Erectile dysfunction in cardiac patients

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Erectile dysfunction (ED) is often caused by endothelial dysfunction (END) and may indicate that the patient has other vascular diseases. Erectile dysfunction in cardiac patients – Risk factors for coronary heart disease, such as lipid metabolism disorders, smoking, diabetes, and hypertension, are also risk factors for ED. Oral ED medications, such as sildenafil, inhibit phosphodiesterase 5 (PDE-5) and the breakdown of cyclic guanosine monophosphate. PDE-5 inhibitors are effective and safe in the treatment of ED, but their use is contraindicated when taking nitrates. These drugs are weak vasodilators, and the possibility of their use in patients with pulmonary hypertension, heart failure and endocrine disorders is currently being studied.

Erectile dysfunction in cardiac patients: Endothelial dysfunction

The early stages of atherosclerosis include END, a condition in which the inner layer of blood vessels loses its function. This includes the loss of normal endothelium-dependent vasodilation. When an acetylcholine-endothelium-dependent vasodilator is injected into normal blood vessels, the endothelium releases nitric oxide (NO), which diffuses into the smooth muscle cells of the vessels, which leads to their relaxation. The blood vessels dilate and the blood flow increases. Similar phenomena occur when the brachial artery is occluded for several minutes (usually with the use of a cuff to measure blood pressure), followed by deflation of the cuff. During the Doppler ultrasound examination, vasodilation is noted with an increase in the diameter of the brachial artery and the speed of blood flow.

erectile dysfunction in cardiac patients

Such a normal response is a consequence of insufficient blood flow, leading to ischemia. However, in END, the vascular response to acetylcholine or temporary compression of the brachial artery with subsequent restoration of blood flow is abnormal. Normal coronary arteries dilate in response to the administration of acetylcholine, which can be detected by angiography. The arteries affected by atherosclerosis do not expand in response to the administration of acetylcholine, or there is a paradoxical narrowing. In patients with vascular diseases caused by atherosclerosis itself or its risk factors, there is a decrease in the severity of vasodilation of the brachial artery after its temporary compression with subsequent reperfusion.

Damage to the endothelium can be the result of a large number of different adverse effects. These include the following common risk factors for atherosclerosis: lipid metabolism disorders (increased total cholesterol, increased low-density lipoprotein (LDL) cholesterol, decreased high-density lipoprotein cholesterol), smoking, diabetes, and hypertension. In addition, inflammatory mediators, infectious agents, and other factors may also be important. These effects can cause damage to the endothelium, leading to impaired NO synthesis/release, increased endothelial permeability to lipids, and increased endothelial thickness, which causes the adhesion of neutrophils and monocytes to its surface. Such endothelial dysfunction occurs before the formation of visible signs of atherosclerosis.

To be continued…

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