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Calcific aortic valve disease (CAVD)—the most common valvular heart disease—is accelerated in diabetes and has no pharmacotherapy. Although it is known that early CAVD is associated with inflammation and osteogenesis, the molecular mechanisms involved in diabetes‐associated CAVD still need to be uncovered. In this context, we have developed a 3D construct based on gelatin populated with human valvular endothelial cells (VEC) and valvular interstitial cells (VIC) and evaluated the effect of high glucose (HG) concentration on osteogenic molecules expression and on calcification mechanisms. First, we characterized the 3D model and assessed VIC remodelling properties at different time‐points. Then, we exposed it to normal glucose (NG) or high glucose (HG) for 7, 14 and 21 days after which the cells were isolated, separated and investigated individually. Our results showed that encapsulated VIC actively remodel the hydrogel, as demonstrated by an increased expression of extracellular matrix (ECM) proteins and matrix metalloproteinases (MMPs). Moreover, exposure of the construct to HG triggered bone morphogenetic protein (BMP) and TGF‐β signalling pathways, up‐regulating expression of osteogenic molecules—BMP‐2/‐4, osteocalcin, osteopontin, SMADs and Runt‐related transcription factor (Runx‐2)—and increased calcium deposits in an osteogenic environment. These findings underline the potential of the developed 3D model as a suitable system to investigate the mechanisms of human CAVD and may help to better understand the calcification mechanisms in CAVD associated to diabetes.

Calcific aortic valve disease (CAVD) is a progressive inflammatory disorder characterized by extracellular matrix remodeling and valvular interstitial cells (VIC) osteodifferentiation leading to valve leaflets calcification and impairment movement. Runx2, the master transcription factor involved in VIC osteodifferentiation, modulates the expression of other osteogenic molecules. Previously, we have demonstrated that the osteoblastic phenotypic shift of cultured VIC is impeded by Runx2 silencing using fullerene (C60)-polyethyleneimine (PEI)/short hairpin (sh)RNA-Runx2 (shRunx2) polyplexes. Since the use of polyplexes for in vivo delivery is limited by their instability in the plasma and the non-specific tissue interactions, we designed and obtained targeted, lipid-enveloped polyplexes (lipopolyplexes) suitable for (1) systemic administration and (2) targeted delivery of shRunx2 to osteoblast-differentiated VIC (oVIC). Vascular cell adhesion molecule (VCAM)-1 expressed on the surface of oVIC was used as a target, and a peptide with high affinity for VCAM-1 was coupled to the surface of lipopolyplexes encapsulating C60-PEI/shRunx2 (V-LPP/shRunx2). We report here that V-LPP/shRunx2 lipopolyplexes are cyto- and hemo-compatible and specifically taken up by oVIC. These lipopolyplexes are functional as they downregulate the Runx2 gene and protein expression, and their uptake leads to a significant decrease in the expression of osteogenic molecules (OSP, BSP, BMP-2). These results identify V-LPP/shRunx2 as a new, appropriately directed vehicle that could be instrumental in developing novel strategies for blocking the progression of CAVD using a targeted nanomedicine approach.

Parathyroid hormone (PTH) is a key regulator of calcium, phosphate and vitamin D metabolism. Although it has been reported that aortic valve calcification was positively associated with PTH, the pathophysiological mechanisms and the direct effects of PTH on human valvular cells remain unclear. Here we investigated if PTH induces human valvular endothelial cells (VEC) dysfunction that in turn could impact the switch of valvular interstitial cells (VIC) to an osteoblastic phenotype. Human VEC exposed to PTH were analyzed by qPCR, western blot, Seahorse, ELISA and immunofluorescence. Our results showed that exposure of VEC to PTH affects VEC metabolism and functions, modifications that were accompanied by the activation of p38MAPK and ERK1/2 signaling pathways and by an increased expression of osteogenic molecules (BMP-2, BSP, osteocalcin and Runx2). The impact of dysfunctional VEC on VIC was investigated by exposure of VIC to VEC secretome, and the results showed that VIC upregulate molecules associated with osteogenesis (BMP-2/4, osteocalcin and TGF-β1) and downregulate collagen I and III. In summary, our data show that PTH induces VEC dysfunction, which further stimulates VIC to differentiate into a pro-osteogenic pathological phenotype related to the calcification process. These findings shed light on the mechanisms by which PTH participates in valve calcification pathology and suggests that PTH and the treatment of hyperparathyroidism represent a therapeutic strategy to reduce valvular calcification.

