Diabetes heart disease

Introduction to Diabetes Heart Disease Diabetic heart disease is one of the leading causes of death in diabetic patients, especially in patients with type 2 diabetes. Generalized diabetes heart disease includes coronary atherosclerotic heart disease (CHD), diabetic cardiomyopathy and diabetic autonomic neuropathy. Diabetic heart disease is often associated with non-diabetic patients. Diabetes patients have a crown Heart disease often manifests as painless myocardial infarction, with large infarct size, more infarcts, more serious conditions, poor prognosis, and higher mortality; such as coronary angiography and clinical exclusion of coronary artery disease, diabetic patients are severe Arrhythmia, cardiac hypertrophy, pulmonary congestion and congestive heart failure, especially refractory heart failure, clinical considerations for diabetic cardiomyopathy. basic knowledge Sickness ratio: 0.5% Susceptible people: no specific population Mode of infection: non-infectious Complications: cardiogenic shock congestive heart failure arrhythmia pneumonia acute myocardial infarction angina pectoris

Diabetes heart disease

Causes

Accelerated atherosclerotic heart disease and cardiomyopathy in diabetic patients, in addition to hyperglycemia, mainly accompanied by abnormal lipid metabolism, increased incidence of hypertension, hemorheological abnormalities and insulin resistance or hyperinsulinemia And so on.

1. Abnormal lipid metabolism:

(1) Cholesterol (Ch): Elevated cholesterol is an important risk factor for atherosclerosis and has been confirmed by numerous epidemiological investigations and clinical studies. Most clinical studies report that compared with non-diabetic patients, there is no significant change in blood cholesterol in diabetic patients, but diabetes, such as diabetic nephropathy, often presents with hypercholesterolemia. Multi-hazard intervention studies have shown that at any given cholesterol level, the risk of cardiovascular death in diabetics is significantly higher than in non-diabetic patients. Interventions also show that lowering blood cholesterol levels can significantly reduce cardiovascular disease and cardiac events in diabetics. happened.

(2) Triglyceride (TG): Hypertriglyceridemia is the most common disorder of lipid metabolism in diabetic patients, especially in patients with early onset and poor glycemic control, and there are more relationships between TG levels and arteriosclerosis. Most studies believe that high triglycerides are definitely associated with the occurrence of arteriosclerosis. The consensus is that if TG is elevated with high-density lipoprotein-cholesterol (HDL-C) decline is definitely a risk factor for cardiovascular disease, in patients with diabetes, simple serum hypertriglyceridemia also indicates an increased risk of cardiovascular disease. Increased TG in diabetic patients can increase the proportion of small low-density lipoprotein (IDL) molecules and promote the occurrence of arteriosclerosis.

(3) Very low-density lipoprotein (VLDL): Diabetic patients often show an increase in VLDL. VLDL is mainly synthesized in the liver, and a small amount is synthesized in the intestinal mucosa. The components contained in it are mainly endogenous TG. The TG in plasma is mainly derived from VLDL. Therefore, the rate of VLDL production and clearance is the main factor determining the concentration of TG in blood. In diabetes, due to the absolute or relative deficiency of insulin, the rate of synthesis of VLDL in the liver is significantly greater than the rate of clearance and decomposition. At the same time, due to the decreased activity of lipoprotein esterase, the decomposition of triglyceride is slow, and the TG-rich VLDL and chylomicrons are decomposed. Metabolic obstruction causes an increase in the concentration of VLDL in the blood.

(4) Low-density lipoprotein cholesterol (LDL-C): Patients with diabetes often have elevated LDL-C, especially non-enzymatic glycation and oxidatively modified LDL-C levels, which significantly increase their toxic effects on vascular endothelial cells and smooth muscle. The degradation product of LDL-based VLDL mainly contains endogenous cholesterol. About 50% of cholesterol is esterified in plasma by cholesterol transacylase. Most of the esterified cholesterol is stored in LDL particles. LDL is extrahepatic tissue. Cell uptake, which is the main source of cell membrane cholesterol. There is an ApoB receptor that recognizes LDL on the extracellular membrane. LDL specifically binds to the receptor and then metabolizes into the cell and catabolizes in the cell, becoming the main source of cholesterol in the whole body tissue. This is also the main route of LDL catabolism. In persistent hyperglycemia, oxidation and saccharification of LDL can impair the recognition of hepatocyte LDL receptors or reduce its affinity for tissue cell receptors, leading to reduced clearance of LDL and preferential recognition by macrophage LDL receptors. Ingestion and degradation, which causes cholesterol esters to accumulate in macrophages to transform into foam cells and promote atherosclerosis. In addition, saccharification of LDL can lead to LDL being easily oxidized. In contrast, saccharification of HDL increases its rate of clearance and shortens its half-life.

(5) High-density lipoprotein cholesterol (HDL-C): A decrease in HDL-C is common in diabetic patients. HDL-C has been shown to have anti-atherosclerotic effects and its anti-atherosclerosis effect has been mainly associated with the HDL-2 subtype, while HDL-3 has little change. The reduction in HDL in diabetic patients is also mainly associated with a decrease in HDL-2 subtype. HDL mainly contains protein, accounting for about 45%, followed by cholesterol and phospholipids, each accounting for about 25%. HDL in plasma can bind to the cell membrane of extrahepatic tissue, and simultaneously take up cholesterol, and then under the action of cholesterol transacylase and Apo AI, promote the conversion of cholesterol from free state to cholesterol ester, and the new HDL disc can be converted into HDL. -3, then with the participation of VLDL, the surface component of VLDL and cholesterol are transferred to HDL-3 by lipoesterase, which may cause a decrease in HDL in patients with HDL-2 diabetes. The insulin may be insufficient or insulin may be impaired. The decrease of lipoprotein esterase activity reduces the synthesis of HDL-2 and the increase of hepatic esterase activity accelerates the decomposition of HDL-2, and the saccharification modification of HDL increases the clearance rate. Because diabetic patients often have high TGemia, the TG content in HDL particles is increased, and TG partially replaces the esterification site of cholesterol in HDL particles, thus further reducing the ability of HDL particles to transport cholesterol from surrounding tissues, so that surrounding tissue cells such as arteries Cholesterol accumulation in the wall promotes the occurrence of atherosclerosis (the key to reverse cholesterol transport is that intracellular free cholesterol must be esterified after being taken up by HDL particles to be exchanged with particles such as VLDL).

