COVID-19 and post-traumatic stress disorder among nurses: a descriptive cross-sectional study in a COVID hospital.

BACKGROUND: In March 2020, the World Health Organisation (WHO) declared the novel coronavirus (COVID-19) outbreak a global pandemic. Healthcare professionals directly involved in diagnosing, treating and caring for patients with COVID-19 are at risk of developing post-traumatic stress disorder (PTSD). OBJECTIVE: This study investigated the prevalence of PTSD among nurses working in a COVID hospital and evaluated associated factors. METHODS: A descriptive cross-sectional study was conducted at Crema Hospital and the Impact of Event Scale - Revised (IES-R) was administered. Data collection took place from July to September 2020, during which 275 questionnaires were distributed. RESULTS: Of the total sample, 39.88% received a provisional PTSD diagnosis deserving of further analysis. Nurses stated that they were predominantly overwhelmed by intrusive thoughts (M = 1.55). Working in the emergency department during the COVID-19 pandemic (OR=2.40; p=0.02), irregular work shifts (OR=5.41; p=0.01) and coming from a mental health ward (OR=3.80; p=0.02) increased the risk of receiving a provisional PTSD diagnosis. Our findings showed significantly higher IES-R scores among women than among men (p = 0.01). The activities that caused the most distress were related to technical skills required for managing ventilation and intubation devices. CONCLUSIONS: The results of the study highlighted the presence of considerable psychological distress in the sample. There is an urgent need to monitor the short- and long-term consequences of the COVID-19 pandemic and implement early intervention measures.

An LDV based method to quantify the error of PC-MRI derived Wall Shear Stress measurement.

Wall Shear Stress (WSS) has been demonstrated to be a biomarker of the development of atherosclerosis. In vivo assessment of WSS is still challenging, but 4D Flow MRI represents a promising tool to provide 3D velocity data from which WSS can be calculated. In this study, a system based on Laser Doppler Velocimetry (LDV) was developed to validate new improvements of 4D Flow MRI acquisitions and derived WSS computing. A hydraulic circuit was manufactured to allow both 4D Flow MRI and LDV velocity measurements. WSS profiles were calculated with one 2D and one 3D method. Results indicated an excellent agreement between MRI and LDV velocity data, and thus the set-up enabled the evaluation of the improved performances of 3D with respect to the 2D-WSS computation method. To provide a concrete example of the efficacy of this method, the influence of the spatial resolution of MRI data on derived 3D-WSS profiles was investigated. This investigation showed that, with acquisition times compatible with standard clinical conditions, a refined MRI resolution does not improve WSS assessment, if the impact of noise is unreduced. This study represents a reliable basis to validate with LDV WSS calculation methods based on 4D Flow MRI.

Left main intervention in myocardial infarction.

We report an 84-year-old patient who suddenly developed nausea, vomiting, hypotension, and needed intubation, assisted ventilation and pharmacological vasopressor support. Admission EKG showed anterior and lateral leads ST segment depression and 2 mm ST segment elevation in avR lead. Angiogram showed unprotected left-main coronary-artery (LM) sub-occlusive disease and totally occluded ostial right-coronary-artery (RCA), distally filled through the left-coronary system. Unprotected LM disease was immediately treated with bare metal stent. The stent jailed the left-circunflex coronary-artery (LCx) ostium but did not compromise the arterial flow. Lately, the patient was discharged in a very good health condition. Ten months angiographic follow-up showed an extremely compromised LCx ostium treated successfully with drug eluted stent (DES) and mid left anterior descendent (LAD) severe lesion, treated with DES.

The abutment duplication technique: a novel protocol for cementable implant-supported restorations.

The purpose of this study was to present a new laboratory technique for cementable implant-supported restorations and to evaluate its efficacy in reducing chair time for both patients and clinicians, while maintaining the precision of an indirect procedure for crown fabrication. The technique consisted of the duplication of the implant portion of a working cast prepared using double-pour or plastic base die systems for single or multiple crowns. For this purpose, a flask previously intended for the production of ceramic inlays and onlays was used. Duplication was obtained using a high-precision addition silicon material and a low-shrinkage polyurethane resin. The duplicated implant abutment was used to finalize the fixed partial denture restorations after the originals were delivered to the patients. Fifty abutments were tested consecutively. The castings (19 single crowns, 31 fixed partial dentures) produced on the original abutments were seated on the duplicate abutments and evaluated by two prosthodontists and two dental technicians using a visual inspection method (laboratory microscope at 163 magnification). Forty-eight restorations were "good" (completely seated, no marginal opening) and 2 were "acceptable" (incomplete seating but amendable), with a 98% success rate. The technique presented demonstrates efficacy and predictability in reducing the number of clinical sessions for delivering precisely fitting cementable implant-supported restorations.

