tunica media of the MSV. This report is the first to describe an unique combination of ECS and thrombophlebitis associated with a leiomyosarcoma in a horse.]]>
Animals ; Biopsy ; Child ; Compartment Syndromes ; Diagnosis ; Emergencies ; Extremities ; Fascia ; Hindlimb ; Horses ; Humans ; Leiomyosarcoma ; Saphenous Vein ; Thrombophlebitis ; Tunica Media

BACKGROUND: Intima-to-intima microanastomotic vascular remodeling was explored, utilizing a polylactide-caprolactone absorbable vein coupler model (PAVCM), which was designed to simulate a non-absorbable counterpart system with the sole exception of being absorbable. METHODS: Six New Zealand white rabbits were used. After transection of the jugular vein, 2 PAVCMs were placed, 1 at each transected end. The stumps were slipped through the PAVCMs, and the venous wall was everted 90° to achieve intima-to-intima contact. Reanastomosis of the transected jugular vein was performed bilaterally in 3 rabbits. In the other 3 rabbits, the jugular vein (20 mm) harvested from one side was interpositionally grafted to the jugular vein on the opposite side to ease the anastomotic tension. Patency testing, ultrasonography, and histologic assessments were conducted postoperatively at weeks 2, 4, 12, 16, 22, and 26. RESULTS: All anastomotic sites were patent, without stenosis, occlusion, or dilatation. In the histologic sections, immature endothelial regeneration was observed at week 2, which was completed by week 4. Regeneration of the tunica media was noted at week 12. Between week 22 and week 26, the tunica media fully regenerated and the coupler dissipated entirely. CONCLUSIONS: Despite the absence of a coupler to act as an anastomotic buttress, the structure and function of all the vessels appeared normal, even histologically. These outcomes are true milestones in the development of an absorbable vein coupler.
Anastomosis, Surgical ; Constriction, Pathologic ; Dilatation ; Jugular Veins ; Microsurgery ; Rabbits ; Regeneration ; Transplants ; Tunica Media ; Ultrasonography ; Vascular Remodeling ; Vascular Surgical Procedures ; Veins

OBJECTIVEVascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima (atherosclerotic calcification) or tunica media (Mönckenberg's sclerosis). Vascular calcification is also closely related to other pathologies, such as diabetes mellitus, dyslipidemia, and chronic kidney disease. It has been concluded that the degree of vascular calcification may vary from person to person, even if the associated pathologies and environmental factors are the same. Therefore, this suggests an important genetic contribution to the development of vascular calcification. This review aimed to find the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.

DATA SOURCESWe conducted an exhaustive search in Scopus, EBSCO, and PubMed with the keywords "genetics and vascular calcification", "molecular pathways, genetic and vascular calcification" and included the main articles from January 1995 up to August 2016. We focused on the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.

STUDY SELECTIONThe most valuable published original and review articles related to our objective were selected.

RESULTSVascular calcification is a multifactorial disease; thus, its pathophysiology cannot be explained by a single specific factor, rather than by the result of the association of several genetic variants, molecular pathway interactions, and environmental factors that promote its development.

CONCLUSIONAlthough several molecular aspects of this mechanism have been elucidated, there is still a need for a better understanding of the factors that predispose to this disease.

Diabetes Mellitus ; metabolism ; physiopathology ; Dyslipidemias ; metabolism ; physiopathology ; Humans ; Kidney Failure, Chronic ; metabolism ; physiopathology ; Renal Insufficiency, Chronic ; metabolism ; physiopathology ; Tunica Intima ; metabolism ; physiopathology ; Tunica Media ; metabolism ; physiopathology ; Vascular Calcification ; metabolism ; physiopathology

