Presyncopal Attacks Research Articles

A Wolff- Parkinson- White Surprise Case

37-year-old-gentleman, who was presented in three occasional times to emergency department for a fast, precordial, and rhythmic symptomatic palpitations, in which the last episode was with a duration that lasted more than an hour with instability vitally that ended in performing emergency electrical cardioversion. All these episodes were symptomatic and last hospitalization was associated with pre syncopal and syncopal attacks. With evidence of Wolff-Parkinson-White syndrome the patient was brought to Electrophysiology Lab to EP study and ablation.

Prevalence of Operation Room‐Related Syncope and Presyncope among Medical Students

Attending the operation room is an essential part of surgical clerkships. Syncope or presyncopal attacks in the operation room may negatively affect students’ learning and career development. This study set out to identify the prevalence of syncope and presyncopal attacks in the operation room during medical students’ surgical clerkships. Data from 420 medical students (303 men and 117 women) in their 3rd year of clerkship were collected between 2014 and 2017. An anonymous questionnaire was distributed to assess the prevalence and degree of syncope and presyncopal symptoms. A total of 27% of the respondents had experienced syncope or presyncopal symptoms, 49.6% of the female students and 18.8% of the male students (p

Novel Genetic Variants in BAG3 and TNNT2 in a Swedish Family with a History of Dilated Cardiomyopathy and Sudden Cardiac Death

Familial dilated cardiomyopathy is a rare cause of dilated cardiomyopathy (DCM), especially in childhood. Our aim was to describe the clinical course and the genetic variants in a family where the proband was a four-month-old infant presenting with respiratory problems due to DCM. In the family, there was a strong family history of DCM and sudden cardiac death in four generations. DNA was analyzed initially from the deceased girl using next-generation sequencing including 50 genes involved in cardiomyopathy. A cascade family screening was performed in the family after identification of the TNNT2 and the BAG3 variants in the proband. The first-degree relatives underwent clinical examination including biochemistry panel, cardiac ultrasound, Holter ECG, exercise stress test, and targeted genetic testing. The index patient presented with advanced DCM. After a severe clinical course, the baby had external left ventricular assist as a bridge to heart transplantation. 1.5 months after transplantation, the baby suffered sudden cardiac death (SCD) despite maximal treatment in the pediatric intensive care unit. The patient was shown to carry two heterozygous genetic variants in the TNNT2 gene [TNNT2 c.518G>A(p.Arg173Gln)] and BAG3 [BAG3 c.785C>T(p.Ala262Val)]. Two of the screened individuals (two females) appeared to carry both the familial variants. All the individuals carrying the TNNT2 variant presented with DCM, the two adult patients had mild or moderate symptoms of heart failure and reported palpitations but no syncope or presyncopal attacks prior to the genetic diagnosis. The female carriers of TNNT2 and BAG3 variants had more advanced DCM. In the family history, there were three additional cases of SCD due to DCM, diagnosed by autopsy, but no genetic analysis was possible in these cases. Our findings suggest that the variants in TNNT2 and BAG3 are associated with a high propensity to life-threatening cardiomyopathy presenting from childhood and young adulthood.

Novel Mutation in the KCNJ2 Gene Is Associated with a Malignant Arrhythmic Phenotype of Andersen‐Tawil Syndrome

