DOCSLIB.ORG

Angina and Myocardial Infarction with Normal Coronary Arteries M.E

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Angina and Myocardial Infarction with Normal Coronary Arteries M.E Postgrad Med J: first published as 10.1136/pgmj.67.783.4 on 1 January 1991. Downloaded from Postgrad Med J (1991) 67, 4 - 8 ) The Fellowship of Postgraduate Medicine, 1991 Leading Article Angina and myocardial infarction with normal coronary arteries M.E. Bourke and D.L.H. Patterson Cardiac Department, Whittington Hospital, Highgate Hill, London N19 SNF, UK. Introduction Coronary ischaemic syndromes, including chest imbalance between myocardial oxygen supply and pain suggestive of angina pectoris, and document- demand might be abnormal haemoglobin oxygen ed myocardial infarction, in the presence of angio- dissociation, as in carbon monoxide poisoning.6 graphically normal coronary arteries, have been Classic angina pectoris usually indicates myocar- the subject of much attention. In contrast to dial ischaemia, secondary to obstructive coronary atheromatous coronary artery disease the patho- artery disease. It can arise when myocardial physiology ofsuch conditions is poorly understood ischaemia is due not to reduction ofcoronary blood and the mechanisms underlying myocardial ischae- flow, but to other mechanisms such as increased mia in these circumstances have been the cause ofa cardiac work as in aortic stenosis; altered blood great deal of conjecture and controversy. oxygen content in severe anaemia; rheological abnormalities of the blood in hypergammaglobin- aemia or, as described in this issue of the Journal, by copyright. Myocardial infarction due to thyrotoxicosis.'5 In Europe, approximately 10% ofpatients refer- A small percentage of patients presenting with red to cardiac units for assessment ofchest pain are acute myocardial infarction are found to have found on diagnostic cardiac catheterization to have angiographically normal epicardial coronary arter- no angiographic evidence of significant coronary ies. The prevalence is high in certain subsets of artery disease.'6 It is important to appreciate that myocardial infarction patients, such as the very coronary angiograms only visualize coronary young,' especially those infarcting during or fol- arteries of greater than 400 gAm diameter. The lowing severe physical exercise,2 and in young majority will have a non-cardiac cause for their http://pmj.bmj.com/ women during pregnancy or using oral contracep- symptoms and in many cases careful reassessment tives and smoking.3 Documented myocardial and investigation will reveal a musculoskeletal, infarction in the presence of normal coronary oesophageal or psychological cause.'7 It may be arteries has been reported in thyrotoxicosis; both difficult to determine whether anxiety-related true and factitious,4 temporally related to cocaine symptoms are a cause or consequence of the use,5 after acute exposure to carbon monoxide,6 current chest pain. In a small minority of patients and in patients with viral myocarditis.7 This issue of there will still be a clinical suspicion that symptoms the Journal contains a case report on a multisystem are due to myocardial ischaemia. on September 23, 2021 by guest. Protected vasculitis leading to myocardial infarction without evidence of coronary artery involvement.8 Amongst suggested mechanisms are defects in Coronary vasospasm clotting factors and platelet activity,9"10 coronary artery spasm," thrombosis with rapid spontaneous In 1959 Prinzmetal et al. introduced the concept of lysis,'2 coronary emboli' and small vessel disease.'3 epicardial artery spasm causing the specific clinical In cases of chronic Chagas' heart disease, where syndrome, 'variant angina', which is characterized there is parasympathetic ganglion destruction it is by angina at rest with elevated ST segments on postulated that transitory sympathetic overdrive electrocardiogram (ECG).'8 Now it is thought that causes myocardial infarction.' In these cases the this mechanism may play a role in other aspects of coronary arteries are not only free ofatheroma but ischaemic heart disease. Spasm can be detected in indeed are larger in comparison to hypertensive angiographically normal segments, or may be and normal patients. Another cause of an extreme superimposed on an atherosclerotic lesion - 'dynamic coronary stenosis'. Unfortunately the Correspondence: D.L.H. Patterson, M.D., F.R.C.P. literature has become confused because the term Received: 6 September 1990 coronary spasm is often applied to any situation of Postgrad Med J: first published as 10.1136/pgmj.67.783.4 on 1 January 1991. Downloaded from NORMAL CORONARY ARTERIES AND ISCHAEMIC SYNDROMES 5 increased coronary vasomotor tone. It should be symptoms. Many patients have a poor response to confined to a situation of focal coronary constric- long acting nitrate therapy, and a good response to tion sufficient to cause transient coronary occlu- calcium