Williams syndrome (WS) is a developmental disorder characterized by vascular abnormalities such as thickening of the vascular media layer in medium- and large-sized arteries. Supravalvular aortic stenosis (SVAS) and peripheral pulmonary artery stenosis (PPAS) are common vascular abnormalities in WS. The natural course of SVAS and PPAS is variable, and the timing of surgery or intervention is determined according to the progression of vascular stenosis. In our patient, SVAS and PPAS showed rapid concurrent progression within two weeks after birth. We report the early manifestation of SVAS and PPAS in the neonatal period and describe the surgical treatment for stenosis relief.
Aorta ; Aortic Stenosis, Supravalvular ; Arteries ; Constriction, Pathologic* ; Heart Defects, Congenital ; Humans ; Parturition ; Pulmonary Artery* ; Tunica Media ; Williams Syndrome*

Mönckeberg sclerosis is a disease of unknown etiology, characterized by dystrophic calcification within the arterial tunica media of the lower extremities leading to reduced arterial compliance. Medial calcinosis does not obstruct the lumina of the arteries, and therefore does not lead to symptoms or signs of limb or organ ischemia. Mönckeberg sclerosis most commonly occurs in aged and diabetic individuals and in patients on dialysis. Mönckeberg arteriosclerosis is frequently observed in the visceral arteries, and it can occur in the head and neck region as well. This report describes a remarkable case of Mönckeberg arteriosclerosis in the head and neck region as detected on dental imaging studies. To the best of our knowledge, this is the first case that has been reported in which this condition presented in the facial vasculature. The aim of this report was to define the radiographic characteristics of Mönckeberg arteriosclerosis in an effort to assist health care providers in diagnosing and managing this condition.
Arteries ; Arteriosclerosis* ; Calcinosis ; Compliance ; Dialysis ; Extremities ; Head* ; Health Personnel ; Humans ; Ischemia ; Lower Extremity ; Monckeberg Medial Calcific Sclerosis ; Neck* ; Tunica Media ; Vascular Calcification

Intimal accumulation of smooth muscle cells contributes to the development and progression of atherosclerotic lesions and restenosis following endovascular procedures. Arterial smooth muscle cells display heterogeneous phenotypes in both physiological and pathological conditions. In response to injury, dedifferentiated or synthetic smooth muscle cells proliferate and migrate from the tunica media into the intima. As a consequence, smooth muscle cells in vascular lesions show a prevalent dedifferentiated phenotype compared to the contractile appearance of normal media smooth muscle cells. The discovery of abundant stem antigen-expressing cells in vascular lesions also rarely detected in the tunica media of normal adult vessels stimulated a great scientific debate concerning the possibility that proliferating vascular wall-resident stem cells accumulate into the neointima and contribute to the progression of lesions. Although several experimental studies support this hypothesis, others researchers suggest a positive effect of stem cells on plaque stabilization. So, the real contribute of vascular wall-resident stem cells to pathological vascular remodelling needs further investigation. This review will examine the evidence and the contribution of vascular wall-resident stem cells to arterial pathobiology, in order to address future investigations as potential therapeutic target to prevent the progression of vascular diseases.
Adult ; Endovascular Procedures ; Humans ; Myocytes, Smooth Muscle ; Neointima ; Pathology* ; Phenotype ; Stem Cells* ; Tunica Media ; Vascular Diseases

Two major vascular pathologies underlie brain damage in patients with disease of small size penetrating brain arteries and arterioles; 1) thickening of the arterial media and 2) obstruction of the origins of penetrating arteries by parent artery intimal plaques. The media of these small vessels may be thickened by fibrinoid deposition and hypertrophy of smooth muscle and other connective tissue elements that accompanies degenerative changes in patients with hypertension and or diabetes or can contain foreign deposits as in amyloid angiopathy and genetically mediated conditions such as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. These pathological changes lead to 2 different pathophysiologies: 1) brain ischemia in regions supplied by the affected arteries. The resultant lesions are deep small infarcts, most often involving the basal ganglia, pons, thalami and cerebral white matter. And 2) leakage of fluid causing edema and later gliosis in white matter tracts. The changes in the media and adventitia effect metalloproteinases and other substances within the matrix of the vessels and lead to abnormal blood/brain barriers in these small vessels. and chronic gliosis and atrophy of cerebral white matter.
Adventitia ; Amyloid ; Arteries ; Arterioles ; Atrophy ; Basal Ganglia ; Brain ; Brain Ischemia ; CADASIL ; Cerebral Amyloid Angiopathy ; Cerebral Small Vessel Diseases ; Connective Tissue ; Edema ; Gliosis ; Humans ; Hypertension ; Hypertrophy ; Metalloproteases ; Muscle, Smooth ; Parents ; Pathology* ; Pons ; Stroke, Lacunar* ; Tunica Media

