Association Between Syncope and Myocardial Bridge Lins TCB1*, Valente LM2, Oliveira KTMN3 and Brandão SCS4
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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. -
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. -
Captain Suffers Sudden Cardiac Death During Physical Fitness Evaluation - Alabama
2007 Death in the 15 Fire Fighter Fatality Investigation and Prevention Program line of duty… A summary of a NIOSH fire fighter fatality investigation January 30, 2008 Captain Suffers Sudden Cardiac Death During Physical Fitness Evaluation - Alabama SUMMARY • Incorporate exercise stress tests into the Fire Department’s medical On April 25, 2007, a 56-year-old male career evaluation program. Captain was participating in the Fire Department’s annual “Fit Check” (physical • Provide fire fighters with medical fitness) evaluation. The Captain successfully evaluations and clearance to wear completed the bench press, sit-ups, and sit self-contained breathing apparatus and-reach portions of the evaluation within the (SCBA). allotted time. During the aerobic capacity (3 mile walk) portion of the evaluation, he • Provide exercise equipment in all fire completed 6 of 12 laps around the ¼-mile stations. track, when he suddenly collapsed. Crew members on the scene responded and found • Ensure that all members participate in him unresponsive, not breathing, and with a the Fire Department’s mandatory weak pulse that stopped shortly thereafter. wellness/fitness program. Approximately 29 minutes later, despite cardiopulmonary resuscitation (CPR) and advanced life support administered on-scene INTRODUCTION and METHODS and at the hospital, the Captain died. The death certificate and the autopsy, completed by the On April 25, 2007, a 56-year-old male Captain County Medical Examiner, listed lost consciousness while participating in the “complications of atherosclerotic Fire Department annual physical fitness cardiovascular disease” as the immediate evaluation. Despite CPR and advanced life cause of death with “cardiomegaly” as a significant condition. The Fire Fighter Fatality Investigation and Prevention NIOSH investigators offer the following Program is conducted by the National Institute for recommendations to address general safety Occupational Safety and Health (NIOSH). -
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 -
Myocardial Bridges a Forgotten Condition: a Review Martín Ibarrola, MD*
ISSN: 2474-3682 Ibarrola. Clin Med Img Lib 2021, 7:162 DOI: 10.23937/2474-3682/1510162 Volume 7 | Issue 1 Clinical Medical Image Library Open Access IMAGE ARTICLE Myocardial Bridges a Forgotten Condition: A Review Martín Ibarrola, MD* Centro Cardiovascular BV, General Cardiology, Argentina Check for updates *Corresponding author: Martín Ibarrola, MD, Centro Cardiovascular BV, General Cardiology, Argentina Abstract Introduction Myocardial Bridging (MB) is a congenital anomaly in which The first reference of MB was Reymann, H, the an- a segment of a coronary artery takes a “tunneled” intramus- atomically description Published in the Dissertationem cular course under a “bridge” of overlying myocardium. The inauguralem De Vasis Cordis Propriis, written in Latin, first reference of MB in coronary arteries, the association with angina and anatomically as referred by Reyman in described anatomically the presence of MB in a descrip- 1737. Considered a “benign” finding since the myocardi- tion and their relationship with angina in 1937. When al bridge causes coronary artery narrowing during systole noted this anatomy in human heart. Described was a therefore myocardial bridges should not compromise blood congenital variant of a coronary artery in which a por- supply to the musculature during diastole. The Left Anterior Descending coronary (LAD) is the most frequently affected tion of an epicardial coronary artery (most frequently vessel (70% in an autopsy series) and in some cases hearts the middle segment of the LAD takes an intramuscular contain more than one bridge, affecting the same vessel or course [1]. The relation of MB in coronary arteries and different coronaries. presence of angina was described by Black S in 1796 [2]. -
Magnetic Resonance Images of Left Ventricular Pseudoaneurysm
Heart 1998;80:101–103 101 SHORT CASES IN CARDIOLOGY Magnetic resonance images of left ventricular pseudoaneurysm R N Chakraborty, A A Nicholson, M F Alamgir A 63 year old woman presented in March 1997 contrast filled the pseudoaneurysm, but it was with a three month history of shortness of diluted in a huge sac. breath while lying flat and in the left lateral The patient had open heart surgery, which position. She had a history of ischaemic heart revealed dense adhesions around the heart. disease and had coronary artery bypass surgery five years ago. In August 1995 she had an infe- rior wall myocardial infarction with postinfarc- tion angina, which responded to medical treat- ment. Echocardiographic window was poor because of obesity; however, there appeared to