DOCSLIB.ORG

Nitric Oxide-Mediated Flow-Dependent Dilation Is Impaired in Coronary Arteries in Patients with Coronary Spastic Angina

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Nitric Oxide-Mediated Flow-Dependent Dilation Is Impaired in Coronary Arteries in Patients with Coronary Spastic Angina View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector 920 JACC Vol. 30, No. 4 October 1997:920–6 Nitric Oxide-Mediated Flow-Dependent Dilation Is Impaired in Coronary Arteries in Patients With Coronary Spastic Angina KIYOTAKA KUGIYAMA, MD, MASAMICHI OHGUSHI, MD, TAKESHI MOTOYAMA, MD, SEIGO SUGIYAMA, MD, HISAO OGAWA, MD, MICHIHIRO YOSHIMURA, MD, YOSHITO INOBE, MD, OSAMU HIRASHIMA, MD, HIROAKI KAWANO, MD, HIROFUMI SOEJIMA, MD, HIROFUMI YASUE, MD Kumamoto City, Japan Objectives. This study sought to examine whether flow- Results. Flow-dependent dilation of the proximal LAD was dependent dilation is impaired at the site of coronary artery found to be less in spasm arteries than in control arteries. G spasm in patients with coronary spastic angina. Infusion of N -monomethyl-L-arginine (L-NMMA) in the proxi- Background. Physiologic stimuli such as exercise and exposure mal LAD suppressed flow-dependent dilation in control arteries to cold have been shown to cause an increase in coronary blood but had no significant effect on spasm arteries. The dilator flow, leading to flow-dependent dilation of coronary arteries in response to nitroglycerin was not impaired in spasm coronary normal subjects, but cause coronary constriction in patients with arteries. coronary spastic angina. Conclusions. Our results indicate that flow-dependent coronary Methods. A maximal increase in blood flow was induced dilation is impaired in spasm arteries, partly due to a deficiency in selectively in the left anterior descending coronary artery (LAD) endothelial nitric oxide bioactivity, which in turn may contribute by infusion of adenosine through a Doppler flow catheter tip in the to the increase in coronary tone during physiologic stimuli in midportion of the LAD in 10 patients with coronary spastic patients with coronary spastic angina. angina, all with angiographically demonstrated spasm of the LAD, (J Am Coll Cardiol 1997;30:920–6) and in 11 control patients. Coronary artery diameter at the ©1997 by the American College of Cardiology proximal site of the LAD (exposed to increased flow but not to adenosine) was measured by quantitative angiography. Coronary artery spasm has been shown (1,2) to play an continuously generates NO, which has been shown (8–14) to important role not only in the pathogenesis of variant angina, maintain basal vascular tone in animals and humans. We but also of ischemic heart disease in general, including other recently showed (14) that there is a deficiency in endothelial forms of angina pectoris, acute myocardial infarction and NO bioactivity at the sites of coronary artery spasm and that sudden death. However, the precise mechanism by which this deficiency plays an important role in the pathogenesis of coronary spasm occurs remains unknown. Nitric oxide (NO) is coronary spasm. Flow-dependent vasodilation is well known to an important vasodilator and is produced from L-arginine by have an important role in the regulation of arterial tone way of the enzyme NO synthase (NOS) (3–7). Analogues of (15–19). Physiological stimuli, such as exercise and the cold G L-arginine, such as N -monomethyl-L-arginine (L-NMMA), pressor test, which induce an increase in coronary blood flow, competitively inhibit NO production and have been widely have been shown (20–23) to dilate coronary arteries in normal used to examine the NO pathway in animals and humans subjects. However, we and others have shown (1,2,24,25) that (6–13). The constitutive NOS in the arterial endothelium spastic coronary arteries have increased basal tone and do not dilate but constrict during exercise and exposure to cold. An increase in blood flow or shear stress has been shown (3– From the Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan. This study was supported in part by Grant-in-Aid for 13,26,27) to produce endothelial release of NO, which causes Scientific Research C05670622 from the Ministry of Education, Science and flow-dependent vasodilation. Thus, the present study aimed to Culture and a Smoking Research Foundation Grant for Biochemical Research, examine whether flow-dependent dilation is impaired at the Tokyo, Japan. Manuscript received February 12, 1997; revised manuscript received May 27, sites of coronary artery spasm in patients with coronary spastic 1997, accepted June 20, 1997. angina and to determine the possible relevance of deficient NO Address for correspondence: Dr. Kiyotaka Kugiyama, Division of Cardiol- ogy, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto City, bioactivity to the abnormal response of coronary tone to blood 860 Japan. E-mail: [email protected]. flow in spasm coronary arteries. ©1997 by the American College of Cardiology 0735-1097/97/$17.00 Published by Elsevier Science Inc. PII S0735-1097(97)00236-2 JACC