DOCSLIB.ORG

Syncope in Patients with Structural Heart Disease

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Syncope in Patients with Structural Heart Disease View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Landspítali University Hospital Research Archive Review Click here for more articles from the SYNCOPE symposium doi: 10.1111/joim.12027 Syncope in patients with structural heart disease David O. Arnar From the Division of Cardiology, Department of Internal Medicine, Landspıtali – The National University Hospital of Iceland, Reykjavik, Iceland Abstract. Arnar DO (Landspıtali – The National syncope is associated with a poor prognosis and University Hospital of Iceland, Reykjavik, may be a predictor of sudden cardiac death. In Iceland). Syncope in patients with structural patients who present with syncope, the presence of heart disease (Review). J Intern Med 2013; 273: structural heart disease and primary electrophys- 336–344. iological disorders should be considered and fur- ther cardiac evaluation performed as indicated by Syncope is a common condition. It is frequently the clinical history, physical examination and due to a benign cause, but may occasionally be due electrocardiographic findings. to a potentially life-threatening disorder. The pres- ence of structural heart disease in patients with Keywords: arrhythmia, heart disease, syncope. more common [6]. Furthermore, conditions such Introduction as orthostatic hypotension and drug-related syn- Syncope is defined as a sudden, but transient loss cope are not uncommon in older age groups. In the of consciousness accompanied by a loss of postural elderly, syncope is also more commonly due to a tone. Recovery is spontaneous and does not combination of factors. The presence of structural require the use of cardiopulmonary resuscitation. heart disease increases the likelihood of a serious Syncope is a common condition and the differential cause of syncope, such as malignant ventricular diagnosis is extensive. It has been reported that the arrhythmias. frequency of syncope amongst users of emergency departments in Europe is approximately 1% [1, 2]. There are two main goals in the evaluation of The causes of syncope are frequently benign, but patients with syncope. The first aim is to establish can occasionally be due to a potentially life-threat- the cause of the syncopal event. Secondly, patients ening disorder [3]. Because of the transient nature are stratified according to risk, including identifi- of syncope and some of its causes, determination of cation of those at high risk of sudden cardiac death the underlying mechanism can be challenging. A or of recurrent syncope or physical injury [5, 6]. comprehensive initial clinical history along with a detailed physical examination and an electrocar- High-risk features of syncope diogram (ECG) are essential for determining the possible causes as well as the need for further Cardiac syncope can predict sudden cardiac death diagnostic testing. However, despite a thorough [7]. Individuals who present with syncope and are evaluation, the cause of syncope may remain at high risk of subsequent sudden cardiac death, unknown in approximately a third of patients. frequently have a history of structural heart dis- ease along with clinical or ECG characteristics The causes of syncope are heterogeneous and vary suggestive of a serious arrhythmia [6]. These with age (Table 1). Neurocardiogenic (vasovagal) characteristics include heart failure with a severely syncope is most common in patients under the age reduced ejection fraction or the presence of myo- of 40 years and usually has a favourable prognosis cardial scar tissue from previous myocardial [4]. More serious, but less frequent causes of infarction. Clinical features suggestive of a serious syncope in those under the age of 40 include cause of syncope include occurrence during either hypertrophic cardiomyopathy and the so-called exertion or whilst supine. Prodromal symptoms of primary electrophysiological disorders, which can chest pain, acute shortness of breath and palpita- result in ventricular tachycardia (VT) and fibrilla- tions with sudden onset of dizziness may all tion [5]. In individuals over the age of 40 years, suggest a possible serious cardiac cause. A higher cardiac mechanical causes, such as heart failure risk of sudden cardiac death is also indicated by an and aortic stenosis, in addition to arrhythmias are ECG showing one or more of the following 336 ª 2013 The Association for the Publication of the Journal of Internal Medicine D. O. Arnar Review: Syncope in heart disease Table 1 Causes