A syncope collared / A "nyakon fogott" syncope esete

Carotid sinus syncope is a temporary, exaggerated circulatory response to carotid massage, characterized by marked drop in arterial pressure, and varying degree of bradycardia, or even asystole lasting for several seconds, resulting in short lasting loss of consciousness. A related reflex mediated disorder is a fainting precipitated by a parapharyngeal space-occupying lesion, manifests in prolonged episodes of hemodynamic instability. We report a case, where the hemodynamic features of the syncope are well documented. The case illustrates the potential overlap between pulseless electrical activity and syncope, and a simple noninvasive solution for the frightening symptoms is also suggested.

Left hemispheric cortical watershed infarcts triggered by carotid sinus self-massage.

A 69-year-old man was presented to our emergency department with acute onset of hemianopsia, aphasia and dizziness. He reported that while he was sitting in front of his computer at home, he had performed a bilateral self-massage of his carotid arteries when suddenly the symptoms occurred. A neurological examination revealed a hemianopsia with a visual field loss on the right side. In addition, a mild aphasic syndrome with agraphia and a word-finding disorder (National Institutes of Health Stroke Scale (NIHSS): 3 points) was diagnosed. The initial brain CT scan with CT angiography showed neither an intracerebral haemorrhage nor a cerebral infarction. Also, no occlusion or any signs of artery dissection or a flow relevant stenosis of the brain supplying arteries were found. After excluding other contraindications, an intravenous thrombolysis with weight-adapted alteplase was performed. The symptoms of the patient significantly improved in the short-term follow-up. Three days after admission no neurological deficits remained. The MRI of the brain revealed multifocal, small, left hemispherical strokes in the middle cerebral artery territory. In general, watershed infarcts after carotid sinus self-massage follow a rare ischaemic stroke mechanism. This case emphasises the importance of a detailed anamnestic evaluation to determine the aetiological classification of ischaemic stroke as well as educating patients' (poststroke) behaviour.

Ischemic stroke secondary to self-inflicted carotid sinus massage: a case report.

BACKGROUND: The risk of stroke after carotid sinus massage is greater if there is preexisting carotid stenosis or carotid plaques. We present the case of a patient with underlying 40% carotid stenosis, who developed a watershed stroke after a self-neck massage in our stroke unit. We show a well-documented case with magnetic resonance images before and after the neck massage. We report a case of a watershed brain infarct after a self-massage of the carotid sinus, with preexisting carotid artery stenosis. Neck massage continues to be a significant cause of stroke and should therefore not be performed by patients. Clinicians must be aware of the implications of a carotid sinus massage in both the outpatient and inpatient settings. CASE PRESENTATION: We admitted a 58-year-old white male patient, with no relevant medical history, to our department with a brain stem infarct. During his stay at our stroke unit, the patient performed a self-neck massage with consecutive bradycardia and asystole, resulting in left-side hemiparesis. The underlying cause of the hemodynamic stroke is believed to be secondary to this intensive neck massage performed by the patient. The patient also suffered from unknown right internal carotid artery stenosis. CONCLUSION: Clinicians and patients must be aware that neck massage can lead to ischemic stroke. We postulate that repetitive impaired cardiac output can lead to a hemodynamic (watershed-type) stroke.

Electrostimulation of the carotid sinus nerve in mice attenuates inflammation via glucocorticoid receptor on myeloid immune cells.

BACKGROUND: The carotid bodies and baroreceptors are sensors capable of detecting various physiological parameters that signal to the brain via the afferent carotid sinus nerve for physiological adjustment by efferent pathways. Because receptors for inflammatory mediators are expressed by these sensors, we and others have hypothesised they could detect changes in pro-inflammatory cytokine blood levels and eventually trigger an anti-inflammatory reflex. METHODS: To test this hypothesis, we surgically isolated the carotid sinus nerve and implanted an electrode, which could deliver an electrical stimulation package prior and following a lipopolysaccharide injection. Subsequently, 90 min later, blood was extracted, and cytokine levels were analysed. RESULTS: Here, we found that carotid sinus nerve electrical stimulation inhibited lipopolysaccharide-induced tumour necrosis factor production in both anaesthetised and non-anaesthetised conscious mice. The anti-inflammatory effect of carotid sinus nerve electrical stimulation was so potent that it protected conscious mice from endotoxaemic shock-induced death. In contrast to the mechanisms underlying the well-described vagal anti-inflammatory reflex, this phenomenon does not depend on signalling through the autonomic nervous system. Rather, the inhibition of lipopolysaccharide-induced tumour necrosis factor production by carotid sinus nerve electrical stimulation is abolished by surgical removal of the adrenal glands, by treatment with the glucocorticoid receptor antagonist mifepristone or by genetic inactivation of the glucocorticoid gene in myeloid cells. Further, carotid sinus nerve electrical stimulation increases the spontaneous discharge activity of the hypothalamic paraventricular nucleus leading to enhanced production of corticosterone. CONCLUSION: Carotid sinus nerve electrostimulation attenuates inflammation and protects against lipopolysaccharide-induced endotoxaemic shock via increased corticosterone acting on the glucocorticoid receptor of myeloid immune cells. These results provide a rationale for the use of carotid sinus nerve electrostimulation as a therapeutic approach for immune-mediated inflammatory diseases.

