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Biomedical subjects

Wouter Wieling

Publications and source records attributed to Wouter Wieling.

At least 37 records · Page 2Linked to original sources
PubMed2004

Long-term effects of unilateral carotid endarterectomy on arterial baroreflex function.

BACKGROUND AND PURPOSE: Carotid endarterectomy (CE) may be complicated by the clinical syndrome of baroreflex failure. Alterations of baroreflex function may also account for the frequently observed blood pressure lability in the first hours following surgery. We investigated the long-term effects of unilateral CE on baroreflex control of function and blood pressure. METHODS: We investigated 14 patients after unilateral CE (13 m:1 f, 64.8 +/- 6.5 years), 9 patients with a surgically untreated uni-/bilateral carotid stenosis (CS, 7 m:2 f, 57.6 +/- 10.7 years) and 12 healthy controls (HC, 11 m:1 f, 60.9 +/- 7.9 years) by means of Valsalva maneuver, active standing, forced breathing, cold face test, cold pressor test and mental arithmetic. Ambulatory blood pressure level and variability were determined from 24-hour Spacelabs and 5-hour beat-to-beat Portapres recordings. RESULTS: Baroreflex sensitivity (derived from phase IV Valsalva maneuver) was significantly lower in CE (1.53 +/- 0.83 ms/mmHg) than in CS (4.39 +/- 2.27, p = 0.002) and HC (5.34 +/- 3.78, p = 0.003). CE patients exhibited a decreased reflex control of heart rate in response to Valsalva's maneuver and active standing without orthostatic hypotension. Office blood pressure levels before and after endarterectomy were similar, as were ambulatory blood pressure levels in the three groups. Ambulatory blood pressure variability was higher in CE and CS than in HC, but not different between CE and CS. CONCLUSIONS: Unilateral CE causes a long-term impairment of baroreflex function, resulting in an attenuated reflex control of heart rate, but no hypertension or blood pressure lability.

Adult↗
PubMed2004

Use of lower abdominal compression to combat orthostatic hypotension in patients with autonomic dysfunction.

The aim of this study was to investigate in patients with neurogenic orthostatic hypotension the mechanism and usefulness of abdominal compression to increase standing blood pressure. In three protocols, 23 patients underwent abdominal compression. Protocol 1 evaluated in a 40-60 degrees head-up-tilt position, the effect of abdominal compression on caval vein and femoral diameter, arterial blood pressure and hemodynamics. Protocol 2 documented the relationship between the level of compression and the arterial pressure response. Protocol 3 investigated the ability to maintain standing blood pressure by an elastic binder. During head-up-tilt, compression (40 mm Hg) resulted in a reduction in diameter of the caval vein (mean -2.6mm, range -1.4 to 0.6), without a change in femoral vein diameter. Stroke volume increased by 14 % (range -1 to 23) and blood pressure (systolic/diastolic) by 30/14 mmHg (range 7/2 to 69/36), both p < 0.05; 40 mmHg compression was associated with a higher pressure response than 20 mmHg (mean 18/8 mmHg, range 6/2 to 43/20 vs. mean 9/4 mmHg, range -1/0 to 18/8, p < 0.05). Elastic abdominal binding increased standing blood pressure with 15/6 mmHg (range -3/3 to 36/14, p < 0.05). We conclude that in patients with neurogenic orthostatic hypotension, abdominal compression increases standing blood pressure to a varying degree by increasing stroke volume.

Abdomen↗
PubMed2004

Defining and classifying syncope.

There is no widely adopted definition or classification of syncope and related disorders. This lack of uniformity harms patient care, research, and medical education. In this article, syncope is defined as a form of transient loss of consciousness (TLOC) due to cerebral hypoperfusion. Differences between syncope and other causes of TLOC such as epilepsy, and disorders mimicking TLOC are described. A pathophysiological classification of syncope is proposed.

Diagnosis, Differential↗
PubMed2004

Exercise related syncope, when it's not the heart.

