Syncopal Episodes Research Articles

Carotid Sinus Syndrome - Case Report

Abstract Syncope caused by carotid sinus syndrome due to malignancy of the head and neck is rare. The aim of this paper is an inspection into current knowledge of this syndrome, its clinical characteristics, differential diagnosis and current treatment modalities. We present a case of recurrent syncope resulting from extreme bradycardia based on a malignant process in the neck area that compresses the carotid sinus. To discover the cause of syncope, an extensive diagnosis was made including electrocardiography, 24h holter electrocardiography, computed tomography of the neck, biopsy of the lump on the right side of the neck. In order to perform the biopsy, the patient was implanted with a temporary pacemaker. Pathohistological processing of biopsy showed the existence of squamous cell carcinoma of the neck region. Due to localization of the malignant change, surgical resection was contraindicated, so the patient was treated with radiotherapy. Syncope based on carotid sinus hypersensitivity caused by a malignant process of the neck region is a significant diagnostic challenge for any clinician. Neck tumor is rarely thought of, since its frequency is rare in the general population. The disease is mostly recognized in the advanced stages when episodes of syncope are more frequent.

Carotid Sinus Syndrome in a Patient of Nasopharyngeal Carcinoma Treated with Palliative Radiotherapy

Carotid sinus syndrome leading to bradycardia, unconsciousness and eventually cardiac arrest is a rare condition. Its pathophysiology is not fully understood. Here, we present a rare case of a 79-year-old male with left cervical lymph node metastasis originating from primary carcinoma of nasopharynx. He was admitted to hospital with history of recurrent syncopal episodes at home. Paroxysms of extreme bradycardia (Heart rate of < 40) were detected during hospital stay. CT-scan and MRI of neck revealed compression of left neck vasculature. This patient was treated with palliative radiotherapy. He showed favorable response in that he became asymptomatic.

Brugada Syndrome: 30 Years of Scientific Ventures.

Thirty years ago, a distinctly new clinical-electrocardiographic syndrome was described, today known as Brugada Syndrome (BrS). Typical treatment for this type of syndrome is electrocardiography with ST-segment elevation in the direct precordial derivations. The clinical presentation of the disease is highly variable: the patients can remain completely asymptomatic, but they can also develop episodes of syncope, atrial fibrillation (AF), sinus node dysfunction (SNF), conduction disorders, asystole, and ventricular fibrillation (VF). This disease is caused by mutations in the genes responsible for the potential action of cardiac cells. The most commonly involved gene is SCN5A, which controls the structure and function of the heart's sodium channel. The description of this new syndrome has shown highly positive implications in all fields of medicine.

Abstract Number ‐ 76: Bow hunter’s syndrome‐ a rare case of hearing loss associated with co‐dominant vertebral artery compression

