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Background
Monckeberg's sclerosis is a disease of unknown aetiology characterised by calcification of the media of small-sized and medium-sized arteries 1 first described by Johann Georg Monckeberg in 1903 2 for whom it is eponymously named. The result is progressive stiffening of the elastic layer of the arterial wall. This loss of elasticity can subsequently lead to systolic hypertension, left ventricular hypertrophy and impaired myocardial perfusion and ultimately increased cardiovascular risk. 3
At first believed to be a benign condition exclusively involving small-sized and medium-sized arteries, without thrombosis and luminal obstruction characteristic of atherosclerotic disease 4 this condition has now been associated with a multitude of systemic conditions, including atherosclerosis, chronic kidney disease and hyperparathyroidism. 5
The aetiology and pathogenesis of Monckeberg's sclerosis remain unclear. Proposed mediators of calcification include abnormal vascular smooth muscle cells with osteoblastic properties, and cytokine modulators of bone mineralisation such as osteoprotegerin, tumour necrosis factor (TNF)-related apoptosis-inducing ligand and receptor activator of nuclear factor kappa B ligand. Monckeberg's sclerosis has also been associated with autonomic neuropathy in diabetics, 6 7 suggesting that autonomic dysfunction might play an important role in medial calcification. This association is further supported by the increased incidence of vascular calcification following lumbar sympathectomy. 8
This case highlights the bidirectional relationship between Monckeberg's sclerosis and coronary artery disease. While ischaemic heart disease is usually looked for in individuals with peripheral arterial calcification, it is equally important to rule out arterial calcification in patients with proven coronary artery disease. Monckeberg's sclerosis can be an unexpected contraindication to arterial puncture in patients planned for coronary angiography and percutaneous intervention.
Case presentation
A 62-year-old man presented with angina at rest since the past 6 days. He was a known diabetic on oral antidiabetic drugs since the past 8 years. There were no other risk factors for ischaemic heart disease. There were also no symptoms suggestive of peripheral arterial insufficiency including paraesthesias and non-healing ulcers in the extremities.
At admission, the patient was haemodynamically stable. All peripheral pulses were palpable; arterial wall thickening was noted in both radial arteries. His hands and feet were warm with no evidence of limb ischaemia. Cardiovascular examination was essentially normal.
Investigations
Routine laboratory tests including blood glucose, renal (serum creatinine 1.0 mg/dl) and...