Syncope or pre-syncope in association with physical exercise may be the first indication of a dangerous underlying cardiovascular condition. Thus, the diagnostic workup of patients presenting with exercise-related syncope must include assessment of the risk for acute cardiac death. When potentially lethal conditions have been ruled out, several hypotensive syndromes that are associated with exercise should be considered. This review aims to give a concise overview of several forms of exercise- related functional hypotensive syndromes causing syncope, including the physiology of post-exercise hypotension. The focus is on underlying mechanisms, clinical considerations, and outlining treatment strategies for these syndromes.

Autonomic Nervous System Diseases↗
PubMed2004

Nonpharmacological treatment of reflex syncope.

Reflex syncope is a common medical problem. Vasovagal reflex syncope is the most frequent form. Although the prognosis of the disorder is excellent, it may impose substantial changes in life style and cause profound psychological distress. Thus, management of this disorder is an important issue. This chapter, based on a review of the literature and the authors' clinical experience, encompasses the non-pharmacological measures used in the management of reflex syncope. The cornerstone of the non-pharmacological management of patients with reflex syncope is education and reassurance regarding the benign nature of the condition. Patients should be instructed to avoid potential triggers. A tilt table test can be employed to teach the patient to recognize early premonitory symptoms. There are several physical maneuvers (e. g., leg crossing, muscle tensing and squatting) that are effective in combating orthostatic intolerance. For the majority of patients this approach is adequate. Patients with frequent attacks of reflex syncope are advised to increase their dietary salt intake. Exercise training also increases orthostatic tolerance. In highly motivated patients with recurrent syncope, raising the head of the bed to permit gravitational exposure during sleep and prolonged periods of enforced maintenance of the upright posture (tilt-training) can be considered. Preliminary data suggest that water drinking may improve orthostatic tolerance. Abdominal belts may also be effective in highly symptomatic subjects with reflex syncope.

Abdomen↗
PubMed2004

Syncope: a clinically guided diagnostic algorithm.

The initial evaluation of a patient with syncope should include a thorough clinical history, physical examination and 12 lead electrocardiogram (ECG). The history is the best diagnostic tool. Clinical findings guide further testing. Patients with syncope and heart disease require echocardiography, Holter monitoring or exercise testing. The tilt test and carotid sinus massage are useful to reproduce reflex syncope. An insertable subcutaneous loop recorder can provide prolonged ECG monitoring.

Algorithms↗
PubMed2004

Syncope.

Syncope is a syndrome consisting of a relatively short period of temporary and self-limited loss of consciousness caused by transient diminution of blood flow to the brain (most often the result of systemic hypotension). Syncope comprises part of a subset of clinical conditions in which loss of consciousness is transient. Other conditions in this group, which are not syncope and should be clearly distinguished from syncope, include, for example, seizure disorders, posttraumatic loss of consciousness, and cataplexy. Recent surveys indicate that syncope accounts for approximately 1% of emergency department visits in Europe, although older reports from the United States placed this number closer to 3%. The reported prevalence of syncope in the population varies: 15% of children before the age of 18 years; 25% of a military population aged 17 to 26 years; 16% and 19%, respectively, in men and women aged 40 to 59 years; and up to 23% in a nursing home population older than 70 years. The highest frequency of syncope occurs in patients with cardiovascular comorbidity and older patients in institutional care settings. The causes of syncope are numerous and, not infrequently, multiple factors may contribute. The diagnostic evaluation is benefited by availability of a detailed medical history and reports of eyewitnesses. In this context, the physician must consider the classification of the causes of syncope, and address the most likely causes first. The principal groups of causes may be summarized as: (1) neurally mediated reflex syncope (eg, vasovagal faint, carotid sinus syndrome); (2) orthostatic (postural) syncope; (3) cardiac arrhythmias; (4) structural cardiac and pulmonary causes; and (5) cerebrovascular disorders (rare). In addition, conditions that may mimic syncope but are not true syncope (eg, psychogenic pseudosyncope) must be considered. Only after a definitive cause is established can appropriate treatment be initiated. In this regard, the syncope evaluation is facilitated by maintaining an organized diagnostic approach. The practitioner should avoid wasteful use of short-term ambulatory electrocardiographic recordings (eg, Holter monitors) and rarely positive neurologic tests (eg, electroencephelography, head magnetic resonance imaging/computed tomography) in the absence of head trauma or evident neurologic signs. In many medical centers the evaluation of patients with syncope is haphazard, and may be substantially enhanced by establishment of a multidisciplinary syncope evaluation unit or team.

