Medicine:Microangiopathy

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Microangiopathy (also known as microvascular disease, small vessel disease (SVD) or microvascular dysfunction) is a disease of the microvessels, small blood vessels in the microcirculation.[1] It can be contrasted to macroangiopathies such as atherosclerosis, where large and medium-sized arteries (e.g., aorta, carotid and coronary arteries) are primarily affected.[2]

Microangiopathy
MVD001.jpg
A case of conjunctival microangiopathy (red dashed-square) secondary to diabetes demonstrating a microaneurysm (orange arrow), vessel dilatation (blue arrows), and vascular tortuosity (yellow arrow).

Small vessel diseases (SVDs) affect primarily organs that receive significant portions of cardiac output such as the brain, the kidney, and the retina. Thus, SVDs are a major etiologic cause in debilitating conditions such as renal failure, blindness, lacunar infarcts, and dementia.[3]

Types

Microangiopathies are involved in a variety of different diseases including:

Pathophysiology

The main target of small vessel diseases is the endothelium, which plays a key role in vascular homeostasis.[3] The pathogenesis of SVDs in various organs is characterized by endothelial dysfunction, capillary rarefaction, microthrombi and microvascular remodeling.[15]

Diabetic microangiopathy, which is the most common cause of microangiopathy, is more prevalent in the kidney, retina and vascular endothelium since glucose transport isn’t regulated by insulin and these tissues cannot stop glucose from entering cells when blood sugar levels are high.[16] Among all biochemical mechanisms involved in diabetic vascular damage such as the polyol pathway and the renin–angiotensin system (RAS), the advanced glycation end products (AGEs) pathway appears to be the most important in the pathogenesis and progression of microvascular complications.[17]

Chronic high blood sugar levels lead to the attachment of sugar molecules to various proteins, including collagen, laminin, and peripheral nerve proteins. This process, called glycosylation, creates advanced glycation end products (AGEs). AGEs formation cross-links these proteins, making them resistant to degradation. This leads to accumulation of AGEs, thickening of the basement membrane, narrowing the blood vessels, reducing blood flow to the tissues and causing ischemic injury.[18][19]

In addition, oxidative stress, caused by AGEs and the other pathways, causes apoptosis of pericytes and podocytes in the retina and the kidneys respectively leading to capillary wall fragility and increased vascular leakage. This results in local swelling (e.g. macular edema) and impaired tissue function.[20]

Microvascular diseases as a multisystem disorder

Some researchers have suggested that SVD may be a multisystem disorder, meaning that it can affect multiple organs in the body, including the heart and brain. This is supported by multiple studies stating that cardiac pathologies are more prevalent in patients with pathological evidence of cerebrovascular SVD and vice versa.[15][21]

Coronary microvascular diseases (CMDs) can be caused by:[5]

  • Structural changes, such as vascular remodeling and increased thickness and hypertrophy of arterial walls present in hypertrophic cardiomyopathy.
  • Functional changes, such as endothelial dysfunction caused by oxidative damage as in smoking.
  • Extravascular changes, such as left ventricular hypertrophy and high left ventricular pressure as a result of aortic stenosis (AS).

On the other hand, Cerebral SVD encompasses a range of vascular pathologies including arteriosclerosis-related CSVD, where lipohyalinosis causes stenosis of the lumen of the arterioles and amyloid-related CSVD, characterized by the build-up of β-amyloid deposits in small- and medium-caliber cerebral vessels.[6]

The vascular anatomy of the heart and brain is similar in that conduit arteries are distributed on the surface of these organs with tissue perfusion achieved through deep penetrating arteries. Both coronary and cerebral microvascular diseases do share some common risk factors such as hypertension. Why some patients with microvascular angina subsequently develop vascular cognitive impairment and others do not is an unanswered question. Potential underpinning mechanisms include premature vascular aging and clustering of vascular risk factors leading to an accelerated cardiovascular risk.[21]

