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ObjectiveThis study assessed whether apolipoprotein CIII-lipoprotein(a) complexes (ApoCIII-Lp(a)) associate with progression of calcific aortic valve stenosis (AS).MethodsImmunostaining for ApoC-III was performed in explanted aortic valve leaflets in 68 patients with leaflet pathological grades of 1–4. Assays measuring circulating levels of ApoCIII-Lp(a) complexes were measured in 218 patients with mild–moderate AS from the AS Progression Observation: Measuring Effects of Rosuvastatin (ASTRONOMER) trial. The progression rate of AS, measured as annualised changes in peak aortic jet velocity (Vpeak), and combined rates of aortic valve replacement (AVR) and cardiac death were determined. For further confirmation of the assay data, a proteomic analysis of purified Lp(a) was performed to confirm the presence of apoC-III on Lp(a).ResultsImmunohistochemically detected ApoC-III was prominent in all grades of leaflet lesion severity. Significant interactions were present between ApoCIII-Lp(a) and Lp(a), oxidised phospholipids on apolipoprotein B-100 (OxPL-apoB) or on apolipoprotein (a) (OxPL-apo(a)) with annualised Vpeak (all p<0.05). After multivariable adjustment, patients in the top tertile of both apoCIII-Lp(a) and Lp(a) had significantly higher annualised Vpeak (p<0.001) and risk of AVR/cardiac death (p=0.03). Similar results were noted with OxPL-apoB and OxPL-apo(a). There was no association between autotaxin (ATX) on ApoB and ATX on Lp(a) with faster progression of AS. Proteomic analysis of purified Lp(a) showed that apoC-III was prominently present on Lp(a).ConclusionApoC-III is present on Lp(a) and in aortic valve leaflets. Elevated levels of ApoCIII-Lp(a) complexes in conjunction with Lp(a), OxPL-apoB or OxPL-apo(a) identify patients with pre-existing mild–moderate AS who display rapid progression of AS and higher rates of AVR/cardiac death.Trial registration NCT00800800.

ObjectivesOptimizing valve implantation depth (ID) plays a crucial role in minimizing conduction disturbances and achieving optimal functional integrity. Until now, the impact of intraprocedural fast (FP) or rapid ventricular pacing (RP) on the implantation depth has not been investigated. Therefore, we aimed to (1) evaluate the impact of different pacing maneuvers on ID, and (2) identify the independent predictors of deep ID.Methods473 TAVR patients with newer-generation self-expanding devices were retrospectively enrolled and one-to-one propensity-score-matching was performed, resulting in a matching of 189 FP and RP patients in each cohort. The final ID was analyzed, and the underlying functional, anatomical, and procedural conditions were evaluated by univariate and multivariate analysis.ResultsThe highest ID was reached under RP in severe aortic valve calcification and valve size 26 mm. Multivariate analysis identified left ventricular outflow (LVOT) calcification [OR 0.50 (0.31–0.81) p = 0.005*], a “flare” aortic root [OR 0.42 (0.25–0.71), p = 0.001*], and RP (OR 0.49 [0.30–0.79], p = 0.004*) as independent highly preventable predictors of a deep ID. In a model of protective factors, ID was significantly reduced with the number of protective criteria (0–2 criteria: − 5.7 mm ± 2.6 vs. 3–4 criteria − 4.3 mm ± 2.0; p < 0.0001*).ConclusionData from this retrospective analysis indicate that RP is an independent predictor to reach a higher implantation depth using self-expanding devices. Randomized studies should prove for validation compared to fast and non-pacing maneuvers during valve delivery and their impact on implantation depth.Trail registrationClinical Trial registration: NCT01805739.Graphic abstractStudy design: Evaluation of the impact of different pacing maneuvers (fast ventricular pacing—FP vs. rapid ventricular pacing—RP) on implantation depth (ID). After one-to-one-propensity-score-matching, independent protective and risk factors for a very deep ID beneath 6 mm toward the LVOT (< − 6 mm) were identified. Stent frame pictures as a courtesy by Medtronic®. AVC aortic valve calcification.

Introduction During arthroscopy, the localization of calcific deposit in patients suffering from calcifying tendinitis can be demanding and time consuming, frequently using ionizing radiation. Intraoperative ultrasound has been recently promoted, facilitating deposit localization and reducing radiation dose. Material and Methods In this prospective, randomized, controlled and clinical observer-blinded pilot trial, 20 patients with calcific tendinitis were operated. In group I, the deposit was localized conventionally. In group II, the deposit was localized using intraoperative ultrasound. The needle punctures to detect the deposit and operation times were noted. Patients were postoperatively evaluated after 2 and 6 weeks and 9 months. Results In group II, the needle punctures to detect the deposit were significantly lower than in group I ( p  < 0.0001). Operation time to localize the deposit was also significantly less in group II ( p  < 0.033). In both groups, patients improved significantly with increased shoulder function ( p  < 0.0001) and decreased pain ( p  < 0.0001) 2 weeks and 9 months ( p  < 0.001) after surgery. The difference between the groups was not significant. Excellent radiological findings were obtained in both groups after 9 months. Conclusions Intraoperative US significantly facilitates the detection of calcific deposits during arthroscopic debridement by speeding up surgery and reducing the number of needle punctures. Hence, we have changed our method of detecting calcific deposits intraoperatively from fluoroscopy to ultrasound.

