What Is Left Ventricular Hypertrophy?

Compared to the right ventricle, the shape of the left ventricle is longer and more like a cone. Its cross section also presents an oval or nearly circular outline. The thoracocostal plane, the front of the heart, is mainly composed of the right ventricle, and a small part is composed of the left ventricle. However, the left ventricle not only forms the apex of the heart, but also forms the majority of the septum of the heart, which is the side where the organ is in contact with the diaphragm. To pump blood with a high blood pressure, the muscles of the left ventricle are thicker and more developed than the right ventricle.

Left ventricular hypertrophy

Overview of left ventricular hypertrophy

The left ventricle receives oxygenated blood from the left atrium and pumps it into the aorta to supply the oxygenated blood to the body. During this journey, oxygenated blood passes through two valves, one is the mitral valve located between the left atrium and the left ventricle, and the other is the aortic valve located in the aorta, both of which are used to prevent blood from flowing backwards.

Left ventricular hypertrophy

Beginning in adolescents, the muscle wall of the left ventricle becomes thicker, making it three to six times thicker than the right ventricle. This also reflects that the left ventricle creates five times more pressure during the pumping process than the right. In each heartbeat, the left ventricle receives blood from the pulmonary veins at approximately 80 Torr (equivalent to a pressure close to 11 kPa), and then raises the blood pressure to approximately 120 Torr (equivalent to 16.3 kPa) to send it in. Aorta. (All pressure values are measured while the heart is at rest, and are relative values relative to the surrounding atmospheric pressure, which is set to a reference pressure of zero).

In a normal heart, the muscles of the left ventricle must be relaxed immediately after each contraction to allow oxygenated blood from the pulmonary veins to fill quickly, which is the relaxation and filling of the diastole. The rapid and intense contraction pushes a large amount of blood into the aorta, overcomes the very high aortic pressure and provides additional pressure to extend the aorta and other major arteries and provide sufficient space for sudden rise in blood volume, which is the systolic Shrink and efflux. Under the control of the central system, its pumping capacity is rapidly increased or decreased. A normal adult heart can pump approximately five liters of blood per minute while resting. The maximum output can be increased from about 25 liters per minute for non-athletes to about 45 liters per minute for athletes reaching Olympic level.

Clinical significance of left ventricular hypertrophy

Left ventricular hypertrophy is not a disease in itself, but it is often a precursor to heart disease. Left ventricular hypertrophy can be a natural response of the myocardium to aerobic exercise and strength training, and it can also be a pathological response to cardiovascular disease and hypertension, but it can also be caused by increased heart load or myocardial disease. There are many causes of cardiac hypertrophy, including hypertensive left ventricular hypertrophy, congestive heart failure, anterior cardiac infarction, athlete's heart, mitral regurgitation, aortic stenosis, proliferative obstructive cardiomyopathy, pulmonary hypertension, and cardiopulmonary disease , Dilated cardiomyopathy, endocarditis, pericardial effusion, left ventricular aneurysm, mitral stenosis and so on.

Clinically common in the following diseases:

1. Rheumatic mitral regurgitation

Rheumatic mitral valve insufficiency is rare and clinically associated with rheumatic mitral stenosis. On auscultation, the apex of the heart can be heard with systolic breeze-like noise of grade 2/6 and above, which is rough and the first heart sound can be masked.

2. Aortic valve insufficiency

Causes of aortic valve insufficiency include rheumatism and syphilis. The former is younger, most often between the ages of 10 and 40, with a history of rheumatic fever, a longer period of cardiac function compensation, and more often with mitral or aortic stenosis; the latter is usually 34-50 years old , Previous history of sexually transmitted diseases, often with angina pectoris.

Aortic stenosis

More common in men, symptoms appear late, syncope and angina pectoris are the prominent symptoms in the later stage, syncope may lead to sudden death.

4. Hypertensive heart disease

The patient had a long history of hypertension and her heart expanded to the lower left. The second sound of the aortic valve area is enhanced, and systolic murmurs can be heard at the apex due to relative mitral regurgitation.

5. Coronary atherosclerotic heart disease (coronary heart disease)

Presented as angina pectoris, myocardial infarction, but also as arrhythmia, heart failure, without any clinical symptoms, or sudden death at the first onset.

6, the arterial duct is not closed

When the arterial duct is not closed, a continuous noise is produced. The noise is bright.

7.Aortic constriction

The narrowing of the aorta narrows the aortic cavity. Its clinical feature is that the lower limb blood pressure is significantly lower than the upper limb, and the upper limb blood pressure, especially the systolic blood pressure, is significantly higher than normal blood pressure. Patients often experience lower limb fatigue, coldness, and numbness.

