Enlargement of the left ventricle itself does not result in signs and symptoms. The underlying pathological causes of LVH, such as hypertension, heart murmurs, and gallops, do present with signs and symptoms on physical exam.
Five major ECG findings that indicate LVH:
The myocardial fibers amplify the voltage generated in LVH. In the horizontal plane, there is an increased amplitude of the positive R wave forces recorded on the left precordial leads (V2 to V6). An increase in the negative force of the S waves is noted over the right precordial leads (V1).
In the frontal plane, the amplitude of the R waves in limb leads I and aVL is also increased with a horizontal or leftward QRS axis.
LVH is associated with a widening of the QRS complex. This change may be associated with an incomplete left bundle branch block (iLBBB).
Most patients with LBBB present with LVH. Some causes of LVH, such as calcification or fibrosis of the proximal ventricular conduction system near the valve ring in calcific aortic stenosis, lead to LBBB.
An ÅQRSF of −30° to ±150° is a common finding in patients with left ventricular hypertrophy.
LVH with a normal or rightward QRS axis may also be seen in young adults or patients with biventricular hypertrophy.
ST depression and T wave inversion are commonly seen in patients with LVH, particularly in the limb and precordial leads where tall R waves are the typical ECG findings. Some interpreters refer to this morphology as left ventricular strain pattern, but it is more correctly termed as left ventricular hypertrophy with associated ST-T wave abnormalities.
These ECG changes may be caused by altered repolarization of the hypertrophied left ventricular myocardium or related to subendocardial ischemia.
Prominent positive T waves in the lateral chest leads may represent LVH with a volume load state secondary to mitral or aortic regurgitation.
Studies involving hypertensive patients with LVH have shown that 15% of patients who have ST-T wave changes with the strain pattern are likely to have coronary heart disease and larger left ventricular mass. In patients without any coronary heart disease, the magnitude of ST depression is positively correlated with increasing left ventricular mass and prevalence of LVH.4
LVH with ST-T wave changes in patients with valvular aortic stenosis presents with more severe hypertrophy, fibrosis, and aortic stenosis.5
Patients with concomitant left atrial abnormality with LVH have an increased duration of the P wave (0.12 seconds or more) in the limb leads and/or biphasic P waves with a prominent negative terminal component in V1 (Chapter 5). These subtle findings are important as they give a major clue to severe mitral regurgitation or dilated cardiomyopathies.
Broad P waves are indicative of intra-atrial conduction delays. The presence of these atrial abnormalities aid in the detection of LVH in cases of concomitant LBBB.
4 Okin PM, Devereux RB, Nieminen MS, et al. Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study. J Am Coll Cardiol. 2001;38(2):514–520.
5 Shah ASV, Chin CWL, Vassiliou V, et al. Left ventricular hypertrophy with strain and aortic stenosis. Circulation. 2014;130(18):1607–1616.
https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.114.011085