜0.0001) especially in males (OR 3.67; 95% CI 2.19–6.14) compared with females (OR, 2.96; 95% CI 1.89–4.64) by sex-specific logistic regression analysis. Conclusion: The risk of CVD was greater in G6PD-deficient subjects after age 60, both in males and females, than those with normal enzyme activity, after adjusting for conventional CVD risk factors and H. pylori infection. The reduction of important protective mechanisms against oxidative stress in the elderly might explain the study findings.

Cardiovascular disorders (CVD) are highly prevalent and the leading cause of death worldwide. Atherosclerosis is responsible for most cases of CVD. The plaque formation and subsequent thrombosis in atherosclerosis constitute an ongoing process that is influenced by numerous risk factors such as hypertension, diabetes, dyslipidemia, obesity, smoking, inflammation, and sedentary lifestyle. Among the various risk and protective factors, the role of glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common inborn enzyme disorder across populations, is still debated. For decades, it has been considered a protective factor against the development of CVD. However, in the recent years, growing scientific evidence has suggested that this inherited condition may act as a CVD risk factor. The role of G6PD deficiency in the atherogenic process has been investigated using in vitro or ex vivo cellular models, animal models, and epidemiological studies in human cohorts of variable size and across different ethnic groups, with conflicting results. In this review, the impact of G6PD deficiency on CVD was critically reconsidered, taking into account the most recent acquisitions on molecular and biochemical mechanisms, namely, antioxidative mechanisms, glutathione recycling, and nitric oxide production, as well as their mutual interactions, which may be impaired by the enzyme defect in the context of the pentose phosphate pathway. Overall, current evidence supports the notion that G6PD downregulation may favor the onset and evolution of atheroma in subjects at risk of CVD. Given the relatively high frequency of this enzyme deficiency in several regions of the world, this finding might be of practical importance to tailor surveillance guidelines and facilitate risk stratification.

Background: The aim of this multicenter prospective study was to evaluate the prognostic weight of preoperative right ventricular assessment on early mortality in cardiac surgery. Methods: This is a multicenter prospective observational study performed by the Italian Group of Research for Outcome in Cardiac Surgery (GIROC) including 11 centers. From October 2017 to March 2019, out of 923 patients undergoing cardiac surgery, 28 patients with some missing data were excluded and 895 patients were enrolled in the study right ventricular dilatation was defined as a basal end-diastolic diameter >42 mm. The right ventricle (RV) function was assessed using the combination of three parameters: fractional area changing (FAC), tricuspid annular plane systolic excursion (TAPSE), and S'-wave using tissue Doppler imaging (TDI-S'); RV dysfunction was defined as the presence of at least two of the following cutoffs: FAC

The role of water hardness on human health is still debated, ranging from beneficial to harmful. Before the rise of drinking bottled water, it was a common habit to obtain supplies of drinking water directly from spring-fed public fountains. According to the geographic location, spring waters are characterized by a variable content of mineral components. In this ecological study, for the first time in Sardinia, Italy, the spatial association between spring water quality/composition and standardized mortality ratio (SMR) for coronary artery disease (CAD) in the decade from 1981 to 1991 was investigated using data retrieved from published databases. In a total of 377 municipalities, 9918 deaths due to CAD, including acute myocardial infarction (AMI), ICD-9 code 410, and ischemic heart disease (IHD), ICD-9 code 411–414, were retrieved. A conditional autoregressive model with spatially structured random effects for each municipality was used. The average SMR for CAD in municipalities with a predominantly “soft” (&lt, 30 mg/L) or “hard” (≥30 mg/L) water was, respectively, 121.4 ± 59.1 vs. 104.7 ± 38.2 (p = 0.025). More specifically, an inverse association was found between elevated calcium content in spring water and cardiovascular mortality (AMI: r = −0.123, p = 0.032, IHD: r = −0.146, p = 0.009) and borderline significance for magnesium (AMI: r = −0.131, p = 0.054, IHD: r = −0.138, p = 0.074) and bicarbonate (IHD: r = −0.126, p = 0.058), whereas weak positive correlations were detected for sodium and chloride. The lowest CAD mortality was observed in geographic areas (North-West: SMR 0.92, South-East: SMR 0.88), where calcium- and bicarbonate-rich mineral waters were consumed. Our results, within the limitation of an ecological study, confirm the beneficial role of waters with high content in calcium and bicarbonate against coronary artery disease.

Background and purpose: pericoronary fat over-inflammation might lead to the development and destabilization of coronary plaque in patients with pre-diabetes (PDM). Notably, pericoronary fat could over-express the sodium-glucose cotransporter 2 (SGLT2) and leptin, along with decreased sirtuin 6 (SIRT6) expression in PDM vs. normoglycemic (NG) patients undergoing coronary artery bypass grafting (CABG) for acute myocardial infarction (AMI). However, in the current study, we evaluated inflammatory markers, SGLT2, SIRT6, and leptin levels in pericoronary fat and, subsequently, 12-month prognosis comparing PDM to NG subjected to CABG for AMI. In addition, we evaluated in PDM patients the effects of metformin therapy on SIRT6 expression, leptin, and SGLT2 levels, and assessed its beneficial effect on nitrotyrosine and inflammatory cytokine levels. Methods: we studied AMI patients referred for CABG, divided into PDM and NG-patients. PDM patients were divided into never-metformin users and metformin users. Finally, we evaluated major adverse cardiac events (MACE) at a 12-month follow-up. Results: the MACE was 9.1% in all PDM and 3% in NG patients (p &lt, 0.05). Metformin users presented a significantly lower MACE rate in PDM than never-metformin users (p &lt, 0.05). PDM showed higher inflammatory cytokines, 3-nitrotyrosine levels, SGLT2, and leptin content, and decreased SIRT6 protein levels in pericoronary fat compared to NG-patients (p &lt, 0.05). PDM never-metformin-users showed higher SGLT2 and leptin levels in pericoronary fat than current-metformin-users (p &lt, 0.05). Conclusions: metformin therapy might ameliorate cardiovascular outcomes by reducing inflammatory parameters, SGLT2, and leptin levels, and finally improving SIRT6 levels in AMI-PDM patients treated with CABG.