(6) Lipoprotein [LP()]: LP () is a large molecular glycoprotein composed of lipid carbohydrates, ApoA and ApoB, which is metabolized by a TG-rich microparticle synthesized by the liver. Both ApoA and ApoB100 are composed of disulfide bonds.

even. The concentrations of Apo () and LP () are both controlled by genetics. The physiological function of LP() is not well understood, but it is closely related to the occurrence of arteriosclerosis. The results of LP() in diabetic patients are still inconsistent. It is generally believed that LP() may be elevated in patients with type 1 diabetes and type 2 diabetes, especially in patients with diabetic nephropathy; in patients with type 2 diabetes with cardiovascular disease, LP () levels are elevated; LP () levels are generally independent of metabolic control in diabetic patients.

A more consistent view is that diabetes with hypercholesterolemia and elevated LDL is a positive risk factor for cardiovascular disease, but in patients with diabetes, especially in type 2 diabetes, elevated serum TG and HDL-C are more common. Increased serum TG with decreased HDL-C is also a positive risk factor for cardiovascular disease; many epidemiological studies have shown that elevated serum TG also indicates a significant increase in the risk of cardiovascular disease, and some scholars believe that TG is elevated in diabetic patients. The risk of cardiovascular disease is closer than that of cholesterol, especially in obese patients with type 2 diabetes. The increase in TG and the amount and quality of HDL and LDL (HDL-TG elevation, HDL-C decline, and LDL-TG elevation) exacerbate the occurrence of arteriosclerosis.

2, abnormal blood rheology:

(1) Hyperfunction of platelets: Studies have shown that platelet aggregation of diabetic patients significantly increases the release of -particle content (thromboglobulin, platelet factor 4 and platelet-derived growth factor) from platelet synthesis compared with non-diabetic patients; Increased sensitivity to platelet agonists such as ADP, collagen arachidonic acid platelet activating factor and thrombin; platelet activation increases the synthesis and release of thromboxane A2, aggravates platelet aggregation when activated by ADP, etc. Expression of glycoprotein IIb-IIIa complex, which binds to fibrinogen, a process that is part of primary platelet aggregation independent of arachidonic acid pathway and release response compared to non-diabetic controls Increased attachment to fibrinogen, which may be related to increased platelet glycoprotein IIb-IIIa molecules on the platelet surface

(2) Abnormal function of coagulation and fibrinolysis system: antithrombin III and serine protease (heparin and heparin sulfate enhance their activity) form a complex and inactivate it; protein C (after activation by thrombin-thromb complex) Coagulation factor V and factor VIII can be inactivated and stimulate tissue plasminogen activator (a regulator of the important endogenous fibrinolysis system of tPA). Decreased antithrombin III activity and relative lack of acquired protein C in diabetic patients, making diabetic patients prone to thrombosis; increased exposure to diabetes due to increased concentrations of coagulation factors XII, XI, VIII and von Willebrand factor (endogenous Coagulation pathway).

A plasminogen activator such as tPA initiates a fibrinolytic system that converts plasminogen to a plasmin-initiating thrombus, a process by tissue plasminogen activator inhibitor-1 (PAI-1 Active form release) blocked by PAI-2 and plasminogen inhibitors (2 antithrombin and 2 macroglobulin). Diabetes patients have normal or elevated tPA levels, but their activity is decreased due to increased connection with PAI-1. On the other hand, PAI-1 activity is increased in diabetic patients, and may also be associated with insulin resistance, hyperlipidemia and endothelial cell damage. In addition, in addition, saccharification of plasminogen reduces the susceptibility to activation and the relative lack of protein C also reduces the release of tPA. The above factors impair the fibrinolytic system of diabetic patients.

Diabetic patients are often accompanied by an increase in Lp(). Clinical observations suggest that elevated Lp() levels are associated with thrombolytic therapy for reperfusion failure. This effect may be partly related to Apo() and plasminogen in Lp(). Structural homology is associated with Lp() competition for receptor binding to endothelial cells and inhibition of the fibrinolytic system.

(3) Red blood cells: Red blood cells of diabetic patients are affected by factors such as saccharification and lipid peroxidation, and the erythrocyte fragility is increased, the discile degeneration ability is decreased, and the whole blood viscosity is increased at high shear speed, so that it is difficult to pass. Capillaries are beneficial for microthrombus formation.