With the introduction into clinical practice and increasingly frequent application of endovascular repair of abdominal aortic aneurysms (EVAR), along with the well-known benefits of minimally invasive interventions, controversies arise associated to new treatment methods. These controversies include the medium and long-term results of EVAR influenced by the potential occurrence of procedure-specific complications. To maintain the long-term success of EVAR, namely to eliminate the risk of aneurysm rupture, lifelong, regular imaging surveillance must redocument and reassure the exclusion of the aneurysm sac from the systemic circulation. We hereby propose an effective and safe duplex ultrasound/contrast-enhanced ultrasound-based surveillance protocol that would lead to a significant reduction in the number of computed tomography scans required as part of the postoperative surveillance with a resultant reduction in exposure to both ionizing radiation and intravenous nephrotoxic contrast and a significant cost saving.

Abdominal aortic aneurysm (AAA) represents a major health problem affecting 2%–8% of males over the age of 60 and 1% of women older than 64 years. A lot of patients with AAA remain asymptomatic until the rupture occurs. Early diagnostic and prophylactic surgical intervention (open or endovascular) is essential to prevent rupture. The open repair remains the most durable intervention but the actual approach moves to endovascular aneurysmal repair (EVAR) in most countries. EVAR is nowadays considered the technique of first choice for infrarenal AAAs with suitable aortic anatomy. There are new evolving technologies making endovascular approach suitable to almost all type of aortic morphology as well as acute or chronic pathologies. Patient selection is crucial in the successful treatment of AAA. We should carefully investigate and consider the anatomy of the abdominal aorta but also the comorbidities of the patient when we establish the treatment we propose. Medium and long-term results have improved over the years both in open and endovascular approaches due to better preoperative planning and postoperative management but also to new and refined devices for endovascular treatment.

Acute massive pulmonary embolism (PE) is a life threatening condition requiring quick diagnosis and intervention. The mortality rate in this acute entity is high despite progress in therapeutically strategies. Acute PE is the third most common cause of death among hospitalized patients. Currently, multidisciplinary teams with cardiovascular surgeons’ involvement have introduced again the surgical embolectomy on cardiopulmonary bypass for high risk patients with PE and also for selected patients with intermediate-high risk, particularly if thrombolysis is contraindicated or failed. There is also recent evidence data that supports prompt multidisciplinary approach and individualized indication of surgery before hemodynamic collapse, while the mortality rates are of 6% or less. Complete removal of thrombotic material from pulmonary arteries is the best predictor to avoid persistent pulmonary artery hypertension. Acute pulmonary embolectomy on cardiopulmonary bypass is safe and it has good and long-lasting results in patients with severe right ventricular dysfunction.

A 55-year-old female who undergone mitral valve replacement eight years ago with a mechanical graft, presented accusing sudden decrease of effort tolerance and two episodes of pulmonary edema in the last month. Anamnesis, physical examination, electrocardiogram (ECG), transthoracic echocardiography and coronarography were performed. The mechanical valve leaflets and the tissue surrounding the prosthetic ring were evaluated by: optical microscopy (hematoxylin eosin stain and immunohistochemistry), scanning electron microscopy (SEM) and EDAX analysis (Energy Dispersive X-ray spectroscopy). Anamnesis: inferior myocardial infarction in 2006, congestive cardiac insufficiency, pulmonary hypertension, and arterial hypertension. Clinical examination and ECG: minimal perimaleolar edema bilateral, sinus rhythm on admission. Transthoracic echocardiography: 55% ejection fraction, a pression gradient across the mitral valve (Gmax/Gmed= 24/11 mmHg), tricuspid regurgitation, and pulmonary hypertension. A mitral prosthetic valve’s leaflet was found immobile. No thrombus was evidenced. Coronarography: an immobile graft’s leaflet, stenoses on the right coronary artery, stenosis on left anterior descending artery and occlusion at the circumflex artery emergence. The prosthesis was replaced, and two coronary artery bypasses were performed. Macroscopic examination: a fibroconjunctive tissue expansion in close contact with the leaflet. Histopathological evaluation: muscle cells with altered phenotypes, fibroblasts along with fibrous connective tissue and calcium depots areas. SEM evaluation: tissue depots on the immobile leaflet, suggesting that the connective tissue expansion was blocking the leaflet’s movements. EDAX analysis: the metallic leaflets surface was made of tantalum; sodium, calcium and chloride deposits were also detected. Graft failure was caused by the tissue proliferation affecting leaflet’s mobility. SEM is a viable method for failed cardiovascular grafts investigation.

