Venous Capacitance Research Articles

A double-blind placebo-controlled cross-over study of the vascular effects of midodrine in neuropathic compared with hyperadrenergic postural tachycardia syndrome

POTS (postural tachycardia syndrome) is a chronic form of OI (orthostatic intolerance). Neuropathic POTS is characterized by decreased adrenergic vasoconstriction, whereas hyperadrenergic POTS exhibits increased adrenergic vasoconstriction. We hypothesized that midodrine, an α1-adrenergic receptor agonist, would increase CVR (calf vascular resistance), decrease C(v) (calf venous capacitance) and decrease orthostatic tachycardia in neuropathic POTS, but not alter haemodynamics in hyperadrenergic POTS. A total of 20 POTS patients (12 neuropathic and eight hyperadrenergic), ages 12-20 years, participated in this randomized placebo-controlled double-blind cross-over study. Of these subjects, 15 were female. POTS subjects received 2 weeks of treatment with midodrine or placebo, with increased dosing from 2.5 to 10 mg three times daily. Following a 7-day drug-washout period, subjects received the cross-over treatment. HR (heart rate), MAP (mean arterial pressure), Q(calf) (calf blood flow) and CVR were measured supine and during 35° HUT (head-up tilt). C(v) was measured supine. In neuropathic POTS, midodrine decreased supine HR, Q(calf) and C(v), while increasing MAP and CVR compared with placebo. During HUT, in neuropathic POTS, midodrine decreased HR, Q(calf) and C(v), while increasing MAP and CVR. In hyperadrenergic POTS, placebo and midodrine both decreased upright HR and increased supine CVR. Placebo also increased supine C(v), compared with midodrine in hyperadrenergic POTS. Therefore midodrine improved postural tachycardia in neuropathic POTS by increasing CVR and decreasing Q(calf) and C(v), whereas these effects were not seen in hyperadrenergic POTS patients who experienced a placebo effect. This suggests that midodrine is probably an effective treatment for neuropathic POTS, but not for hyperadrenergic POTS.

Renal sympathetic denervation significantly reduces blood pressure but not cause orthostatic dysregulation in patients with resistant hypertension

Backround: Patients (pts.) with resistant hypertension have been characterized by increased sympathetic nerve activity when compared to normotensive subjects. Before the introduction of modern antihypertensive drugs patients have been treated with surgical lumbal sympathectomy. However, this procedure was linked with severe side effects such as severe orthostatic dysregulation. Recently, catheter-based bilateral renal denervation (RDN) of sympathetic nerve fibres has been shown to significantly lower blood pressure (BP). However, the effect of RDN on orthostatic blood pressure regulation is not known. Methods: 9 pts. were selected according to the SIMPLICITY criteria and treated with RDN. Follow-up included baseline values and measurements at 3 and 6 months. Office BP was measured with OmeronTM. A Schellong test was performed at baseline, 3 and 6 month after RDN. After being in relaxed supine position for 10 min. BP and heart rate (HR) was measured every 2 minutes. BP and HR were then measured in an upright position over ten min. and after returning into a supine positon. Results: The baseline mean office SBP/DBP was 176/89 mmHg (SEM 5/6 mmHg), after 6 month 141/80 mmHg (SEM 6/4). Pts. were treated with 5.3 antihypertensives mean. As shown by the Schellong test there was no significant difference in the overall orthostatic regulation of the BP, the level of BP was lower 6 month after RDN as compared to baseline. HR did not differ between the two groups. ![Figure][1] Figure 1. SBP at 3 and 6 month Conclusion: (i) In patients with resistant hypertension RDN resulted in a significant blood pressure reduction after 3 and 6 month. (ii) No orthostatic dysregulation or syncope were be identified after RDN using the Schellong-test, indicating that RDN has no effect on venous tone and venous capacity when tilting into an upright position. [1]: pending:yes

