Diabetic cardiomyopathy

Introduction to diabetic cardiomyopathy Diabetic cardiomyopathy refers to a cardiomyopathy that occurs in diabetic patients and cannot be explained by hypertensive heart disease, coronary atherosclerotic heart disease, valvular heart disease, and other heart disease. Increased blood lipids in diabetic patients can promote the uptake of lipids by vascular wall cells. VLDL-c is more likely to be converted into cholesterol esters. LDL saccharification damages the recognition of receptors on hepatocytes and slows down their metabolism, and is combined by other receptors. Macrophages preferentially phagocytose and degrade, accumulate in macrophages to become foam cells and promote the formation of atherosclerotic plaque. Diabetes patients, especially in poor glycemic control, increase triglyceride and increase lipoprotein oxidase activity Increased LDL content of oxidized protein components and small density, which are cytoplasmic toxicities of vascular endothelial cells and smooth muscle cells, and participate in the occurrence of atherosclerosis. The pathological study of diabetic cardiomyopathy also exhibits a wide range of metabolism. Diffuse myocardial damage: cardiomyocyte hypertrophy, degeneration, focal necrosis, necrotic areas replaced by fibrous tissue. Elevated myocardial extracellular glucose levels directly cause changes in intracellular calcium ion concentration. It has been found that sodium-calcium exchange in cardiomyocytes of type 2 diabetes is inhibited, while the sarcoplasmic reticulum Ca pump is normal, so that Ca is gradually concentrated in the sarcoplasmic reticulum. Ca overloaded myocardial sarcoplasmic reticulum can increase the release of spontaneous Ca, increase tension during myocardial relaxation, and decrease cardiac compliance. basic knowledge The proportion of sickness: 0.00253% Susceptible people: no specific population Mode of infection: non-infectious Complications: heart failure, arrhythmia, diabetes, heart disease

Causes of diabetic cardiomyopathy

Cardiomyocyte calcium transport defects (25%):

Elevated extracellular glucose levels directly cause changes in intracellular calcium concentration. It has been found that sodium-calcium exchange in cardiomyocytes of type 2 diabetes is inhibited, while the sarcoplasmic reticulum Ca pump is normal, causing Ca to concentrate in the sarcoplasmic reticulum. Ca overloaded myocardial sarcoplasmic reticulum increases spontaneous Ca release, increases tension during myocardial relaxation, and decreases cardiac compliance.

Cardiomyocyte metabolic disorder (25%):

Increased blood lipids in diabetic patients can promote the uptake of lipids by vascular wall cells. VLDL-c is more likely to be converted into cholesterol esters. LDL saccharification damages the recognition of receptors on hepatocytes and slows down their metabolism, and is combined by other receptors. Macrophages preferentially phagocytose and degrade, accumulate in macrophages to become foam cells and promote the formation of atherosclerotic plaque. Diabetes patients, especially in poor glycemic control, increase triglyceride and increase lipoprotein oxidase activity Increased LDL content of oxidized protein components and small density, which are cytoplasmic toxicities of vascular endothelial cells and smooth muscle cells, and participate in the occurrence of atherosclerosis. The pathological study of diabetic cardiomyopathy also exhibits a wide range of metabolism. Diffuse myocardial damage: cardiomyocyte hypertrophy, degeneration, focal necrosis, necrotic areas replaced by fibrous tissue.

Coronary microvascular disease (20%):

There is a small myocardial lesion in the diffuse myocardium in the myocardium of diabetic patients.

Myocardial interstitial fibrosis (15%):

It is due to the long-term progression of diabetes caused by glycosylated collagen deposition.

Cardiac autonomic neuropathy (10%):

About 83% of diabetic patients develop cardiac autonomic neuropathy.

Pathogenesis

Pathogenesis

(1) Cardiomyocyte metabolic disorder: The study found that the contractile protein or calmodulin of cardiomyocytes in diabetic patients is mediated by the second messenger such as protein kinase c (PK-c) and nitric oxide (NO). Can cause its function to be abnormal.

