Relationship of Clinical Presentation and Calcification of Culprit Coronary Artery Stenoses

Abstract

Abstract-Coronary artery calcification is increased in the presence of atherosclerosis. However, there is great variability in the calcification of individual coronary stenoses, and the clinical significance of this finding remains unknown. We tested the hypothesis that culprit lesions associated with myocardial infarction or unstable angina are less calcified than are stenoses associated with stable angina. The study consisted of 78 patients who underwent intravascular ultrasound imaging of culprit stenoses after the placement of a stent. Seventeen patients presented with stable angina; 43, with unstable angina; and 18, with myocardial infarction. The extent of coronary calcification was measured by the angle of its arc and was quantified with a computer-based protractor. The arc of calcium was measured in the stented area at the point of maximal calcification and also as an average of the calcification found at proximal, middle, and distal stent segments. The maximal arc of calcium decreased progressively from patients with stable angina (91Ϯ10°) to those with unstable angina (59Ϯ8°) and to those with myocardial infarction (49Ϯ11°, Pϭ0.014). Similarly, the average arc of calcium was greatest (32Ϯ7°) in patients with stable angina, less (15Ϯ4°) in patients with unstable angina, and least (10Ϯ5°) in patients with acute myocardial infarction (Pϭ0.014). These associations remained significant after adjustment for other factors that potentially affect arterial calcification. Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina. Key Words: calcinosis Ⅲ calcium Ⅲ coronary vessels Ⅲ ultrasonography, interventional Ⅲ myocardial infarction C oronary artery calcification is an active process that is commonly observed in the setting of atherosclerosis. 1-3 Previous reports have found that arterial calcification is proportional to the overall burden of the atherosclerotic plaque but not necessarily to the severity of luminal narrowing. 3-7 Acute coronary syndromes, including myocardial infarction and unstable angina, arise from rupture or erosion of atherosclerotic plaques. 4 The relationship of lesional calcium toward propensity to plaque rupture and, thus, to the pathogenesis of acute coronary syndromes remains uncertain. 5 See editorial, page 1561Furthermore, the association between coronary calcification and atherosclerosis has stimulated interest in using arterial calcification to detect coronary atherosclerosis. Noninvasive methods of quantifying coronary calcification, eg, electron beam CT (EBCT), have helped to define the relationship between coronary artery calcification and the atherosclerotic burden. Whether such calcium-based approaches can be useful in visualizing the most dangerous, ie, vulnerable plaques, is unknown.In the present study, we tested the hypothesis that calcification of culprit lesions responsible is reduced for acute coronary syndromes compared with lesions associated with stable angina. Accordingl...

Small Coronary Calcium Deposits and Elevated Plasma Levels of Oxidized Low Density Lipoprotein are Characteristic of Acute Myocardial Infarction

“…Hence, one could hypothesize that small and spotty calcium deposits within an atherosclerotic plaque cause differences in tissue stiffness in the plaque, and the junction between the calcified and non-calcified tissues could act as a destabilizer, potentially leading to plaque rupture or fissuring. Indeed, recent clinical studies using IVUS and multislice CT (MSCT) have shown that coronary plaques with small spotty calcium deposits are more prone to rupture than severely calcified plaques [1][2][3]24) . It is conceivable, therefore, that discrete and spotty calcification, which contributes to differences in tissue tensile strength, together with other destabilizing factors such as endothelial dysfunction, plaque inflammation, and lipid accumulation, plays a role in the genesis of coronary plaque instability and the development of acute coronary events, which could cause high levels of plasma ox-LDL.…”

Characterization of Human Atherosclerotic Plaques by Intravascular Magnetic Resonance Imaging

“…In the in vivo studies, both IVMRI and IVUS showed high levels of agreement for identifying the presence and location of calcium, which is unsurprising, because IVUS excels at defining calcifications. 24 However, calcification interferes with measurement of atheroma size by IVUS, because outer vessel boundaries are lost because of acoustic shadowing; calcification poses no such difficulties in interpreting IVMRI. This problem was relatively frequent for IVUS, perhaps because iliac arteries tend to be calcified.…”

18F-sodium fluoride positron emission tomography assessed microcalcifications in culprit and non-culprit human carotid plaques

“…15,16 In contrast, established calcifications are seen as atherosclerotic end stage products and are associated with plaque stability. [17][18][19][20] It has been suggested that 18 F-NaF may additionally be a useful marker for plaque vulnerability. 21 Indeed, a clinical study by Joshi et al showed that ruptured and high-risk coronary plaques have a significantly higher 18 F-NaF uptake than non-culprit and low-risk coronary plaques.…”