Vascular abnormalities in primary amyloidosis

Modesto, Karen; Dispenzieri, Angela; Gertz, Morie A.; Cauduro, Sanderson; Khandheria, Bijoy K.; Seward, James B.; Kyle, Robert A.; Wood, Christina M.; Bailey, Kent R.; Miller, Fletcher A.; Pellikka, Patricia A.; Abraham, Theodore P.

doi:10.1093/eurheartj/ehm066

Cited by 55 publications

(50 citation statements)

References 29 publications

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“…Vasculature with amyloid infiltration cannot respond normally with appropriate vasoconstriction when presented with slight hypovolemia due to mild diuresis. 6 As expected, the patient's hypotension quickly resolved after minimal fluid resuscitation, given the increased vascular rigidity caused by the amyloid infiltration. This allowed for adequate perfusion to the kidneys, resulting in the rapid correction of the patient's acute kidney injury.…”

Section: Discussionsupporting

confidence: 59%

An Unusual Presentation and Etiology of Hypotension Seen in Nephrotic Syndrome

Panagiotides¹,

Hever²,

Sim³

2009

TPJ

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Section: Discussionsupporting

confidence: 59%

An Unusual Presentation and Etiology of Hypotension Seen in Nephrotic Syndrome

Panagiotides¹,

Hever²,

Sim³

2009

TPJ

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“…Increased LV filling pressure, which causes increased wall stress due to diastolic dysfunction in cardiac amyloidosis, compresses myocardial capillaries, with subsequent decrease in their lumen. Endothelial function is impaired by microvascular toxicity induced by light chain in AL amyloidosis 27, 28. These mechanisms cause functional myocardial ischaemia, subclinical impairment of LV systolic function, and cardiac troponin release.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic utility of cardiac troponin T level in patients with cardiac amyloidosis

et al. 2017

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AimThe aim of this study was to evaluate the diagnostic utility of high‐sensitivity cardiac troponin T (hs‐cTnT) levels in discriminating cardiac amyloidosis from patients with cardiac hypertrophy caused by aetiologies other than cardiac amyloidosis.Methods and resultsSerum hs‐cTnT levels were measured in 96 patients with cardiac amyloidosis (light chain: 23, wild‐type transthyretin amyloidosis: 40, and mutated transthyretin amyloidosis: 33), and 91 patients with other causes of cardiac hypertrophy who were confirmed to have no cardiac amyloidosis by endomyocardial biopsy (control group). The diagnostic utility and cut‐off value of hs‐cTnT were evaluated by receiver operating characteristic analysis. The median hs‐cTnT levels were higher in cardiac amyloidosis than the control group [0.048 (0.029–0.073) vs. 0.016 (0.010–0.031) ng/mL; P < 0.001]. High levels of hs‐cTnT were suggestive of cardiac amyloidosis (cut‐off value: 0.0312 ng/mL, sensitivity: 0.74, specificity: 0.76, area under the curve: 0.788; 95% confidence interval: 0.723–0.854, P < 0.001), compared with brain natriuretic peptide and E/e′ ratio. The hs‐cTnT levels were also useful in differentiating each type of amyloidosis from the control group. Multivariate analysis identified log hs‐cTnT as an independent diagnostic factor for cardiac amyloidosis (odds ratio: 2.22; 95% confidence interval: 1.30–3.80; P = 0.004).ConclusionsHigh serum levels of hs‐cTnT are highly suggestive of cardiac amyloidosis, allowing its differentiation from cardiac hypertrophy of other aetiologies. Further refined diagnostic approaches that include imaging modalities and histopathological examination are needed for these patients to avoid underdiagnosis of cardiac amyloidosis.

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“…[9][10][11][12] There are limited data on endothelial function in patients with AL amyloidosis. 9,13 The study of the vascular function is complex, and surrogate markers of endothelial activation could be useful in understanding the potential role of endothelium in the development of symptoms and complications of AL amyloidosis. von Willebrand factor (VWF) is a large multimeric glycoprotein mainly produced (but not exclusively), stored, and secreted by ECs.…”

Section: Introductionmentioning

confidence: 99%