sudden cardiac death and coronary artery disease


Source: Wikipedia


Sudden death is the first presentation of coronary artery disease in a significant proportion of cases – a third of cases in some studies, whilst 72% in one study had no previous cardiac history (Fornes 1993; Chi and Kloner 2003).

Of those who present with sudden cardiac death, between 80-90% have ‘significant’ coronary artery disease (Zipes and Wellens 1998).

Of those who die from sudden cardiac death, coronary artery findings are varied (Davies and Popple 1979; Davies 1992 and 2000; Kolodgie 2004; Fornes 1993);

  • 66% have stenoses
  • Between 15-75% have an acute coronary thrombus. This broad range reflects different inclusion criteria for published studies, but Farb et al (1996) found acute thrombi in 54% of men with coronary disease who died suddenly – a figure suggested by other experts as being a ‘reasonable’ estimate (Gallagher 2002 and personal communication 2005).
  • Those with no thrombus had >75% stenosis of at least one vessel
  • Coronary artery spasm can occur in segments having eccentric plaques, resulting in myocardial ischaemia without occlusion

The mechanism of the terminal event is said to be either VF or acute myocardial infarction, and there is no consensus on the importance of an old infarction (Gaita 2003; de Vreede 1998; Takada 2003).

Acute myocardial infarction has been described (Chandrasekaran and Kurbaan 2002) with angiographically ‘normal’ coronary arteries, typically affecting those under 50 years, where proposed mechanisms include;  

Kumar et al (2005) summarise the pathogenesis of atherosclerosis, and set out the ‘response to injury’ hypothesis. This is a theory describing atherosclerosis as a chronic inflammatory response of the arterial wall initiated by injury to the endothelium. Lesion progression is sustained by the interaction between modified lipoproteins, macrophages, T lymphocytes and the normal constituents of the arterial wall.

Atherosclerotic plaques have a tendency to develop at branch points of vessels, and at ostia, where blood flow is disturbed.

Davies (2000) described the histological features of the ‘typical’ plaque. A connective tissue capsule, together with macrophages and ‘foam cells’ surround a lipid core.

Thrombi form within a coronary artery by either;  

  • Plaque rupture/ fissuring (in >85% of major thrombi in white men with dyslipidaemia) – where the plaque collagen cap tears, exposing the highly thrombogenic core to blood. Thrombus forms within the plaque, and extends into the lumen. These atheromatous lesions tend to be eccentric.
  • Erosion (in 50% of thrombi in women) – where thrombus adheres to a denuded endothelial surface overlying a concentric segment of atheroma.


Progressive atherosclerosis formation

Source: Wikipedia

progression of athersclerosis


'Fatty streak'

micrograph of an artery with a 'fatty streak'

(source - with virtual slide - University of Western Ontario virtual slide box)


Atherosclerotic plaque

atherosclerotic plaque microscopy

(source - with virtual slide - University of Western Ontario virtual slide box )

implications of coronary artery plaque rupture


Studies implicate plaque erosion in 44% of sudden deaths, and ruptures as being responsible for 60 – 75% of acute coronary syndrome. This arises when activated platelets clump on the thrombus surface, and are swept downstream (Davies 2000; Kolodgie 2004; Farb 1996).

The concept of the ‘vulnerable plaque’ or ‘thin cap fibroatheroma’ has developed, which is implicated in sudden cardiac death, particularly in women, with raised cholesterol levels and raised CRP levels.

The ‘vulnerable plaque’ has the following characteristics (Davies 2000; Aikawa and Libby 2004; Kolodgie 2004); 

  • a lack of severe stenosis
  • a large lipid core (>50% of overall plaque volume)
  • inflammatory cell accumulation
  • a thin fibrous cap
  • smooth muscle cell loss
  • collagen loss
  • over-expression of metalloproteinases and other factors

As the thrombus occludes the artery lumen, it responds by increasing cross sectional area, and by a process of ‘remodelling’ maintains a lumen. Thrombi that do not develop rapidly allow a collateral blood supply to develop, whilst rapidly developing thrombi that last for 6 hours or more result in transmural infarction of the myocardium supplied by that vessel. Repetitive insults or platelet emboli from thrombus surfaces result in non-transmural infarcts.  

autopsy assessment of coronary artery stenosis


The majority of sudden cardiac deaths occur on a background of coronary artery disease, manifested by luminal stenosis. The myocardium extracts oxygen at maximum efficiency and increased demand from basal requirements can only be achieved by increasing blood flow. Any degree of stenosis is therefore able to reduce that required increase.

Clinical studies demonstrate reduced coronary blood flow with stenoses >50%, but there is a complex curvilinear relationship between the two, and the length of a lesion and its geometry must also be taken into account. Coronary blood flow decreases rapidly when the stenosis >70% (Stary 1995).