Current State of Endovascular Treatment for Vasculogenic Erectile Dysfunction

Normal erectile function requires adequate penile arterial inflow, normal penile architecture and an intact venous capacitance system. Vascular disease is the dominant etiology of erectile dysfunction (ED) and current medical therapy increases penile blood flow. However, in a large proportion of patients, medical therapy is inadequate or contraindicated requiring the use of mechanical constrictive devices or implantation of a penile prosthesis. Rapid advances in endovascular intervention have allowed safe and effective treatment of small arteries in other vascular beds. A minimally invasive approach targeting penile arterial inflow disease may prove to be safe and effective. In this paper, we discuss the normal arterial blood supply to the penis, describe angiographic findings in patients with ED, and critically review the published data on endovascular and microsurgical approaches at reestablishing penile blood flow. Lastly, we offer a potential algorithm and procedural tips for endovascular intervention for ED.

Nitrates and Arterial Function

In this article we trace the history of nitrites and nitrates from their discovery to their widespread use in clinical medicine. The cardiovascular actions and uses of these molecules [namely endogenous nitric oxide (NO) and exogenous nitroglycerin (NTG)] are described along with their similar mechanisms of action. The major vasodilating effect of both NO and NTG is on muscular arteries with less effect on arterioles and veins. By decreasing arterial stiffness, these agents reduce pulse wave velocity (PWV) and attenuate wave reflection amplitude and duration. These alterations in arterial properties and wave reflection characteristics reduce pulsatile left ventricular (LV) afterload (systolic and pulse blood pressure) and LV wasted energy, which decrease myocardial oxygen requirements. These agents can also increase arteriolar and venous caliber, which decreases distal resistance and increases venous capacity, respectively. These mechanistic effects help to explain the benefit of nitrites and nitrates in control of angina pectoris, congestive heart failure, and systolic hypertension.

Algebraic Approximations for Blood, Interstitial, and Lymph Pressures, Volumes, and Flows During Hemorrhagic Shock and Fluid Resuscitation

The tolerance to hemorrhage, effectiveness of fluid resuscitation, and the transport of inflammatory mediators, all depend on how fluid redistributes between vascular and interstitial compartments. Fluid redistribution depends on the complex interaction of cardiac function, venous and interstitial capacitance, arterial and venous resistances, microvascular filtration and lymphatic function. The promise of mathematical models to elucidate the physiology of shock has suffered from the very complexity they aim to address, leading to numerical solutions that only apply for a particular animal or patient population, are sensitive to assumed parameters, and are difficult to interpret. We therefore applied simplifying assumptions to the standard hemodynamic and fluid balance equations typically used in shock research. The result is the first set of algebraic approximations for the pressure, volumes, and flow of blood, interstitial fluid and lymph during shock and subsequent fluid resuscitation. We thus provide a new tool to address the traditional goals of determining the optimal composition, amount, and timing of fluid resuscitation to restore perfusion and limit extravascular redistribution, as well as the newer goal of preventing acute respiratory distress syndrome by limiting the transport of inflammatory mediators transported in mesenteric lymph.

Chemohypersensitivity and Autonomic Modulation of Venous Capacitance in the Pathophysiology of Acute Decompensated Heart Failure

Heart failure is increasing in prevalence around the world, with hospitalization and re-hospitalization as a result of acute decompensated heart failure (ADHF) presenting a huge social and economic burden. The mechanism for this decompensation is not clear. Whilst in some cases it is due to volume expansion, over half of patients with an acute admission for ADHF did not experience an increase in total body weight. This calls into question the current treatment strategy of targeting salt and water retention in ADHF. An alternative hypothesis proposed by Fallick et al. is that an endogenous fluid shift from the splanchnic bed is implicated in ADHF, rather than an exogenous fluid gain. The hypothesis states further that this shift is triggered by an increase in sympathetic tone causing vasoconstriction in the splanchnic bed, a mechanism that can translocate blood rapidly into the effective circulating volume, generating the raised venous pressure and congestion seen in ADHF. This hypothesis encourages a new clinical paradigm which focuses on the underlying mechanisms of congestion, and highlights the importance of fluid redistribution and neurohormonal activation in its pathophysiology. In this article, we consider the concept that ADHF is attributable to episodic sympathetic hyperactivity, resulting in fluid shifts from the splanchnic bed. Chemosensitivity is a pathologic autonomic mechanism associated with mortality in patients with systolic heart failure. Tonic and episodic activity of the peripheral chemoreceptors may underlie the syndrome of acute decompensation without total body salt and water expansion. We suggest in this manuscript that chemosensitivity in response to intermittent hypoxia, such as experienced in sleep disordered breathing, may explain the intermittent sympathetic hyperactivity underlying renal sodium retention and acute volume redistribution from venous storage sites. This hypothesis provides an alternative structure to guide novel diagnostic and treatment strategies for ADHF.

