What Are the Different Types of Hypertrophy?

Why does an enlarged heart turn to failure? This is a problem that has been discussed and studied for a long time. Currently, compensatory myocardial hypertrophy is considered to be an imbalanced growth form. This kind of imbalanced growth, which has its characteristic manifestations at different levels of organs, tissues, cells, and molecules, is the basis for the turning insufficiency of hypertrophic myocardium.

Cardiac hypertrophy

Myocardial hypertrophy is a powerful form of compensation, but it is not infinite. If the cause cannot be eliminated for a long time, the function of the hypertrophic myocardium cannot remain normal for a long time and eventually turn to heart failure. Chronic heart failure generally develops on the basis of myocardial compensatory hypertrophy.

Myocardial hypertrophy symptoms

Myocardial Hypertrophy (I) Characteristics at the Organ Level

From the perspective of the entire heart, imbalanced growth manifests as an increase in the weight of the heart over the growth of axons of sympathetic neurons that dominate the heart, so the density of sympathetic nerve distribution in the heart is significantly lower than normal. Moreover, the catecholamine synthesis in the hypertrophic myocardium is reduced and the consumption is increased, so the norepinephrine content in the heart is significantly reduced. Such changes in innervation and transmitter content will promote myocardial excitation-contraction coupling disorders, leading to myocardium Reduced contractility.

Myocardial Hypertrophy (II) Characteristics at the Tissue Level

The growth of arterioles and capillaries in the myocardium obviously lags behind the growth of the volume of cardiomyocytes, so the number of capillaries of hypertrophic myocardium per unit weight decreases. Biomass studies of the myocardial microcirculation of mammals show that at rest, normal animal myocardium has approximately 2,300 open capillaries per 1 mm3, and the average spacing of capillaries is 16.8 m. When the heart load is increased or hypoxia, The anterior sphincter of capillaries is relaxed, and about 2,100 capillaries that were originally in reserve are also open. In this way, the total number of functional hair cell tubes can reach 4.400 pieces / mm3, and the capillary spacing is reduced to 5.5 m. Therefore, the increased myocardial oxygen demand due to the increased load is quickly satisfied by the acceleration of the original transportation. However, during myocardial hypertrophy, because the total number of capillaries is relatively reduced, the diffusion interval of oxygen is increased, so myocardial hypoxia. In such patients, most of the reserve capillaries are already open, so when the load increases, the number of functional capillaries can no longer increase significantly, and the diffusion interval of oxygen cannot be significantly reduced. Therefore, the hypertrophic myocardium is often in a state of hypoxia when the load increases, resulting in weakened aerobic metabolism, insufficient energy generation, and reduced myocardial contractility.

Regarding whether the hypertrophic myocardium is hypoxic, there have been different opinions, because some people have measured the coronary arterial and venous blood oxygen content per unit weight of the hypertrophic myocardium, and the results are not significantly different from normal myocardial conditions, indicating that No hypoxia.

Myocardial hypertrophy (three) cell level characteristics

It appears that the increase in cell volume and weight is greater than the increase in its surface area, that is, the ratio of the surface area to the weight of the hypertrophic myocardium is significantly reduced. The membrane on the cell surface (sarcoplasmic membrane) is exactly the part that Na + -K + and Na + -Ca2 + must pass through. Therefore, the relative reduction of the cell area can weaken the cell's ability to transport ions, including the relatively inadequate Ca2 + influx, thereby reducing the function of myocardial cells. Electron microscope observations in recent years have also confirmed that the ratio of the number of mitochondria to the volume of cardiomyocytes in hypertrophic myocardium is reduced, and the ratio of mitochondrial membrane surface area to the weight of myocardial fibers is also significantly reduced, so the biological oxidation in hypertrophic myocardium is relatively weakened. This is also one of the reasons for insufficient energy production in hypertrophic myocardium.

Myocardial hypertrophy (IV) at the molecular level

The ratio of the heavy segment (head) and light segment (tail) of the myosin molecule is reduced, that is, the proportion of the head in the entire molecule is reduced. The head is exactly where the ATPase is located, and a decrease in the specific gravity of the head can reduce the ATPase activity accordingly. In addition, ATPase is activated by Ca2 +. In heart failure, because Ca2 + is slowly transported to the myosin bridge, the ATPase activity can be further reduced. In vitro experiments show that the activity of ATPase in depleted myocardium is reduced by about 20-30%. Decreased ATPase activity impairs myocardial energy utilization, thereby reducing myocardial contractility.

Prevention and treatment of myocardial hypertrophy

Patients with myocardial hypertrophy should pay attention to avoid overwork and prevent excessive stress. Beta blockers and propranolol can reduce myocardial contractility, reduce left ventricular outflow tract obstruction, improve left ventricular wall compliance and left ventricular filling. With anti-arrhythmic effect. Dosage: 10mg orally 3 times a day. It can be gradually increased up to 480mg / day. Can also be used calcium channel blockers, verapamil 40mg orally 3 times a day, nifedipine 10mg, orally, 3 times a day. Can improve ventricular diastolic function, should pay attention to observe blood pressure to prevent blood drops too low. ^[1]