Diagnosis

The diagnosis of microangiopathies can be based on direct visualization of the microcirculation, imaging modalities (e.g. MRI), conventional testings (e.g. ophthalmoscopy for diabetic retinopathy) or other diagnostic measures (e.g. blood smear for schistocytes in thrombotic microangiopathies).[6][8][16]

For assessment of the morphological and functional aspects of microcirculation, nailfold videocapillaroscopy (NVC) can be used, in which videocapillaroscopy is performed at the nailfold, where capillaries are arranged with the longitudinal axis parallel to the skin surface, so that they can be examined along their entire length.[8]

NVC has been largely used not only for investigating peripheral microangiopathy, but also as a sort of “window” to systemic microvascular dysfunction. Although its main application is within the connective tissue diseases such as systemic scleroderma and dermatomyositis, it has been employed in non-rheumatic diseases with microvascular involvement such as diabetes mellitus, essential hypertension and COVID-19 infection.[8]

Nailfold capillaroscopy
Capillaroscopic findings in patients with mild COVID-19
  1. Enlarged loops (Black arrow)
  2. Microhemorrhages (Red arrow)
  3. Microthrombosis (Green arrow)

Optical coherence tomography angiography (OCTA) is another imaging modality that offers high-resolution visualization of the retinal capillary network and can be used to evaluate microcirculation in conditions such as diabetic retinopathy.[22] Many studies have demonstrated that evaluation of the retinal microvascular changes using OCTA or other methods such as fluorescein angiography may reflect the systemic microvascular functions as in patients with coronary microvascular disease, cerebral small vessel diseases or systemic sclerosis (The potential of retinal microvascularopathy as a biomarker for assessing microvascular status of other circulations).[23][24]

Unlike the retinal microcirculation, the coronary microvasculature cannot be directly imaged. Instead, a number of different tests can be used to measure how much blood is flowing through the coronary microvasculature. These tests can be used to assess how well the coronary microvasculature is functioning and to diagnose coronary microvascular disease.[5] They include non-invasive measures such as cardiac MRI and invasive measures such as intracoronary Doppler wire.[25]

Similarly, CSVD is typically recognized on both brain magnetic resonance imaging (MRI) and computed tomography (CT) scans, but MRI has greater sensitivity and specificity. Neuroimaging of CSVD primarily involves visualizing radiological phenotypes of CSVD such as recent subcortical infarcts or cerebral microbleeds (CMBs).[6]

Treatment

Treatment options of microangiopathies can be directed at:

  • Prevention (e.g. maintaining good glycaemic control, screening for retinopathy and neuropathy and testing for albuminuria).[16]
  • Controlling symptoms and preventing further deterioration (e.g. tricyclic antidepressants and gabapentin for diabetic neuropathy).[16]
  • Drug therapy (e.g. antiplatelets (low-dose aspirin) and lipid-lowering therapy (statins) for management of CMDs).[25]
  • Diet and lifestyle modification (e.g. low-protein diet in diabetic nephropathy, smoking cessation, weight loss, improved nutrition, and regular exercise).[16][25][26]
  • Intensive management of coexisting conditions and risk factors (e.g. adequate control of blood pressure, diabetes and related metabolic abnormalities and lipid management).[25][26]
  • Other measures (e.g. photocoagulation in patients with severe proliferative diabetic retinopathy).[16]
  • Young people with extensive CSVD and few or no conventional vascular risk factors may benefit from genetic testing to identify any underlying genetic disorders that may be contributing to their condition (For Fabry disease, there is an enzyme replacement therapy).[26]

A better understanding of the mechanisms leading to damage of small blood vessels may be associated with novel therapeutic approaches, the safety and efficacy of some of which will need to be further investigated. Examples include calcium dobesilate and aldose reductase inhibitors in diabetic microangiopathies and endothelin receptor antagonists for pulmonary hypertension.[16][21][27][28]