Background/objectives Pericoronary adipose tissue inflammation might lead to the development and destabilization of coronary plaques in prediabetic patients. Here, we evaluated inflammation and leptin to adiponectin ratio in pericoronary fat from patients subjected to coronary artery bypass grafting (CABG) for acute myocardial infarction (AMI). Furthermore, we compared the 12-month prognosis of prediabetic patients compared to normoglycemic patients (NG). Finally, the effect of metformin therapy on pericoronary fat inflammation and 12-months prognosis in AMI-prediabetic patients was also evaluated. Methods An observational prospective study was conducted on patients with first AMI referred for CABG. Participants were divided in prediabetic and NG-patients. Prediabetic patients were divided in two groups; never-metformin-users and current-metformin-users receiving metformin therapy for almost 6 months before CABG. During the by-pass procedure on epicardial coronary portion, the pericoronary fat was removed from the surrounding stenosis area. The primary endpoints were the assessments of Major-Adverse-Cardiac-Events (MACE) at 12-month follow-up. Moreover, inflammatory tone was evaluated by measuring pericoronary fat levels of tumor necrosis factor-α (TNF-α), sirtuin 6 (SIRT6), and leptin to adiponectin ratio. Finally, inflammatory tone was correlated to the MACE during the 12-months follow-up. Results The MACE was 9.1% in all prediabetic patients and 3% in NG-patients. In prediabetic patients, current-metformin-users presented a significantly lower rate of MACE compared to prediabetic patients never-metformin-users. In addition, prediabetic patients showed higher inflammatory tone and leptin to adiponectin ratio in pericoronary fat compared to NG-patients (P Conclusion Prediabetes increase inflammatory burden in pericoronary adipose tissue. Metformin by reducing inflammatory tone and leptin to adiponectin ratio in pericoronary fat may improve prognosis in prediabetic patients with AMI. Trial registration Clinical Trial NCT03360981, Retrospectively Registered 7 January 2018

OBJECTIVE To evaluate the effect of metformin therapy on coronary endothelial function and major adverse cardiac events (MACE) in patients with prediabetes with stable angina and nonobstructive coronary stenosis (NOCS). RESEARCH DESIGN AND METHODS Metformin therapy may be needed to reduce coronary heart disease risk in patients with prediabetes. A total of 258 propensity score–matched (PSM) patients with stable angina undergoing coronary angiography were enrolled in the study. Data from 86 PSM subjects with normoglycemia (NG), 86 PSM subjects with prediabetes (pre-DM), and 86 PSM subjects with prediabetes treated with metformin (pre-DM metformin) were analyzed. During coronary angiography, NOCS was categorized by luminal stenosis 0.80. In addition, we assessed the endothelial function, measuring coronary artery diameter of left anterior descending coronary (LAD) at baseline and after the infusion of acetylcholine, by means of an intracoronary Doppler guide wire. MACE, as cardiac death, myocardial infarction, and heart failure, was evaluated at 24 months of follow-up. RESULTS At baseline, NG patients had a lower percentage of LAD endothelial dysfunction compared with pre-DM patients (P < 0.05). The pre-DM patients had a higher percentage of endothelial LAD dysfunction as compared with the pre-DM metformin patients (P < 0.05). At the 24th month of follow-up, MACE was higher in pre-DM versus NG (P < 0.05). In pre-DM metformin patients, MACE was lower compared with pre-DM patients (P < 0.05). CONCLUSIONS Metformin therapy may reduce the high risk of cardiovascular events in pre-DM patients by reducing coronary endothelial dysfunction.

Background Left main (LM) coronary atresia (LMCA) is a rare coronary anomaly where the LM is congenitally absent and a variable clinical spectrum can follow. The diagnosis of LMCA is generally made in youth because of the development of symptoms, but very rarely in adulthood. In symptomatic patients, surgical revascularization is recommended, whereas, in asymptomatic patients with LMCA and without inducible myocardial ischaemia, preventive surgical treatment is controversial. Case summary A 58-year-old male patient with aortic ectasia detected during an echocardiogram performed to evaluate a hypertension-related preclinical cardiac damage and, due to this finding, an echocardiographic follow-up was suggested. Three years later, he was admitted to undergo coronary angiography (CA) after the computed tomography finding of a suspected occlusion of the LM with collateral circulation from right coronary artery (RCA) to left anterior descending and circumflex arteries. CA confirmed an LMCA and the RCA provided blood supply to the left coronary artery through collaterals whose calibre was similar to that of the target left-sided vessels. No obstructive coronary artery disease was detected. In order to detect potential myocardial ischaemia, a technetium-tetrofosmin cardiac single-photon emission computed tomography during maximal exercise-stress test was performed and it did not show a perfusion defect. Medical management with scheduled follow-up visits was deemed to be the best therapeutic option. Discussion LMCA is a rare anomaly where LM is absent and the RCA provides collateral circulation for left coronary artery. In asymptomatic patients, preventive surgical treatment is controversial.

