Loss of Pulmonary Vascular Volume as a Predictor of Right Ventricular Dysfunction and Mortality in Acute Pulmonary Embolism

Background: In acute pulmonary embolism, chest computed tomography angiography derived metrics, such as the right ventricle (RV): left ventricle ratio are routinely used for risk stratification. Paucity of intraparenchymal blood vessels has previously been described, but their association with clinical biomarkers and outcomes has not been studied. We sought to determine if small vascular volumes measured on computed tomography scans were associated with an abnormal RV on echocardiography and mortality. We hypothesized that decreased small venous volume would be associated with greater RV dysfunction and increased mortality. Methods: A retrospective cohort of patients with intermediate risk pulmonary embolism admitted to Brigham and Women’s Hospital between 2009 and 2017 was assembled, and clinical and radiographic data were obtained. We performed 3-dimensional reconstructions of vasculature to assess intraparenchymal vascular volumes. Statistical analyses were performed using multivariable regression and cox proportional hazards models, adjusting for age, sex, lung volume, and small arterial volume. Results: Seven hundred twenty-two subjects were identified of whom 573 had documented echocardiography. A 50% reduction in small venous volume was associated with an increased risk of RV dilation (relative risk: 1.38 [95% CI, 1.18–1.63], P <0.001), RV dysfunction (relative risk: 1.62 [95% CI, 1.36–1.95], P <0.001), and RV strain (relative risk: 1.67 [95% CI, 1.37–2.04], P <0.001); increased cardiac biomarkers, and higher 30-day and 90-day mortality (hazard ratio: 2.50 [95% CI, 1.33–4.67], P =0.004 and hazard ratio: 1.84 [95% CI, 1.11–3.04], P =0.019, respectively). Conclusions: Loss of small venous volume quantified from computed tomography angiography is associated with increased risk of abnormal RV on echocardiography, abnormal cardiac biomarkers, and higher risk of 30- and 90-day mortality. Small venous volume may be a useful marker for assessing disease severity in acute pulmonary embolism.

Influence of Superficial Venous Ablation on Deep Venous Dilation and Reflux in Patients With Saphenous Varicose Veins

Background: To investigate the influence of superficial venous ablation on deep venous dilation and reflux in patients with saphenous varicose veins, and to elucidate the association between superficial venous reflux and deep venous morphology and hemodynamics. Methods: The data of 154 patients with 223 limbs, who underwent endovenous radiofrequency ablation (RFA) of the great saphenous vein for primary varicose veins between September 2014 and March 2016 in Eniwa Midorino Clinic, were retrospectively analyzed. Overall venous hemodynamics of the leg, including functional venous volume (VV) and venous filling index (VFI), was assessed using air-plethysmography. Saphenous and deep vein reflux and diameter were evaluated with duplex scanning. Results: Hemodynamic and morphologic changes were evaluated before and 1 month after RFA. The VV and VFI were significantly decreased in postoperative values than in preoperative values ( P < .001). Limbs with deep venous reflux significantly decreased postoperatively than preoperatively ( P < .001). There were significant differences in the diameter of the common femoral vein (CFV) and popliteal vein (PV) between the preoperative and postoperative values ( P < .001). There were strong to moderate correlations between the VV and the diameter of the CFV or PV (CFV, r = 0.47, P < .001; PV, r = 0.35, P < .001), while there were moderate to weak correlations between the VFI and the diameter of the CFV or PV (CFV, r = 0.23, P < .001; PV, r = 0.33, P <.001). Conclusions: Superficial venous ablation significantly reduced deep venous dilation and reflux in patients with saphenous varicose veins. Significant correlations existed between the VV or VFI, which reflected superficial venous reflux, and the diameter of the deep veins. These findings reveal that volume overload due to superficial venous reflux is associated with deep venous morphology and hemodynamics.

Effects of Silybum marianum Aqueous Extract and L-carnitine on Stereological Changes in Diazinon-Treated Rat Liver

As an organophosphorus, Diazinon (DZN) impairs liver tissue function by inhibiting acetylcholinesterase and causing oxidative stress. In this study, the effects of <em>Silybum</em><em> marianum </em>aqueous extract (SMAE) and L-carnitine (LC) on the stereological and histopathological changes of the liver in DZN-treated male rats were investigated. The rats in this study were placed into 9 groups of 8 each containing control, placebo, and a combination of DZN, SMAE, and LC. The animals received SMAE and chemicals orally for 30 days. At last, the liver tissue of all animals was removed. Then, tissue sections from the liver were provided to study the stereological markers including liver volume and weight, hepatocytes’ volume, central venous volume, sinusoidal volume, connective tissue volume, inflammation rate, and a number of the hepatocytes’ nuclei. Also, the sample tissues were evaluated histopathologically. Treatment with DZN significantly reduced the liver volume and weight, hepatocyte volume, central venous volume, sinusoidal volume, and hepatocyte nucleus number compared to placebo and control but it significantly increased the inflammation and volume of liver’s connective tissue. However, co-administration of SMAE and LC with DZN improved liver volume and weight, hepatocyte volume, central venous volume, sinusoidal volume, connective tissue volume, and hepatocyte nucleus number alone compared to the DZN treatment. Liver inflammation was also significantly decreased compared to the DZN treatment but comparing to the placebo and control groups, it increased significantly. Simultaneous administration of SMAE and LC has protective effects on liver tissue and can reduce DZN-induced liver injury in rats.

