Citations

Abstract Acute carotid terminus occlusion (CTO) is responsible for up to 5% of acute ischemic strokes secondary to emergent large vessel occlusion (ELVO) and up to 20% of acute internal carotid artery (ICA) occlusions. 1 The term “CTO” has also been used to describe occlusions in the supra-clinoid segment or at the bifurcation of the ICA. Compared to other ELVOs, patients with CTO present with higher stroke severity and larger infarct volume, likely to be a result of disruption of direct Circle of Willis collaterals across the anterior communicating artery (AComA) and posterior communicating artery (PComA). 2,3 Similary, CTO is usually associated with worse prognosis compared to other ELVOs in general. With regard to response to treatment, previous studies have reported significantly lower recanalization rates with intravenous alteplase with CTO compared to M1 segment occlusion. With regard to the safety and efficacy of mechanical thrombectomy, prior reports provide conflicting results with some reporting lower successful recanalization rates with CTO compared to M1 occlusion, and others reporting similar results. In our experience, we have found that successful recanalization of CTO can be achieved with a similar approach to M1 occlusions utilizing a direct aspiration first pass technique (ADAPT). 3,4 Herein, we present a case of CTO for which we performed mechanical thrombectomy using ADAPT. This procedure was an emergent standard of care procedure for which a consent was not required and so not obtained.

Aims The outcomes of patients presenting with acute myocarditis and life‐threatening ventricular arrhythmias (LT‐VA) are unclear. The aim of this study was to assess the incidence and predictors of recurrent major arrhythmic events (MAEs) after hospital discharge in this patient population. Methods and results We retrospectively analysed 156 patients (median age 44 years; 77% male) discharged with a diagnosis of acute myocarditis and LT‐VA from 16 hospitals worldwide. Diagnosis of myocarditis was based on histology or the combination of increased markers of cardiac injury and cardiac magnetic resonance (CMR) Lake Louise criteria. MAEs were defined as the relapse, after discharge, of sudden cardiac death or successfully defibrillated ventricular fibrillation, or sustained ventricular tachycardia (sVT) requiring implantable cardioverter‐defibrillator therapy or synchronized external cardioversion. Median follow‐up was 23 months [first to third quartile (Q1–Q3) 7–60]. Fifty‐eight (37.2%) patients experienced MAEs after discharge, at a median of 8 months (Q1–Q3 2.5–24.0 months; 60.3% of MAEs within the first year). At multivariable Cox analysis, variables independently associated with MAEs were presentation with sVT [hazard ratio (HR) 2.90, 95% confidence interval (CI) 1.38–6.11]; late gadolinium enhancement involving ≥2 myocardial segments (HR 4.51, 95% CI 2.39–8.53), and absence of positive short‐tau inversion recovery (STIR) (HR 2.59, 95% CI 1.40–4.79) at first CMR. Conclusions Among patients discharged with a diagnosis of myocarditis and LT‐VA, 37.2% had recurrences of MAEs during follow‐up. Initial CMR pattern and sVT at presentation stratify the risk of arrhythmia recurrence.

Abstract Transfemoral access has long been the main access site for cerebral angiography and neurointerventional procedures. Radial access is accepted as an alternative to the traditional transfemoral approach. Ulnar access may be undertaken if the radial artery is occluded or small caliber, or when radial artery preservation is needed. The safety and feasibility of ulnar access for neuroangiographic procedures has been demonstrated. 1-3 In this operative video, we demonstrate ulnar artery access in a patient in whom radial artery preservation was desired. We further elaborate on the technical nuances of this access. This nontraditional access site offers the same advantages as radial access, avoiding the need to switch to femoral artery access. A preoperative Allen's test is not necessary. Ultrasound imaging is used to aid in the identification and successful puncture of the ulnar artery. A medial to lateral approach for ulnar artery puncture is advised to avoid injury to the ulnar nerve. Careful application of wrist closure bands avoids hematoma accumulation. The patient gave informed consent for the procedure and video recording. Institutional review board approval was deemed unnecessary. Video. © University at Buffalo, May 2021. Used with permission.

