Popliteal vein compression, obesity, and chronic venous disease.

BACKGROUND: Obesity is a known risk factor for the development of chronic venous disease (CVD). However, some obese patients with lower limb skin changes suggestive of venous disease do not demonstrate venous reflux or obstruction. Popliteal vein compression (PVC) caused by knee hyperextension during standing has been postulated by others to be more common in the obese due to the increased adipose content of the popliteal fossa. This compression may contribute to the development of venous disease. The objective was to examine the prevalence of PVC in obese and nonobese subjects, with and without venous disease. METHODS: Participants were recruited across the range of Clinical-Etiology-Anatomy-Pathophysiology (CEAP) clinical classifications and body mass. Those referred for venous studies had full venous ultrasound assessments. To assess for PVC, the popliteal vein was assessed via B-mode ultrasound whilst the subject stood and performed two maneuvers: knee hyperextension and a bilateral toe stand. Video clips of each maneuver were analyzed offline. RESULTS: There were 309 limbs (158 subjects), of which 131 were nonobese (body mass index [BMI]: 26 ± 3 kg/m2) and 178 obese (BMI: 43 ± 8 kg/m2). PVC with toe stand (PVC(toe stand)) was more common in obese limbs (89% vs 64%, P < .001). It occurred mainly in the distal popliteal vein, associated with contraction of the gastrocnemius muscles. PVC with knee hyperextension (PVC(lock)) was also more frequent in obese limbs (39% vs 10%, P < .0001) and was distinct as it occurred more proximally in the popliteal vein. PVC(lock) was significantly more frequent in all C classes of obese patients, most notably in the obese with C4-6 CVD (41% vs 4%, P < .0001), and was associated with more severe Venous Clinical Severity Score (median 8 [range: 0-19] vs 5 [0-21], P = .034). There were 19 limbs with skin changes (C4-6) with no venous reflux or obstruction on ultrasound, exclusively obese limbs. These limbs, designated CEAP Pn limbs, were in older, shorter participants with a higher BMI than their counterparts demonstrating reflux, and they also had more frequent PVC(lock) (63% vs 37%, P = .036). CONCLUSIONS: PVC(toe stand) and PVC(lock) are both functional effects and more common in obese limbs. PVC(toe stand) is likely associated with normal functioning of the calf muscle pump. Although PVC(lock) may contribute to CVD in some obese limbs, the demonstration of PVC(lock) alone is insufficient evidence for direct intervention.

Improved cardiac outcomes with combined atenolol and diazepam intervention in seizure.

OBJECTIVE: Altered autonomic activity has been implicated in the development of cardiac dysfunction during seizures. This study investigates whether intervening in seizure progression with diazepam will reduce seizure-induced cardiomyopathy. Second, this study examines the hypothesis that combining atenolol with diazepam, as an intervention after seizure onset, will combat cardiac injury during status epilepticus. METHODS: Male Sprague-Dawley rats were implanted with electroencephalographic/electrocardiographic electrodes to allow simultaneous recordings during seizures induced by intrahippocampal (2 nmol, 1 µL) kainic acid (KA). Subcutaneous saline, atenolol (5 mg·kg-1 ), diazepam (5 mg·kg-1 ), or atenolol and diazepam (n = 12/group) were administered at 60 minutes post-KA and daily for 7 days, at which point echocardiography, susceptibility to aconitine-induced arrhythmias, and histology were evaluated. RESULTS: Seizure activity was associated with immediately increased heart rate, QTc interval, and blood pressure (BP; 10%-30% across indices). Seven days postseizure, saline-treated animals were found to have reduced left ventricular function, increased fibrotic scarring, and an elevated risk of aconitine-induced arrhythmias. Diazepam treatment significantly reduced cumulative seizure behaviors by 79% compared to saline-treated animals but offered no cardiac protection. Diazepam significantly raised BP (35%) and increased the risk of bigeminal arrhythmias (36%) compared to saline-treated animals. Atenolol administration, either alone or with diazepam, reduced heart rate, QTc interval, and BP back to control levels. Atenolol also preserved cardiac morphology and reduced arrhythmia risk. SIGNIFICANCE: Attenuation of seizure with diazepam offered no cardiac protection; however, coadministration of atenolol with diazepam prevented the development of seizure-induced cardiac dysfunction. This study demonstrates that atenolol intervention should be strongly considered as an adjunct clinical treatment to reduce cardiomyopathy during seizures.

Accuracy and repeatability of the Dopplex Ability.

BACKGROUND: Ankle-brachial index (ABI) and pulse volume recordings (PVR) are non-invasive tests used in diagnosis of peripheral arterial disease (PAD). The Dopplex Ability is an automated ABI/PVR device utilising air plethysmography, offering easy and rapid PAD diagnosis. The accuracy and repeatability of the Dopplex were assessed in comparison to the Doppler/air plethysmography-based Parks Flo-Lab system. METHODS: Sixty-six patients (n = 129 lower limbs) were assessed with both Dopplex and Parks systems. For Dopplex ABI and PVR to be deemed accurate, it had to be within ±10% of the Parks ABI, and the PVR grade (1-4) had to be equal. The coefficient of variation (CV) was calculated from three repeat ABI/PVR readings to assess repeatability. RESULTS: The Dopplex and Parks devices correlated poorly for ABI (R2 = 0.17) with only 43% of ABIs and 69% of PVRs meeting the accuracy criteria compared to the Parks values. The specificity and sensitivity were 56% and 82%, respectively for ABI, and 91% and 89%, respectively for PVRs. The Dopplex showed a significantly higher CV for both ABIs and PVRs compared to the Parks. CONCLUSION: We found the Dopplex device to demonstrate suboptimal accuracy and repeatability in assessing ABI/PVR, and it was deemed unsuitable for use in our community.

Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus.

Seizures are associated with altered autonomic activity, which has been implicated in the development of cardiac dysfunction and structural damage. This study aimed to investigate the involvement of the autonomic nervous system in seizure-induced cardiomyopathy. Male Sprague-Dawley rats (320-350 g) were implanted with EEG/ECG electrodes to allow simultaneous telemetric recordings during seizures induced by intrahippocampal (2 nmol, 1 µl/min) kainic acid and monitored for 7 days. Seizure activity occurred in conjunction with increased heart rate (20%), blood pressure (25%), and QTc prolongation (15%). This increased sympathetic activity was confirmed by the presence of raised plasma noradrenaline levels at 3 h post-seizure induction. By 48 h post-seizure induction, sympathovagal balance was shifted in favor of sympathetic dominance, as indicated by both heart rate variability (LF/HF ratio of 3.5 ± 1.0) and pharmacological autonomic blockade. Functional cardiac deficits were evident at 7 and 28 days, as demonstrated by echocardiography showing a decreased ejection fraction (14% compared with control, P < 0.05) and dilated cardiomyopathy present at 28 days following seizure induction. Histological changes, including cardiomyocyte vacuolization, cardiac fibrosis, and inflammatory cell infiltration, were evident within 48 h of seizure induction and remained present for up to 28 days. These structural changes most probably contributed to an increased susceptibility to aconitine-induced arrhythmias. This study confirms that prolonged seizure activity results in acute and chronic alterations in cardiovascular control, leading to a deterioration in cardiac structure and function. This study further supports the need for modulation of sympathetic activity as a promising therapeutic approach in seizure-induced cardiomyopathy.