References

  1. ↑ "microangiopathy" at Dorland's Medical Dictionary
  2. ↑ Kumar, Vinay; Abbas, Abul K.; Aster, Jon C.; Perkins, James A.; Robbins, Stanley L.; Cotran, Ramzi S. (2015). Robbins and Cotran pathologic basis of disease (Ninth ed.). Philadelphia, Pa: Elsevier; Saunders. ISBN 978-1-4557-2613-4. 
  3. ↑ 3.0 3.1 Hakim, Antoine M. (24 September 2019). "Small Vessel Disease". Frontiers in Neurology 10: 1020. doi:10.3389/fneur.2019.01020. ISSN 1664-2295. PMID 31616367. 
  4. ↑ Sugimoto, Kazuhiro; Murakami, Hiroshi; Deguchi, Takahisa; Arimura, Aiko; Daimon, Makoto; Suzuki, Susumu; Shimbo, Takuro; Yagihashi, Soroku (2019). "Cutaneous microangiopathy in patients with type 2 diabetes: Impaired vascular endothelial growth factor expression and its correlation with neuropathy, retinopathy and nephropathy". Journal of Diabetes Investigation 10 (5): 1318–1331. doi:10.1111/jdi.13020. ISSN 2040-1116. PMID 30719863. 
  5. ↑ 5.0 5.1 5.2 Camici, Paolo G.; Crea, Filippo (22 February 2007). "Coronary microvascular dysfunction". The New England Journal of Medicine 356 (8): 830–840. doi:10.1056/NEJMra061889. ISSN 1533-4406. PMID 17314342. https://pubmed.ncbi.nlm.nih.gov/17314342/. 
  6. ↑ 6.0 6.1 6.2 6.3 Litak, Jakub; Mazurek, Marek; Kulesza, Bartłomiej; Szmygin, Paweł; Litak, Joanna; Kamieniak, Piotr; Grochowski, Cezary (20 December 2020). "Cerebral Small Vessel Disease". International Journal of Molecular Sciences 21 (24): 9729. doi:10.3390/ijms21249729. ISSN 1422-0067. PMID 33419271. 
  7. ↑ Pereira Fontes, Carla; Fonseca, Samuel (2021). "Pseudothrombotic Microangiopathy as a Rare Presentation of Cobalamin Deficiency". Cureus 13 (8): e17184. doi:10.7759/cureus.17184. ISSN 2168-8184. PMID 34540418. 
  8. ↑ 8.0 8.1 8.2 8.3 Gualtierotti, Roberta; Fox, Sharon E.; Da Silva Lameira, Fernanda; Giachi, Andrea; Valenti, Luca; Borghi, Maria Orietta; Meroni, Pier Luigi; Cugno, Massimo et al. (28 May 2023). "Nailfold Videocapillaroscopic Alterations as Markers of Microangiopathy in COVID-19 Patients". Journal of Clinical Medicine 12 (11): 3727. doi:10.3390/jcm12113727. ISSN 2077-0383. PMID 37297922. 
  9. ↑ Prommer, Hans-Ulrich; Maurer, Johannes; von Websky, Karoline; Freise, Christian; Sommer, Kerstin; Nasser, Hamoud; Samapati, Rudi; Reglin, Bettina et al. (28 March 2018). "Chronic kidney disease induces a systemic microangiopathy, tissue hypoxia and dysfunctional angiogenesis". Scientific Reports 8 (1): 5317. doi:10.1038/s41598-018-23663-1. ISSN 2045-2322. PMID 29593228. Bibcode: 2018NatSR...8.5317P. 
  10. ↑ Franzeck, U. K.; Haselbach, P.; Speiser, D.; Bollinger, A. (1993). "Microangiopathy of cutaneous blood and lymphatic capillaries in chronic venous insufficiency (CVI).". The Yale Journal of Biology and Medicine 66 (1): 37–46. ISSN 0044-0086. PMID 8256463. 
  11. ↑ Lambova, Sevdalina Nikolova (10 February 2023). "Microangiopathy in Rheumatic Diseases". Life 13 (2): 491. doi:10.3390/life13020491. ISSN 2075-1729. PMID 36836847. 
