Uremic cardiomyopathy

Introduction to uremic cardiomyopathy Uremia cardiomyopathy (uremiccardiomyopathy) refers to myocardial lesions that occur during renal failure, mostly caused by chronic renal failure (CRF), and a small number can be caused by acute renal failure. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: heart failure, arrhythmia

Causes of uremic cardiomyopathy

(1) Causes of the disease

Because of the causes of chronic renal failure (CRF), in addition to the kidney itself, there are chronic renal failures caused by other diseases, such as diabetic nephropathy, kidney disease of hypertension, kidney damage of rheumatic diseases, etc. In addition to causing kidney damage and chronic kidney failure, it can also cause heart disease. Common factors involved in the onset of uremic heart disease are:

1. Hemodynamic factors, volume overload, renal anemia, arteriovenous fistula, hypertension, secondary heart valve disease.

2. Non-hemodynamic factors ischemic heart disease, autonomic dysfunction, hypocalcemia, myocardial calcification, excessive secretion of parathyroid hormone (PTH), metabolic acidosis, aluminum poisoning, 2 Microglobulin-related amyloidosis, vitamin B1 deficiency, carnitine deficiency, metabolic disorders, uremic toxins, inadequate dialysis, malnutrition, infection, etc.

3. Non-uremia factors include age, smoking, hyperlipidemia and heredity.

(two) pathogenesis

The pathogenesis of uremic cardiomyopathy has not yet been fully elucidated and is currently thought to be related to the following factors:

Pathogenesis

(1) The role of metabolic toxins: uremia, certain toxins such as urea, creatinine, amber sputum and methyl hydrazine discharge disorders, these substances can inhibit myocardial energy metabolism, resulting in myocardial cell dysfunction.

(2) disorders of lipid metabolism and carnitine deficiency: lipid spectroscopy analysis shows that uremia patients with dialysis are often accompanied by elevated levels of blood triglyceride and low-density lipoprotein and decreased high-density lipoprotein levels, prone to atherosclerosis Sclerotherapy and ischemic cardiomyopathy, and can promote cardiomyocyte apoptosis, leading to myocardial contractile dysfunction, hemodialysis patients have carnitine deficiency, the latter involved in transporting fatty acids into mitochondrial oxidative energy supply, affecting myocardial contraction; Ting can reverse some of the cardiac insufficiency.

(3) secondary hyperparathyroidism and calcium and phosphorus metabolism disorders: CRF patients are often associated with hyperparathyroidism, parathyroid hormone (PTH) levels and vitamin D metabolism disorders, associated with myocardial damage If any research finds:

1 removal of parathyroid gland in uremic patients, can reduce the associated myocardial fibrosis; re-administration of PTH, myocardial re-fibrosis, it is believed that PTH plays an important role in uremic myocardial fibrosis, but the mechanism is unknown;

2PTH can cause elevated intracellular calcium concentration and protein kinase C activation, and participate in the regulation of RNA translation process, resulting in changes in the expression of contractile or non-shrinking proteins, leading to left ventricular hypertrophy;

3 Calcium salts can be deposited in the heart and blood vessels, causing calcification, resulting in reduced blood supply and oxygen supply to the heart muscle. In addition, the cardiac conduction system can also undergo fibrosis and calcification, causing various arrhythmias and aggravating myocardial damage.

(4) Effects of stress and volume overload: Hypertension, anemia, sodium water retention and arteriovenous fistula are common in CRF patients, which may cause excessive pressure and volume overload. Excessive pressure overload may lead to left ventricular centripetal hypertrophy. Excessive volume overload often causes left ventricular dilatation, which in turn leads to systolic and diastolic dysfunction.

(5) Effects of hemodialysis on myocardium: Myocardial damage caused by hemodialysis is related to the following factors:

1 arteriovenous fistula shunt;

2 dialysis often causes the body to be in an unstable hemodynamic state, with dialysis hypertension or hypotension;

3 Hemodialysis has poor ability to scavenge PTH, 2-MG and other unknown large and medium molecular weight toxins, so that it gradually accumulates in the body, which can directly damage the myocardium or deposit in the myocardium, causing secondary myocardial amyloid change;

4 dialysis can cause insufficient nutrients for myocardial energy metabolism such as carnitine;

5 The acetic acid effect produced by dialysis with acetic acid dialysate also has myocardial toxicity.

(6) Myocardial ischemia: uremia patients may have angina pectoris and even myocardial infarction, but normal coronary angiography is not uncommon, with statistics up to 27%. The mechanism of analyzing myocardial ischemia in uremic patients may be multi-faceted. In addition to coronary lesions, increased volume and pressure load, left ventricular hypertrophy, arteriovenous fistula, anemia, tachycardia, hemodialysis, hypoxemia, electrolyte abnormalities, etc. can increase myocardial aerobics and / or Reduced oxygen supply, combined with vascular calcification and endothelial cell dysfunction, are involved in the occurrence of myocardial ischemia.