3. Insulin resistance and/or hyperinsulinemia:

Diabetic patients, especially those with type 2 diabetes, often have varying degrees of insulin resistance and/or hyperinsulinemia (compensated hyperinsulinemia due to insulin resistance or due to inappropriate treatment). Epidemiological investigations and clinical studies suggest that insulin resistance and hyperinsulinemia are closely associated with an increased risk of atherosclerotic disease, but the exact mechanism is unknown. Prolonged hyperinsulinemia may work through the following pathways: 1 stimulating arteries Wall smooth muscle and endothelial cells proliferate and narrow the vascular lumen; 2 increase liver VLDL production, promote lipid deposition in the arterial wall; 3 stimulate the synthesis and release of PAI-1 by endothelial cells, damage the body's fibrinolysis system, promote thrombosis; Increase blood pressure through various mechanisms (such as promoting renal tubular epithelial cells to reabsorb sodium and endothelial cells to synthesize and secrete endothelin); 5 increase the excitability of the body's sympathetic nerves, increase the secretion of catecholamines, increase cardiac output and contract blood vessels; Transmembrane ion transport increases intracellular sodium and calcium ion concentrations, thereby increasing the reactivity of arteriolar smooth muscle to vasopressor; in addition, it stimulates arterial wall vascular smooth muscle hypertrophy, narrows small vessel lumen, and increases peripheral resistance Wait. All of the above effects may accelerate the occurrence and progression of arteriosclerosis. Some clinical studies have reported that patients with diabetes often have significant hyperinsulinemia, and the risk of insulin-induced atherosclerosis is significantly higher than that of insulin.

4, low blood pressure inflammation:

In the case of IGT, diabetes or IR, there is often a low vascular inflammatory response. Studies have shown that inflammation is associated with AS and participates in the formation and development of AS plaques and thrombi. The body may appear under the influence of macrovascular disease risk factors such as hyperinsulinemia or proinsulinemia, hypertension, hyperlipidemia and smoking. Endothelial cell dysfunction increases the expression of various adhesion molecules and inflammatory chemokines, attracting inflammatory cells, mainly adhering and migrating monocytes and T lymphocytes to the intima of the artery, and entering the vascular wall, the role of monocytes in cytokines The cells are differentiated into macrophages, which can be inactivated by oxidatively modified low-density lipoproteins and transformed into foam cells. The foam cells can be apoptotic and necrotic and release lipids to form extracellular lipid nucleus. When the lipid nucleus is round, the fibrous cap becomes thinner. When macrophages are dominant, some cytokines such as tumor necrosis factor- (TNF-), interleukin-6, interferon and matrix metalloproteinase are involved in inflammation and decomposition. The effect can lead to erosion or rupture of atherosclerotic plaque, followed by platelet activation and thrombosis, resulting in stenosis or occlusion of the blood vessels. The clinical manifestation of cardiovascular and cerebrovascular events, C-reactive protein (CRF), is a marker of inflammation and itself Direct involvement in the formation of atherosclerotic plaques and thrombi. CRF is found in atherosclerotic plaques that induce complement activation, recruit monocytes, induce tissue factor production, block endothelial cell responsiveness to vasoactive substances, and attenuate endothelial-nitric oxide synthase (eNOS) and NO production. Induces PAI-1 mRNA expression and PAI-1 production, promotes LDL-C oxidation and macrophage uptake of oxLDL. Other markers of inflammation include fibrinogen factor VIII and PAI-1, which are also involved in the formation of AS.

5, high blood sugar:

Hypertension and diabetes are independent risk factors for atherosclerotic disease, and studies from Framinghan report that the risk of an increased atherosclerotic event with two or more risk factors is multiplied rather than additive. Regardless of the increase in systolic and diastolic blood pressure, the risk of cardiovascular disease increases by 40% for every 10 mmHg increase in mean arterial pressure. The clinical meta-analysis suggests that if the blood pressure starts from 115/75mmHg, the systolic blood pressure increases by 20mmHg, and the diastolic blood pressure increases by 10mmHg, the cardiovascular events multiply. 70%-80% of the untreated hypertensive patients in China die from the brain. 10% to 15% of vascular diseases die from coronary heart disease, and 5% to 10% die of renal failure.

6, high blood pressure:

A large number of animal experiments and clinical studies suggest that the incidence, severity, and rate of progression of chronic complications of diabetes (such as diabetic retinopathy, diabetic nephropathy, and neuropathy) are associated with the presence of hyperglycemia, a multicenter prospective review of "diabetes control and concurrency." The clinical study of the "Diabetes Trial" (DCCT) confirmed that 1441 patients (type 1 diabetes) were enrolled in the study, with an average follow-up of 6.5 years. Compared with the conventional treatment group (HbAlc < 9.1%), the intensive glycemic therapy (HbAlc 7.2%) group The incidence and progression of diabetic retinopathy, peripheral neuropathy, and diabetic nephropathy have been significantly reduced to varying degrees; recently, an 11-year prospective study from the UK Prospective Diabetes Study (UKPDS) group further confirmed intensive blood glucose Control (using insulin, sulfonylureas or biguanides) can also significantly reduce microvascular complications in patients with type 2 diabetes. The above results strongly suggest that hyperglycemia is an important risk factor for chronic complications of diabetes. Hyperglycemia may exert its pathophysiological effects through a variety of mechanisms, and may mainly have the following metabolic pathways.

Pathogenesis

The pathogenesis of diabetic heart disease has not been fully elucidated, but from the metabolic disorders of diabetes, pathophysiology, non-invasive cardiac function tests and pathological anatomy data, it is believed that the occurrence of diabetic heart disease is closely related to the following factors:

