Mönckeberg's Disease of the Lower Limb.

Vascular calcification represents a group of several pathological states of differing aetiologies. Mönckeberg medial sclerosis is considered to be more widespread in the lower abdominal region and lower limbs. We present a 59-years-old male patient presented right foot gangrene. At physical exploration, femoral and popliteal pulses were presented and the ankle-brachial pressure index was 0.45, and the toe-brachial index was 0.33. The patient underwent distal angioplasty of anterior and posterior tibial arteries and due to inaccurate evolution a transmetatarsal amputation was required. Mönckeberg's medial sclerosis is diagnosed with an ABI>1.1, however, questions have been raised about the validity and the role of ABI in diagnosis of Mönckeberg's medial sclerosis. Colour-doppler vascular ultrasound allow a non-invasive technique widely available to detect vascular calcification and to differentiation between Mönckeberg's medial sclerosis and the atherosclerosis-related lesions.

Arteriosclerose, aterosclerose, arteriolosclerose e esclerose calcificante da média de Monckeberg: qual a diferença? / Arteriosclerosis, atherosclerosis, arteriolosclerosis, and Monckeberg medial calcific sclerosis: what is the difference?

Resumo A principal causa de óbito na contemporaneidade são as doenças cardiovasculares. Arteriosclerose, aterosclerose, arteriolosclerose e arteriosclerose de Monckeberg são termos frequentemente utilizados como sinônimos, mas traduzem alterações distintas. O objetivo desta revisão foi discutir os conceitos de arteriosclerose, aterosclerose, arteriolosclerose e esclerose calcificante da média de Monckeberg. O termo arteriosclerose é considerado mais genérico, significando o enrijecimento e a consequente perda de elasticidade da parede arterial, abarcando os demais tipos. A aterosclerose é uma doença inflamatória secundária a lesões na camada íntima, que tem como principal complicação obstrução crônica e aguda do lúmen arterial. A arteriolosclerose se refere ao espessamento das arteríolas, particularmente relacionada à hipertensão arterial sistêmica. Já a esclerose calcificante da média de Monckeberg designa a calcificação, não obstrutiva, da lâmina elástica interna ou da túnica média de artérias musculares. As calcificações vasculares, que incluem lesões ateroscleróticas e a esclerose calcificante da média de Monckeberg, vêm sendo estudadas como um fator de risco para a morbimortalidade cardiovascular.

Abstract Cardiovascular diseases are the main cause of death in contemporary times. Arteriosclerosis, atherosclerosis, arteriolosclerosis, and Monckeberg's arteriosclerosis are terms that are often used interchangeably, but they refer to different vascular pathologies. The objective of this study is to review the concepts of atherosclerosis, atherosclerosis, arteriosclerosis and Monckeberg medial calcific sclerosis (MMCS). The term arteriosclerosis is more generic, meaning the stiffening and consequent loss of elasticity of the arterial wall, and encompasses the other terms. Atherosclerosis is an inflammatory disease secondary to lesions in the intimal layer and whose main complication is acute and chronic obstruction of the arterial lumen. Arteriolosclerosis refers to thickening of arterioles, particularly in association with systemic arterial hypertension. MMCS refers to non-obstructive calcification in the internal elastic lamina or the tunica media of muscular arteries. Vascular calcifications, which include atherosclerotic lesions and MMCS, have been studied as a risk factor for cardiovascular morbidity and mortality.

The impact of pre-existing radial artery pathology by histological assessment on the maturation, function and patency of the radiocephalic fistula for hemodialysis.