Objective To investigate the long-term prognostic implications of coronary calcification in patients undergoing percutaneous coronary intervention for obstructive coronary artery disease. Methods Patient-level data from 6296 patients enrolled in seven clinical drug-eluting stents trials were analysed to identify in angiographic images the presence of severe coronary calcification by an independent academic research organisation (Cardialysis, Rotterdam, The Netherlands). Clinical outcomes at 3-years follow-up including all-cause mortality, death—myocardial infarction (MI), and the composite end-point of all-cause death—MI—any revascularisation were compared between patients with and without severe calcification. Results Severe calcification was detected in 20% of the studied population. Patients with severe lesion calcification were less likely to have undergone complete revascularisation (48% vs 55.6%, p<0.001) and had an increased mortality compared with those without severely calcified arteries (10.8% vs 4.4%, p<0.001). The event rate was also high in patients with severely calcified lesions for the combined end-point death—MI (22.9% vs 10.9%; p<0.001) and death—MI— any revascularisation (31.8% vs 22.4%; p<0.001). On multivariate Cox regression analysis, including the Syntax score, the presence of severe coronary calcification was an independent predictor of poor prognosis (HR: 1.33 95% CI 1.00 to 1.77, p=0.047 for death; 1.23, 95% CI 1.02 to 1.49, p=0.031 for death—MI, and 1.18, 95% CI 1.01 to 1.39, p=0.042 for death—MI— any revascularisation), but it was not associated with an increased risk of stent thrombosis. Conclusions Patients with severely calcified lesions have worse clinical outcomes compared to those without severe coronary calcification. Severe coronary calcification appears as an independent predictor of worse prognosis, and should be considered as a marker of advanced atherosclerosis.

Calcific aortic stenosis (AS) is the most prevalent heart valve disorder in developed countries. It is characterized by progressive fibro-calcific remodelling and thickening of the aortic valve leaflets that, over years, evolve to cause severe obstruction to cardiac outflow. In developed countries, AS is the third-most frequent cardiovascular disease after coronary artery disease and systemic arterial hypertension, with a prevalence of 0.4% in the general population and 1.7% in the population >65 years old. Congenital abnormality (bicuspid valve) and older age are powerful risk factors for calcific AS. Metabolic syndrome and an elevated plasma level of lipoprotein(a) have also been associated with increased risk of calcific AS. The pathobiology of calcific AS is complex and involves genetic factors, lipoprotein deposition and oxidation, chronic inflammation, osteoblastic transition of cardiac valve interstitial cells and active leaflet calcification. Although no pharmacotherapy has proved to be effective in reducing the progression of AS, promising therapeutic targets include lipoprotein(a), the renin–angiotensin system, receptor activator of NF-κB ligand (RANKL; also known as TNFSF11) and ectonucleotidases. Currently, aortic valve replacement (AVR) remains the only effective treatment for severe AS. The diagnosis and staging of AS are based on the assessment of stenosis severity and left ventricular systolic function by Doppler echocardiography, and the presence of symptoms. The introduction of transcatheter AVR in the past decade has been a transformative therapeutic innovation for patients at high or prohibitive risk for surgical valve replacement, and this new technology might extend to lower-risk patients in the near future. Calcific aortic stenosis (AS) involves fibro-calcific remodelling of the aortic valve that causes restriction of blood flow. Pibarot and colleagues discuss the mechanisms, diagnosis and management of AS and highlight how the introduction of transcatheter-based valve replacement has transformed patient outcomes.

Surgical management of ductal carcinoma in situ (DCIS), particularly in cases involving suspicious morphology and orientation of microcalcifications, remains a primary treatment option. However, the lack of real-time technical assistance in the form of an intraoperative surgical tool for detection of microcalcifications in the resection margins presents a significant challenge. In the context of breast conserving surgery, ex-vivo imaging of excised breast tissues slices from 12 patients was conducted. By employing a cross-polarized multispectral microcamera setup for tissue visualization an imaging depth of up to 2 mm was achieved. The microcamera provides the clinician with a clear color image with magnification allowing features down to 50 μm to be seen on the resection surface. Mammography images were used for accurate cross-correlation, enabling the identification of microcalcifications in the microcamera images. Detection efficacy of microcalcifications in microcamera images was notably influenced by both calcification clustering and distribution depth within the tissue. Calcifications within the 2 mm range were detected through their distinct optical manifestations in relation to the adjacent tissues. Four independent reviewers—two medical and two technical—achieved an average sensitivity of 77.8%, specificity of 80.0%, and overall accuracy of 79.0%. This study demonstrates the potential of an integrated microcamera and cross-polarized setup for non-invasive, real-time detection of microcalcifications in superficial breast tissues. By focusing on the superficial 2 mm, this approach shows promising results and offers substantial opportunities for future research and clinical applications.