Introduction Bow hunter’s syndrome (BHS), also known as rotational vertebral artery syndrome, refers to symptomatic vertebrobasilar insufficiency (VBI) caused by mechanical compression and severe stenosis or occlusion of the vertebral artery (VA) during neck and head rotation. Etiologies include bony spurs and osteophytes, or hypertrophic muscles and ligaments compressing typically on the dominant vertebral artery. Upon turning their head, patients experience posterior circulation symptoms such as vertigo, dizziness, syncope, nausea, tinnitus, or headache. These patients are at risk of stroke due to repetitive mechanical damage to the vessel and thromboembolism. [1] We present a rare case of BHS associated with hearing loss that was caused by bony spurs compressing on a left co‐dominant vertebral artery seen on turning head to both sides. Methods A woman in her 50s presented with sporadic progressive episodes of dizziness which started about 4 years. In addition, she reported experiencing episodic tinnitus in her left ear, frequent headaches, neck pain, and syncopal episodes. She was diagnosed with severe left ear sensorineural hearing loss (SNHL). Vestibular therapy and multiple neuropathic medications (nortriptyline, gabapentin) only provided her with minimal relief. Results Examination showed left SNHL and neck tenderness. X‐ray of cervical spine showed bony hypertrophy adjacent to the dens and inferior to the anterior arch of C1, suggestive of large osteoarthritic bony spurs. CT angiogram showed narrowing of the left vertebral artery at C1 due to severe hypertrophic arthropathy of the lateral mass articulation. It also showed impingement of the left VA in the left transverse foramen. The intradural portion of the VA (V4) appeared to be co‐dominant with normal size. Dynamic cerebral angiogram revealed near occlusion of the left VA at the level of C1‐C2 with head to the right. Left VA remained patent in neutral position, and experienced reduction in flow with head rotation to the left. The dynamic stenosis of VA caused by mechanical compression upon head turn leading to VBI, and reversal of stenosis when rotating head to neutral position was consistent with diagnosis of Bow hunters syndrome. Conclusions This case report highlights a rare presentation of VBI caused by dynamic stenosis of VA as a sequela of mechanical compression of a co‐dominant VA upon head turn to both sides. Only about 2% of the BHS patients experience symptoms during head turn to both sides [2], which was the finding in our patient. Furthermore, this case illustrates an association between BHS and SNHL. Hearing loss is previously described in vertebral artery atresia [3]; however, we present a novel association between acquired BHS and SNHL. Although we could not prove the causality, the coexistence of the two conditions in this patient may help to elicit further clinical consideration and evaluation in patients with SNHL of unknown etiology.

Abstract Number ‐ 103: Revascularization of a Persistently Occluded Left Vertebral Artery with Ongoing Symptoms and Poor Collaterals

Introduction Ischemic stroke presents a significant burden to health globally, with those in the posterior circulation accounting for 20% of all strokes. [1]. Efforts to attempt endovascular revascularization in a chronically occluded vertebral artery is not prevalent but has been increasing abroad. In a single center in China, 22 subjects had attempted revascularization, with successful revascularization was achieved in 86.36% of patients using balloon dilation combined with stenting in 14 subjects. Improving technology and techniques have made these attempts more feasible. Objective: This report demonstrates a unique case of symptomatic vertebral artery revascularization 3 days after the initial onset of vertebral artery occlusion symptoms using balloon angioplasty and stenting in the proximal portion of the left vertebral artery. Methods Case report Results 58‐year‐old man with history of hypertension, hyperlipidemia, and smoking presented to the Wilson Hospital ER with an abrupt onset syncopal episode. He was found crawling on the highway by EMS. Initial workup included MRI and CTA that were consistent with cerebellar strokes, a hypoplastic right vertebral artery, and occlusion of the left vertebral artery. Three days elapsed between recognition of the vertebral pathology and indication of appropriate endovascular intervention and angiography. Angiography revealed an acute occlusion of the left vertebral artery with significant reduction of anterograde flow. Initial blood flow transit time from VAO to left posterior circulation took 6 seconds compared to 2 seconds in the right posterior circulation. Inadequate vertebral collateral flow was appreciated from costocervical cervical trunk branches. An urgent stenting of the left vertebral artery was performed after informed consent from patient. Before the procedure, the patient was prepared with both aspirin (325mg), Plavix (150mg), and IV heparin to achieve 1.5‐2 times the baseline activated clotting time. Angioplasty was performed with a 2.5×20mm Maverick balloon loaded over a choice PT 14 compatible microwire. Integrilin (5mg) was delivered prior to catheterization to reversibly inhibit GPllb/llla. The left vertebral artery was catheterized, and angioplasty was performed two times with balloon inflation at 12 atmospheres. Using fluoroscopic guidance, a drug‐eluting stent measuring 4×22 was placed across stenotic vertebral artery via the existing vertebral wire. In placement, the balloon was inflated up to 10 atmospheric pressures to obtain an intraluminal diameter of 4.0. Post‐procedure angiogram showed that the lesion decreased from a near complete occlusion to less than 10% occlusion. Additionally, post‐procedure transit time was reduced to 2 seconds. Patient was asymptomatic at discharge and was given aspirin (325mg), clopidogrel (75mg), and was recommended to follow‐up after 4–6 weeks Conclusions This case study gives greater support to endovascular intervention in a delayed setting with revascularization with balloon dilation combined with stent implantation on a case‐by‐case basis. Further investigation of inclusion criteria is needed, as this patient was exceptional in collaterals and anatomy.

