8 research outputs found

    Radiation-induced skin injury after complex endovascular procedures

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    BackgroundRadiation-induced skin injury is a serious potential complication of fluoroscopically guided interventions. Transient erythema occurs at doses of 2 to 5 Gy, whereas permanent epilation, ulceration, and desquamation are expected at doses above this level. Complex endovascular procedures (CEPs), such as fenestrated endovascular aortic aneurysm repair (FEVAR), are associated with high radiation doses, yet the prevalence of radiation-induced skin injury is unknown. We hypothesized that skin injury after these exposures is likely to be underrecognized and underreported. This study examined the frequency and severity of deterministic effects and evaluated patient characteristics that might predispose to radiation injury in CEP.MethodsCEP was defined as a procedure with a radiation dose ≄5 Gy (National Council on Radiation Protection and Measurements threshold for substantial radiation dose level [SRDL]). Radiation dose and operating factors were recorded for all CEPs performed in a hybrid room during a 30-month period. Patient medical records were retrospectively reviewed for evidence of skin injury. Patients were seen in follow-up daily until discharge and then at weeks 2 and 6, months 3 and 6, and 1 year. Phone interviews were conducted to determine the presence of any skin-related complaints. Peak skin dose (PSD) distributions were calculated for FEVARs with custom software employing input data from fluoroscopic machine logs. These calculations were validated against Gafchromic film (Ashland Inc, Covington, Ky) measurements. Dose was summed for the subset of patients with multiple procedures within 6 months of the SRDL event, consistent with Joint Commission recommendations.ResultsSixty-one CEPs reached a reference air kerma (RAK) of 5 Gy (50 FEVARs, six embolizations, one thoracic endovascular aortic repair, one endovascular aneurysm repair, one carotid intervention, and two visceral interventions). The patient cohort was 79% male and had a mean body mass index of 31. The average RAK was 8 ± 2 Gy (5.0-15.9 Gy). Sixteen patients had multiple CEPs within 6 months of the SRDL event, with a mean cumulative RAK of 12 ± 3 Gy (7.0-18.4 Gy). The mean FEVAR PSD was 6.6 ± 3.6 Gy (3.7-17.8 Gy), with a mean PSD/RAK ratio of 0.78. Gafchromic film dose measurements were not statistically different from PSD estimations, with a constant of proportionality of 0.99. Three patients were lost to follow-up before their first postoperative visit. No radiation skin injuries were found.ConclusionsThis study represents the largest analysis of deterministic skin injury after CEPs, and our results suggest that it is less frequent than expected and not increased in CEPs

    Differential effects of eplerenone versus amlodipine on muscle metaboreflex function in hypertensive humans

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    Abstract Numerous studies have demonstrated that sympathetic nervous system overactivation during exercise in hypertensive rodents and humans is due, in part, to an exaggerated reflex response known as the exercise pressor reflex. Our prior studies have implicated a key role of mineralocorticoid receptor activation in mediating an augmented exercise pressor reflex in spontaneously hypertensive rats, which is mitigated by blockade with eplerenone. However, the effect of eplerenone on exercise pressor reflex has not been assessed in human hypertension. Accordingly, the authors performed a randomized crossover study to compare the effects of eplerenone to another antihypertensive drug from a different class amlodipine on sympathetic nerve activity (SNA) in 14 patients with uncomplicated hypertension. The authors found that amlodipine unexpectedly augmented the increase in SNA during the second minute of isometric handgrip, which persisted into the post‐exercise circulatory arrest period (∆ SNA, from rest of 15 ± 2 vs. 9 ± 2 vs. 10 ± 2 bursts/min, amlodipine vs. baseline vs. eplerenone, respectively, p < .01), suggesting an exaggerated muscle metaboreflex function. Eplerenone did not alter sympathetic responses to exercise or post‐exercise circulatory arrest in the same hypertensive individuals. In conclusions, our studies provide the first direct evidence for a potentially unfavorable potentiation of muscle metaboreflex by amlodipine during isometric handgrip exercise in hypertensive patients whereas eplerenone has no significant effect. Our study may have clinical implications in terms of selection of antihypertensive agents that have the least detrimental effects on sympathetic neural responses to isometric exercise

    Functional sympatholysis is impaired in hypertensive humans

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    In healthy individuals, sympathetic vasoconstriction is markedly blunted in exercising muscles to optimize blood flow to the metabolically active muscle fibres. This protective mechanism, termed functional sympatholysis, is impaired in rat models of angiotensin-dependent hypertension. However, the relevance of these findings to human hypertension is unknown. Therefore, in 13 hypertensive and 17 normotensive subjects we measured muscle oxygenation and forearm blood flow (FBF) responses to reflex increases in sympathetic nerve activity (SNA) evoked by lower body negative pressure (LBNP) at rest and during moderate-intensity rhythmic handgrip exercise. In the normotensives, LBNP caused decreases in oxygenation and FBF (−16 ± 2% and −23 ± 4%, respectively) in resting forearm but not in exercising forearm (−1 ± 2% and −1 ± 3%, respectively; P < 0.05 vs. rest). In the hypertensives, LBNP evoked decreases in oxygenation and FBF that were similar in the resting and exercising forearm (−14 ± 2%vs.−12 ± 2% and −20 ± 3%vs.−13 ± 2%, respectively; P > 0.05), indicating impaired functional sympatholysis. In the hypertensives, SNA was unexpectedly increased by 54 ± 11% during handgrip alone. However, when SNA was experimentally increased during exercise in the normotensives, sympatholysis was unaffected. Treatment for 4 weeks with the angiotensin receptor blocker irbesartan, but not with the thiazide-type diuretic chlorthalidone, restored sympatholysis in the hypertensives. These data provide the first evidence that functional sympatholysis is impaired in hypertensive humans by a mechanism that appears to involve an angiotensin-dependent increase in sympathetic vasoconstriction in the exercising muscles
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