Pathology-validated prevalence and clinical characteristics of coronary medial arterial calcification

Yuki Matsumoto1, Sho Torii1, Kazuki Aihara1

  • 1Department of Cardiology, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan.

Insights

True coronary medial arterial calcification (MAC) is rare, with most imaging findings actually representing deep intimal calcification (DIC). Distinguishing these conditions is crucial for accurate diagnosis and patient care.

Area of Science:

  • Cardiovascular Pathology
  • Arterial Disease Research
  • Histopathology

Background:

  • Medial arterial calcification (MAC) is well-documented in peripheral arteries, but its prevalence and characteristics in the coronary arteries are not well-established.
  • Deep intimal calcification (DIC) can mimic MAC on intravascular imaging due to its proximity to the internal elastic lamina (IEL), complicating diagnosis.

Purpose of the Study:

  • To determine the pathology-validated prevalence of true coronary MAC.
  • To morphologically characterize DIC as a potential mimic of coronary MAC.
  • To differentiate between primary MAC and DIC in coronary arteries.

Main Methods:

  • Analysis of 4508 histologic sections from 327 coronary arteries in 112 autopsy cases.
  • Precise identification of the IEL and external elastic lamina using Movat Pentachrome and EVG stains.
  • Evaluation of a high-risk cohort with 85% cardiac deaths.

Main Results:

  • Pathology-confirmed coronary MAC was rare (1.0% of sections, 3.6% of patients).
  • Two distinct MAC phenotypes were observed: secondary nodular protrusion (3 patients) and rare primary medial disease (1 patient).
  • Deep intimal calcification (DIC) was significantly more prevalent, found in 35.7% of patients.

Conclusions:

  • True primary coronary MAC is exceptionally rare.
  • Clinical imaging findings of coronary 'MAC' predominantly represent DIC, not true medial calcification.
  • Accurate interpretation of coronary artery imaging requires recognition of DIC, secondary nodular protrusions, and Mönckeberg-type MAC.
Abstract

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