Long-Term Prognostic Value of Coronary Calcification Detected by Electron-Beam Computed Tomography in Patients Undergoing Coronary Angiography

Keelan, Paul C.; Bielak, Lawrence F.; Ashai, Khalid; Jamjoum, Lama S.; Denktaş, Ali E.; Rumberger, John A.; Sheedy, Patrick F.; Peyser, Patricia A.; Schwartz, Robert S.

doi:10.1161/hc2901.093112

Cited by 358 publications

(220 citation statements)

References 36 publications

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“…6,15,16) Moreover, the amount of calcium and the rapid progression of calcification at the coronary arteries level have been associated in previous works with a higher risk of cardiovascular events. [17][18][19][20][21] Therefore, carotid calcifications could reflect diffuse coronary artery disease. Our study demonstrates that the presence of an extensively calcified carotid plaque is strongly suggestive of the likelihood of an acute coronary event or at least a warning sign of advanced coronary artery disease.…”

Section: Discussionmentioning

confidence: 99%

Can Carotid Plaque Histology Selectively Predict the Risk of an Acute Coronary Syndrome?

et al. 2011

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SummaryThe aim of this study was to assess whether carotid plaque morphology is an independent predictive factor of stroke and, innovatively, of acute coronary syndrome (ACS). We analyzed morphological aspects of carotid atherosclerotic plaque associated with an increased risk of ACS and stroke. We examined 72 carotid endarterectomy (CEA) specimens obtained between January 2005 and February 2009. All patients underwent follow-up for 12 months after the revascularization treatment to assess the occurrence of ACS and stroke. Data obtained showed that in patients with a previous ACS and in those who had developed an ACS during follow-up after CEA, the degree of carotid plaque calcification was more severe than in patients who did not develop an ACS, either before CEA or during follow-up. However, plaques of patients with ACS were mostly devoid of a significant inflammatory component, whereas a rich infiltrate, mainly consisting of monocytes-macrophages and lymphocytes, was present in plaques of subjects who did not develop an ACS. This element was particularly important since strokes occurred only in the latter group of patients (62% versus 0%). Therefore, we deduced that inflammation, from the histological point of view, is more correlated with cerebral circulation disorders than with coronary disease. In conclusion, while the finding of a soft plaque with a large necrotic core and a marked inflammatory component, often characterized by acute complications, may be predictive of an increased risk of cerebrovascular events, a heavily calcified plaque may be indicative of a high risk of coronary events. (Int Heart J 2011; 52: 72-77)

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Section: Discussionmentioning

confidence: 99%

Can Carotid Plaque Histology Selectively Predict the Risk of an Acute Coronary Syndrome?

et al. 2011

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“…5 CAC quantity is an independent predictor of angiographically defined CAD after controlling for established CAD risk factors, 6,7 and CAC predicts future CAD end points in asymptomatic and symptomatic adults. 8,9 Many established CAD risk factors, such as male sex, older age, smoking, abnormal lipid levels, high blood pressure, and ponderosity are related to CAC quantity. 7,10 -13 Much variation in CAC quantity, however, remains unexplained after accounting for these factors.…”

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confidence: 99%

Heritability of Coronary Artery Calcium Quantity Measured by Electron Beam Computed Tomography in Asymptomatic Adults

et al. 2002

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Background-Electron beam computed tomography is an accurate, noninvasive method to detect and quantify coronary artery calcification (CAC), a marker of subclinical and clinical coronary artery atherosclerosis. CAC quantity predicts future coronary artery disease end points in asymptomatic adults, but measured risk factors explain less than half the variability in CAC quantity. Although several candidate genes for CAC have been identified, the relative importance of genetic influences on CAC quantity has not been assessed in asymptomatic adults in a community. Methods and Results-We quantified the relative contributions of measured risk factors and genetic influences on CAC quantity measured by electron beam computed tomography in 698 asymptomatic white adults from 302 families. Before adjusting for any risk factors, 43.5% of the variation in CAC quantity was attributable to genetic factors (Pϭ0.0007). Independent predictors of CAC quantity were identified with stepwise linear regression. After adjusting for these risk factors, including age, sex, fasting glucose level, systolic blood pressure, pack-years of smoking, and LDL cholesterol, 41.8% of the residual variation in CAC quantity was attributable to genetic factors (Pϭ0.0003). Conclusions-These results demonstrate the importance of genetic factors in subclinical coronary atherosclerosis variation as measured by CAC quantity. The presence of genetic effects suggests that unknown genes that influence CAC quantity are yet to be identified. (Circulation. 2002;106:304-308.)

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“…56 The presence of coronary calcification is strongly predictive of ischemic heart disease despite absence of significant luminal obstruction. 57,58 Fibroblast growth factor (FGF)-23 is an emerging factor that appears to play a central role in the regulation of phosphorus and vitamin D homeostasis. 59 Increased FGF-23 observed in CKD enhances phosphaturia by downregulating renal expression of sodium phosphate cotransporters and it reduces 1,25-dihydroxyvitamin D production by inhibiting renal 1-α hydroxylase.…”

Section: Dysregulation Of Calcium and Phosphate Homeostasismentioning

confidence: 99%

Cardiorenal Syndrome

Lekawanvijit

Kompa

Wang

et al. 2012

Circulation Research

149

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Cardiorenal syndrome is a condition in which a complex interrelationship between cardiac dysfunction and renal dysfunction exists. Despite advances in treatment of both cardiovascular and kidney disease, cardiorenal syndrome remains a major global health problem. Characteristic of the pathophysiology of cardiorenal syndrome is bidirectional cross-talk; mediators/substances activated by the disease state of 1 organ can play a role in worsening dysfunction of the other by exerting their biologically harmful effects, leading to the progression of the syndrome. Accumulation of uremic toxins is a hallmark of renal excretory dysfunction. Removal of some toxins by conventional dialysis is particularly problematic because of their high protein binding. In this review, we demonstrate that protein-bound uremic toxins may play an important role in progression of cardiovascular disease in the setting of chronic kidney disease. The highly protein-bound uremic toxin indoxyl sulfate has emerged as a potent toxin adversely affecting both the kidney and heart. Direct cardiac effects of this toxin have been recently demonstrated both in vitro and in vivo. Specifically, potent fibrogenic and prohypertrophic effects, as well as oxidative stress-inducing effects, appear to play a central role in both renal and cardiac pathology. Many of these adverse effects can be suppressed by use of a gut adsorbent, AST-120. Potential mechanisms underlying indoxyl sulfate−induced cardiorenal fibrosis are discussed. Future research and clinical implications conclude this review.

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Long-Term Prognostic Value of Coronary Calcification Detected by Electron-Beam Computed Tomography in Patients Undergoing Coronary Angiography

Cited by 358 publications

References 36 publications

Can Carotid Plaque Histology Selectively Predict the Risk of an Acute Coronary Syndrome?

Can Carotid Plaque Histology Selectively Predict the Risk of an Acute Coronary Syndrome?

Heritability of Coronary Artery Calcium Quantity Measured by Electron Beam Computed Tomography in Asymptomatic Adults

Cardiorenal Syndrome

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