Vol. 30, No. 4 KUGIYAMA ET AL. 921 October 1997:920–6 FLOW-INDUCED DILATION IN SPASM CORONARY ARTERY Table 1. Clinical Characteristics of Study Patients* Abbreviations and Acronyms Patients Control ACh 5 acetylcholine With CSA Patients ECG 5 electrocardiogram (n 5 10) (n 5 11) LAD 5 left anterior descending coronary artery Age (yr) 59 11 57 10 LCx 5 left circumflex coronary artery 6 6 G Women/men 4/6 3/8 L-NMMA 5 N -monomethyl-L-arginine NO 5 nitric oxide Total serum cholesterol (mg/dl) 181 6 36 191 6 33 NOS 5 nitric oxide synthase HDL cholesterol (mg/dl) 39 6 846614 Serum triglyceride (mg/dl) 127 6 69 140 6 41 Hypercholesterolemia† 0 1 Hypertension‡ 3 2 Diabetes mellitus§ 0 2 Methods Current smokeri 24 *p 5 NS for all comparisons. †Total serum cholesterol $240 mg/dl. ‡Blood Study patients. The study included 10 patients with coro- pressure $140/90 mm Hg or taking antihypertensive medication. §Fasting blood nary spastic angina (mean age 59 years, range 43 to 71; six men, glucose $140 mg/dl or taking antidiabetic medication. i$10 cigarettes/day for four women) who fulfilled the following inclusion criteria: 1) $10 years. Data presented are mean value 6 SD or number of patients. CSA 5 spontaneous chest pain in association with ST segment eleva- coronary spastic angina. tion or depression on the 12-lead electrocardiogram (ECG) or the ambulatory ECG at rest, usually in the middle of the night or early morning and more than two times a day during the spasm (,50% decrease in coronary diameter from baseline) study; 2) coronary spasm (total or subtotal occlusion) of the after intracoronary injection of ACh. Neither nitrates nor left anterior descending coronary artery (LAD) demonstrated calcium channel blockers were effective in relieving chest pain angiographically during chest pain, with ST segment changes in any control patient. after intracoronary injection of acetylcholine (ACh), as previ- The clinical characteristics of the study patients are shown ously reported (28,29); 3) no organic coronary artery stenosis in Table 1. All medications except sublingual nitroglycerin on angiography. Five patients had transient ST segment ele- were withdrawn at least 3 days before the study, and no patient vation and five ST segment depression during the spontaneous had taken nitroglycerin within6hofthestudy. No patient had attacks. All 10 patients with coronary spastic angina performed a previous myocardial infarction, congestive heart failure or treadmill exercise and hyperventilation tests. Anginal attacks other serious diseases. Written informed consent was obtained of chest pain with ST segment changes occurred in two patients from all patients before the study. The study was approved by during the treadmill test (ST segment elevation in one, ST the ethics committee of our institution. segment depression in the other) and in four during the Study protocol. Coronary angiography was performed with hyperventilation test (ST segment elevation in three, ST seg- the Judkins technique using contrast material (Ioxaglate, ment depression in one). The spontaneous attacks were Guerbet S.A.) in the morning when the patients were fasting. promptly resolved by the administration of sublingual nitro- After heart rate and blood pressure measurements, control glycerin and were almost completely prevented by calcium angiography of the left main and right coronary arteries was channel blocking agents in all 10 patients with coronary spastic performed. Thereafter, incremental doses of ACh were in- angina. In patients with coronary spastic angina, the proximal jected into the left main coronary artery (20, 50 and 100 mg) LAD diameter at baseline angiography was .1.5 mm, so the and subsequently into the right coronary artery (20 and 50 mg). Doppler catheter was allowed to avoid catheter-induced coro- The method of injecting ACh for provocation of coronary nary spasm in these patients. All study patients had ambulatory spasm has been detailed elsewhere (28,29). Coronary spasm ECG monitoring for at least 48 h. ST segment changes on resolved spontaneously without the use of nitroglycerin in all 12-lead and ambulatory electrocardiography were considered patients with coronary spastic angina in this study. significant if transient ST segment elevation (.0.2 mV) or Flow-dependent dilation in human coronary arteries in vivo depression (.0.1 mV) versus baseline levels occurred at 60 to was assessed similar to previously reported methods (18,19). In 80 ms after the J point. brief, 15 min after completion of the intracoronary injection of This study also included 11 control patients who underwent ACh, when systemic hemodynamic variables and angiographic diagnostic cardiac catheterization for evaluation of atypical coronary artery diameters had returned to baseline levels, an chest pain (mean age 57 years, range 39 to 70; eight men, three additional 5,000 U of heparin was given intravenously, and an women) and were matched for coronary artery disease risk 8F guiding catheter was positioned in the ostium of the left factors to patients with coronary spastic angina.
