- Email: [email protected]
The Valvular Apparatus in Venous Insufficiency: A Problem of Quantity?
The Valvular Apparatus in Venous Insufficiency: A Problem of Quantity? Clifford M. Sales, MD, David Rosenthal, MD, Kathleen A. Petrillo, RVT, Hilde S. Jerivs, MD, John Matsuura, MD, Michael D. Clark, MD, Michael A. Pontoriero, MD, Donald C. Syracuse, MD, and Norman L. Luka, MD, Livingston, New Jersey, and Atlanta, Georgia
Abnormal venous valvular function may produce venous reflux and venous insufficiency. While valvular agenesis is a known, but rare cause of venous insufficiency. While valvular agenesis is a known, but rare cause of venous insufficiency, little work has been done on the relative number of greater saphenous vein (GSV) valves in patients with venous insufficiency. This study investigates whether the GSV in patients with symptomatic venous insufficiency has fewer valves than the GSV of patients without venous insufficiency. The number of GSV valves in patients (n = 51) with symptomatic venous insufficiency undergoing saphenectomy (VI) were compared with the number of GSV valves in patients (n = 26) without venous insufficiency undergoing in situ GSV bypass under angioscopic surveillance who served as a control group. The two groups differed, as expected, in age and sex distribution. The VI group had a mean of 25.7 ± 11.0 centimeters of GSV between valves, while the control group had 19.0 ± 9.7 centimeters of GSV between valves (F = 6.99; p = 0.01). The mean number of valves in the saphenous veins of the two groups also differed significantly: VI = 2.3 ± 0.83 versus control (CTRL) = 4.8 ± 2.01 (F = 61.86; p < 0.0001). That properly functioning valve leaflets help maintain physiologic antegrade venous flow is indisputable. This study, however, suggests that the relative lack of valves may be related to the development of venous insufficiency. This report documents that patients with symptomatic reflux in the GSV have significantly fewer valves than patients with apparently normal functioning saphenous veins. (Ann Vasc Surg 1998;12:153-155.)
INTRODUCTION Technological advances in the past decade have provided new information regarding the pathophysiology of venous insufficiency.1-3 Duplex ultra-
From the Saint Barnabas Health Care System, Livingston, NJ (C.M.S., K.A.P., M.A.P., M.A.P., D.C.S., N.L.L.) and the Georgia Baptist Medical Center, Atlanta, GA (D.R., H.S.J., J.M., M.D.C.). Presented at the Twenty-second Annual Meeting of the Peripheral Vascular Surgery Society, Boston, MA, May 31, 1997. Correspondence to: C. M. Sales, MD, Saint Barnabas Health Care System, 5 Franklin Avenue, Suite 302, Belleville, NJ 07109, USA.
sonography has allowed the clinician to localize the site of venous valvular incompetence and plethysmographic techniques have better elucidated the function of the calf muscle pump.4,5 Both valvular dysfunction and ineffective propulsion of blood from the calf have been cited as the primary causes of chronic venous insufficiency, while postphlebitic valvular destruction has also been indicted as a cause. Although these causes of venous disease have been well documented, a more simplistic explanation has received little attention—the total valve number. While valvular agenesis is a recognized cause of venous insufficiency, there has been little reported in the medical literature relating chronic venous insufficiency to the number of valves within 153
154
Sales et al.
Annals of Vascular Surgery
Table I. Differences in greater saphenous veins Mean
Control
Venous insufficiency
p
GSV length (cm) Number valves identified Distance between valves (cm)
75.0 ± 6.8 4.8 ± 2.0 19.0 ± 9.66
52.3 ± 14.3 2.3 ± .8 25.7 ± 11.1
<0.0001 <0.0001 0.01
the saphenous vein. This report examines the relationship of total valve number as a function of saphenous vein competency.
nique.7 The average length of saphenous vein studied, the number of valves identified, and the average distance between valves are indicated in Table I.
