Prinzmetals Angina Masquerading As Acute Pericarditis
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J Wave and Cardiac Death in Inferior Wall Myocardial Infarction
ORIGINAL ARTICLES Arrhythmia 2015;16(2):67-77 J Wave and Cardiac Death in Inferior Wall Myocardial Infarction Myung-Jin Cha, MD; Seil Oh, MD, ABSTRACT PhD, FHRS Background and Objectives: The clinical significance of J wave Department of Internal Medicine, Seoul National University presentation in acute myocardial infarction (AMI) patients remains Hospital, Seoul, Korea unclear. We hypothesized that J wave appearance in the inferior leads and/or reversed-J (rJ) wave in leads V1-V3 is associated with poor prognosis in inferior-wall AMI patients. Subject and Methods: We enrolled 302 consecutive patients with inferior-wall AMI who were treated with percutaneous coronary in- tervention (PCI). Patients were categorized into 2 groups based on electrocardiograms before and after PCI: the J group (J waves in in- ferior leads and/or rJ waves in leads V1-V3) and the non-J group (no J wave in any of the 12 leads). We compared patients with high am- plitude (>2 mV) J or rJ waves (big-J group) with the non-J group. The cardiac and all-cause mortality at 6 months and post-PCI ventricular arrhythmic events ≤48 hours after PCI were analyzed. Results: A total of 29 patients (including 19 cardiac death) had died. Although all-cause mortality was significantly higher in the post-PCI J group than in the non-J group (p=0.001, HR=5.38), there was no difference between the groups in cardiac mortality. When compar- ing the post-PCI big-J group with the non-J group, a significant dif- ference was found in all-cause mortality (n=29, p=0.032, HR=5.4) and cardiac mortality (n=19, p=0.011, HR=32.7). -
Unstable Angina with Tachycardia: Clinical and Therapeutic Implications
Unstable angina with tachycardia: Clinical and therapeutic implications We prospectively evaluated 19 patients with prolonged chest pain not evolving to myocardiai infarction and accompanied with reversible ST-T changes and tachycardia (heart rate >lOO beats/min) in order to correlate heart rate reduction with ischemic electrocardiographic (ECG) changes. Fourteen patients (74%) received previous long-term combined treatment with nifedipine and nitrates. Continuous ECG monitoring was carried out until heart rate reduction and at least one of the following occurred: (1) relief of pain or (2) resolution of ischemic ECG changes. The study protocol consisted of carotid massage in three patients (IS%), intravenous propranolol in seven patients (37%), slow intravenous amiodarone infusion in two patients (lo%), and intravenous verapamil in four patients (21%) with atrial fibrillation. In three patients (16%) we observed a spontaneous heart rate reduction on admission. Patients responded with heart rate reduction from a mean of 126 + 10.4 beats/min to 64 k 7.5 beats/min (p < 0.005) and an ST segment shift of 4.3 k 2.13 mm to 0.89 k 0.74 mm (p < 0.005) within a mean interval of 13.2 + 12.7 minutes. Fifteen (79%) had complete response and the other four (21%) had partial relief of pain. A significant direct correlation was observed for heart rate reduction and ST segment deviation (depression or elevation) (f = 0.7527 and 0.8739, respectively). These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate. Conventional vasodilator therapy may be deleterious, and heart rate reduction Is mandatory. -
The J Wave of the ECG. Concepts Compiled by Dr
The J wave of the ECG. Concepts Compiled by Dr. Andrés R. Pérez Riera The J wave is a positive deflection in the ECG normal (present in 2%–14% of healthy individuals and is more prevalent in young males, particularly if athletic and African descent. Additionally, ERP is a common finding in young teen athletes (the prevalence in the athletic population rises to 20-90%.).1 In this population ERP in both inferior and lateral leads is more common (18.2%) than isolated inferior (9.1%) or lateral (8.2%) ERP. Young age might be a contributing factor in causing a more diffuse repolarization abnormality. 2 or pathological that occurs approximately (There is an overlap of ≈10 msec. 3) after the junction between the end of the QRS complex and the beginning of the ST segment, also known as the J point (junction point), QRS end, J-junction, ST0 [zero millisecond] or ST beginning to occur after the notch/slur or J wave 4. It is described as J deflection as slurring/lambda 5 or notching of the terminal portion of QRS complex. Currently, J waves, is defined as an elevation of the QRS-ST junction ≥1 mm either as QRS slurring or notching in at least 2 contiguous leads. Additionally, when it becomes more accentuated, it may appear as a small, R wave (R′) or ST segment elevation. The term J deflection or J-wave has been used to designate the formation of the wave produced when there is a large, prominent deviation of the J point from the baseline with two shapes: notching/spike-and- slurring/lambda 5 or dome 6 variety. -