Objectives: We examined the association of the coronary thrombus microbiota and relative metabolites with major adverse cardiovascular events (MACE) in hyperglycemic patients with ST segment elevation myocardial infarction (STEMI). Background: Hyperglycemia during STEMI may affect both development and progression of coronary thrombus via gut and thrombus microbiota modifications. Methods: We undertook an observational cohort study of 146 first STEMI patients treated with primary percutaneous coronary intervention (PPCI) and thrombus-aspiration (TA). Patients were clustered, based on admission blood glucose levels, in hyperglycemic (≥140 mg/dl) and normoglycemic (

Objectives. We examined the association of the coronary thrombus microbiota and relative metabolites with major adverse cardiovascular events (MACE) in hyperglycemic patients with ST segment elevation myocardial infarction (STEMI).Background. Hyperglycemia during STEMI may affect both development and progression of coronary thrombus via gut and thrombus microbiota modifications. Methods. We undertook an observational cohort study of 146 first STEMI patients treated with primary percutaneous coronary intervention (PPCI) and thrombus-aspiration (TA). Patients were clustered, based on admission blood glucose levels, in hyperglycemic (>140 mg/dl) and normoglycemic (Prevotellaspp and TMAO terziles and MACE. MACE endpoint at 1 year included death, re-infarction, unstable angina.Results. In fecal and thrombus samples, we observed a significantly different prevalence of both Prevotellaspp and Alistipesspp. between patients with hyperglycemia (n=56) and those with normal glucose levels (n=90). The abundance of Prevotella increased in hyperglycemic vs normoglycemic patients whereas the contrary was observed for Alistipes. Interestingly, in coronary thrombus, the content of Prevotella was associated with admission blood glucose levels (pPrevotella and TMAO in coronary thrombus as compared to patients with low levels of Prevotella and TMAO, after 1-year follow up.Conclusions. Hyperglycemia during STEMI may increase coronary thrombus burden via gut and thrombus microbiota dysbiosis characterized by an increase of Prevotella and TMAO content in thrombi.

Background The aim of this multicenter retrospective study was to compare early and midterm clinical and hemodynamic results of aortic valve replacement with rapid-deployment bioprostheses performed through conventional full-sternotomy vs mini-sternotomy. Methods Data from the Italian multicenter registry of aortic valve replacement with rapid-deployment bioprostheses (INTU-ITA registry) were analyzed. Patients were divided into 2 groups: full sternotomy (FS) and ministernotomy (MS). Primary endpoint was the comparison of early and midterm mortality. Secondary endpoints were: comparison of intraoperative variables, complications, and hemodynamic performance. A propensity score weighting approach was used for data analysis. Results A total of 1057 patients were analyzed: 435 (41.2%) and 622 (58.8%) in group FS and MS, respectively. Thirty-day mortality was 1.6% and 0.6% in FS and MS groups, respectively (P = .074). cardiopulmonary bypass time was 78.5 minutes and 83 minutes in FS and MS groups, respectively (P = .414). In the overall cohort, the incidence of intraoperative complications and of device success was 3.8% (40 patients) and 95.9% (1014 patients), respectively, with no significant differences between groups. Survival at 1, 3, and 5 years was 94.1%, 98.1%, 88.5% and 91.8%, 85.2%, and 84.8% in FS and MS groups, respectively (P = .412). The 2 groups showed similar postoperative gradients (median mean gradient, FS: 10.0 mm Hg, MS: 11.0 mm Hg; P = .170) and also similar incidence of patient–prosthesis mismatch (FS: 7%, MS: 6.4%, P = .647). Conclusions According to our data, rapid-deployment bioprostheses allow the performance of minimally invasive aortic valve replacement with similar surgical times and similar clinical and hemodynamic outcomes to conventional surgery and should be considered the first choice in these procedures.

Anticoagulation is of paramount importance during left atrial appendage occlusion procedure (LAAOP) to prevent periprocedural stroke. We present the case of a 66-year-old male patient who was scheduled to undergo LAAOP because of a prior intracranial bleeding. After transesophageal echocardiography-guided transseptal puncture, intravenous heparin 5,000 IUs were administered obtaining an ACT greater than 300 s. We planned to implant an Amplatzer-Amulet 25 mm LAA occluder through the dedicated 12F delivery sheath. After starting the tug test, TEE suddenly showed a floating thrombus whose proximal part was connected to the delivery cable. Because transesophageal echocardiography showed a good position of the device, we decided to release it and to quickly retrieve as a unit into the right atrium both the delivery cable with attached thrombus and the delivery sheath. We discuss about periprocedural anticoagulation dosing and monitoring and the importance to have specific studies in the setting of LAAOP.

Traumatic mitral valve regurgitation is a rare and often insidious condition. Clinical presentation is variable and influenced by the anatomic structures injured; when papillary muscles are damaged, the clinical presentation is often acute, whereas, in the case of involvement of other anatomic structures of the valvular apparatus (e.g. chordae tendinae), the onset of symptoms may be delayed (days, weeks, or months). Therefore, diagnosis may be belated because of the heterogeneous clinical presentation. Traumatic mitral valve injury should be excluded in patients admitted to the emergency services with blunt chest trauma, in particular when signs or symptoms of acute heart failure occur. Echocardiography, particularly with the transoesophageal approach, may play a pivotal role in this setting. Herein, we present a case of severe mitral regurgitation because of blunt chest trauma and a systematic review of the literature. We examined 192 described cases, classified according to epidemiology, aetiology, anatomic features, clinical presentation, diagnosis, surgical/clinical management and prognosis.