Load more

Recommended publications
  • Young Adults. Look for ST Elevation, Tall QRS Voltage, "Fishhook" Deformity at the J Point, and Prominent T Waves
    EKG Abnormalities I. Early repolarization abnormality: A. A normal variant. Early repolarization is most often seen in healthy young adults. Look for ST elevation, tall QRS voltage, "fishhook" deformity at the J point, and prominent T waves. ST segment elevation is maximal in leads with tallest R waves. Note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2- 6 is concave upwards, another characteristic of this normal variant. Characteristics’ of early repolarization • notching or slurring of the terminal portion of the QRS wave • symmetric concordant T waves of large amplitude • relative temporal stability • most commonly presents in the precordial leads but often associated with it is less pronounced ST segment elevation in the limb leads To differentiate from anterior MI • the initial part of the ST segment is usually flat or convex upward in AMI • reciprocal ST depression may be present in AMI but not in early repolarization • ST segments in early repolarization are usually <2 mm (but have been reported up to 4 mm) To differentiate from pericarditis • the ST changes are more widespread in pericarditis • the T wave is normal in pericarditis • the ratio of the degree of ST elevation (measured using the PR segment as the baseline) to the height of the T wave is greater than 0.25 in V6 in pericarditis. 1 II. Acute Pericarditis: Stage 1 Pericarditis Changes A. Timing 1. Onset: Day 2-3 2. Duration: Up to 2 weeks B. Findings 1.
    [Show full text]
  • Veno-Occlusive Unloading of the Heart Reduces Infarct Size in Experimental
    www.nature.com/scientificreports OPEN Veno‑occlusive unloading of the heart reduces infarct size in experimental ischemia–reperfusion Esben Søvsø Szocska Hansen2, Tobias Lynge Madsen1, Gregory Wood1, Asger Granfeldt3, Nikolaj Bøgh2, Bawer Jalal Tofg1, Peter Agger4, Jakob Lykke Lindhardt1, Christian Bo Poulsen1, Hans Erik Bøtker1 & Won Yong Kim1,2* Mechanical unloading of the left ventricle reduces infarct size after acute myocardial infarction by reducing cardiac work. Left ventricular veno‑occlusive unloading reduces cardiac work and may reduce ischemia and reperfusion injury. In a porcine model of myocardial ischemia–reperfusion injury we randomized 18 pigs to either control or veno‑occlusive unloading using a balloon engaged from the femoral vein into the inferior caval vein and infated at onset of ischemia. Evans blue and 2,3,5‑triphenyltetrazolium chloride were used to determine the myocardial area at risk and infarct size, respectively. Pressure–volume loops were recorded to calculate cardiac work, left ventricular (LV) volumes and ejection fraction. Veno‑occlusive unloading reduced infarct size compared with controls (Unloading 13.9 ± 8.2% versus Control 22.4 ± 6.6%; p = 0.04). Unloading increased myocardial salvage (54.8 ± 23.4% vs 28.5 ± 14.0%; p = 0.02), while the area at risk was similar (28.4 ± 6.7% vs 27.4 ± 5.8%; p = 0.74). LV ejection fraction was preserved in the unloaded group, while the control group showed a reduced LV ejection fraction. Veno‑occlusive unloading reduced myocardial infarct size and preserved LV ejection fraction in an experimental acute ischemia–reperfusion model. This proof‑of‑concept study demonstrated the potential of veno‑occlusive unloading as an adjunctive cardioprotective therapy in patients undergoing revascularization for acute myocardial infarction.