Progressive Right Ventricular Obstruction Caused by a Double-Chambered Right Ventricle Resulting in Shunt-Reversal via a Concomitant Congenital Ventricular Septal Defect and Subsequent Erythrocytosis in a Dog

A 3-year-old Chihuahua was presented because of exercise intolerance, respiratory distress, and syncopal episodes. At the age of 10 weeks, the dog was diagnosed with a congenital small left-to-right shunting ventricular septal defect and a mild right ventricular outflow tract obstruction via echocardiography. At that time, the dog was asymptomatic, but the breeder's veterinarian heard a murmur. Both cardiac defects were judged to be clinically non-relevant at that time. However, at 3 years of age, echocardiography revealed a severe right ventricular obstruction, known as a double-chambered right ventricle, along with right-to-left shunting via the ventricular septal defect. Because of chronic hypoxemia due to the right-to-left shunting, erythrocytosis developed. Flow reversal via the shunt was caused by a progressively worsening right ventricular obstruction leading to a supra-systemic right ventricular systolic pressure. Because of the poor prognosis, the dog was euthanized, and the heart was submitted for post-mortem examination. Gross pathologic findings revealed the close proximity of the right ventricular obstructive lesion to the ventricular septal defect. Histopathology revealed localized muscular hypertrophy and severe endocardial fibrosis. The suspected pathogenesis of the progressive obstruction was infiltrative myocardial fibrosis due to turbulent blood flow from the left-to-right shunting ventricular septal defect, as described in humans.

Survived 80 seconds of asystole without damage! : Consequences for better Holter diagnostics

A67-year old women suffered multiple syncope episodes during a vacation trip. The emergency 12-lead electrocardiogram revealed a sinusrhythm, AV block I° and left bundle branch block. After admission to the base hospital, a Holter ECG system was implemented. The next morning, the woman collapsed unnoticed. By chance, she was found and stabilized by nurses. The Holter report showed a total AV block over 80 seconds without ventricular replacement rhythm. The patient recovered without neurological damage and got a pacemacer system (DDDR). To the best of our knowledge, this is the longest documented total AV block survived without clinical damage.Conclusion: 1.The emergency 12-lead electrocardiogram (Index ECG) has prognostic power. 2.It is absolutely necessary to integrate alert functions in Holter ECG systems to enable external help in case of threatening arrhythmias.

Riesgo arrítmico en episodios únicos o recurrentes de síncope inexplicado con bloqueo completo de rama

Introduction and objectivesPatients with a single syncopal episode (SSE) and complete bundle branch block (cBBB) are frequently managed more conservatively than patients with recurrent episodes (RSE). The objective of this study was to analyze if there are differences between patients with single or recurrent unexplained syncope and cBBB in arrhythmic risk, the diagnostic yield of tests, and clinical outcomes. MethodsCohort study of consecutive patients with unexplained syncope and cBBB with a median follow-up time of 3 years. The patients were evaluated via a stepwise workup protocol based on electrophysiological study (EPS) and long-term follow-up with an implantable cardiac monitor. ResultsOf the 503 patients included in the study, 238 (47.3%) had had only 1 syncopal episode. The risk of an arrhythmic syncope was similar in both groups (58.8% in SSE vs 57.0% in RSE; P=.68), also after adjustment for possible confounding variables (HR, 1.06; 95%CI, 0.81-1.38; P=.674). No significant differences between the groups were found in the EPS results and implantable cardiac monitor diagnostic yield. A total of 141 (59.2%) patients with SSE and 154 (58.1%) patients with RSE required cardiac device implantation (P=.797). After appropriate treatment, 35 (7%) patients had recurrence of syncope. The recurrence rate and mortality were also similar in both groups. ConclusionsPatients with cBBB and unexplained syncope are at high risk of an arrhythmic etiology, even after the first syncopal episode. Patients with SSE and RSE have a similar arrhythmic risk and similar outcomes, and therefore there is no clinical justification for not managing them in the same manner.Full English text available from:www.revespcardiol.org/en

