Yunnan sudden death syndrome is a label used to define unexplained cases of cardiac arrest, which afflicted significant numbers of rural villagers in Yunnan province, in southwest China. Cases occurred almost always during the midsummer rainy season (from June to August), at an altitude of . The cause turned out to be a mushroom now blamed for an estimated 400 deaths in the past three decades.

The mysterious fatalities were recorded for decades before researchers from the Chinese Center for Disease Control and Prevention isolated a significant factor common in every case: a tiny unknown mushroom which was unintentionally gathered and consumed during wild mushroom harvests in the region. Previously the syndrome was thought to be caused by Keshan disease, caused by the Coxsackie virus.

The mushroom, "Trogia venenata", is also known as 'Little White'. It has been determined that families collecting fungi to sell have been eating these Little White mushrooms as they have no commercial value. Three amino acids present in the mushrooms have been shown to be toxic. The mushrooms have also been shown to contain very high quantities of barium, and it may be that some of the deaths are simply from barium poisoning.

In the hours before death, about two-thirds of the victims had such symptoms as nausea, dizziness, heart palpitations, seizures and fatigue.

However, in December 2012 it was announced that Dr Xu Jianping (徐建平) has been collecting samples of "Trogia venenata" in Yunnan for the past three years, and his research now shows that barium levels in the wild mushroom are no higher than those of common foods such as poultry and fish. Nonetheless, it appears the mushroom will still likely play a role. Since publication of the widely circulated 2010 "Science" article, no instances of Yunnan sudden death syndrome have been reported.

Breastfeeding is associated with a lower risk of SIDS. It is not clear if co-sleeping among mothers who breastfeed without any other risk factors increased SIDS risk.

SIDS rates decrease with increasing maternal age, with teenage mothers at greatest risk. Delayed or inadequate prenatal care also increases risk. Low birth weight is a significant risk factor. In the United States from 1995 to 1998, the SIDS death rate for infants weighing 1000–1499 g was 2.89/1000, while for a birth weight of 3500–3999 g, it was only 0.51/1000. Premature birth increases the risk of SIDS death roughly fourfold. From 1995 to 1998, the U.S. SIDS rate for births at 37–39 weeks of gestation was 0.73/1000, while the SIDS rate for births at 28–31 weeks of gestation was 2.39/1000.

Anemia has also been linked to SIDS (note, however, that per item 6 in the list of epidemiologic characteristics below, extent of anemia cannot be evaluated at autopsy because an infant's total hemoglobin can only be measured during life.). SIDS incidence rises from zero at birth, is highest from two to four months of age, and declines toward zero after the infant's first year. Baby boys have a ~50% higher risk of SIDS than girls.

The sudden cardiac deaths of 387 young American athletes (under age 35) were analyzed in a 2003 medical review:

While most causes of sudden cardiac death relate to congenital or acquired cardiovascular disease, an exception is commotio cordis, in which the heart is structurally normal but a potentially fatal loss of rhythm occurs because of the accident of timing of a blow to the chest. Its fatality rate is about 65% even with prompt CPR and defibrillation, and more than 80% without.

Age 35 serves as an approximate borderline for the likely cause of sudden cardiac death. Before age 35, congenital abnormalities of the heart and blood vessels predominate. These are usually asymptomatic prior to the fatal event, although not invariably so. Congenital cardiovascular deaths are reported to occur disproportionately in African-American athletes.

After age 35, acquired coronary artery disease predominates (80%), and this is true regardless of the athlete's former level of fitness.

Cardiomyopathies are generally inherited as autosomal dominants, although recessive forms have been described, and dilated cardiomyopathy can also be inherited in an X-linked pattern. Consequently, in addition to tragedy involving an athlete who succumbs, there are medical implications for close relatives. Among family members of index cases, more than 300 causative mutations have been identified. However, not all mutations have the same potential for severe outcomes, and there is not yet a clear understanding of how these mutations (which affect the same myosin protein molecule) can lead to the dramatically different clinical characteristics and outcomes associated with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM).

Since HCM, as an example, is typically an autosomal dominant trait, each child of an HCM parent has a 50% chance of inheriting the mutation. In individuals without a family history, the most common cause of the disease is a "de novo" mutation of the gene that produces the β-myosin heavy chain.

The risk factors for SCD are similar to those of coronary artery disease and include age, cigarette smoking, high blood pressure, high cholesterol, lack of physical exercise, obesity, diabetes, and family history. A prior episode of sudden cardiac arrest also increases the risk of future episodes.

Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers risk was closer to that of those who had never smoked.

Marine-derived omega-3 polyunsaturated fatty acids (PUFAs) has been promoted for the prevention of sudden cardiac death due to its postulated ability to lower triglyceride levels, prevent arrhythmias, decrease platelet aggregation, and lower blood pressure. However, according to a recent systematic review, omega-3 PUFA supplementation are not being associated with a lower risk of sudden cardiac death.