BACKGROUND: We prospectively analyzed the effect of preexisting structural changes of the radial artery (RA) wall by histological examination on the wrist radiocephalic fistula (RCF) outcomes. METHODS: During RCF creation, one segment of the RA wall was collected and its histomorphometric analysis was performed. The RCF function was evaluated by measuring blood flow rate. RESULTS: At the end of follow-up, 75.7% of the thirty-seven patients enrolled were performing hemodialysis by using their successful RCF and 24.3% of them showed early RCF failure. Compared to patients with a healthy RA, the RCF of those with medial RA microcalcification reached up a lower flow and a shorter primary patency (P=0.005 and P=0.040, respectively). The RA microcalcification was predictive of the RCF function (coefficient -614.9, 95% CI: -994.7 to -235.1, P=0.003). Compared to patients with successful RCF, those with failed RCF had a greater frequency of weak RCF thrill after releasing the clamps (P=0.045). Dependence on hemodialysis during RCF placement was predictive of its early failure (OR: 23.2, 95% CI: 1.76 to 306.9, P=0.017). Both having at least one cardiovascular comorbidity (HR 4.30, 95% CI: 1.29 to 14.39, P=0.018) and a thicker media layer of the RA (HR 1.60, 95% CI: 1.87 to 2.15, P=0.002) were predictive of primary RCF patency. CONCLUSIONS: The function and survival of the successful RCF were related to preoperative RA abnormalities such as microcalcification and media layer thickness. Both dependence on hemodialysis during RCF placement and an attenuated RCF thrill were associated with early RCF failure.

Media sclerosis drives and localizes atherosclerosis in peripheral arteries.

Media sclerosis (MS) and peripheral artery disease (PAD) may coincide, particularly in type 2 diabetics (T2D) and in patients with chronic kidney disease (CKD). In contrast to non-diabetics, in T2D PAD is more severe and more distal. Although MS is suspected to play a role, the underlying pathophysiological reasons for the differences still remain elusive today. We tested the hypothesis that MS is a promoter of atherosclerosis as it occurs in T2D with PAD by interfering with arterial remodeling using an in-silico simulation. We confirmed that MS aggravates PAD by promoting negative remodeling. We found that the effect is more pronounced in smaller distal arteries compared to larger proximal ones. Our results suggest that the degree of this divergence depends on the ratio between the thickness of the intima relative to the thickness of the media/adventitia of the individually affected arteries.

Roles of High Mobility Group Box 1 in Cardiovascular Calcification.

Calcific disease of the cardiovascular system, including atherosclerotic calcification, medial calcification in diabetes and calcific aortic valve disease, is an important risk factor for many adverse cardiovascular events such as ischemic cardiac events and subsequent mortality. Although cardiovascular calcification has long been considered to be a passive degenerative occurrence, it is now recognized as an active and highly regulated process that involves osteochondrogenic differentiation, apoptosis and extracellular vesicle release. Nonetheless, despite numerous studies on the pathogenesis of cardiovascular calcification, the underlying mechanisms remain poorly understood. High mobility group box 1 (HMGB1), a nuclear protein bound to chromatin in almost all eukaryotic cells, acts as a damage-associated molecular pattern (DAMP) when released into the extracellular space upon cell activation, injury or death. Moreover, HMGB1 also functions as a bone-active cytokine participating in bone remodeling and ectopic calcification pathogenesis. However, studies on the roles of HMGB1 in promoting cardiovascular calcification are limited to date, and the mechanisms involved are still unclear. In this review, we summarize recent studies investigating the mechanism of cardiovascular calcification and discuss multiple roles of HMGB1 in its development.

[When the tissue tolerance fiber tears]. / Wenn der Gewebegeduldsfaden reisst .

We report a 65 year old patient who presented with both an aneurysm of the axillary artery and, some years later, with an acute aortic dissection type Stanford A. After surgical intervention of the dissection in the further workup, no specific etiology could be found. The most likely reason for the two aneurysms was the inadequately treated hypertension. Therefore, follow-up strategies aim to treat the risk factors which are known to promote aneurysm growth.

Correlation of pre-existing radial artery macrocalcifications with late patency of primary radiocephalic fistulas in diabetic hemodialysis patients.

