An Overview on Microvascular Dysfunction in the Coronary Arteries

Christine Pacheco^*
*Correspondence: Christine Pacheco, Cardiovascular Division, University of Florida, Gainesville, Florida, USA, Email:

Commentary

Patients with Coronary Microvascular Dysfunction (CMVD) are prevalent, and despite the favourable prognosis, many of them suffer from angina symptoms that limit their everyday activities. This page summarises the most prevalent clinical presentation pictures, such as stable and unstable microvascular angina. The most important risk factors are covered, followed by the most up-to-date knowledge on the subject, such as pathogenic hypotheses, diagnostics, and treatment possibilities [1]. Microvascular anomalies that aren't completely understood, such as slow flow and no reflow, as well as prognosis and the disease's impact on quality of life, are investigated. Angina without coronary artery disease (CAD) is associated with severe morbidity and can be identified in 10% to 30% of those who have an angiography.

Coronary Microvascular Dysfunction (CMD) is present in 50 to 65 percent of these patients. This group's optimum treatment is uncertain. We conducted a systematic review to investigate treatment options for reliably diagnosed CMD in the absence of CAD. In human subjects with angina and a coronary flow reserve or myocardial perfusion reserve of 2.5 in the absence of coronary artery stenosis of 50% or structural heart disease, we included studies using positron emission tomography, cardiac magnetic resonance imaging, dilution methods, or intracoronary Doppler. Only eight papers met the strict criteria for inclusion. In the studies, different treatments, results, and definitions of CMD were employed [2]. The tiny sample sizes of this research severely limit the power of the findings. Studies looking at the effects of sildenafil, quinapril, oestrogen, and transcutaneous electrical nerve stimulation all yielded encouraging results.

There was no benefit from L-arginine, doxazosin, pravastatin, or diltiazem. There is minimal evidence to recommend CMD therapy, according to our systematic review. We assess previously published data that is related but not included and evaluate material that meets severe inclusion conditions. We also discuss the next steps in narrowing this research gap, which include a standardised definition of CMD, routine CMD assessment in studies of chest pain without obstructive CAD, and specialised therapeutic assessment in the case of obstructive CAD. We don't know enough about the importance, mechanisms, and effects of coronary microvascular dysfunction in diabetes mellitus right now. Diabetes-induced endothelial dysfunction in multiple artery beds is well established for contributing to a wide range of issues and impairing microcirculatory regulation [3,4]. A number of interconnected physiological mechanisms regulate coronary microcirculation, with the goal of adapting local blood flow to myocardial metabolic needs. The deregulation of this network could have a range of pathological consequences.

This conveys the most relevant scientific and clinical findings linked to diabetes-associated coronary microvascular dysfunction. When the left myocardial mass swells due to an increase in cardiomyocyte size, it is known as left ventricular hypertrophy (LVH). LVH is a physiological response to physical activity, as well as a primary (genetic) or secondary (environmental) pathological condition (i.e. caused by LV ovulation). There are signs of coronary microvascular dysfunction in both primary and secondary LVH patients (CMD). Due to medial wall thickening and an increased wall/lumen ratio, the latter is induced by capillary rarefaction and unfavourable remodelling of intramural coronary arterioles.

Coronary Microvascular Dysfunction (CMD) is characterised as an enhanced sensitivity to vasoconstrictor stimuli and a diminished ability for microvascular vasodilation in a significant number of these patients. The coronary microvasculature has been studied more fully in the last two decades thanks to the development of non-invasive and invasive methods. CMD has been identified as a cause of myocardial ischemia in addition to typical atherosclerotic disease and vasospastic sickness. CMD can occur alone or in combination with obstructive CAD. Many risk factors are shared by CMD and macrovascular CAD. The disorder is diagnosed by the reduction of coronary blood flow in response to vasodilatory medications [5]. Imaging technologies such as cardiovascular magnetic resonance, positron emission tomography, and transthoracic Doppler echocardiography have not yet completely replaced traditional intracoronary vaso-reactivity testing.

The management of risk factors and a change in lifestyle are the first steps in CMD treatment. Traditional antianginal and anti-atherosclerotic medications, as well as some innovative therapies, may be beneficial; nevertheless, clinical trials are required to determine the efficacy of pharmacologic and nonpharmacologic treatment options. Longer-term trials are also needed to evaluate the prognostic benefits of these drugs. CMD epidemiology, prognosis, pathogenesis, diagnosis, risk factors, and current therapies are all explored in detail.

References

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2. De Vita, Antonio, Laura Manfredonia, Priscilla Lamendola, and Angelo Villano, et al. "Coronary microvascular dysfunction in patients with acute coronary syndrome and no obstructive coronary artery disease." Clin Res Cardiol 108 (2019): 1364-1370.

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3. Michelsen, Marie M., Adam Pena, Naja D. Mygind, and Jan Bech, et al. "Coronary microvascular dysfunction and myocardial contractile reserve in women with angina and no obstructive coronary artery disease." Echocardiography 35 (2018): 196-203.

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4. Safdar, Basmah, Gail D’Onofrio, James Dziura, and Raymond R. Russell, et al. "Prevalence and characteristics of coronary microvascular dysfunction among chest pain patients in the emergency department." Eur Heart J Acute Cardiovasc Care 9 (2020): 5-13.

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5. Ford, Thomas J., Paul Rocchiccioli, Richard Good, and Margaret McEntegart, et al. "Systemic microvascular dysfunction in microvascular and vasospastic angina." Eur Heart J  39, no. 46 (2018): 4086-4097.

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