Takotsubo cardiomyopathy is rare, affecting between 1.2% and 2.2% of people in Japan and 2% to 3% in western countries who suffer a myocardial infarction. It also affects far more women than men with 90% of cases being women, most postmenopausal. Scientists believe one reason is that estrogen causes the release of catecholamine and glucocorticoid in response to mental stress. It is not likely for the same recovered patient to experience the syndrome twice, although it has happened in rare cases. The average ages at onset are between 58 and 75 years. Less than 3% of cases occurred in patients under age 50.

Risk factors for long QT syndrome include the following:

- female sex

- increasing age

- liver or renal impairment

- family history of congenital long QT syndrome

- pre-existing cardiovascular disease

- electrolyte imbalance: especially hypokalemia, hypocalcemia, hypomagnesemia

- concurrent administration of interacting drugs

Anorexia nervosa has been associated with sudden death, possibly due to QT prolongation. It can lead a person to have dangerous electrolyte imbalances, leading to acquired long QT syndrome and can in turn result in sudden cardiac death. This can develop over a prolonged period of time, and the risk is further heightened when feeding resumes after a period of abstaining from consumption. Care must be taken under such circumstances to avoid complications of refeeding syndrome.

Despite the grave initial presentation in some of the patients, most of the patients survive the initial acute event, with a very low rate of in-hospital mortality or complications. Once a patient has recovered from the acute stage of the syndrome, they can expect a favorable outcome and the long-term prognosis is excellent. Even when ventricular systolic function is heavily compromised at presentation, it typically improves within the first few days and normalises within the first few months. Although infrequent, recurrence of the syndrome has been reported and seems to be associated with the nature of the trigger.

Holiday heart syndrome is an irregular heartbeat pattern presented in individuals who are otherwise healthy. Coined in 1978 the term is defined as "abnormal heart rhythms sometimes following excessive alcohol consumption; usually temporary".

Holiday heart syndrome can be the result of stress, dehydration, and drinking alcohol. It is sometimes associated with "binge drinking" common during the holiday season. The condition can also occur when individuals consume only moderate amounts of alcohol.

Irregular heartbeats can be serious. If palpitations continue for longer than a few hours patients should seek medical attention. Some arrhythmias associated with HHS after binge drinking can lead to sudden death, which may explain some of the sudden death cases commonly reported in alcoholics. Atrial fibrillation is the most common arrhythmia in holiday heart syndrome. Symptoms usually resolve themselves within 24 hours.

Holiday heart can also cause abnormal burning sensation whilst urinating and/or the feeling of passing blood similar to a kidney stone. This generally subsides in days or weeks.

Porcine stress syndrome, also known as malignant hyperthermia or PSS, is a condition in pigs. It is characterised by hyperthermia triggered by stress, anaesthesia with halothane or intense exercise. PSS may appear as sudden death in pigs, often after transport. It is an inherited, autosomal recessive disorder due to a defective ryanodine receptor leading to huge calcium influx, muscle contracture and increase in metabolism.

PSS can manifest itself in the abattoir as the production of Pale, Soft and Exudative meat due to a rapid fall in muscle pH and degradation of muscle proteins and structure. This meat is usually rejected after inspection.

This disorder is most common in Landrace, Piétrain and crossbreeds of these breeds of pig. The genes may have been favoured in the past due to a larger muscle bulk in these breeds. However this is not standard protocol in developed countries these days.

After return of heart function, there has been a moderately higher risk of death in the hospital when compared to MI patients without PVF. Whether this still holds true with the recent changes in treatment strategies of earlier hospital admission and immediate angioplasty with thrombus removal is unknown. PVF does not affect the long-term prognosis.

The number of people affected by Brugada ECG is higher in Asia than in the United States and Europe. Specifically, Brugada Type 1 ECG appears more frequently in Asia (0%–0.36% of the population) and Europe (0%–0.25%) than in the United States (0.03%). Type 2 and Type 3 ECG is more prevalent in Asia (0.12%–2.23%) than in Europe (0.0%–0.6%) or the United States (0.02%).

It is the most common cause of sudden death in young men without known underlying cardiac disease in Thailand and Laos.

The cause of short QT syndrome is unclear at this time. A current hypothesis is that short QT syndrome is due to increased activity of outward potassium currents in phase 2 and 3 of the cardiac action potential. This would cause a shortening of the plateau phase of the action potential (phase 2), causing a shortening of the overall action potential, leading to an overall shortening of refractory periods and the QT interval.

In the families afflicted by short QT syndrome, mutations have been described in three genes, KvLQT1, the "human ether-a-go-go gene (HERG)", and KCNJ2.

Removing the pig from the stressful situation can prevent the episode.

Sedation and glucocorticoids may be beneficial.