Towards quantitative evaluation of wall shear stress from 4D flow imaging.

Wall shear stress (WSS) is a relevant hemodynamic indicator of the local stress applied on the endothelium surface. More specifically, its spatiotemporal distribution reveals crucial in the evolution of many pathologies such as aneurysm, stenosis, and atherosclerosis. This paper introduces a new solution, called PaLMA, to quantify the WSS from 4D Flow MRI data. It relies on a two-step local parametric model, to accurately describe the vessel wall and the velocity-vector field in the neighborhood of a given point of interest. Extensive validations have been performed on synthetic 4D Flow MRI data, including four datasets generated from patient specific computational fluid dynamics simulations on carotids. The validation tests are focused on the impact of the noise component, of the resolution level, and of the segmentation accuracy concerning the vessel position in the context of complex flow patterns. In simulated cases aimed to reproduce clinical acquisition conditions, the WSS quantification performance reached by PaLMA is significantly higher (with a gain in RMSE of 12 to 27%) than the reference one obtained using the smoothing B-spline method proposed by Potters et al. (2015) method, while the computation time is equivalent for both WSS quantification methods.

Functional Tricuspid Regurgitation Model in a Beating Heart Platform.

Currently, clinicians are seeking new, minimally invasive treatment options for functional tricuspid regurgitation (FTR). Challenging tricuspid complexity requires the evaluation of the treatment techniques in adequate and realistic preclinical scenario. The purpose of this article is to describe the design and functional assessment of a novel passive beating heart model of the pulmonary circulation with the possibility to tightly control FTR. The model housed porcine hearts actuated by a volumetric pump that cyclically pressurized the right ventricle. The in-vitro FTR model exploited the tendency of the ventricle to dilate under pressure. The dilation entailed papillary muscles displacement and valve annulus enlargement, thus inducing tricuspid valve insufficiency. Employment of constraint bands allowed to restore valve competency. The system provided consistent replication of the main determinants of the pulmonary hemodynamics in a wide range of working conditions. The experimental model of FTR was reliable, easily controllable, and showed good stability-over-time. Echocardiography and fiberscope imaging provided a unique opportunity to investigate valve dynamics. These features make the platform suitable for realistic training purposes and testing of the upcoming FTR therapies.

Incidence, location, magnitude, and clinical correlates of saphenous vein graft calcification: an intravascular ultrasound and angiographic study.

BACKGROUND: The pattern of saphenous vein graft (SVG) calcification before percutaneous intervention has not been studied. METHODS AND RESULTS: We used diagnostic and preintervention intravascular ultrasound (IVUS) to determine the incidence and magnitude of SVG calcification in 334 SVG lesions in 274 consecutive patients. Calcium was found in 133 SVGs (40%). Calcium was uniformly distributed among 48 lesion sites (14%), 43 proximal references (13%), and 42 distal references (13%). Calcium was superficial in 20 (40%) and deep in 28 (60%). Over the entire length of the SVGs, the maximum arc and length of calcium (in calcium-containing SVGs) averaged 174+/-107 degrees and 6.8+/-4.8 mm, respectively. In calcium-containing SVGs, lesion site arc and length of calcium measured 151+/-107 degrees and 4.1+/-3.7 mm, similar to the proximal and distal references (175+/-121 degrees and 4.0+/-2.3 mm and 177+/-121 degrees and 4.1+/-2.5 mm, respectively). Graft age (7.5+/-4.7 versus 10.5+/-4.7 years, P<0.0001), insulin-treated diabetes mellitus (40% versus 60%, P=0.02), and tobacco use (44% versus 55%, P=0.06) were clinical independent predictors of SVG calcification. CONCLUSIONS: Sixty-five percent of calcium-containing SVGs had reference calcium in the absence of lesion calcium. Calcium was located primarily in SVG wall and not at the plaque. These data suggest that SVG calcium is not just part of lesion formation and maturation. SVG calcium occurred more commonly in older grafts, in insulin-treated diabetic patients, and in smokers.

Akt controls vascular smooth muscle cell proliferation in vitro and in vivo by delaying G1/S exit.