(2) Cardiomyocyte calcium transport defect: The increase of extracellular glucose level in cardiomyocytes directly causes changes in intracellular calcium ion concentration. Allo et al found that the sodium-calcium exchange of cardiomyocytes in type 2 diabetes is inhibited, while the sarcoplasmic reticulum Ca2 pump is normal. Ca2 gradually concentrates on the sarcoplasmic reticulum, Ca2 overload myocardial sarcoplasmic reticulum, can increase the release of spontaneous Ca2, increased tension during myocardial relaxation, so the heart of type 2 diabetes is mainly decreased, type 1 diabetes The cardiomyocytes, the sodium-calcium exchange and the Ca2 pump were inhibited. Although the intracellular Ca2 concentration was not significantly increased, the diastolic phase could not be reduced in time, so the heart of patients with type 1 diabetes was mainly diastolic dysfunction.

(3) Coronary microvascular disease: The microvascular system refers to the capillary and microvascular network between the tiny artery and the tiny vein. The autopsy found that the myocardium of diabetic patients has diffuse myocardial wall small vessel disease, while the myocardial wall has larger coronary artery. Normally, histological examination showed that infiltration of fat around small blood vessels, proliferation of endothelial and subendothelial fibers, thickening of the basement membrane, and observation of microcirculation after cardiac perfusion, found that 50% of patients had microangioma, which was similar to retina and Small blood vessel lesions in the kidney also exist in the heart. These pathological changes can reduce the reactivity of myocardial small blood vessels to vasoactive substances and affect the coronary reserve function.

(4) myocardial interstitial fibrosis: a longer course of diabetes, can show myocardial fibrosis and increased PAS staining positive substance and other histological changes, caused by glycosylated collagen deposition, in addition, and diabetic microangiopathy Reduced myocardial blood supply, increased fibrosis formation.

(5) Cardiac autonomic neuropathy: About 83% of patients with diabetes develop cardiac autonomic neuropathy. The early stage of the disease is mainly vagus nerve damage. When the disease is advanced, the vagus and sympathetic nerves can be involved. Electrocardiography can find persistent tachycardia. Prolonged QT interval, decreased heart rate variability and severe ventricular arrhythmia, severe cases of asymptomatic myocardial infarction and sudden cardiac death.

(6) Other:

1 Increased use of fatty acids: Recent studies suggest that diabetic patients are associated with decreased glucose utilization, while increased fatty acid utilization leads to accumulation of toxic fatty acid intermediates, further inhibiting myocardial glucose utilization, which may lead to ATP depletion, prevent lactic acid production, and increase myocardial oxygen consumption. All of these cause impaired myocardial function.

2 microcirculatory disorders cause myocardial ischemia and hypoxia: circulatory disorders can occur in early stage of diabetes, resulting in insufficient perfusion of blood in the myocardium, causing ischemia, hypoxia, aggravating secondary damage of cardiomyocytes, enabling myocardial cells to supply The accumulation of oxygen and metabolites is getting worse.

2. Pathology

(1) Cardiomyocyte lesions: cardiomyocyte hypertrophy, degeneration, focal necrosis, necrotic fibrosis, myocardial myosin ATPase activity decreased, sarcoplasmic reticulum decreased calcium ion uptake, diastolic cardiomyocyte intracellular free calcium As the ion concentration increases, the myocardial diastolic compliance decreases.

(2) vascular lesions: one of the characteristic changes of diabetic cardiomyopathy, mainly involving the intermuscular arterioles, while the epicardial coronary artery is completely normal (except those with coronary heart disease), mainly characterized by small intima of the arterioles and Subendal hyperplasia, fibrosis and deposition of PAS-positive substances, narrowing of the lumen, diminished diastolic function, reduced coronary circulation reserve, capillary basement membrane thickening and capillary hemangioma formation, and a large amount of glycogen deposition Affects the exchange function of capillaries.

(3) Interstitial lesions: Some scholars have found that diabetic cardiomyopathy is associated with interstitial, such as fibrosis of myocardial interstitial and deposition of PAS-positive substances.

(4) hemodynamic changes: can be expressed as two types of restrictive cardiomyopathy and dilated cardiomyopathy, the former is more common in the early stage, mainly diastolic dysfunction, the latter more common in the late stage, mainly left ventricular enlargement, left ventricle Hypertrophy, impaired systolic function and increased left ventricular end-diastolic pressure, combined with left ventricular diastolic dysfunction.

Diabetic cardiomyopathy prevention

1. The prevention of diabetic cardiomyopathy focuses on the secondary prevention of diabetes and prevents the occurrence of various complications. Therefore, it is necessary to control the development of diabetes and the basic stability of blood sugar, which can reduce the chain reaction of the "three high phenomenon" and reduce the cells. The shrinkage and edema effect can maintain the function of normal cell membranes.