METHODS This prospective study contrasts the number of valves in the greater saphenous veins (GSV) of patients with documented valvular incompetence in comparison to the number of valves identified in a ‘‘control’’ group whose GSV was utilized as a conduit for lower extremity revascularization. The study group consisted of 51 consecutive patients who underwent greater saphenectomy in 1996 (January–December) for symptomatic venous insufficiency. The length of saphenous vein removed was calculated based on the two skin incisions and the location of the valvular apparatus was carefully identified. No attempt was made to determine the function of the identified valves on gross examination. The control group consisted of 21 consecutive patients with normal GSV who underwent in situ bypass under angioscopic surveillance. 6 Valves were clearly identified angioscopically and valvulotomy carried out under direct visualization. The length of saphenous vein harvested and the number of valves lysed were recorded. Data was collected and analyzed with the assistance of an IBM-compatible computer with a Pentium processor. Statistical analysis was performed with the use of Graph Pad In Stat. Analysis of variance was used to calculate F- and p values.
RESULTS The control group (CTRL) consisted of 26 patients undergoing lower extremity revascularization under angioscopic surveillance. This group consisted of 17 men (65%) and the average age of the group was 71.5 years. The study group (VI) was composed of 51 consecutive patients (65% women; average age 43.5 years) who were examined and who underwent saphenectomy for symptomatic venous insufficiency by the inversion saphenectomy tech-
DISCUSSION Physiologic venous flow necessitates properly functioning valve leaflets. The ability of the lower extremity venous system to return blood cephalad to the heart is dependent on the calf muscle pump and unidirectional flow maintained by the venous valvular apparatus. Valve destruction and the inability of valve leaflets to coapt properly are the principal documented causes of venous insufficiency; while valvular agenesis, a rare anomaly, may cause venous insufficiency as well. The marked difference, demonstrated in this report, in the number of GSV valves between legs with ‘‘normal’’ venous systems and those with documented venous incompetence is significant. The concept that venous insufficiency may be related to a decrease in the number of GSV valves was first reported by Cotton8 in 1961, but has since received little attention. A pending report by Ortega et al.,9 however, describes an increase in the number of normal valves in cadaveric normal GSV as compared to GSV valves found in patients with documented venous incompetence. Although the demographics of the two groups reported herein differ, it is unlikely that this contributed to the noted differences. The total number of valves within the GSV does not change with time—only the number of functioning valves may diminish. Therefore, the greater number of valves identified in the older control group is not a function of age. It is conceivable, however, that sex differences account for part of the discrepancy between the two groups. The control group, consisting of 65% male, and the VI group, with 65% female, may have differed on the basis of sex differences alone. Previous reports failed to document any differences in the number of valves between the genders.10 The use of angioscopy to identify valve leaflets in
Vol. 12, No. 2, 1998
the control group would likely underestimate the total valve number since incompetent valves would not be lysed and, therefore, not be counted. Conversely, visual inspection of the inverted GSV in the venous insufficiency group would lead to a falsely elevated calculation of the valve number as it is possible that intimal defects could be mistaken for a valve cusp. These errors would skew the two groups incorrectly towards one another—not away as the findings are reported. It is important to realize that, while the lengths of veins compared differ significantly between the two groups, it is not this difference that accounts for the difference in valve distribution. The average length between valves in the VI group is significantly greater than that in the control group. The possibility remains, however unlikely, that the distal segment of saphenous vein left unremoved in the saphenectomy (VI) group, may harbor an unusually high number of valves. This is not the clinical impression of the authors although hard data to dispute this possibility is absent. The findings presented in this report correlate the presence of venous insufficiency with a relative decrease in the number of GSV valves. One hypothesis regarding this difference may be that those limbs with fewer valves are at a greater risk to develop chronic venous insufficiency. This may be attributed to the relatively greater importance that each valve has in a ‘‘normal’’ lower extremity venous system. A normal GSV (6-8 valves) may be able to function without symptoms of venous insufficiency if one valve is nonfunctional as the competency of the remaining valves are able to prevent venous reflux from occurring over a lengthy distance. However, in a GSV with fewer valves (2-3), incompetence of a single valve may result in a long segment of vein being subject to reflux ‘‘conditions’’ which may lead to incompetence of contiguous valves that produces the symptoms of venous insufficiency. Alternatively, it is possible that patients with venous insufficiency and a decreased number of valves may simply represent an ‘‘incomplete expression’’ of valvular agenesis. Thus, the few valves that are present are incompletely developed and, therefore, incompetent. This report cannot offer data to support either of these hypotheses; how-
Valvular apparatus in venous insufficiency 155
ever, a longitudinal study of patients with a strong genetic predisposition towards venous insufficiency may provide further insight. While absolute valve number may not be the direct cause of venous insufficiency, it may signify its inevitable development in some patients. Since the valvular apparatus can be accurately identified utilizing duplex ultrasonography, perhaps quantitating the number of valves in patients at risk for developing venous insufficiency (i.e., those with a family history) may have a predictive value.