    [Show full text]
  • Angelmed Guardian System
    Angel Medical Systems, Inc. Guardian® System Executive Summary Circulatory System Devices Panel AngelMed Guardian® System for the Alerting of Patients to ST Segment Changes Indicative of Coronary Artery Occlusion PMA P150009 SPONSOR EXECUTIVE SUMMARY CIRCULATORY SYSTEM DEVICES PANEL MEETING DATE: March 16, 2016 Sponsored by Angel Medical Systems, Inc. 1 Angel Medical Systems, Inc. Guardian® System Executive Summary Circulatory System Devices Panel Table of Contents 1 Synopsis .......................................................................................................................1 2 Unmet Need for Earlier Treatment of Heart Attacks .............................................5 2.1 Epidemiology of Recurrent Heart Attacks ...................................................................5 2.2 Impact of Treatment Delay on Clinical Outcomes .......................................................6 2.3 Inadequacy of Reliance on Symptoms to Prompt Treatment for Heart Attacks ..........................................................................................................................6 2.4 Rationale for Continuous ST Segment Monitoring to Identify Coronary Occlusion ......................................................................................................................7 3 AngelMed Guardian System ......................................................................................9 3.1 Overview of the Guardian System ................................................................................9 3.2
    [Show full text]
  • Effect of Nitroglycerin and Dipyridamole on Regional Left Ventricular Blood Flow During Coronary Artery Occlusion
    Effect of Nitroglycerin and Dipyridamole on Regional Left Ventricular Blood Flow during Coronary Artery Occlusion LEWIS C. BECKER From the Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27514 and Johns Hopkins University School of Medicine, Department of Medicine, Baltimore, Maryland 21205 A B S T R A C T Coronary vasodilators have been vari- INTRODUCTION or have no effect ously reported to increase, decrease, Coronary vasodilators increase myocardial blood flow upon blood flow to ischemic myocardium. Conse- in hearts with normal coronary arteries and may also quently, the effects of two different types of dilators, increase flow when coronary artery occlusive disease nitroglycerin (TNG) and dipyridamole, were studied is present (1). However, in the latter situation, in- with radioactive microspheres in open-chested dogs be to after coronary artery ligation. Given as a bolus i.v. creased flow may merely going myocardial injection, 0.4 mg TNG resulted in an increase in regions fed by normal vessels rather than areas sup- blood flow to nonischemic areas of myocardium and a plied by obstructed vessels. While some investigators preservation of flow to ischemic regions, despite a fall have found that vasodilators increase flow to com- blood pressure and promised myocardium (2-8), others have found a de- in blood pressure. 5 min later crease or no change (9-14). Fam and McGregor (11) nonischemic flow were back to base line, and a small be re- selective increase in flow to ischemic myocardium have pointed out that these discrepancies may per g, P < 0.05).
    [Show full text]
  • Dysrhythmias
    CARDIOVASCULAR DISORDERS DYSRHYTHMIAS I. BASIC PRINCIPLES OF CARDIAC CONDUCTION DISTURBANCES A. Standard ECG and rhythm strips 1. Recordings are obtained at a paper speed of 25 mm/sec. 2. The vertical axis measures distance; the smallest divisions are 1 mm ×1 mm. 3. The horizontal axis measures time; each small division is 0.04 sec/mm. B. Normal morphology Courtesy of Dr. Michael McCrea 1. P wave = atrial depolarization a. Upright in leads I, II, III, aVL, and aVF; inverted in lead aVR b. Measures <0.10 seconds wide and <3 mm high c. Normal PR interval is 0.12–0.20 seconds. 2. QRS complex = ventricular depolarization a. Measures 0.06-0.10 seconds wide b. Q wave (1) <0.04 seconds wide and <3 mm deep (2) Abnormal if it is >3 mm deep or >1/3 of the QRS complex. c. R wave ≤7.5 mm high 3. QT interval varies with rate and sex but is usually 0.33–0.42 seconds; at normal heart rates, it is normally <1/2 the preceding RR interval. 4. T wave = ventricular repolarization a. Upright in leads I, II, V3–V6; inverted in aVR b. Slightly rounded and asymmetric in configuration c. Measures ≤5 mm high in limb leads and ≤10 mm high in the chest leads 5. U wave = a ventricular afterpotential a. Any deflection after the T wave (usually low voltage) b. Same polarity as the T wave c. Most easily detected in lead V3 d. Can be a normal component of the ECG e. Prominent U waves may indicate one of the following: (1) Hypokalemia (<3 mEq/L) (2) Hypercalcemia (3) Therapy with digitalis, phenothiazines, quinidine, epinephrine, inotropic agents, or amiodarone (4) Thyrotoxicosis f.
