risks and triggers

 

The risks of sudden cardiac death generally reflect the risks of ischaemic heart disease:

(Zipes 1998; and see also Cardiovascular risk prediction charts reproduced in the British National Formulary (BNF))

 

  • Age – peak incidence 45-75
  • Sex – M>F (3 – 4 fold difference)
  • Elevated serum cholesterol
  • Smoking – 2.5 times risk of sudden death in those smoking >20 cigarettes per day, possibly due to increased platelet adhesiveness and catecholamine release
  • Glucose intolerance
  • Weight
  • Hypertension
  • Heart rate
  • Left Ventricular Hypertrophy
  • Impaired left ventricular function (particularly in men) – non-sustained ventricular tachycardia (VT) may be an independent marker of increased mortality risk in those with severe heart failure
  • Intraventricular conduction block/ Atrio-ventricular (AV) block in survivors of out-of-hospital cardiac arrest
  • Alcohol– heavy drinking, binge drinking, overt cardiomyopathy and alcoholic fatty liver all associated with sudden death.
  • Post myocardial infarction – unique set of predictive factors, elucidated by Multicentre Automatic Defibrillator Implantation Trial (MADIT) eg. spontaneous non-sustained VT, inducible VT not suppressed by IV procainamide and an ejection fraction <35%
  • Autonomic state and Carotid sinus pressure (CSP) – baroreflex sensitivity is reduced in patients at risk of sudden death. Myocardial infarction produces regional autonomic dysfunction, predisposing to arrhythmias. CSP also linked to sudden cardiac death.
  • Mitochondrial DNA mutations – an apparent association between a common mitochondrial DNA mutation (mtDNA4977) and cardiac muscle damage has been reported. (Polisecki 2004).
  • Type of water – soft water areas have been linked with an excess of sudden cardiac deaths (Davies and Popple 1979)
  • Relationship with food – an association has been reported between sudden cardiac death and the hour following a meal, particularly the main evening meal. (Myers and Dewar 1975)
  • Myocardial fibrosis

   

Transient risks

It is thought that structural cardiac abnormalities provide the substrate upon which the following transient risk factors operate, (Zipes 1998);

 

  • Time of day – many researchers have established a circadian rhythm associated with sudden cardiac death, as well as strokes and myocardial infarction, transient ischaemic events and arrhythmias. (Chi and Kloner 2003; Willich 1993; Myers and Dewar 1975). The peak times appear to be in the hours immediately after waking, and in the evening. This could be mediated by the waking sympathetic discharge in response to venous pooling with increases in blood pressure and blood coagulability. (Leor 1996).
  • Day of the week – an increased incidence of myocardial infarction has been noted on Mondays, possibly indicating an increased risk on returning to work after a weekend break. (Chi and Kloner 2003).
  • Emotional stress/ arousal – folklore has long held that emotional stress, and in particular fear and anger can result in sudden death. Researchers have appeared to validate this, linking increases in cardiac arrest, arrhythmias and sudden death with natural disasters such as earthquakes, and war, as well as sporting events, and other life events. (Lecomte 1996; Reich 1981; Chi and Kloner 2003; Leor 1996; Meisel 1991; Willich 1993). (See also ‘Issues and controversies’ section).
  • Transient effects of drugs, toxins or alcohol– Flecainide, an anti-arrhythmic drug was found to exacerbate arrhythmias in the Cardiac Arrhythmia Suppression Trial (CAST) in certain circumstances.
  • Reperfusion
  • Haemodynamic dysfuction
  • Electrolyte abnormalities (hypokalaemia and hypomagnesaemia)
  • Changes in pH or p02
  • Influence of central or peripheral neurophysiological actions
  • Transient ischaemia eg. during coronary artery spasm or platelet microemboli from intracoronary plaque thrombi

 

references

 

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