Carotid sinus nerve stimulation attenuates alveolar bone loss and inflammation in experimental periodontitis.

Baroreceptor and chemoreceptor reflexes modulate inflammatory responses. However, whether these reflexes attenuate periodontal diseases has been poorly examined. Thus, the present study determined the effects of electrical activation of the carotid sinus nerve (CSN) in rats with periodontitis. We hypothesized that activation of the baro and chemoreflexes attenuates alveolar bone loss and the associated inflammatory processes. Electrodes were implanted around the CSN, and bilateral ligation of the first mandibular molar was performed to, respectively, stimulate the CNS and induce periodontitis. The CSN was stimulated daily for 10 min, during nine days, in unanesthetized animals. On the eighth day, a catheter was inserted into the left femoral artery and, in the next day, the arterial pressure was recorded. Effectiveness of the CNS electrical stimulation was confirmed by hypotensive responses, which was followed by the collection of a blood sample, gingival tissue, and jaw. Long-term (9 days) electrical stimulation of the CSN attenuated bone loss and the histological damage around the first molar. In addition, the CSN stimulation also reduced the gingival and plasma pro-inflammatory cytokines induced by periodontitis. Thus, CSN stimulation has a protective effect on the development of periodontal disease mitigating alveolar bone loss and inflammatory processes.

Complementary effectiveness of carotid sinus massage and tilt testing for the diagnosis of reflex syncope in patients older than 40 years: a cohort study.

AIMS: Indications, methodology, and diagnostic criteria for carotid sinus massage (CSM) and tilt testing (TT) have been standardized by the 2018 Guidelines on Syncope of the European Society of Cardiology. Aim of this study was to assess their effectiveness in a large cohort which reflects the performance under 'real-world' conditions. METHODS AND RESULTS: We analysed all patients who had undergone CSM and TT in the years 2003-2019 for suspected reflex syncope. Carotid sinus massage was performed according to the 'Method of Symptoms'. Tilt testing was performed according to the 'Italian protocol' which consists of a passive phase followed by a sublingual nitroglycerine phase. For both tests, positive test was defined as reproduction of spontaneous symptoms in the presence of bradycardia and/or hypotension. Among 3293 patients (mean age 73 ± 12 years, 48% males), 2019 (61%) had at least one test positive. A bradycardic phenotype was found in 420 patients (13%); of these, 60% were identified by CSM, 37% by TT, and 3% had both test positive. A hypotensive phenotype was found in 1733 patients (53%); of these, 98% were identified by TT and 2% had both TT and CSM positive. CONCLUSION: The overall diagnostic yield of the tests in patients >40-year-old with suspected reflex syncope was 61%. Both CSM and TT are useful for identifying those patients with a bradycardic phenotype, whereas CSM has a limited value for identifying the hypotensive phenotype. Since the overlap of responses between tests is minimal, both CSM and TT should be performed in every patient over 40 years receiving investigation for unexplained but possible reflex syncope.

Supraventricular tachydysrhythmias in the emergency department.

Diagnosing and treating supraventricular tachycardias is routine in emergency medicine, and new strategies can improve efficiency and outcomes. This review provides an overview of supraventricular tachycardias, their pathophysiology, differential diagnosis, and electrocardiographic features. Clinical evidence guiding contemporary practice is determined largely by multiple observational studies, with few randomized controlled trials. Current prehospital and emergency department management strategies beyond the use of adenosine and calcium channel blockers are addressed. Diagnostic and therapeutic recommendations are provided, based on the best available evidence.

Implant-Mediated Therapy of Arterial Hypertension.