Influence of patient positioning and pneumoperitoneum on lower limbs venous haemodynamics during laparoscopic cholecystectomy

The introduction of laparoscopic surgery has dramatically changed the management of gallstone disease, establishing laparoscopic cholecystectomy as the method of choice for treating cholelithiasis. The aim of this study is to review the significance of patient positioning and pneumoperitoneum in laparoscopic cholecystectomy as potential risk factors for the development of postoperative venous thromboembolism (VTE), with the use of impedance plethysmography (IPG). We studied 40 consecutive patients undergoing selective laparoscopic cholecystectomy. Seventeen patients of our study group were positioned on the operating table in the lithotomy (French) position and 23 in the supine (American) position. Femoral venous capacitance (VC) and maximum venous outflow (MVO) from both legs of the patient was obtained using an impedance ple-thysmography (IPG) device. These parameters were measured: a) the day before operation, b) after French or American positioning on the surgical table, c) at the time of inflation to produce pneumoperitoneum, d) 30 minutes after pneumoperitoneum, and e) 24 hours after surgery. Our study confirms that the patient’s position on the surgical table (French or American position) does not affect venous haemodynamics of the legs. Peritoneal carbon dioxide insufflations to an intrabdominal pressure of 12 mm Hg produce haemodynamic changes, significantly increased after the beginning of peritoneal insufflations.VC and MVO were significantly increased during surgery in both positions. However, after exsufflation and at the first postoperative day, all haemodynamic parameters returned to preoperative values. Our study advocates no difference between French or American positioning during laparoscopic cholecystectomy in measurements obtained from both legs of the patient using an impedance plethysmography device.

Impact of physiological aging on lower limb venous compliance

AimWe aimed to evaluate changes in venous physiologic parameters with aging in healthy volunteers. MethodsSixty subjects (29 women, 31 men, mean age 63.1±4.4, 24 subjects aged over 75years) with no history of deep venous thromboembolism, venous insufficiency, deep venous thrombosis, peripheral arteriopathy, lower limb edema, atrial fibrillation or acute medical condition within the last 7days were enrolled. Subjects remained in the supine position for 15min before and during data acquisition. Mercury strain gauge was put around the calf and connected to the EC6 plethysmograph. We measured the venous parameters by inflating the collecting cuff up to 50mmHg pressure for 4min. The data were implemented in the NIVP3 software to measure compliance, maximum venous outflow (MVO) and half-emptying time (T1/2). ResultsThe venous capacitance, compliance and MVO significantly decreased with age (P=0.023, P=0.01 and P=0.02, respectively, ANOVA) while T1/2 increased with age (P=0.02, ANOVA). There was a negative correlation between age and respectively, compliance (rs=−0.21, P=0.01) and MVO (rs=−0.25, P=0.0003), and a positive correlation between T1/2 and age (rs=0.14, P=0.0003). Using logistic regression analysis, calf circumference (P=0.0001), venous capacitance (P=0.012) and MVO (P=0.033) were the only variables independently associated to age. ConclusionUsing a sensitive, non-invasive, painless, reproducible and easily repeatable computerized method, we successfully forecasted changes of venous physiological parameters over age and provided valuable information in the field of physiological aging.

