Carmine Sessa

Treatment of Primary Venous Insufficiency by Endovenous Saphenous Vein Obliteration

The objective of this paper is to evaluate treatment of primary venous insufficiency by endovenous saphenous vein obliteration. Three hundred one limbs were treated in 206 women and 67 men with a mean CEAP Clinical Class of 2.4 ±0.9. Endovenous obliteration was combined with high ligation in 67 limbs (22%) and with stab avulsion phlebectomies in 181 (60%). Acute occlusion was achieved in 290 limbs (96%). Obliteration failures in 11 limbs were treated by saphenous stripping or managed expectantly. Paresthesias followed 15% of treatments confined to the thigh and upper leg and affected 30% of limbs when treatment extended to the ankle (p < 0.001). Eight potentially preventable thermal skin injuries occurred, five in particularly superficial venous segments, of which four were in men. At a mean follow-up of 4.9 months, 21 (7.2%) of successfully treated veins have partially or totally (n = two) recanalized, but only 11 (3.8% of 290) have Doppler-detectable reflux. Ninety-one patients have been followed up for 6 months to 1 year, showing significant improvement in CEAP class and progressive relief from clinical symptoms. At their latest visit, 94% rated themselves as being symptom-free or substantially improved. These midterm results with endovenous obliteration in the treatment of primary varicose veins suggest that it may be as effective as surgical stripping in eliminating greater saphenous vein reflux and delaying the appearance of new varicose veins. Simple procedural modifications, such as not treating to the ankle, prophylactic infiltration about superficially placed veins, and early duplex surveillance should diminish the complications observed in this early experience.

European Society of Hypertension scientific newsletter: hypertension and aortic diseases.

Hypertension, one of the major cardiovascular risk factors, promotes the formation of atheromatous lesions in the large arteries, including the aorta. It also favors aortic aneurysm and acute aortic syndrome such as aortic dissection or hematoma. In patients with aortic disease, beta-blockers and/or renin–angiotensin–aldosterone system inhibitors should be preferentially used to decrease blood pressure and improve arterial wall properties.

Postoperative systemic artery to pulmonary vessel fistula: analysis of three cases.

BACKGROUNDnSystemic artery to pulmonary vessel fistulas (SAPVF) occur through pleural adhesions from miscellaneous origin. We report 3 cases of acquired SAPVF that developed late after thoracotomy.nnnMETHODSnThere was one pleurectomy for pneumothorax, one sleeve main bronchial resection, and one lower-middle bilobectomy. These SAPVF were discovered 4, 18, and 21 years after surgery.nnnRESULTSnOne patient underwent two unsuccessful embolizations. One patient underwent an unsuccessful attempt at surgical treatment after a previous embolization. Both have persistent SAPVF with minimal clinical discomfort 5 and 13 years later. One patient remains without treatment.nnnCONCLUSIONSnIn the literature 13 cases of SAPVF have been reported after lung resection, pleural drainage, axillary abcess drainage, closed chest trauma, parietal pleurectomy, and talc poudrage. Potential treatments of SAPVF include embolization, resection of pleural adhesion, and artery ligation. The effectiveness of these techniques is uncertain and the follow-up is too short to draw any clear conclusions. Embolization seems to be a useful tool in case of a single afferent artery. Surgical treatment seems to achieve more durable results than embolization but carries a higher risk of bleeding in the case of large SAPVF. Because SAPVF are well tolerated and complications are uncommon, clinical follow-up may be warranted in most cases.

Vasoconstrictor effects of iso-prostaglandin F2α type-III (8-iso-prostaglandin F2α) on human saphenous veins