Acute Coronary Vasospasm Secondary to Industrial Nitroglycerin Withdrawal
158 SA MEDIESE TYDSKRIF DEEL 63 29 JANUARIE 1983 Acute coronary vasospasm secondary to industrial nitroglycerin withdrawal A case presentation and review J. Z. PRZYBOJEWSKI, M. H. HEYNS Clinical presentation Summary The patient, a Black man, was apparently quite healthy Ilntil July A Black employee exposed to industrial nitrogly 1977 when he' noted the onset ofdyspnoea on moderate exertion cerin (NG) in an explosives factory presented with and nonspecific chest pain. A chest radiograph then showed severe precordial pain. The clinical presentation 'bilateral basal segment pleuropneumonitis with pleural effu was that of significant transient anteroseptal and sions', cardiomegaly and pulmonary congestion. Therapy for anterolateral transmural myocardial ischaemia cardiac failure was begun but the patient's clinical condition did which responded promptly to sublingual isosorbide not improve significantly and he began experiencing dyspnoea dinitrate. Despite being removed from exposure to on minimal exertion, orthopnoea, paroxysmal cardiac dyspnoea, industrial NG and receiving therapy with long swelling of the ankles, and some abdominal distension. At this acting oral nitrates and calcium antagonists, the time he was 41 years old and had been employed atan explosives patient continued to experience repeated attacks of factory for many years whe:re he came into contact with indus severe retrosternal pain, although transient myo trial nitroglycerin (NG). cardial ischaemia was not demonstrated electro There was no past history of rheumatic fever or any other cardiographically during these episodes. Cardiac cardiac disease; he did not indulge in the consumption ofalcohol catheterization revealed cl normal myocardial hae and his diet was normal. Since his condition was not improving modynamic sy~tem and selective coronary arterio he was referred for admission to another university hospital, graphy delineated coronary arteries free from any where a diagnosis of significant constrictive pericarditis was obstructive lesions. -
The Management of Acute Coronary Syndromes in Patients Presenting
CONCISE GUIDANCE Clinical Medicine 2021 Vol 21, No 2: e206–11 The management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: key points from the ESC 2020 Clinical Practice Guidelines for the general and emergency physician Authors: Ramesh NadarajahA and Chris GaleB There have been significant advances in the diagnosis and international decline in mortality rates.2,3 In September 2020, management of non-ST-segment elevation myocardial the European Society of Cardiology (ESC) published updated infarction over recent years, which has been reflected in an Clinical Practice Guidelines for the management of ACS in patients international decline in mortality rates. This article provides an presenting without persistent ST-segment elevation,4 5 years after overview of the 2020 European Society of Cardiology Clinical the last iteration. ABSTRACT Practice Guidelines for the topic, concentrating on areas relevant The guidelines stipulate a number of updated recommendations to the general or emergency physician. The recommendations (supplementary material S1). The strength of a recommendation and underlying evidence basis are analysed in three key and level of evidence used to justify it are weighted and graded areas: diagnosis (the recommendation to use high sensitivity according to predefined scales (Table 1). This focused review troponin and how to apply it), pathways (the recommendation provides learning points derived from the guidelines in areas to facilitate early invasive coronary angiography to improve relevant to general and emergency physicians, including diagnosis outcomes and shorten hospital stays) and treatment (a (recommendation to use high sensitivity troponin), pathways paradigm shift in the use of early intensive platelet inhibition). -
