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Rotational atherectomy: re-emergence of an old technique
  1. Adam J de Belder
  1. Correspondence to Dr Adam J de Belder, Department of Cardiology, Brighton and Sussex University Hospitals NHS Trust, Eastern Road, Brighton, UK; adam.debelder{at}bsuh.nhs.uk

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Learning objectives

  • Understand the incidence, pathophysiology and treatment options for human coronary arterial calcification.

  • Understand the different imaging options for determining the extent of coronary vascular calcification and their role in planning treatment.

  • Understand the role and limitations of rotational atherectomy in the management of obstructive calcific coronary disease.

Introduction

The generation of mineralised matrix within arterial conduits is common (see Figure 1). About 10%–20% of atherosclerotic vessels contain architecturally complete trabecular bone with fully formed marrow cavities with haematopoietic cells and vascular sinusoids. Although it is recognised that bone formation and arterial vessel calcification have common biochemical pathways, this so-called vascular calcification is a complex and incompletely understood phenomenon, which has proved difficult to prevent and treat.1 The process of extraskeletal ossification is not unlike embryonic ossification pathways which can be triggered by a variety of metabolic, inflammatory and genetic factors. For example, it is likely that proteins that normally restrict biomineralisation to skeletal bone are diminished (eg, fetuin A, matrix GIa, among others), and raise the prospect of identifying targets for therapeutic intervention. The two types of calcification—atherosclerotic (intimal calcification) and medial artery calcification—have different mechanisms, but both affect arterial stiffness and physiology, and increase the risk of adverse cardiovascular events.2

Figure 1

Three-dimensional reconstruction showing extensive aortic and coronary calcification (image courtesy of Dr V Parish).

Vascular calcification: therapeutic targets

Vascular calcification is more common with ageing, patients with diabetes mellitus, hypertension, renal dysfunction, hypercalcaemia and hyperphosphataemia, but can occur in patients without any of these characteristics. Patients with a high calcium diet do not have an increased risk of coronary calcification, suggesting that the pathogenesis lies in dysfunctional regulatory pathways. There is a substantial literature on the potential genetic and acquired mechanisms for this process, but specific mechanisms leading to therapeutic prevention have proved elusive. For example, small studies using statins, calcium blockers, hormonal therapies, phosphate …

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