of syncope according to age Table 2 Structural heart diseases that can lead to syncope Patients < 40 years of age Patients 40 years of age Commonly cause syncope Rarely cause syncope Neurocardiogenica Cardiacc Ischaemic heart disease Myocarditis Psychiatrica Mechanical Nonischaemic dilated Pulmonary embolism Long QT syndromeb Arrhythmic cardiomyopathy (tachy- or Aortic stenosis Cardiac tamponade bradyarrhythmias) Hypertrophic cardiomyopathy Atrial myxoma Brugada syndromeb Orthostatic hypotensiona Arrhythmogenic right Severe pulmonary Wolf–Parkinson–White Drug relateda ventricular cardiomyopathy hypertension syndromeb (Primary electrophysiological Aortic dissection Arrhythmogenic right Multifactoriala disorders: long QT Congenital heart ventricular syndrome, short QT disease cardiomyopathyb syndrome, Brugada Ventricular syndrome, cardiomyopathyb catecholaminergic Hypertrophic polymorphic ventricular cardiomyopathyb tachycardia) aUsually benign. bInfrequent, but not benign. (especially if associated with depressed left ven- cGenerally not benign. tricular function), nonischaemic dilated cardiomy- opathy and severe aortic stenosis. Other less abnormalities: nonsustained VT, bifascicular block frequent, but nevertheless important causes are or intraventricular conduction delay (QRS > 120 hypertrophic cardiomyopathy and arrhythmogenic ms), a pre-excited QRS, abnormally prolonged or right ventricular cardiomyopathy (previously short QT interval, a Brugada syndrome pattern or termed dysplasia). Although not classified as struc- negative T waves in the precordial leads along with tural heart diseases, but rather as genetic disor- an epsilon wave consistent with arrhythmogenic ders that underlie primary electrophysiological right ventricular cardiomyopathy [6, 8]. Patients disease, the long QT interval syndrome (LQTS), presenting with syncope and one or more of the short QT syndrome, catecholaminergic polymor- above ECG abnormalities are candidates for hos- phic VT and Brugada syndrome are also worth pital admission. These individuals should receive considering as relatively infrequent, but serious continuous ECG monitoring and further diagnostic causes of syncope. Similarly, an accessory atrio- evaluation whilst in hospital; consultation with an ventricular pathway causing delta wave on the arrhythmia specialist should also be considered. ECG may represent uncommon causes of severe syncope. In the latter case, atrial fibrillation can be A diagnosis of a cardiac cause of syncope has associated with extremely high ventricular rates important prognostic implications. Studies com- due to rapid conduction over the accessory path- paring mortality after syncope according to likely way, which may sometimes lead to syncope and mechanism have consistently shown that patients even cardiac arrest. with a cardiac cause have a higher mortality than those with a noncardiac cause [9]. In the largest Myocarditis, pulmonary embolism, cardiac tamp- such study of over 400 patients with a follow-up of onade, atrial myxoma, severe pulmonary hyper- more than 60 months, the mortality rate during tension and certain congenital heart diseases follow-up was 50% in patients with a cardiac cause (including those previously repaired) are structural compared with rates of 31% and 24%, respectively, heart disorders that are occasionally associated in those with a noncardiac or unknown cause [10]. with syncope [6]. A variety of structural heart diseases can result in A family history of sudden cardiac death, especially syncope (Table 2) [6]. Disorders commonly associ- at a young age, should alert to the possibility of an ated with syncope include ischaemic heart disease inherited arrhythmogenic disease [5]. Likewise, ª 2013 The Association for the Publication of the Journal of Internal Medicine 337 Journal of Internal Medicine, 2013, 273; 336–344 D. O. Arnar Review: Syncope in heart disease any history of cardiovascular problems in the 8–10 s usually produces loss of consciousness, individual presenting with syncope may be impor- although briefer pauses can cause near syncope tant when attempting to narrow the differential [7]. In individuals with a pacemaker, a device diagnosis. malfunction needs to be ruled out. However, it is noteworthy that the presence of Other possible causes of cardiogenic syncope structural heart disease per se does not neces- include low output states, for example with either sarily imply that the syncopal event is caused by ischaemic or dilated cardiomyopathy, which can the underlying heart disorder. Patients with an sometimes be further exacerbated if the patient is underlying heart condition can also have rela- taking vasoactive medications, as is common in tively benign causes of syncope, such as neuro- those who have these disorders. Conditions such cardiogenic or drug-induced syncope. Drug- as aortic stenosis and severe hypertrophic cardio- induced syncope can be overlooked, especially myopathy may cause mechanical outflow obstruc- in elderly patients who may be taking a number tion from the left ventricle,