The aim of this retrospective multicenter study was to compare early clinical and hemodynamic outcomes of Perceval-S sutureless (Livanova, London, United Kingdom) and Intuity rapid-deployment (Edwards Lifesciences, Irvine, Calif) bioprostheses.Data from patients who underwent isolated or combined aortic valve replacement with Perceval-S and with Intuity bioprostheses at 18 cardiac surgical institutions were analyzed. Propensity matching was performed to identify similar patient cohorts.We included 911 patients from March 2011 until May 2017. Perceval-S and Intuity valves were implanted in 349 (38.3%) and in 562 (61.7%) patients, respectively. Propensity score identified 117 matched pairs. In the matched cohort, device success was 99.1% and 100% in Perceval-S and Intuity group, respectively (P = 1.000). Thirty-day Valve Academic Research Consortium mortality occurred in 2 (1.7%) and 4 (3.4%) patients in the Perceval-S and in Intuity group, respectively (P = .6834). The rate of postoperative new permanent pacemaker implantation was 6% (7 patients) and 6.8% (8 patients) in the Perceval-S and in Intuity group, respectively (P = .7896). Perceval-S valve implantation requires significantly shorter aortic crossclamp and cardiopulmonary bypass times than Intuity valve implantation (aortic crossclamp time for isolated, 52 ± 14 minutes vs 62 ± 24 minutes; P .0001). Peak transaortic gradients were 22.4 ± 8.1 mm Hg and 19.6 ± 6.7 mm Hg (P = .0144), whereas mean gradients were 11.8 ± 4.7 mm Hg and 10.5 ± 3.9 mm Hg (P = .0388) in the Perceval-S and Intuity groups, respectively.Sutureless Perceval-S and rapid-deployment Intuity bioprostheses provide good and similar early clinical and hemodynamic outcomes. Perceval-S valve implantation requires shorter crossclamp and cardiopulmonary bypass times, whereas Intuity valve implantation provides lower transaortic peak and mean gradients.

We evaluate whether the thrombus aspiration (TA) before primary percutaneous coronary intervention (PPCI) may improve STEMI outcomes in hyperglycemic patients.The management of hyperglycemic patients during STEMI is unclear.We undertook an observational cohort study of 3166 first STEMI. Patients were grouped on the basis of whether they received TA or not. Moreover, among these patients we selected a subgroup of STEMI patients with hyperglycemia during the event (glycaemia 140 mg/dl). The endpoint at 1 year included all-cause mortality, cardiac mortality and re-hospitalization for coronary disease, heart failure and stroke.One-thousand STEMI patients undergoing PPCI to plus TA (TA-group) and 1504 STEMI patients treated with PPCI alone (no-TA group) completed the study. In overall study-population, Kaplan-Meier-analysis demonstrated no significant difference in mortality rates between patients with and without TA (P = 0.065). After multivariate Cox-analysis (HR: 0.94, 95% CI 0.641-1.383) and the addition of propensity matching (HR: 0.86 95% CI 0.412-1.798) TA was still not associated with decreased mortality. By contrast, in hyperglycemic subgroup STEMI patients (TA-group, n = 331; no-TA group, n = 566), Kaplan-Meier-analysis demonstrated a significantly lower mortality (P = 0.019) in TA-group than the no-TA group. After multivariate Cox-analysis (HR: 0.64, 95% CI 0.379-0.963) and the addition of propensity matching (HR: 0.54, 95% CI 0.294-0.984) TA was still associated with decreased mortality.TA was not associated with lower mortality in PPCI for STEMI when used in our large all-comer cohort. Conversely, TA during PPCI for STEMI reduces clinical outcomes in hyperglycemic patients. Trial registration NCT02817542. 25th, June 2016.

Objectives We evaluate whether the thrombus aspiration (TA) before primary percutaneous coronary intervention (PPCI) may improve STEMI outcomes in hyperglycemic patients. Background The management of hyperglycemic patients during STEMI is unclear. Methods We undertook an observational cohort study of 3166 first STEMI. Patients were grouped on the basis of whether they received TA or not. Moreover, among these patients we selected a subgroup of STEMI patients with hyperglycemia during the event (glycaemia > 140 mg/dl). The endpoint at 1 year included all-cause mortality, cardiac mortality and re-hospitalization for coronary disease, heart failure and stroke. Results One-thousand STEMI patients undergoing PPCI to plus TA (TA-group) and 1504 STEMI patients treated with PPCI alone (no-TA group) completed the study. In overall study-population, Kaplan–Meier-analysis demonstrated no significant difference in mortality rates between patients with and without TA (P = 0.065). After multivariate Cox-analysis (HR: 0.94, 95% CI 0.641–1.383) and the addition of propensity matching (HR: 0.86 95% CI 0.412–1.798) TA was still not associated with decreased mortality. By contrast, in hyperglycemic subgroup STEMI patients (TA-group, n = 331; no-TA group, n = 566), Kaplan–Meier-analysis demonstrated a significantly lower mortality (P = 0.019) in TA-group than the no-TA group. After multivariate Cox-analysis (HR: 0.64, 95% CI 0.379–0.963) and the addition of propensity matching (HR: 0.54, 95% CI 0.294–0.984) TA was still associated with decreased mortality. Conclusions TA was not associated with lower mortality in PPCI for STEMI when used in our large all-comer cohort. Conversely, TA during PPCI for STEMI reduces clinical outcomes in hyperglycemic patients. Trial registration NCT02817542. 25th, June 2016

Pectus excavatum can be associated with coronary artery diseases that can become difficult to manage in urgent situations. We describe the use of an off-pump minimally invasive direct coronary artery bypass (MIDCAB) through the fourth intercostal space incision in a patient with pectus excavatum and acute coronary syndrome who previously underwent a cosmetic prosthesis implantation. The patient refused any surgical procedure that could compromise the integrity of his cosmetic prosthesis and a left mini-thoracotomy was a good option to avoid the removal of the prosthesis. The preservation of the integrity of the thoracic cage enhanced chest wall stability and pulmonary function and permitted avoidance of inadvertent cardiac structure iatrogenic injuries. MIDCAB was optimal for the exposure of the left internal thoracic artery and the left anterior descending artery. The deformity of the chest should not be considered as an absolute contraindication to off-pump MIDCAB when other surgical options are not viable, even in emergency situations.