Multicentre open label randomised controlled trial of immediate enhanced ambulatory ECG monitoring versus standard monitoring in acute unexplained syncope patients: the ASPIRED study

IntroductionDiagnosing underlying arrhythmia in emergency department (ED) syncope patients is difficult. There is a evidence that diagnostic yield for detecting underlying arrhythmia is highest when cardiac monitoring devices are applied...

Male Adolescent With Syncope and Abnormal Chest X-Ray.

A 16-year-old man presented after an episode of syncope and an abnormal chest radiography at an urgent care. He reported chest wall pain after an injury at football practice. On examination, he was awake and alert with reproducible tenderness of the left lateral ribs and a normal cardiac exam. Laboratory study results, including complete blood count, basic metabolic panel, and troponin were at normal levels. The chest radiography (Figure 1) revealed cardiomegaly. After transfer to a tertiary care center, a point-of-care echocardiogram was performed (Figure 2), which prompted pericardiocentesis, and, eventually, magnetic resonance lymphangiography (Figure 3).Figure 2Subxiphoid ultrasound view peering through the liver (†) revealed a large pericardial effusion (#) causing a collapsed right ventricle (∗), surrounded by the pericardium (‡).View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 3Magnetic resonance lymphangiography of the heart (∗) revealed a large, entirely chylous, pericardial effusion (#).View Large Image Figure ViewerDownload Hi-res image Download (PPT) Traumatic chylous pericardial effusion. Pediatric cardiology was consulted, and he ultimately underwent pericardiocentesis and pericardial drain placement. Abundant (>600 mL) milky (chylous) fluid was drained from the pericardium, and he was admitted to investigate the cause. While primary or idiopathic cases exist, chylopericardium is commonly secondary to thoracic duct injury, surgery, neoplasm, or congenital cysts.1Rochefort M.M. Review of chylopericardium.Mediastinum. 2022; 6: 3Crossref PubMed Google Scholar Pericardial fluid triglyceride levels >500 mg/dL is pathognomonic.2Dib C. Tajik A.J. Park S. et al.Chylopericardium in adults: a literature review over the past decade (1996-2006).J Thorac Cardiovasc Surg. 2008; 136: 650-656Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Other findings suggestive of chylopericardium include a milky-white appearance, the cholesterol: triglyceride ratio <1, and fat globules seen with staining.2Dib C. Tajik A.J. Park S. et al.Chylopericardium in adults: a literature review over the past decade (1996-2006).J Thorac Cardiovasc Surg. 2008; 136: 650-656Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Lymphoscintigraphy can confirm an anomalous connection between the thoracic duct and the pericardial space.1Rochefort M.M. Review of chylopericardium.Mediastinum. 2022; 6: 3Crossref PubMed Google Scholar As seen here, in cases of progressive chylous accumulation, patients can develop tamponade physiology requiring a pericardial drain or a window creation.3Akamatsu H. Amano J. Sakamoto T. et al.Primary chylopericardium.Ann Thorac Surg. 1994; 58: 262-266Abstract Full Text PDF PubMed Scopus (65) Google Scholar Management may also include depending surgical thoracic duct obliteration or even diet modifications in very mild chronic cases.4Han Z. Li S. Jing H. et al.Primary idiopathic chylopericardium: a retrospective case series.BMC Surg. 2015; 15: 61Crossref PubMed Scopus (10) Google Scholar This patient underwent lymphatic intervention to obliterate the fistula and was subsequently started on a low-fat diet with minimal recurrence of disease to date.