Risk Stratification in Acute Coronary Syndrome: Focus on Unstable Angina/Non-ST Segment Elevation Myocardial Infarction R Bugiardini
729 EDITORIAL Heart: first published as 10.1136/hrt.2004.034546 on 14 June 2004. Downloaded from Risk stratification in acute coronary syndrome: focus on unstable angina/non-ST segment elevation myocardial infarction R Bugiardini ............................................................................................................................... Heart 2004;90:729–731. doi: 10.1136/hrt.2004.034546 Although there have been advances in the management of fashion. Experts in a variety of fields make decisions using a more intuitive process of unstable angina/non-ST segment elevation myocardial recognising patterns and applying their own infarction syndromes, the rate of cardiovascular mortality rules. In varying proportions, pathophysiologic after discharge is still unacceptably high. With many reasoning, personal clinical experience, and recent published research each play a role in therapeutic options available, the clinician is challenged to the development of our own clinical rules. This identify the safest and most effective treatment for long term approach may produce incorrect use of tools of survival of each individual patient risk stratifications and inappropriate use of treatment strategies and procedures. However, ........................................................................... errors are more often due to ‘‘failure’’ of the system, not of the doctors. Most errors occur at the transfer of care, and particularly at the transfer from the outpatient to the inpatient ‘‘Simple, but not too simple’’—Albert Einstein sites. There are a number of programs now focusing on errors and strategies to reduce errors welve million individuals in the USA and (GAP, CRUSADE QI, JACHO).5–7 All of these 143 million worldwide have coronary artery programs focus on education of physicians, Tdisease. Two million US patients are better interaction between health care organisa- admitted annually to cardiac care units with tions and physicians, and appropriate use of care acute coronary syndromes (ACS). -
Intraoperative Coronary Artery Vasospasm: a Twist in the Tale!
INTRAOPERATIVE CORONARY ARTERY VASOSPASM: A TWIST IN THE TALE! INTRAOPERATIVE CORONARY ARTERY VASOSPASM: A TWIST IN THE TALE! * MICHAEL S. GREEN, D.O. AND SHELDON GOMES, MD Abstract The cause of variant angina is localized hyperresponsiveness of the vascular smooth muscle cells caused by non-specific stimuli of vasoconstriction. Autonomic imbalance can be one of the mechanisms of spontaneous vasospasm, and sympathetic or parasympathetic stimulation can induce Coronary Artery Spasm (CAS). Although various reports of CAS events have been described, episodes associated with untwisting or manipulation of a visceral structure remains unique. We report one such case of CAS in association with intraoperative untwisting of a torted ovarian cyst treated with intracoronary nitroglycerine in the catheterization laboratory. Vasospastic or variant angina is a well known clinical condition first described by prinzmetal and colleagues, characterized by CAS in normal and diseased coronary arteries. General anesthesia can be a triggering event. This case demonstrates unique etiology in that spasm was provoked by surgical manipulation of a torted ovarian cyst. CAS has been implicated as a cause of sudden, unexpected circulatory collapse and death during surgery, cardiopulmonary bypass, and other non-cardiac surgical procedures. There are few reports of coronary vasospasm during regional anesthesia and neuroaxial block. Many factors are involved in the occurrences of perioperative CAS including activated sympathetic activity, activated parasympathetic activity, cocaine, alkalosis, hypercalcemia, magnesium deficiency, succinylcholine, vasopressors, essential hypertension, Hyperthyroidism, epidural anesthesia, spinal anesthesia, smoking, lipid metabolic disorder, coronary artery aneurysm, commercial weight loss products. We describe a rare case of CAS during general anesthesia, in a patient with no past history of coronary artery disease, possibly provoked by surgical manipulation of a torted ovarian cyst, which was diagnosed and treated promptly via cardiac catheterization. -
