Impaired peripheral vasoconstrictor response to orthostatic stress in patients with multiple system atrophy

Suzuki, Junichiro; Nakamura, Tomohiko; Hirayama, Masaaki; Mizutani, Yasuaki; Okada, Ayaka; Ito, Mizuki; Watanabe, Haruo; Sobue, Gen

doi:10.1016/j.parkreldis.2015.05.023

Cited by 12 publications

(6 citation statements)

References 31 publications

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“…The total peripheral resistance at 60° tilt was increased compared with the baseline levels in all normal subjects (14) but was lower than at baseline in all examined patients. The absence of an increase in the total peripheral resistance in these patients suggests an impaired peripheral vasoconstrictor response to orthostatic stress due to denervation of efferent sympathetic nerves (18,20). Figure shows the sequential changes over time in the systolic blood pressure, diastolic blood pressure, heart rate, and total peripheral resistance at the fifth minute of the 20°, 40°, and 60° tilts, as measured by impedance cardiography.…”

Section: Resultsmentioning

confidence: 86%

“…After resting in a supine position for at least 5 minutes, subjects were tilted up to 60° in a stepwise manner (20°, 40°, and 60° for 5 minutes each) to assess the change in systolic blood pressure at 60° compared with the baseline level in the supine position. Cardiovascular recordings were performed using a noninvasive monitoring device (Task Force Monitor, CNSystems, Medizintechnik, Graz, Austria) during the head-up tilt test to examine the total peripheral resistance (18,20). Total peripheral resistance was calculated using the cardiac output, mean arterial pressure, and central venous pressure (18,20).…”

Section: Methodsmentioning

confidence: 99%

“…Cardiovascular recordings were performed using a noninvasive monitoring device (Task Force Monitor, CNSystems, Medizintechnik, Graz, Austria) during the head-up tilt test to examine the total peripheral resistance (18,20). Total peripheral resistance was calculated using the cardiac output, mean arterial pressure, and central venous pressure (18,20). Cardiac parameters were obtained at every beat from impedance cardiography, and the average of the last 30 seconds at baseline, the fifth minute of the 20°, 40°, and 60° tilts, and the third minute after the return to the supine position were used for the analysis.…”

Section: Methodsmentioning

confidence: 99%

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Widespread Cardiac and Vasomotor Autonomic Dysfunction in Non-Val30Met Hereditary Transthyretin Amyloidosis

et al. 2018

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Objective The autonomic functions of hereditary transthyretin (ATTRm) amyloidosis, traditionally referred to as familial amyloid polyneuropathy, have primarily been investigated in patients with Val30Met mutations, and information regarding non-Val30Met patients is scarce. The aim of this study was to systematically investigate the cardiac and peripheral vasomotor autonomic functions in non-Val30Met patients. Methods The coefficient of variation of R-R intervals (CVR-R), responses to the Valsalva manoeuvre, head-up tilt test results, noradrenaline infusion test results, and the (123) I-metaiodobenzylguanidine (MIBG) uptake on myocardial scintigraphy were assessed in five patients. The predominant manifestations were neuropathy in three patients (Val94Gly, Val71Ala, and Pro24Ser), cardiomyopathy in one (Thr60Ala), and oculoleptomeningeal involvement in one (Tyr114Cys). Results Although one patient with predominant cardiomyopathy did not manifest orthostatic hypotension during the head-up tilt test, the CVR-R, responses to the Valsalva manoeuvre, and myocardial MIBG uptake indicated the presence of cardiac sympathetic and parasympathetic dysfunction in all patients. The total peripheral resistance at 60° tilt did not increase from the baseline values in any of the examined patients. An infusion of low-dose noradrenaline induced an increase in the systolic blood pressure, except in one patient with mild neuropathy. Conclusion Cardiac and peripheral vasomotor autonomic dysfunctions were prevalent in non-Val30Met patients, irrespective of their phenotype, suggesting a common pathology of autonomic involvement. However, the vasoconstrictor function was preserved, even in a patient with advanced neuropathy.

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Section: Resultsmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Widespread Cardiac and Vasomotor Autonomic Dysfunction in Non-Val30Met Hereditary Transthyretin Amyloidosis

et al. 2018

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“…One unexpected finding in nOH was a decrease of TPR in the upright position, measured from a baseline supine position (64)(65)(66)(67). This upright decrease in TPR, apparently stronger in PAF than in MSA, was unexpected because a change to the upright position should cause TPR to increase, or at least remain the same if it cannot increase.…”

Section: Pathophysiology Of Coh/nohmentioning

confidence: 98%

Timing of Circulatory and Neurological Events in Syncope

Dijk

Rossum

Thijs

2020

Front. Cardiovasc. Med.

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Syncope usually lasts less than a minute, in which short time arterial blood pressure temporarily falls enough to decrease brain perfusion so much that loss of consciousness ensues. Blood pressure decreases quickest when the heart suddenly stops pumping, which happens in arrhythmia and in severe cardioinhibitory reflex syncope. Loss of consciousness starts about 8 s after the last heart beat and circulatory standstill occurs after 10-15 s. A much slower blood pressure decrease can occur in syncope due to orthostatic hypotension Standing blood pressure can then stabilize at low values often causing more subtle signs (i.e., inability to act) but often not low enough to cause loss of consciousness. Cerebral autoregulation attempts to keep cerebral blood flow constant when blood pressure decreases. In reflex syncope both the quick blood pressure decrease and its low absolute value mean that cerebral autoregulation cannot prevent syncope. It has more protective value in orthostatic hypotension. Neurological signs are related to the severity and timing of cerebral hypoperfusion. Several unanswered pathophysiological questions with possible clinical implications are identified.

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“…We are writing with respect to the recent article by Suzuki et al, “Impaired peripheral vasoconstrictor response to orthostatic stress in patients with multiple system atrophy,” [1] in which the authors report an overall decrease in total peripheral resistance to blood flow (TPR) during orthostasis in multiple system atrophy (MSA). This is potentially important, because if this interpretation of the data were correct then MSA might involve a heretofore unrecognized reflexive systemic vasodilator response to decreased venous return to the heart.…”

Section: To the Editormentioning

confidence: 99%