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Sudden Cardiac Arrest and Cardiopulmonary Resuscitation (CPR)

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  1. Introduction to sudden cardiac arrest and resuscitation
    4 Chapters
  2. Resuscitation physiology and mechanisms
    2 Chapters
  3. Causes of sudden cardiac arrest and death
    2 Chapters
  4. Cardiopulmonary Resuscitation
    10 Chapters
  5. Special Circumstances
    11 Chapters
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It is commonly stated that approximately 80% of all cardiac arrests are caused by acute or chronic coronary artery disease, with the latter being the most common. The figure 80% occurs in most textbooks in the field. However, contemporary data suggest that the current figure is approximately 60%. The discrepancy between traditional figures and recent studies is due to the dramatic decrease in the incidence of acute coronary syndromes over the past decades. Furthermore, early revascularization in acute coronary syndromes (STEMI, NSTEMI, unstable angina) has increased, resulting in fewer cardiac arrests caused by these conditions (Jerkeman et al).

It is often difficult to determine the cause of an out-of-hospital cardiac arrest. Autopsies are recommended when the underlying cause is unknown, particularly among young individuals. Yet, autopsies are often not performed due to the high costs. The difficulties in determining the cause of out-of-hospital cardiac arrest are reflected in the classification recommended according to the Utstein guidelines (Table 1). The broad categories of causes are considered necessary due to the uncertainties prevailing in the pre-hospital setting (Perkins et al.). Figure 1 presents data from the Swedish Cardiac Arrest Registry, which has recorded causes of cardiac arrest with a separate category for cardiac etiologies.

Medical causeIncludes cardiac arrest caused by heart disease, other medical conditions (pulmonary embolism, bleeding, stroke, etc.) as well as cases where the cause does not fall into the other categories.
TraumaCardiac arrest caused by violence, accidents, burns, or other trauma.
DrowningCardiac arrest due to drowning
ElectrocutionCardiac arrest due to electrical current through the heart.
AsphyxiaAsphyxia as a result of external causes, for example foreign body, hanging or strangulation.
Drug overdoseIntentional or accidental overdose of medications, drugs or other substances (including alcohol) causing cardiac arrest.
Table 1. Classification of causes of cardiac arrest according to the Utstein protocol.
Figure 1. Data from the Swedish Cardiopulmonary Resuscitation Registry (SCRR), showing presumed causes of out-of-hospital cardiac arrest in 130’000 cases (Rawshani et al).

Cardiac etiology

Cardiac arrests caused by cardiovascular conditions and events are highly stochastic events. This is due to the fact that the vast majority of these arrests are caused by ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation), whose occurrence is highly stochastic. This is evident from the fact that the vast majority of all myocardial infarctions and episodes of myocardial ischemia, do not cause ventricular arrhythmias and cardiac arrest. It is clear that only a negligible fraction of all episodes of myocardial ischemia result in cardiac arrest. In order for an infarction or ischemic episode to result in ventricular arrhythmia, it must coincide with other pro-arrhythmogenic factors. The emergence of ventricular tachycardia or ventricular fibrillation is, therefore, the result of a perfect storm scenario, where ischemia, hemodynamics, the autonomous nervous system, electrolyte concentrations, and other factors (potentially also genetic predisposition) interact to trigger ventricular tachycardia or ventricular fibrillation. These factors interact and vary over time. Some factors vary from second to second (e.g. degree of ischemia, parasympathetic and sympathetic tone) while others take months or years to develop (e.g. myocardial remodeling in heart failure or after myocardial infarction).

Ventricular arrhythmias are easier to induce in the presence of arrhythmogenic substrates. A substrate is defined as a physiological or anatomical factor that can trigger or sustain arrhythmias, such as necrotic tissue after myocardial infarction (refer to Mechanisms of cardiac arrhythmias).