Atrial fibrillation (AF) is the most common arrhythmia and its prevalence is increasing due to the progressive aging of the population. About 20% of strokes are attributable to AF and AF patients are at five-fold increased risk of stroke. The mainstay of treatment of AF is the prevention of thromboembolic complications with oral anticoagulation therapy. Drug treatment for many years has been based on the use of vitamin K antagonists, but recently newer and safer molecules have been introduced (dabigatran etexilate, rivaroxaban, apixaban, and edoxaban). Despite these advances, many patients still do not receive adequate anticoagulation therapy because of contraindications (relative and absolute) to this treatment. Over the last decade, percutaneous closure of left atrial appendage, main site of thrombus formation during AF, proved effective in reducing thromboembolic complications, thus offering a valid medical treatment especially in patients at increased bleeding risk. The aim of this consensus document is to review the main aspects of left atrial appendage occlusion (selection and multidisciplinary assessment of patients, currently available methods and devices, requirements for centres and operators, associated therapies and follow-up modalities) having as a ground the significant evolution of techniques and the available relevant clinical data.

Atrial fibrillation (AF) is the most common arrhythmia and its prevalence is increasing due to the progressive aging of the population. About 20% of strokes are attributable to AF and AF patients are at 5-fold increased risk of stroke. The mainstay of treatment of AF is the prevention of thromboembolic complications with oral anticoagulation therapy. Drug treatment for many years has been based on the use of vitamin K antagonists, but recently newer and safer molecules have been introduced (dabigatran etexilate, rivaroxaban, apixaban and edoxaban). Despite these advances, many patients still do not receive adequate anticoagulation therapy because of contraindications (relative and absolute) to this treatment. Over the last decade, percutaneous closure of left atrial appendage, main site of thrombus formation during AF, proved effective in reducing thromboembolic complications, thus offering a valid medical treatment especially in patients at increased bleeding risk. The aim of this consensus document is to review the main aspects of left atrial appendage occlusion (selection and multidisciplinary assessment of patients, currently available methods and devices, requirements for centers and operators, associated therapies and follow-up modalities) having as a ground the significant evolution of techniques and the available relevant clinical data.

Spontaneous coronary artery dissection is a rare condition usually encountered in young women without risk factors for atherosclerotic disease but with tortuous coronary artery or contemporary presence of fibromuscular dysplasia. Sometimes spontaneous coronary dissection occurs in patients with atherosclerotic disease, although without significant epicardial coronary artery stenosis. We report a case of a patient who underwent minimally invasive mitral valve repair, whose initially uneventful postoperative course was complicated by spontaneous coronary artery dissection of the left main causing a life threatening condition. A subsequent emergency sternotomy was required to perform a coronary artery bypass.

CONTEXT: A strong association between subclinical hypothyroidism (SCH) and atherosclerotic diseases, independent of the traditional risk factors, was noted. OBJECTIVE: The objective of the study was to evaluate the association between SCH and the inflammatory potential of atherosclerotic plaques as well as the role of L-T(4) replacement therapy (LTR) on regulation of plaque inflammation. EXPERIMENTAL DESIGN AND MAIN OUTCOME MEASURES: We examined the differences in macrophage content, proinflammatory cytokine infiltration, and oxidative stress between asymptomatic carotid plaques of patients with and without SCH and LTR. SETTING AND PARTICIPANTS: Plaques were obtained from 23 SCH patients with LTR (treated), 34 untreated SCH patients, and 30 control patients without SCH enlisted to undergo carotid endarterectomy for extracranial high-grade (>70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T lymphocytes, human leukocyte antigen (HLA)-DR(+) cells, nuclear factor-κB (NF-κB), inhibitory-κBβ (IκBβ), TNF-α, nitrotyrosine, matrix metalloproteinase-9 (MMP-9), and collagen content (immunohistochemistry and ELISA). RESULTS: Compared with control plaques, SCH plaques had more macrophages, T lymphocytes, and HLA-DR(+) cells, TNF-α, NF-κB, markers of oxidative stress (nitrotyrosine and O(2-) production), and MMP-9 (P < 0.01, for all), along with a lesser collagen content and IκBβ levels (P < 0.001). Compared with plaques from treated patients, plaques from untreated patients had more macrophages, T lymphocytes, HLA-DR(+) cells, TNF-α, NF-κB (P < 0.001), nitrotyrosine, O(2-) production, and MMP-9 (P < 0.01, for all), along with a lesser collagen content and IκBβ levels (P

