News "Vulnerable plaque screening and risk prediction"

Computed tomography (CT scanning of the heart, CT coronary angiogram) or cardiac computed tomography angiography (CCTA) is used to examine occlusion in coronary arteries. Although not routinely used in clinical practice, it provides important prognostic information. CCTA permits visualization of the vessel wall which has a crucial role in the development of the acute coronary syndrome. It was concluded that this tool may improve risk stratification in patients. Hadamitzky et al. provided in their study long-term follow-up (5.6 years) data on prognosis: The severity of coronary artery disease (CAD) and the total plaque score were the best predictors of death and non-fatal myocardial infarction. The annual event rate ranged from 0.24% for patients with no CAD to 1.1% for patients with obstructive CAD and 1.5% for patients with CAD and extensive plaque load. Hadamitzky et al. concluded that CCTA imaging may be a valuable tool in the assessment of long-term prognosis in patients with suspected CAD.

MRI imaging of carotid plaques: can future cerebral ischemia be predicted?

Methods are needed that can identify vulnerable plaques. In case of carotid artery stenosis, vulnerable plaques are expected to be associated with an increased risk of cerebral events. Esposito-Bauer et al. show that MRI plaque imaging has indeed the potential to identify patients with asymptomatic carotid stenosis who are particularly at risk of developing future cerebral ischemia. Event-free survival was higher among patients with the MRI-defined stable lesion types. It was concluded that MRI could improve selection criteria for invasive therapy in the future.

PLoS One. 2013 Jul 24;8(7):e67927. doi: 10.1371/journal.pone.0067927. Print 2013.
MRI plaque imaging detects carotid plaques with a high risk for future cerebrovascular events in asymptomatic patients.
Esposito-Bauer L, Saam T, Ghodrati I, Pelisek J, Heider P, Bauer M, Wolf P, Bockelbrink A, Feurer R, Sepp D, Winkler C, Zepper P, Boeckh-Behrens T,
Riemenschneider M, Hemmer B, Poppert H.
Department of Neurology, Technische Universität München, Munich, Germany; Department of Psychiatry and Psychotherapy, Universitätsklinikum des Saarlandes,
Homburg, Germany.

High C-reactive protein: are increased adverse cardiovascular events just a consequence of ongoing coronary narrowing?
C-reactive protein (CRP) is used as a marker of systemic inflammation that can increase up to 50 thousand fold in acute infection. It remains, however, unclear to what extent CRP is involved in ongoing atherosclerosis. The study of Patel et al. provides evidence that coronary narrowing is not monitored by CRP in postmenopausal women. However, adverse cardiovascular events are increased among patients with higher CRP levels.

Clin Cardiol. 2013 Jun 10. doi: 10.1002/clc.22155. [Epub ahead of print]
Discordant Association of C-Reactive Protein With Clinical Events and Coronary Luminal Narrowing in Postmenopausal Women: Data From the Women's Angiographic
Vitamin and Estrogen (WAVE) Study.
Patel D, Jhamnani S, Ahmad S, Silverman A, Lindsay J.
Department of Internal Medicine, Washington Hospital Center, Washington, DC; Department of Internal Medicine, Division of Cardiology, Virginia Commonwealth
University Hospital, Richmond, Virginia.

Is a stable plaque turned into a vulnerable plaque by cardiac dilatation?
Although great progress has been made in the prevention of myocardial infarction, mechanisms predisposing to plaque rupture remain greatly unresolved. In case that mechanisms hve been identified, they are often inadequately treated. As discussed previously, increased pulse pressure which raises shear stress increases the vulnerability of a plaque. It is in this context an important observation by Burgmaier et al. that left ventricular dilation which is known to be associated with an increase in overall wall stress (for an overview, see heartimaging) is associated with decreased fibrous cap thickness of coronary lesions. Enddiastolic volume predicted plaque vulnerability and it was concluded that this parameter may be a useful adjunct to the risk-stratification of patients with type 2 diabetes. It can be inferred that an increase in wall stress underlies the relationship between chamber dilation and plaque vulnerability. A raised wall stress of the myocardial wall is expected to be transmitted to plaques leading to plaque cap thinning. One of the conclusions is that factors promoting chamber dilatation should be identified and treated more rigorously. For a potential target, see HUFA deficiency found in dilative heart failure requiring replacement of HUFAs.

