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The left internal mammary artery (LIMA) bypass grafts to the left anterior descending artery (LAD) are superior to saphenous venous grafts because of…

Background:Deep venous thrombosis (DVT), even though resolved, may damage the valves and may lead to chronic venous insufficiency (CVI). We designed the present study to examine the thrombotic markers or other ultrasound features in the absence of active thrombosis in patients presenting with features suggestive of CVI.Materials and Methods:It was a cross-sectional study of 50 DVT patients. We collected a detailed history of presenting symptoms (onset, progression, and duration) and associated history of aggravating factors. After classifying the patients, color Doppler investigation for DVT and venous incompetence and blood investigations such as Factor V, D-Dimer, total cholesterol, total triglycerides, homocysteine, high-density lipoproteins, low-density lipoproteins (LDL), and very LDL were done.Results:We found a raised Factor V significantly more in patients classified as severe under clinical classification compared with nonsevere (19% and 0%; P = 0.05) and in patients with a high Venous Severity Clinical Score (VSCS) compared to those with a low VSCS score (17% and 0%; P = 0.03). We also found that perforators were significantly more in patients with a high VSCS score (88% and 58%; P = 0.02), in patients with a primary venous etiology compared with those without any venous etiology (97% and 1%; P < 0.0001), in patients with obstruction/reflux compared to those without any pathology (95% and 0%; P < 0.0001), and in patients with severe clinical classification compared with nonsevere patient (95% and 55%; P = 0.002).Conclusions:Clinical or subclinical DVT, an important cause of CVI, may not always be seen on ultrasound, especially after resolution. However, they may have the presence of blood parameters (Factor V and hyperhomocysteinemia) suggestive of DVT; these can be used as proxy markers for the current or previous DVT.

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Endarterectomy of common femoral artery lesions (CFA) carries favorable longterm results and is currently still considered the gold standard for treating these lesions. Although routine stenting has been considered an option for treating the CFA, it has yielded conflicting results and is currently reserved for a bailout of suboptimal endovascular results. Newer therapies with atherectomy or lithoplasty in conjunction with pharmacologic antiproliferative therapies are promising with less bailout stenting and dissections but randomized trials are needed to confirm their effectiveness and safety.