Objectives. We analyzed the molecular mechanisms evoked by tight glycemic control during post-infarction remodeling in human hearts. Background. The molecular mechanisms by which tight glycemic control improves heart remodeling during acute myocardial infarction (AMI) are still largely unknown. Methods. Eighty-eight patients with first AMI undergoing coronary bypass surgery were studied: 38 normoglycemic patients served as the control group; hyperglycemic patients (glucose =140 mg/dl) were randomized to intensive glycemic control (IGC) (n = 25; glucose 80 to 140 mg/dl) or conventional glycemic control (CGC) (n = 25; glucose 180 to 200 mg/dl) for almost 3 days before surgery, with insulin infusion followed by subcutaneous insulin treatment. Echocardiographic parameters were investigated at admission and after treatment period. During surgery, oxidative stress (nitrotyrosine, superoxide anion [O2 –] production, inducible nitric oxide synthase [iNOS]),inflammation (nuclear factor kappa B [NF_B], tumor necrosis factor [TNF]-a, and apoptosis (caspase-3) were analyzed in biopsy specimens taken from the peri-infarcted area. Results. Compared with normoglycemic patients, hyperglycemic patients had higher myocardial performance index (MPI) (p < 0.05), reduced ejection fraction (p 0.05), more nitrotyrosine, iNOS, and O2 _ production, more macrophages, T-lymphocytes, and HLA-DR (Dako, Milan, Italy) cells, and more NF_B-activity, TNF-a, and caspase-3 levels (p < 0.01) in peri-infarcted specimens. After the treatment period, plasma glucose reduction was greater in the IGC than in the CGC group (p < 0.001). Compared with IGC patients, CGC patients had higher MPI (p _0.02), had lower ejection fraction (p < 0.05), and had more markers of oxidative stress, more inflammation and apoptosis (p < 0.01) in peri-infarcted specimens. Conclusions. Tight glycemic control, by reducing oxidative stress and inflammation, might reduce apoptosis in peri-infarcted areas and remodeling in AMI patients.

Whether morning blood pressure surge influences the molecular mechanisms of plaque progression toward instability is not known. Recently, we have demonstrated enhanced activity of the ubiquitin–proteasome system in human plaques and evidenced that it is associated with inflammatory-induced plaque rupture. We evaluated the inflammatory infiltration and ubiquitin–proteasome activity in asymptomatic carotid plaques of hypertensive patients with different patterns of morning blood pressure surge. Plaques were obtained from 32 hypertensive patients without morning blood pressure surge and 28 with morning blood pressure surge enlisted to undergo carotid endarterectomy for extracranial high-grade (>70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T-lymphocytes, human leukocyte antigen–DR+cells, ubiquitin–proteasome activity, nuclear factor-κB, inhibitor kB-β, tumor necrosis factor-α, nitrotyrosine, matrix metalloproteinase-9, and collagen content (immunohistochemistry and ELISA). Compared with plaques obtained from hypertensive patients without morning blood pressure surge, plaques from with morning blood pressure surge had more macrophages, T-lymphocytes, human leukocyte antigen–DR+cells ( P P P P

Pseudoaneurysm formation some years after aortic root or ascending aorta surgery, complicated by fistula formation through a branch of the pulmonary artery, is a rare condition described only in case reports. We describe a case of this rare complication in a 58-year-old man, which occurred 13 years after aortic surgery and was characterized by a huge pseudoaneurysm of 70 mm that fistulized into the right pulmonary artery, causing a life-threatening situation.

Increased Activity of the Ubiquitin-Proteasome System in Patients With Symptomatic Carotid Disease Is Associated With Enhanced Inflammation and May Destabilize the Atherosclerotic Plaque: Effects o...

The role of ubiquitin-proteasome system in the accelerated atherosclerotic progression of diabetic patients is unclear. We evaluated ubiquitin-proteasome activity in carotid plaques of asymptomatic diabetic and nondiabetic patients, as well as the effect of rosiglitazone, a peroxisome proliferator–activated receptor (PPAR)-γ activator, in diabetic plaques. Plaques were obtained from 46 type 2 diabetic and 30 nondiabetic patients undergoing carotid endarterectomy. Diabetic patients received 8 mg rosiglitazone (n = 23) or placebo (n = 23) for 4 months before scheduled endarterectomy. Plaques were analyzed for macrophages (CD68), T-cells (CD3), inflammatory cells (HLA-DR), ubiquitin, proteasome 20S activity, nuclear factor (NF)-κB, inhibitor of κB (IκB)-β, tumor necrosis factor (TNF)-α, nitrotyrosine, matrix metalloproteinase (MMP)-9, and collagen content (immunohistochemistry and enzyme-linked immunosorbent assay). Compared with nondiabetic plaques, diabetic plaques had more macrophages, T-cells, and HLA-DR+ cells (P < 0.001); more ubiquitin, proteasome 20S activity (TNF-α), and NF-κB (P < 0.001); and more markers of oxidative stress (nitrotyrosine and O2− production) and MMP-9 (P < 0.01), along with a lesser collagen content and IκB-β levels (P < 0.001). Compared with placebo-treated plaques, rosiglitazone-treated diabetic plaques presented less inflammatory cells (P < 0.01); less ubiquitin, proteasome 20S, TNF-α, and NF-κB (P < 0.01); less nitrotyrosine and superoxide anion production (P < 0.01); and greater collagen content (P < 0.01), indicating a more stable plaque phenotype. Similar findings were obtained in circulating monocytes obtained from the two groups of diabetic patients and cultured in the presence or absence of rosiglitazone (7.0 μmol/l). Ubiquitin-proteasome over-activity is associated with enhanced inflammatory reaction and NF-κB expression in diabetic plaques. The inhibition of ubiquitin-proteasome activity in atherosclerotic lesions of diabetic patients by rosiglitazone is associated with morphological and compositional characteristics of a potential stable plaque phenotype, possibly by downregulating NF-κB-mediated inflammatory pathways.