Association of Venous Function and Post-Exercise Oxygen Consumption

Excess post-exercise oxygen consumption (EPOC) has been attributed to metabolic, hemodynamic, neuroendocrine, and pulmonary factors. Interestingly, few studies have examined the role of venous system on EPOC. The purpose of this study was to examine the relationship between measures of vascular function and EPOC. Measures of vascular function and VO2 recovery kinetics were examined in 20 individuals [age=22+2.41 yrs]. Nondominant forearm arterial inflow, venous capacitance and venous outflow were evaluated at rest and after 5 minutes of upper arm occlusion, using strain gauge plethysmography. VO2 recovery kinetics was assessed using gas exchange analysis following a six-minute constant work rate protocol at 60 percent of VO2peak (VO2@60%), on a cycle ergometer. The average VO2peak was 33.48±8.22 ml×kg-1×min-1 (Range: 18.7 to 46.1 ml×kg-1×min-1). Following the six-minute constant work rate protocol, recovery half-time (T1/2VO2) and Tau were 17.01±3.51 seconds and 54.45±11.28 seconds, respectively. Arterial resting inflow was 2.77±1.51 ml×100ml-1×min-1, reactive hyperemic blood flow was 17.72±3.65 ml×100ml-1×min-1, venous capacitance was 2.86±0.72 percent, and venous outflow was 34.19±10.03 ml×100ml-1×min-1. Bivariate correlations revealed significant inverse associations between T1/2VO2 and the reactive hyperemic response (r=-0.48, p=0.03) and T1/2VO2 and venous outflow post-occlusion (r=-0.50, p=0.02). In conclusion, these findings suggest an important role of both the arterial and venous circulation on EPOC.

Heritability of Venous Biomechanics

Altered venous biomechanics may contribute to the pathogenesis of venous diseases, and their heritability is less known. Seventy-eight monozygotic twin pairs (aged 42.4 ± 16.8 years) and 24 same-sex dizygotic twin pairs (aged 50.5 ± 16.1 years) were examined. Anteroposterior and mediolateral diameters of the common femoral vein were measured by ultrasonography. Measurements were made both in supine and in standing body positions, with or without controlled forced expiration (Valsalva test). High correlation of diameter, capacity, and distensibility values was found between twin pairs. The univariate heritability (A), shared (C), and unshared (E) environmental effects model has shown 39.3% genetic component of the variance of low pressure, 37.9% of high-pressure venous capacity, and 36.4% of maximal capacity changes, even after elimination of sex, age, and body weight effects. Bivariate Cholesky analysis revealed substantial covariance of inherited body weight and venous capacity components (57.0%-81.4%). Femoral vein capacity and elasticity depend ≈30% to 40% on genetic factors, and this value in the standing body position can reach 50%. A relatively high genetic covariance was found between weight and femoral vein capacity and elasticity. Our work might yield some new insights into the inheritance of venous diseases that are associated with altered venous biomechanics and help elucidate the involved genes.

Visualization of peripheral vasodilative indices in human skin by use of red, green, blue images

We propose a method to visualize the arterial inflow, the vascular resistance, and the venous capacitance in the skin tissue from red, green, blue (RGB) digital color images. The arterial inflow and the venous capacitance in the skin tissue are visualized based on an increase in the rate of change in the total blood concentration and the change of the total blood concentration during upper limb occlusion at a pressure of 50 mmHg. The resultant arterial inflow with the measured mean arterial pressure also provides an image of the vascular resistance in human skin. The arterial inflow, the vascular resistance, and the venous capacitance acquired by the method are well correlated with those obtained from the conventional strain-gauge plethysmograph. The correlation coefficients R between the estimated values by the method and the measurements by the SPG are calculated to be 0.83 (P<0.001) for the arterial inflow, 0.77 (P<0.01) for the vascular resistance, and 0.77 (P<0.01) for the venous capacitance. The arterial inflow and the venous capacitance in the skin tissue are significantly higher in active subjects compared with the sedentary subjects, whereas the vascular resistance was significantly lower in the active subjects compared with the sedentary subjects. The results of the present study indicate the possibility of using the proposed method for evaluating the peripheral vascular functions in human skin.