1. Macrovascular disease: Diabetic macrovascular disease is accelerated by the development of atherosclerosis. It is the cause of increased myocardial infarction, stroke, and gangrene in diabetic patients. The exact cause of the accelerated formation of arteriosclerosis and the increase of myocardial infarction in diabetic patients is still unclear. Abnormalities in platelet, certain coagulation factors, red blood cells, lipid metabolism and other factors are considered to be effective. In addition, smoking and hypertension Risk factors such as coexistence may also play an important role in the development of the disease. Metabolic disorders such as lipids and mucopolysaccharides, especially elevated plasma LDL, triglycerides, etc., HDL, etc., often compared with diabetic patients without this group of lesions or non-diabetic patients with such lesions, suggesting lipid metabolism in diabetes, etc. Disorder is an important factor in the pathogenesis of arteriosclerosis. The well-known heart prevention study (HPS) has confirmed that patients who are given statins to strictly control blood lipids (especially LDL) have a significantly lower incidence of cardiovascular events than those with poor lipid control. Benefit more. Type 2 diabetes often has hyperinsulinemia secondary to insulin resistance. Excessive insulin levels increase renal retention of sodium, aggravate or cause hypertension, and hyperinsulinemia also promotes liver low-density lipoprotein ( Increased production of VLDL) leads to hypertriglyceridemia (which in turn causes a decrease in HDL-cholesterol levels), resulting in a series of changes in metabolic syndrome (hyperglycemia, hyperinsulinemia, lipid metabolic disorders, and hypertension). Hyperinsulinemia can also stimulate the proliferation of endothelial and vascular smooth muscle cells - the role of insulin in the growth factor receptors leads to atherosclerosis; the study found that diabetes itself and diabetes are complicated by glucose, fat metabolism disorders and neurofibrosis Is a high risk factor for coronary atherosclerotic heart disease (CHD). It has been clearly stated in the recently published report on the detection, evaluation and treatment of adult hypercholesterolemia (ATPIII): it is recommended that there will be no CHD-free diabetes. The patient is treated to a height equivalent to the risk of CHD (ie, the equivalent of CHD).

2, microvascular disease: refers to the capillary due to capillary thickening caused by capillary and pre-capillary vascular lesions myocardial microvascular disease and myocardial metabolic disorders caused by myocardial ischemia, focal necrosis fibrosis called diabetic cardiomyopathy. Animal experiments in BB mouse chain Zuoxing and alloxan have shown that the earliest manifestation of diabetic heart disease is myocardial lesions, and the mechanism remains to be studied. Clinical observations have found that some patients with diabetes can develop severe heart failure and congestive cardiomyopathy. However, coronary artery disease is not seen in angiography. Even after autopsy, there is no coronary artery occlusion and myocardial infarction. In some cases, extensive myocardial lesions (focal necrosis) can be seen. ), suggesting that it may be related to microvascular disease in the myocardium. The pathogenesis of microvascular disease includes a variety of factors, such as hemorheological changes, hyperperfusion, hyperfiltration of microvascular basement membrane thickening, increased blood viscosity, abnormal blood coagulation mechanisms, microcirculatory disorders, and increased oxidative stress And non-enzymatic glycosylation of various plasma and tissue proteins, such as glycated hemoglobin (HbA1c) glycated lipoprotein, glycated collagen, increased free radical production, and finally the accumulation of glycation end products (AGE), Tissue damage and hypoxia. The development and progression of microvascular disease is directly related to the state of blood glucose control. If blood glucose is well controlled, the occurrence of microvascular disease can be delayed, alleviated or even reversed.

3, autonomic neuropathy: autonomic neuropathy is common in diabetic patients with a long history, can affect multiple organ functions, can occur in erect hypotension, fixed tachycardia in a quiet state, cardiovascular system for Valsalva action Decreased responsiveness, mild phlegm, diarrhea (often at night) and intermittent constipation of bladder emptying and impotence in patients with impaired myocardial infarction, autopsy found that the heart's sympathetic and parasympathetic nerves have different degrees of morphology Learning changes, such as nerve bead-like thickening with increased argyrophilicity, nerve fibers in a fusiform shape with fragmentation, the number can be reduced by 20% to 60%. The main change in diabetic autonomic neuropathy is Schwann cell degeneration, often accompanied by demyelination and axonal degeneration of nerve fibers, which is similar to the pathological changes of diabetic peripheral nerves. Clinical observations show that early vagal nerve damage, prone to tachycardia in the late sympathetic nerve can also be involved, forming a transplanted heart similar to no neuromodulation, resulting in painless myocardial infarction, severe arrhythmia, often leading to cardiogenic shock, Acute heart failure and even sudden death

In conclusion, diabetic patients can cause organic and functional changes in the heart due to coronary atherosclerosis, microangiopathy, cardiac autonomic dysfunction, abnormal blood rheology of myocardial metabolism, and combined hypertension.

Pathophysiology

The pathological changes of diabetic heart disease are as follows:

1, myocardial capillary basement membrane thickening (100 ~ 110) × 10-9m [generally (63 ~ 95) × 10-9m];

2, myocardial fibrosis, including interstitial fibrosis perivascular fibrosis and focal scar fibrosis 3;

3, myocardial fiber gap has more PAS staining positive substance deposition and lipid accumulation, which can affect myocardial compliance;

4, extensive myocardial small artery lesions, endothelial cell hyperplasia mucopolysaccharide deposition under the endothelium, narrowing of the lumen;

5. Cardiomyocyte hypertrophy;

6, blood viscosity increased, red blood cell deformability decreased, which affect tissue perfusion and oxygenation, but also aggravated abnormal blood rheology leading to heart disease.

In summary, cardiomyocyte hypertrophy, myocardial fibrosis, and myocardial small artery lesions are characteristic of diabetic cardiomyopathy. Diabetic patients not only have coronary atherosclerosis in the heart, but also extensive microvascular, small and medium vascular lesions leading to myocardial focal necrosis, fibrosis, thickening of myocardial vascular wall, more fatty calcium salts and glycoprotein deposition, making the lumen Narrow, myocardial insufficiency, dysfunction. Therefore, this disease is not caused by coronary atherosclerosis alone.

The pathogenesis of diabetic heart disease has not been fully elucidated, but from the metabolic disorders of diabetes, pathophysiology, non-invasive cardiac function tests and pathological anatomy, it is believed that the early stage of this disease may be caused by autonomic dysregulation of the cardiovascular system. Functional disorders, sequential myocardial lesions, and coronary atherosclerosis is often a late manifestation.

