What are the strategies to prevent and treat cardiovascular complications in maintenance dialysis patients?

  In uremic patients on maintenance dialysis. The incidence of cardiovascular complications and death rate are high. The quality of life and survival time of dialysis patients are seriously threatened, so it is necessary to actively prevent and treat cardiovascular complications.  I. Risk factors There are many risk factors for cardiovascular complications in uremic patients on maintenance dialysis. These include the same traditional risk factors as in the general population, as well as risk factors specific to patients with chronic kidney disease (CKD) and associated with hemodialysis.  1. Traditional risk factors: hypertension, hyperglycemia, hyperuricemia, dyslipidemia, smoking, old age, male, low activity, stress, postmenopause, family history of coronary artery disease, and existing left ventricular hypertrophy.  2. Risk factors specific to CKD patients: proteinuria, RAS system activation, water and sodium retention, anemia, disorders of calcium and phosphorus metabolism, uremic toxins, hyperhomocysteinemia, oxidative stress, malnutrition, infection and inflammatory response, thrombosis factors, reduced partial pressure of oxygen, metabolic acidosis, etc.  3. Risk factors associated with hemodialysis: arteriovenous endovascular fistula, quality of dialysis fluid and dialysis water, dialyzer biocompatibility, hypotension in dialysis, hypoxemia, rapid changes in extracellular fluid in dialysis, rapid changes in electrolytes and pH, metastatic calcification causing vascular, myocardial and soft tissue calcification, carnitine deficiency, etc.  II. Signs and symptoms Common cardiovascular complications in dialysis patients include intractable hypertension, cardiac insufficiency (systolic and diastolic function), coronary artery disease, acute coronary syndrome (unstable angina, acute myocardial infarction), cerebrovascular lesions (stroke, cerebral artery insufficiency), and peripheral vascular lesions (abdominal aortic atherosclerosis, thoracoabdominal aortic coarctation aneurysm, intermittent claudication). The main causes of death in dialysis patients are acute left heart insufficiency, acute coronary syndrome, and cerebral hemorrhage. Dialysis patients often have no autonomic symptoms in the presence of acute coronary syndrome. It is characterized by silent, painless myocardial ischemia, which is most evident in elderly, diabetic nephropathy dialysis patients.  III. PREVENTION RECOMMENDATIONS The cardiovascular status of each patient should be evaluated before or initially before the patient enters dialysis.  1. First, electrocardiogram and echocardiogram should be performed. Find out whether the patient has cardiac hypertrophy, myocardial ischemia and abnormal cardiac function.  2.Serum high-sensitivity c-a-reactive protein (hs.CRP), troponin T (c-TnT), lipid levels, calcium, phosphorus and iPTH levels were examined to evaluate the risk of cardiovascular events.  3. Carotid ultrasonography was performed to understand the intima-media thickness, stenosis and atheromatous plaque formation of large arteries, thus indirectly evaluating the condition of systemic arteries. Through the above multiple comprehensive examinations, we can evaluate whether the patient has existing cardiovascular lesions and the risk level of concomitant cardiovascular complications, so as to determine the prevention and treatment strategies. For young and middle-aged dialysis patients, the feasibility of kidney transplantation can also be evaluated.  Prevention and control measures (a) Pharmacological treatment 1. Lowering blood pressure: It has been debated at what level blood pressure should be maintained in dialysis patients. It is recommended that the blood pressure level should be controlled according to the individual condition of the patient, such as age factor, cardiovascular and cerebrovascular pathology and systemic condition, <135/85 mmHg during the day and <120/80 mmHg at night. methods: strict control of dry weight to reduce the volume load; reduce the level of weight gain between two dialysis sessions; low salt diet, low sodium dialysis or application of adjustable sodium dialysis (sodium concentration from 150 to 135 mmol/L), or increasing the duration or frequency of dialysis, such as slow dialysis for 6-8 h each time, or 2-3 h daily, or switching to peritoneal dialysis (CAPD). In Europe, it has been reported that patients rarely develop hypertension when dialysis is applied by the above methods. In addition, for recalcitrant hypertension, HDF, HF or high-flux dialyzers can be applied to remove vasoconstrictive substances from the body. The antihypertensive drugs can be CCB, ACEI, ARB, 13 receptor blocker, instrument and p receptor combination blocker.  2, correct renal anemia: reasonable application of oral or intravenous iron, folic acid and B vitamins and erythropoietin to correct anemia, so as to improve the ischemic and hypoxic conditions of various organs, relieve ventricular wall hypertrophy and reduce the onset of angina pectoris. The hemoglobin level should be maintained at 110-120 g/L and the erythrocyte volume should be maintained at 0.33-0.36. 