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Updated: Apr 28, 2026
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Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance
Published on: March 21, 2013
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Arrhythmic syncope in neurogenic orthostatic hypotension: two case reports
Cristina Di Stefano1, Valeria Milazzo, Gabriele Sobrero
1Autonomic Unit and Hypertension Unit, Medical Sciences Department, University of Turin, Corso Bramante 88, 10126, Turin, Italy, cris86_d@libero.it.
Summary
Patients with autonomic failure can experience fainting due to low blood pressure upon standing (orthostatic hypotension) or heart rhythm problems (arrhythmias). This report details two cases of primary autonomic neuropathy presenting with both severe orthostatic hypotension and arrhythmic syncope.
Area of Science:
- Cardiology
- Neurology
- Autonomic Nervous System Research
Background:
- Autonomic failure can lead to orthostatic hypotension (OH), a condition causing a significant drop in blood pressure upon standing.
- Orthostatic hypotension is frequently associated with syncope (fainting) in patients with autonomic dysfunction.
- Arrhythmias are another critical cause of syncope, carrying a substantial risk of mortality.
Observation:
- Two patients diagnosed with primary autonomic neuropathy were studied.
- Both patients presented with severe symptoms of orthostatic hypotension.
- Concurrently, both patients experienced syncope attributed to cardiac arrhythmias.
Findings:
- The cases highlight a co-occurrence of severe orthostatic hypotension and arrhythmic syncope in primary autonomic neuropathy.
- This dual presentation suggests complex interactions between autonomic dysfunction and cardiac electrical stability.
- The findings underscore the potential for multiple syncope mechanisms in this patient population.
Implications:
- Recognizing both OH and arrhythmias is crucial for managing syncope in autonomic failure.
- Comprehensive cardiovascular and neurological assessment is warranted for patients with primary autonomic neuropathy.
- Further research may elucidate shared pathophysiological pathways and inform targeted therapeutic strategies.
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