It should also be noted that neither stenoses nor thrombi are necessary to cause myocardial ischaemia – coronary artery spasm is well documented, and is the basis for Prinzmetal’s variant angina and microvascular angina (Aikawa and Libby 2004).

However, 40-86% of cardiac arrest survivors do have >75% stenosis of at least one coronary artery, and some researchers conclude that this is the minimum degree of stenosis required to be present before a cardiac cause of death can be reasonably ascribed. However, there is confusion in the literature about what constitutes ‘pin-point’ stenosis – either 75% or 85% (Davies and Popple 1979; Davies 1999).

Heavily calcified coronary arteries make any meaningful assessment of degree of stenosis difficult, and some authors recommend perfusion fixation followed by decalcification. The arteries are then sliced at 2-3 mm intervals. Others have produced visual charts allowing comparison of degrees of stenosis, without the need for complex planimetry assessment (Champ and Coghill 1989).

The presence of calcification is thought to be a marker for complex atherosclerotic lesions (Chandrasekaran and Kurbaan 2002), and Davies and Popple (1979) stated that ‘it is reasonable to assume that in the under 65 years age group, heavy calcification is likely to be associated with enough stenosis to cause death', whereas the correlation for those over 65 was not so good.

Further disagreement exists in the literature regarding the significance or otherwise of different patterns of stenoses. Some consider the right coronary artery to be at the basis of fatal arrhythmias (Myers and Dewar 1975), whilst for others the Left Anterior Descending artery is the ‘artery of sudden death’ (Davies and Popple 1979). Still others consider there to be no pattern (Zipes 1998).

Davies (1999) produced guidance on the ‘roughly estimated’ probability of death being due to IHD based on the degree of stenosis, and this guidance was produced in a modified form (Sheppard and Davies 1998) to provide probability ranges (high, medium, low and very low probability). No data is provided upon which these probabilities are based, however.



Approximate probability of death being due to IHD (Davies 1999)

Modified Probability of death being due to IHD

(Sheppard and Davies 1998)

Pericardial tamponade

Rupture of acute infarct

Coronary thrombus


High probability

Acute MI/ coronary thrombus

Coronary thrombosis alone

Healed previous infarct scar – no thrombus



No thrombus – no scars

X3 vessels with >75% stenosis

X2 vessels with >75% stenosis

X1 vessel with >75% stenosis


Medium probability (>75% diameter stenosis with old infarction and/or LVH)


Low probability

(high grade stenosis but normal myocardium)

Stenosis <75% alone

Less than 50%

Very low probability

(<50% stenosis, no scars or LVH)


Cardiology view of assessing coronary artery stenosis?

See discussion on, and examples of percutaneous coronary angiographic assessment of the coronary circulation at PCIpedia, for example an occlusion of the proximal LAD. For an overview of angiography, see Ask Dr wiki.

myocardial infarction and evolution of ECG changes


evolution of an infarct on an ECG:

  • (a) normal QRST complex
  • (b) ST elevation
  • (c) and (d) Q wave formation and T wave inversion
  • (e) normalisation with persistent Q wave.


source: ECGpedia


Source: ECGpedia

Acute anterior left ventricular wall infarction

  • extending into the interventricular septum following left anterior descending coronary artery occlusion- correlates within hours with ST elevation and inverted T waves (NB. in the hyperacute phase, within minutes of infarction, there is ST elevation with tall T waves).



Healing anterior myocardial infarction

  • with thinning of the left ventricular free wall and anterior septum, due to scar formation. This correlates with pathologic Q waves on an ECG.

Source: ECGpedia



Pathologic Q wave

Source: ECGpedia

infarct localisation

see the full-size illustration of infarct localisation by Tor Ercleve (@ Life in the fastlane blog)

myocardial infarction due to atherosclerotic occlusion of the proximal left anterior descending coronary artery


ECG - anterior myocardial infarction (proximal LAD occlusion)

See ECGpedia for a detailed account of ECG changes observed in myocardial infarction, including anterior infarcts.

Source: PCIpedia


pcipedia prox lad occlusion angiography.avi (1,3 MB)

Imaging during angiography and percutaneous coronary artery stenting procedure (PCI) -  proximal left anterior descending artery occlusion  causing anterior myocardial infarction

Source: PCIpedia


myocardial infarction microscopy


Acute infarction

acute haemorrhagic myocardial infarction

(source - with virtual slide - University of Western Ontario virtual slide box)


Healing (and well-healed) myocardial infarction

healing and well healed myocardial infarction

(source - with virtual slide - University of Western Ontario virtual slide box)


Healed myocardial infarct

healed (scarred) myocardial infarct

(source - with virtual slide - University of Western Ontario virtual slide box)



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