Sudden Cardiac Death (SCD)

The football world lost another young player to sudden death in Spain last weekend.A seperate incident in the Leicester game could easily have made it a double jeopardy weekend.
These stories have brought memories of similar deaths in the past:Mark Vivien Foe and Sam Oparaji readily springs to mind.Let's not forget the Kanu Heart foundation....and Kalilou Fadiga still wears an Implantable Cardioverter-Defibrillator(ICD).
Today,I dug up a little information on this dreaded killer.

Sudden cardiac death remains a leading cause of death in the United States. The annual incidence has been estimated at approximately 450,000 cases annually, which translates to about half of all heart-related deaths . These estimates are based on death certificates, however, which can be inaccurate. The true number may be as low as 184,000, but this still represents a significant cause of death. As total cardiac mortality has decreased over the past decade, sudden cardiac death has increased by about 12% as a proportion of all cardiac deaths. Coronary artery disease is by far the most common cause, accounting for approximately 75% of cases, with cardiomyopathies and primary electrical disturbances making up the remainder.

The most important risk factors for sudden cardiac death, in descending order, are left ventricular ejection fraction of less than 40%, congestive heart failure, frequent PVCs, ischemia, and left ventricular hypertrophy. Inherited disorders associated with a high risk of sudden death include the long QT syndromes, Brugada syndrome, and exercise-induced polymorphic ventricular tachycardia.

Most cases of SCD occur in patients with structural abnormalities of the heart, related to either a prior myocardial infarction (MI) or a congenital abnormality. Acute thrombosis in an atherosclerotic coronary artery may present as unstable angina, acute myocardial infarction (MI), or SCD. Although more than 80% of SCD events occur in individuals with coronary artery disease (CAD), evidence of acute MI is far less common. Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) both are associated with increased risk of SCD. Heart failure and various valvular diseases such as aortic stenosis are associated with increased risk of SCD. The strongest predictor of SCD is left ventricular dysfunction of any cause. Acute illnesses, such as myocarditis, may provide both an initial and sustained risk of SCD due to inflammation and fibrosis of the myocardium.

Less commonly, SCD happens in patients who may not have apparent structural heart disease. These conditions usually are inherited arrhythmia syndromes.
At the molecular level, VT and VF can be caused by altered Ca hemodynamics, neurohormonal changes, altered K hemodynamics especially in ischemia, or mutations resulting in dysfunction of a sodium channel (Na channelopathy) resulting in enhanced automaticity or reentry with unidirectional block. In patients who survive a myocardial infarction (MI), it has been demonstrated that the presence of premature ventricular contractions (PVCs), particularly complex forms, such as multiform PVCs, short coupling intervals (R-on-T phenomenon), or VT (salvos of 3 or more ectopic beats), reflect an increased risk of sudden cardiac death.

ref:MKSAP14 and emedicine.com
OMC