Load more

Recommended publications
  • Abdominal Coarctation in a Hypertensive Female Collegiate Basketball Player B Sloan, S Simons, a Stromwall
    1of2 Br J Sports Med: first published as 10.1136/bjsm.2002.004176 on 23 September 2004. Downloaded from CASE REPORT Abdominal coarctation in a hypertensive female collegiate basketball player B Sloan, S Simons, A Stromwall ............................................................................................................................... Br J Sports Med 2004;38:e20 (http://www.bjsportmed.com/cgi/content/full/38/5/e20). doi: 10.1136/bjsm.2002.004176 INVESTIGATIONS The purpose of the preparticipation examination is to identify A chest radiograph was within normal limits except for rib health conditions that might adversely affect an athlete while notching. Complete blood count, electrolytes, serum urea participating in sport. Hypertension is the most common. This nitrogen and creatinine, and thyroid stimulating hormone case report details a female basketball player found to be were within normal limits. Urinalysis showed 300 mg/l hypertensive, and complaining of fatigue, at her prepartici- protein. Electrocardiography showed sinus bradycardia with pation physical examination. Presentation, diagnostics, occasional premature atrial contractions. Echocardiography treatment, and final outcome of coarctation involving the revealed mitral valve prolapse, no mitral insufficiency, and an abdominal aorta are summarised. ejection fraction of 69%. One month after the initial presentation, an aortogram was performed. It confirmed the diagnosis of abdominal coarcta- tion, which was about 10 cm in length and 6 mm in diameter reparticipation sports physical examinations have at its greatest stenotic segment. The left renal and coeliac become routine for many institutions at the high school arteries were mildly stenotic. Internal mammary and inter- Pand collegiate level. Their main purpose is to identify costal arteries were dilated. The superior and inferior health conditions that might adversely affect an athlete while mesenteric arteries were patent, and the distal abdominal participating in a particular activity.
    [Show full text]
  • Pulmonary Arteriopathy in Patients with Mild Pulmonary Valve Abnormality Without Pulmonary Hypertension Or Intracardiac Shunt Karam Obeid1*, Subeer K
    Original Scientific Article Journal of Structural Heart Disease, June 2018, Received: September 13, 2017 Volume 4, Issue 3:79-84 Accepted: September 27, 2017 Published online: June 2018 DOI: https://doi.org/10.12945/j.jshd.2018.040.18 Pulmonary Arteriopathy in Patients with Mild Pulmonary Valve Abnormality without Pulmonary Hypertension or Intracardiac Shunt Karam Obeid1*, Subeer K. Wadia, MD2, Gentian Lluri, MD, PhD2, Cherise Meyerson, MD3, Gregory A. Fishbein, MD3, Leigh C. Reardon, MD2, Jamil Aboulhosn, MD2 1 Department of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA 2 Department of Internal Medicine, Ahmanson/UCLA Adult Congenital Heart Disease Center, Los Angeles, California, USA 3 Department of Pathology, Ronald Reagan/UCLA Medical Center, Los Angeles, California, USA Abstract benign course without episodes of dissection or rup- Background: The natural history of pulmonary artery ture despite 6/11 patients with PAA ≥ 5 cm. PA dilation aneurysms (PAA) without pulmonary hypertension, progresses slowly over time and does not appear to intracardiac shunt or significant pulmonary valvular cause secondary events. Echocardiography correlates disease has not been well studied. This study looks to well with magnetic resonance imaging and computed describe the outcome of a cohort of adults with PAA tomography and is useful in measuring PAA over time. without significant pulmonic regurgitation and steno- Copyright © 2018 Science International Corp. sis. Imaging modalities utilized to evaluate pulmonary artery (PA) size and valvular pathology are reviewed. Key Words Methods: Patients with PAA followed at the Ahmanson/ Pulmonary artery aneurysm • Pulmonary stenosis • UCLA Adult Congenital Heart Disease Center were in- Pulmonary hypertension • Aortic aneurysm cluded in this retrospective analysis.
