Association of infrapopliteal medial arterial calcification with lower-limb amputations in high-risk patients: A systematic review and meta-analysis

Losurdo, Fabrizio; Ferraresi, Roberto; Ucci, Alessandro; Zanetti, Anna; Clerici, Giacomo; Zambon, Antonella

doi:10.1177/1358863x20979738

Cited by 20 publications

(13 citation statements)

References 47 publications

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“…The extension of medial calcification is associated with an increased mortality risk, irrespective of the revascularization method used [ 23 ]. A meta-analysis, including more than 6500 patients, showed that the presence of MAC on below-knee arteries is associated with a more than two-fold greater risk of lower limb amputation [ 24 ].…”

Section: Clinical Relevance Of Mac In Patients With Padmentioning

confidence: 99%

Inflammatory, Metabolic, and Coagulation Effects on Medial Arterial Calcification in Patients with Peripheral Arterial Disease

Nikolajević

Šabovič

2023

IJMS

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Calcium deposits in the vessel wall in the form of hydroxyapatite can accumulate in the intimal layer, as in atherosclerotic plaque, but also in the medial layer, as in medial arterial calcification (MAC) or medial Möenckeberg sclerosis. Once considered a passive, degenerative process, MAC has recently been shown to be an active process with a complex but tightly regulated pathophysiology. Atherosclerosis and MAC represent distinct clinical entities that correlate in different ways with conventional cardiovascular risk factors. As both entities coexist in the vast majority of patients, it is difficult to estimate the relative contribution of specific risk factors to their development. MAC is strongly associated with age, diabetes mellitus, and chronic kidney disease. Given the complexity of MAC pathophysiology, it is expected that a variety of different factors and signaling pathways may be involved in the development and progression of the disease. In this article, we focus on metabolic factors, primarily hyperphosphatemia and hyperglycemia, and a wide range of possible mechanisms by which they might contribute to the development and progression of MAC. In addition, we provide insight into possible mechanisms by which inflammatory and coagulation factors are involved in vascular calcification processes. A better understanding of the complexity of MAC and the mechanisms involved in its development is essential for the development of potential preventive and therapeutic strategies.

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Section: Clinical Relevance Of Mac In Patients With Padmentioning

confidence: 99%

Inflammatory, Metabolic, and Coagulation Effects on Medial Arterial Calcification in Patients with Peripheral Arterial Disease

Nikolajević

Šabovič

2023

IJMS

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“…Surprisingly, in patients with diabetes, medial arterial calcification is a stronger predictor of cardiovascular mortality compared with intimal calcification [31]. A recent meta-analysis showed that limb amputation is associated with below-the-knee medial arterial calcification [32].…”

Section: Aortic and Peripheral Arterial Disease (Pad)mentioning

confidence: 99%

Biomolecules Orchestrating Cardiovascular Calcification

2021

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Vascular calcification, once considered a degenerative, end-stage, and inevitable condition, is now recognized as a complex process regulated in a manner similar to skeletal bone at the molecular and cellular levels. Since the initial discovery of bone morphogenetic protein in calcified human atherosclerotic lesions, decades of research have now led to the recognition that the regulatory mechanisms and the biomolecules that control cardiovascular calcification overlap with those controlling skeletal mineralization. In this review, we focus on key biomolecules driving the ectopic calcification in the circulation and their regulation by metabolic, hormonal, and inflammatory stimuli. Although calcium deposits in the vessel wall introduce rupture stress at their edges facing applied tensile stress, they simultaneously reduce rupture stress at the orthogonal edges, leaving the net risk of plaque rupture and consequent cardiac events depending on local material strength. A clinically important consequence of the shared mechanisms between the vascular and bone tissues is that therapeutic agents designed to inhibit vascular calcification may adversely affect skeletal mineralization and vice versa. Thus, it is essential to consider both systems when developing therapeutic strategies.

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“… 14 They are also common in the leg arteries in patients with genetic syndromes, renal dysfunction, diabetes, and ageing. 15 Here they predict amputations. A plausible mechanism is that the ‘Windkessel function’ of our arterial system is disturbed by these calcifications and that the high pulse pressure leads to organ failure.…”

Section: Medial Arterial Calcification and Cardiovascular Diseasementioning

confidence: 99%