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Myocardial contusion is a rare and potentially fatal complication of chest trauma. There is no unique definition for this entity: some authors define myocardial contusion as a mild increase in cardiac biomarkers in the context of chest trauma, while for others the diagnosis requires evidence of pathologic findings at cardiac imaging. Consequently, the real incidence of myocardial contusion remains unknown, varying in reports between 8% and 71%. We describe a case of cardiac contusion secondary to a low-energy blunt chest trauma, manifesting as persistent ST-elevation associated with elevation of myocardial necrosis markers, with consequent myocardial stunning of the right ventricular free wall. As there is no consensus regarding the diagnostic pathway, it is essential to integrate first-level exams (ECG and laboratory findings) with cardiac magnetic resonance imaging, to define the presence of cardiac contusion and its extent, particularly if the echocardiographic data are unconclusive.

Objective- Aim of this study was to evaluate changes in LCAT (lecithin:cholesterol acyltransferase) concentration and activity in patients with an acute coronary syndrome, to investigate if these changes are related to the compromised capacity of HDL (high-density lipoprotein) to promote endothelial nitric oxide (NO) production, and to assess if rhLCAT (recombinant human LCAT) can rescue the defective vasoprotective HDL function. Approach and Results- Thirty ST-segment-elevation myocardial infarction (STEMI) patients were enrolled, and plasma was collected at hospital admission, 48 and 72 hours thereafter, at hospital discharge, and at 30-day follow-up. Plasma LCAT concentration and activity were measured and related to the capacity of HDL to promote NO production in cultured endothelial cells. In vitro studies were performed in which STEMI patients' plasma was added with rhLCAT and HDL vasoprotective activity assessed by measuring NO production in endothelial cells. The plasma concentration of the LCAT enzyme significantly decreases during STEMI with a parallel significant reduction in LCAT activity. HDL isolated from STEMI patients progressively lose the capacity to promote NO production by endothelial cells, and the reduction is related to decreased LCAT concentration. In vitro incubation of STEMI patients' plasma with rhLCAT restores HDL ability to promote endothelial NO production, possibly related to significant modification in HDL phospholipid classes. Conclusions- Impairment of cholesterol esterification may be a major factor in the HDL dysfunction observed during acute coronary syndrome. rhLCAT is able to restore HDL-mediated NO production in vitro, suggesting LCAT as potential therapeutic target for restoring HDL functionality in acute coronary syndrome.

Furfural is a high-value chemical, being the precursor of compounds such as furfuryl alcohol and tetrahydrofurfuryl alcohol. Pt is known as active for furfural hydrogenation, but the high price limits its exploitation and imposes the search for alternatives. Here we presented a Pt/Mo bimetallic system with enhanced catalytic activity for furfural hydrogenation. For comparison, monometallic Mo- and Pt-supported on activated carbon have been prepared by impregnation and sol-immobilization. The bimetallic Pt/Mo was prepared impregnating the Mo-AC catalyst with Pt, using Na2PtCl4 as a precursor, PVA, and NaBH4 as reducing agent. HR-TEM analyses on Pt/Mo catalyst showed Mo-containing agglomerates embedded in the carbon matrix, displaying diffraction fringes with spacing typical of Mo4O11 in the orthorhombic phase, as well as Pt nanoparticles more evenly dispersed in the Mo-AC system compared to bare AC. The Pt/Mo catalyst showed higher activity than both monometallic ones, and it converted 92% of furfural to furfuryl alcohol and ethyl furfuryl ether with 20% and 80% selectivity, respectively. However, despite a lower initial activity, the monometallic Mo/AC catalyst showed a complete selectivity to the ether.

This paper investigates the influence of TSV noise coupling on nearby devices based on an extended 3D TSV circuit model. This model not only takes into account the complex RF field distributions in bulk Si, but also incorporates the anomalous TSV capacitance inversion behavior, which has been found to occur due to the presence of fixed charges in the backside passivation layer after wafer thinning. The extended 3D TSV circuit model is validated by the excellent agreement between the simulation results and experimental data. It demonstrates that the inversion behavior of the TSV capacitance increases the noise coupling to adjacent devices mainly in the low frequency range. Furthermore, we show that noise mitigation techniques can be easily implemented in this 3D circuit model to predict the extent of noise coupling alleviation.

