Cardiac hypertrophy

Introduction This is a slower but more effective compensatory function, mainly in the case of long-term stress overload, increased myocardial volume, increased contractility, allowing the heart to maintain a normal blood circulation, while having considerable reserve . However, this compensatory function also has its disadvantages, mainly because of hypertrophic myocardial aerobic increase, and the coronary blood supply is often unable to be met, resulting in myocardial ischemia, which will eventually lead to a decline in myocardial contractility. Hypertrophic cardiomyopathy is characterized by cardiac hypertrophy. It is characterized by ventricular muscle hypertrophy, typically in the left ventricle, with interventricular septum, occasionally concentric hypertrophy.

Cause

The cause is unknown. It is currently believed that genetic factors are the main cause, based on the obvious familial morbidity of this disease, often combined with other congenital cardiovascular malformations. Some patients have this disease at birth, and the genetics of HLA antigen can be seen in patients with this disease. type. The lesion is mainly composed of cardiac hypertrophy and the weight of the heart is increased. Cardiac hypertrophy can be seen in the ventricular septum and free wall. The former is often asymmetrical (non-concentric) hypertrophy, that is, the left ventricle is common in the ventricular wall with different degrees of hypertrophy, and the right ventricle is rare. The hypertrophy of the interventricular septum is prominent in the left ventricular cavity, and the left ventricular outflow tract obstruction is caused by contraction, which is called "hypertrophic obstructive cardiomyopathy". It is called "the idiopathic hypertrophic aortic subvalvular stenosis". The ventricular septal hypertrophy is mild, and the systolic period does not cause obvious obstruction of the left ventricular outflow tract, which is called "hypertrophic non-obstructive cardiomyopathy". The anterior papillary muscles can also be hypertrophic and often displaced to affect normal valve function. When the myocardium is highly hypertrophied, the left ventricular cavity is reduced. Disproportionate cardiac hypertrophy often results in a ratio of ventricular septal thickness to left ventricular posterior wall thickness 1.3, with a few up to 3.

There is a variant of hypertrophic cardiomyopathy, with cardiac hypertrophy in the apical region. This type of pericardial coronary artery is normal, but the number of coronary arteries in the ventricular wall is increased and the lumen is narrow. Under the microscope, the arrangement of myocardial cells was disordered, the nucleus was abnormal, the branches of the cells were many, the mitochondria increased, the cardiomyocytes were extremely hypertrophied, and the intracellular glycogen content increased. In addition, there was interstitial fibrosis. Under the electron microscope, the arrangement of myofibrils was also disordered. In 2/3 patients, the mitral leaflets increased and a fibrous plaque on the left ventricular wall opposite the anterior mitral valve was caused by mitral valve and ventricular septal impact. The disease can occur at all ages, but the cardiac hypertrophy is more serious in people under 40 years old than those over 40 years old. The cause of this relationship between fatness and age is unknown. With the development of the disease, myocardial fibrosis increased, the ventricular wall hypertrophy decreased, and the degree of cardiac cavity was also reduced, showing a late performance.

an examination

Related inspection

Electrocardiographic angiography selective cardiovascular angiography

The onset is slow. About 1/3 have a family history. Most of the symptoms begin before the age of 30, and both men and women suffer.

The main symptoms are:

1, breathing difficulties, more often after fatigue, is due to decreased left ventricular compliance, increased end-diastolic pressure, followed by elevated pulmonary venous pressure, lungs and blood stasis. The mitral regurgitation associated with ventricular septal hypertrophy can aggravate pulmonary sputum.

2, chest pain, more often after exertion, like angina, but can not be typical, due to increased hypertrophic myocardial aerobics, and relatively insufficient coronary blood supply.

3, fatigue, dizziness and fainting, mostly occur during activities, is due to the increase in heart rate, so that the left ventricular diastolic phase of the original diastolic filling is further shortened, so that the diastolic phase of the left ventricle, which has been poorly filled during diastole, is further shortened. Increased filling is insufficient and cardiac output is reduced. When active or emotional, due to the sympathetic effect, the hypertrophic myocardial contraction is strengthened, the outflow obstruction is aggravated, and the cardiac output is suddenly reduced to cause symptoms.

4, palpitations, due to cardiac dysfunction or arrhythmia.

5, heart failure, more common in advanced patients, due to decreased myocardial compliance, ventricular end-diastolic pressure increased significantly, followed by elevated atrial pressure, and often combined with atrial fibrillation. In advanced patients, myocardial fibrosis is extensive, ventricular systolic function is also weakened, and heart failure and sudden death are prone to occur.

Common signs are:

1. The heart of the voiced voice expands to the left. The apex beats to the left and down, and there is a lifting impulse. Or there is a pacing of the apex, which is the pulsation generated by the atrium to the ventricle with reduced compliance, which is touched before the apex beats.

2, the lower part of the left sternal apex can be seen inside the systolic or late jet murmur, to the apex of the heart but not to the bottom of the heart, may be associated with systolic tremor, seen in patients with ventricular outflow obstruction. Measures to increase myocardial contractility or reduce cardiac load, such as digitalis, isoproterenol (2g/min), isoamyl nitrite, nitroglycerin, Valsalva action, physical labor or premature beats The noise is enhanced. Measures that weaken myocardial contractility or increase cardiac load, such as vasoconstrictors, beta blockers, squats, and clenched palms can alleviate murmurs. About half of the patients can hear the murmur of mitral regurgitation at the same time.

3, the second sound can be abnormally split, due to obstruction of the left ventricle, the aortic valve delayed closure. The third sound is common in patients with mitral regurgitation.

Differential diagnosis

Differential diagnosis

Myocardial infarction: refers to the interruption of coronary blood flow on the basis of coronary artery disease, causing severe and long-lasting acute ischemia in the corresponding myocardium, eventually leading to myocardial ischemic necrosis.

Myocardial hypoxia: The heart is deprived of oxygen due to insufficient blood supply. The main manifestations are: palpitations, heart discomfort, sometimes heart pain or appreciation of colic; shortness of breath, exercise, fullness or agitation is more serious, the body is weak; in severe cases, short-term shock.

Myocardial abscess: Myocardial edema is one of the main clinical symptoms of dilated cardiomyopathy.

Myocardium is gray and relaxed: it is a kind of myocardial damage, which may be related to immune myocardial damage after viral infection, and is generally seen in ultrasound examination of dilated cardiomyopathy. Can be used as a differential diagnosis with other cardiomyopathy.

Myocardial stunning, also known as myocardial dysfunction after ischemia, means that myocardial transient ischemia has not caused myocardial necrosis, but mechanical resilience after reperfusion returns to normal blood flow requires hours, days or weeks. The phenomenon of complete recovery. The onset is slow. About 1/3 have a family history. Most of the symptoms begin before the age of 30. Men and women are equally suffering.

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