: Free radical generation can initiate the peroxidation of arachidonic acid, resulting in a non-cyclooxygenase-dependent production of bioactive prostaglandin F2-like compounds. We have investigated the effects of iso-prostaglandin F2alpha type III, (iPF2alpha-III, formerly named 8-iso prostaglandin F2alpha) on human saphenous veins, and characterized the underlying mechanisms. In organ baths, the contractile effects of iPF2alpha-III were tested on saphenous vein rings coming from 22 patients. iPF2alpha-III induced concentration-dependent contractions of isolated human saphenous veins. The maximal contraction did not differ significantly from that of prostaglandin F2alpha (PGF2alpha). The pD2 values for iPF2alpha-III, PGF2alpha, endothelin-1 (ET-1), and U46619 (a stable thromboxane A2 mimetic) were 6.31+/-0.12, 5.66+/-0.13, 7.37+/-0.08, and 7.99+/-0.31, respectively (p < 0.001 for U46619 vs. iPF2alpha-III and PGF2alpha; and ET-1 vs. PGF2alpha). Emax values of iPF2alpha-III, PGF2alpha, ET-1, and U46619 were 137.7+/-24.3%, 145.9+/-7.5%, 92.9+/-16.8%, and 238.7+/-23.7%, respectively (p < 0.001 for U46619 vs. iPF2alpha-III, PGF2alpha and ET-1; and for PGF2alpha vs. ET-1). The responses to iPF2alpha-III were inhibited by GR 32191 10(-7) M, a TP-receptor antagonist, without affecting the maximal response (pD2 values were 5.98+/-0.06 in the absence, and 5.22+/-0.05 in the presence of GR32191; p < 0.001). Concentration-effect curves to iPF2alpha-III were not affected by phosphoramidon 10(-5) M (an endothelin converting enzyme inhibitor), BQ123 10(-6) M (a selective ET(A)-receptor antagonist), BQ788 10(-6) M (a selective ET(B)-receptor antagonist), and indomethacin 10(-5) M (a cyclooxygenase inhibitor). Finally, the contractile response of iPF2alpha-III did not involve the release of thromboxane B2 and ET-1, measured using enzyme immunoassays. This study demonstrates that iPF2alpha-III is a vasoconstrictor of human saphenous veins, with a potency fourfold greater than that of PGF2alpha, and 50 times less than that of the thromboxane A2 mimetic, U46619. These effects are mediated at least in part by TP-receptor stimulation, but do not involve thromboxane A2 or ET-1 release.

Antagonistic effects of losartan on thromboxane A2-receptors in human isolated gastroepiploic artery and saphenous vein

In addition to its AT1-receptor antagonist activity, losartan has been shown to antagonize thromboxane A2 (TXA2)-induced contraction of animal vessels. We investigated for the first time in human isolated gastroepiploic artery (GEA) and saphenous vein (SV) the TXA2/PGH2-receptor antagonist activity of losartan in the presence of indomethacin (1 microM) and N(omega)-nitro-L-arginine (100 microg). Losartan at concentrations of > or =1 microM on GEA and from 10 microM on SV significantly shifted U46619-induced contractions to the right. In addition, 100 microM losartan decreased by 34% the amplitude of the contraction to U46619 on both GEA and SV. The potency of losartan for the TXA2 receptor was 50- and 80-fold lower than that for the AT1 receptor on human GEA and SV, respectively. This inhibitory effect of losartan appeared selective for angiotensin II and TXA2-induced contractions because 100 microM losartan did not modify either endothelin-1- or KCl-induced contraction in human SV, although a reduction of norepinephrine- and 5-hydroxytryptamine-induced contraction was observed in human GEA and SV, respectively. In conclusion, losartan is an antagonist of TXA2 receptor on human GEA and SV. However, this antagonist activity occurred for a relative high dose of losartan, suggesting that it contributes at a low level, if any, to its antihypertensive effect.

Cyclosporine a and Cremophor EL induce contractions of human saphenous vein : Involvement of thromboxane A2 receptor-dependent pathway

Chronic treatment with Sandimmune (cyclosporine A [CsA] dissolved in Cremophor EL [CrEL]) is often associated with hypertension and nephrotoxicity. The aims of the present study were to assess the effect of Sandimmune and its two main components (CsA and CrEL) on human saphenous veins and to study the underlying mechanism of their contractile responses. In organ bath, concentration-response curves for Sandimmune (36 ng/ml-120 microg/ml of CsA). CsA (36 ng/ml-120 microg/ml), or CrEL (2.4 microg/ml-8 mg/ml) were elicited in the presence of a thromboxane A2 (TXA2) receptor antagonist (GR32191, 0.3 microM), a cyclooxygenase inhibitor (indomethacin, 1 microM), a 5-lipoxygenase inhibitor (AA861, 10 microM), or their respective vehicles. In addition, the production of TXA2 after CsA challenge was assessed by enzyme immunoassay. Sandimmune, CsA, and CrEL induced concentration-dependent contractions on human saphenous veins. In terms of potency, CsA was a more potent vasoconstrictor agent than CrEL (EC50 values: 11.9+/-3.7 microg/ml (CsA, n = 12) vs. 1.2+/-0.4 mg/ml (CrEL, n = 16), p < 0.05). In contrast, in terms of efficacy, CrEL induced greater contractions than CsA (Emax (% of KCl 90 mM-induced contraction): 98.1+/-16.1% (CrEL, n = 16) vs. 17.0+/-4.3% (CsA, n = 12) p < 0.05). Pretreatment with GR32191 significantly reduced by 85% and 56% the contractions elicited by CsA and CrEL, respectively, whereas indomethacin had no effect. Finally, CsA (12 and 120 microg/ml) failed to stimulate TXA2 production. These in vitro data suggest that Sandimmune-induced contractions on human vascular smooth muscle appear to be mediated by CsA in the therapeutic ranges of doses and by both CsA and CrEL, which, in supratherapeutic doses, acted through a TXA2 receptor-dependent pathway.