It is often difficult to clarify the exact mechanism causing cardiac arrest, even if a substrate is known. A patient with ischemic cardiomyopathy may have multiple substrates – e.g. necrotic tissue in the myocardium, heart failure with dilatation and myocardial remodeling, and repeated episodes of ischemia due to coronary artery stenoses – making it difficult to determine the exact trigger.

Chronic and acute coronary syndromes

  • Acute myocardial ischemia can induce ventricular tachycardia and ventricular fibrillation, thereby causing cardiac arrest. This can occur at any time during the natural course of coronary artery disease, including as the first manifestation of coronary heart disease. The arrhythmia mechanism is, in most cases, re-entry around the ischemic zone.
  • Acute myocardial infarction can also cause ventricular tachycardia and ventricular fibrillation. The arrhythmia mechanism is also re-entry. The risk of ventricular tachycardia and ventricular fibrillation is highest during the first minutes and hour and then diminishes rapidly.
  • Chronic total occlusions (CTO) are complete and chronic occlusions of coronary arteries. Virtually all CTOs have collateral vessels (from other arteries) that reperfuse the occluded artery, such that the myocardium at risk can be perfused. However, the myocardium is likely to have developed arrhythmia substrates (e.g. infarction) despite the support from collateral vessels. Collaterals may prevent or limit additional infarction and enable full contractile function at rest. However, the functional reserve in collaterals is limited, and the vast majority of patients with CTOs experience ischemic symptoms related to the myocardium supplied by the CTO. Recent studies show that roughly 35% of patients with out-of-hospital cardiac arrest, with an initial shockable rhythm, have CTOs (Lemkes et al.).
  • Ischemic cardiomyopathy. Ischemic cardiomyopathy is characterized by remodeling, scar formation, and heart failure, which pose a very high risk of malignant ventricular arrhythmias. Patients with ischemic cardiomyopathy have a high risk of sudden cardiac arrest.

Among patients who experience cardiac arrest, previous myocardial infarction is significantly more common than acute myocardial infarction. A previous infarction is seen in 40–70% of all out-of-hospital cardiac arrests, while acute or recent infarction is observed in 20% of cases. In the POST-SCD study, only 30% of all cases had acute coronary syndrome (Tseng et al.). Thus, among cases with coronary artery disease as the underlying cause of cardiac arrest, old infarctions constitute the majority of the substrates.

The risk of cardiac arrest increases with the extent of the ischemia or infarction. The risk also increases with electrolyte imbalance, hypotension, hypertension, left ventricular load, and with sympathetic activation.

  • Congenital coronary artery anomalies
    • Congenital variants in the origination of coronary arteries occur in 5% of all individuals (Angelini et al.). Some variants are associated with an increased risk of sudden cardiac arrest, particularly during strenuous exercise.
    • Myocardial bridges (prevalent in 1% of the population) are believed to increase the risk of sudden cardiac arrest, especially during exercise. Bridges are defined as epicardial segments of the coronary artery running within the myocardium, resulting in compression of the coronary artery segment (Figure 1).
  • Embolism to the coronary arteries
    • Embolism from endocarditis (aortic valve, mitral valve).
    • Embolism from thrombi in the proximal aorta.
    • Embolism from mural thrombi in the left ventricle.
    • Embolism from thrombi formed in the left atrial appendage.
  • Arteritis (inflammation of the coronary arteries)
    • Kawasaki’s disease.
    • Polyarteritis nodosa (PAN).
  • Coronary artery spasm can cause sudden cardiac arrest due to ventricular arrhythmias. The risk appears to be higher if the spasm occurs in atherosclerotic coronary arteries with stenoses.
  • Proximal aortic dissection with occlusion of the coronary ostium can lead to extensive ischemia and ventricular arrhythmias.
Figur 1. Myocardial bridge
Figure 2. Myocardial bridge in LAD (left anterior descending artery). LAD viewed from different angles. The arrow indicates the compressed segment. A1 is recorded during systole. A2 is recorded during diastole. Source.