Through large-scale epidemiological investigations and studies, it is found that compared with the same age control group, the incidence and mortality of cardiovascular disease in diabetic patients is 2 to 3 times higher than that of non-diabetics, and heart disease occurs earlier and develops faster. The condition is heavier and the prognosis is worse. The incidence of myocardial infarction in diabetic patients is 3 to 5 times higher, and more than 70% of diabetic patients die of cardiovascular complications or concomitant myocardial infarction, which is the leading cause of death in patients with type 2 diabetes.

Diabetes heart disease prevention

1. Primary prevention or primary prevention

Primary prevention of coronary heart disease in diabetes is actually a probable cause of prevention of atherosclerosis. Autopsy has proven that atherosclerosis has occurred from childhood, and some youth have been quite serious, so prevention should start from childhood and inheritance. It has been proved that diabetes is a polygenic genetic disease. After the 1970s, coronary heart disease has noticed its genetic problems abroad. Some survey data reported that one parent has coronary heart disease and his child's coronary heart disease occurs. The rate is 2 times that of families without coronary heart disease; 2 parents have coronary heart disease, and the incidence of coronary heart disease in their children is 5 times that of families without coronary heart disease. It can be seen that the occurrence of coronary heart disease is closely related to genetic family factors. Therefore, there are close relatives in the family. People with diabetes, coronary heart disease and high blood pressure should take active primary prevention measures to prevent the occurrence of diabetic coronary heart disease.

2. Secondary prevention

Also known as secondary prevention, all those who have diabetes coronary heart disease should be avoided for the factors that induce or promote the development of their disease. For those with symptoms, they should actively treat, control angina, correct heart failure and arrhythmia, improve heart. Features.

3. Three levels of prevention

According to the cause and pathogenesis of pathogenesis, prevention of diabetes complications has its specific causes. Prevention of these causes and the evolution of pathogenesis are important measures to prevent the development of diabetic coronary heart disease.

(1) Pay attention to the rationalization of diet and nutrition, and avoid regular drug: Many data indicate that people with body weight are prone to diabetes and coronary heart disease. The two are like sisters in the image of obesity. According to the survey of urban and rural areas in Shijiazhuang, more than 10% of the standard weight For high body weight; those with a body weight below 10% are low body weight; those with a standard body weight are normal weight, resulting in a high prevalence of high body weight (8.33% to 8.97%) and low prevalence of low body weight ( 2.33%2.92%); the prevalence of normal weight is between the two (3.06%~5.10%); among the three prevalence rates, the lower limit is the rural prevalence rate, and the high limit is the urban prevalence rate. In Beijing, the incidence of coronary heart disease and angina pectoris was 49.2% in obese people and 10.1% in lean body. The results of the two groups suggest that the weight of the patients is closely related to the prevalence rate, especially for diabetic coronary heart disease. Thus, prevention of overweight of body fat is an important measure to prevent coronary heart disease in diabetes.

(2) Regular exercise to prevent leisure and leisure: Diabetes is a lifelong metabolic disease. Exercise is one of the four basic therapies for diabetes. Exercise can improve the function of cell membranes, improve the function of organelles, and improve various systems. The function of organs, therefore, exercise is an important measure to prevent and treat coronary heart disease and reduce weight. It is especially important to pay attention to the regularization of sports. Life is a famous saying, and it should be avoided. This is the reduction of physical activity and mental activity. In the hotbed, it has been counted that from the Qin Shihuang to the end of the Qing Dynasty, the emperor had 210 people who could test the birth and death, of which only 10 were over 70 years old, accounting for 4.76%; 120 short-lived emperors died within 40 years old, accounting for 57.14. %, an important reason for its early death is that it is easy to idle.

(3) Establish a reasonable living system: quit smoking, bad hobbies, avoid mental stress, emotional excitement, and develop a stable psychological quality.

Mainly including lifestyle and exercise interventions, appropriate participation in exercise or physical labor, maintaining normal weight, avoiding overweight and obesity, especially abdominal obesity, helping to improve cardiovascular function in diabetic patients, and reporting the risk of cardiovascular disease in routine exercise participants Reduced sexuality by 35% to 50%; low salt (recommended daily intake of salt does not exceed 6g) low-fat diet (more intake of unsaturated fatty acids); smoking cessation, smoking is an important risk factor for cardiovascular disease, and non-smokers Compared with smokers, cardiovascular disease occurs earlier, non-smokers live in a smoking environment (passive smoking), and are also prone to cardiovascular disease. Stop smoking can significantly reduce the risk of cardiovascular disease; There is some controversy about the impact of drinking on cardiovascular disease. It is believed that a small amount of alcohol (30 ~ 60ml / d) may reduce the incidence of cardiovascular disease, but heavy drinking can increase high blood pressure and blood lipids, drinking alcohol in diabetes may interfere with glucose metabolism, Avoid drinking or not drinking as much as possible.

In 1996, the American College of Cardiology proposed to reduce the risk of cardiovascular disease. It is recommended that the general population's diet and lifestyle should strive to achieve the following goals: 1 quit smoking; 2 appropriate calorie intake and physical activity to prevent obesity, overweight weight loss 3 fat intake accounts for 30% or less of the total calorie intake per day, saturated fatty acids account for 8% to 10% of the total daily intake, and polyunsaturated fatty acid intake accounts for 10% of the total daily calories. The monounsaturated fatty acid intake accounts for 15% of the total daily calories, the cholesterol intake should be below 30 mg/d; the 55% to 60% of the 4 calories should come from complex carbohydrates; 5 drinkers and alcoholists, Do not drink more than 1 or 2 alcohol units a day. Do not let non-drinkers start drinking or increase their alcohol consumption.

