Left ventricular hypertrophy

Generally speaking, if we don’t go to the hospital for a check-up, we won’t know our physical condition. Especially myocardial hypertrophy. Without professional equipment and professional knowledge, we will not know whether our myocardium has hypertrophy. Even if we don't know, we can judge through some symptoms. For example, difficulty breathing, dizziness, fatigue and palpitations.

This is a slower but more effective compensatory function that mainly occurs when there is long-term excessive pressure load. The total myocardial volume increases and the contractility strengthens, allowing the heart to maintain normal blood circulation while having considerable reserve capacity. However, this compensatory function also has its disadvantages, mainly because the hypertrophic myocardium requires increased oxygen, but the blood supply of the coronary arteries is often unable to meet it, causing myocardial ischemia, which will ultimately lead to a decrease in myocardial contractility.

Clinical symptoms

1. Dyspnea often occurs after exertion. It is caused by decreased left ventricular compliance, increased end-diastolic pressure, and subsequent increased pulmonary venous pressure, resulting in pulmonary congestion. Mitral regurgitation associated with ventricular septal hypertrophy can aggravate pulmonary congestion.

2. Chest pain, which often occurs after fatigue, is similar to angina pectoris, but may be atypical. It is caused by increased oxygen demand of the hypertrophic myocardium and relatively insufficient blood supply to the coronary arteries.

3. Fatigue, dizziness and fainting mostly occur during activities. They are due to the accelerated heart rate, which further shortens the diastolic period of the left ventricle, which already has poor diastolic filling, aggravating the insufficient filling and reducing cardiac output. When active or emotionally excited, the sympathetic nerves act to increase the contraction of the hypertrophic myocardium, aggravate outflow tract obstruction, and cause a sudden drop in cardiac output, resulting in symptoms.

4. Palpitations are caused by decreased heart function or arrhythmia.

5. Heart failure is more common in late-stage patients. Due to decreased myocardial compliance, the ventricular end-diastolic pressure increases significantly, followed by increased atrial pressure, and is often accompanied by atrial fibrillation. In late-stage patients, myocardial fibrosis is extensive and ventricular contractile function is weakened, making them prone to heart failure and sudden death.

Clinical signs

1. The boundary of cardiac dullness expands to the left. The apex beat is displaced to the lower left, with a lifting impulse. Or there may be an apical doublet, a beat produced when the atria eject blood into the less compliant ventricles and is touched before the apical beat.

2. A mid-systolic or late-systolic ejection murmur can be heard on the inner side of the apex at the lower left edge of the sternum. It propagates toward the apex rather than the base of the heart and may be accompanied by systolic tremor. It is seen in patients with ventricular outflow tract obstruction. Any measures that increase myocardial contractility or reduce cardiac load, such as administration of digitalis, isoproterenol (2 μg/min), amyl nitrite, nitroglycerin, Valsalva maneuver, after physical labor or premature beats, can intensify the murmur. Any measures that weaken myocardial contractility or increase cardiac workload, such as vasoconstrictors, beta-blockers, squatting, and clenching the palms, can reduce the murmur. In about half of patients, a murmur of mitral regurgitation can also be heard.

3. The second sound may be abnormally split, which is caused by obstruction of left ventricular blood ejection and delayed closure of the aortic valve. The third tone is common in patients with mitral regurgitation.