Constitutive activation of serine/threonine kinase Akt causes uncontrolled cell-cycle progression in different cell types and in malignancy. To investigate how Akt activation modulates cell-cycle progression in vascular smooth muscle cells (SMCs) in vitro and in the intact animal, we inhibited Akt-dependent signaling by adenovirus-mediated transfection of a dominant-negative Akt mutant (AA-Akt). We observed reduced proliferation rate (P<0.01), DNA synthesis (P<0.01), and a significant arrest in G1/S exit (P<0.01) both in vitro in response to serum stimulation and in vivo after vascular injury. In vivo transfection of the balloon-injured vessel with AA-Akt reduced SMC proliferation, resulting in decreased neointima compared with control virus (P<0.01). These effects were at least in part modulated, both in vitro and in vivo, by increased p21Cip1 expression, as demonstrated by lack of effect of AA-Akt on cell proliferation in p21-/- mouse SMCs. In conclusion, this study demonstrates that Akt-dependent signaling enhances cell-cycle progression of nontransformed SMCs in vitro and in response to vascular injury in the intact animal. These results suggest a role for Akt signaling in modulating the response of normal tissues to stress and the response of the arterial wall to acute and possibly repetitive injuries that ultimately contribute to restenosis and atherosclerosis.

Predictors of subacute stent thrombosis: results of a systematic intravascular ultrasound study.

BACKGROUND: Factors leading to subacute stent thrombosis after percutaneous coronary intervention (PCI) have not been well established. We assessed the pre- and post-PCI intravascular ultrasound (IVUS) characteristics of subacute stent thrombosis. METHODS AND RESULTS: We analyzed 7484 consecutive patients without acute myocardial infarction who were treated with PCI and stenting and underwent IVUS imaging during the intervention. Twenty-seven (0.4%) had angiographically documented subacute closure <1 week after PCI (median time to subacute closure, 24 hours). Subacute closure lesions were compared with a control group (selected to be 3 times the abrupt closer group) matched by procedure date (within 6 months), age, gender, stable or unstable angina, lesion location, and additional treatment (balloon angioplasty or atherectomy). Postintervention IVUS did not identify a cause in 22% and did identify at least 1 cause for abrupt closure in 78% of patients (versus 33% in matched lesions, P=0.0002). In 48% of the patients, there were multiple causes in 48% (versus 3% in matched lesions, P<0.0001). Causes included dissection (17%), thrombus (4%), and tissue protrusion within the stent struts leading to lumen compromise lumen (4%). A total of 83% of patients with >1 of these abnormal morphologies also had reduced lumen dimensions post-PCI (final lumen <80% reference lumen). Preprocedural lesion characteristics were not different from matched lesions. CONCLUSIONS: Subacute stent thrombosis is infrequently related to the preintervention lesion characteristics. Inadequate postprocedure lumen dimensions, alone or in combination with other procedurally related abnormal lesion morphologies (dissection, thrombus, or tissue prolapse), contribute to this phenomenon.

Incidence, morphology, angiographic findings, and outcomes of intramural hematomas after percutaneous coronary interventions: an intravascular ultrasound study.

BACKGROUND: Intramural hematomas during percutaneous coronary intervention (PCI) have not been well studied. METHODS AND RESULTS: We used intravascular ultrasound to determine the incidence, morphology, and clinical features of post-PCI intramural hematomas. In 905 patients with 1025 consecutive native coronary artery, non-in-stent restenosis lesions undergoing PCI, 72 hematomas were detected in 69 arteries in 68 patients. The incidence of intramural hematomas per artery was 6.7% (69 of 1025); 36% (26 of 72) involved the proximal reference artery, 18% (13 of 72) were confined to the lesion, and 46% (33 of 72) involved the distal reference artery. The entry site from the lumen into the hematoma was identified in 86% of hematomas (62 of 72) and had the appearance of a dissection into the media. Conversely, a re-entry site was identifiable in only 8% (6 of 72). The axial extension of the hematoma was distal in 63% and proximal in 37%. In 60% of the hematomas (42 of 72) the angiogram had the appearance of a dissection; in 11% (8 of 72), it appeared to be a new stenosis; and in 29% (22 of 72), no significant abnormality was detected. Non-Q-wave myocardial infarctions occurred in 26% of patients (17 of 65). In 3 patients, the creatine kinase-MB was not measured during the hospital stay. Repeat revascularization occurred in 2 patients in-hospital, 2 additional patients at 1 month, and 8 additional patients at 1 year. There were 3 sudden deaths at 1 year. CONCLUSIONS: Intravascular ultrasound identified intramural hematomas after 6.7% of PCIs. The mechanism appeared to be a dissection into the media where blood accumulated because of a lack of re-entry. A third of ultrasound-identified hematomas showed no angiographic abnormalities. There was a high rate of non-Q-wave myocardial infarction, need for repeat revascularization, and sudden death in patients with hematomas.

Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction.

BACKGROUND: Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI). METHODS AND RESULTS: We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries [IRAs] with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P&M) area. Positive remodeling was defined as lesion/mean reference EEM >1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5+/-10.1, 9.8+/-4.0, and 10.3+/-5.7 mm, respectively; P<0.0001), had larger EEM area (15.0+/-6.0, 11.5+/-5.7, and 12.6+/-5.6 mm2, respectively; P=0.0353) and P&M area (13.0+/-6.0, 7.5+/-3.7, 9.3+/-4.3 mm2, respectively; P<0.0001), smaller lumens (2.0+/-0.9, 4.1+/-3.1, and 3.4+/-2.5 mm2, respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging. CONCLUSIONS: Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.

The outcome of percutaneous coronary intervention in patients with in-stent restenosis who failed intracoronary radiation therapy.

OBJECTIVES: This study reports the outcome of patients who failed intracoronary radiation therapy (IRT) for the treatment of in-stent restenosis (ISR). BACKGROUND: Intracoronary radiation therapy has demonstrated a reduction in the recurrence rate of restenosis for patients with ISR. However, 10% to 30% of these patients require repeat intervention to the irradiated site. METHODS: Of 961 patients who were assigned to gamma or beta radiation for the treatment of diffuse ISR, we evaluated the outcome of 282 (29%) consecutive patients who failed IRT and compared them with the 679 (71%) patients who had successful IRT. For patients who failed radiation, the mean time to the first target vessel revascularization (TVR) was 173 +/- 127 days after the index procedure and the total duration of follow-up was 494 +/- 304 days. RESULTS: Patients who failed IRT were younger (60 +/- 10 vs. 63 +/- 11 years, p = 0.002) and had a higher incidence of restenting (51% vs. 41%, p = 0.003). The majority (55%) of the restenotic lesions after IRT failure were focal (< or =10 mm), with a mean lesion length of 11.9 +/- 1.9 mm. Of the 257 patients who had subsequent TVR after failed IRT, 68 (26%) underwent coronary artery bypass grafting and 189 (74%) underwent percutaneous coronary intervention using balloon in 61%, restenting in 26%, atheroablation in 11%, and the cutting balloon in 2% of cases. At six months, 6% of patients died, 1% had Q-wave MI, 17% had repeat TVR, and the overall rate of major adverse cardiac events was 21%. CONCLUSIONS: The predominant angiographic pattern of lesions in patients who failed IRT is focal restenosis, with these lesions responding well to conventional revascularization methods.

Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound.

OBJECTIVES: This study was designed to report the clinical and angiographic correlates of plaque rupture detected by intravascular ultrasound (IVUS). BACKGROUND: Acute coronary syndromes result from spontaneous plaque rupture and thrombosis. METHODS: We report 300 plaque ruptures in 257 arteries in 254 patients. Plaque ruptures were detected during pre-intervention IVUS. Standard clinical, angiographic, and IVUS parameters were collected and/or measured. One lesion per patient was analyzed. RESULTS: Multiple ruptures were observed in 39 of 254 patients (15%), 36 in the same artery. Plaque rupture occurred not only in patients with unstable angina (46%) or myocardial infarction (MI, 33%), but also stable angina (11%) or no symptoms (11%). The tear in the fibrous cap could be identified in 157 of 254 patients; 63% occurred at the shoulder of the plaque and 37% in the center of the plaque. Thrombi were more common in patients with unstable angina or MI (p = 0.02) and in multiple ruptures (p = 0.04). The plaque rupture site contained the minimum lumen area (MLA) site in only 28% of patients; rupture sites had larger arterial and lumen areas and more positive remodeling than MLA sites. Intravascular ultrasound plaque rupture strongly correlated with complex angiographic lesion morphology: ulceration in 81%, intimal flap in 40%, thrombus in 7%, and aneurysm in 7%. CONCLUSIONS: Plaque ruptures occur with varying clinical presentations, strongly correlate with angiographic complex lesion morphology, may be multiple, and usually do not cause lumen compromise.

