Benita Tjoe, MD, Lili Barsky, MD, Janet Wei, MD, Bruce Samuels, MD, Babak Azarbal, MD, C. Noel Bairey Merz, MD and Chrisandra Shufelt, MD, MS
Lay Summary – Diagnosis and Treatment in Coronary Microvascular Dysfunction
Both CMVD and CAS may caused prolonged myocardial ischaemia leading to myocardial infarction. So, both mechanisms may be associated with permanent cardiac damage through multiple episodes or prolonged episodes
Myocardial ischaemia has been traditionally perceived as the consequence of atherosclerotic obstructions of the coronary vessels. More recently an overwhelming body of evidence has proven that atherosclerotic obstructions are just one of several mechanisms that can precipitate myocardial ischaemia. CAS, CMVD and Endothelial Dysfunction are included among the mechanisms that, in isolated fashion or in combination, may cause myocardial ischaemia
The wall of the blood vessel (coronary artery) supplying the heart muscle has got three layers: the innermost layer contains endothelial cells, the middle layer contains the smooth muscle cells and the outermost layer contains collagen fibres for support.
The endothelial cells naturally release a substance called nitric oxide (NO), that then diffuses along into the neighbouring smooth muscle cells and causes these cells to relax. This leads to the coronary artery dilating, which results in an increased blood flow to the heart muscle. This is an important physiological response to exertion.
Endothelium-dependent CMD essentially means an inability of the endothelial cells to produce nitric oxide. As a result, the smooth muscle cells are unable to relax and the coronary artery is unable to dilate as required. This results in blunted increase in blood flow to the heart muscle during times of stress, which results in angina.
Endothelium-independent (or non-endothelium dependent) CMD refers to an inability of the smooth muscle cells to relax despite an adequate amount of nitric oxide. This, again, results in blunted increase in blood flow to the heart muscle during times of stress, which results in angina.
Therefore, both group of patients have an inability to dilate their coronary arteries in response to stress, which reduces the blood flow to the heart muscle during times of stress, leading to angina
Michael T Corban, Lilach O Lerman, Amir Lerman
Lay Summary – Discusses if Endothelial Dysfunction could be in other parts of the body.
http://academic.oup.com/eurheartj/article/39/46/4098/5079860
Angela H.E.M Maas, Dejan Milasinovic, Colin Berry, Javier Escaned
Lay Summary – As stated in the title of the publication
http://www.emjreviews.com/interventional-cardiology/article/microvascular-angina-diagnosis-assessment-and-treatment
Haseeb Rahman, David Corcoran, Muhammad Aetesam-ur-Rahman, Stephen P Hoole, Colin Berry, Divaka Perera.
Lay Summary – Defining the specific type of CMVD in patients can improve management
https://heart.bmj.com/content/105/20/1536
Peter Ong, Paolo G. Camici, John F Beltrame, Filippo Crea, Hiroaki Shimokawa, Udo Sechtem, Juan-Carlos Kaski, C. Noel Bairey Merz
Lay Summary – Defines standard criteria to investigate & diagnose microvascular angina
https://www.researchgate.net/publication/319612722_International_standardization_of_diagnostic_criteria_for_microvascular_angina
Professor Thomas F Lüscher
Lay Summary – What the term Acute Coronary Syndrome should now include.
https://academic.oup.com/eurheartj/article/40/15/1169/5450090
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