Diabetic heart disease complications Complications cardiogenic shock congestive heart failure arrhythmia pneumonia acute myocardial infarction angina pectoris

The symptom of diabetic myocardial infarction is sudden myocardial infarction based on the symptoms of diabetes, so the condition should be more serious and complicated, but the symptoms of diabetic myocardial infarction are often lighter than non-diabetic myocardial infarction. Bradly compared 100 cases of diabetic myocardial infarction. 100 cases of non-diabetic myocardial infarction, found that diabetic myocardial infarction was mild, moderate chest pain was more common, only 6 patients in the non-diabetic group without chest pain, 46 in the diabetes group, and the mortality rate in the diabetic group was higher than that in the non-diabetic group, 1975 Solen analyzed the clinical symptoms of 285 patients with diabetic myocardial infarction. As a result, 33% had no typical angina symptoms, and 40% died within one month after the onset. In fact, the symptoms of diabetic myocardial infarction were not mild, but because diabetes patients were accompanied by The findings of peripheral neuritis and autonomic dysfunction have concealed the symptoms of pain and often become a painless myocardial infarction, so the mortality rate is higher, which is a noteworthy clinical feature after the occurrence of diabetic myocardial infarction.

Diabetic myocardial infarction

(1) aura symptoms: some have chest tightness, shortness of breath, or the original paroxysmal becomes persistent; some have angina or pre-palm discomfort, according to the general myocardial infarction observation, its aura symptoms are early and late, its 56.9% of aura symptoms were 1 week before onset; 21.6% were 2 weeks before onset; 6.6% were 3 weeks before onset; the rest were 4 weeks before onset or earlier.

The symptoms of aura are mainly angina pectoris, accounting for 61.8%. It is characterized by frequent pain, increased pain, and prolonged attack time. It should be closely observed for aura symptoms and treated in time, which is beneficial to the prognosis of myocardial infarction.

(2) Chest pain: Chest pain is the main symptom of myocardial infarction. It occurs mostly in emotional excitement. After stress or tiredness, after moving heavy objects, sometimes it occurs in deep sleep. The painful nature and location resembles angina, but the pain is very intense. Long duration, usually 0.5 ~ 24h, sometimes a few patients with atypical pain, such as the abdomen, jaw, shoulder and toothache, there are still some patients, especially the elderly without any pain, called painless myocardial infarction, these are not Typical symptoms or no pain are easily missed, misdiagnosed, and should be paid attention to.

(3) Digestive tract symptoms: After the onset of diabetic myocardial infarction, about one-third of patients have nausea, vomiting, abdominal distension, and occasionally even diarrhea. These gastrointestinal symptoms may be related to autonomic dysfunction, or ischemic involvement. Caused by mesenteric artery.

(4) Signs: acute illness, anxiety, face gray, sweating, breathing tightness, after the onset of 12, may have fever, the next day body temperature can reach 38 ° C, or even 39 ° C, then gradually decline, return to normal after about 1 week , pulse fineness, most of more than 100 times / min, blood pressure decreased, systolic blood pressure is often 70 ~ 100mmHg (9 ~ 13kPa), sometimes blood pressure drops, indicating that shock may occur, most of the heart rhythm, heart sounds often have a second heart sound split, Sometimes galloping, systolic murmurs in the apex, most suggest impaired papillary muscle function, a small number of patients may have pericardial friction, about 20% of the pericarditis after a few days after the infarction.

(5) Electrocardiogram examination: Electrocardiogram examination is of great significance for the diagnosis of confirmed myocardial infarction. More than 90% of patients can show clear abnormal electrocardiogram within a few hours or even ten hours after onset. However, sometimes typical ECG often appears after 24h. Or more obvious, the electrocardiogram of acute myocardial infarction is often ischemic, and the lesion and necrosis are combined.

1 pathological Q wave: suggesting necrotic changes, the main feature is that the lead to the myocardial necrosis area shows pathological Q wave, width > 0.04s, can be QR or QS type and its depth > 1/4R wave.

2S-T segment elevation: It is a damage type change, which is characterized by a guide to the damaged part, showing an abnormal rise of the ST segment, which can be as high as 2 to 15 mm and convex, with the arch back up and its starting point R wave The descending branch is different from the tip of the R wave, sometimes close to the peak, and is curved upwards of the convex arch, and then descends to the isobar. Therefore, the electrocardiogram is called a unidirectional curve, and the ST segment is raised. It is a wave pattern that occurs early in myocardial infarction, and sometimes it can last for ten hours or several days before gradually returning to the isobar.

3 ischemic T wave: also known as inverted T wave, suggesting subepicardial ischemia. When the ST segment of the electrocardiogram is in a unidirectional curve, the ST segment and the T wave are merged, which is difficult to distinguish. After a few days, the ST segment is restored to When the isobar is pressed, the T wave is inverted and becomes deeper and deeper. After a long time, the T wave gradually becomes shallower and erect.

The lead diagram of the electrocardiogram facing the infarct area, the above three typical patterns appear, and the corresponding lead in the infarct area, the R wave is increased, the ST segment is lowered and the T wave is high, which is called a specular pattern.

4 subendocardial myocardial infarction pattern: some subendocardial myocardial infarction, only a thin layer of infarcted endocardium, unlike the complete necrosis of the wall, the degree of necrosis is less than 1/3 of the thickness of the epicardium, There is no wave on the ECG, but there is a significant ST-segment drop on the corresponding lead, which can sometimes drop to 3~5mm, accompanied by T-wave inversion, and often R-wave becomes low. It usually lasts for a few days or even weeks.