Tests for the identification of reflex syncope mechanism

ABSTRACT Introduction Treatment efficacy of reflex syncope is mainly related to the mechanism underlying syncope rather than its etiology or clinical presentation. The predominant mechanism underlying reflex syncope can be assigned to hypotensive or to bradycardic phenotypes. Areas covered Methodology and diagnostic criteria of the most useful tests for the identification of hypotensive and bradycardic phenotypes are discussed. Diagnostic tests for the hypotensive phenotype include office blood pressure measurement with active standing test, home, and wearable blood pressure monitoring, 24-h ambulatory blood pressure monitoring and tilt table test. Diagnostic tests for the bradycardic phenotype include carotid sinus massage, tilt table test and prolonged ECG monitoring. Expert opinion In reflex syncope, the documentation of bradycardia/asystole during a syncopal episode does not rule out the possibility that a preceding or parallel hypotensive reflex plays an important role. Similarly, even when a hypotensive mechanism is established, the possibility of an associated cardioinhibitory reflex should be investigated. Investigating the mechanism of reflex syncope is mandatory in patients with severe recurrent episodes, with the final aim to develop a personalized treatment strategy. Recent trials have demonstrated the benefits of personalized mechanism-based therapy, thus highlighting the importance of a comprehensive assessment of the mechanisms underlying syncope.

Correlation between percutaneous patent foramen ovale closure and recurrence of unexplained syncope.

The relationship between patent foramen ovale (PFO) and unexplained syncope remains to be illustrated. Therefore, this study aimed to explore the outcomes and prognostic factors for syncope recurrence after PFO closure. Patients with both large right-to-left shunting (RLS) PFO and unexplained syncope who visited the cardiovascular department of Xiangya Hospital Central South University from 1 January 2017 to 31 December 2021 were consecutively enrolled in our study. The recurrence rate of syncope was compared between the non-closure group (n = 20) and the closure group (n = 91). A total of 111 patients were finally included. After 31.11 ± 14.30 months of follow-up, only 11% of patients in the closure group had recurrent syncope, which was much lower than that of the non-closure group (11.0 vs. 35%, P = 0.018). We further investigated the possible prognostic factors for syncope recurrence in the closure group and found syncope occurring more than five times preoperatively, hypertension, and residual RLS at 12-month follow-up were significantly correlated with a higher number of recurrences. PFO closure reduced the recurrence rate of unexplained syncope. The efficacy of prevention was prognosticated by factors including the presence or absence of syncope induction, the frequency of syncope episodes, and the presence or absence of hypertension. Syncope recurrence was also related to residual shunts post closure.

Successful Clindamycin Therapy of an Infected Subcutaneous Permanent Pacing Lead in a Dog after a Failed Course with Potentiated Amoxicillin and Enrofloxacin

Though permanent pacemaker implantation is the only effective therapy for certain bradyarrhythmias in dogs, it is not without risks. Bacterial infection of the device is one of the most common complications. Human guidelines recommend besides systemic antibiotics, surgical explantation of the pacing lead and pulse generator in case of device-infection. This report describes a 13.5-year-old dog that received a transvenous endocardial permanent pacemaker because of syncopal episodes resulting from paroxysmal third-degree atrio-ventricular block. Five days after an uneventful surgery, a painful swelling appeared around the subcutaneous part of the lead where this was inserted into the jugular vein. A 4-week course of amoxicillin and clavulanic acid combined with enrofloxacin failed to clear the infection on long-term. Ultrasound-guided puncture of the abscess was performed to gain a sample for bacterial culture and antibiogram. Oral clindamycin of 4 weeks' duration successfully resolved the infection with Staphylococcus aureus without having to explant the device. Repeated ultrasonographic examinations and fine-needle aspiration biopsies were used to evaluate for persistent local inflammation, guiding the length of the antibiotic therapy. Though the described approach has traditionally been ill-advised because of the risk of introducing bacteria and damaging the pacemaker lead, it was successful in our case.

