Vulnerable plaque

The term vulnerable plaque ( French plaque [ plak ], German “plate, spot, shield” ; Latin vulnus “ wound ” or vulnerable “wound”) describes a form of atherosclerotic plaque , which increases the risk of thrombotic complications such as strokes or myocardial infarction having. Plaques that show a particularly rapid progression are also referred to as vulnerable . If a thromboembolic event such as a heart attack or stroke is caused by a vulnerable plaque, then a “culprit plaque” (English pronunciation [ kʌlprɪt ], German literally “guilty”, meaning “the plaque causing an event”) is spoken of .

Criteria for a vulnerable plaque

In a consensus document published in 2003 by a group of recognized and internationally known atherosclerosis scientists (including pathologists , radiologists , molecular biologists , neurologists , internists ) , 5 main and 5 secondary criteria of vulnerable plaque were defined. It was generally stated that knowledge of the degree of stenosis of an atherosclerotic plaque alone is not sufficient to determine its vulnerability . In contrast, it is important to know the composition of the plaque and its morphology in order to be able to draw conclusions about its vulnerability.

Main criteria

• Active inflammation within the plaque ( infiltration by monocytes / macrophages , less often by T cells )
• Large fat core (“lipid / necrotic core”) with a thin fibrous cap
• Endothelial denudation with aggregation of platelets on the surface
• Plaque rupture (tear in the thin endothelial layer over a plaque)
• Stenosis of the vascular lumen in the plaque area> 90%

Secondary criteria

• Calcifications protruding into the vessel lumen
• Yellowish aspect of the plaque ( angioscopic ), as an indication of a high fat content
• Hemorrhage into the plaque (either from rupture of the fibrous cap or from unstable neovasculature sprouting into the plaque)
• Endothelial dysfunction
• Expansive (positive) remodeling (outward plaque growth without severe narrowing of the vascular lumen)

Pathophysiology

In the context of atherosclerosis of arterial blood vessels , presumably as part of an endothelial dysfunction, extra- and intracellular lipid deposits lead to thickening in the subendothelial layers of the tunica intima of the vessel wall. These thickenings within the vascular wall, if they occur in the form of foci, are also referred to as atherosclerotic plaques. Are mainly of the oxidized LDL existing particles lipid deposits by macrophage phagocytosis , so they become foam cells transformed. The formation of foam cells in turn causes an inflammatory reaction, in the course of which through various processes u. a. through proliferation of smooth muscle cells, calcifications, increased formation of collagen fibers and cell necrosis, a gradual tissue remodeling takes place. This creates a connective tissue-like cap (fibrous cap) over a lipid core in the artery. As the process continues, there may be increasing thinning of the fibrous cap. A vulnerable plaque develops. If the fibrous cap ruptures , the highly thrombogenic fat core is exposed to the bloodstream. This leads to the activation and aggregation of platelets , which results in the formation of a thrombus . This blood clot can either relocate the vascular lumen directly on site or be washed away as an embolus and lead to a vascular occlusion further distal to the flow path. If the blood supply to an organ is interrupted or critically reduced due to the vascular occlusion so that cells die, it is called an infarction . Particularly critical here is an acute vascular occlusion of the arteries supplying the brain, which leads to a stroke if the blood supply to the brain tissue is insufficient , or an acute occlusion of the coronary vessels supplying the myocardium , which results in a heart attack .

Epidemiology

Various studies have shown that 65-75% of myocardial infarctions with ST elevation on the electrocardiogram result from rupture of a vulnerable plaque and that the majority of myocardial infarctions occur in vessels without significant pre-existing stenosis (i.e. stenosis <50%). Similar data are also available on the pathogenesis of ischemic, macroangiopathic stroke. It is known that only around 10% of ischemic strokes of macroangiopathic origin occur as a result of severe stenoses in the course of the vessels supplying the brain, which then cause characteristic border zone infarcts. The majority is caused by ruptured plaques, which mostly occur in the area of ​​the carotid bifurcation, but in rare cases can also be located in the aortic arch or in the area of ​​the intracranial internal carotid artery . Recent imaging studies, e.g. B. MRI (magnetic resonance imaging) was able to show that vulnerable plaques occur significantly more frequently in arteries supplying the brain on the side of the stroke than on the unaffected side and that the presence of vulnerable plaques is associated with an up to 6-fold increased risk of cerebrovascular events, regardless of the degree of stenosis . In addition, it could also be shown in vivo that vulnerable or bleeding plaques are associated with a faster progression of atherosclerosis.

Diagnostics and therapy

The aim is, on the one hand, through preventive measures such as B. a reduction of cardiovascular risk factors , to prevent or delay the development of atherosclerotic lesions and on the other hand to identify patients with vulnerable plaques in good time and to give them a suitable drug, surgical or interventional therapy before serious complications occur. A contribution to this can u. a. the imaging processes, especially the field of plaque imaging, which aims to diagnose critical atherosclerotic changes at an early stage using various modalities such as color duplex sonography , CT and MRT .

