Circadian rhythm of blood pressure reflects the severity of cardiac impairment in familial amyloid polyneuropathy

Algalarrondo, Vincent; Eliahou, Ludivine; Thierry, Isabelle; Bouzeman, Abdeslam; Dasoveanu, Madalina; Sébag, C; Moubarak, Ghassan; Guludec, Dominique Le; Samuel, Didier; Adams, David H.; Dinanian, S.; Slama, Michel

doi:10.1016/j.acvd.2012.03.004

Cited by 11 publications

(6 citation statements)

References 33 publications

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“…Rhythm disturbances and conduction defects are frequent consequences of cardiac amyloidal infiltration. Such as other studies, 14,26 we observed an increase in their occurrence with the worsening of TTR-FAP. It has been suggested that conduction defects can be relatively dissociated from LV thickening 14 and may even worsen after liver transplantation.…”

Section: Discussionsupporting

confidence: 60%

“…As in other studies, abnormalities in circadian BP variation were frequently detected. 26,27 High BP and the decrease in nocturnal systolic BP drop were the most common cardiovascular abnormalities and were more pronounced in patients with neurological involvement.…”

Section: Discussionmentioning

confidence: 99%

“…23 ABPM measurements were performed using SpaceLabs 90207 monitors (Healthcare, Inc) as described elsewhere. 24 Daytime, nighttime, and circadian systolic BP variation were determined. High BP was classified as mean daytime BP≥140/90 mm Hg or nighttime BP≥125/75 mm Hg.…”

Section: Cardiovascular Evaluationmentioning

confidence: 99%

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Reduced Myocardial 123-Iodine Metaiodobenzylguanidine Uptake

Coutinho

Cortez-Dias

Cantinho

et al. 2013

Circ: Cardiovascular Imaging

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Background-Transthyretin familial amyloid polyneuropathy is a hereditary form of amyloidosis characterized by sensorimotor and autonomic neuropathy, cardiac conduction defects, and infiltrative cardiomyopathy. Previous studies have suggested that myocardial sympathetic denervation assessed by 123-iodine metaiodobenzylguanidine (MIBG) imaging occurs early in disease progression. However, its prognostic significance was never evaluated. We aimed to study the long-term prognostic value of myocardial sympathetic denervation detected by MIBG imaging in transthyretin familial amyloid polyneuropathy. Methods and Results-A total of 143 individuals with V30M transthyretin mutation underwent Holter, ambulatory blood pressure monitoring, echocardiography, and MIBG imaging. Time to all-cause death was compared with late heart-tomediastinum MIBG uptake ratio (H/M; either in relation to the estimated lower limit of normal [

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

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Reduced Myocardial 123-Iodine Metaiodobenzylguanidine Uptake

Coutinho

Cortez-Dias

Cantinho

et al. 2013

Circ: Cardiovascular Imaging

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“…Ambulatory BP monitoring (ABPM) can help in the diagnosis and management of nOH [99]. Affected patients typically have a reversal of the normal circadian blood pressure pattern with higher BP during the night when the patient is supine in bed than during the day (i.e., non-dipping BP) [5, 22]. Nocturnal supine hypertension causes pressure natriuresis with exaggerated sodium and water loss causing overnight depletion of intravascular volume, worsening OH in the morning.…”

Section: Diagnosis Of Neurogenic Ohmentioning

confidence: 99%

Orthostatic hypotension in hereditary transthyretin amyloidosis: epidemiology, diagnosis and management