A methodology for the public health surveillance and epidemiologic analysis of outdoor falls that require an emergency medical services response

BackgroundFalls are a common cause of injury with significantly associated medical costs yet public health surveillance of injuries from falls is underdeveloped. In addition, the epidemiologic understanding of outdoor falls, which have been reported to account for 47% of all injurious falls, is scant. Here we present methods to use emergency medical services (EMS) data as a public health surveillance tool for fall injuries, including those that occur secondary to syncope and heat illness, with a focus on the scope and epidemiology of outdoor fall injuries.MethodsUsing the 2019 National Emergency Medical Services Information System (NEMSIS) data, we developed an approach to identify EMS encounters for fall injuries, syncope and heat illness. NEMSIS variables used in our algorithm included the EMS respondent’s impression of the encounter, the reported major symptoms and the cause of injury. With these data we identified injuries from falls and, using the NEMSIS data on the location of the encounter, we identified fall injuries as occurring indoors or outdoors. We present the descriptive epidemiology of the identified patients.ResultsThere were 1,854,909 injuries from falls that required an EMS response identified in the NEMSIS data, with 4% of those injuries secondary to episodes of syncope (n = 73,126) and heat illness. Sufficient data were available from 94% of injurious falls that they could be assigned to indoor or outdoor locations, with 9% of these fall injuries occurring outdoors. Among fall injuries identified as occurring outdoors, 85% occurred on streets and sidewalks. Patient age was the primary sociodemographic characteristic that varied by location of the injurious fall. Sixty-six percent of fall injuries that occurred indoors were among those age 65 years or older, while this figure was 34% for fall injuries occurring outdoors on a street or sidewalk.ConclusionThe occurrence of outdoor fall injuries identified in the NEMSIS data were substantially lower than reported in other data sets. However, numerically fall injuries occurring outdoors represent a substantial public health burden. The strengths and weaknesses of using this approach for routine public health surveillance of injuries from falls, syncope and heat illness are discussed.

Giant intrapericardial lipoma: Clinical and forensic implications

Introduction. Even though lipomas are the most common benign tumors, they are rarely found in the pericardial cavity. Although histopathologically benign, they can cause life-threatening complications by rapid growth and may there-fore be clinically considered malignant. Case report. We present an 80-year-old female who was injured during a syncopal episode when falling from a standing height and suffered bodily injuries for which she was hospitalized. In the further course of her short-term hospital treatment, death occurred, and the cause of death was marked as ?un-known?. At the autopsy, a dilated and tense pericardium filling up a large part of the chest cavity was noted. A well-encapsulated soft tissue mass, 2 0 ? 1 8 ? 3 cm in size, weighing 820 g, was visualized in the pericardial cavity. Histopathological examination revealed that the mass was a lipoma and showed acute myocardial necrosis; therefore, it was assumed that the cause of death was probably due to the compression of lipoma on coronary arteries. Conclusion. Even though intrapericardial lipomas are benign tumors, they can cause life-threatening complications and sudden cardiac death. There are numerous diagnostic methods capable of detecting intrapericardial lipomas, and with timely treatment, the patient can be cured.

Acute Esophageal Necrosis Presenting as Acute Blood Loss Anemia

An elderly male with coronary artery disease as well as atrial fibrillation on rivaroxaban presented following a syncopal episode. Workup revealed acute non–ST-elevation myocardial infarction. Aspirin and clopidogrel were administered followed by coronary angiography. Twelve hours after his procedure, he developed delirium, fever, tachycardia, and hypotension. Urgent chest computed tomography revealed acute subsegmental pulmonary emboli for which heparin drip was initiated. Empiric antibiotics were also started due to concern for sepsis; ultimately, no infectious source was identified.