An Educational Training Simulator for Advanced Perfusion Techniques Using a High‐Fidelity Virtual Patient Model

The operation of cardiopulmonary bypass procedure requires an advanced skill in both physiological and mechanical knowledge. We developed a virtual patient simulator system using a numerical cardiovascular regulation model to manage perfusion crisis. This article evaluates the ability of the new simulator to prevent perfusion crisis. It combined short-term baroreflex regulation of venous capacity, vascular resistance, heart rate, time-varying elastance of the heart, and plasma-refilling with a simple lumped parameter model of the cardiovascular system. The combination of parameters related to baroreflex regulation was calculated using clinical hemodynamic data. We examined the effect of differences in autonomous-nerve control parameter settings on changes in blood volume and hemodynamic parameters and determined the influence of the model on operation of the control arterial line flow and blood volume during the initiation and weaning from cardiopulmonary bypass. Typical blood pressure (BP) changes (hypertension, stable, and hypotension) were reproducible using a combination of four control parameters that can be estimated from changes in patient physiology, BP, and blood volume. This simulation model is a useful educational tool to learn the recognition and management skills of extracorporeal circulation. Identification method for control parameter can be applied for diagnosis of heart failure.

Medical simulation in ‘my world’

I read with great interest the editorial by Dr Gilpin and colleagues [1], as we have recently changed the manikin in our centre from one that was ‘fixed’ and had ‘deductive modelling’ to one that is now ‘wireless’ and is controlled ‘on the fly’ (where the instructor changes the manikin’s physiology based on the actions of the candidates in the scenario). I recognise the problems involved in programming an overly complicated ‘deductive model’, for example, in having to change the manikin’s venous capacitance to drop its blood pressure, the oxygen consumption to prevent a desaturation or the ‘ischaemic index sensitivity’ to prevent a cardiac arrest, which detracts from faculty’s concentrating on controlling the scenario, and sometimes resulting in manikin ‘death’ despite correct simulated intervention. During a newer, high-fidelity simulation scenario, candidates only see parameters displayed on a monitor, which can be adapted readily by the controller to achieve a realistic physiological change. The internal physiological programming of the manikin plays no actual part in the scenario provided. A well-delivered scenario can be achieved by ensuring an experienced and well-trained faculty. A typical complex trauma scenario at our centre requires at least five members of faculty and although this requires a large investment in time and manpower, we are able to deliver a realistic scenario using a manikin that is a third of the price of a typical ‘deductive model’. Typical faculty roles are as follows: one overall scenario controller (usually the course director); a manikin controller; a manikin voice operator (so as not to distract the controller); a phone operator; and a facilitator who is able to direct the scenario (receiving headset instructions from the scenario controller) and act in a health and safety role. Pre-planned, fixed manikin programs can become unstuck if candidates do something unpredictable, such as giving the wrong drug or drug dose or decompressing a tension pneuomthorax that does not exist. Newer manikins allow the experienced controller to change parameters appropriately, without spoiling the fidelity of a simulation as a result of having to reprogram a deductive model. Advances in technology should be welcomed, particularly new software provided for handheld devices, but the future lies in well-trained controllers and faculty who have the experience to alter the manikin during scenarios and achieve the pre-determined learning objectives.

Clevidipine: a review of its use in the management of acute hypertension.

Clevidipine: a review of its use in the management of acute hypertension.

Collateral Perfusion: Time for Novel Paradigms in Cerebral Ischemia

Collateral circulation and associated potential compensation in downstream perfusion have been recognized long before arterial occlusions were known to cause ischemic stroke. Arterial aspects and the venous capacity of collaterals to offset potentially devastating effects of blocking a cerebral artery have been studied in various animal species and even human populations with stroke, providing a framework for translational research. The time has come for collaterals to move from the periphery to a central position in stroke therapeutics, propelled by the momentum of imaging data and culminating in novel paradigms with respect to time, imaging approaches and treatment strategies. It is time for a concerted focus on collateral perfusion to harness potential therapeutic advances from acute stroke to chronic cerebrovascular disorders.