OBJECTIVE: The aim of this study was to evaluate the impact of pre-existing radial artery macrocalcification (Mönckeberg type of arteriosclerosis) on patency rates of radiocephalic fistulas (RCFs) in diabetic end-stage renal disease (ESRD) patients undergoing hemodialysis. METHODS: In this observational prospective study, the long-term patency rates (primary outcome measures) of RCFs in ESRD diabetics who had Mönckeberg radial (±brachial) artery disease (calcified [C] group) were compared with those obtained in ESRD diabetics who had healthy, noncalcified vessels before RCF construction (healthy [H] group). Vessel calcification was assessed by plain two-dimensional radiography. For inclusion in the C-group, uniform linear railroad track-type macrocalcifications of at least 6 cm in length, in the medial wall of the radial artery ipsilateral to RCF creation, were required. Patients were included in the H-group if the radial artery ipsilateral to the RCF creation was free of any macrocalcification, of either intima or media type. Any intimal-like plaque with irregular and patchy distribution was an exclusion criterion for both groups. Patients in both groups also were required to have suitable upper limb vascular anatomy on the basis of ultrasound imaging before RCF creation (cephalic vein of minimum diameter of 1.6 mm, without stenosis or thrombosis in all outflow areas, and radial artery of minimum diameter of 1.5 mm, without proximal hemodynamically significant stenosis). Secondary outcome measures included all-cause mortality. Kaplan-Meier statistics were used for comparison between groups. RESULTS: The arm radiograph at the site of possible fistula construction showed abnormality in 39 patients (C-group, 47 RCFs), whereas 33 patients had noncalcified ("healthy") vascular anatomy (H-group, 40 RCFs). Mean duration of the diabetic disease at the time of RCF creation was 8.9 ± 5.6 years (range, 2-25 years) for the H-group and 14 ± 9.9 years (range, 1-40 years) for the C-group (P = .018). The mean follow-up period for H-group and C-group was 51.9 ± 35.9 months (range, 0.1-126 months) and 26.1 ± 31.6 months (range, 0.1-144 months), respectively (P = .0006). Forty-four patients died during the follow-up period. Primary patency rates at 12, 24, 36, and 48 months for C-group vs H-group were 50.2% vs 80%, 36.5% vs 72.3%, 32.4% vs 67.9%, and 29.1% vs 59.3% (P = .0019). Respective values for secondary patency rates were 52.4% vs 87.5%, 40.9% vs 82.4%, 36.6% vs 78.1%, and 33.2% vs 72.8% (P = .00064). Patient survival rates at 24 and 48 months were 56.1% and 46.4% for C-group and 92.4% and 67.4% for H-group, respectively (P = .05). CONCLUSIONS: ESRD diabetics with radial artery Mönckeberg calcifications receiving RCFs had worse late clinical outcomes compared with ESRD diabetics with healthy distal arm vessels receiving the same access. The long-term benefit of RCFs may be lost in diabetics with extensively calcified vessels, and preferably the brachial artery should be used instead.

Medial vascular calcification revisited: review and perspectives.

Vascular calcifications (VCs) are actively regulated biological processes associated with crystallization of hydroxyapatite in the extracellular matrix and in cells of the media (VCm) or intima (VCi) of the arterial wall. Both patterns of VC often coincide and occur in patients with type II diabetes, chronic kidney disease, and other less frequent disorders; VCs are also typical in senile degeneration. In this article, we review the current state of knowledge about the pathology, molecular biology, and nosology of VCm, expand on potential mechanisms responsible for poor prognosis, and expose some of the directions for future research in this area.

Impact of atherosclerotic risk factors on different ankle-brachial-index criteria--results of the Heinz Nixdorf RECALL study.

BACKGROUND: On the basis of the Heinz Nixdorf RECALL Study (HNR) we estimated the impact of classical atherosclerotic risk factors on different ankle-brachial-index (ABI) criteria. PATIENTS AND METHODS: In a subgroup of participants (n = 2586) who had normal ABI at baseline ABI measurement was repeated at a 5 years follow-up and 3 different ABIs were defined: "ABI-high" calculated from the higher pressure, "ABI-low" from the lower pressure of both foot arteries of each leg. "Pure-ABI-low" was defined by exclusion of participants with ABI-high from those with ABI-low. Mönckebergs mediacalcinosis (MC) was accepted in case of ABI-high > 1.4 in one leg. RESULTS: According to ABI-high 2 %, to ABI-low 7.8 % and pure-ABI-low 5.8 % of the participants developed peripheral arterial disease (PAD) (ABI < 0.9) and 3.6 % developed MC within the 5 years. Age did not play any role whereas female gender, diabetes mellitus and smoking were associated with an increased relative risk of pathologic ABI-high and ABI-low. Looking at the pure-ABI-low group only, female gender and smoking showed significant associations. None of the analysed risk factors except gender had an impact on the development of MC. CONCLUSIONS: Classical risk factors have different impact on incidence of PAD as defined by different ABI criteria.