2. The right amount of physical exercise can not only enhance blood circulation, improve microcirculation function, wash and massage the intima of the blood vessels, but also improve cell membrane function, which is conducive to maintaining blood sugar stability.

3. Regularly check myocardial antinuclear antibodies to rule out autoimmune reactions. If autoimmune cardiomyopathy is found, measures should be taken early to prevent further damage to the myocardium.

4. Prevent infection and avoid infectious cardiomyopathy. If there are signs of infection, anti-infective treatment should be carried out in time.

Diabetic cardiomyopathy complications Complications heart failure arrhythmia diabetes heart disease

Complications such as heart failure and arrhythmia can occur.

1. Heart Failure Framingham study found that the incidence of heart failure in male patients with diabetes was 2.4 times higher than that of the control group, and that of female patients was 5.1 times higher. In hospitalized heart failure patients, diabetes accounted for 24% to 47%.

2. Arrhythmia Diabetic cardiomyopathy can be seen in different types of arrhythmias, the incidence of arrhythmia in diabetic patients is 40% to 75%.

Symptoms of diabetic cardiomyopathy Common symptoms Tachycardia heart failure Heart enlargement Angina pectoris Arrhythmia Standing heart rate difference apical beat diffusion conduction block apex apex...

1. Congestive heart failure is the main clinical manifestation of diabetic cardiomyopathy. Patients with insulin-dependent diabetes mellitus (IDDM) are more likely to develop cardiomyopathy than adults with type 2 diabetes. In diabetic patients, the probability of concomitant heart failure is about Two times male, after considering factors such as age, blood pressure, body weight and cholesterol, the risk of heart failure in women with diabetes is more than 5 times that of the control group, and about 2 times for men. If the patient has a history of myocardial infarction, it is very Difficulties and heart failure after myocardial infarction, need to be confirmed by pathological biopsy, patients with hypertension need to be differentiated from hypertensive heart disease.

2. Arrhythmia may be due to myocardial focal necrosis, fibrous scar formation, causing myocardial electrophysiological heterogeneity and arrhythmia, which may be manifested as atrial fibrillation, sick sinus syndrome, atrioventricular block, ventricular premature contraction And ventricular tachycardia, etc., different from coronary heart disease mainly in various ventricular arrhythmias.

3. Angina pectoris in addition to subcardiac coronary artery disease, but also due to occlusion of small coronary artery occlusion in the wall, Liu Yunzhi and other reports, according to the international disease code diagnosis of diabetic cardiomyopathy in 7 patients with angina There were 3 cases of medical history.

Examination of diabetic cardiomyopathy

1. Blood sugar and glycated hemoglobin are significantly increased: Most glucose peaks are significantly delayed if the glucose tolerance test is performed.

2. Increased plasma osmotic pressure: significantly exceeds the normal range.

3. Increased blood viscosity : whole blood viscosity (low cut) 10.00, plasma specific viscosity 1.70 (this test may vary with laboratory conditions and instrument methods, if the control can be seen to increase the phenomenon).

4. Echocardiography : left ventricular diastolic dysfunction, in patients with diabetes without clinical heart failure, characterized by abnormal left ventricular diastolic function, earlier and more obvious than systolic dysfunction, isovolumic diastolic time (IVRT) prolonged, Peak filling rate decreases and the rapid filling period increases, the E/A ratio decreases, and the left ventricular end diastolic diameter (LVEDD) decreases. When diabetic patients develop congestive heart failure, there is cardiac enlargement, left ventricular systolic dyskinesia, left ventricular contraction. Echocardiographic findings of dilated cardiomyopathy with impaired function.

The intersystolic phase and M-mode ultrasound have always been an important means for scholars to study the clinical cardiac function of diabetic patients. However, due to the difference in methods and patient selection, the results are contradictory. In 1975, Ahmed et al found that patients with diabetes without heart failure showed The left ventricular ejection (PEP) was prolonged, the ejection duration (LVET) was shortened, and the PEP/LVET ratio was higher than normal. It was considered to be unrelated to the course of diabetes and treatment, but related to the combined microvascular disease. Syked et al reported in 1977. Ventricular PEIP was shortened, LVET was prolonged, and PEP was reversed after oral hypoglycemic or diet therapy. Some scholars found that LVET was normal at rest, but only 43% abnormal after exercise, and no abnormality in the control group. Other scholars believe that Both rest and activity are elevated.