  12. ↑ Martinelli, Anthony W.; Dunn, William; McClure, Mark E.; Walker, Ieuan; Stewart, Andrew; Karia, Sumit; Preston, Stephen D.; Thiru, Sathia et al. (November 2022). "A Case of Thrombotic Microangiopathy and Acute Sarcoidosis". Chest 162 (5): e245–e248. doi:10.1016/j.chest.2022.06.023. ISSN 0012-3692. PMID 36344132. 
  13. ↑ Koike, Haruki; Katsuno, Masahisa (5 February 2019). "Ultrastructure in Transthyretin Amyloidosis: From Pathophysiology to Therapeutic Insights". Biomedicines 7 (1): 11. doi:10.3390/biomedicines7010011. ISSN 2227-9059. PMID 30764529. 
  14. ↑ Cesarone, M. R.; Belcaro, G.; Geroulakos, G.; Griffin, M.; Ricci, A.; Brandolini, R.; Pellegrini, L.; Dugall, M. et al. (April 2003). "Flight microangiopathy on long-haul flights: prevention of edema and microcirculation alterations with Venoruton". Clinical and Applied Thrombosis/Hemostasis 9 (2): 109–114. doi:10.1177/107602960300900203. ISSN 1076-0296. PMID 12812378. 
  15. ↑ 15.0 15.1 Feuer, Daniel S.; Handberg, Eileen M.; Mehrad, Borna; Wei, Janet; Merz, C. Noel Bairey; Pepine, Carl J.; Keeley, Ellen C. (2022). "Microvascular dysfunction as a systemic disease: A review of the evidence". The American Journal of Medicine 135 (9): 1059–1068. doi:10.1016/j.amjmed.2022.04.006. ISSN 0002-9343. PMID 35472396. PMC 9427712. https://www.amjmed.com/article/S0002-9343(22)00341-2/fulltext. 
  16. ↑ 16.0 16.1 16.2 16.3 16.4 16.5 16.6 Khalil, H. (November 2017). "Diabetes microvascular complications-A clinical update". Diabetes & Metabolic Syndrome 11 (Suppl 1): S133–S139. doi:10.1016/j.dsx.2016.12.022. ISSN 1878-0334. PMID 27993541. https://www.sciencedirect.com/science/article/abs/pii/S1871402116302648. 
  17. ↑ Mengstie, Misganaw Asmamaw; Chekol Abebe, Endeshaw; Behaile Teklemariam, Awgichew; Tilahun Mulu, Anemut; Agidew, Melaku Mekonnen; Teshome Azezew, Muluken; Zewde, Edgeit Abebe; Agegnehu Teshome, Assefa (15 September 2022). "Endogenous advanced glycation end products in the pathogenesis of chronic diabetic complications". Frontiers in Molecular Biosciences 9: 1002710. doi:10.3389/fmolb.2022.1002710. ISSN 2296-889X. PMID 36188225. 
  18. ↑ Cecil, Russell La Fayette; Goldman, Lee; Schafer, Andrew I. (2012). Goldman's Cecil medicine (24th ed.). Philadelphia: Elsevier/Saunders. ISBN 978-1-4377-1604-7. 
  19. ↑ Somboonwong, Juraiporn; Yusuksawad, Mariem; Keelawat, Somboon; Thongruay, Sirima; Poumsuk, Ubon (2016). "Minimization of the Risk of Diabetic Microangiopathy in Rats by Nigella sativa". Pharmacognosy Magazine 12 (Suppl 2): S175–S180. doi:10.4103/0973-1296.182169. ISSN 0973-1296. PMID 27279704. 
  20. ↑ Madonna, Rosalinda; Balistreri, Carmela Rita; Geng, Yong-Jian; De Caterina, Raffaele (March 2017). "Diabetic microangiopathy: Pathogenetic insights and novel therapeutic approaches". Vascular Pharmacology 90: 1–7. doi:10.1016/j.vph.2017.01.004. ISSN 1879-3649. PMID 28137665. https://core.ac.uk/reader/98114493?utm_source=linkout. 
