Sudden cardiac death

Classification according to ICD-10
I21-I22	Sudden death from myocardial infarction
I44-I45	Sudden death from conduction disorder
I46.0	Cardiac arrest with successful resuscitation
I46.1	Sudden cardiac death, as described
R96.-	Sudden death without further information
ICD-10 online (WHO version 2019)

Sudden cardiac death (SCD) (also second cardiac death or Sekundentod ) is a medical term for a sudden and unexpected death occurred cardiac cause. However, a study by the American Heart Association shows that every second patient suffers from warning symptoms such as chest pain, shortness of breath or dizziness before sudden cardiac death . In the Anglo-American language area the term Sudden Cardiac Death (SCD) is common.

Death is usually the result of persistent ventricular fibrillation or persistent ventricular tachycardia , which then lead to cardiac arrest . If one of these conditions is successfully and permanently ended by defibrillation or resuscitation measures, the phrase “survived sudden cardiac death” or “post-resuscitation state” is used.

frequency

Sudden cardiac death is the most common fatal manifestation of heart disease. In Germany, 100,000 to 200,000 people die from it every year. This proportion remains constant despite a reduction in general cardiovascular mortality . If a clinically relevant heart disease is present, the risk of developing PHT is 6 to 10 times higher; Coronary heart disease alone increases the risk 2 to 4 times.

Men die from sudden cardiac death more often than women (men / women per 100,000: 411/275), and mortality increases with age (men / women per 100,000: 35 to 44 years 34/12; 75 to 84 years 1363/929). The risk of sudden cardiac death is 2.5 times as high for competitive athletes as for non-athletes, whereby sport is not the cause of the higher disease rate, but must be understood as the cause of the disease in the presence of congenital heart diseases.

Among young people

For the age group of young people up to 35 years of age, studies show a frequency of 1.3 per 100,000 person-years in Australia and New Zealand , 1.8 in England and Wales and 2.8 in Denmark . In the Australian-New Zealand study with 490 cases examined, the incidence was highest in the age group between 31 and 35 years with 3.2 cases per 100,000 person-years, mainly caused by coronary artery disease . Across all age groups, this was found in 24% of all cases, cardiomyopathy was found in 16%, and in 40% no cause could be determined at autopsy . In this group, however, a gene mutation was found in 27% of the cases examined, which in most cases affected proteins of the ion channels . The mean age was 24 years with a standard deviation of 10 years. Boys or men were affected in 72%. Most of the cases occurred during sleep (38%) or at rest (27%), only 11% during exercise and 4% after stopping sport.

See also : Sudden cardiac death while exercising

causes

As a rule, three components are required for a PHT to occur:

• Structural heart disease
• Temporary trigger
• Arrhythmia Mechanism

There is a cardiac arrhythmia , an electromechanical decoupling or even an immediate asystole . At the beginning of a rhythm disturbance there is often a ventricular tachycardia , which then turns into ventricular fibrillation . Hypoxia-related asystole then follows with no electrical activity in the heart. More rarely, bradycardia , e.g. B. as part of an AV block III ° or bradyarrhythmia , develop an asystole.

Structural heart disease

Coronary heart disease (approx. 80% of cases)

• In 15% to 50% of the patients (numbers vary greatly depending on the literature) it is the first manifestation of coronary heart disease (CHD).
• Acute heart attack : There is a 15 percent chance of sudden cardiac death (PHT) within the first 48 hours after an untreated heart attack. This risk drops to 3% in the next few days. 80% of all episodes of ventricular fibrillation occur in the first six hours after the onset of pain (maximum in the first hour) in an acute myocardial infarction.
• Chronic CHD: 50% of patients have already had a heart attack . Here play ventricular tachycardias an essential role in the scar areas.

Non-ischemic cardiomyopathies (approx. 10% to 15% of cases)

This is understood to mean heart muscle diseases that are not caused by coronary heart disease, e.g. B. as part of a heart attack. These include:

• Dilated cardiomyopathy (DCM): 30% of all deaths in patients with DCM occur suddenly.
• Hypertrophic cardiomyopathy (HCM): Particular risk factors may include a. a badly thickened wall of the left heart and an insufficient increase in blood pressure during exercise. HCM is the most common cause of sudden cardiac death in young people.

