II. Advanced venous disease session
II. Advanced venous disease session
Role of elevated central venous pressures in chronic venous insufficiency
Raghu Kolluri (Columbus, OH, US)
Marked changes in intrathoracic pressure lead to decreased intrathoracic pressure, resulting in central hypovolemia (from pulmonary vasoconstriction) and an increase in peripheral fluid retention. Intermittent nocturnal right ventricular failure leads to venous pressure within the lower extremities and manifests as edema. Activation of the renin-angiotensin- aldosterone system leads to periodic left ventricular dysfunction during apnea and results in lower extremity edema. Apneic episodes increase systolic blood pressure during sleep, which leads to left ventricular diastolic dysfunction and peripheral edema. The relationship between obesity and edema was analyzed in 20 ambulatory patients with severe chronic venous insufficiency (CVI) and a mean body mass index of 52; 25 limbs had venous ulcers. An ultrasound analysis revealed no evidence of venous insufficiency in 75% of the patients. Elevated central venous pressure by echocardiogram in patients with CVI was evaluated. Every patient underwent a duplex ultrasound to assess reflux and a simultaneous and limited echocardiogram. Demographics revealed body mass index and other important causes that may result in edema and CVI, including obstructive sleep apnea (OSA) documented in the past medical history. Diabetes, older age, and right-sided CVI symptoms may be clues to trigger a work up and treatment of elevated central venous pressure in patients presenting with a diagnosis of CVI. In conclusion, patients with a diagnosis of CVI cannot ignore the 22.7% and 26% prevalence of elevated central venous pressure and OSA, respectively; when summed, 40% have either OSA or a moderate-to-severe risk for underlying OSA.
Chronic venous hypertension: what to do when there is no venous disease to treat Sergio Gianesini (Ferrara, Italy)
A study about hemodynamic changes in iliofemoral disease revealed higher, but variable pressure values in patients with postthrombotic syndrome compared with the control patients. Raju1 studied peripheral venous pressure before and after iliac vein stenting and noted that 12 mm Hg iliac pressure gradients were pathological and showed that, before stenting, the pressure did not correlate with the stenosis area, while, after stenting, 55% of patient’s pressure improved or normalized. In general, foot venous pressure measurements showed a good correlation with clinical severity and degree of venous reflux. Although dorsal foot venous pressure may be normal, deep venous pressure may decrease or even increase. Ron Eifel2 showed that mean walking pressure and walking pressure fall were more reliably associated with anatomic distribution of reflux and the clinic severity of chronic venous insufficiency than the gold-standard ambulatory venous pressure and 90% recover time. Sergio Gianesini’s group showed an elevation in the circulating cytokine-chemokine profile in chronic venous disease, while they are downregulated after intervention and elevated again during recurrence. Bergan,3 in his study for venous active drugs, showed that there is no solid evidence for drugs to protect venous hypertension from becoming venous disease. Horner4 pointed out the value of graduated compression stockings for deep venous insufficiency as ambulatory venouspressure was reduced by 20% to 30%. Again, Sergio Gianesini’s group showed the beneficial effects of aquatic exercise on reducing chronic lower limb edema.
References:
1. Raju S, Knight A, Buck W, May C, Jayaraj A. Caliber-targeted reinterventional overdilation of iliac vein Wallstents. J Vasc Surg Venous Lymphat Disord. 2019;7(2):184-194.
2. Eifell RK, Ashour HY, Lees TA. Comparison of new continuous measurements of ambulatory venous pressure (AVP) with conventional tiptoe exercise ambulatory AVP in relation to the CEAP clinical classification of chronic venous disease. J Vasc Surg. 2006;44(4):794-802.
3. Bergan JJ, Pascarella L, Schmid-Schönbein GW. Pathogenesis of primary chronic venous disease: Insights from animal models of venous hypertension. J Vasc Surg. 2008;47(1):183-92.
4. Horner J, Fernandes J, Fernandes E, Nicolaides AN. Value of graduated compression stockings in deep venous insufficiency. Br Med J. 1980;280(6217):820-821