    [Show full text]
  • Stroke Mimics and Chameleons: Quandaries in the Field
    Stroke Mimics and Chameleons: Quandaries in the Field Madeleine Geraghty, MD Rockwood Multicare What’s the difference Stroke mimic: Looks like a stroke, is something else Stroke chameleon: Looks like something else, is really a stroke! Scope of the Mimic Recent eval by Briard, et al: ◦ 960 patients transported by EMS during an 18 month period ◦ 42% mimics 55% other neurologic diagnoses 20% seizures, 19% migraines, 11% peripheral neuropathies 45% non-neurologic diagnoses Cardiac 16%, psychiatric 12%, infectious 9% ◦ Neurologic mimics were younger (~64 years) than non-neurologic mimics (~70 years) Entering a new era Large vessel occlusions Now a 24 hour time window for mechanical thrombectomy ◦ Most centers will likely activate the > 6 hour patients from within the ED, still working out those details Volume of stroke mimics/chameleons in the new time window? Effects on resource management? ◦ At the hospital level? ◦ At the regional level with distance transports? Need Emergency Responder Impressions now more than ever in order to learn for the future!! General Principles Positive symptoms Indicate an excess of central nervous system neuron electrical discharges Visual: flashing lights, zig zag shapes, lines, shapes, objects sensory: paresthesia, pain motor: jerking limb movements Migraine, Seizure are characterized with having “positive” symptoms Negative symptoms Indicate a loss or reduction of central nervous system neuron function – loss of vision, hearing, sensation, limb power. TIA/Stroke present with “negative” symptoms.
    [Show full text]
  • Shovlin Wilmshurst and Jackson.Pdf
    Eur Respir Mon 2011; 54: 218–245. DOI: 10.1183/1025448x.10008410 Pulmonary arteriovenous malformations and other pulmonary aspects of hereditary haemorrhagic telangiectasia Claire L Shovlin, 1 2 Peter Wilmshurst 3 4 and James E. Jackson 5 1NHLI Cardiovascular Sciences, Imperial College, London, UK. 2Respiratory Medicine, 5Imaging, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London UK. 3 Department of Cardiology, Royal Shrewsbury Hospital, UK; 4 University of Keele, UK Corresponding author: Dr Claire L. Shovlin PhD FRCP, HHTIC London, Respiratory Medicine, Hammersmith Hospital, Du Cane Rd, London, W12 0NN, UK. Phone (44) 208 383 4831; Fax (44) 208 383 1640; [email protected] CLS and JEJ acknowledge support from the NIHR Biomedical Research Centre Funding Scheme. The authors have no conflicts of interest to declare KEY WORDS: Contrast echocardiography, diving, hypoxaemia, pulmonary hypertension, stroke. 1 SUMMARY: Pulmonary arteriovenous malformations (PAVMs) are vascular structures that provide a direct capillary-free communication between the pulmonary and systemic circulations. The majority of patients have no PAVM-related symptoms, but are at risk of major complications that can be prevented by appropriate interventions. More than 90% of PAVMs occur as part of hereditary haemorrhagic telangiectasia (HHT), the genetic condition most commonly recognised by nosebleeds, anaemia due to chronic haemorrhage, and/or the presence of arteriovenous malformations in pulmonary, hepatic or cerebral circulations. Patients with HHT are also at higher risk of pulmonary hypertension and pulmonary embolic disease, management of which can be compounded by other aspects of their HHT. This chapter primarily addresses PAVMs and pulmonary HHT in the clinical setting, in order to improve patient care.