    [Show full text]
  • ST-Segment Elevation in Conditions Other Than Acute Myocardial Infarction
    The new england journal of medicine review article current concepts ST-Segment Elevation in Conditions Other Than Acute Myocardial Infarction Kyuhyun Wang, M.D., Richard W. Asinger, M.D., and Henry J.L. Marriott, M.D. From the Hennepin County Medical Cen- cute myocardial infarction resulting from an occlusive ter, University of Minnesota, Minneapolis thrombus is recognized on an electrocardiogram by ST-segment elevation.1 (K.W., R.W.A.); and the University of South a 2-4 Florida, Tampa (H.J.L.M.). Address reprint Early reperfusion therapy has proved beneficial in such infarctions. The requests to Dr. Wang at the Hennepin earlier the reperfusion, the greater the benefit, and the time to treatment is now consid- County Medical Center, Cardiology Division, ered to indicate the quality of care. These days, when thrombolytic treatment and per- 701 Park Ave., MC 865A, Minneapolis, MN 55415. cutaneous intervention are carried out so readily, it is important to remember that acute infarction is not the only cause of ST-segment elevation. The purpose of this review is N Engl J Med 2003;349:2128-35. to describe other conditions that mimic infarction and emphasize the electrocardio- Copyright © 2003 Massachusetts Medical Society. graphic clues that can be used to differentiate them from true infarction. normal st-segment elevation and normal variants The level of the ST segment should be measured in relation to the end of the PR seg- ment, not the TP segment.5 In this way, ST-segment deviation can still be detected ac- curately, even if the TP segment is not present because the P wave is superimposed on the T wave during sinus tachycardia or if the PR segment is depressed or there is a prominent atrial repolarization (Ta) wave.
    [Show full text]
  • Angiogenesis and Myogenesis in a Chronic Ischemic Heart. Esha Ibrahim East Tennessee State University
    East Tennessee State University Digital Commons @ East Tennessee State University Electronic Theses and Dissertations Student Works 8-2005 Angiogenesis and Myogenesis in a Chronic Ischemic Heart. Esha Ibrahim East Tennessee State University Follow this and additional works at: https://dc.etsu.edu/etd Part of the Medical Sciences Commons Recommended Citation Ibrahim, Esha, "Angiogenesis and Myogenesis in a Chronic Ischemic Heart." (2005). Electronic Theses and Dissertations. Paper 1058. https://dc.etsu.edu/etd/1058 This Thesis - Open Access is brought to you for free and open access by the Student Works at Digital Commons @ East Tennessee State University. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of Digital Commons @ East Tennessee State University. For more information, please contact [email protected]. Angiogenesis and Myogenesis in a Chronic Ischemic Heart A thesis presented to the faculty of the Department of Physiology East Tennessee State University In partial fulfillment of the requirements for the degree Master of Science in Biomedical Science by Esha Ibrahim August 2005 Race L. Kao, Ph.D., Chair Brian Rowe, Ph. D. Krishna Singh, Ph. D. Keywords: TMR, angiogenesis, myogenesis, myocardial ischemia, ventricular function ABSTRACT Angiogenesis and Myogenesis in a Chronic Ischemic Heart by Esha Ibrahim Miniswine underwent procedures to evaluate treating chronic ischemia with the implantation of autologous satellite cells and laser transmyocardial revascularization (TMR). The objective was to combine two therapies to restore cardiac function. This experiment involved three surgical procedures: (1) placing a constrictor on the coronary artery; (2) producing channels and implanting cells; (3) obtaining samples. The swine were divided into groups: Group 1, Ischemia; Group 2, Ischemia + Laser TMR; Group 3, Ischemia + Laser TMR+ Cells; Group 4, Ischemia + Cells.
