Linking Coronary Microvascular Dysfunction to Cardiac Troponin Elevation in Transthyretin Amyloid Cardiomyopathy

Transthyretin amyloid cardiomyopathy (ATTR-CM) is frequently accompanied by persistent elevation of high-sensitivity cardiac troponin T (hs-cTnT) and coronary microvascular dysfunction (CMD), yet their pathophysiological link remains incompletely defined.

To identify the structural and functional correlates of hs-cTnT elevation in ATTR-CM.

We retrospectively studied 71 hospitalized patients with left ventricular hypertrophy (LVH) who underwent invasive physiological assessment of the left anterior descending artery, right heart catheterization, and endomyocardial biopsy as part of the etiological evaluation. ATTR-CM was histologically confirmed in 51 patients; the remaining 20 patients, who had no cardiac amyloidosis and alternative causes of LVH, served as a contextual reference group. The primary interpretation therefore focused on within-ATTR-CM associations. Coronary flow reserve (CFR), index of microcirculatory resistance (IMR), myocardial capillary density (MCD), and sampled transthyretin deposition were quantified and analysed in relation to hs-cTnT and haemodynamic and imaging parameters. Within the ATTR-CM cohort, higher hs-cTnT levels were independently associated with higher pulmonary artery wedge pressure (standardized β = 0.46, p = 0.0001), lower CFR (β = -0.26, p = 0.027), and lower MCD (β = -0.24, p = 0.037), but not with IMR or sampled histological transthyretin burden.

In this selected invasive cohort with histologically confirmed ATTR-CM, higher hs-cTnT levels were independently associated with lower biopsy-derived MCD, impaired perfusion reserve, and elevated filling pressure, suggesting an integrated microvascular-haemodynamic substrate of persistent myocardial injury.