This paper investigates the influence of TSV noise coupling on nearby devices based on an extended 3D TSV circuit model. This model not only takes into account the complex RF field distributions in bulk Si, but also incorporates the anomalous TSV capacitance inversion behavior, which has been found to occur due to the presence of fixed charges in the backside passivation layer after wafer thinning. The extended 3D TSV circuit model is validated by the excellent agreement between the simulation results and experimental data. It demonstrates that the inversion behavior of the TSV capacitance increases the noise coupling to adjacent devices mainly in the low frequency range. Furthermore, we show that noise mitigation techniques can be easily implemented in this 3D circuit model to predict the extent of noise coupling alleviation. Index Terms — TSV, 3D circuit model, inversion layer, inversion behavior of TSV capacitance, noise coupling.

Radiotherapy for breast cancer may expose heart and vessels to late radiation-induced complications. Although recent technical progress in radiation therapy (RT) has been associated with drastic reduction in cardiovascular (CV) mortality, the prolonged life expectancy of patients with cancer requires CV evaluation for many years. The aim of our study was to evaluate local changes in vascular and cardiac function because of previous breast RT. We enrolled 43 patients treated with RT 15 years ago for breast cancer. CV risk factors and atherosclerotic carotid damage were investigated in all women. We divided patients into 2 groups: R (n = 25) treated to right breast and L (n = 18) to left breast. All subjects were submitted to standard echocardiography and functional arteries evaluation by carotid-radial pulse-wave velocity (crPWV; Complior) and AIx (Sphygmocor; Atcor Medical). Global mean age was 69.5 ± 8 years old. CV risk factors were equally allocated in 2 groups. No patients had history of cardiac or artery disease. R had a significantly increased crPWV (9.9 ± 1.4 vs 8.9 ± 1.1, p = 0.001) on right arm compared with left arm, and in L group, crPWV was similarly higher on the left arm than on right arm (9.6 ± 1.5 vs 8.9 ± 1.4, p = 0.011). AIx was significantly increased in the ipsilateral arm only in L (32.1 ± 7.6 vs 28.3 ± 6.8, p = 0.05). Central blood pressure estimation was not different in the right and left arms. No correlations were found with hormone therapy or chemotherapy. Our data show a local arterial stiffening because of radiation that can be involved in increased CV risk in breast cancer–treated patients.

BACKGROUND In the last 2 decades, new drugs that oppose the effects of vascular endothelial growth factor receptor (VEGFR), and thus angiogenesis, have considerably improved treatment of solid tumors. These anti-VEGFR drugs, however, are burdened by several side effects, particularly relevant on heart and vessels. The aim of this study was to analyze the changes in cardiovascular structure and function associated with use of anti-VEGFR drugs. METHODS Twenty-nine patients (27 affected by renal and 2 by thyroid cancer), received treatment with anti-VEGFR drugs. Brachial blood pressure (BP), central BP, carotid-femoral pulse wave velocity (cfPWV), augmentation index (Aix), and several echocardiographic markers of systolic and diastolic left ventricular functions including global longitudinal strain were measured before starting treatment (T0), after 2 (T1), and 6 weeks (T2) of treatment. RESULTS Anti-VEGFR treatment was accompanied by a significant increase of both peripheral (systolic BP +13±15.5mm Hg, diastolic BP +7.1±9.3mm Hg, P < 0.001) and central BP (systolic BP +14±14.2mm Hg, diastolic BP +7.3±10.4mm Hg, P < 0.001) and a significant raise of cfPWV (+1.3±1.8 m/sec, P = 0.003). There was also a significant alteration of markers of diastolic and subclinical left ventricular systolic function, including global longitudinal strain (-19.9±3.8% at T0, -17.8±2.6% at T2, P < 0.05). All the changes were already evident at T1, worsened at T2 in patients who maintained oncological treatment, but disappeared at T2 in patients in whom treatment was stopped. CONCLUSIONS All the changes regarding BP and cfPWV appear early after treatment initiation and seem to be reversible if treatment is stopped, instead diastolic and systolic left ventricular function are persistently altered by anti-VEGFR drugs.

