Amyloid deposits in prostate biopsy as an opportunity to diagnose early cardiac amyloidosis

Abstract

Background: The diagnostic delay of cardiac amyloidosis (CA) is known to be substantially long. A prolonged time from symptoms onset to diagnosis negatively impacts quality of life and life expectancy of the affected patients. We aim to describe the role of the incidental finding of amyloid deposits in prostatic tissue as an early marker of CA.

Methods: A systematic cardiological evaluation, comprising ECG, echocardiogram and 99mTc-DPD scintigraphy, was offered to a cohort of 19 patients with incidental prostatic amyloidosis (PA) findings, propectively detected between 2014-2023, to assess cardiac involvement.

Results: The median age of the patients was 80.2 years (IQR: 74.9 -82.6 years). Histopathological study revealed amyloid deposits within the walls of small vessels (predominantly small arteries) in 18 patients and mainly in the stroma in the remaining case. All of them were immunohistochemically positive for transthyretin (ATTR) except one patient, with known myeloma, which was unconclusive fo ATTR. Clonal dyscrasia was excluded in the rest of the patients. Thirteen patients (68.4%) underwent all cardiological tests, 4 patients (21.1%) underwent only ECG and echocardiographic evaluation and two patients (10.5%) refused to undergo any cardiological study. Among 13 individuals undergoing the complete evaluation, six patients were eventually diagnosed with CA (46.15%). All of them were asymptomatic from a cardiovascular point of view at the time of the prostate biopsy.

Conclusion: The finding of PA should prompt a complete cardiovascular examination, given the significant percentage of patients eventually diagnosed with early-stage CA. Multidisciplinary collaboration among different medical specialists must be encouraged, given the potential clinical impact of CA early diagnosis.

Figure 1

Amyloid deposits found in prostate specimens. (A): Amyloid deposition inside the wall of a small vessel in a prostate needle biopsy (black arrow); (B): Amyloid positivity in Congo Red Stain; (C): TTR immunohistochemical reactivity. TTR: transthyretin.

Figure 2

Study population workflow. From the initial cohort, 13 patients underwent a complete systematic cardiovascular evaluation, including ECG, transthoratic echocardiogram and scintingraphy. Among them, 6 patients (46.2%) were eventually diagnosed with ATTR-CA. ATTR-CA: transthyretin cardiac amyloidosis.

Figure 3

Diagnostic accuracy of electrophysiological, echocardiographic and clinical manifestations evaluated in the study. The presence of any electrophysiological, echocardiographic and clinical manifestations performed with low diagnostic accuracy for ATTR-CA. ATTR-CA: transthyretin cardiac amyloidosis. BBB: bundle branch block; GLS: global longitudinal strain; TAPSE: tricuspid annular plane systolic excursion.

Figure 4

Distribution of electrophysiological, echocardiographic and clinical manifestations among patients with cardiac amyloidosis. Six patients with the final diagnosis of ATTR-CA are shown in the diagram. Check marks indicate the presence of any electrophysiological, echocardiographic and clinical manifestation for each individual. BBB: bundle branch block; BT: biceps tendon; CA: cardiac amyloidosis; CD: conduction disturbances; CTS: carpal tunnel syndrome; DD: diastolic dysfunction; GLS: global longitudinal strain; Pat.: pattern; RWT: relative wall thickness; TAPSE: Tricuspid annular plane systolic excursion.