Individual evidence

1. ^ PR Moreno: Vulnerable plaque: definition, diagnosis, and treatment. In: Cardiology clinics. Volume 28, number 1, February 2010, ISSN  1558-2264 , pp. 1-30, doi: 10.1016 / j.ccl.2009.09.008 , PMID 19962047 (review).
2. ^ AA Alsheikh-Ali, GD Kitsios, EM Balk, J. Lau, S. Ip: The vulnerable atherosclerotic plaque: scope of the literature. In: Annals of Internal Medicine . Volume 153, Number 6, September 2010, ISSN  1539-3704 , pp. 387-395, doi: 10.7326 / 0003-4819-153-6-201009210-00272 , PMID 20713770 (review).
3. ↑ AV Finn, M. Nakano, J. Narula, FD Kolodgie, R. Virmani: Concept of vulnerable / unstable plaque. In: Arteriosclerosis, Thrombosis, and Vascular Biology . Volume 30, Number 7, July 2010, ISSN  1524-4636 , pp. 1282-1292, doi: 10.1161 / ATVBAHA.108.179739 , PMID 20554950 (review).
4. ↑ M. Naghavi, P. Libby et al. a .: From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. In: Circulation . Volume 108, Number 14, October 2003, ISSN  1524-4539 , pp. 1664-1672, doi: 10.1161 / 01.CIR.0000087480.94275.97 , PMID 14530185 (review).
5. ↑ Welsch: Textbook Histology . Urban & Fischer / Elsevier, Munich 2003, pp. 241–242.
6. ^ GK Hansson: Inflammation, atherosclerosis, and coronary artery disease. In: The New England Journal of Medicine . Volume 352, Number 16, April 2005, ISSN  1533-4406 , pp. 1685-1695, doi: 10.1056 / NEJMra043430 , PMID 15843671 (review).
7. ↑ E. Arbustini, B. Dal Bello et al. a .: Plaque erosion is a major substrate for coronary thrombosis in acute myocardial infarction. In: Heart . Volume 82, Number 3, September 1999, pp. 269-272, PMID 10455073 , PMC 1729173 (free full text).
8. ↑ E. Falk: Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. In: British Heart Journal . Volume 50, Number 2, August 1983, pp. 127-134, PMID 6882602 , PMC 481384 (free full text).
9. ↑ A. Farb, AP Burke et al. a .: Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. In: Circulation. Volume 93, Number 7, April 1996, ISSN  0009-7322 , pp. 1354-1363, PMID 8641024 (review).
10. ^ LG Spagnoli, A. Mauriello u. a .: Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke. In: Journal of the American Medical Association . Volume 292, Number 15, October 2004, pp. 1845-1852, doi: 10.1001 / jama.292.15.1845 , PMID 15494582 .
11. ↑ JP Parmar, WJ Rogers et al. a .: Magnetic resonance imaging of carotid atherosclerotic plaque in clinically suspected acute transient ischemic attack and acute ischemic stroke. In: Circulation. Volume 122, number 20, November 2010, ISSN  1524-4539 , pp. 2031-2038, doi: 10.1161 / CIRCULATIONAHA.109.866053 , PMID 21041694 , PMC 3008416 (free full text).
12. ^ TM Freilinger, A. Schindler et al. a .: Prevalence of nonstenosing, complicated atherosclerotic plaques in cryptogenic stroke. In: JACC: Cardiovascular Imaging . Volume 5, Number 4, April 2012, ISSN  1876-7591 , pp. 397-405, doi: 10.1016 / j.jcmg.2012.01.012 , PMID 22498329 .
13. ↑ T. Saam, H. Hetterich, V. Hoffmann, C. Yuan, M. Dichgans, H. Poppert, T. Koeppel, U. Hoffmann, MF Reiser, F. Bamberg: meta-analysis and systematic review of the predictive value of carotid plaque hemorrhage on cerebrovascular events by magnetic resonance imaging. In: Journal of the American College of Cardiology . Volume 62, number 12, September 2013, pp. 1081-1091, doi: 10.1016 / j.jacc.2013.06.015 , PMID 23850912 (review).
14. ↑ N. Takaya, C. Yuan et al. a .: Presence of intraplaque hemorrhage stimulates progression of carotid atherosclerotic plaques: a high-resolution magnetic resonance imaging study. In: Circulation. Volume 111, Number 21, May 2005, ISSN  1524-4539 , pp. 2768-2775, doi: 10.1161 / CIRCULATIONAHA.104.504167 , PMID 15911695 .
15. ↑ D. Vancraeynest, A. Pasquet et al. a .: Imaging the vulnerable plaque. In: Journal of the American College of Cardiology. Volume 57, Number 20, May 2011, ISSN  1558-3597 , pp. 1961-1979, doi: 10.1016 / j.jacc.2011.02.018 , PMID 21565634 (review).
16. ↑ T. Saam, TS Hatsukami et al. a .: The vulnerable, or high-risk, atherosclerotic plaque: noninvasive MR imaging for characterization and assessment. In: Radiology. Volume 244, Number 1, July 2007, ISSN  0033-8419 , pp. 64-77, doi: 10.1148 / radiol.2441051769 , PMID 17581895 (review).

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