    [Show full text]
  • Advanced EKG Interpretation JUNCTIONAL RHYTHMS and NURSING INTERVENTIONS Objectives
    Advanced EKG Interpretation JUNCTIONAL RHYTHMS AND NURSING INTERVENTIONS Objectives ♥ Identify specific cardiac dysrhythmias ♥ Describe appropriate nursing interventions for specific dysrhythmias Junctional Rhythms ▪ Junctional rhythms are named such because their impulse originates from the AV node (AV junction) instead of the SA node. ▪ The SA node may be impaired secondary to drug toxicity or underlying cardiac disease. ▪ When the AV node does not sense an impulse coming down from the SA node, it will become the pacemaker of the heart. Characteristics of all Junctional Rhythms ▪ Inverted (negative) or absent P waves are seen before each QRS complex OR ▪ P wave can be hidden in the QRS complex OR ▪ P wave may follow the QRS complex ▪ PR interval of <0.12 seconds (remember normal is 0.12-0.2) ▪ QRS complex within normal measurements Most Common Variations ▪ Junctional (escape) rhythm: 40 - 60 bpm ▪ Accelerated junctional rhythm: 61 – 100 bpm ▪ Junctional tachycardia: >100 bpm ▪ Premature junctional complexes (PJCs) Junctional Rhythm ♥ Junctional (escape) rhythms originate at or around the AV node and the Bundle of His. The impulse travels up the atria and down to the ventricles resulting in inverted P waves that can occur prior to, during or after the QRS. ♥ P waves can also be absent if the impulse does not travel up into the atria. Inverted P wave 5 Steps to Identify Junctional Rhythm 1. What is the rate? 40-60 bpm 2. What is the rhythm? Regular 3. Is there a P wave before each QRS? Are P waves upright Usually inverted or absent, may be before, during or after and uniform? QRS complex 4.
    [Show full text]
  • Establishing a Myocardial Ischemia-Reperfusion Injury Model in Mice and Rats Using Left Anterior Descending Artery Ligation and Isolated Heart Experiments
    Philadelphia College of Osteopathic Medicine DigitalCommons@PCOM PCOM Biomedical Studies Student Scholarship Student Dissertations, Theses and Papers 2020 Establishing a Myocardial Ischemia-Reperfusion Injury Model in Mice and Rats using Left Anterior Descending Artery Ligation and Isolated Heart Experiments Alexander Papa Philadelphia College of Osteopathic Medicine Follow this and additional works at: https://digitalcommons.pcom.edu/biomed Part of the Medicine and Health Sciences Commons Recommended Citation Papa, Alexander, "Establishing a Myocardial Ischemia-Reperfusion Injury Model in Mice and Rats using Left Anterior Descending Artery Ligation and Isolated Heart Experiments" (2020). PCOM Biomedical Studies Student Scholarship. 195. https://digitalcommons.pcom.edu/biomed/195 This Thesis is brought to you for free and open access by the Student Dissertations, Theses and Papers at DigitalCommons@PCOM. It has been accepted for inclusion in PCOM Biomedical Studies Student Scholarship by an authorized administrator of DigitalCommons@PCOM. For more information, please contact [email protected]. Philadelphia College of Osteopathic Medicine Graduate Program in Biomedical Sciences Department of Bio-Medical Sciences Establishing a Myocardial Ischemia-Reperfusion Injury model in mice and rats using Left Anterior Descending Artery ligation and Isolated Heart experiments. A Thesis in Biomedical Sciences by Alexander Papa We, the undersigned, duly appointed committee have read and examined this manuscript and certify it is adequate in scope and
    [Show full text]
  • Descending Necrotizing Mediastinitis Mimicking Acute ST Segment Elevation Myocardial Infarction
    Case Report DNM Mimicking Acute STEMI Acta Cardiol Sin 2010;26:123-6 Descending Necrotizing Mediastinitis Mimicking Acute ST Segment Elevation Myocardial Infarction Hung-Yu Chang,1 Yung-Nien Yang,1 Wei-Hsian Yin1 and Mason-Shing Young2 Descending necrotizing mediastinitis (DNM) is a rare but lethal disease. Despite prompt use of broad-spectrum antibiotics and proper surgical drainage, the mortality is still high. High vigilance for disease presentation is helpful to early diagnosis. A 59-year-old female with a history of hypertension, diabetes and dyslipidemia came to our emergency room. Her initial presentation of chest pain, elevated troponin-I level and ST segment elevation in electrocardiogram (ECG) mimicked acute ST segment elevation myocardial infarction. However, DNM was suspected by her atypical clinical presentation and imaging studies. The ST segment elevation in ECG resolved immediately after pigtail catheter drainage. Finally, DNM was proved by right thoracotomy with mediastinal exploration. Klebsiella pneumoniae was isolated from pus and necrotic tissue. Key Words: Coronary artery disease · Descending necrotizing mediastinitis · Myocardial infarction INTRODUCTION CASE REPORT Descending necrotizing mediastinitis (DNM) is a A 59-year-old woman presented at the emergency rare but lethal disease. This disease results from odon- room of our institution with progressive, substernal dull togenic, pharyngeal, or cervical infection extending chest pain for three days and mild drowsiness for one downward into the mediastinum via pretracheal, para- day. Within the previous two weeks, she had experi- pharyngeal and retrovisceral spaces of the neck. The in- enced non-productive cough and snuffle. She had his- fection is often polymicrobial in etiology, with gas-pro- tory of hypertension, type 2 diabetes and dyslipidemia, ducing organisms.