Placental growth factor (PlGF) is a potent dilator of uterine and mesenteric veins isolated from pregnant rats

PlGF, a member of the VEGF family, is produced by the placenta; impairment of its signalling has been reported in preeclampsia. We tested the effect of PlGF on uterine and mesenteric veins to evaluate its vasoactive properties in reproductive vs. non‐reproductive tissues. Uterine (pre‐myometrial, pre‐placental) and third order mesenteric veins isolated from pregnant rats (n=12) were cannulated and pressurized (6 mmHg) in an arteriograph. All vessels were preconstricted 40–50% with U46619 prior to being exposed to PlGF (10pM–3nM). PlGF produced vasodilation in a concentration‐dependent manner in all veins. Similar maximal relaxations were observed in pre‐myometrial (32 ± 5%) and pre‐placental (36 ± 10%) veins, while greater efficacy (52 ± 10%, p&lt;0.05) was noted in mesenteric veins. The kinetics of the vasodilatory response were also different, with half times on the order of 20 vs. 10 minutes in uterine vs. mesenteric vessels. In mesenteric veins, inhibition of NOS + COX reduced vasodilation by 65% on average, to 18 ± 9% (p = 0.03). Thus, PlGF is a potent vasodilator of both reproductive and systemic veins, with significantly more potent and rapid effects in the mesenteric circulation, suggesting an important role for the tissue VEGFR‐1 (Flt‐1) receptor in regulating maternal gestational hemodynamic changes, e.g. venous capacitance and return, and cardiac output.This study was supported by NIH HL79253

Type 1 Diabetes in young women is associated with decreased circulatory response to hypovolemic stress

ObjectiveDiabetes is associated with hemodynamic instability, e.g. during anaesthesia. Young men with type 1 diabetes (DM‐1) have impaired circulatory response to hypovolemic stress. The effect of DM‐1 on cardiovascular response to hypovolemia in young women is unknown however.Design and MethodsLower body negative pressure (LBNP) of 30 cm H2O was used to create rapid hypovolemic stress in fifteen young women with DM‐1 as well as sixteen healthy women. Cardiovascular response and the compensatory mobilisation of venous capacitance blood (capacitance response) and net fluid absorption were measured with volumetric technique.ResultsCapacitance response was both reduced and developed slower in DM‐1, P &lt; 0.01. Fluid absorption was almost halved in women with DM‐1, P &lt; 0.01. Arterial vasoconstriction also developed slower in DM‐1, P &lt; 0.05.ConclusionsYoung women with DM‐1 present with decreased as well as slower mobilisation of venous capacitance blood and decreased net fluid absorption that could make women with type 1 diabetes prone to hemodynamic instability. Cardiovascular autonomic neuropathy could play a role, but also differences in the venous circulation and microcirculation.

Requirement for Functional BK Channels in Maintaining Oscillation in Venomotor Tone Revealed by Species Differences in Expression of the β1 Accessory Subunits

We determined the possible role of large-conductance Ca2+-activated K (BK) channels in regulation of venous tone in small capacitance veins and blood pressure. In rat mesenteric venous smooth muscle cells (MV SMC), BK channel α- and β1-subunits were coexpressed, unitary BK currents were detected, and single-channel currents were sensitive to voltage and [Ca2+]i. Rat MV SMCs displayed Ca sparks and iberiotoxin-sensitive spontaneous transient outward currents. Under resting conditions in vitro, rat MV exhibited nifedipine-sensitive spontaneous oscillatory constrictions. Blockade of BK channels by paxilline and Ca2+ sparks by ryanodine constricted rat MV. Nifedipine caused venodilation and blocked paxilline-induced, KCl-induced (20 mM), and BayK8644-induced contraction. Acute inhibition of BK channels with iberiotoxin in vivo increased blood pressure and reduced venous capacitance, measured as an increase in mean circulatory filling pressure in conscious rats. BK channel α-subunits and L-type Ca2+ channel α1-C subunits are expressed in murine MV. However, these channels are not functional because murine MV lack nifedipine-sensitive basal tone and rhythmic constrictions. Murine MV were also insensitive to paxilline, ryanodine, KCl, and BayK8644, consistent with our previous studies showing that murine MV do not have BK β1-subunits. These data show that not only there are species-dependent properties in ion channel control of venomotor tone but also BK channels are required for rhythmic oscillations in venous tone.

