Key result
Cardiac amyloidosis patients show transcardiac biomarker gradients reflecting ongoing cardiac damage and sympathetic activation.
Why the study?
Cardiac amyloidosis is an important cause of heart failure in the elderly, yet the pathophysiological drivers of cardiac damage in cardiac amyloidosis remain poorly understood.
Does transcardiac blood sampling reveal significant gradients of cardiac remodelling and sympathetic activation markers in patients with cardiac amyloidosis?
Does transcardiac blood sampling reveal significant gradients of cardiac remodelling and sympathetic activation markers in patients with cardiac amyloidosis?
Cardiac amyloidosis is characterized by significant transcardiac gradients of natriuretic peptides, troponins, and norepinephrine, suggesting a key role for sympathetic activation in amyloid-related cardiac damage.
Answers are grounded in this paper and cite their sources.
Sympathetic activation may drive ongoing injury in cardiac amyloidosis; hypothesis-generating and should not yet change practice.
Background Cardiac amyloidosis (CA) results from the deposition of misfolded proteins in the heart, leading to progressive organ damage. CA is an important cause of heart failure (HF) in the elderly, yet the pathophysiological drivers of cardiac damage in CA remain poorly understood. Purpose To investigate the determinants of cardiac damage in CA through the assessment of transcardiac blood sampling of relevant analytes. Methods Patients with CA or CA phenocopies underwent simultaneous coronary sinus (CS) and peripheral artery (ART) blood sampling. The transcardiac gradient of analytes was determined by the difference between the two sites. Peripheral venous sampling served as a control. Analytes related to cardiac remodelling (natriuretic peptides, troponins), neurohormonal activation (norepinephrine, epinephrine, aldosterone, renin), and amyloidogenic precursors (transthyretin, light chains) were assessed. All patients underwent comprehensive clinical evaluation, including ECG and echocardiography, before the procedure. Results A total of 17 patients (9 with light chain [AL]-CA, 7 with wild-type transthyretin [ATTR]-CA, and 1 with variant ATTR-CA) and 2 phenocopies underwent the procedure. CA patients exhibited a significant transcardiac gradient of natriuretic peptides (BNPART 379 [192-974] vs. BNPCS 1328 [680-2480] ng/L, p<0.0001) and troponins (hsTnTART 49 [26-76] vs. hsTnTCS 60 [31-98] ng/L, p<0.0001), indicating ongoing cardiac damage, with no significant differences between AL-CA and ATTR-CA. CA patients also showed a significant transcardiac gradient of norepinephrine (NEART 624 [254-970] vs. NECS 731 [353-1832] ng/L, p<0.001), with a trend towards higher values in AL-CA compared to ATTR-CA (p=0.072) and median values comparable to those found in non-CA HF patients. The transcardiac gradient of norepinephrine correlated with BNP levels and indices of diastolic dysfunction. No meaningful transcardiac gradient of aldosterone, renin, or amyloidogenic precursors was detected. Conclusions CA is characterized by high-level ongoing cardiac remodelling. The sympathetic nervous system may play a key role in amyloid-related cardiac damage.
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Castiglione et al. (2025) studied this question. Cardiac amyloidosis patients showed significant transcardiac gradients of natriuretic peptides, troponins, and norepinephrine indicating ongoing cardiac damage and sympathetic activation (p<0.001).
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