Rare causes (<5%)

• Arrhythmogenic right ventricular cardiomyopathy (ARVCM): The risk is particularly increased with impaired right ventricular pump function.
• Long QT syndrome : Syncope is the most common manifestation. The younger the patient when the first syncope occurs, the worse the prognosis. 20% die within a year of the first syncope.
• Brugada syndrome : PHT is caused by rapid polymorphic ventricular tachycardias, preferably during periods of rest or sleep.
• Idiopathic ventricular fibrillation: This is a so-called exclusion diagnosis , which is made in about 8% of the survivors of a sudden cardiac arrest with a structurally healthy heart.
• Aortic stenosis (AS): Before aortic valve surgery, AS was a common non-coronary cause of sudden cardiac death. 73% of the patients with high-grade AS died from it. After aortic valve replacement , 18 to 21% of all deaths are sudden cardiac deaths (frequency peak 3 weeks to 8 months after surgery).
• Coronary anomalies, coronary artery embolisms, coronary arteritis, coronary spasms and muscle bridges
• peripartum cardiomyopathy (mortality within pregnancy 20%)
• Inflammatory and infiltrative diseases of the heart ( myocarditis , autoimmune diseases , amyloidosis , hemochromatosis , Chagas cardiomyopathy)
• neuromuscular diseases.
• Genetic causes: The hereditary disease ARVC (arrhythmogenic right ventricular cardiomyopathy) can also be responsible.

Temporary triggers

• Electrolyte disorders (changes in blood salts):
  • Hypokalaemia <2.5 mmol / l, hyperkalemia > 6.5 mmol / l
  • Hypercalcemia
  • Hypomagnesaemia : As a cofactor, it can promote the occurrence of PHT (e.g. torsades de pointes ), but is never the sole cause of ventricular fibrillation.
• Acidosis , e.g. B. in renal insufficiency or respiratory insufficiency (insufficient respiratory function)
• Hypoxia (insufficient oxygen supply)
• Acute and subacute ischemia (circulatory disorders), most common during myocardial infarction and up to 48 hours after the start of the painful event
• Reperfusion (flooding of metabolic products after blood circulation has been restored)
• Antiarrhythmics and drugs:
  • A prolonged QTc interval in the resting ECG and a slow basic rhythm are indications of a drug-induced torsade de pointes.
  • Drugs such as B. cocaine, can lead to vascular spasms with subsequent ischemia-related cardiac arrhythmias.
• Electricity accident
• Stress (increased sympathetic tone )
• Vagus irritation or strong vagotonic reaction:
  • swallowed solids stuck in the throat ( bolus death )
  • sleep
  • Urination (also known as micturition syncope )
  • Recovery immediately after finishing vigorous physical exertion

Arrhythmia Mechanisms

• Circling excitement (reentry)
• increased automatism , e.g. B. in the transition tissue between scar and healthy heart muscle, for example after a heart attack or in HCM
• triggered activity

treatment

The impending sudden cardiac death is treated with resuscitation measures whenever possible. In addition to restoring a minimal circulation through chest compressions , the cardiac rhythm will be displayed as early as possible with the help of the EKG function of a defibrillator . If there is a treatable rhythm disturbance (VT, KF), defibrillation takes place.

Course and prognosis of sudden cardiac arrest

found rhythm	successful resuscitation	Leaving the clinic
Asystole	<10%	0% to 2%
Decoupling	approx. 20%	11%
Ventricular fibrillation	> 25%	11%
Ventricular tachycardia	> 75%	65% to 70%
noncardiac causes	40%	11%

There is often no resuscitation outside the hospital . Resuscitation is only successful in about 30% of cases. The success and likelihood of keeping the hospital healthy, d. H. without leaving hypoxic brain damage depends on the heart rhythm when the patient is found and on the quality of first aid ( lay resuscitation ). The mild therapeutic hypothermia , i.e. the cooling of the body after successful resuscitation, shows positive effects.

Prevention

A distinction is made between primary prevention in the absence of a serious arrhythmia and secondary prevention after surviving cardiac arrest.

Primary prevention

Most studies on primary prevention of PHT have been conducted with post-infarction patients and with patients with structural heart disease such as DCM and CHD. Primary prevention is possible through optimal therapy for the underlying heart disease. In CHD, this includes consistent therapy of the risk factors and revascularizing (restoring blood flow) measures such as coronary angioplasty and bypass surgery . After a sleep apnea syndrome should be sought and, if it is present, treated.