Diagnosis, Differential↗
PubMed2004

The role of carotid chemoreceptors in the sympathetic activation by adenosine in humans.

The direct vasodilatory and negative chronotropic effects of adenosine in humans are counterbalanced by a reflex increase in sympathetic nerve traffic. A suggested mechanism for this reflex includes peripheral chemoreceptor activation. We, therefore, assessed the contribution of carotid chemoreceptors to sympatho-excitation by adenosine. Muscle sympathetic nerve activity was recorded during adenosine infusion (140 microg.kg(-1).min(-1) for 5 min) in five patients lacking carotid chemoreceptors after bilateral carotid body tumour resection (one male and four female, mean age 51 +/- 11 years) and in six healthy controls (two male and four female, mean age 50 +/- 7 years). Sympathetic responses to sodium nitroprusside injections were assessed to measure baroreceptor-mediated sympathetic activation. In response to adenosine, controls showed no change in blood pressure, an increase in heart rate (+48.2 +/- 13.2%; P<0.003) and an increase in sympathetic nerve activity (+195 +/- 103%; P<0.022). In contrast, patients showed a decrease in blood pressure (-14.6 +/- 4.9/-17.6 +/- 6.0%; P<0.05), an increase in heart rate (+25.3 +/- 8.4%; P<0.032) and no significant change in sympathetic activity. Adenosine-induced hypotension in individual patients elicited less sympathetic activation than equihypotensive sodium nitroprusside injections. In humans lacking carotid chemoreceptors, adenosine infusion elicits hypotension due to the absence of significant sympatho-excitation. Chemoreceptor activation is essential for counterbalancing the direct vasodilation by adenosine. In addition, blunting of the baroreflex sympathetic response to adenosine-induced hypotension may indicate a direct sympatho-inhibitory effect of adenosine.

Adenosine↗
PubMed2004

Cardiovascular responses to stress after carotid baroreceptor denervation in humans.

Iatrogenic bilateral denervation of carotid sinus baroreceptors may occur as a complication of carotid body tumor resection and radiation therapy of the neck. The acute phase of the resulting syndrome of baroreflex failure is characterized by a limited blood pressure buffering capacity against excessive rise or fall in response to emotional and physical stimuli like sexual arousal and cold. Paroxysms of severe hypertension and tachycardia, accompanied by excessive increments in sympathetic tone and catecholamine plasma levels, were ascribed to loss of tonic inhibitory influence of baroreceptors on sympathetic tone. Bilateral anesthetic blockade of baroreceptor afferent nerves was shown to result in a strong increase in muscle sympathetic nerve activity and disruption of its normal patterning. This chapter reviews our findings on the long-term effects of iatrogenic baroreflex trauma on the hemodynamic responses to pharmacological, physical, and emotional stress in the autonomic function laboratory as well as under daily life conditions. Chronic attenuation of baroreflex sensitivity after carotid body tumor resection and neck irradiation results in an increased blood pressure variability. However, unopposed sympathetic activation in response to physical and emotional stress appears to be limited to the acute phase of baroreflex failure.

Carotid Arteries↗
PubMed2003

Denervation of carotid baro- and chemoreceptors in humans.

Experimental denervation in animals has shown that carotid baro- and chemoreceptors play an eminent role in maintaining blood pressure and blood gas homeostasis. Denervation of carotid sinus baro- and chemoreceptors in humans may occur as a complication of invasive interventions on the neck or after experimental surgical treatment in asthma. In this topical review, the short- and long-term effects of carotid baro- and chemoreceptor denervation on the control of circulation and ventilation in humans are discussed. Carotid baroreceptor denervation in humans causes a persistent decrease in vagal and sympathetic baroreflex sensitivity and an increase in blood pressure variability; however, carotid denervation does not lead to chronic hypertension. Therefore, although carotid baroreceptors contribute to short-term blood pressure control, other receptors are able to maintain normal chronic blood pressure levels in the absence of carotid baroreceptors. Conversely, carotid chemoreceptor denervation leads to permanent abolition of normocapnic ventilatory responses to hypoxia and reduced ventilatory responses to hypercapnia.