antagonists. The incidence ofsudden death sion, which gives rise to attacks ofischaemic pain at in patients with documented coronary artery rest. spasm is unknown. Since episodes of complete Although various neural'9 and humoral202' heart block and ventricular tachycardia are known mechanisms have been proposed, the genesis of to occur during coronary artery spasm, it may be coronary spasm is as yet undefined. Maseri and his that some patients have died as a result of these co-workers postulate a focal hyperreactivity to a rhythm disturbances. Overall the prognosis of a variety of coronary vasoconstrictive stimuli acting patient with severe coronary atherosclerosis and on different receptors.22 It has been observed that in coronary artery spasm depends upon the degree of variant angina, coronary spasm usually occurs at atherosclerosis.29,30 the site ofatheromatous plaques,23 but the fact that such plaques are common and classical variant Syndrome X angina rare, suggests that some additional factor other than the presence of plaque is required. In a The term Syndrome X was first used by Kemp3' in large study of patients with chronic coronary 1973 in an editorial discussion of a paper by ischaemic syndromes other than variant angina, Arbogast and Bourassa,32 who performed pacing Bertrand et al.24 showed that when stenosis existed studies in patients with chest pain and normal there was no correlation between the degree of coronary arteries and showed ST depression dur- underlying stenosis and the occurrence of spasm. ing atrial pacing. No mention was made ofexercise- Bertrand could demonstrate ergonovine-induced induced ST segment changes in these patients. The angina in only 4% of those with chronic stable authors designated their patient cohort as group X. angina and 6% with old myocardial infarction. In The phrase was later popularized by Opherk et al.33 contrast 20% ofpatients with recent infarction and The term has been widely used, but with a lack of 30% ofthose experiencing angina at rest developed agreed hard diagnostic criteria. This has resulted in by copyright. focal coronary occlusion in response to ergono- a confusing picture as each study has used it own vine. It may be that in these acute situations there is terms of reference, making comparisons very a focal hyperreactivity to coronary vasoconstrictor difficult. agents. Less than 1% of those who present to a cardiac Recent studies have shown that vasoactive com- unit with possible angina, and in whom a non- pounds affect segments of the human coronary cardiac cause has been excluded, will fulfil the circulation differentially.22 This has implications in diagnostic criteria of a tight, albeit empirical, the pathophysiology of both focal coronary artery definition of Syndrome X:34 (a) typical angina on spasm and of 'Syndrome X', which has been effort; (b) positive exercise test; (c) no demonstrable http://pmj.bmj.com/ suggested to be due to a more diffuse disturbance of coronary stenosis; (d) no other obvious cause, such coronary blood flow. Intracoronary injection of as hypertension, valve disease or overt cardio- organic nitrates causes marked dilatation ofepicar- myopathy. Even applying these strict criteria will dial vessels, suggesting a resting coronary motor not give an infallible diagnosis, since, for instance tone. In contrast these doses have little affect on exercise testing has its limitations. total coronary blood flow, implying little effect on An alternative approach to the diagnosis is to use intramural resistance vessels. Adenosine displays a conceptual definition, i.e. inducible ischaemia in the opposite pattern, with a marked distal dilating the absence of large coronary artery stenosis or on September 23, 2021 by guest. Protected effect but relatively minor actions on the epicardial haemodynamic overload. This approach intro- vessels. duces practical problems because ofthe difficulty in Studies ofthe effects ofintracoronary infusion of demonstrating ischaemia unequivocally. various endogenous vasoactive substances, includ- Several studies have used the demonstration of ing calcitonin gene related peptide,25 neuropeptide stimulation ofanaerobic metabolism as evidence of y,26 acetylcholine27 and substance P,28 point to a ischaemia. This is a specific but not sensitive heterogeneity of responses within the human cor- marker. In studies of patients with postulated onary circulation, and may allow some pharma- Syndrome X, 12-100% demonstrated myocardial cological intervention of coronary blood flow lactate production in response to pacing or dipyrid- regulation. It is difficult to validate their relevance amole infusion.34'35 to the pathophysiology of conditions under con- A fall in coronary sinus oxygen saturation in sideration here. response
Load more

Recommended publications
  • 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).
    [Show full text]
  • 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.