Endovascular aneurysm repair (EVAR) is an attractive alternative to open surgical approach in treating abdominal aortic aneurysms (AAA). In Nuerenberg in our 14-year experience of 1502 cases (ending December 2007) we used 13 different endografts. The median follow-up was 41 months (1.0-98) and the AAA had a mean diameter of 52.4 mm. Five-hundred and nineteen cases were done using Powerlink grafts. The 30 day mortality was 1.7%. The total reintervention rate was 5.3%, while no distal migration, conversion or post EVAR rupture occurred. At the Army's Center for Cardiovascular Diseases, Bucharest, between July 2008 and December 2009, 15 patients underwent EVAR for AAA. We used the following types of endografts: one Anaconda, three Medtronic Talent, seven Endologix Powerlink and four EVITA Jotec. The mean hospitalization time was three days. Follow-up was done by CT-scan at one, three, six, and 12 months. No endoleaks or infection were seen in the short and medium term follow-up. EVAR is an appropriate treatment for selected patients, especially those at high risk for open surgical repair. The future of EVAR as the potential gold standard for aortic aneurysm therapy rests upon the vision and creativity of both surgeons and technology innovators to realize the potential of endovascular interventions.

The approach to aortic pathology is nowadays more and more endovascular at both thoracic and abdominal levels. Thoracic stenting has gained worldwide acceptance as first intention to treat pathologies of the descending thoracic aorta. Indications have been extended to aortic arch aneurysms and also to diseases of the ascending aorta. The current devices in use for thoracic endovascular repair (TEVAR) are Medtronic Valiant, Gore TAG, Cook Tx2 and Jotec. The choice of the endograft depends on the thoracic aortic pathology and the anatomical suitability. The technological evolution of the abdominal aortic endografts was very rapid, arriving now at the fourth generation. We report the results of 55 elective cases of endovascular abdominal aortic repair (EVAR) performed in two vascular surgical centers in Romania and Germany. The prostheses used were 16 E-vita Abdominal XT, 12 Excluder, eight Talent, seven PowerLink, three Endurant and nine custom-made, fenestrated or branched from Jotec. The mean follow-up was 18 months with CT-scan, duplex ultrasound and contrast-enhanced ultrasound. The mortality was 2%. EVAR tends to become the gold standard for abdominal aortic aneurysm repair. Technological development of the devices with lowest profile introduction systems will permit to extend the anatomical indications to new frontiers.

Background In order to elucidate the diagnosis and the correct therapeutic approaches, the present high degree of specialization, as well as the complex, frequent “borderline” pathology, impose an inter-disciplinary cooperation. We presented the main infections that imposed an inter-disciplinary cooperation; we enunciate the main imposed problems, as well as a unitary vision for these approaches.

Cardiovascular disease is a leading cause of death in all developed countries. In response to this need, endovascular management techniques have been developed across a large range of medical specialties. Minimally invasive percutaneous interventions were initially complex and challenging, but with the continued development of equipment and expertise their use has become routine in many fields. With routine use, it has become important to establish the safety and efficacy of endovascular treatments against the respective "gold standard" procedures, especially in light of their initial intended use for the management of patients at unacceptably high risk for standard therapy only. Such evaluation has to take into account the variety and diversity of devices and techniques, as well as the effects of operator dependability. Endovascular techniques are increasingly recognised as valid alternative management options for a variety of conditions, and it is anticipated that the current trend towards minimally invasive techniques will continue in the future, with moves towards increasingly complex endovascular techniques and hybrid interventions.