Under anaesthesia, dantrolene sodium is a very effective treatment.

Genetic testing enables animals to be removed from the herd if they are positive for the gene. This means that the disorder is rare in the developed world these days.

Stress at slaughter should be minimised in all cases.

The survival of PVF largely depends on the promptness of defibrillation. The success rate of prompt defibrillation during monitoring is currently higher than 95%. It is estimated that the success rate decreases by 10% for each additional minute of delay.

Brugada syndrome (BrS) is a genetic condition that results in abnormal electrical activity within the heart, increasing the risk of sudden cardiac death. Those affected may have episodes of passing out. Typically this occurs when a person is at rest.

It is often inherited from a person's parent with about a quarter of people having a family history. Some cases may be due to a new mutation or certain medications. The abnormal heart rhythms can be triggered by a fever or increased vagal tone. Diagnosis is typically by electrocardiogram (ECG), however, the abnormalities may not be consistently present.

Treatment may be with an implantable cardioverter defibrillator (ICD). Isoproterenol may be used in those who are acutely unstable. In those without symptoms the risk of death is much lower, and how to treat this group is unclear. Testing people's family members may be recommended.

Between 1 and 30 per 10,000 people are affected. Onset of symptoms is usually in adulthood. It is more common in people of Asian descent. Males are more commonly affected than females. It is named after the Spanish cardiologists Pedro and Josep Brugada who described the condition in 1992. Their brother Ramon Brugada described the underlying genetics in 1998.

Short QT syndrome is a genetic disease of the electrical system of the heart. It consists of a constellation of signs and symptoms, consisting of a short QT interval on an EKG (≤ 300 ms) that does not significantly change with heart rate, tall and peaked T waves, and a structurally normal heart. Short QT syndrome appears to be inherited in an autosomal dominant pattern, and a few affected families have been identified.

Consistent risk factors include:

- Severity of seizures, increased refractoriness of epilepsy and presence of generalized tonic-clonic seizures: the most consistent risk factor is an increased frequency of tonic–clonic seizures.

- Poor compliance. Lack of therapeutic levels of anti-epileptic drugs, non-adherence to treatment regimens, and frequent changes in regimens are risk factors for sudden death.

- Young age, and early age of seizures onset.

- Male gender

- Poly-therapy of epilepsy. It remains unclear whether this is an independent risk factor or a surrogate marker for severity of epilepsy.

- Being asleep during a seizure is likely to favour SUDEP occurrence.

Athlete's heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy, a genetic disorder.

No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete’s heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.

Knowledge that TdP may occur in patients taking certain prescription drugs has been both a major liability and reason for retirement of these medications from the marketplace. Examples of compounds linked to clinical observations of TdP include amiodarone, fluoroquinolones, methadone, lithium, chloroquine, erythromycin, amphetamine, ephedrine, pseudoephedrine, methylphenidate, and phenothiazines. It has also been shown as a side effect of certain anti-arrhythmic medications, such as sotalol, procainamide, and quinidine. The gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes. In many cases, this effect can be directly linked to QT prolongation mediated predominantly by inhibition of the hERG channel.

In September 2011 (subsequently updated in March 2012 and February 2013), the FDA issued a warning concerning increased incidence of QT prolongation in patients prescribed doses of the antidepressant Celexa (citalopram) above 40 mg per day, considered the maximum allowable dosage, thereby increasing the risk of Torsades. However, a study, "Evaluation of the FDA Warning Against Prescribing Citalopram at Doses Exceeding 40 mg," reported no increased risk of abnormal arrhythmias, thus questioning the validity of the FDA's warning.

The treatment for auto-brewery syndrome is a change in diet requiring low carbohydrates and high protein. Sugar is fermented into alcohol, and a diet that effectively lowers sugars also lowers the alcohol that can be fermented from it. Anything that causes an imbalance between the beneficial and harmful bacteria in the gut can help increase the chance that fermentation in the gut will develop. This can include not only antibiotics, but also overindulgence in sugars and carbohydrates. Watching what you eat could lower the risk of gut fermentation syndrome, and taking probiotics could further protect you by increasing the number of good bacteria in your system.

The following is a list of factors associated with an increased tendency towards developing torsades de pointes:

- Hypokalemia (low blood potassium)

- Hypomagnesemia (low blood magnesium)

- Hypocalcemia (low blood calcium)

- Bradycardia (slow heartbeat)

- Heart failure

- Left ventricular hypertrophy

- Hypothermia

- Subarachnoid hemorrhage

- Hypothyroidism

The Registry has been enrolling new patients from participating institutions that are member of the Congenital Heart Surgeons' Society. Hospitals from across North America continue to join the study group and enroll patients. Over 140 patients with AAOCA have been enrolled by June 2011, making it the largest cohort ever assembled of this anomaly.