3. Improve homocysteinemia: Dialysis patients have a reduced ability to excrete homocysteine, and the amount of vitamins required for cysteine metabolism in the body is reduced, resulting in an increase in serum homocysteine levels. High homocysteine can damage vascular endothelial cells and promote atherosclerosis and thrombosis. However, these views are still controversial, and it has been observed that dialysis patients with low or normal serum homocysteine concentrations also have a high mortality rate. The current K/DOQI guidelines recommend a treatment regimen of folic acid 15 mg/d, vitamin B6 100 mg/d, and vitamin B12 1 mg/d. 4. Adjustment of lipid metabolism abnormalities: See Table 1 for definitions. lipid metabolism disorders in dialysis patients are characterized by normal LDL cholesterol, low HDL cholesterol, and elevated triglyceride (TG) levels. TG levels were reduced by lifestyle improvement, application of fibrates and/or niacin. When TG > 5, 65 mmol/L, acute pancreatitis is highly likely to occur. For high Tc and high LDL-C, statin lipid-regulating drugs need to be applied. Statin lipid regulators not only have lipid-lowering effects, but also organ-protective effects. It achieves renal and cardiac protection through anti-inflammatory, immunomodulatory, anti-proliferative, and inhibiting extracellular matrix deposition effects. Statins not only protect blood vessels and promote atheromatous plaque stability, but also up-regulate nitric oxide synthase activity and improve vascular endothelial diastolic function, in addition to reducing the inflammatory response and lowering CRP levels.  6, antioxidant therapy: the presence of excessive free radical products in the body of uremic patients, cytokine production increased. Decreased clearance of pro-inflammatory factors, increased volume load, endotoxemia, and low levels of antioxidant substances can aggravate oxidative stress, which leads to impaired endothelial cell function, inflammation and atherosclerosis. Most current clinical studies have used vitamin E, vitamin C, and B carotene supplementation alone or in combination to reduce oxidative stress and prevent coronary heart disease, but have not yielded positive beneficial results and thus are not recommended for use in the general population. However, supplementation with vitamin E or the application of dialyzers made of membranes containing vitamin E can be beneficial in uremic dialysis patients. It should be emphasized that supplementation with high doses of vitamin E (>400 IU/d) has the potential to increase mortality from a variety of diseases.  7. Anti-inflammatory therapy: Inflammation related to vascular access, biocompatibility of dialyzer, impurity or contamination of dialysis water and dialysis fluid, and various toxins of uremia can aggravate oxidative stress, leading to complement activation and cytokine production, increased production of endothelial cell adhesion factors, pro-inflammatory factors, and ultimately increased CRP levels, promoting atherogenesis and formation of atherosclerosis. increased CRP levels predict Patients are at high risk for acute myocardial infarction, ischemic stroke, and peripheral vascular disease in the short or long term. It is a strong predictor of death from cardiovascular lesions. In addition, an increase in IL.6 is often accompanied by an increase in death in dialysis patients. Therefore, aggressive anti-inflammatory therapy can reduce CRP levels, achieve protection of endothelial cell function, improve oxidative stress, reduce the occurrence of cardiovascular events, and decrease morbidity and mortality. A significantly increased risk of cardiovascular events has been reported after acute infections. The risk of myocardial infarction (MI) and ischemic stroke increased by 4.95 and 3.19 times, respectively, within 3 d after respiratory tract infection. The increased risk after urinary tract infection was 1.66-fold and 2.72-fold, respectively. Clinical studies reported so far have initially demonstrated that statins, ACEI, VitE, certain anti-platelet aggregation drugs and the application of biocompatible dialysis membranes and ultra-pure dialysis fluid can improve the inflammatory state and reduce CRP levels.  8, correction of calcium and phosphorus metabolism disorders: dialysis patients due to inappropriate application of active vitamin D, excessive consumption of calcium and phosphorus-containing binding agents, or the application of high-calcium dialysis fluid, high phosphorus diet, resulting in hypercalcemia or hyperphosphatemia, so that the calcium and phosphorus product in the blood > 65 mg. 2 / dl: when, very easy to occur metastatic calcification. For example, calcification occurs in internal organs, around joints, eyes, skin, arteries and heart muscle. Calcium salt deposition in the inner and middle layers of blood vessels and atheromatous plaque fast can further aggravate coronary artery lesions and aggravate vascular sclerosis. Therefore, we need to actively control both hyperphosphatemia. We should also pay attention to the prevention of hypercalcemia, and control the calcium and phosphorus product below 55 m92/dlz as recommended by K/DOQI guidelines.  