5T wave inversion: In some patients with mild myocardial infarction, the wave does not appear on the ECG. Only the T wave gradually becomes inverted under dynamic observation, becoming a symmetric deep T wave, sometimes accompanied by mild ST segment elevation. After a few weeks, gradually recover, from two-way, flat to erect, this situation suggests that may be subendocardial infarction, or its infarct size is small, so-called small focal infarction, there are still normal myocardial fibers in the infarct, Therefore, the wave does not appear.

The pathological wave lasts for the longest time, often lasts for several years or even disappears for a lifetime. However, when the connective tissue shrinks in the lesion, its area will gradually shrink, and with the good collateral circulation, the wave will gradually become smaller, even in the Some leads can disappear completely and gamma waves appear.

2. Cardiogenic shock

There was no special report on the incidence of myocardial infarction complicated with cardiogenic shock. The data in Beijing was 20.6% and the shock mortality was 56.1%.

3. Congestive heart failure

Heart failure is one of the important complications of acute myocardial infarction. The analysis of acute myocardial infarction in Beijing from 1971 to 1975, the incidence of heart failure was 16.1% to 23.8%, and the mortality rate of myocardial infarction was 18.2% to 45.1%. Acute myocardial infarction complicated with heart failure is mainly left heart failure, but the disease continues to develop, which can lead to bilateral heart failure or heart failure.

4. Arrhythmia

Arrhythmia is a common complication of myocardial infarction, accounting for about 80% of the incidence, about 80% to 100% of the type of arrhythmia is ventricular premature contraction, the use of electronic monitoring system and coronary care unit for more than a decade ( The development of CCU), the early detection of arrhythmia and timely treatment, has greatly reduced the mortality of myocardial infarction complicated with arrhythmia.

5. Heart rupture and papillary muscle dysfunction

Cardiac rupture is one of the most critical complications of acute myocardial infarction. It is divided into two types according to its rupture: one is rupture of the ventricular wall, penetrating the pericardial cavity, causing pericardial tamponade, sudden cardiac death; and second, myocardial structural rupture Including papillary muscle rupture and interventricular septal perforation, heart failure or shock often occurs suddenly.

6. Late complications

(1) ventricular aneurysm: ventricular aneurysm is not a real tumor, and its mechanism is mainly due to myocardial necrosis, the lesion is replaced by connective tissue to form a scar.

(2) post-infarction syndrome: in the recovery period of acute myocardial infarction, usually in the second to 11 weeks after myocardial infarction, fever, chest tightness, fatigue, cough and other symptoms, known as post-infarction syndrome, often accompanied by triad , that is, pericarditis, pleurisy (pleural effusion), pneumonia, most of which are caused by autoimmunity, the incidence rate is 1% to 4%.

Diabetes complicated with acute myocardial infarction is a serious acute and chronic mixed disease. The condition is heavy and complicated, difficult to control, and the mortality is high. Therefore, the treatment should be comprehensive and timely, and diabetes should always be thought of when rescuing myocardial infarction. In the treatment of diabetes, the severity of myocardial infarction should be considered in order to achieve the purpose of treatment.

Diabetes heart disease symptoms common symptoms fatigue high blood pressure coma arrhythmia heart failure powerless angina pectoris ventricular fibrillation threshold lower hand cramps

1. tachycardia at rest

Early diarrhea may involve the vagus nerve, and the sympathetic nerve is in a state of relative excitement, so the heart rate tends to increase. Anyone who has a heart rate of more than 90 beats/min during rest should be suspicious and autonomic dysfunction. This heart rate is often fixed. It is not easily affected by various conditioning reactions. Sometimes the heart rate can reach 130 beats/min, which is more suggestive of vagus nerve injury.

2. Painless myocardial infarction

Because diabetic patients often have autonomic neuropathy, cardiac afferent afferent nerve function, the incidence of painless myocardial infarction is high, up to 24% to 42%, patients only have nausea, vomiting, congestive heart failure, or performance For arrhythmia, cardiogenic shock, some only fatigue, weakness, dizziness and other symptoms, no obvious pain in the precordial area, it is easy to miss diagnosis and misdiagnosis, the mortality rate is as high as 26% to 58%, diabetic patients with acute myocardial infarction More than non-diabetic patients, the disease is heavier, the prognosis is poor, and easy to re-infarction, the prognosis is worse, prone to cardiac arrest, must be vigilant, usually not strict control of diabetes is more likely to occur, some patients Ventricular fibrillation occurs due to oral hypoglycemic drugs.

3. Upright hypotension

When the patient stands up from the supine position, such as systolic blood pressure drop > 4kPa (30mmHg) or diastolic blood pressure drop > 2.67kPa (20mmHg) called orthostatic hypotension (or orthostatic hypotension, positional hypotension), sometimes systolic And diastolic blood pressure decreased, especially diastolic blood pressure decreased significantly, even decreased to O, often accompanied by dizziness, weakness, palpitations, sweating, visual impairment, fainting, and even shock, especially with hypertension and oral antihypertensive drugs, or Diuretics, vasodilators and tricyclic antidepressants are more likely to occur. It can also be seen after insulin injection. At this time, attention should be paid to the identification of hypoglycemia. The cause of orthostatic hypotension may be multi-faceted. Any link of the reflex arc can cause hypotension, but in most patients, sympathetic damage is the main cause of orthostatic hypotension. The causes of orthostatic hypotension in diabetic autonomic neuropathy may be: 1 After standing, the effective circulating blood volume is reduced, and the reflex heart rate cannot be accelerated; 2 the peripheral blood vessels are not reflexively contracted or contracted poorly; 3 catecholamines and renin-vessels The Zhangsu-aldosterone system can not rapidly regulate the response, mainly sympathetic nerve damage. This type of manifestation is seen in patients with advanced cardiovascular autonomic neuropathy. The main pathogenesis is caused by efferent nerve damage in the blood pressure regulating reflex arc. When standing from the supine position, due to sympathetic neuropathy, the release of norepinephrine is reduced, and the peripheral vasoconstriction is not compensated. The amount of adrenaline is also insufficient to reduce the cardiac output, resulting in contraction. Both pressure and diastolic pressure are reduced.

