Sudden cardiac death causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2]
Overview
Sudden cardiac arrest may be caused by coronary artery abnormality such as coronary atherosclerosis, acute MI, coronary artery embolism, coronary arteritis , hypertrophy of myocardium such as HCM, hypertensive heart disease, primary or secondary pulmonary hypertension , myocardial disease such as ischemic cardiomyopathy, non-ischemic cardiomyopathy, myocarditis ,valvular heart disease such as aortic stenosis, aortic insufficiency, mitral valve prolapse, endocarditis , congenital heart disease such as congenital septal defect with eisenmenger physiology , abnormality in conducting system such as Wolf-Parkinson-White syndrome , electrical instability such as (CPVT, LQTS)
Causes
Sudden cardiac arrest may be caused by :
- Coronary artery abnormality such as coronary atherosclerosis, acute MI, coronary artery embolism, coronary arteritis[1][2]
- Hypertrophy of myocardium such as HCM, hypertensive heart disease, primary or secondary pulmonary hypertension
- Myocardial disease such as ischemic cardiomyopathy, non-ischemic cardiomyopathy, myocarditis[3]
- Valvular heart disease such as aortic stenosis,aortic insufficiency, mitral valve prolapse, endocarditis [4]
- Congenital heart disease such as congenital septal defect with Eisenmenger physiology[5]
- Abnormality in conducting system such as Wolf-Parkinson-White syndrome
- Electrical instability such as (CPVT, LQTS)
Differentaitindg diagnosis of sudden cardiac death | Coronary Artery Disease | Ideopathic dilated cardiomyopathy | Hypertrophic cardiomyopathy | Arrhythmogenic right ventricular cardiomyopathy | Valvular Heart Disease | Congenital Heart Disease | Long QT syndrome | WPW syndrome | Ideopathic monomorphic VT | Ideopathic polymorphic VT | Primary VF | Sudden unexpected nocturnal death | Drugs]] |
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Incidence of SCD | Atherosclirosis: 80% | 10% | 2-4% per year in adult, 4-6% in children and adolescence | 2% | 20% of post operative death after valvular replacement | 1/1000 patient-year follow- up | Rare | ||||||
Mechanism | Atherosclerosis in coronary arteries: 3 vessels disease in 40-86% patients with stenosis > 75%, MI < 50%, Qwave MI < 25%, recent coronary thrombosis 15-64% (plaque, fissure, hemorrhage, thrombosis), healed infarct>50% in autopsy or survivors of SCD, Non atherosclerotic changes including coronary emboli, coronary arthritis, coronary dissection in few cases | Myocardial stretch, neuroendocrine factors, electrolyte abnormality, proarrhythmic effect of antiarrhythmic drugs, excessive activation of sympathetic and renin angiotensin system | Arrhythmia, abrupt hemodynamic deterioration, ischemia | Fatty and fibrofaty myocardial infiltration, patchy myocarditis, apoptosis of left ventricle, left ventricular septum (50-67%), right ventricular inflow, outflow tract and apex( triangle of dysplasia) | Arrhythmia, prosthetic valve dysfunction,Coexisting CAD | Tetralogy of fallot, Transposition of the great arteries, Aortic stenosis, Pulmonary vascular obstruction. SCD is late presentation after surgical repair of complex congenital heart disease | Prolongation of repolarization, early after depolarization | In 10% of patients, SCD is first presentation. development of AF rapid conduction to the ventricle through accessory pathway caused VF | Normal heart structure, Originated from RV outflow tract (more common), or LV outflow tract. SCD is rare | Initiation of arrhythmia with coupled premature complex,SCD is more common than monomorphic VT, sporadic or familiar | |||