JS-NG-8: CASE REPORT: POSSIBLE NEW CHANNELOPATHY ASSOCIATED WITH ELEVATED ALDOSTERONE LEVELS

Background: Potassium channelopathies are associated with prolonged QT cardiac syndrome. New potassium channelopathies in somatic cells, including KCNJ5 mutations, also underlie some forms of primary hyperaldosteronism. We present a first-in-human report of an association between a KCNQ1 loss of function mutation manifesting with life threatening-ventricular tachycardia (VT), severe hypokalemia and presumed hyperaldosteronism. Case Presentation: The patient is a 51-year-old Asian woman known for obesity, Wolff-Parkinson-White post ablation, and recurrent syncopal episodes with polymorphic VT due to prolonged QTc, requiring an implantable cardioverter defibrillator. On initial presentation for syncope, spontaneous hypokalemia was discovered at 3.1 mmol/L. She had multiple hospitalizations for torsade storms and persistent hypokalemia resistant to aggressive potassium supplementation until addition of spironolactone. Investigations revealed a suppressed plasma renin activity &lt; 0.05 ng/L/s, serum aldosterone concentration at 302 pmol/L, and an aldosterone to renin ratio (ARR) &gt; 6040. Repeated ARR was &gt; 10980. Confirmatory saline suppression testing or adrenal vein sampling were not performed due to risk of recurrent VT associated with spironolactone cessation. A comprehensive evaluation for the etiology of this patient's clinical presentation revealed a mutation in the KCNQ1 gene type 1. Literature review: The voltage-dependent K(+) channel responsible for activating delayed K(+) current is composed of pore-forming KCNQ1 and regulatory KCNE1/3 subunits which loss of function predispose to sustained torsade de pointes. Animal models demonstrate that KCNQ1 and KCNE1 mRNAs are expressed in the zona glomerulosa of adrenal glands where potassium channels directly participate in the control of aldosterone production. Although KCNE3 is not expressed in mouse adrenals, its deletion is thought to cause activation of lymphocytes targeting adrenal glands, leading to hyperaldosteronism. Furthermore, administration of spironolactone to KCNE3 knockout mice ameliorates their QT prolongation and predisposition to VT. There have been no case reports of an association between KCNQ1/E1/E3 loss of function and hyperaldosteronism in humans. Conclusion: This raises the question if this mechanism can also be a component of human KCNQ1 and KCNE1/3-linked arrhythmogenesis and hyperaldosteronism. Alternatively, we can further speculate that patients with hyperaldosteronism who develop malignant arrhythmias during hypokalemia are subjects with impaired repolarization reserve as a consequence of variants in genes known to cause long QT syndrome. The variants, leading to subclinical ion channel dysfunction, are typically silent until unmasked by electrolytes abnormalities such as hypokalemia. To our knowledge, this case is a first report of a potentially novel channelopathy associated with hyperaldosteronism in humans. These findings are hypothesis generating and require further investigations.

Human granulocytic anaplasmosis complicated by hemophagocytic syndrome and coinfection.

KEY POINTS A 74-year-old man with end-stage renal disease was admitted to hospital in the spring after an episode of syncope that occurred during a hemodialysis session 1 day after he returned from his cottage in eastern Ontario. Within 24 hours of admission, he developed a fever (38.6°C) and

Arrhythmic risk in single or recurrent episodes of unexplained syncope with complete bundle branch block