Angina: Contemporary Diagnosis and Management Thomas Joseph Ford ,1,2,3 Colin Berry 1
Education in Heart CHRONIC ISCHAEMIC HEART DISEASE Heart: first published as 10.1136/heartjnl-2018-314661 on 12 February 2020. Downloaded from Angina: contemporary diagnosis and management Thomas Joseph Ford ,1,2,3 Colin Berry 1 1BHF Cardiovascular Research INTRODUCTION Learning objectives Centre, University of Glasgow Ischaemic heart disease (IHD) remains the leading College of Medical Veterinary global cause of death and lost life years in adults, and Life Sciences, Glasgow, UK ► Around one half of angina patients have no 2 notably in younger (<55 years) women.1 Angina Department of Cardiology, obstructive coronary disease; many of these Gosford Hospital, Gosford, New pectoris (derived from the Latin verb ‘angere’ to patients have microvascular and/or vasospastic South Wales, Australia strangle) is chest discomfort of cardiac origin. It is a 3 angina. Faculty of Health and Medicine, common clinical manifestation of IHD with an esti- The University of Newcastle, ► Tests of coronary artery function empower mated prevalence of 3%–4% in UK adults. There Newcastle, NSW, Australia clinicians to make a correct diagnosis (rule- in/ are over 250 000 invasive coronary angiograms rule- out), complementing coronary angiography. Correspondence to performed each year with over 20 000 new cases of ► Physician and patient education, lifestyle, Dr Thomas Joseph Ford, BHF angina. The healthcare resource utilisation is appre- medications and revascularisation are key Cardiovascular Research Centre, ciable with over 110 000 inpatient episodes each aspects of management. University of Glasgow College year leading to substantial associated morbidity.2 In of Medical Veterinary and Life Sciences, Glasgow G128QQ, UK; 1809, Allen Burns (Lecturer in Anatomy, Univer- tom. -
Pathogenic Mechanisms of Takotsubo Cardiomyopathy Or Broken Heart Syndrome Devorah Leah Borisute Devorah Leah Borisute Is Graduating June 2018 with a B.S
Pathogenic Mechanisms of Takotsubo Cardiomyopathy or Broken Heart Syndrome Devorah Leah Borisute Devorah Leah Borisute is graduating June 2018 with a B.S. in Biology and will be attending the SUNY Downstate Physician Assistant Program. Abstract Takotsubo Cardiomyopathy (TTC) is a temporary heart-wall motion abnormality with the clinical presentation of a myocardial infarction Found predominantly in postmenopausal women, TTC most often appears with apical ballooning and mid-ventricle hypokinesis Often induced by an emotional or physical stress, TTC is reversible and excluded as a diagnosis in patients with acute plaque rupture and obstructive coronary disease The transient nature and positive prognosis of this cardiomyopathy leaves a dilemma as to what precipitates it This paper explores the theories of the pathogenesis of TTC including coronary artery spasm, microvascular dysfunction, and catecholamine excess A thorough analysis of the pathogenesis was conducted using online data- bases The coronary artery spasm theory involves an occlusion of a blood vessel caused by a sudden vasoconstriction of a coronary artery. This condition was confirmed in some patients with TTC using provocative testing, but failure to induce a coronary artery spasm in many patients led to its dismissal as a primary pathogenic mechanism. It is however a significant occurrence in patients with TTC and cannot be dismissed entirely The microvascular dysfunction theory is challenged in the limited and underdeveloped methods of testing for its presence However, using -
Coronary Artery Disease Management
HealthPartners Inspire® Special Needs Basic Care Clinical Care Planning and Resource Guide CORONARY ARTERY DISEASE MANAGEMENT The following Evidence Base Guideline was used in developing this clinical care guide: National Institute of Health (NIH); American Heart Association (AHA) Documented Health Condition: Coronary Artery Disease, Coronary Heart Disease, Heart Disease What is Coronary Artery Disease? Coronary artery disease (CAD) is a disease in which a waxy substance called plaque builds up inside the coronary arteries. These arteries supply oxygen‐rich blood to your heart muscle. When plaque builds up in the arteries, the condition is called atherosclerosis (ATH‐er‐o‐skler‐O‐sis). The buildup of plaque occurs over many years. Over time, plaque can harden or rupture (break