CONCLUSIONS This report demonstrates that the total number of valves in patients with symptomatic GSV insufficiency is significantly less than the total number of valves in patients with normal GSV. The importance of this, and its direct relation to the development of venous insufficiency, remains to be fully elucidated, but warrants further investigation. REFERENCES 1. Welch HJ, Faliakou EC, McLaughlin RL, et al. Comparison of descending phlebography with quantitative photoplethysmography, air plethysmography, and duplex quantitative valve closure time in assessing deep venous reflux. J Vasc Surg 1992;16:913-920. 2. van Bemmelen P, Bedford G, Beach K, Strandness D. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg 1989;10:425-431. 3. Labropoulos N, Leon M, Nicolaides AN, et al. Superficial venous insufficiency: Correlation of anatomic extent of reflux with clinical signs and symptoms. J Vasc Surg 1994;20: 953-958. 4. Vasdekis SN, Clarke GH, Nicolaides AN. Quantification of venous reflux by means of duplex scanning. J Vasc Surg 1989;10:670-677. 5. Christopoulos D, Nicolaides AN, Cook A, et al. Pathogenesis of venous ulceration in relation to calf muscle pump function. Surgery 1989;106:829-835. 6. Rosenthal D, Herring MB, O’Donovan TG, et al. Endovascular infrainguinal in situ saphenous vein bypass: A multicenter preliminary report. J Vasc Surg 1992;16:453-458. 7. van der Stricht J. Saphenectomy par invagination sur fil. Presse Med 1963;71:1081-1082. 8. Cotton LT. Varicose veins: Gross anatomy and development. Br J Surg 1961;48:589-598. 9. Ortega F, Mompeo B, Sarmiento L, et al. Comparison of saphenous veins removed for primary venous insufficiency with cadaver saphenous veins. Vasc Surg 1997. In Press. 10. Kosinski C. Observation on the superficial venous system of the lower extremity. J Anat 1926;60:131.
Abnormal venous valvular function may produce venous reflux and venous insufficiency. While valvular agenesis is a known, but rare cause of venous insufficiency. While valvular agenesis is a known, but rare cause of venous insufficiency, little work has been done on the relative number of greater saphenous vein (GSV) valves in patients with venous insufficiency. This study investigates whether the GSV in patients with symptomatic venous insufficiency has fewer valves than the GSV of patients without venous insufficiency. The number of GSV valves in patients (n = 51) with symptomatic venous insufficiency undergoing saphenectomy (VI) were compared with the number of GSV valves in patients (n = 26) without venous insufficiency undergoing in situ GSV bypass under angioscopic surveillance who served as a control group. The two groups differed, as expected, in age and sex distribution. The VI group had a mean of 25.7 ± 11.0 centimeters of GSV between valves, while the control group had 19.0 ± 9.7 centimeters of GSV between valves (F = 6.99; p = 0.01). The mean number of valves in the saphenous veins of the two groups also differed significantly: VI = 2.3 ± 0.83 versus control (CTRL) = 4.8 ± 2.01 (F = 61.86; p < 0.0001). That properly functioning valve leaflets help maintain physiologic antegrade venous flow is indisputable. This study, however, suggests that the relative lack of valves may be related to the development of venous insufficiency. This report documents that patients with symptomatic reflux in the GSV have significantly fewer valves than patients with apparently normal functioning saphenous veins. (Ann Vasc Surg 1998;12:153-155.)