OBJECTIVE: After transplantation heart is denervated, resulting in increased resting heart rate (HR) and altered physiologic response to exercise. In heart transplant (HTX) recipients, absence of blood pressure (BP) dipping phenomenon has been reported, but information on central blood pressure, pulse wave velocity (PWV) and Augmentation Index (Aix) is scanty. Aim of our study was to investigate 24 h modulation not only of brachial BP but also of central-aortic BP (CABPM), HR, PWV and Aix in hypertensive HTX patients. DESIGN AND METHOD: We enrolled 24 hypertensive patients, 12 HTX recipients (Ht-HTX), at a mean time after HTX of 10,4 years, and 12 matched controls (Ht-C). All the patients were clinically stable and had normal LV systolic function. Ambulatory brachial BP, CABPM, PWV and Aix were recorded over 24 hours by Mobilograph device. RESULTS: Baseline brachial and central BP were similar in Ht-HTX vs Ht-C, as were 24 h brachial (128/78 mmHg ± 11/8Vs124/79mmHg ± 14/2) and central BP (119/81 mmHg ± 12/8 vs114/79 mmHg ± 13/7), HR (74.5 ± 11 vs 69 ± 10 bpm), PWV (8.15 ± 1.8 vs 8.2 ± 1.3 m/s) and Aix (23.6 ± 7.5 vs 22.8 ± 5.8%). PWV showed a dipping phenomenon in Ht-C (daily 8.3 ± 1.2, night 7.9 ± 1.4 m/s), p < 0.001) but not in Ht-HTX (daily 8.15 ± 1.8, night 8.15 ± 1.8). This was the case also for HR. Central systolic BP remained unchanged from day to night in Ht-HTX (118 ± 12 vs 119 ± 16 mmHg) but not in Ht-C (117 ± 15 vs 95 ± 33 mmHg), with night central systolic BP being higher in Ht-HTX vs Ht-C (p < 0.05). An index of 24 h variability (standard deviation) of BP and HR was lower in Ht-HTX than in Ht-C, reaching statistical significance only for 24h-HR (4.3 ± 1.7 vs 6.7 ± 2.3, p: 0.01). CONCLUSIONS: Our study shows for the first time that in Ht-HTX there is no nocturnal dipping not only of brachial BP and HR but also of CABPM, and PWV up to 10 years after HTX, probably due to persistent cardiac denervation and/or interference by immunosuppressant drugs. Altered

OBJECTIVE: In the last two decades new drugs that oppose the effects of vascular endothelial growth factor receptor (VEGFR), and thus angiogenesis, have considerably improved treatment of solid tumors. These anti-VEGFR drugs, however, are burdened by several side effects, particularly relevant on heart and vessels. Aim of this study was to analyze the changes in cardiovascular structure and function associated with use of anti-VEGFR drugs. DESIGN AND METHOD: 29 patients (27 affected by renal and 2 by thyroid cancer), received treatment with antiVEGFR drugs. Hemodynamic, non invasive arterial investigation (Pulse Wave velocity -cfPWV-, Augmentation Index-Aix- and Aortic Pressure) and echocardiography with global longitudinal strain (gLS) were performed before starting therapy (T0), after 2 (T1) and 6 weeks (T2). Oncologic outcome was determined by the assessment of the neoplastic lesions at CT scans, according to Response Evaluation Criteria in Solid Tumors Guidelines. RESULTS: A significant increase of both peripheral and central blood pressure (BP) was observed. We documented a significant raise of cfPWV from T0 (9.9 ± 2.5m/sec) to T1 (10.6 ± 2.3m/sec); at T2 cfPWV still increased in patients who continued treatment (10.8 ± 2.3m/sec), while decreased in patients who stopped therapy (9.8 ± 1.9m/sec). At the on-treatment CT scan (available in 22 patients) 12 patients had a stable disease (StD), 5 showed a reduction of the lesions (responders -PR-) and 5 showed a disease progression (PD). PD patients showed a lower cfPWV at T2 than StD-PR patients (cfPWV: 9.3 ± 2.8 Vs 13.3 ± 1.5 m/sec; p value 0.02). Aix at T1 was higher in PD than in StD-PR (Aix: 36 ± 2.8% Vs 24.6 ± 9.2%; p value 0.02). CONCLUSIONS: Anti-VEGFR treatment is associated with a marked increase in both brachial and central BP. Moreover it early induces an aortic reversible stiffening. The evidence that cfPWV and AIx changes are early and sensitive cardio-vascular effects of anti-angiogenic treatment and t

Early vascular aging is a process characterized by a reduction in arterial elastin with an increase in collagen that has been related to cardiovascular risk factor and can determine an increased arterial stiffness and central blood pressure. It can be measured by several non invasive methods and in different arterial segment. The present paper will focus on functional (local stiffness parameter) and structural (intima media thickness) carotid arteries alterations typically evaluated by ultrasound methods. Methodological, research and clinical issue has been reviewed.