PURPOSE OF REVIEW: To give an overview on recent developments in permanent implant-based therapy of resistant hypertension. RECENT FINDINGS: The American Heart Association (AHA) recently updated their guidelines to treat high blood pressure (BP). As elevated BP now is defined as a systolic BP above 120 mmHg, the prevalence of hypertension in the USA has increased from 32% (old definition of hypertension) to 46%. In the past years, device- and implant-mediated therapies have evolved and extensively studied in various patient populations. Despite an initial drawback in a randomized controlled trial (RCT) of bilateral carotid sinus stimulation (CSS), new and less invasive and unilateral systems for baroreflex activation therapy (BAT) with the BAROSTIM NEO® have been developed which show promising results in small non-randomized controlled (RCT) studies. Selective vagal nerve stimulation (VNS) has been successfully evaluated in rodents, but has not yet been tested in humans. A new endovascular approach to reshape the carotid sinus to lower BP (MobiusHD™) has been introduced (baroreflex amplification therapy) with favorable results in non-RCT trials. However, long-term results are not yet available for this treatment option. A specific subgroup of patients, those with indication for a 2-chamber cardiac pacemaker, may benefit from a new stimulation paradigm which reduces the AV latency and therefore limits the filling time of the left ventricle. The most invasive approach for resistant hypertension still is the neuromodulation by deep brain stimulation (DBS), which has been shown to significantly lower BP in single cases. Implant-mediated therapy remains a promising approach for the treatment of resistant hypertension. Due to their invasiveness, such treatment options must prove superiority over conventional therapies with regard to safety and efficacy before they can be generally offered to a wider patient population. Overall, BAROSTIM NEO® and MobiusHD™, for which large RCTs will soon be available, are likely to meet those criteria and may represent the first implant-mediated therapeutical options for hypertension, while the use of DBS probably will be reserved for individual cases. The utility of VNS awaits appropriate assessment.

Efficacy of Electrical Baroreflex Activation Is Independent of Peripheral Chemoreceptor Modulation.

Arterial baroreflex activation through electrical carotid sinus stimulation has been developed for the treatment of resistant hypertension. Previous studies suggested that the peripheral chemoreflex is tonically active in hypertensive patients and may inhibit baroreflex responses. We hypothesized that peripheral chemoreflex activation attenuates baroreflex efficacy evoked by electrical carotid sinus stimulation. We screened 35 patients with an implanted electrical carotid sinus stimulator. Of those, 11 patients with consistent acute depressor response were selected (7 men/4 women, age: 67±8 years, body mass index: 31.6±5.2 kg/m2, 6±2 antihypertensive drug classes). We assessed responses to electrical baroreflex stimulation during normoxia, isocapnic hypoxia (SpO2: 79.0±1.5%), and hyperoxia (40% end-tidal O2 fraction) by measuring heart rate, blood pressure, ventilation, oxygen saturation, end-tidal CO2 and O2 fractions, and muscle sympathetic nerve activity. During normoxia, baroreflex activation reduced systolic blood pressure from 164±27 to 151±25 mm Hg (mean±SD, P<0.001), heart rate from 64±13 to 61±13 bpm (P=0.002), and muscle sympathetic nerve activity from 42±12 to 36±12 bursts/min (P=0.004). Hypoxia increased systolic blood pressure 8±12 mm Hg (P=0.057), heart rate 10±6 bpm (P<0.001), muscle sympathetic nerve activity 7±7 bursts/min (P=0.031), and ventilation 10±7 L/min (P=0.002). However, responses to electrical carotid sinus stimulation did not differ between hypoxic and hyperoxic conditions: systolic blood pressure: -15±7 versus -14±8 mm Hg (P=0.938), heart rate: -2±3 versus -2±2 bpm (P=0.701), and muscle sympathetic nerve activity: -6±4 versus -4±3 bursts/min (P=0.531). We conclude that moderate peripheral chemoreflex activation does not attenuate acute responses to electrical baroreflex activation therapy in patients with resistant hypertension. These patients provided insight into human baroreflex-chemoreflex interactions that could not be gained otherwise.

Carotid baroreceptor stimulation in obese rats affects white and brown adipose tissues differently in metabolic protection.

The sympathetic nervous system (SNS) regulates the functions of white adipose tissue (WAT) and brown adipose tissue (BAT) tightly. Carotid baroreceptor stimulation (CBS) efficiently inhibits SNS activation. We hypothesized that CBS would protect against obesity. We administered CBS to obese rats and measured sympathetic and AMP-activated protein kinase (AMPK)/ PPAR pathway responses as well as changes in perirenal WAT (PWAT), epididymal WAT (EWAT), and interscapular BAT (IBAT). CBS alleviated obesity-related metabolic changes, improving insulin resistance; reducing adipocyte hypertrophy, body weight, and adipose tissue weights; and decreasing norepinephrine but increasing acetylcholine in plasma, PWAT, EWAT, and IBAT. CBS also downregulated fatty acid translocase (CD36), fatty acid transport protein (FATP), phosphorylated and total hormone sensitive lipase, phosphorylated and total protein kinase A, and PPARγ in obese rats. Simultaneously, CBS upregulated phosphorylated adipose triglyceride lipase, phosphorylated and total AMPK, and PPARα in PWAT, EWAT, and IBAT. However, BAT and WAT responses differed; although many responses were more sensitive in IBAT, responses of CD36, FATP, and PPARγ were more sensitive in PWAT and EWAT. Overall, CBS decreased chronically activated SNS and ameliorated obesity-related metabolic disorders by regulating the AMPK/PPARα/γ pathway.