Risk factors of SCD | Frequent episodes of non sustain VT, syncope | Family history of SCD, recurrent syncope, sustained VT, history of SCA, massive LVH, multiple episodes of non sustained VT | Asymptomatic aotric valve disease is low risk for [[SCD].Risk factors of SCD in MVP: myxomatous degeneration of the valve, coexisting mitral regurgitation, LV dysfunction | Risk factors of SCD in TOF: QRS prolongation, dilated RV | Incidence of cardiac event in LQTS1, LQTS2> LQTS3 Lethality of cardiac event in LQTS3>LQTS1,LQTS2 | Predictors of VF: AF with shortest interval between ventricle beats less than 250 msec | Cathecolamine release after stressful emotional or physical event | ||||||
Arrhythmia | VT, VF (75%), bradycardia, asystole(25%) | Mechanism of VT: bundle branch reentry tachycardia, terminal event: asystole, [[electromechanical dissociation in advanced LV dysfunction | 9 | ECG in normal sinus rhythm:inverted T waves in V1-V3, complete, incomplete RBBB, epsilone wave ( terminal notch on QRS complex), VT is LBBB contour | Arrhythmia:Torsadepoints, Normal ECG findings: abnormal Twaves contour, Twaves alternance, sinus bradycardia | RV outflow tract VT is LBBB contour, inferior axis, Termination with vagal maneuver such as adenosine. LVOT VT or fasciculated VT is RBBB contour with left axis deviation, originated from left posterior septum, Termination with calcium channel blocker | SCD in the presence of polymorphic VT and normal LV function without torsadepoints, Termination of cathecolaminergic polymorphic VT (CPVT) with betablocker, No response to betablocker in the presence of ideopathic VF or short coupled of torsadepoints |
- Causes of acquired Long QT syndrome include the following:
- Antiarrhythmic agents
- Class IA: quinidine, procainamide, N-acetyl procainamide, disopyramide
- Class III: amiodarone, low risk of torsade de points
- Class IV: bepridil,mibefradil
- Antihistamines
- Terfenadine
- Astemizole
- Antimicrobials
- Erythromycin
- Trimethoprim-sulfamethoxazole
- Clarithromycin
- Cotzimoxazole
- Azithromycin
- Ketoconazole
- Pentamidine
- Chloroquine
- Gastrointestinal
- Cisapride
- Liquid protein diets
- Anorexia nervosa
- Lipid-lowering
- Probucol
- Psychotropic agents
- Tricyclic and tetracycline antidepressants
- Haloperidol
- Phenothiazines
- Risperidone
- Selective serotonin reuptake inhibitors
- Other agents
- Organophosphates
- Diuretics (reduced K+, Mg2+)
- Vasopressin (severe bradycardia)
- Chloral hydrate amantadine
- Electrolyte abnormalities
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Causes of Sudden Death Including Sudden Cardiac Death by Organ System
Differentiating sudden cardiac death from non-cardiac causes
References
- ↑ Mehta, Davendra; Curwin, Jay; Gomes, J. Anthony; Fuster, Valentin (1997). "Sudden Death in Coronary Artery Disease". Circulation. 96 (9): 3215–3223. doi:10.1161/01.CIR.96.9.3215. ISSN 0009-7322.
- ↑ Eisenberg MS, Mengert TJ (2001). "Cardiac resuscitation". N. Engl. J. Med. 344 (17): 1304–13. PMID 11320390. Unknown parameter
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ignored (help) - ↑ . doi:10.1080/2F20961790.2019.1595352. Missing or empty
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(help) - ↑ 4.0 4.1 Basso, Cristina; Perazzolo Marra, Martina; Rizzo, Stefania; De Lazzari, Manuel; Giorgi, Benedetta; Cipriani, Alberto; Frigo, Anna Chiara; Rigato, Ilaria; Migliore, Federico; Pilichou, Kalliopi; Bertaglia, Emanuele; Cacciavillani, Luisa; Bauce, Barbara; Corrado, Domenico; Thiene, Gaetano; Iliceto, Sabino (2015). "Arrhythmic Mitral Valve Prolapse and Sudden Cardiac Death". Circulation. 132 (7): 556–566. doi:10.1161/CIRCULATIONAHA.115.016291. ISSN 0009-7322.
- ↑ Yap, Sing-Chien; Harris, Louise (2014). "Sudden cardiac death in adults with congenital heart disease". Expert Review of Cardiovascular Therapy. 7 (12): 1605–1620. doi:10.1586/erc.09.153. ISSN 1477-9072.