    [Show full text]
  • Hypertension and Cardiac Arrhythmias: a Consensus Document from The
    Europace (2017) 19, 891–911 CONSENSUS DOCUMENT doi:10.1093/europace/eux091 Hypertension and cardiac arrhythmias: a consensus document from the European Heart Rhythm Association (EHRA) and ESC Council on Hypertension, endorsed by the Heart Rhythm Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS) and Sociedad Latinoamericana de Estimulacion Cardıaca y Electrofisiologıa (SOLEACE) Gregory Y.H. Lip1,2, Antonio Coca3, Thomas Kahan4,5, Giuseppe Boriani6, Antonis S. Manolis7, Michael Hecht Olsen8, Ali Oto9, Tatjana S. Potpara10, Jan Steffel11, Francisco Marın12,Marcio Jansen de Oliveira Figueiredo13, Giovanni de Simone14, Wendy S. Tzou15, Chern-En Chiang16, and Bryan Williams17 Reviewers: Gheorghe-Andrei Dan18, Bulent Gorenek19, Laurent Fauchier20, Irina Savelieva21, Robert Hatala22, Isabelle van Gelder23, Jana Brguljan-Hitij24, Serap Erdine25, Dragan Lovic26, Young-Hoon Kim27, Jorge Salinas-Arce28, Michael Field29 1Institute of Cardiovascular Sciences, University of Birmingham, UK; 2Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark; 3Hypertension and Vascular Risk Unit, Department of Internal Medicine, Hospital Clınic (IDIBAPS), University of Barcelona, Barcelona, Spain; 4Karolinska Institutet Department of Clinical Sciences, Danderyd Hospital, Stockholm, Sweden; 5Department of Cardiology, Danderyd University Hospital Corp, Stockholm, Sweden; 6Cardiology Department, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy; 7Third Department of Cardiology, Athens
    [Show full text]
  • Syncope Fainting, Or Syncope, Is the Sudden Loss of Consciousness and Ability to Stand
    Northwestern Memorial Hospital Patient Education CONDITIONS AND DISEASES Syncope Fainting, or syncope, is the sudden loss of consciousness and ability to stand. It is also called “passing out.” This common If you have any problem is the cause of many falls and injuries. One third of people faint at least once during their life. Syncope may occur questions, ask without warning or can be signaled by: ■ Feelings of weakness your physician ■ Feeling hot or sweating ■ Dizziness or nurse. ■ Visual changes ■ Nausea ■ Palpitations Causes of syncope Fainting is due to a sudden decrease in blood flow and oxygen to the brain. There are many causes of syncope, but most fall into 1 of 3 major types. Abnormal nerve reflex Nerves that control heart rate, blood pressure and other body functions may respond in an abnormal way and cause syncope. This can be triggered by: ■ Standing ■ Pain ■ Unpleasant sight or smell ■ Stress, anxiety or emotional distress ■ Coughing, sneezing or swallowing ■ Urinating or having a bowel movement Fainting due to an abnormal nerve reflex is more likely to occur under certain conditions, such as dehydration, viral infection, after prolonged bed rest or a lack of sleep or regular food intake. Types of syncope that involve an abnormal nerve reflex include: ■ Vasovagal (neurocardiac) syncope is the most common type and can occur at any age. It often occurs when blood pools in the leg veins. This triggers a reflex where the heart rate, blood pressure or both may suddenly fall. It generally is not a dangerous condition and can be prevented by avoiding situations that can trigger syncope.
    [Show full text]
  • Latest Diagnostic and Treatment Strategies for the Congenital Long QT Syndromes
    Latest Diagnostic and Treatment Strategies for the Congenital Long QT Syndromes Michael J. Ackerman, MD, PhD Windland Smith Rice Cardiovascular Genomics Research Professor Professor of Medicine, Pediatrics, and Pharmacology Director, Long QT Syndrome Clinic and the Mayo Clinic Windland Smith Rice Sudden Death Genomics Laboratory President, Sudden Arrhythmia Death Syndromes (SADS) Foundation Learning Objectives to Disclose: • To RECOGNIZE the “faces” (phenotypes) of the congenital long QT syndromes (LQTS) • To CRITIQUE the various diagnostic modalities used in the evaluation of LQTS and UNDERSTAND their limitations • To ASSESS the currently available treatment options for the various LQT syndromes and EVALUATE their efficacy WINDLAND Smith Rice Sudden Death Genomics Laboratory Conflicts of Interest to Disclose: • Consultant – Boston Scientific, Gilead Sciences, Medtronic, St. Jude Medical, and Transgenomic/FAMILION • Royalties – Transgenomic/FAMILION Congenital Long QT Syndrome Normal QT interval QT QT Prolonged QT 1. Syncope 2. Seizures 3. Sudden death Torsades de pointes Congenital Long QT Syndrome Normal QT interval QT QT ♥ 1957 – first clinical description – JLNS ♥ 1960s – RomanoProlonged-Ward QT syndrome ♥ 1983 – “Schwartz/Moss score”1. Syncope ♥ 1991 – first LQTS chromosome locus 2. Seizures ♥ March 10, 1995 – birth of cardiac 3. Sudden channelopathies death Torsades de pointes Congenital Long QT Syndrome Normal QT interval QT QT Prolonged QT 1. Syncope 2. Seizures 3. Sudden death Torsades de pointes Congenital Long QT Syndrome Normal
    [Show full text]
  • The Carotid Bruit on September 25, 2021 by Guest