BACKGROUND: Angioleiomyoma, a vascular leiomyoma, is a rare, benign smooth-muscle tumor that originates in the tunica media of vessels. It occurs anywhere in the body, most frequently in the lower extremities. METHODS: We reviewed the medical records of 16 patients who were treated for angioleiomyoma between 2000 and 2012. The clinical features of angioleiomyoma and the correlation between symptoms and pathological subtypes were investigated. RESULTS: There were 9 males and 6 females. Ages of the patients ranged from 21 to 61. Pain was the primary symptom in 44% of the patients. Tumors were smaller than 2.0 cm in all dimensions and were located in the face in 4 patients, whereas 5 lesions occurred in the upper extremities and the remaining 7 in the lower extremities. Three histologic subtypes were identified: solid, venous, and cavernous. The subtypes did not correlate with the clinical symptoms. CONCLUSIONS: Angioleiomyoma appears to be a rare tumor that occurs in the face and the extremities. The tumor usually occurs in middle age. A differential diagnosis of this tumor is difficult, but the tumor should be considered in the diagnosis of painful subcutaneous masses. Ultrasonography and magnetic resonance imaging can be helpful in the diagnosis of angioleiomyoma. These tumors can be successfully treated with simple excision, with a low recurrence rate.
Angiomyoma* ; Diagnosis ; Diagnosis, Differential ; Extremities ; Female ; Humans ; Leiomyoma ; Leiomyomatosis ; Lower Extremity ; Magnetic Resonance Imaging ; Male ; Medical Records ; Middle Aged ; Recurrence ; Tunica Media ; Ultrasonography ; Upper Extremity

OBJECTIVETo analyze the impact of atorvastatin on blood lipids and arterial media thickness (IMT) in new-onset type 2 diabetes patients.

METHODS333 patients, 30-70 years old and diagnosed within one year as type 2 diabetes, were selected from the Chinese Diabetes Complication Prevention Study (CDCPS) to take part in this study. Changes of blood lipids and IMT of carotid, femoral and iliac artery pre and post the administration of atorvastatin were tested and followed for 24 months.

RESULTSTotal cholesterol, triglycerides and low-density lipoprotein decreased significantly (P = 0.000) and maintained at a low level. The carotid artery IMT decreased significantly (P = 0.022) at the end of this study, but the femoral and iliac artery IMT did not show any obvious change. There were no serious adverse events noticed, during the study period.

CONCLUSIONLong-term use of atorvastatin seemed to be safe and effective in reducing blood lipids in patients with type 2 diabetes thus could delay the development of atherosclerosis.

Adult ; Aged ; Atorvastatin Calcium ; Diabetes Mellitus, Type 2 ; drug therapy ; Female ; Follow-Up Studies ; Heptanoic Acids ; therapeutic use ; Humans ; Lipids ; blood ; Male ; Middle Aged ; Pyrroles ; therapeutic use ; Tunica Media ; pathology

Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p<0.05). Nicotine-treated group showed significant (p<0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group (ED50=1.44x10(5) M vs. 4.9x10(6) M) (p<0.05~0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group (ED50=6.17x10(7) M vs. 2.82x10(7) M) (p<0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p<0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.
Acetylcholine ; Animals ; Aorta ; Aorta, Thoracic ; Arterial Pressure ; Blood Circulation ; Blood Pressure ; Glutathione ; Humans ; Hypertension ; Lipid Peroxidation ; Male ; Malondialdehyde ; Nicotine ; Oxidation-Reduction ; Oxidative Stress ; Phenylephrine ; Rats* ; Rats, Sprague-Dawley ; Relaxation ; Superoxide Dismutase ; Tobacco Products ; Tunica Media