Medication

For patients with severely restricted pumping function (ejection fraction <35%):

• The success of primary drug prevention with amiodarone is not considered certain. The large primary prevention studies show a favorable effect on the incidence (frequency of occurrence) of PHT in post-infarction patients without significantly influencing the overall mortality.
• Beta blockers reduce the rate of sudden cardiac death after myocardial infarction by up to 30% (MERIT-HF study).
• Aldosterone antagonists (spironolactone, eplerenone) show a 15% reduction in PHT after a heart attack (EPHESUS study).
• Angiotensin converting enzyme inhibitors (ACEH) reduce the risk of PHT after infarction by 20%, according to the results of a meta-analysis.
• The primary preventive effect of other antiarrhythmics is not considered to be certain with regard to all-cause mortality; an increase in mortality in post-infarction patients has been confirmed for sotalol (SWORD study).

Implantable Cardioverter Defibrillator (ICD)

The implantation of an ICD is only valid for the following clinical pictures with regard to its primary preventive effect (MADIT-I study):

• short-term (<30 seconds) ventricular tachycardia
• limited pumping function
• Artificially triggered ventricular fibrillation or ventricular tachycardia, survived infarction or CHD, whereby no suppression of cardiac arrhythmias is possible with class I antiarrhythmics

or

• Severely restricted pumping function (ejection fraction <30%) at least 1 month after myocardial infarction or 3 months after bypass surgery (MADIT-II study).

Secondary prevention of sudden cardiac death (after surviving sudden cardiac arrest)

Sudden cardiac arrest survivors have a risk of recurrence of up to 30% within the first year, provided that the event did not occur in the context of an acute myocardial infarction. After two years, the risk increases to up to 45%.

Medication

Secondary drug prevention with antiarrhythmics is clearly inferior to ICD implantation.

• Despite acute and chronic suppression of ventricular tachycardias and ventricular fibrillation with class I antiarrhythmics and sotalol, the risk of recurrence within the first two years after the event is 30% to 40%.
• Amiodarone is superior to class I antiarrhythmics, but the recurrence rate after two years is 18%.

Implantable Cardioverter Defibrillator (ICD)

An ICD is absolutely indicated for secondary prevention after surviving sudden cardiac arrest with ventricular fibrillation or ventricular tachycardia without evidence of a reversible cause.

• A meta-analysis shows a 27% reduction in all-cause mortality within six years after the event (AVID, CASH and CIDS study)
• only patients with a restricted pump function (ejection fraction <40%) benefit significantly from an ICD implantation compared to an amiodarone medication. ICD therapy is not superior to amiodarone therapy in patients with little or no impaired pumping function (ejection fraction> 40%) (AVID subgroup analysis). Nevertheless, amidarone therapy is currently only recommended as an adjunct therapy to the ICD for a resuscitated patient in order to minimize the frequency of shock delivery or for patients who refuse an ICD or cannot receive an ICD for other reasons.

Sudden death from noncardiac cause

A number of non-cardiac causes can also cause sudden death. For example, a pulmonary embolism, acute internal bleeding or acute poisoning can also lead to sudden death.

Sudden Cardiac Death Cost

Exact statements on the costs of the PHT are not known due to the unclear initial data situation. Estimates by the Cologne Business School put the indirect costs of sudden cardiac death due to the loss of production for the German economy at 4.37 billion euros per year. According to the study, North Rhine-Westphalia incurs annual, indirect costs of around 940 million euros with an estimated average number of cases of around 25,500 deaths. For Austria, indirect costs of almost 702 million euros per annum are estimated in a further short study.

