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Background: The increase in troponin is a cardiac amyloidosis (CA) peculiarity. The most acclaimed hypothesis is direct toxicity of amyloid fibrils on cardiomyocytes, but a subendocardial ischemia due to discrepancy between oxygen supply and demand imbalance has not been investigated yet. Methods: 129 outpatients attending the Pavia Amyloid Center were enrolled, 66 of them were affected by CA.Aortic stiffness was assessed measuring carotid-femoral pulse wave velocity (PWV).The subendocardial viability ratio (SEVR) was used to quantify the relationship between subendocardial oxygen supply and demand. Echocardiogram data were used to quantify left ventricular diastolic pressure and left ventricular mass index (LVMI). Results: Troponin was higher in CA (p<0.0001); there was an inverse correlation between troponin and SEVR (p = 0.0002). Troponin was strongly correlated with LVMI (p = 0.0003). Both the increase in TnI and the reduction of SEVR were related to low values of ejection fraction. The ROC curves showed that SEVR had a greater sensitivity and specificity (AUC = 0.778) than EF% and PWV in identifying pathological troponin values. Conclusions: There is a close relationship in CA between troponin values and the reduction in the SEVR. Ischemic suffering, with undamaged coronary arteries, may be a cause of cardiac myocytes damage in amyloidosis. LVMI increases with disease progression. On the other hand, amorphous amyloid mass modifies the microcirculation. These two phenomena may seriously affect myocardial perfusion. Moreover, amyloid alters the macrostructural organization of myofibrils, thus heart may need an increased energy-metabolic supply. SEVR assessment may improve the identification of subclinical myocardial damage in cardiac amyloidosis.