Andersen-Tawil syndrome (ATS) is a rare inherited multisystem disorder associated with mutations in KCNJ2 and low prevalence of life-threatening ventricular arrhythmias. Our aim was to describe the clinical course of ATS in a family, in which the proband survived aborted cardiac arrest (ACA) and genetic screening revealed a previously unknown mutation (c.271_282del12[p.Ala91_Leu94del]) in the KCNJ2 gene. A cascade family screening was performed in a 5-generation family after identification of the KCNJ2 mutation in the proband. Subsequently, 10 of 21 screened individuals appeared to be mutation carriers (median age 38 [range 10-75] years, 3 female). Mutation carriers underwent clinical examination including biochemistry panel, cardiac ultrasound, Holter ECG, and exercise stress test. (1) At baseline, 2 patients had survived ACA, 3 had syncope or presyncopal attacks, and 2 reported palpitations. Exercise-induced nonsustained bidirectional ventricular tachycardia was documented in 4 patients, 2 received implantable cardioverter-defibrillators (ICD) for primary prevention and 2 for secondary prevention. (2) During follow-up, 1 primary prevention and 1 secondary prevention patient received in total 4 adequate ICD shocks. Life-threatening ventricular arrhythmias were documented during childhood in 5 of 10 mutation carriers. (3) All mutation carriers presented with characteristic mild dysmorphic features. Only 1 patient suffered from periodic paralysis. All had normal serum potassium level at repeated assessments and none had any other extracardiac disease manifestation. Our findings suggest that the novel KCNJ2 mutation is associated with a predominantly cardiac phenotype of Andersen-Tawil syndrome with high propensity to life-threatening ventricular arrhythmias presenting from childhood and young adulthood.

A dumbbell thrombus entrapped in patent foramen ovale

A 75-year-old lady came to emergency room due to dizziness and presyncopal attacks during exertion since two days prior to admission. Transesophageal echocardiography revealed a thrombus like mass in right atrium traversing patent foramen ovale and extending to left atrium. Spiral chest CT scan showed bilateral pulmonary thromboemboli. Operative and pathological findings confirmed the diagnosis.

Primary Left Ventricular Angiomatosis First Description of a Rare Vascular Tumor in the Left Heart

A 24 year-old male who presented with palpitations and presyncopal attacks had monomorphic ventricular tachycardia and a well-defined huge mass within the inferoposterior wall of the left ventricle proved by transthoracic echocardiography. The mass was completely resected and shown to be proliferative angiomatosis by histopathologic examination. This is the first reported case of primary left ventricular angiomatosis in the literature.

Congenital long QT syndrome: 50 years of electrophysiological research from cell to bedside

Congenital long QT syndrome (LQTS) is a group of ion channel disorders of ventricular myocytes due to genetic mutations. The main symptoms of LQTS are pre-syncopal or syncopal attacks and cardiac arrest. Anti-adrenergic therapy with beta-blockers has been the mainstay of treatment. Left cardiac sympathectomy has also been used as an alternative in those in whom beta-blockers failed. ICDs are highly effective in preventing mortality and should be the first choice of therapy for those with cardiac arrest as the first symptom or those with LQT3 genotype not responding to anti-adrenergic therapy alone. Research on new therapeutic options, specifically those targeting at defective genes or mutant ion channels, may provide more effective treatment for this rare but potentially fatal electrophysiological disorder.

Vasovagal syncope: a prospective, randomized, crossover evaluation of the effect of propranolol, nadolol and placebo on syncope recurrence and patients’ well-being

ObjectivesWe sought to assess the relative therapeutic efficacy of propranolol, nadolol and placebo in recurrent vasovagal syncope (VVS). BackgroundCentral and peripheral mechanisms have been implicated in the pathogenesis of VVS. Propranolol, nadolol and placebo have different sites of action on central and/or peripheral mechanisms. It has not yet been clarified whether one of the aforementioned treatments is more efficient than the others in reducing clinical episodes and exerting a beneficial effect on patients’ well-being. MethodsWe studied 30 consecutive patients with recurrent VVS and a positive head-up tilt test. All were serially and randomly assigned to propranolol, nadolol or placebo. Therapy with each drug lasted three months. On the day of drug crossover, patients reported the total number of syncopal and presyncopal attacks during the previous period. They also gave a general assessment of their quality of life, taking into account: 1) symptom recurrence; 2) drug side effects; and 3) their personal well-being during therapy (scale 0 to 4: 0 = very bad/discontinuation; 1 = bad; 2 = good; 3 = very good; 4 = excellent). At the end of the nine-month follow-up period, they reported whether they preferred a specific treatment over the others. ResultsSpontaneous syncopal and presyncopal episode recurrence during each three-month follow-up period was reduced by all drugs tested (analysis of variance [ANOVA]: chi-square = 67.4, p < 0.0001 for syncopal attacks; chi-square = 60.1, p < 0.0001 for presyncopal attacks) No differences were observed in the recurrence of syncope and presyncope among the three drugs. All drugs improved the patients’ well-being (ANOVA: chi-square = 61.9, p < 0.0001). ConclusionsPropranolol, nadolol and placebo are equally effective treatments in VVS, as demonstrated by a reduction in the recurrence of syncope and presyncope, as well as an improvement in the patients’ well-being.

