gouty cardiomyopathy

Introduction

Introduction to gouty cardiomyopathy Gout is a "crystal disease" in which urate accumulates in the body and forms crystals caused by long-term disturbance of sputum metabolism. The majority of heart disease in gout patients is gout heart disease caused by urate accumulation in the heart, crystallization and even formation of stones. And more is due to gout easily combined with coronary atherosclerosis and high blood pressure caused by heart disease. basic knowledge The proportion of illness: 0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: atherosclerosis, coronary heart disease, angina pectoris, myocardial infarction

Cause

Causes of gouty cardiomyopathy

Primary gout (45%):

For the congenital and idiopathic sputum metabolism abnormalities, most of the molecular defects are unclear, and the multi-gene inheritance is either excessive uric acid production or too little excretion, or both, and a few are considered to be due to specific enzyme defects. For example, an increase in the activity of phosphoribosyl pyrophosphate kinase causes excessive production of uric acid, which is a sexual inheritance.

Secondary gout (40%):

The most common causes are kidney disease (polycystic kidney disease, pyelonephritis, glomerulonephritis, lead-toxic nephropathy, etc.), hypertension, myeloproliferative diseases, blood diseases, malignant tumors and various drugs.

Metabolic syndrome (15%):

High uric acid is often associated with obesity, insulin resistance, hypertriglyceridemia and the like.

Pathogenesis

1. The pathogenesis of Lesch-Nyhan syndrome is hypoxanthine-guanine phosphoribosyltransferase deficiency, which reduces the production of guanine nucleotides and hypoxanthine nucleotides, and reduces the utilization of 1-pyrophosphate-5-phosphate ribose. The amide-transferase-catalyzed reaction is strengthened, the sputum synthesis is increased, and the production of uric acid is increased. Most of the patients are young males, although normal at birth, but after 4 to 6 months, neurological dysfunction, such as muscle rigidity, muscle Powerless, hand and foot dance, joint contracture, lower limbs are scissors-like, hip dislocation, mental retardation, often bite the cheeks and cheeks after the teeth, if it can survive, gouty arthritis, gouty kidney stones, etc. , autosomal recessive glycogen accumulation disease type Ia (von Gierke disease) is due to the lack of glucose-6-phosphatase, patients with increased uric acid production and decreased excretion, in addition to hyperuricemia, hepatosplenomegaly, Slow growth, severe hypoglycemia, acidosis and hyperlipidemia.

2. The most common causes of secondary gout are kidney disease (polycystic kidney, pyelonephritis, glomerulonephritis, lead-toxic nephropathy, etc.), hypertension, myeloproliferative diseases, blood diseases, malignant tumors and various drugs. If patients with these diseases have a longer survival time, hyperuricemia will last longer, which may cause symptoms similar to those of primary gout. If the symptoms are mild, they may be easily covered by the signs of primary disease.

Prevention

Gouty cardiomyopathy prevention

1. Strict diet control

Strict diet control can reduce uric acid by 1~2mg/dl. To do "three principles": don't drink alcohol; don't eat animal internal organs; eat less seafood, and fully replenish water.

(1) Limit the intake of sputum, do not exceed 100 ~ 150mg per day, limit the protein intake, not more than 0.8 ~ 1g per kilogram of body weight, limit the total calories, body fat to reduce 50g staple food per day is appropriate, do not eat sorghum Food, such as animal offal, fish, not stewed meat, lean meat, poultry meat boiled to soup, appropriate to limit fat intake.

(2) Vegetables except dried mushrooms, dried seaweed should not be eaten in large quantities, can be eaten, fruit is not taboo, avoid eating a lot of fructose and vitamin C.

(3) Limit the strong stimulation of spices, spices; salt limit, 2 ~ 5g per day.

2. Drink plenty of water

Keep 2,000 to 3000 ml per day to promote the elimination of uric acid and avoid urinary calculi. It is best to maintain a urine volume of 1500 ml per day.

3. Prohibition of alcohol

Alcohol is metabolized to lactic acid in the body, which tends to cause lactic acid to accumulate in the body. A large amount of lactic acid inhibits the excretion of uric acid by the kidneys. At the same time, alcohol itself promotes the decomposition of ATP to produce uric acid, which is easy to induce gout, especially beer is most likely to cause gout attacks. .

4. On the basis of diet control, adhere to drug treatment.

5. Prevention and treatment of complications of gout.

Complication

Gouty cardiomyopathy complications Complications atherosclerosis coronary heart disease angina pectoris myocardial infarction

Complications such as atherosclerosis, coronary heart disease (angina pectoris, myocardial infarction) can occur earlier.

Symptom

Symptoms of gouty cardiomyopathy Common symptoms Gout nodules Hypertension Cardiac hypertrophy Angina ventricular hypertrophy

Gouty myocardial lesions are as follows:

Gout cardiomyopathy, heart gout stones

As a part of the whole body, the heart can occasionally accumulate urate, crystallize and even form nodules, destroying the heart structure and forming heart disease. It is reported that the endocardium, valve, myocardium, myocardial interstitial, conduction system, and extracardiac Membrane can be affected. In 1940, Bunik et al reported a case of gout on the mitral valve in gout patients. In 1933, Hech et al reported that a patient had complete atrioventricular block due to conduction system gout stones, but clinical There are not many cases of gout directly involving the heart. Since 1856, Bencojones first described it to 1933 and only 11 cases were reported.