Dose heterogeneity may not affect the neointimal proliferation after gamma radiation for in-stent restenosis: a volumetric intravascular ultrasound dosimetric study.

OBJECTIVES: The goal of this study was to use serial (postirradiation and follow-up) volumetric intravascular ultrasound (IVUS): 1) to evaluate the actual distribution of gamma radiation in human in-stent restenosis (ISR) lesions, and 2) to analyze the relationship between neointimal regrowth and the delivered radiation dose. BACKGROUND: The relationship between the neointimal regrowth and delivered dose during the treatment of ISR remains unknown. METHODS: We analyzed 20 actively (gamma emitter) treated, native artery ISR patients from the Washington Radiation for In-Stent restenosis Trial (WRIST) that met the following criteria: on both postirradiation and six-month follow-up IVUS imaging, > or =80% of the external elastic membrane circumference could be identified throughout the treated length including the lesion and proximal and distal reference segments. Intravascular ultrasound images were digitized every 1 mm. Proximal and distal reference and stented segment luminal and adventitial contours were imported and reconstructed. The source was placed circumferentially at the site of the IVUS catheter and longitudinally according to the relationship between the radioactive seeds and stent edges. Using Monte Carlo simulations, dose volume histograms for the adventitia and intima were calculated. The relationship between the neointimal regrowth and calculated doses were evaluated. RESULTS: There was large dose heterogeneity at both the intimal and adventitial levels. Most of the sites (93%) received >4 Gy at the adventitia, and all of the sites received >4 Gy at the intima. There was no relationship between neointimal regrowth and radiation dose. CONCLUSIONS: Although there may be large dose heterogeneity, gamma irradiation (using a fixed dose prescription) appears to deliver a sufficient dose to prevent neointimal regrowth.

Usefulness of periprocedural creatinine phosphokinase-MB release to predict adverse outcomes after intracoronary radiation therapy for in-stent restenosis.

We aimed to analyze periprocedural creatinine phosphokinase (CPK)-MB elevation in patients treated with intracoronary radiation therapy (IRT) for in-stent restenosis (ISR) to risk stratify these patients. The clinical significance of periprocedural CPK-MB elevation after IRT for ISR is unknown. An elevated CPK-MB has been associated with increased mortality after conventional angioplasty. We evaluated 1,326 patients who were enrolled in radiation trials for ISR at the Washington Hospital Center using gamma- and beta-emitters. Patients were analyzed according to degree of CPK-MB increase within 24 hours of the index IRT procedure (normal CPK-MB, CPK-MB 1 to 3 times the upper limit of normal, or CPK-MB >3 times the upper limit of normal). Patients with CPK-MB >3 times the upper limit of normal were older (64 +/- 12 years, p = 0.04), more likely to be smokers (64%, p = 0.04), hypertensive (85%, p <0.01), and diabetic (49%, p = 0.04). The cohort with the highest CPK-MB release (CPK-MB >3 times the upper limit of normal) had significantly higher rates of adverse clinical events at 12 months (major adverse cardiac events 40%, p <0.01), including death (9.3%, p <0.01) and late thrombosis (6.3%, p <0.01). Periprocedural CPK-MB elevation is of prognostic importance in patients treated with IRT for ISR, and its analysis appears to be mandatory to risk stratify these patients. The impact of glycoprotein IIb/IIIa antagonists in reducing periprocedural CPK-MB release awaits evaluation.

Spontaneous coronary artery dissection in a patient with systemic lupus erythematosis.

Spontaneous coronary artery dissection (SCAD) is an uncommon condition that may lead to sudden coronary artery occlusion resulting in a fatal acute myocardial infarction. It usually affects young to middle age women. A Medline search from 1966 to 2001 (using keywords: coronary artery dissection and systemic lupus erythematosis) revealed no prior reports of coronary dissection in a patient with systemic lupus erythematosis (SLE). We describe a 48-year old woman with SLE who sustained a fatal spontaneous left main coronary artery dissection. Coronary angiogram was notable for marked variability in the size of coronary lumen from systole to diastole. This case demonstrates the need to consider SCAD in the evaluation of chest pain and myocardial infarction in patients with SLE. Furthermore, in the absence of classical angiographic findings of coronary dissection, a detailed review of phasic changes in coronary lumen during a cardiac cycle could help reach this diagnosis.