Magnetic stimulation of carotid sinus as a treatment for hypertension.

Previously, we reported that magnetic stimulation of carotid sinus (MSCS) could lower arterial pressure in rabbits. In this randomized, sham-controlled pilot study, we evaluated the effects of MSCS on blood pressure in pre-hypertensive and hypertensive subjects. A total of 15 subjects with blood pressure higher than 130/80 mm Hg were randomized to receive sham or 1Hz MSCS. The changes of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MAP) during treatment were compared between groups. The heart rate variability (HRV) and baroreflex sensitivity (BRS) before, during, and after treatments were analyzed. Reduction of SBP was significantly greater in subjects with MSCS than those with sham stimulation (6.6 ± 0.4 vs -2.5 ± 0.4 mm Hg, P < 0.001). Reduction of DBP was significantly greater in subjects with MSCS than those with sham stimulation (1.2 ± 0.2 vs -2.8 ± 0.2 mm Hg, P < 0.001). Reduction of MAP was significantly greater in subjects with MSCS than those with sham stimulation (1.4 ± 0.3 mm Hg vs -4.0 ± 0.3 mm Hg, P < 0.001). Reduction of HR was significantly greater in subjects with MSCS than those with sham stimulation (0.5 ± 0.5 vs -1.9 ± 0.3 beats/min, P = 0.002). BRS increased from 6.85 ± 0.77 to 8.79 ± 0.95 ms/mm Hg after MSCS compared with that at baseline (P = 0.027). Thus, MSCS can lower blood pressure and heart rate in pre-hypertensive and hypertensive subject, warranting further study for establishing MSCS as a treatment for hypertension.

Pilot study for a novel delta carotid sinus massage in increasing parasympathetic tone: a randomized, prospective, cross-over, comparative study with conventional method

OBJECTIVE: This study examined the efficacy of new delta carotid sinus massage (CSM) versus conventional CSM (CM). METHODS: This prospective, cross-over study was conducted on 26 healthy volunteers with a normal sinus rhythm. CM and delta CSM (DM) were performed in all participants. In both cases, the CSM was performed, where the maximal carotid pulse was palpated. DM differed from CM in that the physician moves the palpating finger in the opposite direction of the carotid pulse at least twice. The mean and longest R-R intervals and mean and lowest heart rates (HRs) at the baseline and during the procedure for each technique were compared. The mean differences between the baseline and procedure R-R intervals and the HRs for each technique were also evaluated. RESULTS: The baseline mean and longest R-R intervals and baseline mean and lowest HRs were similar both groups (P>0.05). The procedure DM mean and longest R-R intervals (22.7±3.1, 26.4±4.9) were significantly greater than the CM corresponding values (22.0±3.1, 24.6±3.5; P<0.001, P=0.003). Procedure DM mean and lowest HRs (67.3±9.7, 58.6±10.7) were significantly lower than the CM corresponding values (69.4±10.0, 61.8±8.9; P=0.001, P=0.003). The differences in the R-R interval and HR between the procedure and baseline were significant (mean and longest R-R intervals with CM [1.3±1.5 and 2.1±1.9] vs. DM [2.0±1.4 and 3.8±3.1], P<0.001, P=0.004; mean and lowest HRs with CM [4.2±4.3 and 5.8±4.6] vs. DM [6.3±4.6 and 9.1±6.5], P<0.001, P=0.005). CONCLUSION: DM is more effective in generating a more potent vagal tone than CM.

Usefulness of Tilt Testing and Carotid Sinus Massage for Evaluating Reflex Syncope.

Thirty years ago Tilt Testing (TT) was described as a tool in the diagnostic work-up of vasovagal syncope; after its initial success, some flaws have become evident. The concept of hypotensive susceptibility has provided the test a new relevance, shifting from diagnosis only, to therapeutic management. Carotid Sinus Massage (CSM) was introduced at the beginning of the XX century; the technique has evolved over years, whereas the concept of carotid sinus syndrome (CSS) has remained unchanged and uncontested for more than half a century. Nowadays, CSS is a matter of debate, with new classifications and criteria coming on the scene. Recently, a common central etiological mechanism has been hypothesized for reflex syncope, manifesting as CSS, vasovagal syncope or both. In this context, TT and CSM acquire an important role in clinical practice, being essential for a complete diagnosis and treatment. Recalling their historical background, the present paper illustrates an actual interpretation of TT and CSM.