    AUGUST 2002 221 Pract Neurol: first published as 10.1046/j.1474-7766.2002.00078.x on 1 August 2002. Downloaded from INTRODUCTION When faced with a patient who may have had a NEUROLOGICAL SIGN stroke or transient ischaemic attack (TIA), one needs to ask oneself some simple questions: was the event vascular?; where was the brain lesion, and hence its vascular territory?; what was the cause? A careful history and focused physical examination are essential steps in getting the right answers. Although one can learn a great deal about the state of a patient’s arteries from expensive vascular imaging techniques, this does not make simple auscultation of the neck for carotid bruits redundant. In this brief review, we will therefore defi ne the place of the bruit in the diagnosis and management of patients with suspected TIA or stroke. WHY ARE CAROTID BRUITS IMPORTANT? A bruit over the carotid region is important because it may indicate the presence of athero- sclerotic plaque in the carotid arteries. Throm- boembolism from atherosclerotic plaque at the carotid artery bifurcation is a major cause of TIA and ischaemic stroke. Plaques occur preferentially at the carotid bifurcation, usually fi rst on the posterior wall of the internal carotid artery origin. The growth of these plaques and their subsequent disintegration, surface ulcera- tion, and capacity to throw off emboli into the Figure 1 Where to listen for a brain and eye determines the pattern of subse- bifurcation/internal carotid quent symptoms. The presence of an arterial http://pn.bmj.com/ artery origin bruit – high up bruit arising from stenosis at the origin of the under the angle of the jaw.
    [Show full text]
  • Problems in Family Practice Heart Murmurs in Infants and Children
    Problems in Family Practice Heart Murmurs in Infants and Children Thomas A. Riemenschneider, MD Sacramento, California A system is presented for evaluation of heart murmurs in in­ fants and children. The system places emphasis on identifica­ tion of functional murmurs, which the physician encounters so frequently in daily practice. A three-part approach is presented which includes: (1) evaluation of cardiovascular status, (2) as­ sessment of the heart murmur, and (3) decision regarding the need for further evaluation. This approach relieves the physi­ cian of the necessity to remember the multiple details of the many congenital cardiac lesions, and requires only the knowl­ edge of a few easily remembered details about functional murmurs. The system enables the physician to confidently distinguish organic and functional murmurs and to decide which children need further evaluation and referral to the pediatric cardiologist. The physician who cares for infants, children, with “normal” murmurs for reassurance to the and adolescents will frequently encounter heart parents.2 Using his/her knowledge of the myriad murmurs during the course of a careful physical details of the many congenital cardiac malforma­ examination. It has been estimated that a heart tions, the pediatric cardiologist seeks evidence murmur may be heard at some time in almost that the murmur is due to an organic lesion. The every child.1 Murmurs may be classified as “func­ family physician cannot expect to retain all of tional” (physiologic, normal, benign, or innocent), these details, and therefore often feels in­ or “organic” (associated with an anatomic car­ adequately prepared to assess the child with a diovascular abnormality).
    [Show full text]
  • Risk for Systemic Embolization of Atrial Fibrillation Without Mitral Stenosis
    Risk for Systemic Embolization of Atrial Fibrillation Without Mitral Stenosis Henry S. Cabin, MD, K. Soni Clubb, BS, Cynthia Hall, MD, Robin A. Perlmutter, MPH, and Alvan R. Feinstein, MD trial fibrillation (AF) has often been associated The risk for systemic embolixation was studied in with systemic embolization.*-I’ In studies of ce- 272 patients wlthout mitral stenosis or prosthetic A rebrovascular events, 6 to 23% of strokes have valves who were referred to the echocardlography been attributed to cardiogenic emboli,8~12+13almost half laboratory with atrial fibrillation (AF). During a of which were in patients with AF.‘*Y’~Although it was mean follow-up perfod of 33 months (range <I to reportedly highest in patients with mitral stenosis and 83), 27 (10%) patients had a systemic embolic AF,3,4,15,16the risk of systemic embolization has also event, which was cerebral in 23 patients (85%) and been suggestively increased when AF occurred without peripheral in 4 (15%). In the analysis of individual mitral stenosis.4v’5T17The increasedrisk of embolization variables, the risk of embolixation was increased by has been reported in patients with AF alone* and in female sex, underlying heart disease and left atrial those with associatedcoronary artery disease,4thyro- she 14.0 cm, but not by age, hypertension or type toxicosis,* 8 systemic hypertensionl 9 or dilated left of AF (paroxysmal vs chronic). In multivariable atria.*O Patients with AF have seldom been followed, analysis, left atrial size 14.0 cm was the single however,to identify risk factors for subsequentsystemic strongest predkitor of htcreased risk for embolixa- embolization.
