Editorial for “Clinical Application of Non‐Contrast‐Enhanced Dixon Water‐Fat Separation Compressed SENSE Whole‐Heart Coronary MR Angiography at 3.0 T With and Without Nitroglycerin”

Editorial for “Clinical Application of Non-Contrast-Enhanced Dixon Water-Fat Separation Compressed SENSE Whole-Heart Coronary MR Angiography at 3.0 T With and Without Nitroglycerin” Nitric oxide (NO), a free radical, is synthesized by the family of NO synthases from L-arginine and oxygen; L-citrulline is generated as a coproduct. NO is a powerful vasodilator that induces the formation of cyclic guanosine monophosphate (cGMP) by activating soluble guanylyl cyclase in vascular smooth muscle cells. cGMP can bind to protein kinase G and enhance its activity, promoting the movement of calcium from the intracellular to the extracellular environment and the opening of calcium-activated potassium channels. The reduction in intracellular calcium impairs the phosphorylation of myosin by myosin light chain kinase, relaxing smooth muscle cells and reducing vascular tone. NO also has several other important roles in the cardiovascular system, such as cell permeability, platelet function, and inflammation. In the blood vessel wall, NO is mainly produced by endothelial nitric oxide synthase (eNOS); thus, endothelial dysfunction has been attributed to a reduction in NO bioactivity. Organic nitrates, such as nitroglycerin, isosorbide dinitrate, and isosorbide mononitrate, have been used to demonstrate endothelium-independent vasodilation and as a positive control for endothelium-dependent vasodilation. Nitrates are rapidly absorbed in several sites, including the gastrointestinal tract, mucous membranes, and the skin, causing the release of NO to act on vascular smooth muscle cells and the cardiovascular system. Nitrates have several hemodynamic effects, primarily by reducing left ventricular oxygen requirements through a NO-mediated dilatation of capacitance veins. Nitrates dilate epicardial coronary arteries and arterioles, improving coronary blood flow and increasing blood flow in coronary collaterals by decreasing the resistance to collateral flow. Therefore, nitrates are often used to manage acute coronary syndrome, and nitroglycerin is most frequently used to treat acute angina episodes. An impaired vasodilatory response to nitroglycerin is associated with risk factors for coronary artery disease and increase in future cardiac events. Nitrate is also commonly used to dilate coronary lumens in coronary computed tomography angiography (CCTA), such as invasive X-ray coronary angiography, intravascular ultrasound, and magnetic resonance angiography. In clinical practice, sublingual nitroglycerin is the routine and preferred method of administration during CCTA since it is the most efficacious technique and associated with fewer side effects. Several research groups have investigated the influences of nitroglycerin on CCTA and found that sublingual nitroglycerin increases both the diameter and luminal attenuation of coronary arteries, especially peripheral small coronary arteries. Consequently, the evaluable number of coronary segments is increased on sublingual nitroglycerin CCTA. Although nitrates dilate epicardial coronary arteries entirely, it has a greater effect on nonstenotic segments and a lesser effect on stenotic segments. As a result, nitrates can enhance the detection of obstructive lesions. Vasospastic angina is caused by the abnormal spontaneous or induced constriction of coronary vessels. Invasive coronary angiography with spasm provocation ergonovine testing is the diagnostic standard according to the recent management guidelines. However, several groups have demonstrated the detection of coronary spasm by CCTA and attempted to improve the diagnostic accuracy of CT protocols with nitrate infusion during scanning. Dual-acquisition CCTA spasm protocols, with high specificity for spasm detection, improve the diagnostic accuracy and provide quantitative information on the coronary vessel distensibility of the segments with spasm, which is higher than that of normal reference segments. These observations suggest the hyper-reactivity of the segments with spasm to nitroglycerin is probably due to lack of baseline production or release of NO from the endothelium. However,