Aim Th1 cells have potent pro‐inflammatory properties and have been shown to play an important role in the development and progression of acute renal injury to chronic renal disease. The aim of this study is to test the hypothesis that chronic renal damage in mice with renal artery stenosis (RAS) would be ameliorated in mice with homozygous deletion of the Th1 transcription factor T‐bet. Methods C57BL6/J (WT) and C57BL6/J mice with homozygous deletion of T‐bet (KO) were obtained from Jackson Laboratory. Renal artery stenosis surgery (RAS) was performed by placement of a polytetrafluoroethylene cuff on the right renal artery of KO (KO RAS group, n =5) and WT mice (WT RAS group, n =6). Sham (SH) surgery was performed with manipulation of the right renal artery without cuff placement in KO (KO SH group, n =4) and WT mice (WT SH group, n =5). Renal blood perfusion and oxygenation (R2*) were measured using 16.4T MRI. Blood pressure measurements were done using tail‐cuff method. Kidneys were harvested at 28 days after RAS for assessment of histology. Results Baseline intra‐renal perfusion in both KO RAS and WT RAS mice was reduced to a similar extent following cuff placement. In KO RAS group, baseline intra‐renal perfusion (795 ± 57 ml/100g/min) was reduced to 234 ± 22 ml/100g/min ( p <0.0001 vs baseline, mean reduction 71%) and in WT RAS group, baseline intra‐renal perfusion (836 ± 87 ml/100g/min) was reduced to 220 ± 21 ml/100g/min ( p =0.002 vs baseline, mean reduction 74%). Both KO RAS and WT RAS mice developed hypertension, which persisted throughout the 4 week study. WT RAS group showed significant elevation in cortical R2*, a measure of hypoxia, following RAS compared to their baseline ( p =0.002). KO RAS mice showed slightly higher R2* value, which was not significantly different from their baseline values. The weight of the stenotic kidney of the KO RAS group (105 ± 11.6 mg) was significantly lower than the KO SH mice (178 ± 14.1 mg, p =0.0021) but significantly higher than the WT RAS group (51.7 ± 7.9 mg, p =0.0010). On histologic and immune‐histochemical analysis, we observed that the stenotic kidney of the KO RAS group had significantly lower (%) cortical tubular atrophy (15% ± 6.7, p <0.0001) compared to WT RAS mice (81.7% ± 7). KO RAS group had significantly lower macrophage (MQ) ( p =0.0016) and T cell influx ( p =0.0052) compared to the WT RAS, as assessed by the % of cortical surface areas staining positive for F4/80 (MQ) and CD3 (T cell). When compared to their respective shams, KO RAS showed no significant differences in the % cortical tubular atrophy, MQ and CD3+ T cell influx. Conclusion We conclude that deficiency of Th1 transcription factor T‐bet, protects against chronic renal injury as evidenced by the less cortical atrophy in KO RAS compared to WT RAS group, despite a similar elevation in blood pressure and reduction in perfusion. This model may provide a novel therapeutic target to prevent renal disease progression in patients with renovascular hypertension. Support or Funding Information National Institutes of Health Grant AI 100911 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

The objective of this study was to identify signaling pathways leading to the development of interstitial fibrosis and tubular atrophy in the stenotic kidney and compensatory hypertrophy/hyperplasia of the contralateral kidney in a murine 2 kidney 1 clip model of hypertensive nephrosclerosis. Mice were studied 2, 5, and 11 weeks after undergoing surgery to establish unilateral renal artery stenosis (RAS). RAS animals, but not sham controls, became hypertensive within 1 week. Compensatory enlargement of the contralateral kidney was associated with a transient increase in proliferation (as assessed by PCNA and Mib‐1), p‐ERK, caspase 3, p27, p53, and TGF‐β expression at early time points, with return to baseline levels by 11 weeks. Tubular atrophy in the stenotic kidney was associated with a persistent increase in p‐ERK, Mib‐1, p53, p21, and p27 expression through 11 weeks. Proliferative activity was observed in tubular epithelial cells and in inflammatory cells. The atrophic kidneys had little apoptotic activity (caspase 3, TUNEL staining). The atrophic kidneys showed progressive increases in TGF‐β and α‐SMA expression and extracellular matrix deposition throughout 11 weeks. Interstitial inflammation was associated with increased MCP‐1 expression. Mechanisms underlying this differential response to unilateral RAS await definition.

Renal artery stenosis (RAS) is a common disorder associated with both cardiovascular and renal morbidity and mortality. Recent studies have shown that stenting of the stenotic kidney fails to improve renal or cardiovascular outcomes, prompting a search for more effective therapies. Strain‐specific variability in renal outcomes is a well recognized problem associated with murine models of chronic injury. The objective of this study was to define strain specific differences in renal outcome and correlation with parameters of injury in a murine model of RAS. We used a 0.25 mm polytetrafluoroethylene cuff to establish RAS in mice (n=292 total). We examined the correlation between age, time following surgery, body weight, blood pressure, heart and kidney weights, ratio of STK/CLK weight, and plasma angiotensin level in 3 murine strains. Percent atrophy in the STK as a function of time following RAS surgery is summarized in the table below: Strain 1 Week 2 Week 4 Week 6 Week 129 21% 31% XX 45% C57BLKS/J 25% 51% 63% 72% C57BL/6J XX XX 39% 41% The right kidney weight and the STK/CLK weight ratio correlated with %atrophy in all strains, with the strongest correlation observed in C57BL/6J mice. In C57BL/6J mice, blood pressure correlated with %atrophy. CLK weight correlated with heart weight, with the strongest correlation observed in 129Sv mice. In BLKS mice, the time following surgery and age correlated with CLK weight and %atrophy in the STK; blood pressure correlated with plasma angiotensin level. We conclude that RAS produces severe chronic renal injury in the STK of all strains studied, with the most severe injury observed in C57BLKS/J mice.The STK/CLK weight ratio correlated most strongly with %atrophy and can be used to predict development of chronic renal damage in all strains. Hypertrophy of the CLK, as measured by CLK weight, strongly correlated with heart weight.