Sudden death

Patients with this disease may have sudden death due to various stresses such as infection, surgery, anesthesia, etc. Clinical manifestations of severe arrhythmias (such as ventricular fibrillation, flutter, etc.) or cardiogenic shock, sudden onset, patients only Feeling short-term chest tightness, palpitations, rapid development to severe shock or coma, blood pressure decreased significantly during physical examination, paroxysmal tachycardia or heartbeat, cardiac arrest, often died within a few hours, accompanied by infection, symptoms often Covered by the primary disease and delayed diagnosis and treatment.

Diabetes heart disease check

1. ECG examination ST segment is reduced horizontally or downwardly, and 0.05mV, T wave is flat, biphasic or inverted.

2. 24-hour dynamic electrocardiogram and/or cardiac load test (such as active plate test, treadmill exercise test, atrial pacing isoproterenol intravenous drip, two-step exercise test, etc.).

3. X-ray, electrocardiogram, echocardiography and heart vector map examination suggest that the heart is enlarged, and myocardial enzyme examination can play an auxiliary diagnostic role for myocardial infarction.

4. CT examination of cardiac morphology, cardiac function, myocardial tissue examination and myocardial perfusion quantitative and qualitative analysis to determine the presence of coronary heart disease.

5. Magnetic resonance imaging suggests cardiac macrovascular disease and clear myocardial infarction; PET can show early myocardial metabolic abnormalities, but it is expensive and economical conditions permit.

6. Radionuclide cardiac imaging includes dynamic visualization of myocardial development at rest and combined exercise test, "cold spot" development with 201Tl or 99mTc-MIBI for normal myocardium development and ischemic area development, and 99mTc coke The "hot spot" development method in which phosphate is used to develop newly necrotic myocardium and normal myocardium is not developed, and myocardial infarction and early diagnosis of coronary heart disease are performed. Newer imaging methods include single photon emission computed tomography.

7. Coronary angiography is a gold indicator for the diagnosis of coronary atherosclerotic lesions, which can be diagnosed and localized, guide the choice of treatment plan, and judge the prognosis, but it should be noted that patients with syndrome X can have typical angina manifestations, but coronary angiography results May be negative as it may be caused by small blood vessels.

Diagnostic diagnosis of diabetic heart disease

diagnosis

1. The diagnostic criteria for diabetic coronary heart disease are similar to those of non-diabetic patients, but the incidence of painless myocardial ischemia and myocardial infarction is higher in diabetic patients; should be vigilant, the diagnosis conditions are as follows: 1 Diabetes diagnosis is clear; 2 angina has occurred , myocardial infarction, arrhythmia or heart failure; 3 electrocardiogram showed ST segment was horizontal or hypotonic depression, and amplitude 0.05 ~ 0.1mV, T wave low, inverted or biphasic; 4 Doppler ultrasound prompted left ventricular diastolic And systolic dysfunction, wall segmental motion is weakened; 5 coronary angiography suggests luminal stenosis >50%; is the most accurate method for diagnosing coronary heart disease; 6 radionuclide (such as 201 Tl) examination of myocardial perfusion defects, combined Single photon emission computed tomography (SPECT) or positron emission tomography (PET) can detect abnormalities in myocardial metabolism and help improve the accuracy of diagnosis; 7 nuclear magnetic resonance imaging (MI) can indicate cardiac macrovascular Lesions and myocardial infarction sites; 8 exclude other structural heart disease.

2. The clinical diagnosis of diabetic cardiomyopathy is difficult, and it is sometimes difficult to distinguish it from other cardiomyopathy such as hypertensive cardiomyopathy. The following points can be used as reference: 1 diagnosis of diabetes; 2 arrhythmia, heart enlargement or heart failure; 3 ultrasound Cardiogram suggests left ventricular enlargement, diastolic or systolic dysfunction, decreased myocardial compliance; 4 radionuclide or MI suggestive of cardiomyopathy; 5 chest X-ray showing enlarged heart, may be associated with pulmonary congestion; 6 coronary angiography exclusion Coronary artery stenosis; 7 exclude other causes of cardiomyopathy.

3. Diabetic cardiac autonomic neuropathy lacks specific criteria. The clinical diagnosis can refer to the following indicators: 1 Diabetes diagnosis is established; 2 The heart rate is greater than 90 beats/min at rest, or the heart rate is fast and fixed and is not affected by other various conditions. Exclude other leading factors such as cardiac insufficiency, anemia and fever; 3 erect hypotension, systolic blood pressure decreased by 30mmHg and diastolic blood pressure decreased by 20mmHg; 4 heart rate difference per minute when deep breathing was 10 times; The heart rate difference is 10 times; the fatigue response index is 1.1; the ratio of the 30th heart beat RR interval to the RR interval of the 15th heart beat is <1.03.

Differential diagnosis

Diabetes combined with coronary heart disease and diabetic cardiomyopathy.

1. Identification of myocardial ischemia caused by coronary artery lesions caused by other causes such as coronary arteritis (rheumatic, vascular occlusive vasculitis), embolism, congenital malformation, sputum, etc.

2. Identify other diseases that cause heart failure and heart enlargement such as congenital heart disease, rheumatic heart disease, pulmonary heart disease, and primary cardiomyopathy.

3. Identification of other diseases that cause pain in the precordial area, such as intercostal neuralgia, cardiac neurosis, etc.

The above various diseases can be clearly identified by careful clinical analysis combined with various laboratory tests.

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