Troponin for differential diagnosis of cardiac arrest

Cardiac-specific Troponin T (TnT) and Troponin I (TnI) are often analyzed in cases of out-of-hospital cardiac arrest to determine whether the cardiac arrest was caused by an acute myocardial infarction. The rationale behind this is that myocardial necrosis commences after 20 minutes of complete myocardial anoxia. Thus, cardiac arrests due to causes other than acute myocardial infarction should present with low levels of troponins, as opposed to infarction-caused cardiac arrests, which should result in high troponin levels. However, it is questionable whether troponin can be used for this purpose. In a study of 145 patients who regained circulation after cardiac arrest and underwent serial troponin measurements and echocardiographic examinations, all individuals had elevated troponin levels, and the levels could not be used to distinguish infarction-related cardiac arrest from other causes. Troponin levels also did not correlate with survival or left ventricular function (Agusala et al.).

Suggested reading: Cardiac troponin I (TnI) and T (TnT): Interpretation and evaluation in acute coronary syndromes

Hypertrophy and hypertrophic cardiomyopathy

All types of hypertrophy, regardless of etiology and localization, increase the risk of ventricular arrhythmias and sudden cardiac arrest. The most common cause of ventricular hypertrophy is arterial hypertension, which results in left ventricular hypertrophy. Since hypertension also causes coronary artery disease, these individuals often exhibit both hypertrophy and ischemia, which increases the risk of arrhythmias. Risk factors for atherosclerosis are strongly linked to aortic stenosis, which is also common among these patients. However, the absolute risk of sudden cardiac arrest in left ventricular hypertrophy is low.

Right ventricular hypertrophy is usually the result of pulmonary hypertension. These patients also have an increased risk of sudden cardiac arrest.

Hypertrophic cardiomyopathy (HCM) is a genetic cardiomyopathy defined by localized or generalized left ventricular hypertrophy. The hypertrophy is usually localized (septal hypertrophy, apical hypertrophy, lateral wall hypertrophy). In septal hypertrophy, LVOT (left ventricular outflow tract) obstruction may occur, resulting in a condition called hypertrophic obstructive cardiomyopathy (HOCM). HOCM is one of the most common causes of sudden cardiac arrest in young individuals, especially athletes. In HOCM, sudden cardiac arrest is likely not caused by the outflow obstruction, but rather a result of ventricular arrhythmias.

Hypertrophy, regardless of etiology, is an independent risk factor for ventricular arrhythmias and sudden cardiac arrest. The risk of arrhythmias correlates with the degree of hypertrophy, left ventricular function (ejection fraction) and ventricular size. Reduced ejection fraction and ventricular dilatation increase the risk of sudden cardiac arrest.


All cardiomyopathies are associated with an increased risk of sudden cardiac death. In general, a history of syncope, family history of cardiac arrest or sudden cardiac death, recurrent ventricular arrhythmias, and early onset of cardiomyopathy are associated with a high risk of sudden cardiac arrest. In patients with cardiomyopathy, unexplained syncope should always raise suspicion of ventricular arrhythmia.

Among patients with HFREF (heart failure with reduced ejection fraction), approximately 50% die from sudden cardiac arrest (Packer et al.). The lower the ejection fraction, the higher the risk of sudden cardiac arrest. The vast majority of sudden deaths in heart failure are caused by ventricular tachyarrhythmias (ventricular tachycardia, ventricular fibrillation). A minority are caused by bradyarrhythmias. Among patients with HFPEF (heart failure with preserved ejection fraction), approximately one-third die from sudden cardiac arrest (Vaduganathan et al.).

Ischemic cardiomyopathy with heart failure is associated with a significantly increased risk of sudden cardiac arrest, likely more than any other cardiomyopathy.

Other types of cardiomyopathies also carry an increased risk of sudden cardiac arrest:

  • Dilated cardiomyopathy (DCM)
  • Restrictive cardiomyopathy (RCM)
  • Alcohol cardiomyopathy
  • Diabetes cardiomyopathy
  • Peripartum cardiomyopathy

Myocarditis is usually a benign condition, but it can be complicated by acute heart failure, ventricular arrhythmias, and cardiac arrest.

