• Information
  1. Causes
  2. Sudden Death in Young Athletes
  3. Athersclerosis and Sudden Death
  4. Sudden Cardiac Death

A. Causes

1. Generally divided into cardiac and non-cardiac causes
2. Cardiac causes should be evaluated based on patient's age (SCD=sudden cardiac death)
3. Common Causes of Sudden Death in Older Persons
   1. Almost all causes are related to coronary artery disease (CAD)
   2. Tachyarrhythmias in patients with ischemia or post-infarction (MI) are most common [4]
   3. Acute Coronary Thrombosis (MI) - usually due to unstable plaque rupture, thrombus [3]
   4. Exertion-related sudden death due to acute plaque rupture in patients with CAD [10]
4. Sudden Death in Young Adults [2]
   1. Study in military recruits age 18-35
   2. Rate ~13 per 100,000 person-years
   3. 86% associated with exercise
   4. Cardiac anomalies found in ~50% of deaths
   5. Coronary artery anomalies 60%, myocarditis 20%, hypertrophic cardiomyopathy (HCM) 13%
   6. Deaths unexplained in 35%
5. Sudden Death in Young Athletes [1,6]
   1. Rate is ~1/200,000 high school athletes per academic year
   2. HCM is most common cause or association
   3. Coronary artery malformations are the second most common
   4. Sudden, non-penetrating chest (thoracic) trauma increases risk of arrhythmia
6. Non-Cardiac Causes of Sudden Death
   1. Massive Stroke
   2. Asphyxiation - anaphylaxis, smoke inhalation, bronchospasm, foreign body
   3. Drug (usually recreational) Induced - cocaine, heroin, others
7. QTc Prolongation
   1. Congenital QTc prolongation can lead to Torsades, other arrhythmias, and/or death
   2. Certain drugs may prolong the QT interval
   3. Certain sudden infant death syndrome (SIDS) cases may be caused by QTc prolongation [5]
8. Overall, ~300,000 cases per year in USA
9. Automated external defibrillators can be used with minimal training and save lives [12]

B. Sudden Death in Young Athletes [1,6]

1. About 80% of cases are due to cardiac causes
2. About 20% are caused by commotio cordis (thoracic non-penetrating abrupt trauma)
3. Other causes include bronchospasm (asthma, anaphylaxis) and drug-induced
4. Cardiac Causes
   1. Hypertrophic Cardiomyopathy (HCM; ~35%)
   2. Increasing LV wall thickness is proportional to risk of sudden death in HCM [11]
   3. Coronary Artery Abnormalities (~20%)
   4. Abnormal increase in cardiac mass (~10%)
   5. Ruptured Aorta (5%)
   6. Tunneled Left Anterior Descending Artery (LAD) (5%)
   7. Aortic Stenosis (4%)
   8. Prolonged QT Syndromes
   9. Arrhythmogenic right ventricular dysplasia (ARVD) may also play a significant role, particularly in persons of Italian descent [26,27]
   10. Others: myocarditis, dilated cardiomyopathy, mitral valve prolapse
5. Sudden, Non-Penetrating Chest (Thoracic) Trauma [24]
   1. Increases risk of severe arrhythmia and suddent death
   2. Also called commotio cordis
6. Less than 10% of athletes who died of sudden cardiac death had physical exam findings
7. VTach in Healthy Hearts [9]
   1. Usually presents in young persons
   2. VTach originates in RV outflow tract or in LV near the septum
   3. Present with specific abnormal ECG depending on origin of VTach
   4. For RV outflow tract, ECG shows LBBB and inferior or right axis deviation
   5. For LV septum, ECG shows RBBB and left axis deviation
   6. Radiofrequency catheter ablation is >90% effective in these patients
8. Screening Young Athletes for Sports' Participation [1,6,27]
   1. American Heart Association Consensus Panel Preparticipation Screening Exams
   2. Family history of premature suddent death or heart disease in surviving relatives
   3. History of heart murmer, systemic hypertension, syncope, exertional dyspnea
   4. History of fatigability, exertional chest pain
   5. Parenteral verification of the patient and family history is strongly recommended
   6. Physical examination for heart murmer (both supine and sitting)
   7. Exam for femoral pulses, stigmata of Marfan syndrome
   8. Blood pressure measurement
   9. Preparticipation ECG with standard history and physical reduced associated with reduced risk of sudden death ~90% in Veneto, Italy [27]
   10. Strongloy consider preparticipation in ECG in all young persons initiating athletics
9. Evaluation in Suspected High Risk Persons
   1. History and Physical Examination - as described
   2. Echocardiography - much more sensitive than physical exam for detecting abnormalities
   3. Stress Testing - goal is to reproduce arrhythmia
   4. Tilt Table Testing - uncertain value in evaluation for SCD; used for evaluating syncope
   5. Electrophysiologic Studies - to induce arrhythmias