A 76-year-old female with a known medical history of treated essential hypertension, hyperlipidemia, and obesity presented to her primary care provider for 2 months of worsening left-sided vision loss. Ophthalmologic evaluation demonstrated a left retinal artery branch occlusion leading to echocardiographic evaluation which revealed a large mobile echodensity on the mitral valve. Given specific clinical features and echocardiographic characteristics, the suspicion was highest for calcified amorphous tumor (CAT). Excision of this mass confirmed the diagnosis of CAT. There is currently clinical equipoise in literature regarding the best treatment strategy for these tumors therefore a multidisciplinary approach should be used to formulate individualized treatment plans.

Background This study aimed to determine the relationship between mammographic calcifications and magnetic resonance imaging (MRI) tumoral enhancement before and after neoadjuvant chemotherapy (NAC) and to assess the impact of these findings on surgical management. Methods This Institutional Review Board-approved, Health Insurance Portability and Accountability Act (HIPAA)-compliant retrospective study involved breast cancer patients who underwent NAC between 2009 and 2015. The study cohort comprised 90 patients with pre- and posttreatment MRI and mammograms demonstrating calcifications within the tumor bed either at presentation or after treatment. The data gathered included pre- and post-NAC imaging findings and post-NAC histopathology, particularly findings associated with calcifications. Comparisons were made using Fisher’s exact test, with p values lower than 0.05 considered significant. Results Complete resolution of MRI enhancement occurred for 44% of the patients, and a pathologic complete response (pCR) was achieved for 32% of the patients. No statistically significant correlation between changes in mammographic calcifications and MRI enhancement was found ( p = 0.12). Resolution of enhancement was strongly correlated with pCR ( p < 0.0001). The majority of the patients with pCR demonstrated complete resolution of enhancement (79%, 23/29). No statistically significant relationship was found between changes in calcifications and rates of pCR ( p = 0.06). A pCR was achieved most frequently for patients with resolution of enhancement and new, increasing, or unchanged calcifications ( p < 0.0001). Conclusions Although calcifications seen on post-NAC mammography may be associated with benign disease, loss of MRI enhancement does not predict the absence of residual tumor with sufficient accuracy to leave calcifications in place. Complete excision of tumor bed calcifications remains standard practice and a substantial limitation to NAC use for downstaging patients to be eligible for breast conservation treatment.

Transcatheter aortic valve implantation (TAVI) can treat symptomatic patients with calcific aortic stenosis. However, the severity and distribution of the calcification of valve leaflets can impair the TAVI efficacy. Here we tackle this issue from a biomechanical standpoint, by finite element simulation of a widely adopted balloon-expandable TAVI in three models representing the aortic root with different scenarios of calcific aortic stenosis. We developed a modeling approach realistically accounting for aortic root pressurization and complex anatomy, detailed calcification patterns, and for the actual stent deployment through balloon-expansion. Numerical results highlighted the dependency on the specific calcification pattern of the “dog–boning” of the stent. Also, local stent distortions were associated with leaflet calcifications, and led to localized gaps between the TAVI stent and the aortic tissues, with potential implications in terms of paravalvular leakage. High stresses were found on calcium deposits, which may be a risk factor for stroke; their magnitude and the extent of the affected regions substantially increased for the case of an “arc–shaped” calcification, running from commissure to commissure. Moreover, high stresses due to the interaction between the aortic wall and the leaflet calcifications were computed in the annular region, suggesting an increased risk for annular damage. Our analyses suggest a relation between the alteration of the stresses in the native anatomical components and prosthetic implant with the presence and distribution of relevant calcifications. This alteration is dependent on the patient-specific features of the calcific aortic stenosis and may be a relevant indicator of suboptimal TAVI results.

Background Dystrophic calcification affecting cardiac structures secondary to hyperadrenocorticism (HAC) is rare in dogs. This case report describes the clinical, imaging, surgical, and pathological findings of a 9-year-old spayed female Maltese dog with severe mitral regurgitation and HAC-related systemic calcification presenting as an intracardiac calcified mass. Case presentation Severe mitral valve thickening and a mobile hyperechoic mass attached to the chordae tendineae were detected on echocardiography. Mitral valvuloplasty was performed, and the calcified mass was excised. Histopathology confirmed a non-neoplastic calcified lesion. Computed tomography revealed extensive calcification in various tissues. The dog developed postoperative aspiration pneumonia and died on postoperative day 2. Conclusions This case highlights the potential for intracardiac dystrophic calcification in dogs with HAC and severe mitral valve disease.