be a large echo free space postero-inferior to the left ventricle leading to suspicion of left ventricular pseudoaneurysm. Magnetic reso- nance images of the heart performed in a 0.5 Tesla GE Vectra (IGF Medical, Milwaukee, Wisconsin, USA) magnetic resonance scanner were consistent with this diagnosis (figs 1–4). The clinical presentation did not suggest a diagnosis of left ventricular pseudoaneurysm. Chest radiography showed cardiomegaly with left sided pleural eVusion. In view of her previ- ous heart attack and coronary artery bypass operation transoesophageal echocardiography was performed followed by a transthoracic echocardiography. The patient was consider- ably breathless while manoeuvring the probe. However, from a limited study there was a very Figure 2 In midsystole a communication between the strong suspicion of left ventricular pseudo- postero-basal area of the left ventricle (LV) and the thin aneurysm. -
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 -
Myocardial Bridge: Harmless Or Harmful
□ EDITORIAL □ Myocardial Bridge: Harmless or Harmful Key words: myocardial ischemia, coronary spasm, myocar- diameter reduction by the myocardial bridge. Quantitative dial infarction, coronary flow reserve, vascular analysis of the Doppler flow profile shows a highly charac- dysfunction teristic pattern in approximately 90% of the patients with an abrupt early diastolic flow acceleration, which has been termed as the “finger-tip” phenomenon, a rapid mid-diastolic deceleration and mid-to-late diastolic plateau. The abrupt The coronary arteries and their major branches usually run early diastolic flow acceleration is due to the persistent dia- on the surface of the heart in the subepicardial tissue. stolic diameter reduction. This is followed by a rapid dia- Sometimes, a portion of the artery runs under a “bridge” of stolic lumen gain leading to a plateau during late diastole. superficial myocardial fibers for a short distance. This condi- This characteristic flow pattern has been well described by tion has been given various terms “myocardial bridge”, “intr Bourassa et al (2). It is not hard to believe that a myocardial amural coronary artery”, “mural coronary artery”, “coronary bridge may cause flow limitation leading to myocardial artery overbridging” and “myocardial loop” (1). The inci- ischemia in such patients with a rapid heart rate where the dence of myocardial bridge has been reported to vary between diastolic phase is relatively shortened or in cases with maxi- 15% and 85% in autopsy, and 0.5% to 2.5% in angiographic mal coronary arterial dilation in which flow velocity is maxi- series (2). The length varies widely from 4 to 40 mm, the mal and any minor resistance against flow could cause flow thickness also varies from 1 to 4 mm (2). -
Update on the Diagnosis and Management of Familial Long QT Syndrome
Heart, Lung and Circulation (2016) 25, 769–776 POSITION STATEMENT 1443-9506/04/$36.00 http://dx.doi.org/10.1016/j.hlc.2016.01.020 Update on the Diagnosis and Management of Familial Long QT Syndrome Kathryn E Waddell-Smith, FRACP a,b, Jonathan R Skinner, FRACP, FCSANZ, FHRS, MD a,b*, members of the CSANZ Genetics Council Writing Group aGreen Lane Paediatric and Congenital Cardiac Services, Starship Children’s Hospital, Auckland New Zealand bDepartment[5_TD$IF] of Paediatrics,[6_TD$IF] Child[7_TD$IF] and[8_TD$IF] Youth[9_TD$IF] Health,[10_TD$IF] University of Auckland, Auckland, New Zealand Received 17 December 2015; accepted 20 January 2016; online published-ahead-of-print 5 March 2016 This update was reviewed by the CSANZ Continuing Education and Recertification Committee and ratified by the CSANZ board in August 2015. Since the CSANZ 2011 guidelines, adjunctive clinical tests have proven useful in the diagnosis of LQTS and are discussed in this update. Understanding of the diagnostic and risk stratifying role of LQTS genetics is also discussed. At least 14 LQTS genes are now thought to be responsible for the disease. High-risk individuals may have multiple mutations, large gene rearrangements, C-loop mutations in KCNQ1, transmembrane mutations in KCNH2, or have certain gene modifiers present, particularly NOS1AP polymorphisms. In regards to treatment, nadolol is preferred, particularly for long QT type 2, and short acting metoprolol should not be used. Thoracoscopic left cardiac sympathectomy is valuable in those who cannot adhere to beta blocker therapy, particularly in long QT type 1. Indications for ICD therapies have been refined; and a primary indication for ICD in post-pubertal females with long QT type 2 and a very long QT interval is emerging. -
Cardiovascular Risk After Hospitalisation for Unexplained