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

ARVC increases the risk of ventricular arrhythmias (monomorphic VT, polymorphic VT, ventricular fibrillation) and sudden cardiac death. The cardiomyopathy usually affects the right ventricle, but may also involve the left ventricle. These patients should not subject themselves to strenuous physical activity. Syncope is a strong predictor of future risk of sudden cardiac arrest.

Acute heart failure

Numerous conditions, such as acute myocardial infarction, acute-on-chronic heart failure, endocarditis, hypertensive crisis, etc., can cause acute heart failure. The risk of sudden cardiac arrest is high. This is due to ventricular arrhythmias and/or cardiogenic shock. In acute heart failure, there is an acute load on the left ventricle along with a powerful sympathetic response and potentially other factors that increase the risk of arrhythmias.

Inflammatory causes and storage diseases

  • Giant cell myocarditis carries a high risk of cardiac arrest.
  • Eosinophilic myocarditis also carries a high risk of cardiac arrest.
  • Cardiac involvement occurs in 20% of individuals with sarcoidosis, with half of these experiencing cardiac symptoms (Ekström et al.). Ventricular tachycardia is common and the risk of cardiac arrest is significantly increased.
  • Systemic sclerosis (scleroderma) also carries an increased risk of cardiac arrest.
  • Amyloidosis (AL, ATTR) also increases the risk of cardiac arrest.

Valvular heart disease

Left-sided valvular lesions are clearly associated with sudden cardiac arrest, particularly aortic stenosis which carries a 1% annual risk of sudden cardiac arrest. The risk increases with the severity of aortic stenosis but can be halved by interventions (surgical valve replacement or TAVI). However, an increased risk persists even after the intervention, which may be explained by coexisting coronary artery disease, heart failure, hypertrophy, and prosthesis dysfunction.

Both surgical procedures and TAVI may cause high-degree AV block, but sudden cardiac arrest is a rare complication since these patients are ECG monitored for several days.

Mitral valve prolapse is also associated with an increased risk of sudden cardiac arrest. A variant called mitral annular disjunction (MAD) may be associated with a higher risk of cardiac arrest, although the scientific evidence is limited (Bennett et al).

Aortic regurgitation and mitral regurgitation carry a slightly increased risk of sudden cardiac arrest.


Endocarditis rarely leads to ventricular arrhythmias. The presence of such arrhythmias should raise suspicion of septic emboli to the coronary arteries, which can cause ventricular arrhythmias (VT, VF).

Congenital heart disease

Congenital heart diseases that increase the risk of sudden cardiac arrest include:

  • Congenital aortic stenosis
  • Shunts that increase pulmonary vascular resistance (PVR)
  • Eisenmenger syndrome
  • Tetralogy of Fallot
  • Transposition of the great arteries
  • AV canal defects

After corrective surgery, scar tissue can result in ventricular arrhythmias and sudden cardiac arrest.

Conduction defects (AV-blocks)

AV block is a less common cause of sudden cardiac arrest. This is due to the heart’s pacemaker hierarchy. Failure of the sinus node almost always leads to the emergence of an escape rhythm originating in the atria, AV node, His-Purkinje system, or ventricular myocardium, in that order. However, escape rhythms are not reliable in the long term since they can fail at any time. High-degree AV blocks should therefore be considered as potentially life-threatening, even in the presence of an apparently stable escape rhythm. High-grade AV blocks are treated with atropine and/or isoproterenol, or a temporary pacemaker until a permanent system is implanted (if needed).

Note that AV block 1 and AV block 2 type 1 can progress to high-grade AV block (AV block 2 type 2, AV block 3). The risk is, however, considered to be very low in AV block 1 and low in AV block 2 type 1. Myocardial infarction complicated by right bundle branch block and fascicular block indicates an increased risk of complete AV block.