    [Show full text]
  • TREATMENT of VASOVAGAL SYNCOPE Where to Go for Help Syncope: HRS Definition
    June 8, 2018, London UK TREATMENT OF VASOVAGAL SYNCOPE Where to go for help Syncope: HRS Definition ▪ Syncope is defined as: —a transient loss of consciousness, —associated with an inability to maintain postural tone, —rapid and spontaneous recovery, —and the absence of clinical features specific for another form of transient loss of consciousness such as epileptic seizure. 3 Syncope Cardiac Vasovagal Orthostatic Carotid sinus 4 Vasovagal Syncope: HRS Definition ▪ Vasovagal syncope is defined as a syncope syndrome that usually: 1. occurs with upright posture held for more than 30 seconds or with exposure to emotional stress, pain, or medical settings; 2. features diaphoresis, warmth, nausea, and pallor; 3. is associated with hypotension and relative bradycardia, when known; and 4. is followed by fatigue. 5 Physiology of Symptoms and Signs Decreased cardiac output Hypotension • Weakness • Lightheadness Retinal hypoperfusion • Blurred vision, grey vision, coning down Physiology of Symptoms and Signs Decreased cardiac output Reflex cutaneous vasoconstriction • Maintains core blood volume • Pallor, looks grey or very white Physiology of Symptoms and Signs Vasovagal reflex Worsened hypotension • More weakness • More lightheadness Vagal • Nausea and vomiting • Diarrhea • Abdominal discomfort Physiology of Symptoms and Signs Increase arterial conductance Rapid transit of core blood to skin • Hot flash • Warmth and discomfort • Lasts seconds • Pink skin SYNCOPE 9 Physiology of Symptoms and Signs Collapse • Preload restored • Reflexes end • Skin
    [Show full text]
  • The Apical Systolic Murmur in Mitral Stenosis
    Br Heart J: first published as 10.1136/hrt.16.3.255 on 1 July 1954. Downloaded from THE APICAL SYSTOLIC MURMUR IN MITRAL STENOSIS BY PATRICK MOUNSEY AND WALLACE BRIGDEN From the Cardiac Department of the London Hospital Received January 11, 1954 The purpose of this work was to determine how reliable a guide an apical systolic murmur can be to the finding at mitral valvotomy of incidental mitral regurgitation complicating dominant mitral stenosis. The history of the systolic murmur in mitral stenosis is a confused one, since general agreement was not reached about the timing of systolic and diastolic murmurs in mitral stenosis for nearly a century after Laennec (1819) first described the " bruit de souffiet " and " bruit de scie." Thus Ormerod (1864), Dickinson (1887), and Brockbank (1910) held that the characteristic murmur in mitral stenosis was in early systole and due to associated mitral regurgitation. On the other hand, Fauvel (1843), Gairdner (1861), and Fagge (1870) believed that the murmur was in late diastole and resulted from obstruction to the passage of blood through the mitral valve, as Laennec had originally suggested. With the advent of the electrocardiogram and phonocardiogram, the time of the murmur was fixed more accurately in the cardiac cycle. It became accepted that both diastolic and systolic murmurs were heard in mitral stenosis, the diastolic murmur being of chief importance as indicating stenosis, the systolic murmur, when present, being of secondary signifi- cance only, since it indicated merely a degree of incidental mitral regurgitation. With the intro- http://heart.bmj.com/ duction of mitral valvotomy and the consequent need for more detailed knowledge of the functional pathology of the mitral valve, interest has been re-awakened in the systolic murmur as one possible guide to the presence of regurgitation complicating mitral stenosis (Baker et al., 1952; Froment and Gravier, 1952; Abelmann et al., 1953; Sellors et al., 1953).
    [Show full text]