INTRODUCTION Technological advances in the past decade have provided new information regarding the pathophysiology of venous insufficiency.1-3 Duplex ultra-
From the Saint Barnabas Health Care System, Livingston, NJ (C.M.S., K.A.P., M.A.P., M.A.P., D.C.S., N.L.L.) and the Georgia Baptist Medical Center, Atlanta, GA (D.R., H.S.J., J.M., M.D.C.). Presented at the Twenty-second Annual Meeting of the Peripheral Vascular Surgery Society, Boston, MA, May 31, 1997. Correspondence to: C. M. Sales, MD, Saint Barnabas Health Care System, 5 Franklin Avenue, Suite 302, Belleville, NJ 07109, USA.
sonography has allowed the clinician to localize the site of venous valvular incompetence and plethysmographic techniques have better elucidated the function of the calf muscle pump.4,5 Both valvular dysfunction and ineffective propulsion of blood from the calf have been cited as the primary causes of chronic venous insufficiency, while postphlebitic valvular destruction has also been indicted as a cause. Although these causes of venous disease have been well documented, a more simplistic explanation has received little attention—the total valve number. While valvular agenesis is a recognized cause of venous insufficiency, there has been little reported in the medical literature relating chronic venous insufficiency to the number of valves within 153
154
Sales et al.
Annals of Vascular Surgery
Table I. Differences in greater saphenous veins Mean
Control
Venous insufficiency
p
GSV length (cm) Number valves identified Distance between valves (cm)
75.0 ± 6.8 4.8 ± 2.0 19.0 ± 9.66
52.3 ± 14.3 2.3 ± .8 25.7 ± 11.1
<0.0001 <0.0001 0.01
the saphenous vein. This report examines the relationship of total valve number as a function of saphenous vein competency.
nique.7 The average length of saphenous vein studied, the number of valves identified, and the average distance between valves are indicated in Table I.
METHODS This prospective study contrasts the number of valves in the greater saphenous veins (GSV) of patients with documented valvular incompetence in comparison to the number of valves identified in a ‘‘control’’ group whose GSV was utilized as a conduit for lower extremity revascularization. The study group consisted of 51 consecutive patients who underwent greater saphenectomy in 1996 (January–December) for symptomatic venous insufficiency. The length of saphenous vein removed was calculated based on the two skin incisions and the location of the valvular apparatus was carefully identified. No attempt was made to determine the function of the identified valves on gross examination. The control group consisted of 21 consecutive patients with normal GSV who underwent in situ bypass under angioscopic surveillance. 6 Valves were clearly identified angioscopically and valvulotomy carried out under direct visualization. The length of saphenous vein harvested and the number of valves lysed were recorded. Data was collected and analyzed with the assistance of an IBM-compatible computer with a Pentium processor. Statistical analysis was performed with the use of Graph Pad In Stat. Analysis of variance was used to calculate F- and p values.
RESULTS The control group (CTRL) consisted of 26 patients undergoing lower extremity revascularization under angioscopic surveillance. This group consisted of 17 men (65%) and the average age of the group was 71.5 years. The study group (VI) was composed of 51 consecutive patients (65% women; average age 43.5 years) who were examined and who underwent saphenectomy for symptomatic venous insufficiency by the inversion saphenectomy tech-
DISCUSSION Physiologic venous flow necessitates properly functioning valve leaflets. The ability of the lower extremity venous system to return blood cephalad to the heart is dependent on the calf muscle pump and unidirectional flow maintained by the venous valvular apparatus. Valve destruction and the inability of valve leaflets to coapt properly are the principal documented causes of venous insufficiency; while valvular agenesis, a rare anomaly, may cause venous insufficiency as well. The marked difference, demonstrated in this report, in the number of GSV valves between legs with ‘‘normal’’ venous systems and those with documented venous incompetence is significant. The concept that venous insufficiency may be related to a decrease in the number of GSV valves was first reported by Cotton8 in 1961, but has since received little attention. A pending report by Ortega et al.,9 however, describes an increase in the number of normal valves in cadaveric normal GSV as compared to GSV valves found in patients with documented venous incompetence. Although the demographics of the two groups reported herein differ, it is unlikely that this contributed to the noted differences. The total number of valves within the GSV does not change with time—only the number of functioning valves may diminish. Therefore, the greater number of valves identified in the older control group is not a function of age. It is conceivable, however, that sex differences account for part of the discrepancy between the two groups. The control group, consisting of 65% male, and the VI group, with 65% female, may have differed on the basis of sex differences alone. Previous reports failed to document any differences in the number of valves between the genders.10 The use of angioscopy to identify valve leaflets in