2019

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PurposeNeurogenic orthostatic hypotension is a prominent and disabling manifestation of autonomic dysfunction in patients with hereditary transthyretin (TTR) amyloidosis affecting an estimated 40–60% of patients, and reducing their quality of life. We reviewed the epidemiology and pathophysiology of neurogenic orthostatic hypotension in patients with hereditary TTR amyloidosis, summarize non-pharmacologic and pharmacological treatment strategies and discuss the impact of novel disease-modifying treatments such as transthyretin stabilizers (diflunisal, tafamidis) and RNA interference agents (patisiran, inotersen).MethodsLiterature review.ResultsOrthostatic hypotension in patients with hereditary transthyretin amyloidosis can be a consequence of heart failure due to amyloid cardiomyopathy or volume depletion due to diarrhea or drug effects. When none of these circumstances are apparent, orthostatic hypotension is usually neurogenic, i.e., caused by impaired norepinephrine release from sympathetic postganglionic neurons, because of neuronal amyloid fibril deposition.ConclusionsWhen recognized, neurogenic orthostatic hypotension can be treated. Discontinuation of potentially aggravating medications, patient education and non-pharmacologic approaches should be applied first. Droxidopa (Northera®), a synthetic norepinephrine precursor, has shown efficacy in controlled trials of neurogenic orthostatic hypotension in patients with hereditary TTR amyloidosis and is now approved in the US and Asia. Although they may be useful to ameliorate autonomic dysfunction in hereditary TTR amyloidosis, the impact of disease-modifying treatments on neurogenic orthostatic hypotension is still uninvestigated.

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“…Mean late HMR in patients without neuropathy 2.2 ± 0.5 vs patients with neuropathy 1.5 ± 0.4 ( P = 0.001) N/A 9 Delahaye et al 11 31 patients 300 MBq (8 mCi) [I-123]-MIBG LE 4 hours p.i. hATTR Mean late HMR 2 years after liver transplantation 1.46 ± 0.28 vs 6 months before liver transplantation 1.45 ± 0.29, P = not significant No cardiac death or lethal arrhythmia reported 10 Algalarrando et al 36 32 patients 300 MBq (8 mCi) [I-123]-MIBG LE 4 hours p.i. hATTR Late HMR ≤1.6 in 26 out of 32 patients No cardiac death or lethal arrhythmia reported 11 Noordzij et al 12 61 patients, 9 healthy control subjects 185 MBq (5 mCi) [I-123]-MIBG ME 4 hours p.i.…”

Section: Imaging Of Cardiac Innervation In Amyloidosismentioning

confidence: 99%

Imaging cardiac innervation in amyloidosis

Slart

Glaudemans

Hazenberg

et al. 2019

Journal of Nuclear Cardiology

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Cardiac amyloidosis is a form of restrictive cardiomyopathy resulting in heart failure and potential risk on arrhythmia, due to amyloid infiltration of the nerve conduction system and the myocardial tissue. The prognosis in this progressive disease is poor, probably due the development of cardiac arrhythmias. Early detection of cardiac sympathetic innervation disturbances has become of major clinical interest, because its occurrence and severity limits the choice of treatment. The use of iodine-123 labelled metaiodobenzylguanidine ([I-123]MIBG), a chemical modified analogue of norepinephrine, is well established in patients with heart failure and plays an important role in evaluation of sympathetic innervation in cardiac amyloidosis. [I-123]MIBG is stored in vesicles in the sympathetic nerve terminals and is not catabolized like norepinephrine. Decreased heart-to-mediastinum ratios on late planar images and increased wash-out rates indicate cardiac sympathetic denervation and are associated with poor prognosis. Single photon emission computed tomography provides additional information and has advantages for evaluating abnormalities in regional distribution in the myocardium. [I-123]MIBG is mainly useful in patients with hereditary and wild-type ATTR cardiac amyloidosis, not in AA and AL amyloidosis. The potential role of positron emission tomography for cardiac sympathetic innervation in amyloidosis has not yet been identified. Electronic supplementary material The online version of this article (doi:10.1007/s12350-017-1059-9) contains supplementary material, which is available to authorized users.

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Circadian rhythm of blood pressure reflects the severity of cardiac impairment in familial amyloid polyneuropathy

Cited by 11 publications

References 33 publications

Reduced Myocardial 123-Iodine Metaiodobenzylguanidine Uptake

Reduced Myocardial 123-Iodine Metaiodobenzylguanidine Uptake

Orthostatic hypotension in hereditary transthyretin amyloidosis: epidemiology, diagnosis and management

Imaging cardiac innervation in amyloidosis

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