5. Electrocardiogram : common sinus tachycardia, ST-T changes and various arrhythmias, left ventricular high voltage.

6. X-ray chest X-ray : Most patients with diabetic cardiomyopathy have normal heart size, and left ventricular enlargement can be seen in patients with heart failure or hypertension.

7. Myocardial biopsy : Endometrial biopsy can be performed on suspected patients, and it is helpful to diagnose when characteristic microangiopathy and/or interstitial PAS-positive substances are deposited.

8. Interventional cardiac catheterization : Studies have shown that patients with diabetic cardiomyopathy generally have elevated left ventricular end-diastolic pressure (LVEDP), normal or increased end-diastolic volume (LVEDV), the ratio of the former to the latter (LVEDP / LVEDV) liter High, this ratio reflects left ventricular stiffness and left ventricular diastolic function. In addition, the patient's stroke volume and ejection fraction decreased, and some patients' left ventricular contraction movement was diffusely weakened.

9. Heart rate variability test (HRV) It has been reported that about 50% of diabetic patients have weakened or disappeared heart rate variability within 24 hours. Studies have shown that the field analysis of HRV has been used to predict the accidental death of autonomically injured patients with diabetes. Bemardi reported that the blood pressure fluctuation of diabetic patients disappeared at 24 hours, that is, the blood pressure trough disappeared at night. This phenomenon is mainly attributed to the supernormal excitability of nocturnal sympathetic nerves, which may indicate that the death of diabetic patients due to cardiovascular disease is particularly common at night.

10. Cardiac autonomic function test can be used as a clinical evaluation of the degree of sympathetic nerve damage in diabetic patients. Evidence for autonomic neuropathy: 1 standing, lying position test, heart rate difference <10 times / min. 2Valsalva action index 1.0. 3 orthostatic hypotension, when erected within 5s of supine position, systolic blood pressure decreased by >30mmHg (3.99kPa), diastolic blood pressure decreased by >20mmHg (2.66kPa), with symptoms such as dizziness. 4 pathological examination of cardiac autonomic nerve fiber reduction, segmentation, local nucleus and spheroidal thickening.

11. Cardiac function examination Diabetic cardiomyopathy, most or all of the ventricular muscles, the overall ventricular contractility is generally reduced, ventricular wall compliance is reduced, myocardial contraction is not coordinated.

(1) The left ventricular ejection fraction (LVEF) of diabetic cardiomyopathy is decreased. The left ventricular ejection fraction of diabetic cardiomyopathy is lower than the normal value. The damage of diabetic cardiomyocytes is the main reason for the decrease of myocardial cell contraction.

(2) Diabetic cardiomyopathy The left ventricular ejection time is shortened, the pre-ejection period (PEP) is prolonged, and the PEP/LVET ratio is increased. This value is negatively correlated with the stroke volume, and the left ventricular systolic function is decreased, then the PEP is prolonged and the LVET is shortened. The ratio is increased, and it is generally considered that the ratio >0.40 has clinical significance.

(3) Cardiac diastolic dysfunction in diabetic cardiomyopathy According to echocardiography, left ventricular end-diastolic pressure (LVEDP) in diabetic cardiomyopathy was significantly higher than normal.

Diagnosis and diagnosis of diabetic cardiomyopathy

Diagnostic criteria

There is no uniform diagnostic criteria for diabetic cardiomyopathy. The following points are available for reference:

1. Diagnosis of diabetes (especially type 1 diabetes).

2. Have clinical manifestations of heart failure.

3. Heart enlargement with impaired systolic function, diastolic dysfunction in patients with no enlarged heart.

4. Exclude heart failure caused by hypertensive heart disease, coronary heart disease and rheumatic valvular heart disease.

5. If necessary, myocardial biopsy, found that microvascular disease and positive PAS staining can be diagnosed.

6. Other microvascular lesions, such as the retina, renal vascular disease, support the diagnosis.

Differential diagnosis

Mainly differentiated from coronary atherosclerotic heart disease, coronary angiography showed that the presence of stenotic lesions in the main branches can help the diagnosis of this disease, can be identified.

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