2. Coronary atherosclerotic heart disease

Patients with gout are prone to coronary atherosclerosis. Clinically, obesity, hypertension, diabetes, coronary heart disease, and gout are common in the same patient. Many scholars have pointed out that about half of gout patients have high blood pressure, and hypertension is a coronary heart disease. Risk factors can increase left ventricular pressure load and promote left ventricular hypertrophy to form hypertensive heart disease. In recent years, some scholars have pointed out that hypertension can stimulate hypertrophy of heart muscle. Gout patients suffer from insufficient joint activity due to lesions involving joints. About half of them Patients with obesity, in addition, gout patients with hyperlipidemia can reach 21% to 83%, impaired glucose tolerance by 21% to 73%, Bluhm reported increased platelet surface activity, hypercoagulable state accounted for gout patients 51 %.

In recent years, many scholars have pointed out that the increase of blood uric acid itself is also a risk factor for coronary atherosclerosis, and there is a positive correlation between the two.

Many scholars believe that atherosclerosis is almost an inevitable complication of gout patients. The age of atherosclerosis in gout patients is earlier than normal. Ogryzlo reported that 51 of 195 gout patients had angina pectoris, myocardial infarction, Bluhm 280 cases of gout were followed up for 5 to 10 years, of which 22 cases had myocardial infarction. Ji Village analyzed the electrocardiogram of 185 patients with gout, including 14% of patients with coronary insufficiency and 12% of left ventricular hypertrophy. Hypertrophy accounts for 9%. As early as 1927, the autopsy data of 77 cases of gout provided by Gudzent et al. have indicated a high incidence of coronary heart disease, of which 29 cases have coronary atherosclerosis and 22 cases die directly from cardiovascular disease.

Examine

Examination of gouty cardiomyopathy

1. Determination of blood uric acid on fasting for more than 8h (fasting after 12 o'clock in the evening, but drinking water), normal value of blood uric acid: 210 ~ 420mol / L or <7mg / dl, or male: 0.38 ~ 0.42mmol / L (6.4 ~ 7mg / dl), female: 0.309mmol / L, when more than 0.38mmol / L, it is easy to form crystals and deposited in the tissues of the human body, leading to gout, blood uric acid often exceeds 420mol / L during acute attack of gout ( 7mg/dl), the remission period is normal.

2. Urine examination urinary pH can be detected, with or without hematuria, proteinuria, etc., often in the late urine of the disease.

3. Blood test The total number of white blood cells can be increased during the attack period, and the erythrocyte sedimentation rate is increased.

4. Joint X-ray film The recurrence of gout can be seen in the destruction of articular cartilage margin, irregular articular surface, and then the joint cavity is narrow, and the tortstone deposition can be seen in the subchondral bone and bone marrow. Osteoporosis, the bone of the adjacent joint is not Uniformly pierced or round transparent defect area, the size is different, the edge is sharp and semi-circular or continuous curved, the edge may have hyperplastic calcification, and severe cases have fractures.

5 abdominal X-ray film kidney visible stone shadow.

6. Joint cavity puncture examination In the acute attack period, the joint cavity puncture, taking the bursal fluid for optical microscopy, can be found that the urate crystal is needle-shaped in the white blood cells or free, with weak refractive phenomenon.

Diagnosis

Diagnosis and diagnosis of gouty cardiomyopathy

Diagnostic criteria

The diagnosis of primary gout is mainly based on clinical symptoms, hyperuricemia and treatment response, except for secondary gout. Generally, clinical diagnosis can be made. Diagnosis should be made from joint cavity puncture, tissue biopsy or gout stone puncture to find uric acid. Salt crystallizes.

After the diagnosis of gout, you should carefully look for signs of heart involvement. For patients with suspected heart gout stones, you should actively follow up the treatment. After the illness, you should seek an autopsy to confirm the diagnosis. If you can confirm the heart disease through imaging, you can pass coronary angiography. Coronary heart disease can also be diagnosed clinically.

Differential diagnosis

Mainly related to a variety of common arthritis identification, should be excluded from cardiomyopathy, valvular disease caused by other causes, cardiovascular degeneration and amyloidosis cardiomyopathy.

1. Rheumatoid arthritis occurs mostly in large joints, showing anaging pain, and the anti-chain "O" often increases.

2. Rheumatoid arthritis is more common in young women, occurs in the proximal joints of the hand and foot, the joint swelling is fusiform, symmetrical, rheumatoid factor-positive, rheumatoid arthritis in the late X-ray, articular surface stenosis, bone defect And osteoporosis.

3. Gout chronic arthritis must be differentiated from pseudogout. The incidence of pseudogout is older, most involving the knee joint. The joint bursa contains calcium pyrophosphate crystals or phosphorish white, X-ray shows cartilage ossification, blood uric acid is not high.

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