Heart Online First, published on August 3, 2017 as 10.1136/heartjnl-2017-311857 Cardiac risk factors and prevention ORIGINAL RESEARCH ARTICLE Heart: first published as 10.1136/heartjnl-2017-311857 on 3 August 2017. Downloaded from Cardiovascular risk after hospitalisation for unexplained syncope and orthostatic hypotension Ekrem Yasa,1,2 Fabrizio Ricci,3,4 Martin Magnusson,1,2 Richard Sutton,5 Sabina Gallina,3 Raffaele De Caterina,3 Olle Melander,1 Artur Fedorowski1,2 1Department of Clinical ABSTRACT The diagnosis of syncope (R55.9, Interna- Sciences, Lund University, Objective To investigate the relationship of hospital tional Classification of Diseases (ICD)-10) is Clinical Research Center, Skåne often referred to as a synonym for reflex syncope, University Hospital, Malmö, admissions due to unexplained syncope and orthostatic Sweden hypotension (OH) with subsequent cardiovascular events the most common cause of T-LOC, accounting 2Department of Cardiology, and mortality. for about 50%–60% of cases. Conversely, OH Skåne University Hospital, Methods We analysed a population-based prospective is believed to coexist with 10%–15% of T-LOC Malmö, Sweden episodes,3 which are then defined as syncope due to 3Institute of Cardiology, cohort of 30 528 middle-aged individuals (age 58±8 University 'G. d’Annunzio', years; males, 40%). Adjusted Cox regression models OH or autonomic failure. It is universally accepted Chieti, Italy were applied to assess the impact of unexplained that recurrent reflex syncope and OH are different 4 Department of Neuroscience syncope/OH hospitalisations on cardiovascular events clinical manifestations of cardiovascular (CV) auto- and Imaging and ITAB – and mortality, excluding subjects with prevalent nomic dysfunction. -
Diagonal 1 and Mid-LAD Myocardial Bridge with Elevated Troponin Enzymes
HCA Healthcare Scholarly Commons Cardiology Research & Publications 2-28-2020 Diagonal 1 and Mid-LAD Myocardial Bridge with Elevated Troponin Enzymes Ronak Patel DO Lewis Gale Hospital Montomery, [email protected] Follow this and additional works at: https://scholarlycommons.hcahealthcare.com/cardiology Part of the Cardiology Commons, Cardiovascular Diseases Commons, and the Congenital, Hereditary, and Neonatal Diseases and Abnormalities Commons Recommended Citation Patel R. Diagonal 1 and Mid-LAD myocardial bridge with elevated Troponin enzymes. Poster presented at: VCOM Research Day; February 28, 2020; Blacksburg, VA. This Abstract is brought to you for free and open access by the Research & Publications at Scholarly Commons. It has been accepted for inclusion in Cardiology by an authorized administrator of Scholarly Commons. Diagonal 1 and Mid-LAD Myocardial Bridge with Elevated Troponin Enzymes Ronak Patel, DO| HCA Introduction Key Points Discussion 7 • Myocardial bridges have been consider benign. But this case serves • Most of the research on a left anterior descending (LAD) myocardial as an example of some potential detrimental effects of a myocardial bridges are localized and documented to the middle portion of the 6.152 6 bridge LAD. • I hypothesize this patient is more inclined to ischemic events and 5 • The limited research thus far has proposed that this condition is 4.72 4.62 symptoms just based of the proximal to mid anatomic location of the benign. 4 patient’s myocardial bridge. This could explain why the patient also • In this case presentation, the patient was found to Diagonal 1 and Mid- had elevated troponins. LAD myocardial bridge which border and partially encompasses the 3 • Being able to recognize a young individual with severe “classic signs” proximal portion of the LAD. -
Premature Ventricular Contractions Ralph Augostini, MD FACC FHRS
Premature Ventricular Contractions Ralph Augostini, MD FACC FHRS Orlando, Florida – October 7-9, 2011 Premature Ventricular Contractions: ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death J Am Coll Cardiol, 2006; 48:247-346. Background PVCs are ectopic impulses originating from an area distal to the His Purkinje system Most common ventricular arrhythmia Significance of PVCs is interpreted in the context of the underlying cardiac condition Ventricular ectopy leading to ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, is one of the common mechanisms for sudden cardiac death The treatment paradigm in the 1970s and 1980s was to eliminate PVCs in patients after myocardial infarction (MI). CAST and other studies demonstrated that eliminating PVCs with available anti-arrhythmic drugs increases the risk of death to patients without providing any measurable benefit Pathophysiology Three common mechanisms exist for PVCs, (1) automaticity, (2) reentry, and (3) triggered activity: Automaticity: The development of a new site of depolarization in non-nodal ventricular tissue. Reentry circuit: Reentry typically occurs when slow- conducting tissue (eg, post-infarction myocardium) is present adjacent to normal tissue. Triggered activity: Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated PVCs, but also with ischemia and electrolyte disturbance. Triggered Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158. Epidemiology Frequency The Framingham heart study (with 1-h ambulatory ECG) 1 or more PVCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD Among patients with CAD, the prevalence rate of 1 or more PVCs was 58% in men and 49% in women.