Introduction and objectivesPatients with a single syncopal episode (SSE) and complete bundle branch block (cBBB) are frequently managed more conservatively than patients with recurrent episodes (RSE). The objective of this study was to analyze if there are differences between patients with single or recurrent unexplained syncope and cBBB in arrhythmic risk, the diagnostic yield of tests, and clinical outcomes. MethodsCohort study of consecutive patients with unexplained syncope and cBBB with a median follow-up time of 3 years. The patients were evaluated via a stepwise workup protocol based on electrophysiological study (EPS) and long-term follow-up with an implantable cardiac monitor. ResultsOf the 503 patients included in the study, 238 (47.3%) had had only 1 syncopal episode. The risk of an arrhythmic syncope was similar in both groups (58.8% in SSE vs 57.0% in RSE; P=.68), also after adjustment for possible confounding variables (HR, 1.06; 95%CI, 0.81-1.38; P=.674). No significant differences between the groups were found in the EPS results and implantable cardiac monitor diagnostic yield. A total of 141 (59.2%) patients with SSE and 154 (58.1%) patients with RSE required cardiac device implantation (P=.797). After appropriate treatment, 35 (7%) patients had recurrence of syncope. The recurrence rate and mortality were also similar in both groups. ConclusionsPatients with cBBB and unexplained syncope are at high risk of an arrhythmic etiology, even after the first syncopal episode. Patients with SSE and RSE have a similar arrhythmic risk and similar outcomes, and therefore there is no clinical justification for not managing them in the same manner.

946 TAKOTSUBO SYNDROME TRIGGERED BY REFLEX SYNCOPE: A POTENTIALLY FATAL COMPLICATION OF A BENIGN CONDITION

Abstract Introduction Vasovagal syncope is traditionally considered a benign condition due to parasympathetic nervous system activation. Here is a case of reflex syncopal episodes that triggered recurrent Takotsubo Syndrome (TS) with life–threatening presentation. Report of a Case A 71-year-old female presented to the Emergency Department (ED) complaining with dyspnoea and chest pain developed half an hour after a vasovagal syncope. Her past medical history was consistent with arterial hypertension, dyslipidaemia, and well-tolerated reflex syncopal episodes since she was a child. At hospital admission, a 12-leads ECG showed T-wave inversion in anterior leads while transthoracic echocardiogram (TTE) showed hypokinesia of the mid-apical segments, reduced left ventricular ejection fraction (LVEF) [40%], and severe mitral regurgitation (MR). Blood tests revealed increased hs-troponin I values [peak value: 1500 ng/L]. A coronary angiography (CA) was thus performed in the suspect of NSTEMI, showing non obstructive coronary disease. A diagnosis of TS was eventually made with ECG normalisation and resolution of echocardiographic abnormalities at 6 month follow-up. Five years later, the patients presented to the ED because of a new syncopal episode followed by severe pulmonary oedema. Since the presence of electrocardiographic T-wave inversion, apical segments akinesia and elevated hs-troponin I were consistent with NSTEMI, a CA was performed revealing (again!) normal coronary vessels. A suspect of TS relapse was thus made. Three months after discharge, ECG and echocardiogram were normal and a syncope diagnostic work–up was suggested. A 24/h ambulatory blood pressure monitoring demonstrated normal pressure values and a tilt test confirmed the well-established history of reflex syncope showing a remarkable cardioinhibitory response. A pacemaker implant was thus indicated. Discussion TS is a heart syndrome characterized by transient contractile dysfunction historically related to catecholamine activation of alpha and beta receptors. While sympathetic system involvement in the development of TS is clearly established, new evidence is emerging about the vagal role in the etiopathogenesis of the disease. Although syncopal episodes could be related to TS, because of LVOT obstruction or major arrhythmias, according to our experience, TS may be triggered by vagal hypertonus [i.e., after vasovagal syncopal episodes]. In similar situation, the implantation of a pace-maker could be considered to prevent future dangerous complications related to recurrent reflex syncope even if well tolerated by the patients. Conclusion In our experience, recurrent episodes of TS appeared triggered by reflex syncope. A condition traditionally considered benign may instead have life-threatening consequences. Moreover, the role of parasympathetic and vagal tone in the development of TS needs further investigation that may lead to the design of new strategies of clinical diagnosis and management.