    [Show full text]
  • Cardiovascular Disease and Rehab
    EXERCISE AND CARDIOVASCULAR ! CARDIOVASCULAR DISEASE Exercise plays a significant role in the prevention and rehabilitation of cardiovascular diseases. High blood pressure, high cholesterol, diabetes and obesity can all be positively affected by an appropriate and regular exercise program which in turn benefits cardiovascular health. Cardiovascular disease can come in many forms including: Acute coronary syndromes (coronary artery disease), myocardial ischemia, myocardial infarction (MI), Peripheral artery disease and more. Exercise can improve cardiovascular endurance and can improve overall quality of life. If you have had a cardiac event and are ready to start an appropriate exercise plan, Cardiac Rehabilitation may be the best option for you. Please call 317-745-3580 (Danville Hospital campus), 317-718-2454 (YMCA Avon campus) or 317-456-9058 (Brownsburg Hospital campus) for more information. SAFETY PRECAUTIONS • Ask your healthcare team which activities are most appropriate for you. • If prescribed nitroglycerine, always carry it with you especially during exercise and take all other medications as prescribed. • Start slow and gradually progress. If active before event, fitness levels may be significantly lower – listen to your body. A longer cool down may reduce complications. • Stop exercising immediately if you experience chest pain, fatigue, or labored breathing. • Avoid exercising in extreme weather conditions. • Drink plenty of water before, during, and after exercise. • Wear a medical identification bracelet, necklace, or ID tag in case of emergency. • Wear proper fitting shoes and socks, and check feet after exercise. STANDARD GUIDELINES F – 3-5 days a week. Include low weight resistance training 2 days/week I – 40-80% of exercise capacity using the heart rate reserve (HRR) (220-age=HRmax; HRmax-HRrest = HRR) T – 20-60mins/session, may start with sessions of 5-15 mins if necessary T – Large rhythmic muscle group activities that are low impact (walking, swimming, biking) Get wellness tips to keep YOU healthy at HENDRICKS.ORG/SOCIAL..
    [Show full text]
  • 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.
    [Show full text]
  • Myocardial Infarction (Heart Attack)
    Sacramento Heart & Vascular Medical Associates February 19, 2012 500 University Ave. Sacramento, CA 95825 Page 1 916-830-2000 Fax: 916-830-2001 Patient Information For: Only A Test Myocardial Infarction (Heart Attack) What is a myocardial infarction (MI)? Myocardial infarction (MI) is a heart attack. It happens when blood flow to a part of the heart is suddenly blocked. How does it occur? Myocardial infarction may occur at any time and often occurs without warning. As we grow older, our coronary arteries may become narrowed by the buildup of cholesterol plaque. When the arteries narrow, less blood can go through them, and less oxygen gets to the heart muscle. The process of narrowing is called atherosclerosis. The narrower the artery becomes, the more likely it is that a blood clot may form and block the artery completely, causing a heart attack. Sometimes sudden blockages can occur even in places where the artery was not narrow before. A heart attack may also occur when the heart muscle needs more oxygen than the blood vessels can provide. This might happen, for example, during hard exercise such as shoveling snow, or with a sudden increase in blood pressure. Less commonly, a heart attack can occur due to coronary spasm. Coronary spasm is a sudden and temporary narrowing of a small part of an artery that supplies blood to the heart. It may be caused by smoking or drugs such as cocaine. Risk factors for heart disease include: - cigarette smoking - a family history of heart attack - diabetes - overweight - high blood pressure - high blood cholesterol - low HDL cholesterol (that is, too little "good" cholesterol) - stress - a lifestyle that does not include much physical activity.
    [Show full text]
  • 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).
    [Show full text]
  • 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).
    [Show full text]
  • Treatment of Acute Coronary Syndrome
    Acute Coronary Syndrome: Current Treatment TIMOTHY L. SWITAJ, MD, U.S. Army Medical Department Center and School, Fort Sam Houston, Texas SCOTT R. CHRISTENSEN, MD, Martin Army Community Hospital Family Medicine Residency Program, Fort Benning, Georgia DEAN M. BREWER, DO, Guthrie Ambulatory Health Care Clinic, Fort Drum, New York Acute coronary syndrome continues to be a significant cause of morbidity and mortality in the United States. Family physicians need to identify and mitigate risk factors early, as well as recognize and respond to acute coronary syn- drome events quickly in any clinical setting. Diagnosis can be made based on patient history, symptoms, electrocardi- ography findings, and cardiac biomarkers, which delineate between ST elevation myocardial infarction and non–ST elevation acute coronary syndrome. Rapid reperfusion with primary percutaneous coronary intervention is the goal with either clinical presentation. Coupled with appropriate medical management, percutaneous coronary interven- tion can improve short- and long-term outcomes following myocardial infarction. If percutaneous coronary interven- tion cannot be performed rapidly, patients with ST elevation myocardial infarction can be treated with fibrinolytic therapy. Fibrinolysis is not recommended in patients with non–ST elevation acute coronary syndrome; therefore, these patients should be treated with medical management if they are at low risk of coronary events or if percutaneous coronary intervention cannot be performed. Post–myocardial infarction care should
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]