open). Hardened plaque narrows the coronary arteries and reduces the flow of oxygen‐rich blood to the heart. If the plaque ruptures, a blood clot can form on its surface. A large blood clot can mostly or completely block blood flow through a coronary artery. Over time, ruptured plaque also hardens and narrows the coronary arteries. Common Causes of Coronary Artery Disease? If the flow of oxygen‐rich blood to your heart muscle is reduced or blocked, angina or a heart attack can occur. Angina is chest pain or discomfort. It may feel like pressure or squeezing in your chest. The pain also can occur in your shoulders, arms, neck, jaw, or back. Angina pain may even feel like indigestion. A heart attack occurs if the flow of oxygen‐rich blood to a section of heart muscle is cut off. If blood flow isn’t restored quickly, the section of heart muscle begins to die. -
Ventricular Tachycardia Associated Syncope in a Patient of Variant
Case Report http://dx.doi.org/10.4070/kcj.2016.46.1.102 Print ISSN 1738-5520 • On-line ISSN 1738-5555 Korean Circulation Journal Ventricular Tachycardia Associated Syncope in a Patient of Variant Angina without Chest Pain Soo Jin Kim, MD, Ji Young Juong, MD, and Tae-Ho Park, MD Department of Cardiology, Dong-A University Medical Center, Busan, Korea A 68-year-old man was admitted for a syncope workup. After routine evaluation, he was diagnosed with syncope of an unknown cause and was discharged from the hospital. He was readmitted due to dizziness. On repeated Holter monitoring, polymorphic ventricular tachycardia was detected during syncope. We performed intracoronary ergonovine provocation test; severe coronary spasm was induced at 70% stenosis of the proximal left anterior descending artery. The patient was treated with percutaneous coronary intervention. We present a rare case of syncope induced by ventricular arrhythmia in a patient with variant angina without chest pain. (Korean Circ J 2016;46(1):102-106) KEY WORDS: Prinzmetal’s variant angina; Coronary vasospasm; Tachycardia, ventricular. Introduction Case Variant angina commonly manifests as chest pain and transient A 68-year-old man visited our emergency room due to recurrent ST elevation by coronary spasm, and generally follows a benign syncope. He had experienced four episodes of syncope with clinical course.1) Rarely, syncope induced by ventricular arrhythmia dizziness and chest discomfort during the prior 2 months. The associated with transient myocardial ischemia can be developed episodes were evoked when he was preparing his boat for sailing by coronary spasm.2)3) If the cause of syncope is not correctly in early morning. -
Angina Symptoms Describe Angina As Feeling Like a Vise Is Squeezing Their Chest Or Feeling Like a Heavy Weight Has Been Placed on Their Chest
Diseases and Conditions Angina By Mayo Clinic Staff Angina is a term used for chest pain caused by reduced blood flow to the heart muscle. Angina (an-JIE-nuh or AN-juh-nuh) is a symptom of coronary artery disease. Angina is typically described as squeezing, pressure, heaviness, tightness or pain in your chest. Angina, also called angina pectoris, can be a recurring problem or a sudden, acute health concern. Angina is relatively common but can be hard to distinguish from other types of chest pain, such as the pain or discomfort of indigestion. If you have unexplained chest pain, seek medical attention right away. Symptoms associated with angina include: Chest pain or discomfort Pain in your arms, neck, jaw, shoulder or back accompanying chest pain Nausea Fatigue Shortness of breath Sweating Dizziness The chest pain and discomfort common with angina may be described as pressure, squeezing, fullness or pain in the center of your chest. Some people with angina symptoms describe angina as feeling like a vise is squeezing their chest or feeling like a heavy weight has been placed on their chest. For others, it may feel like indigestion. The severity, duration and type of angina can vary. It's important to recognize if you have new or changing chest discomfort. New or different symptoms may signal a more dangerous form of angina (unstable angina) or a heart attack. Stable angina is the most common form of angina, and it typically occurs with exertion and goes away with rest. If chest discomfort is a new symptom for you, it's important to see your doctor to find out what's causing your chest pain and to get proper treatment.