Animals↗
PubMed2003

Baroreflex control of muscle sympathetic nerve activity after carotid body tumor resection.

Bilateral carotid body tumor resection causes a permanent attenuation of vagal baroreflex sensitivity. We retrospectively examined the effects of bilateral carotid body tumor resection on the baroreflex control of sympathetic nerve traffic. Muscle sympathetic nerve activity was recorded in 5 patients after bilateral carotid body tumor resection (1 man and 4 women, 51+/-11 years) and 6 healthy control subjects (2 men and 4 women, 50+/-7 years). Baroreflex sensitivity was calculated from changes in R-R interval and muscle sympathetic nerve activity in response to bolus injections of phenylephrine and nitroprusside. In addition, sympathetic responses to the Valsalva maneuver and cold pressor test were measured. The integrated neurogram of patients and control subjects contained a similar pattern of pulse synchronous burst of nerve activity. Baroreflex control of both heart rate and sympathetic nerve activity were attenuated in patients as compared with control subjects [heart rate baroreflex sensitivity: 3.68+/-0.93 versus 11.61+/-4.72 ms/mm Hg (phenylephrine, P=0.011) and 2.53+/-1.36 versus 5.82+/-1.94 ms/mm Hg (nitroprusside, P=0.05); sympathetic baroreflex sensitivity: 3.70+/-2.90 versus 7.53+/-4.12 activity/100 beats/mm Hg (phenylephrine, P=0.10) and 3.93+/-4.43 versus 15.27+/-10.03 activity/100 beats/mm Hg (nitroprusside, P=0.028)]. The Valsalva maneuver elicited normal reflex changes in muscle sympathetic nerve activity, whereas heart rate responses were blunted in the patients with bilateral carotid body tumor resection. Maximal sympathetic responses to the cold pressor test did not differ between the two groups. Denervation of carotid sinus baroreceptors as the result of bilateral carotid body tumor resection produces chronic impairment of baroreflex control of both heart rate and sympathetic nerve activity. During the Valsalva maneuver, loss of carotid baroreflex control of heart rate is less well compensated for by the extra carotid baroreceptors than the control of muscle sympathetic nerve activity.

Adult↗
PubMed2003

Baroreflex and chemoreflex function after bilateral carotid body tumor resection.

OBJECTIVE: To investigate whether bilateral carotid body tumor resection invariably and chronically affects arterial baroreflex or peripheral chemoreflex function. METHODS: We studied eight consecutive patients (two men and six women; ages 48.1 +/- 11.8 years), a median time of 3.4 years (range 1.3-20.6 years) after bilateral carotid body tumor resection, and 12 healthy control individuals (eight men and four women; ages 53.7 +/- 10.1 years). Baroreflex sensitivity (phenylephrine), blood pressure and its variability (24 h Spacelabs and 5 h Portapres recordings), responses to standard cardiovascular reflex tests and the ventilatory responses to normocapnic and hypercapnic hypoxia were assessed. RESULTS: Baroreflex sensitivity was lower in patients (6.4 +/- 7.2 ms/mmHg) than in controls (14.7 +/- 6.6 ms/mmHg; P +/- 0.011). Mean office blood pressure and heart rate were normal in patients (123.3 +/- 11.9/79.0 +/- 7.3 mmHg and 67.5 +/- 9.4 beats/min, respectively) and controls (117.8 +/- 10.6/74.0 +/- 6.8 mmHg and 61.1 +/- 9.2 beats/min, respectively). Blood pressure variability was increased during ambulatory measurements. Three patients exhibited orthostatic hypotension. The Valsalva ratio, an index of baroreflex-mediated cardiovagal innervation, was lower in patients (1.4 +/- 0.2) than in controls (1.8 +/- 0.5; P +/- 0.008). The normocapnic ventilatory response to hypoxia was absent in all patients, whereas a small residual response to hypoxia was observed under hypercapnic conditions in two patients. CONCLUSIONS: Bilateral carotid body tumor resection results in heterogeneous expression of arterial baroreflex dysfunction, whereas the normocapnic hypoxic drive is invariably abolished as a result of peripheral chemoreflex failure.

Adult↗