(7) The role of angiotensin-aldosterone and endothelin: angiotensin II is involved in cardiomyocyte hypertrophy; some scholars have found aldosterone receptors in cardiac fibroblasts, suggesting that aldosterone can induce myocardial fibrosis; studies have found that CRF Plasma endothelin levels can be increased, the latter is a strong vasoconstrictor, can increase the heart afterload, participate in the occurrence of cardiac hypertrophy, and is related to the severity of renal failure.

(8) Malnutrition and anemia: long-term loss of appetite, nausea, vomiting, and dialysis leading to hypoproteinemia, amino acid and vitamin deficiency, trace element metabolism disorders, etc., are involved in the occurrence and development of dystrophic cardiomyopathy, so that cardiac function Further deterioration, in addition, malnutrition is prone to viral or bacterial infection, causing myocarditis or endocarditis, aggravating myocardial damage; anemia increases cardiac output, myocardial oxygen supply, increased oxygen consumption, cardiac dysfunction; trace elements Metabolic disorders such as zinc deficiency, aluminum poisoning and cobalt poisoning can cause chronic inflammation and necrosis of the heart muscle.

Pathological interstitial fibrosis is the most important pathological change of uremic cardiomyopathy. Fibroblast proliferation and collagen matrix increase between hypertrophic cardiomyocytes, but the number of myocardial cells is not reduced, resulting in an increase in collagen matrix. Proportion, myocardial necrosis can lead to ventricular dilatation, and then develop into a pathological change similar to dilated cardiomyopathy, and can also find a variety of other pathological changes, according to statistics, the incidence of various pathological changes are: heart weight increased (male 96%) , female 86%), left ventricular hypertrophy (66%, asymmetrical left ventricular posterior hypertrophy), coronary and aortic atherosclerosis (86%), pericardial effusion and myocardial fibrosis (31%), valve Lesion (28%).

Uremia cardiomyopathy prevention

Uremia-induced myocarditis is caused by a variety of factors, and to improve its prognosis, in addition to the cause of treatment, comprehensive treatment and preventive measures should be used.

Uremia cardiomyopathy complications Complications heart failure arrhythmia

Can be complicated by heart failure, arrhythmia, dialysis hypotension.

1. The main causes of cardiac insufficiency are:

1 hypertension can increase the heart afterload, while sodium water retention increases the heart preload; abnormal lipid metabolism can cause coronary heart disease, affecting myocardial blood supply; and uremic pericarditis can limit ventricular filling and relaxation;

2 anemia can aggravate myocardial hypoxia;

3 secondary hyperparathyroidism is involved in vascular calcification, and may involve the conduction system and the valve, resulting in cardiac insufficiency.

2. Arrhythmia

Cardiomyocyte hypertrophy, autonomic increase in hypoxia; myocardial cell necrosis, interstitial fibrosis is easy to produce reentry; myocardial cell membrane dysfunction, myocardial depolarization repolarization abnormalities, can lead to a variety of tachyarrhythmias; pacing conduction system Calcification can cause a variety of slow arrhythmias; hypokalemia or hyperkalemia causes or aggravates arrhythmias.

3. Dialysis hypotension

In the case of dialysis ultrafiltration dehydration, if the myocardial contractile function has been severely damaged, the myocardial can not undergo compensatory contraction enhancement, diarrhetic hypotension can occur; in addition, left ventricular hypertrophy is often accompanied by decreased left ventricular compliance, dialysis When the left ventricle returns to the heart, the amount of blood is reduced, the cardiac output is decreased, and the occurrence of hypotension is involved.

Symptoms of uremic cardiomyopathy Common symptoms Arrhythmia Heart failure Hypertension Tachycardia Heart palsy oliguric pericarditis Blood hypoxia edema conduction block

Uremia cardiomyopathy is the symptoms and signs of cardiovascular system damage based on the original kidney disease. The main manifestations are as follows:

Congestive heart failure

It is one of the serious manifestations of uremic cardiomyopathy. Hypertension, anemia, hypoproteinemia, severe sodium retention and myocardial damage, etc., increased cardiac load and/or decreased myocardial contractility, which is the main cause of heart failure. Clinical manifestations of edema, oliguria with palpitations, dyspnea and other symptoms and signs of heart failure, the incidence of end-stage renal disease heart failure is higher (30.0% to 52.9%), is the main cause of death.