Cardiovasc Diabetol. 2013 Jul 11;12(1):102. [Epub ahead of print]
Plaque vulnerability of coronary artery lesions is related to left ventricular dilatation as determined by optical coherence tomography and cardiac magnetic
resonance imaging in patients with type 2 diabetes.
Burgmaier M, Frick M, Liberman A, Battermann S, Hellmich M, Lehmacher W, Jaskolka A, Marx N, Reith S.

Coronary calcium: a marker of atherosclerosis and of plaque vulnerability?

Calcification of coronary plaques is thought to contribute to their instability. The study of Servadei et al. indicates that coronary artery calcium can define the risk of acute coronary events but surprisingly does not identify the vulnerable plaque. Clearly more research is needed to unravel adverse molecular mechanisms associated with coronary calcium:

Plaques are exposed to shear stress of the flowing blood which can be crucial for the rupture of a vulnerable plaque. One might, therefore, expect, that increased pulse pressure, i.e. high systolic and low diastolic blood pressure due to adverse vascular remodeling that involves also large arteries contributes to plaque rupture. In the study of Selwaness et al. it is indeed shown that pulse pressure is the strongest determinant of intraplaque hemorrhage which is associated with ischemic stroke. The combination of systolic hypertension and smoking was associated with 2.5 times increased risk of intraplaque hemorrhage:

Hypertension. 2013;61:76-81.
Blood pressure parameters and carotid intraplaque hemorrhage as measured by magnetic resonance imaging: The Rotterdam Study.
Selwaness M, van den Bouwhuijsen QJ, Verwoert GC, Dehghan A, Mattace-Raso FU, Vernooij M, Franco OH, Hofman A, van der Lugt A, Wentzel JJ, Witteman JC.
Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands.

Prediction of inflamed plaques by FDG-PET?
How to predict a high risk of ischemic stroke? How to identify vulnerable plaques? It might not be surprising that techniques that use information from the altered metabolism of inflamed plaque provide such information. In the study by Saito et al. it is shown that fluorodeoxyglucose (FDG) positron emission tomography (PET) can indeed predict the lipid-rich and inflamed plaque:

Cerebrovasc Dis. 2013;35:370-7.
Validity of Dual MRI and F-FDG PET Imaging in Predicting Vulnerable and Inflamed Carotid Plaque.
Saito H, Kuroda S, Hirata K, Magota K, Shiga T, Tamaki N, Yoshida D, Terae S, Nakayama N, Houkin K.
Department of Neurosurgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Plaque volume as risk predictor?
It remains a great challenge to rate cardiovascular risk during progression of atherosclerosis. While various methods have emerged for monitoring subclinical atherosclerosis ranging from measurement of intima-media thickness to arterial stiffness and flow-mediated vasodilatation, the transition from stable to vulnerable plaque remains greatly unexplored. In the prospective study of Wannarong et al. it is shown that total plaque volume is superior in predicting cardiovascular events compared with intima-media thickness and total plaque area:

Stroke. 2013 Jun 4. [Epub ahead of print]
Progression of Carotid Plaque Volume Predicts Cardiovascular Events.
Wannarong T, Parraga G, Buchanan D, Fenster A, House AA, Hackam DG, Spence JD.
From the Stroke Prevention and Atherosclerosis Research Centre, Robarts Research Institute (T.W., D.G.H., J.D.S.), Imaging Research Group, Robarts Research Institute (G.P., D.B., A.F., J.D.S.), Department of Medicine (A.A.H., D.G.H.), and Department of Epidemiology and Biostatistics (D.G.H.), Western University, London, Canada; and Department of Internal Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand (T.W.).

21.12.2013 (HR)