Heart failure patients present an important thrombo-embolic risk, including symptomatic or silent peripheral arterial embolism, pulmonary embolism, and stroke. Patients in sinus rhythm who have concomitant depressed (< 35%) left ventricular ejection fraction have a 4% rate of embolic events. Several prospective randomized trials of anticoagulation in this group of patients were either underpowered or had a short period of follow-up. Even though in two studies warfarin had a slight advantage over aspirin (in the WATCH and WARCEF trials), it was at the cost of an increased risk in major hemorrhage. To decrease bleeding rates and to improve anticoagulant effect, new treatment strategies have to be tested. Novel anticoagulants (dabigatran, rivaroxaban, and apixaban) seem to be a promising alternative.

Abdominal aortic aneurysms are identified in the elderly population; only a few patients die because of AAA rupture prior to the age of 60. The incidence of the disease in the general population is 60/1000 inhabitants [4] and between 1.8% and 6.6% in autopsies studies. In studies of natural history of AAA the rate of aneurysm rupture and death could exceed 60% within 3 years of the initial diagnosis. [5]

The optimal management for pericardial effusions with cardiac tamponade remains controversial. This study compares the results after two commonly performed techniques: subxiphoid surgical pericardial drainage (DPSS) and percutaneous catheter drainage (DPPK).We conducted a 5-year retrospective study to analyse the outcome after DPSS and DPPK in patients with non-traumatic pericardial effusions with cardiac tamponade.Patients with non-traumatic cardiac tamponade were treated with DPSS (N=138) and DPPK (N=54). There were no statistical differences between groups regarding: age, drainage volume and duration of drainage. The etiology was malignant in 72 patients and benign in 120 patients. The 2-year survival was statistically non-significant: 55,1% in the surgical group and 44,4% in the percutaneous group, but there was a slight prevalence of malignant diagnosis in the first group (38% versus 35%). The 1-year survival in patients with proved cyto- hystological malignancy was statistically poorer than in patients with malignant diagnosis and with both negative cytology and hystology (7% versus 33%). The 1-year freedom of re-intervention for recurrence of pericardial effusion was statistically better in the surgical group as in the percutaneous one (92.8% versus 79,6%).DPSS and DPPK can be both safely performed. DPSS appears to decrease intervention-necessitating recurrence, but it brings a minimal advantage for the malignant diagnosis over cytology alone.

The aim of this study was to determine the relations between myocardial revascularization therapy--coronary artery bypass graft (CABG) and coronary angioplasty (PTCA)--and ventricular potentially malignant arrhythmia (VPMA) (coupled VPC, VPC10/hour, NSVT--Morganroth classification), in patients (pts) with stable CAD.765 patients with stable angina and ventricular potentially malignant arrhythmia were evaluated angiochoronarographically, echographically, by programmed electrical stimulation (PES), standard ECG, Holter ECG, radiologically, and by stress test. From 765 patients with CAD and VPMA 169 pts. (22.9% of cases) were revascularized, 77 pts. (10.06% of cases) by CABG surgery and 82 pts. (10.71% of cases) by PTCA with or without stenting.From pts. with inducible sustained ventricular tachycardia by programmed electrical stimulation PES + (129 pts. 16.86% of cases), 19 pts. (2.5% of cases) were with CABG vs 9 pts. (1.17% of cases) with PTCA (p0.05). In 333 pts. with arrhythmogenic myocardic ischemia detected by Holter ECG/24 hours (Holter +) the distribution of myocardial revascularization was similar (40 pts., 5.22% of cases with CABG vs 46 pts., 6.01% of cases with PTCA) (p0.05). The study included 225 pts. with positive stress test, 45 pts. were revascularized, 18 pts. (2.35% of cases) with CABG and 27 pts. (3.52% of cases) with PTCA (p0.05). Revascularized pts. represent an increased percent with prior myocardial infarction in the subgroup with CABG vs. PTCA (39% of cases, p0.05 vs. 25% of cases, p0.05). Revascularized pts. presented similar distributions of VPMA in subgroups with CABG and PTCA.VPMA was not influenced by myocardial revascularization, CABG or PTCA, the incidence being similar (50.94% vs 47.2%; p0.05) with pts. drug treated.