2. Arrhythmia

The occurrence of arrhythmia is related to ventricular dysfunction and electrolyte and/or acid-base balance disorders. All kinds of arrhythmia can occur. Sinus tachycardia, pre-systolic and conduction block are more common, pacing system calcification and A variety of slow arrhythmias are associated with the occurrence.

3. Ischemic myocardial damage

The increase of coronary vascular bed is not compatible with the increase of myocardial mass, which can lead to myocardial ischemia and hypoxia. The clinical manifestations are mainly angina pectoris and even myocardial infarction.

Anemia

Most commonly, hemoglobin levels are inversely related to serum creatinine levels. The main cause of anemia is the reduction of erythropoietin (EPO) in CRF. Other factors include insufficient hematopoietic materials, secondary hyperparathyroidism, and aluminum poisoning. , red blood cell damage increased and so on.

5. Other

Valvular lesions are more common, some patients may have infective endocarditis, pericarditis, systemic embolism, etc., the incidence of valvular calcification can be as high as 70%, exudative pericarditis and left atrial thrombus are 7%.

Examination of uremic cardiomyopathy

blood test:

1. Blood routine is generally positive pigmentation, positive cell anemia, and reduced hematocrit.

2. Renal function test blood urea nitrogen, creatinine, uric acid increased, creatinine clearance decreased, blood gas analysis showed metabolic acidosis.

3. Blood lipids are more common in type IV hyperlipidemia, VLDL, IDL, LDL increase, HDL decrease, apo AI and apo AII decrease, apo A4, apo B48 and apo CIII-containing VLDL, LDL and HDL increase, while HTGL and LCAT activity decreased.

4. Increased parathyroid hormone.

Other auxiliary inspections:

1. Electrocardiogram myocardial hypertrophy, a variety of arrhythmia.

2. The chest shadow of the heart is obviously enlarged, the proportion of heart and chest is >60%, the heart beat is weakened; the lung is blocked.

3. Echocardiographic left ventricular end-diastolic volume increased and left ventricular internal diameter increased, ejection fraction and cardiac output decreased, a good non-invasive method for the diagnosis of uremic cardiomyopathy, Foley analysis of 433 patients with this disease, Left ventricular systolic dysfunction was found to account for 15%, left ventricular hypertrophy and normal systolic function accounted for 76%, left atrial enlargement accounted for 30%, left ventricular enlargement accounted for 23%, some patients can see valvular calcification and reflux, pericardial effusion , the formation of neoplasms, etc.

4. Nuclide myocardial imaging using 99m-methoxyisobutyl isocyanide (99mTc-MIBI) myocardial imaging, calculation of left heart / myocardial count ratio (CMR) and lung / heart count ratio (LHR), found that LHR increased Lower CMR helps to evaluate left ventricular function and prognosis in uremic cardiomyopathy.

5. Endomyocardial biopsy showed different degrees of myocardial hypertrophy, myocardial cell focal dissolution, interstitial fibrosis, myocardial calcification and oxalate deposition, consistent with the above performance, and excluded primary cardiomyopathy and other secondary Cardiomyopathy can be diagnosed.

Diagnosis and diagnosis of uremic cardiomyopathy

diagnosis

The disease is characterized by the clinical manifestations of cardiomyopathy after CRF, combined with medical history, physical signs and laboratory tests, the diagnosis is generally not difficult.

Differential diagnosis

Hypertensive heart disease

This disease has obvious myocardial damage in the early stage of renal function damage, and has fundus, cerebral blood vessels and other lesions. Before uremia, there is a long history of primary hypertension and heart enlargement. Echocardiography helps. Identification: The myocardial weight of patients with uremic cardiomyopathy is significantly greater than that of hypertensive patients, and the performance of overweight is more obvious.

2. Systemic lupus erythematosus and myocardial amyloidosis

The common feature of both is systemic injury. Cardiomyopathy, renal function damage and anemia are often found in the early stage, but the kidneys do not shrink or even enlarge. Systemic lupus erythematosus is often accompanied by fever, arthritis and resistance. Positive for nuclear antibodies, decreased for complement, etc., amyloidosis may be idiopathic or secondary, the latter often have chronic infectious diseases, multiple myeloma history, and hepatosplenomegaly and lymphadenopathy, in liver or kidney biopsy There may be amyloid deposits in the tissue.

3. Primary cardiomyopathy

Myocardial damage occurs earlier, more anemia and severe renal dysfunction. Renal dysfunction can occur when cardiac dysfunction is severe. Renal function can be improved after cardiac function improvement. Generally, dialysis treatment is not needed.

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