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.

A Review of the Role of Breast Arterial Calcification for Cardiovascular Risk Stratification in Women.

Cardiovascular disease continues to be the leading cause of death among women in the United States. One of the barriers to improving cardiovascular disease outcomes in women is the lack of reliable, effective screening modalities. Breast arterial calcification has emerged as a potential risk stratification tool. Localized deposition in the media of the artery, known as Mönckeberg medial calcific sclerosis, is notably different from the intimal atherosclerotic process commonly associated with coronary artery disease. Nonetheless, studies favor a correlation between breast arterial calcification and cardiovascular risk factors or coronary artery disease, defined as coronary artery calcification on computed tomography scan or both nonobstructive and obstructive lesions on angiography. Since a majority of women over the age of 40 undergo yearly breast cancer screening with mammography, measurement of breast arterial calcification may offer a personalized, noninvasive approach to risk-stratify women for cardiovascular disease at no additional cost or radiation. Mammography has the potential to alter the course of the leading cause of death in women, heart disease, through the evaluation of breast arterial calcification and identification of opportunities for prevention. Current evidence supports the universal reporting of breast arterial calcifications and personalized patient-provider discussions to more aggressively treat cardiac risk factors through targeted medical therapies or healthy lifestyle changes.

Arteriosclerosis: facts and fancy.

Arterial vascular diseases comprise the leading cause of death in the industrialized world. Every physician learns about the pathology of these diseases in medical school. All pathologists evaluate arterial disease in surgical pathology and/or autopsy specimens. All clinicians encounter patients with clinical manifestations of these diseases. With such a common and clinically-important group of entities one would think there would be a general understanding of the "known" information that exists. That is, physicians and scientists should be able to separate what is fact and what is fancy. This review article is intended to generate thought in this regard.

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.

Peripheral arterial calcification: prevalence, mechanism, detection, and clinical implications.

Vascular calcification (VC), particularly medial (Mönckeberg's medial sclerosis) arterial calcification, is common in patients with diabetes mellitus and chronic kidney disease and is associated with increased cardiovascular morbidity and mortality. Although, the underlying pathophysiological mechanisms and genetic pathways of VC are not fully known, hypocalcemia, hyperphosphatemia, and the suppression of parathyroid hormone activity are central to the development of vessel mineralization and, consequently, bone demineralization. In addition to preventive measures, such as the modification of atherosclerotic cardiovascular risk factors, current treatment strategies include the use of calcium-free phosphate binders, vitamin D analogs, and calcium mimetics that have shown promising results, albeit in small patient cohorts. The impact of intimal and medial VC on the safety and effectiveness of endovascular devices to treat symptomatic peripheral arterial disease (PAD) remains poorly defined. The absence of a generally accepted, validated vascular calcium grading scale hampers clinical progress in assessing the safety and utility of various endovascular devices (e.g., atherectomy) in treating calcified vessels. Accordingly, we propose the peripheral arterial calcium scoring system (PACSS) and a method for its clinical validation. A better understanding of the pathogenesis of vascular calcification and the development of optimal medical and endovascular treatment strategies are crucial as the population ages and presents with more chronic comorbidities.

Clinical decision-making for vitamin K-1 and K-2 deficiency and coronary artery calcification with warfarin therapy: are diet, factor Xa inhibitors or both the answer?

Coronary artery calcification is a recognised risk factor for ischaemic heart disease and mortality. Evidence is now strong that Mönckeberg's arteriosclerosis, a form of vascular calcification, can be attributable to vitamin K deficiency, but that vitamin K-2, especially the MK-4 form from foods like cheese can be protective. Warfarin blocks the recycling of hepatic and peripheral vitamin K leading to secondary vitamin K deficiency with adverse effects on vasculature, bone, kidneys, brain and other tissues and systems (inflammatory, immune function and neoplasia at least). There is individual susceptibility to vitamin K deficiency and warfarin sensitivity, partly explicable in terms of genetic polymorphisms, epigenetics, diet and pharmacotherapy. The emergence of extensive coronary calcification in a man with atrial fibrillation treated for a decade with warfarin is described by way of illustration and to raise the present clinical management conundrums. Finally, a putative set of recommendations is provided.