  21. ↑ 21.0 21.1 21.2 Berry, Colin; Sidik, Novalia; Pereira, Anthony C.; Ford, Thomas J.; Touyz, Rhian M.; Kaski, Juan-Carlos; Hainsworth, Atticus H. (2 February 2019). "Small-Vessel Disease in the Heart and Brain: Current Knowledge, Unmet Therapeutic Need, and Future Directions". Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 8 (3): e011104. doi:10.1161/JAHA.118.011104. ISSN 2047-9980. PMID 30712442. 
  22. ↑ Le, Patrick H.; Patel, Bhupendra C. (2023). "Optical Coherence Tomography Angiography". StatPearls (StatPearls Publishing). PMID 33085382. https://www.ncbi.nlm.nih.gov/books/NBK563235/. Retrieved 29 September 2023. 
  23. ↑ Sideri, Anna-Maria; Kanakis, Menelaos; Katsimpris, Andreas; Karamaounas, Aristotelis; Brouzas, Dimitrios; Petrou, Petros; Papakonstaninou, Evangelia; Droutsas, Konstantinos et al. (5 May 2023). "Correlation Between Coronary and Retinal Microangiopathy in Patients With STEMI". Translational Vision Science & Technology 12 (5): 8. doi:10.1167/tvst.12.5.8. ISSN 2164-2591. PMID 37145590. 
  24. ↑ Tang, Qian; Zhang, Yanli; Yang, Zhengfang; Li, Siou; Wu, Meini; Guo, Yongming; Zhao, Weina; Yin, Changhao (9 June 2022). "Study on the Interaction between the Characteristics of Retinal Microangiopathy and Risk Factors for Cerebral Small Vessel Disease". Contrast Media & Molecular Imaging 2022: 9505945. doi:10.1155/2022/9505945. ISSN 1555-4309. PMID 35800241. 
  25. ↑ 25.0 25.1 25.2 25.3 Taqueti, Viviany R.; Di Carli, Marcelo F. (27 November 2018). "Coronary Microvascular Disease Pathogenic Mechanisms and Therapeutic Options: JACC State-of-the-Art Review". Journal of the American College of Cardiology 72 (21): 2625–2641. doi:10.1016/j.jacc.2018.09.042. ISSN 0735-1097. PMID 30466521. 
  26. ↑ 26.0 26.1 26.2 Chojdak-Łukasiewicz, Justyna; Dziadkowiak, Edyta; Zimny, Anna; Paradowski, Bogusław (March 2021). "Cerebral small vessel disease: A review". Advances in Clinical and Experimental Medicine 30 (3): 349–356. doi:10.17219/acem/131216. ISSN 1899-5276. PMID 33768739. 
  27. ↑ Zhang, XinYuan; Liu, Wei; Wu, ShanShan; Jin, JingLong; Li, WeiHong; Wang, NingLi (2014-12-20). "Calcium dobesilate for diabetic retinopathy: a systematic review and meta-analysis" (in en). Science China Life Sciences 58 (1): 101–107. doi:10.1007/s11427-014-4792-1. ISSN 1674-7305. PMID 25528255. 
  28. ↑ Haller, Hermann; Ji, Linong; Stahl, Klaus; Bertram, Anna; Menne, Jan (2017). "Molecular Mechanisms and Treatment Strategies in Diabetic Nephropathy: New Avenues for Calcium Dobesilate—Free Radical Scavenger and Growth Factor Inhibition" (in en). BioMed Research International 2017: 1909258. doi:10.1155/2017/1909258. ISSN 2314-6133. PMID 29082239. 

External links

Classification



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