Intraventricular conduction defects with broad QRS complexes indicate an increased risk of sudden cardiac arrest among patients with coronary artery disease. The presence of pathological Q waves indicates a previous large myocardial infarction, which represents a significant substrate for malignant ventricular arrhythmias (VT, VF).

Pre-excitation (Wolff-Parkinson-White syndrome, WPW) can cause hemodynamically significant tachyarrhythmias (orthodromic AVRT, antidromic AVRT) but very rarely sudden cardiac arrest. Yet, the risk of sudden cardiac arrest should be considered high among patients whose accessory pathway has a short anterograde refractory period (i.e. can conduct impulses from the atrium to the ventricle with a short refractory period), since atrial fibrillation in these patients may be transduced to ventricular fibrillation (VF) and thus cause sudden cardiac arrest.

Long QT syndrome (LQTS)

Prolongation of the QT interval may induce torsades de pointes ventricular tachycardia, which can be self-terminating (cease spontaneously) but there is a high risk of progression to ventricular fibrillation. Torsade de pointes should be considered a highly unstable arrhythmia. The majority of individuals with prolonged QT interval have acquired it as a result of side effects of medications (see below). Congenital prolongation of the QT interval is much less common. The characteristic ECG changes in congenital LQTS types 1, 2, and 3 are shown below. Regardless of the genesis of torsades de pointes, there is a high risk of ventricular fibrillation.

Congenital LQTS (long QT syndrome)

Long QT syndrome (LQTS) is a disorder of cardiac repolarization, characterized by a prolonged QT interval, which increases the risk of ventricular arrhythmias and sudden cardiac arrest. LQTS is a heterogeneous disorder with various genetic mutations causing the disorder.

LQTS type 1 (LQT1) is the most common type of congenital LQTS and is caused by a mutation in the KCNQ1 gene, resulting in a loss of function of the cardiac potassium channel. Arrhythmias typically occur during physical exertion, particularly swimming, and other sympathetic triggers. The ECG findings include broad-based T waves.

LQTS type 2 (LQT2) is caused by a mutation in the KCNH2 gene, which also leads to a loss of function of the potassium channel. Arrhythmias typically occur with sudden surprises (such as sudden loud noises or fear), stress, physical exertion, or during sleep. The ECG findings in LQT2 include a low-amplitude T wave with an extra hump or notch. Postpartum, the risk of torsades de pointes is high.

LQTS type 3 (LQT3) is caused by a mutation in the SCN5A gene, which leads to increased sodium influx. Sudden death during sleep is typical, and bradyarrhythmias can also give rise to malignant arrhythmias. The ECG findings in LQT3 include a late onset of the T wave (with a long and distinct ST segment) and a pointed T wave.

LQTS type 4 (LQT4) is rare and accounts for only 1% of cases. It is caused by a mutation in the ANKB gene, which codes for a protein that anchors membrane proteins to the cytoskeleton. LQT4 can cause various arrhythmias, such as familial catecholaminergic polymorphic ventricular tachycardia, atrial fibrillation, conduction disturbances, sinus node dysfunction, and bradycardia.

Other variants of LQTS are very rare and often part of more extensive syndromes involving multiple organ systems (Jervell and Lange-Nielsen syndrome, Romano-Ward syndrome). Patients with congenital LQTS should not use drugs that prolong the QT interval (see below).

It is difficult to predict the risk of cardiac arrest in LQTS. Some individuals never experience arrhythmias while others have repeated cardiac arrests. The following are risk factors or warning signs for cardiac arrest in LQTS:

  • Syncope
  • Markedly prolonged QT interval
  • QT alternans (varying QTc interval)
  • Family history of sudden cardiac death
  • Occurrence of torsade de pointes, other ventricular tachycardia, ventricular fibrillation

Acquired LQTS

Many conditions and drugs can induce QT prolongation, leading to acquired LQTS. This type of LQTS is more common than the congenital form. Medical conditions, situations, and drugs that can cause or exacerbate LQTS are discussed in List of drugs and conditions causing long QT syndrome.