Dural sinus volume in children with syndromic craniosynostosis and intracranial hypertension

OBJECTIVEIntracranial hypertension is a major concern in children with syndromic craniosynostosis (sCS). Cerebral venous hypertension caused by cerebral venous outflow obstruction is believed to contribute to intracranial hypertension. The authors therefore hypothesized that cerebral venous volume would be increased in those children with sCS and intracranial hypertension.METHODSIn a case series of 105 children with sCS, of whom 32 had intracranial hypertension, cerebral MRI techniques were used to quantify the volume of the superior sagittal sinus, straight sinus (StrS), and both transverse sinuses.RESULTSLinear regression showed that total cerebral venous volume increased by 580.8 mm3 per cm increase in occipitofrontal head circumference (p < 0.001). No significant difference was found between the intracranial hypertension group and the nonintracranial hypertension group (p = 0.470). Multivariate ANOVA showed increased StrS volume (as a proportion of total volume) in the intracranial hypertension group (8.5% vs 5.1% in the nonintracranial hypertension group, p < 0.001). Multivariate logistic regression showed that a 100-mm3 increase in StrS volume is associated with increased odds of having intracranial hypertension by 60% (OR 1.60, 95% CI 1.24–2.08).CONCLUSIONSAlthough intracranial hypertension was not associated with total cerebral venous volume increase, it was associated with an isolated increase in StrS volume. Hence, it is unlikely that general cerebral venous outflow obstruction is the mechanism of intracranial hypertension in sCS. Rather, these findings indicate either a central cerebral vulnerability to intracranial hypertension or a mechanism involving venous blood redistribution.

Cardiovascular responses to exercise when increasing skin temperature with narrowing of the core-to-skin temperature gradient

The decline in stroke volume (SV) during exercise in the heat has been attributed to either an increase in cutaneous blood flow (CBF) that reduces venous return or an increase in heart rate (HR) that reduces cardiac filling time. However, the evidence supporting each mechanism arises under experimental conditions with different skin temperatures (Tsk; e.g., ≥38°C vs. ≤36°C, respectively). We systematically studied cardiovascular responses to progressively increased Tsk (32°C–39°C) with narrowing of the core-to-skin gradient during moderate intensity exercise. Eight men cycled at 63 ± 1% peak oxygen consumption for 20–30 min. Tsk was manipulated by having subjects wear a water-perfused suit that covered most of the body and maintained Tsk that was significantly different between trials and averaged 32.4 ± 0.2, 35.5 ± 0.1, 37.5 ± 0.1, and 39.5 ± 0.1°C, respectively. The graded heating of Tsk ultimately produced a graded elevation of esophageal temperature (Tes) at the end of exercise. Incrementally increasing Tsk resulted in a graded increase in HR and a graded decrease in SV. CBF reached a similar average plateau value in all trials when Tes was above ~38°C, independent of Tsk. Tsk had no apparent effect on forearm venous volume (FVV). In conclusion, the CBF and FVV responses suggest no further pooling of blood in the skin when Tsk is increased from 32.4°C to 39.5°C. The decrease in SV during moderate intensity exercise when heating the skin to high levels appears related to an increase in HR and not an increase in CBF. NEW & NOTEWORTHY This study systematically investigated the effect of increasing skin temperature (Tsk) to high levels on cardiovascular responses during moderate intensity exercise. We conclude that the declines in stroke volume were related to the increases in heart rate but not the changes in cutaneous blood flow (CBF) and forearm venous volume (FVV) during moderate intensity exercise when Tsk increased from ~32°C to ~39°C. High Tsk (≥38°C) did not further elevate CBF and FVV compared with lower Tsk during moderate intensity exercise.

The inability of venous occlusion air plethysmography to identify patients who will benefit from stenting of deep venous obstruction

Background The aim of this study was to assess whether venous occlusion plethysmography can be used to identify venous obstruction and predict clinical success of stenting. Method Receiver operated characteristic curves were used to determine the ability of venous occlusion plethysmography to discriminate between the presence and absence of obstruction, measured by duplex ultrasound and magnetic resonance venography, and to discriminate between successful and non-successful stenting, measured by VEINES-QOL/Sym. Result Two hundred thirty-seven limbs in 196 patients were included. Areas under the curve for post-thrombotic obstruction were one-second outflow volume 0.71, total venous volume 0.69 and outflow fraction 0.59. Stenting was performed in 45 limbs of 39 patients. Areas under the curve for identifying patients with successful treatment at one year after stenting were 0.57, 0.54 and 0.63, respectively. Conclusion Venous occlusion plethysmography cannot be used to identify venous obstruction proximal to the femoral confluence or to distinguish which patients will benefit from treatment.

Removal of Arterial Vessel Contributions in Susceptibility-Weighted Images for Quantification of Normalized Visible Venous Volume in Children with Sickle Cell Disease

Purpose. To evaluate a new postprocessing framework that eliminates arterial vessel signal contributions in the quantification of normalized visible venous volume (NVVV, a ratio between venous and brain volume) in susceptibility-weighted imaging (SWI) exams in patients with sickle cell disease (SCD). Materials and Methods. We conducted a retrospective study and qualitatively reviewed for hypointense arterial vessel contamination in SWI exams from 21 children with SCD. We developed a postprocessing framework using magnetic resonance angiography in combination with SWI to provide a more accurate quantification of NVVV. NVVV was calculated before and after removing arterial vessel contributions to determine the error from hypointense arterial vessels in quantifying NVVV. Results. Hypointense arterial vessel contamination was observed in 86% SWI exams and was successfully corrected by the proposed method. The contributions of hypointense arterial vessels in the original SWI were significant and accounted for approximately 33% of the NVVV [uncorrected NVVV = 0.012 ± 0.005 versus corrected NVVV = 0.008 ± 0.003 (mean ± SD), P<0.01]. Conclusion. Hypointense arterial vessel contamination occurred in the majority of SWI exams and led to a sizeable overestimation of the visible venous volume. A prospective longitudinal study is needed to evaluate if quantitation of NVVV was improved and to assess the role of NVVV as a biomarker of SCD severity or stroke risk.