Aim The aim of this study was to define the functional correlates of reversibilitiy following restoration of blood flow in the murine 2K1C model of renovascular hypertension. Method : Renal artery stenosis surgery (RAS) was performed by placement of a polytetrafluoroethylene cuff on the right renal artery (N=18). Sham surgery was performed without cuff placement (N=6). In two groups the cuff was removed at 7 days (7D cuff‐off, N=6) and 14 days (14D cuff‐off, N=6) after surgery. In the RAS group, cuff was left in place for 28 days (28D RAS, N=6). Kidneys were harvested at 28 days for assessment of histology and microvessel density (MVD). Renal blood perfusion and oxygenation were measured using 16.4T MRI. Blood pressure measurements were done using tail cuff method. Results In 7D cuff‐off group, baseline intra‐renal perfusion (891±142.8 ml/100g/min) was significantly reduced (311±73.4 ml/100g/min, p<0.0001) following cuff placement. Perfusion was restored to normal level (810±81.2 ml/100g/min) at 28 days following cuff removal at 7 days after RAS. In 14D cuff‐off group, baseline intra‐renal perfusion (846±74.5 ml/100g/min) was also significantly reduced (304±45.9 ml/100g/min, p=0.0002) following cuff placement with non‐significant improvement (579±112.9 ml/100g/min) at 28 days after cuff removal at 14 days after RAS. Baseline intra‐renal perfusion (905±54.9 ml/100g/min) in the 28D RAS group was significantly reduced (455±56.4 ml/100g/min, p<0.0034) following cuff placement and the reduction was maintained throughout the study period (478±22.2 ml/100g/min). 7D cuff‐off group (142±8.2 mg) showed no significant difference in kidney weights measured at 28 days compared to the sham group (154±4.8 mg), but was significantly higher compared to the 28D RAS group (67±10.5 mg, p=0.0010). The kidney weights of the 14D cuff‐off group (86±18.3 mg) measured at 28 days was not significantly different from the 28D RAS group. The 7D cuff‐off group had a significantly lower % atrophy (7±2.2%, p=0.0042) and higher MVD count (152±6.5, p=0.0045) compared to 28D RAS group (% atrophy 66±13%, MVD count 78±15.2). The 14D cuff‐off group had severe atrophy (56±16.6%) and reduced MVD count (94±20.1) similar to that seen in 28D RAS group. 50% of mice that developed hypoxia at day 3 had an improvement in their oxygenation after cuff removal at day 7, whereas, mice undergoing cuff removal at day 14 and 28 day ras mice remained hypoxic. Conclusion Based on these results, we conclude that the renal architecture and microvessel density are preserved when the cuff is removed no longer than 7 days post surgery. We Identified that 2 weeks after cuff placement is the “point of no return” in the renal injury in murine RAS model due to their reduction in microvessel density. Studies to identify biomarkers associated with irreversible renal injury in this model are currently being performed. Support or Funding Information NIH AI 100911 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

The objective of this study was to define a role for chemokine generation by parenchymal cells versus circulating inflammatory cells in the initiation of renal damage in the 2K1C model of renovascular hypertension. 129 SV mice were subjected to renal artery stenosis (RAS) by placement of a polytetraethylene cuff on the right renal artery. Systolic blood pressure increased within 2 days of surgery. The cuffed kidney developed tubular atrophy, whereas the contralateral kidney developed compensatory enlargement. Immunohistochemical staining of the cuffed kidney revealed less than 2 CD3+ T cells per 200x field, and rare F4/80+ macrophages or CD20+ B cells in the first 2 weeks following RAS, with progressive increases in macrophages and T cells throughout the 6‐week observation period. Despite the relative paucity of infiltrating inflammatory cells, there was a dramatic increase in chemokine generation within the first week following RAS, as assessed by qPCR analysis of renal cortical homogenates, with 25‐fold induction of MCP‐1, 47‐fold induction of RANTES, and 15‐fold induction of MIP‐2. Chemokine generation continued to increase throughout the 6 weeks, during which circulating inflammatory cells infiltrated the cuffed kidney. Increased expression of MCP‐1 was detected in tubular epithelial cells within 1 week of RAS. We conclude that chemokine generation precedes inflammatory cell influx in RAS.