Hypertrophy

The healthy human heart accounts for about 0.5% of body weight. Pathological hypertrophy can develop in the left or the right side.

In living patients, cardiac MRI is the best way to determine the weight of the heart. However, although less exact, estimation of hypertrophy by transthoracic echocardiography is much more cost-efficient. In routine practice, you can measure various wall sections in 2D sections, and then use these measurements to estimate total heart muscle mass. The thickness of the normal LV myocardium is less than 10mm. Hypertrophy of more than 20mm is rare, even in pronounced, longstanding arterial hypertension or severe aortic valve stenosis.

Left ventricular hypertrophy, or LVH for short, is a common disorder. In addition to primary hypertrophic cardiomyopathy, it usually occurs secondary to conditions such as long-term pressure and/or volume overload of the left ventricle. Pressure overload with increased afterload occurs in arterial hypertension or aortic valve stenosis, for example, while volume load occurs in disorders such as severe aortic or mitral regurgitation.

Depending on the cause of the hypertrophy, there are certain common additional findings. In hypertensive heart disease, for instance, an enlargement of the left atrium, diastolic dysfunction, and a dilation of the ascending aorta are common.

The wall of the right ventricle is markedly thinner than that of the left ventricle.

Just like the left heart, the right heart hypertrophy develops in response to long-term pressure and / or volume load. The wall of the right ventricle is considered hypertrophic if its thickness is more than 5mm.

Severe tricuspid regurgitation can lead to significant right ventricular volume load. The same is true for an atrial or ventricular septal defect with left right shunt.

The most common cause of right ventricular pressure overload is pulmonary hypertension.

How does the ECG help us to diagnose right and left ventricular hypertrophy?

The ECG is not the means of choice for the diagnosis of myocardial hypertrophy. Nevertheless, we should be aware of, and make use of, all of the information that can be generated through quick, inexpensive and non-invasive tools. The final diagnosis can then be confirmed using echocardiography.

Unfortunately, ECG signs of hypertrophy are not particularly reliable; its sensitivity is less than 50%, although specificity is almost 90%.

What changes occur?

1.) QRS complex

The thickening of the myocardium results in a longer "journey" for the wave of depolarization through the ventricular myocardium. We thus see a higher RS amplitude and a widening of the QRS complex.

2.) Heart axis

In severe hypertrophy, a change in the electrical heart axis may occur.

The electrical heart axis becomes directed towards the hypertrophied ventricle. Therefore left ventricular hypertrophy will lead to left axis deviation, while right ventricular hypertrophy will lead to right axis deviation.

3.) Signs of ischemia

The distribution of the coronary arteries in the myocardium runs from the epicardium inwards. If hypertrophy is severe, the coronary arteries can no longer ensure a sufficient supply of oxygen to the entire width of the wall. Relative ischemia can occur at rest, but is more likely on exertion. Clinically, stress-induced angina pectoris or dyspnea can occur. In severe hypertrophy, this ischemia can even lead to a connective tissue transformation of the heart muscle, that is to myocardial fibrosis. This is not uncommon in patients with hypertrophic cardiomyopathy, where the myocardium thickness can be more than 30mm. Diseases leading to left ventricular hypertrophy often cause diastolic dysfunction, with increased left ventricular filling pressures. Again, the high pressures lead to poorer perfusion of the ventricular myocardium.

In the ECG, ST depressions and negative T waves can occur. Myocardial hypertrophy is, of course, only one differential diagnosis, and it is necessary to think primarily of coronary heart disease when signs of ischemia are detected.

Let’s look briefly now at a simple way of confirming a clinical suspicion of left or right ventricular hypertrophy. All it requires is a quick glance at the ECG. Remember to think of the different ECG leads as cameras, and which sections of the myocardium are being filmed by each lead.

The leads v1 and v2 are located close to the right heart. So, an increased R amplitude in these leads indicates right ventricular hypertrophy.

The leads v5 and v6 are located directly in front of the left heart. So, an increased R amplitude in these leads indicates left ventricular hypertrophy.

For the assessment of the left ventricular myocardium, the amplitude of the R wave in either v5 or v6 (the higher amplitude counts) is added to the amplitude of the S wave in v1. If the sum is greater than 3.5 millivolts, the index is positive. This is suggestive of hypertrophy of the left ventricle.

For the assessment of the right ventricular myocardium, the R wave in v1 and the S wave in v5 are considered. If the sum exceeds 1.05 millivolts, this is suggestive of RVH.

The limits of the Sokolow-Lyon method are manifold, as reflected by its low sensitivity. If the index is positive, however, an explanation must be sought. This means that more diagnostic tests are necessary, starting with transthoracic echocardiography.

One rare phenomenon is paradoxical LVH, which is sometimes seen in cardiac amyloidosis.

Cardiac amyloidosis is a rare disease in which amyloid depositions in the heart muscle lead to wall thickening. In echocardiography, the walls appear massively thickened, with wall thicknesses of more than 20mm. Since the hypertrophy results from amyloid depositions rather than muscle hypertrophy, the ECG shows no signs of hypertrophy. Instead, very low QRS complexes are found. This is therefore called paradoxical LVH.

Myocardial hypertrophy, especially of the left ventricle, is a very common finding in internal medicine. The diagnosis cannot be made using an ECG, and a normal ECG does not exclude it.

BUT: If the Sokolow-Lyon index is positive and this is not explained by a known underlying illness, a structural cardiac disease must be excluded.

When signs of ischemia are present, such as changes in the ST segments or T wave inversion, further diagnostic tests should be carried out.

If LVH remains the only explanation for signs of ischemia after a comprehensive diagnostic work-up, understanding of the concept of relative ischemia secondary to myocardial hypertrophy will be reassuring to physician and patient alike.