Differing haemodynamic and catecholamine responses to exercise in three groups with peripheral autonomic dysfunction: Insulin-dependant diabetes mellitus, familial amyloid polyneuropathy and pure autonomic failure

Smith, George J.; Watson, Laura; Mathias, C. J.

doi:10.1016/s0165-1838(98)00132-5

Cited by 3 publications

(1 citation statement)

References 33 publications

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“…In turn, physical immobility worsens OH, leading to a “vicious cycle” of deconditioning [41]. Physical exercise is therefore a key component of the therapeutic regimen, but because physical activity in the standing position can worsen nOH in patients with hereditary transthyretin amyloidosis [81, 110, 122–124], exercise should be performed in the recumbent or sitting position using a recumbent stationary bicycle or rowing machine. The exception is exercise in a pool as the hydrostatic pressure of water allows upright exercise without hypotension [111].…”

Section: Management Of Neurogenic Oh In Hereditary Ttr Amyloidosismentioning

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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Section: Management Of Neurogenic Oh In Hereditary Ttr Amyloidosismentioning

confidence: 99%

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

2019

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Exercise-induced hypotension in autonomic disorders

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Nóbrega

2012

Autonomic Neuroscience

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Effects of midodrine on exercise-induced hypotension and blood pressure recovery in autonomic failure

Schrage

Eisenach²,

Dinenno

et al. 2004

Journal of Applied Physiology

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We tested the hypothesis that the oral alpha1-adrenergic agonist, midodrine, would limit the fall in arterial pressure observed during exercise in patients with pure autonomic failure (PAF). Fourteen subjects with PAF underwent a stand test, incremental supine cycling exercise (25, 50, and 75 W), and ischemic calf exercise, before (control) and 1 h after ingesting 10 mg midodrine. Heart rate (ECG), beat-to-beat blood pressure (MAP, arterial catheter), cardiac output (Q, open-circuit acetylene breathing), forearm blood flow (FBF, Doppler ultrasound), and calf blood flow (CBF, venous occlusion plethysmography) were measured. The fall in MAP after standing for 2 min was similar ( approximately 60 mmHg; P = 0.62). Supine MAP immediately before cycling was greater after midodrine (124 +/- 6 vs 117 +/- 6 mmHg; P < 0.03), but cycling caused a workload-dependent hypotension (P < 0.001), whereas increases in Q were modest but similar. Midodrine increased MAP and total peripheral resistance (TPR) during exercise (P < 0.04), but the exercise-induced fall in MAP and TPR were similar during control and midodrine (P = 0.27 and 0.14). FBF during cycling was not significantly reduced by midodrine (P > 0.2). By contrast, recovery of MAP after cycling was faster (P < 0.04) after midodrine ( approximately 25 mmHg higher after 5 min). Ischemic calf exercise evoked similar peak CBF in both trials, but midodrine reduced the hyperemic response over 5 min of recovery (P < 0.02). We conclude midodrine improves blood pressure and TPR during exercise and dramatically improves the recovery of MAP after exercise.

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Differing haemodynamic and catecholamine responses to exercise in three groups with peripheral autonomic dysfunction: Insulin-dependant diabetes mellitus, familial amyloid polyneuropathy and pure autonomic failure

Cited by 3 publications

References 33 publications

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

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

Exercise-induced hypotension in autonomic disorders

Effects of midodrine on exercise-induced hypotension and blood pressure recovery in autonomic failure

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