Short QT Syndrome (SQTS)

SQTS is a rare condition characterized by a QTc interval <300 ms, which also increases the risk of ventricular arrhythmias and cardiac arrest.

J-Wave Syndromes

There are two J-wave syndromes that increase the risk of cardiac arrest, namely Brugada syndrome and Early Repolarization Syndrome.

Brugada Syndrome

Brugada syndrome is an autosomal dominant inherited condition. There are 12 known gene mutations that affect the transport of sodium or calcium across the cell membrane. The individual is usually asymptomatic until 20-55 years of age and presents with syncope, ventricular fibrillation, ventricular tachycardia, cardiac arrest, and/or sudden cardiac death. Since the syndrome is hereditary, there is often a family history of syncope and unexpected cardiac arrests. The characteristic ECG changes are intermittent. ECG changes and arrhythmias appear to occur more frequently at rest, during sleep, with fever, and in situations with high vagal tone. Physical exertion does not appear to increase the risk of arrhythmias. Men are overrepresented among cases who suffer cardiac arrest, as are those with type 1 Brugada syndrome. ECG changes and arrhythmias can be induced with ajmaline, flecainide, and procainamide.

Types of Brugada Syndrome

Type 1 Brugada syndrome is characterized by a coved-shaped ST-segment elevation ≥2 mm which transitions to a negative T-wave. If this pattern is present in leads V1 and/or V2, the diagnosis is confirmed. Type 2 Brugada syndrome is characterized by a saddleback-shaped ST-segment elevation with an elevated J-point ≥2 mm. The terminal portion of the ST segment is elevated ≥1 mm. Type 3 Brugada syndrome is similar to Type 2, but the terminal portion of the ST segment is elevated <1 mm.

Figure 10. The three types of Brugada syndrome and the characteristic ST segment elevations.
Figure 3. The three types of Brugada syndrome and the characteristic ST segment elevations.

Early Repolarisation Syndrome

Approximately 5-13% of the general population display early repolarization on the ECG (70% of whom are men). Early repolarization, especially in leads II, aVF, and III, is associated with idiopathic ventricular fibrillation and a 3-5 times increased risk of cardiac arrest. Although the relative risk of cardiac arrest is high compared to individuals without early repolarization, the absolute risk is very low.

The ST elevations usually have a concave ST segment and are most pronounced in the chest leads. The T waves are high. The main finding is the presence of a hump or slope at the transition from the R wave to the ST segment (see figure). The hump is completely above the baseline, and the slope begins before the baseline is reached.

The ECG pattern is considered benign if it occurs in anterior chest leads (V3-V4). The higher the J points, the higher the risk of ventricular fibrillation. It is likely that early repolarization is a predisposing factor for ventricular arrhythmias in situations that can trigger such arrhythmias, such as myocardial ischemia and myocardial infarction.

Figure 1. Early repolarization pattern on ECG. Note the end-QRS notches and slurs, as well as the ST segment elevations.
Figure 4. Early repolarization pattern on ECG. Note the end-QRS notches and slurs, as well as the ST segment elevations.

Catecholaminergic polymorphic ventricular tachycardia (CPVT)

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited condition with high mortality due to sudden cardiac death. The prevalence in the population is approximately 1 in 10000 individuals. There is a high risk for polymorphic and bidirectional VT. Ventricular tachycardia is caused by catecholamines, which makes beta-blockers an effective treatment. The resting ECG is typically completely normal.

Takotsubo cardiomyopathy

Takotsubo cardiomyopathy is thought to be caused by an extreme catecholaminergic surge, leading to widespread myocardial stunning, typically localized to the apex, which becomes ballooned and temporarily loses contractility. The prognosis is generally good, and it is unclear whether the condition is associated with an increased risk of sudden cardiac arrest. It can cause QT prolongation. Mortality is increased primarily due to hemodynamic collapse rather than ventricular arrhythmias.