Vol. 12, No. 2, 1998
the control group would likely underestimate the total valve number since incompetent valves would not be lysed and, therefore, not be counted. Conversely, visual inspection of the inverted GSV in the venous insufficiency group would lead to a falsely elevated calculation of the valve number as it is possible that intimal defects could be mistaken for a valve cusp. These errors would skew the two groups incorrectly towards one another—not away as the findings are reported. It is important to realize that, while the lengths of veins compared differ significantly between the two groups, it is not this difference that accounts for the difference in valve distribution. The average length between valves in the VI group is significantly greater than that in the control group. The possibility remains, however unlikely, that the distal segment of saphenous vein left unremoved in the saphenectomy (VI) group, may harbor an unusually high number of valves. This is not the clinical impression of the authors although hard data to dispute this possibility is absent. The findings presented in this report correlate the presence of venous insufficiency with a relative decrease in the number of GSV valves. One hypothesis regarding this difference may be that those limbs with fewer valves are at a greater risk to develop chronic venous insufficiency. This may be attributed to the relatively greater importance that each valve has in a ‘‘normal’’ lower extremity venous system. A normal GSV (6-8 valves) may be able to function without symptoms of venous insufficiency if one valve is nonfunctional as the competency of the remaining valves are able to prevent venous reflux from occurring over a lengthy distance. However, in a GSV with fewer valves (2-3), incompetence of a single valve may result in a long segment of vein being subject to reflux ‘‘conditions’’ which may lead to incompetence of contiguous valves that produces the symptoms of venous insufficiency. Alternatively, it is possible that patients with venous insufficiency and a decreased number of valves may simply represent an ‘‘incomplete expression’’ of valvular agenesis. Thus, the few valves that are present are incompletely developed and, therefore, incompetent. This report cannot offer data to support either of these hypotheses; how-
Valvular apparatus in venous insufficiency 155
ever, a longitudinal study of patients with a strong genetic predisposition towards venous insufficiency may provide further insight. While absolute valve number may not be the direct cause of venous insufficiency, it may signify its inevitable development in some patients. Since the valvular apparatus can be accurately identified utilizing duplex ultrasonography, perhaps quantitating the number of valves in patients at risk for developing venous insufficiency (i.e., those with a family history) may have a predictive value.
CONCLUSIONS This report demonstrates that the total number of valves in patients with symptomatic GSV insufficiency is significantly less than the total number of valves in patients with normal GSV. The importance of this, and its direct relation to the development of venous insufficiency, remains to be fully elucidated, but warrants further investigation. REFERENCES 1. Welch HJ, Faliakou EC, McLaughlin RL, et al. Comparison of descending phlebography with quantitative photoplethysmography, air plethysmography, and duplex quantitative valve closure time in assessing deep venous reflux. J Vasc Surg 1992;16:913-920. 2. van Bemmelen P, Bedford G, Beach K, Strandness D. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg 1989;10:425-431. 3. Labropoulos N, Leon M, Nicolaides AN, et al. Superficial venous insufficiency: Correlation of anatomic extent of reflux with clinical signs and symptoms. J Vasc Surg 1994;20: 953-958. 4. Vasdekis SN, Clarke GH, Nicolaides AN. Quantification of venous reflux by means of duplex scanning. J Vasc Surg 1989;10:670-677. 5. Christopoulos D, Nicolaides AN, Cook A, et al. Pathogenesis of venous ulceration in relation to calf muscle pump function. Surgery 1989;106:829-835. 6. Rosenthal D, Herring MB, O’Donovan TG, et al. Endovascular infrainguinal in situ saphenous vein bypass: A multicenter preliminary report. J Vasc Surg 1992;16:453-458. 7. van der Stricht J. Saphenectomy par invagination sur fil. Presse Med 1963;71:1081-1082. 8. Cotton LT. Varicose veins: Gross anatomy and development. Br J Surg 1961;48:589-598. 9. Ortega F, Mompeo B, Sarmiento L, et al. Comparison of saphenous veins removed for primary venous insufficiency with cadaver saphenous veins. Vasc Surg 1997. In Press. 10. Kosinski C. Observation on the superficial venous system of the lower extremity. J Anat 1926;60:131.