OBJECTIVE—Stress hyperglycemia has been associated with increased mortality in patients with myocardial infarction (MI). We examined the association between plasma glucose levels, circulating inflammatory markers, T-cell activation, and functional cardiac outcome in patients with first MI. RESEARCH DESIGN AND METHODS—Echocardiographic parameters, circulating levels of interleukin-18 (IL-18), C-reactive protein (CPR), and the percent of CD16-CD56, CD4/CD8, CD152, and HLA-DR expression were investigated in 108 patients with acute MI on admission to the emergency ward. RESULTS—Our review found that 31 new hyperglycemic patients (glycemia ≥7 mmol/l) had higher infarct segment length (P < 0.05) and myocardial performance index (P < 0.02) and reduced transmitral Doppler flow (P < 0.05), pulmonary flow analysis (P < 0.02), and ejection fraction (P < 0.05) compared with 36 hyperglycemic diabetic patients and 41 normoglycemic patients. Plasma IL-18 and CRP were higher in the hyperglycemic than in the normoglycemic patients (P < 0.005), with the highest values in patients with new hyperglycemia (P < 0.05). Hyperglycemic patients had a higher percent of CD16+/CD56+ cells and CD4/CD8 ratio (P < 0.01), whereas they had lower CD152 expression (which has a negative regulatory function in T-cell activation) compared with normoglycemic patients (P < 0.001). CONCLUSIONS—During MI, hyperglycemia is associated with increased levels of inflammatory markers, enhanced expression of cytotoxic T-cells, and reduced expression of T-cells, which are implicated in limiting the immune process. An increased inflammatory immune process seems a likely mechanism linking acute hyperglycemia to poor cardiac outcome in MI patients.

Bronchial artery embolization is a well-known treatment for hemoptysis. Adverse events of this procedure include multiple systemic embolism and infarction. Myocardial infarction has been recently reported during bronchial artery embolization, owing to the presence of a coronary-to-bronchial artery fistula. We report the management of an ischemic left ventricular free wall rupture caused by bronchial artery embolization in a patient with massive hemoptysis, bronchiectasis, and undetected coronary-to-bronchial artery anomalous connection.

An imbalance of Nuclear Factor Kappa B (NFкB) and Inhibitor Kappa B (IкB) is involved in various human diseases including atherogenesis. We aimed to evaluate the relationship between NFKB1 and NFKBIA polymorphism and susceptibility to myocardial infarction (MI).Genotyping was performed for NFKB1 and NFKBIA gene variants in 253 subjects (86 patients affected by myocardial infarction and 167 control subjects). In 40 patients, biopsy specimens were taken from the left ventricle area of presumed ischemia for p50, p65 and IкBα quantification. The allele frequency and genotype distribution of NFKBIA gene polymorphism did not differ between MI and control group while control subjects had a higher D allele frequency of -94 ins/del ATTG NFKB1 polymorphism, compared to the MI group (P0.001; OR=0.304; 95% CI=0.177-0.522). Subjects carrying the D allele had significantly lower plasma fibrinogen and CRP (C-reactive protein) levels compared to no carriers (P0.05). Fibrinogen-genotype interaction was found to have a significant effect on susceptibility to myocardial infarction. Myocardial p50 (r=0.627; P=0.012) and p65 (r=0.683; P=0.005) levels significantly correlated with plasma fibrinogen levels while subjects carrying the D allele of the NFкB1 gene variant had lower myocardial p50 (P=0.007) and p65 (P=0.009) levels compared to no carriers.-94 ins/del ATTG NFKB1 gene variant may contribute to lower MI susceptibility via the potential reduction of activated NFкB which in turn is related to plasma inflammatory marker reduction.

Eighteen years after its first introduction for coronary artery revascularization, the radial artery (RA) was reinvestigated because of unexpected good long-term results in the early series. Since July 1989, 104 patients underwent myocardial revascularization using 122 RA grafts (18 patients received two grafts). The left internal mammary artery (IMA) was concomitantly used as a pedicled graft in 100 cases and the right IMA in 19 cases; a free IMA graft was used in 29 cases and a saphenous vein graft in 24 cases. A mean of 2.8 grafts per patient were performed. Nine patients underwent associated procedures: carotid endarterectomy (3), aortic valve replacement (3), Bigelow procedure (1), and mitral valve repair (2). The target artery receiving the RA was the circumflex (n = 59), diagonal (n = 29), right coronary (n = 27), and left anterior descending (n = 7). One patient died (0.96%) and 2 had perioperative myocardial infarct. Sternal wound infection was noted in 3 cases of double IMA implantation. No ischemia of the hand was observed. All patients received diltiazem started intraoperatively and continued after discharge. In addition aspirin (100 mg/day) was given at discharge. Early angiographic controls (less than 2 weeks) were obtained in the first 50 consecutive patients and revealed 56 of 56 patent RA grafts, 48 of 48 patent left IMA grafts, 11 of 11 patent right IMA grafts, 14 of 18 patent free IMA grafts, and 8 of 9 patent vein grafts.(ABSTRACT TRUNCATED AT 250 WORDS)

Reports concerning unruptured, isolated aneurysms of one sinus of Valsalva are rare. These aneurysms usually protrude inside the heart and are very rarely extracardiac. We report 4 cases of isolated, unruptured extracardiac aneurysms of the noncoronary sinus of Valsalva. Clinical symptoms were nonspecific. Operation was performed by patch reconstruction of the dilated aortic sinus without replacement of the ascending aorta. Microscopic examination of the diseased aortic wall revealed absence of medial elastic fibers. Late follow-up in all 4 cases revealed a normal ascending aorta with no dilatation of the aortic root and no aortic regurgitation.