Sudden infant death syndrome (SIDS)

Sudden infant death syndrome (SIDS) is defined as an unexpected death between birth and 6 months of age. This was more common in the past when infants slept on their stomachs, which is now discouraged, resulting in a halving of the incidence of SIDS. The mechanism is thought to be obstructive sleep apnea, but a proportion of these infants may have LQTS.

Sudden cardiac arrest during sports and physical activity

Sports and physical activity is associated with a slightly increased risk of acute myocardial infarction and sudden cardiac arrest during and after physical activity. The risk of sudden cardiac arrest during sports is extremely low. In young individuals, cardiomyopathies (HCM, HOCM, ARVD/ARVC, myocarditis) should be suspected in the event of unexplained syncope or sudden cardiac arrest. Less commonly, ion channel disorders and Brugada syndrome may be the cause. In middle-aged and older individuals, coronary artery disease is the most common cause. After myocarditis, physical activity is prohibited for 3 to 6 months because the risk of ventricular arrhythmias is highest during this time.

Other causes of cardiac arrest

  • Other causes of cardiac arrest include commotio cordis (trauma to the thorax can cause ventricular tachycardia and ventricular fibrillation).
  • Malignant hyperthermia, including during physical exertion in heat.
  • Idiopathic VF (ventricular fibrillation without underlying cause).
  • Pulmonary embolism.
  • Air embolisms.
  • Sleep apnea causes cardiac arrest via apnea.
  • Aortic dissection.
  • Tamponade.


Sadie Bennett, Ritu Thamman, Timothy Griffiths, Cheryl Oxley, Jamal Nasir Khan, Thanh Phan, Ashish Patwala, Grant Heatlie, Chun Shing Kwok. Mitral annular disjunction: A systematic review of the literature Sadie Bennett. Echocardiography . 2019 Aug;36(8):1549-1558.

Vaduganathan M, Patel R.B, Michel A, et al. Mode of death in heart failure with preserved ejection fraction.  J Am Coll Cardiol . 2017;69:556–569.

Ekstrom K, Lehtonen J, Nordenswan H.K, et al. Sudden death in cardiac sarcoidosis: an analysis of nationwide clinical and cause-of-death registries.  Eur Heart J . 2019;40:3121–3128.

Finocchiaro G, Papadakis M, Robertus J.L, et al. Etiology of sudden death in sports: insights from a United Kingdom regional registry.  J Am Coll Cardiol . 2016;67:2108–2115.

Minners J, Rossebo A, Chambers J.B, et al. Sudden cardiac death in asymptomatic patients with aortic stenosis.  Heart . 2020;106:1646–1650

Urena M, Webb J.G, Eltchaninoff H, et al. Late cardiac death in patients undergoing transcatheter aortic valve replacement: incidence and predictors of advanced heart failure and sudden cardiac death.  J Am Coll Cardiol . 2015;65:437–448.

Fulton B.L, Liang J.J, Enriquez A, et al. Imaging characteristics of papillary muscle site of origin of ventricular arrhythmias in patients with mitral valve prolapse.  J Cardiovasc Electrophysiol . 2018;29:146–153.

Myerburg R.J. Physiological variations, environmental factors, and genetic modifications in inherited LQT syndromes.  J Am Coll Cardiol . 2015;65:375–377.

Sollazzo F, Palmieri V, Gervasi S.F, et al. Sudden cardiac death in athletes in Italy during 2019: Internet-based epidemiological research.  Medicina (Kaunas) . 2021;57.

Tseng Z.H, Olgin J.E, Vittinghoff E, et al. Prospective countywide surveillance and autopsy characterization of sudden cardiac death: post scd study.  Circulation . 2018;137:2689–2700.

Coronary Artery Anomalies An Entity in Search of an Identity Paolo Angelini Originally published13 Mar 2007 Circulation. 2007;115:1296–1305

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