literature

• Mewis, Riessen, Spyridopoulos (Ed.): Cardiology compact - Everything for ward and specialist examination . 2nd Edition. Thieme, Stuttgart / New York 2006, ISBN 3-13-130742-0 , pp. 629-649 ( books.google.de ).
• D. Corrado et al .: Does sports activity enhance the risk of sudden death in adolescents and young adults? In: J Am Coll Cardiol. 2003, 42 (11), pp. 1959-1963, PMID 14662259 .
• W. Dichtl et al .: An uncommon coronary artery fistula causing survived sudden cardiac death in a young woman. In: Int J Cardiovasc Imaging. 2005, 21 (4), pp. 387-390, PMID 16047119 .
• Wilfried Kindermann, Axel Urhausen : Sudden cardiac death while exercising . Federal Institute for Sport Science, Cologne 2000, ISBN 3-89001-131-4 , p. 1–55 ( bisp.de [PDF]).
• AT Mills et al .: Brugada syndrome: syncope in the younger patient and the risk of sudden cardiac death. In: Emerg Med J. 2005, 22 (8), pp. 604-606, PMID 16046779 .
• SG Priori et al .: Task Force on Sudden Cardiac Death of the European Society of Cardiology. In: Eur Heart J. 2001 Aug, 22 (16), pp. 1374-1450, PMID 11482917 .
• A. Tabib et al .: Circumstances of death and gross and microscopic observations in a series of 200 cases of sudden death associated with arrhythmogenic right ventricular cardiomyopathy and / or dysplasia. In: Circulation. 2003, 108 (24), pp. 3000-5, PMID 14662701 .

Individual evidence

1. ↑ Many sudden cardiac arrests preceded by warning signs . ( Memento of the original from November 25, 2013 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. AHA 
2. ^ ZJ Zheng, et al: Sudden Cardiac Death in the United States, 1989 to 1998 . In: Circulation . 104, No. 18, 2001, pp. 2158-2163. PMID 11684624 .
3. ^ D Corrado, et al: Does sports activity enhance the risk of sudden death in adolescents and young adults? . In: J Am Coll Cardiol . 42, No. 11, December 3, 2003, pp. 1959-1963. PMID 14662259 .
4. ↑ Richard D. Bagnall, Robert G. Weintraub, Jodie Ingles, Johan Duflou, Laura Yeates, Lien Lam, Andrew M. Davis, Tina Thompson, Vanessa Connell, Jennie Wallace, Charles Naylor, Jackie Crawford, Donald R. Love, Lavinia Hallam , Jodi White, Christopher Lawrence, Matthew Lynch, Natalie Morgan, Paul James, Desirée du Sart, Rajesh Puranik, Neil Langlois, Jitendra Vohra, Ingrid Winship, John Atherton, Julie McGaughran, Jonathan R. Skinner, Christopher Semsarian: A Prospective Study of Sudden Cardiac Death among Children and Young Adults New England Journal of Medicine 2016, Volume 374, Issue 25 of 23; June 2016, pages 2441-2452, doi: 10.1056 / NEJMoa1510687
5. ^ Gorgels, Anton, et al .: Out-of-hospital cardiac arrest-the relevance of heart failure. The Maastricht Circulatory Arrest Registry . In: Eur Heart J . 24, No. 13, 2003, pp. 1204-1209.
6. ↑ Erich and Hanna Klessmann Institute for Cardiovascular Research and Development, Heart and Diabetes Center NRW, Bad Oeynhausen .
7. ↑ ^{a b} Gerd Herold : Internal Medicine . Cologne 2007, p. 530, 532 .
8. ↑ Sudden Cardiac Death - Heart-Safe Solutions That Save Lives! (No longer available online.) In: www.herzsicherheit.info. Archived from the original on May 10, 2016 ; accessed on May 9, 2016 . Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice.  
9. ↑ K. Brinkmann, H. Schaefer: The electrical accident . Springer-Verlag, 2013, ISBN 978-3-642-68227-8 ( limited preview in the Google book search).
10. ↑ AJ Moss, et al .: Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators (MADIT) . In: N Engl J Med . 335, No. 26, December 26, 1996, pp. 1933-1940. PMID 8960472 .
11. ^ AJ Moss, et al .: Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction (MADIT II) . In: N Engl J Med . 346, No. 12, March 21, 2002, pp. 877-883. PMID 11907286 .
12. ^ Andreas Lueg-Arndt: The indirect costs of sudden cardiac death in North Rhine-Westphalia and Germany . Ed .: Definetz e. V. Bönen 2012 ( definetz.de [PDF; 142 kB ]).
13. ^ Andreas Lueg-Arndt: The indirect costs of sudden cardiac death in Austria . Ed .: Definetz e. V. Bönen 2012 ( definetz.de [PDF; 128 kB ]).

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