To the editor: Treatment with thiazolidinedione (TZD), an agonist of peroxisome proliferator-activated receptor-γ (PPARγ), has been associated with a significant increase in heart failure in type 2 diabetic patients.1 These ligand-activated nuclear transcription factors (rosiglitazone and pioglitazone) are implicated in adipogenesis and tissue lipid accumulation.2 Indeed, myocyte overexpression of PPARγ, leads to lipotoxic cardiomyopathy in both transgenic mice overexpressing PPARγ and TZD-treated diabetic mice.3 Thus, while PPARγ agonists appear to have beneficial effects on metabolic control,4 their direct actions on myocardium may impair heart function, inducing lipid accumulation. To examine these concerns, we analysed lipid accumulation and PPARγ expression in myocardial biopsy specimens obtained from type 2 diabetic patients with and without TZD treatment who underwent surgical valve replacement for mitral stenosis (MS), and related them to the heart function. Nineteen non-TZD-treated and 13 TZD-treated (⩾24 weeks of monotherapy in the previous year) type 2 diabetic patients who underwent mitral valve replacement (area⩽1.2 cm2) participated in the study. Patients …

I read with interest the increasing number of scientific articles involving transcatheter aortic valve replacement. The meaning of the term “replacement” is to substitute something with something else. Yet, at present, the only way to substitute a stenotic aortic valve is to take away the calcific or fibrotic tissue and put in a new prosthetic valve, which is a surgical (traditional or minimally invasive) approach. I believe this is not merely a semantic question. As a matter of fact, the presence of the native valve left in situ could be one of the major potential issues affecting the outcome of the transcatheter procedures: peri-procedural risk of stroke and perivalvular leak or infection could be highly related to this aspect. For these reasons, I believe that the transcatheter procedure could be defined as “implant, insertion, overlapping or therapy,” but not as aortic valve replacement.

Background: Because the ubiquitin-proteasome pathway (UPS) is required for activation of nuclear factor kappa beta (NFkB), a transcription factor that regulates inflammatory genes, we evaluated the UPS activity, NFkB activation, and tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, in ischemic specimens of diabetic myocardium and relate them to the glycemic control (HbA1c), oxidative stress (nitrotyrosine, a modified amino acid produced by reactive O2), and cardiac outcome (echocardiographic parameters). Moreover, the role of UPS, NFkB, and TNF-alpha in the cardiac tissue injury of acute ischemia/reperfusion (I/R) was evaluated in streptozotocin (STZ)-hyperglycemic rats. Finally, this study aimed to elucidate whether an intervention on UPS with bortezomib, an inhibitor of UPS, may counteract the extensive myocardial infarction and increased inflammatory reaction into the hyperglycemic myocardium. Methods: Ventricular biopsy specimens from 16 nondiabetic and 18 type 2 diabetic patients presenting with unstable angina who underwent coronary artery bypass were collected during coronary bypass surgery. Ejection fraction (EF); myocardial performance index (MPI), which measures both systolic and diastolic function, immunostaining, and cardiac levels of nitrotyrosine; UPS activity; NFkB; and TNF-alpha were investigated in both ischemic human myocardium and heart tissue from STZ-hyperglycemic rats subject to a myocardial ischemia/reperfusion procedure. Results: We found that diabetic patients had higher MPI (P

We evaluated the role of sterol-regulatory element binding protein (SREBP)-1c/peroxisome proliferator activated receptor-gamma (PPARgamma) pathway on heart lipotoxicity in patients with metabolic syndrome (MS) and aortic stenosis (AS). Echocardiographic parameters of heart function and structural alterations of LV specimens were studied in patients with (n = 56) and without (n = 61) MS undergoing aortic valve replacement. Tissues were stained with hematoxylin-eosin (H and E) and oil red O for evidence of intramyocyte lipid accumulation. The specimens were also analyzed with PCR, Western blot, and immunohistochemical analysis for SREBP-1c and PPARgamma. Ejection fraction (EF) was lower in MS compared with patients without MS (P < 0.001); no difference was found in aortic orifice surface among the groups. H and E and oil red O staining of specimens from MS patients revealed several myocytes with intracellular accumulation of lipid, whereas these alterations were not detected in biopsies from patients without MS. Patients without MS have low levels and weak immunostaining of SREBP-1c and PPARgamma in heart specimens. In contrast, strong immunostaining and higher levels of SREBP-1c and PPARgamma were seen in biopsies from the MS patients. Moreover, we evidenced a significative correlation between both SREBP-1c and PPARgamma and EF and intramyocyte lipid accumulation (P < 0.001). SREBP-1c may contribute to heart dysfunction by promoting lipid accumulation within myocytes in MS patients with AS; SREBP-1c may do it by increasing the levels of PPARgamma protein.

Familial hypercholesterolemia is an inherited disorder with incidences of approximately 1:500 and 1:1,000,000 in heterozygous and homozygous form respectively. Affected patients usually show early coronary artery disease and severe aortic root calcification, despite optimization of therapy. We report a case of a 64-year-old woman affected by heterozygous familial hypercholesterolemia which presented dyspnea and anginal symptoms due to a severely calcified aortic root causing valve stenosis and narrowed sinotubular junction. Aortic valve replacement and aortic root enlargement were performed using the Manougian procedure. Even for experiences surgeons, this surgery could prove challenging for this group of patients due to aggressive degenerative tissue calcification of the aortic root, which often presents an extremely calcified aortic valve with a small annulus associated to a narrowed sinotubular junction.