Sympathetically Mediated Changes in Capacitance

“To be accepted as a paradigm, a theory must seem better than its competitors, but it need not, and in fact never does, explain all the facts with which it can be confronted.” Thomas Kuhn, The Structure of Scientific Revolutions ### Heard on Rounds “A 57-year-old patient with a history of heart failure states that she began experiencing worsening shortness of breath 4 days prior to admission, with lower extremity edema developing 1 day prior to admission. She is compliant with her medications, though has had similar admissions previously. She states that her weight at home increased by “a couple of pounds” 2 days ago and that she increased her diuretic dose but her symptoms worsened. She says that she generally adheres to her low salt diet, but admits to eating pretzels 5 days ago. The physical examination showed BP 136/84, HR 94, weight 3 lbs above baseline, elevated JVP, basilar rales, and 1+ pedal edema.” As the intern finishes the presentation, the Senior expresses surprise that the patient's weight had increased only 3 pounds, and comments about salt and volume overload leading to acute decompensated heart failure (ADHF). The Attending adds that recent data reveal that many patients presenting with ADHF have minimal or no weight gain, but that there is no clear mechanism to explain this phenomenon. They set in place plans for diuresis, increasing vasodilators, and further patient education. On the surface, there is nothing remarkable about this case, and the usual approaches to treat this entity have remained remarkably consistent since the advent of loop diuretics over 50 years ago: salt restriction, patient education, uptitration of medications if not already at optimal doses, and diuresis. However, approximately 1 in 4 such patients are readmitted to the hospital within 30 days,1 and the disease continues to progress. It is clear …

Does Distal Venous Hypertension Affect Lower-Extremity Venous Pulsatility?

Introduction Pulsatile flow in the lower-extremity venous system is commonly attributed to various cardiac abnormalities. In patients with significant venous insufficiency and resultant venous hypertension, venous capacitance may be drastically reduced. We have noted multiple patterns of venous pulsatility and theorized that the hemodynamic state of the lower-extremity venous system could in fact play a role in these patterns. If venous reflux is isolated to the superficial system, ablation of these veins could resolve the venous hypertension and potentially influence the pulsatile flow pattern. Methods We compared the presence and pattern of lower extremity venous pulsatility in 293 consecutive patients suffering from chronic venous insufficiency (Mean CEAP 3.2). Of these, 242 limbs underwent endovenous thermal ablation (EVTA) of a refluxing truncal vein. Duplex ultrasound was used to evaluate these limbs approximately 3 days post procedure and the results of 101 limbs were available for comparison with the initial exam and provide the basis of this study. Results Of the 101 limbs, 47 (46.5%) had evidence of pulsatile flow in the lower extremity venous system preoperatively which was graded into one of three categories. Forty-eight (47.5%) had deep venous insufficiency of either the femoral vein (n = 16) or popliteal vein (n = 32), which was graded as normal, &gt;1 second, or &gt;2 seconds. The remaining had no evidence of deep vein reflux. Paired observations using the Wilcoxon method showed no difference in the venous pulsatility post ablation. Additionally, isolating patients with no evidence of deep venous reflux also revealed no difference in pulsatility following ablation. Conclusion Ablation of refluxing truncal veins did not appear to influence the presence or pattern of venous pulsatility in the lower extremities regardless of deep system valve function.