8. Tricuspid atresia with atrial septal defect

Patients often have severe cyanosis, clubbing fingers (toes), and squatting positions. Hypoxic attacks are also common.

9, heart disease caused by nodular polyarteritis

Presented as angina pectoris or myocardial infarction, similar to coronary heart disease. If the lesion affects the kidney, it can cause high blood pressure, which can increase the degree of heart damage.

x Left ventricular hypertrophy x-ray manifestations

The apex extends downward to the left.

The opposite beat point moves up.

The left heart segment is extended, rounded and expanded to the left.

The left ventricle overlaps with the spine.

In the left position, the posterior cardiac space narrows or even disappears, and the anterior esophageal space at the posterior margin of the heart disappears.

ECG manifestations of left ventricular hypertrophy

The position of the normal left ventricle is located at the left rear of the heart, and the left ventricle wall is significantly thicker than the right ventricle. Therefore, the normal ventricular depolarization comprehensive vector shows the characteristics of the dominant left ventricle. When left ventricular hypertrophy, the situation of left ventricular advantage can be made more prominent, and the following changes on the electrocardiogram can appear:

1. Increased QRS complex voltage: chest lead Rv5 or Rv6> 2, 5mV; Rv5 + Sv1> 4, 0mV (male) or> 3, 5Mv (female). In limb leads, R1> 1, 5Mv; RaVL> 1,2Mv; RaVF> 2, 0Mv; RI + SIII> 2, 5Mv.

In recent years, some scholars have established Cornell voltage standards: RaVL + Sv3> 2, 8mV (male) or 2,0V (female). The standard is reported to increase the sensitivity to detect left ventricular hypertrophy and improve the accuracy of ECG diagnosis.

2. The left side of the frontal ECG axis may appear.

3. The QRS complex time is extended to 0, 10 ~ 0, 11s, but generally <0, 12s.

4. In the R wave-based lead, the ST segment is down-slope down to more than 0,05mV, and the T wave is flat, bidirectional or inverted. In the S wave-based lead (such as V1 lead), the upright T wave can be seen instead. When the QRS complex voltage increases and is accompanied by changes in ST-T, left ventricular hypertrophy is associated with strain.

A diagnosis of left ventricular hypertrophy can generally be established on the basis of meeting one or more of the QRS voltage increase criteria, combined with one of the other positive indicators. The more conditions are met, the greater the diagnostic reliability. If only the QRS voltage is increased, and no other person has any positive indicators, the diagnosis of left ventricular hypertrophy should be cautious.

Left ventricular hypertrophy treatment

Left ventricular hypertrophy is divided into primary and secondary. Primary refers to hypertrophic cardiomyopathy. Drug treatment includes Beta receptor blockers and calcium channel blockers. Chemical ablation can achieve better results. Secondary is mainly secondary to hypertension, valvular disease, etc., mainly to treat the primary disease.

Left ventricular hypertrophy is generally compensatory hypertrophy of the heart caused by hypertension. Failure to actively treat blood pressure may eventually lead to heart failure. Treatment should actively control hypertension. Have a low-salt, low-fat diet in your life and take antihypertensive drugs. Blood lipids need to be taken if the diet is not well controlled.

Always pay attention, do not work quickly, be stable, the choice of antihypertensive drugs should be based on the principle of individualization, according to the patient's age, blood biochemical changes, target organ damage, blood pressure and its complications and other factors to choose medication.

1. Among those with no target organ damage in hypertension, young patients are mostly sympathetic, such as hyperdynamic type, increased cardiac output, large pulse pressure, large blood pressure fluctuations, and tachycardia. -blockers should be preferred. Elderly patients should choose ACEI or calcium antagonists or angiotensin II receptor antagonists because of increased topical vascular resistance;

2. People with hyperlipidemia, diabetes and gout should not use beta blockers and thiazide diuretics;

3. For patients with left ventricular hypertrophy and angina pectoris, -blockers and calcium antagonists can be selected;

4. Patients with heart failure associated with hypertension and heart disease should choose ACEI or angiotensin II receptor antagonist or diuretics;

5, combined arrhythmia including pre-ventricular contraction, supraventricular tachyarrhythmia should choose blockers or verapamil;

6. Patients with renal insufficiency should choose diuretics or calcium antagonists. When serum creatinine <3mg / dl, ACEI or angiotensin II receptor antagonists can be selected;

7, patients with cerebral infarction should choose calcium antagonists or ACEI or angiotensin II receptor antagonists.