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- Kohno, Ritsuko, et al.
(författare)
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Mast Cell Activation Disorder and Postural Orthostatic Tachycardia Syndrome : A Clinical Association
- 2021
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Ingår i: Journal of the American Heart Association. - 2047-9980. ; 10:17
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Tidskriftsartikel (refereegranskat)abstract
- Background Recently there has been increased interest in a possible association between mast cell activation (MCA) disorder and postural orthostatic tachycardia syndrome (POTS). This study examined the frequency with which symptoms and laboratory findings suggesting MCA disorder occurred in patients diagnosed with POTS. Methods and Results Data were obtained from patients in whom symptoms and orthostatic testing were consistent with a POTS diagnosis. Individuals with <4 months symptom duration, evident ongoing inflammatory disease, suspected volume depletion, or declined consent were excluded. All patients had typical POTS symptoms; some, however, had additional nonorthostatic complaints not usually associated with POTS. The latter patients underwent additional testing for known MCA biochemical mediators including prostaglandins, histamine, methylhistamine, and plasma tryptase. The study comprised 69 patients who met POTS diagnostic criteria. In 44 patients (44/69, 64%) additional nonorthostatic symptoms included migraine, allergic complaints, skin rash, or gastrointestinal symptoms. Of these 44 patients, 29 (66%) exhibited at least 1 laboratory abnormality suggesting MCA disorder, and 11/29 patients had 2 or more such abnormalities. Elevated prostaglandins (n=16) or plasma histamine markers (n=23) were the most frequent findings. Thus, 42% (29/69) of patients initially diagnosed with POTS exhibited both additional symptoms and at least 1 elevated biochemical marker suggesting MCA disorder. Conclusions Laboratory findings suggesting MCA disorder were relatively common in patients diagnosed with POTS and who present with additional nonorthostatic gastrointestinal, cutaneous, and allergic symptoms. While solitary abnormal laboratory findings are not definitive, they favor MCA disorder being considered in such cases.
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| 2. |
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| 3. |
- Sutton, Richard, et al.
(författare)
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Tilt testing remains a valuable asset
- 2021
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X.
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Forskningsöversikt (refereegranskat)abstract
- Head-up tilt test (TT) has been used for >50 years to study heart rate/blood pressure adaptation to positional changes, to model responses to haemorrhage, to assess orthostatic hypotension, and to evaluate haemodynamic and neuroendocrine responses in congestive heart failure, autonomic dysfunction, and hypertension. During these studies, some subjects experienced syncope due to vasovagal reflex. As a result, tilt testing was incorporated into clinical assessment of syncope when the origin was unknown. Subsequently, clinical experience supports the diagnostic value of TT. This is highlighted in evidence-based professional practice guidelines, which provide advice for TT methodology and interpretation, while concurrently identifying its limitations. Thus, TT remains a valuable clinical asset, one that has added importantly to the appreciation of pathophysiology of syncope/collapse and, thereby, has improved care of syncopal patients.
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| 4. |
- Torabi, Parisa, et al.
(författare)
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Impact of Cardiovascular Neurohormones on Onset of Vasovagal Syncope Induced by Head-up Tilt.
- 2019
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Ingår i: Journal of the American Heart Association. - 2047-9980. ; 8:12
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundVasovagal reflex is the most common form of syncope, but the pathophysiological mechanisms that initiate the reflex are not well understood. We aimed to study supine and early orthostatic levels of the neurohormones involved in control of circulatory homeostasis in relation to the onset of tilt‐induced vasovagal syncope (VVS).Methods and ResultsA total of 827 patients who were investigated for unexplained syncope with head‐up tilt test (HUT) and optional nitroglycerin provocation (Italian protocol) had blood samples collected while supine and after 3‐minutes of HUT. Of these, 173 (20.9%) patients developed VVS during drug‐free HUT, 161 of whom (males 44.7%; age 45±21 years) had complete data. We analyzed levels of epinephrine, norepinephrine, C‐terminal pro–arginine vasopressin, C‐terminal endothelin‐1, and midregional fragments of pro–atrial natriuretic peptide and pro‐adrenomedullin in relation to time from tilt‐up to onset of VVS. We applied a linear regression model adjusted for age and sex. The mean time to syncope was 11±7 minutes. Older age (β=0.13; SE=0.03, P<0.001), higher supine systolic blood pressure (β=0.06; SE=0.03, P=0.02), and higher supine midregional fragment of pro‐adrenomedullin predicted longer time to syncope (β=2.31; SE=0.77, P=0.003), whereas supine levels of other neurohormones were not associated with time to syncope. Among 151 patients who developed VVS later than 3 minutes of HUT, increase in epinephrine (β=−3.24; SE=0.78, P<0.001) and C‐terminal pro–arginine vasopressin (β=−2.07; SE=0.61, P=0.001) at 3 minutes of HUT were related to shorter time to syncope.ConclusionsOlder age, higher blood pressure, and higher level of pro‐adrenomedullin are associated with later onset of VVS during tilt testing, whereas greater increase of tilt‐induced epinephrine and vasopressin release correlate with shorter time to syncope.
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