Carotid Artery Revascularisation Following Neck Irradiation: Immediate and Long-Term Results

OBJECTIVEnCarotid artery stenosis is a complication of neck irradiation. We describe the immediate and long-term results of surgical treatment.nnnMETHODSnThis was a retrospective single centre study. From 1996 to 2009, 24 consecutive patients who had in the past received neck radiation therapy (mean 12 years, 1-41 years) underwent 27 primary carotid artery revascularisation procedures. Six patients (23%) had previous radical neck dissection, three permanent tracheostomies and one cervicoplasty with pectoral muscle flap. Indications for surgery included symptomatic (five transient ischaemic attacks (TIAs), four strokes; 34%) and asymptomatic (18 patients, 66%) stenosis. Four patients had occlusion of the contralateral carotid. General anaesthesia without shunting was used with measurement of stump pressure. Carotid interposition bypass grafting included 23 vein grafts and three polytetrafluoroethylene (PTFE) grafts.nnnRESULTSnNo perioperative deaths or central neurological events occurred. Three patients suffered transient cranial nerve injuries. Eleven patients died during follow-up, mean interval of 28 months (range 6-120 months), of causes unrelated to surgery. Five patients had recurrent bypass stenosis with one TIA and one stroke. All other surviving patients remained asymptomatic.nnnCONCLUSIONnDespite no comparative study as evidence, we think that the perioperative risk of stroke is at least comparable with the risk encountered for angioplasty procedures.

Functional comparison of the antagonistic properties of some Angiotensin II type 1 receptor blockers on the contraction elicited by Angiotensin II and thromboxane A2 on human saphenous veins.

&NA; We previously described on human vascular preparations that, in addition to its antagonistic properties on Angiotensin II type 1 (AT1) receptor, losartan could also inhibit the contraction elicited by the stable thromboxane A2 mimetic U46619. The present study was designed (1) to investigate, in human vascular preparations (the saphenous veins) whether these antagonistic properties on thromboxane A2/prostaglandin H2 (TP) receptor were shared by some other AT1 receptor antagonists (irbesartan and valsartan) and the active metabolite of losartan EXP3174, and (2) to compare their antagonistic properties on TP receptors to their antagonistic properties on AT1 receptors. In the presence of indomethacin (10 &mgr;M) and N‐nitro‐L‐arginine (100 &mgr;M), irbesartan, valsartan, and EXP3174 induced a rightward shift of U46619‐ and angiotensin II‐induced contraction. The inhibitory effect of irbesartan, valsartan, and EXP3174 on U46619‐induced contraction was significant from 100 μM while their inhibitory effect on the contraction elicited by angiotensin II was significant from 1 nM. With regard to the plasma therapeutic concentrations of irbesartan, valsartan, and EXP3174, these data suggest that TP receptor blockade does not account for the antihypertensive effects of these AT1 receptor blockers.

Endovascular Treatment of Aortic and Primitive Iliac Artery Aneurysms Associated With Behçet Disease

Behçet disease is a systemic vasculitis that can cause vascular complications. We describe a 42-year-old woman with an aortic aneurysm and common right iliac aneurysm, both saccular and complicating Behçet disease. The patient was successfully treated by an endovascular method, which currently seems to be the best therapeutic choice given the frequent anastomotic complications of conventional surgical treatment.

Video-Assisted Removal of a Ventricular Mass through the Mitral Valve

Abstractu2002 We report the case of 31‐year‐old man who was admitted for cerebellar ischemia. The echocardiography showed an intraventricular mass, mobile with the cardiac activity compatible with a thrombus or a myxoma. He successfully underwent a video‐assisted removal of the mass, through the mitral valve