    [Show full text]
  • Guidelines for the Interpretation of the Neonatal Electrocardiogram
    European Heart Journal (2002) 23, 1329–1344 doi:10.1053/euhj.2002.3274, available online at http://www.idealibrary.com on Task Force Report Guidelines for the interpretation of the neonatal electrocardiogram A Task Force of the European Society of Cardiology P. J. Schwartz1 (Chair), A. Garson, Jr2, T. Paul3, M. Stramba-Badiale4, V. L. Vetter5, E. Villain6 and C. Wren7 1Department of Cardiology, University of Pavia and IRCCS Policlinico S. Matteo, Pavia, Italy; 2University of Virginia, Charlottesville, VA, U.S.A.; 3The Children’s Heart Program of South Carolina, Medical University of South Carolina, Charleston, SC, U.S.A.; 4Pediatric Arrhythmias Center, IRCCS Istituto Auxologico Italiano, Milan, Italy; 5Division of Pediatric Cardiology, Department of Pediatrics, Children’s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA, U.S.A.; 6Division of Pediatric Cardiology, Department of Pediatrics, Hoˆpital Necker Enfants Malades, Paris, France; 7Department of Paediatric Cardiology, Freeman Hospital, Newcastle upon Tyne, U.K. Introduction.............................................................1329 Left ventricular hypertrophy............................1338 Normal electrocardiogram in the newborn .............1330 Low QRS voltage.............................................1338 Normal values......................................................1330 Ventricular repolarization....................................1338 Technology ..........................................................1330 QT prolongation:
    [Show full text]
  • Non Specific S-T Segment Variations During Intravenous Induction in Anesthesia in Hypertensive Patients Treated with Renin Angiotensin System Antagonists
    Journal of Anesthesia & Critical Care: Open Access Research Article Open Access Non specific S-T segment variations during intravenous induction in anesthesia in hypertensive patients treated with renin angiotensin system antagonists Abstract Volume 8 Issue 1 - 2017 Background: induction in anesthesia and airway‘s manipulations are stressful events for Marija Sholjakova,1 Marija Jovanovski-Srceva2 patients undergoing surgery, producing consecutive changes in blood pressure and pulse 1Department for Doctoral studies University “Ss. Cyril & rate. There are several reports indicating that hypertensive patients treated with Renin Methodius” Faculty of Medicine, Republic of Macedonia angiotensin system (RAS) antagonists show greater hemodynamic changes during these 2University Clinic of Anesthesiology, University “Ss. Cyril & periods which may imply that coronary circulation is compromised and variations in the Methodius” Faculty of Medicine, Republic of Macedonia ST-T segment might be noticed. The aim of this study was to evaluate and report the ST changes appeared during intravenous induction to anesthesia in hypertensive patients. Correspondence: Marija Sholjakova, Full professor of Anesthesiology, Department for Doctoral studies University Ss. Method and material: In prospective, randomized clinical study, Sixty patients undergoing Cyril & Methodius Faculty of Medicine, Bul. Marks I Engels 2 elective surgery in general anesthesia, ASA I and II, BMI <30m were randomized into 1/5-16, 1000 Skopje, Republic of Macedonia, Tel +389 71 24 34
    [Show full text]