9, NO: In dialysis patients, ADMA (asymmetric dimethylarginine) is increased, which is an endogenous NO synthesis inhibitor, and NO synthesis is reduced. It makes vasoconstriction and hypertension occur in dialysis patients. Increased blood levels of ADMA predict poor prognosis and death from coronary artery disease. Nitric oxide inhalation, which is currently used clinically, has the effect of dilating vascular smooth muscle, lowering blood pressure, increasing blood flow, lowering cholesterol, and preventing thrombosis and cardiovascular injury. Inhalation of low dose of NO can dilate bronchial smooth muscle and reduce pulmonary hypertension, which is a new therapy for the treatment of severe ARDS.  10, acute coronary syndrome (ACS) drug treatment: when there are dynamic changes in ECG sT-T (with or without Q waves), myocardial enzyme profile, CK.mb, cTnT significantly increased, with or without anterior heart pain. The diagnosis of ACS should be considered. In this case, electrocardiographic monitoring, bed rest, reduced activity, oxygenation, B-blockers to reduce myocardial oxygen consumption, nitrates for coronary expansion, heparin anticoagulation, anti-platelet aggregation, ACEI or ARB to improve myocardial remodeling should be applied. Anti-platelet aggregation drugs also have the effect of reducing IL.6, CRP, macrophage colony-stimulating factor levels and inhibiting the inflammatory response. When the condition allows, UCG, nuclear myocardial scan and coronary angiography are feasible to clarify whether interventional treatment can be performed.  (B) Interventional treatment Coronary angioplasty includes coronary artery bypass surgery (CABG) and percutaneous transluminal coronary balloon dilation (PTCA) and stenting (STANT), the latter 2 also known as coronary intervention (PCI). To date, there are no clear indications and contraindications for CABG and PCI alone in patients with chronic renal failure, and all indications and contraindications apply to the general population. The same applies to patients with chronic renal failure.  The ideal indications for PCI are: (1) poor drug therapy, frequent angina pectoris or recurrent myocardial infarction with surviving myocardium at the lesion site; (2) high expected mortality and incidence of myocardial infarction without PCI; (3) single or multiple vessel lesions with limited stenosis, located in large vessels or large branches, and insignificant vascular calcification; (4) low expected risk of adverse events . The presence of significant active bleeding prior to anticoagulation therapy is an absolute contraindication to PCI. Relative contraindications include bleeding tendency, anatomically unsuitable coronary lesions or lesions at high risk (e.g., chronic total occlusive vasculopathy, diffuse distal vasculopathy, left main stem stenosis), recurrent restenosis of multiple vessels, diffuse stenotic vasculopathy, end-stage lesions with heavy vascular calcification, or poorly anticipated survival. Coronary lesions that are not suitable for stent placement. PTCA is now widely used in clinical practice because of its minimal invasiveness and rapid postoperative recovery. Coronary artery bypass grafting requires open-heart surgery, which is highly damaging to the organism, and should be considered carefully because of the poor coagulation function of uremic patients. Japanese scholars suggest that PTCA and stenting should be preferred for coronary artery flow reconstruction in uremic dialysis patients. According to the postoperative follow-up of 10 uremic dialysis patients who underwent PTCA with stent placement, no one died during the perioperative period. In one case, four stents were placed and the patient has survived for 5 years. We believe that proper selection of contrast agent, appropriate dosage (no more than 200 m1 per dose), attention to hydration before and after PCI, and enhanced hemodialysis are better ways to prevent the aggravation of renal damage by contrast agent. Coronary intervention in uremic dialysis patients is feasible and safe, which helps to improve the quality of survival and reduce the occurrence of cardiovascular events in uremic patients. Prevention and reduction of cardiogenic death rate.       In conclusion, for uremic patients on maintenance dialysis active? effective blood pressure control, blood glucose control, smoking cessation, maintenance of appropriate dry weight, lifestyle changes, application of B-blockers, ACEI or ARB, statin lipid regulators, aspirin and other drugs, correction of calcium and phosphorus metabolism disorders, improvement of nutrition and inflammation status, thus preventing cardiovascular complications, reducing cardiovascular events and improving the quality of survival of dialysis patients.