Plaque rupture and sudden death related to exertion in men with coronary artery disease
ABSTRACT Exertion has been reported to acutely increase the risk of sudden coronary death, but the underlying mechanisms are unclear.
To determine the frequency of plaque rupture in sudden deaths related to exertion compared with sudden deaths not related to exertion.
Autopsy survey. Coronary arteries were perfusion fixed and segments with more than 50% luminal narrowing were examined histologically. Ruptured plaques were defined as intraplaque hemorrhage with disruption of the fibrous cap and luminal thrombus. Exertion before death was determined by the investigator of the death.
Medical examiner's office.
A total of 141 men with severe coronary artery disease who died suddenly, including 116 whose deaths occurred at rest (mean [SD] age, 51  years) and 25 who died during strenuous activity or emotional stress (age, 49  years).
The frequency and morphology of plaque rupture was compared in men dying at rest vs those dying during exertion. Independent association of risk factors (total cholesterol, high-density lipoprotein cholesterol, glycosylated hemoglobin, cigarette smoking) in addition to acute exertion with plaque rupture were determined.
The mean (SD) number of vulnerable plaques in the coronary arteries of men in the exertional-death group was 1.6 (1.5) and in the at-rest group was 0.9 (1.2) (P=.03). The culprit plaque in men dying during exertion was plaque rupture in 17 (68%) of 25 vs 27 (23%) of 116 men dying at rest (P<.001). Hemorrhage into the plaque occurred in 18 (72%) of 25 men in the exertional-death group and 47 (41%) of 116 men in the rest group (P=.007). Histological evidence of acute myocardial infarction was present in 0 of 25 in the exertion group and in 15 (13%) of 116 in the rest group. Men dying during exertion had a significantly higher mean (SD) total cholesterol-high-density lipoprotein cholesterol ratio (8.2 [3.0]) than those dying at rest (6.2 [ 2.7]; P=.002), and the majority (21/25) were not conditioned. In multivariate analysis, both exertion (P=.002) and total cholesterol-high-density lipoprotein cholesterol ratio (P=.002) were associated with acute plaque rupture, independent of age and other cardiac risk factors.
In men with severe coronary artery disease, sudden death related to exertion was associated with acute plaque rupture.
SourceAvailable from: R.M.C. SoCommunications in Computational Physics 01/2013; 14(1):126-152. · 1.78 Impact Factor
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ABSTRACT: To provide data on the risk factors and characteristics of subjects who experience sudden cardiac death (SCD) during physical exercise. We assessed the characteristics and the medico-legal autopsy findings of SCD victims who had experienced a witnessed fatal cardiac arrest at rest (n = 876) or in relation to physical exercise (n = 328) in the Finnish Study of Genotype and Phenotype Characteristics of SCD (FinGesture). A total of 876 (73%) witnessed SCDs occurred at rest (R group) and 328 (27%) during or immediately after physical exercise (PE group). Male gender was more common in the PE group compared to the R group (309/328, 94% versus 678/876, 77%, P < 0.001). Coronary artery disease was a more common structural heart disease than non-ischemic disease at autopsy when SCD was exercise-triggered (299/328, 91% versus 657/876, 75%, P < 0.001). Myocardial scarring and cardiac hypertrophy were more commonly found at autopsy in the PE group (194/328, 59% versus 370/876, 42%, P < 0.001; 243/328, 74% versus 585/876, 67%, P = 0.012, respectively). Skiing, cycling, and snow shoveling were the most common modes of exercise at the time of SCD. SCD during or immediately after exercise is related to male gender, ischemic heart disease, cardiac hypertrophy, and myocardial scarring.Annals of Medicine 04/2015; DOI:10.3109/07853890.2015.1025824 · 4.73 Impact Factor
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ABSTRACT: The presence of microcalcifications (µCalcs) >5 µm within the cap of human fibroatheroma has been shown to produce a 200-700 % increase in peak circumferential stress, which can transform a stable plaque into a vulnerable one, whereas µCalcs < 5 µm do not appear to increase risk. We quantitatively examine the possibility to distinguish caps with µCalcs > 5 µm based on the gross morphological features of fibroatheromas, and the correlation between the size and distribution of µCalcs in the cap and the calcification in the lipid/necrotic core beneath it. Atherosclerotic lesions (N = 72) were imaged using HR-μCT at 2.1-μm resolution for detailed analysis of atheroma morphology and composition, and validated using non-decalcified histology. At 2.1-μm resolution one observes four different patterns of calcification within the lipid/necrotic core, and is able to elucidate the 3D spatial progression of the calcification process using these four patterns. Of the gross morphological features identified, only minimum cap thickness positively correlated with the existence of µCalcs > 5 µm in the cap. We also show that µCalcs in the cap accumulate in the vicinity of the lipid/necrotic core boundary with few on the lumen side of the cap. HR-μCT enables three-dimensional assessment of soft tissue composition, lipid content, calcification patterns within lipid/necrotic cores and analysis of the axial progression of calcification within individual atheroma. The distribution of µCalcs within the cap is highly non-uniform and decreases sharply as one proceeds from the lipid pool/necrotic core boundary to the lumen.The international journal of cardiovascular imaging 04/2015; DOI:10.1007/s10554-015-0650-x · 2.32 Impact Factor