C. Athersclerosis and Sudden Death [4]

1. Atherogenesis is associated with SCD [8]
   1. Acute ischemia imposed on susceptible tissue is probable underlying mechanism
   2. Both partial and total coronary occlusions are associated with SCD
2. Most SCD occurs with dyslidemia, atherogenesis, inflammation
   1. Dyslipidemias are all associated with systemic inflammation
   2. Platelet activation, leucocytosis are common
   3. TNF alpha, IL-1, IL-6 and IL-8 are expressed
   4. Fibrinogen, plasminogen activator inhibitor (PAI) and Factor VII increased
   5. Peroxisome proliferator activated receptor (PPAR) alpha pathway upregulated by lipids
   6. Platelet activating factor (PAF) may be released in response to oxidized-LDL
   7. In addition, hepatocytes and macrophages exposed to high cholesterol greatly increase their synthesis of choline phospholipids
3. Suggested Pathways for Suppressing SCD Potential [4,8]
   1. Likely that agents which reduce harmful lipids and/or inflammation will reduce SCD
   2. Reduction in cholesterol with HMG-CoA Reductase Inhibitors (statins)
   3. ß-adrenergic blockers clearly reduce risk of SCD post-MI
   4. Estrogens reduce risk of SCD in post-menopausal women [7]
   5. ACE inhibitors may reduce the risk of SCD by reducing cariac hypertrophy
   6. PPAR alpha modulators such as leukotriene antagonists
   7. Cyclooxygenase (prostaglandin synthetase) inhibitors such as aspirin
   8. PAF-receptor antagonists
   9. Cytokine antagonists - note that glucocorticoids can suppress plaque formation

D. Sudden Cardiac Death (SCD) [13]

1. SCD accounts for ~50% of all cardiovascular deaths
2. In general, VTach or VF are believed to be major pre-morbid arrhythmias
3. Causes
   1. Most cases occur in patients with acute MI within first 72 hours
   2. Many cases occur in patients with previous MI and scar tissue
   3. 10-15% of cases in hypertrophic or dilated cardiomyopathy
   4. Other genetic syndromes associated with VTach or VF in <5% [14]
   5. Blunt impact (including sports, violence injuries) may predisopse to SCD [15]
   6. Earthquake may also trigger SCD [16]
   7. Neuro-cardiac interactions may play a role in some cases
4. Antihypertensive Therapy and SCD
   1. Non-potassium sparing diuretics appear to increase risk of SCD [17,18]
   2. This occurs more frequently within 1 year of initiating therapy than subsequently
   3. May be related to potassium and/or magnesium depletion
   4. ß-Blockers may increase risk of SCD in patients without coronary artery disease (CAD)
   5. However, ß-blockers protect from diuretic (and CAD) associated SCD
5. Prevention of SCD in Patients with CAD [13]
   1. Patients at risk for arrhythmias should be evaluated for arrhythmia potential
   2. Electrophysiology study should be performed to guide therapy
   3. ß-Adrenergic blockers are the most effective post-MI preventive therapy available [19]
   4. In general, implantable cardioverter defibrillator (ICD) is preferred therapy [25]
   5. Amiodarone and ICD may have similar efficacy in primary prevention of SCD in patients with ventricular arrhythmia [20]
   6. Other anti-arrhythmic agents do not substantially prevent post-MI arrhythmias
   7. Antiarrhythmic agents (except for ß-blockers and amiodarone) are associated with increased events in EPS-inducible patients who have CAD [21]
   8. No anti-arrhythmic agent (including ß-blockers and amiodarone) prevent recurrence of life-threatening arrhythmic events
   9. Only ICD have prevented recurrence of life-threatning arrhythmic events [25]
6. In post-resuscitation cardiac arrest patients, hypothermia to 32-34°C for 12-24 hours improves mortality and neurologic recovery [22,23]

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