A free floating ball thrombus in the left atrial cavity

A 65-year-old woman with a medical history of mitral valve stenosis was admitted to our hospital with paroxysmal dyspnea, orthopnea, and presyncopal attacks, which started 24 hours before admission. The patient was in atrial fibrillation and had been treated with digitalis, diuretic, β-blockers, and dicumarole (the last international normalized ratio, 3 days earlier, had been 2.5). Results of physical examination, chest radiography, and electrocardiography were consistent with the underlying mitral valve stenosis. Routine transthoracic echocardiography revealed a stenotic mitral valve and a large left atrium with an occasional appearance of a floating mass within the atrium but not well visible. Transesophageal evaluation soon after revealed a large, round ball-like thrombus with well-demarcated borders, which was free floating in the left atrial cavity, occluding the stenotic mitral valve transiently but completely. The stenotic mitral valve seemed to protect the patient from systemic embolization by the thrombus. The variation in position was not coincident with the cardiac cycle, and the motion of the thrombus was unpredictable (Fig 1). The patient subsequently underwent urgent cardiac operation with removal of the circular mass from the left atrium and mitral valve replacement. Indeed, no attachment of the mass was found at operation, and the histologic examination proved that it was a thrombus. She was discharged on postoperative day 7 in stable condition. Discussion. Left atrial ball thrombus appears to be an unusual occurrence. Wood, who first applied the term ball thrombus to this entity in 1814, described autopsy findings in From the Department of Cardiology, University of Athens, Hippokration Hospital, Athens, Greece. Received for publication July 12, 1999; accepted for publication Aug 11, 1999. Address for reprints: Costas Tsioufis, MD, 4, Athanasiou Diakou St, 15127 Melissia, Greece. J Thorac Cardiovasc Surg 1999;118:1120-2

Concurrent Monitoring of Brainstem Auditory and Somatosensory Evoked Potentials During Carotid Endarterectomy

Intraoperative management of a 68-year-old man with a 3-month history of presyncopal attacks presenting for left carotid endarterectomy is reported. Preoperative angiograms revealed that the patient had a 90% stenosis of his left internal carotid artery and a 35% stenosis of right internal carotid artery, absent posterior communicating arteries, a totally occluded left vertebral artery, and a right vertebral artery that became compressed upon turning his head to the right, often precipitating the presyncopal attacks. The surgical procedure was managed with intraoperative monitoring of both brainstem auditory and somatosensory evoked potentials. The patient had an uneventful outcome. The anesthetic management is discussed.

Rate Dependent Depression of Subsidiary Ventricular Impulse Formation—Cause of Stokes‐Adams Attacks in a Patient with Rate Modulated Pacing

Following His bundle ablation and implantation of a rate adaptive pacemaker (Vitatron TX 911) a 52-year-old gentleman experienced several presyncopal attacks while driving a car. On examination pectoralis muscle contraction caused temporary pacemaker inhibition. Incremental overdrive stimulation demonstrated progressive depression idioventricular automaticity and was associated with similar symptoms following overdrive at high pacing rates. Following appropriate pacemaker programming the patient remained symptom free.