Assessment of Ventricular Hypertrophies from an ECG
Essentials
Ventricular hypertrophy refers to the thickening of the ventricular wall: left ventricle > 12 mm, right ventricle > 5 mm.
Hypertension is the main cause of left ventricular hypertrophy (LVH), and LVH is an independent risk factor for coronary heart disease. The target blood pressure for patients with LVH is less than 130/80 mmHg.
Right ventricular hypertrophy (RVH) indicates severe heart or lung disease and is usually not encountered in asymptomatic patients.
Accurate diagnosis of ventricular hypertrophy, or its exclusion, is possible with echocardiography Echocardiography as an Outpatient Procedure or, in special cases, with magnetic imaging.
General remarks
Ventricular hypertrophy may be
eccentric, where also the volume and outer dimension of the ventricle are increased
concentric, where the wall thickness ”grows inwards”, i.e. the outer dimension of the ventricle does not increase
asymmetric, where the wall thickness is increased only at certain sites (septum, apex).
Ventricular hypertrophy can occur
secondary to any heart disease that exposes the ventricle to either pressure or volume overload
as a primary condition, due to idiopathic cardiomyopathy.
Ventricular hypertrophy may be reversible if the causative condition improves or the overload is significantly reduced.
ECG changes
The ECG criteria for ventricular hypertrophy (in order of appearance)
The most important change: an increase in the QRS amplitude (voltage criterion)
Shift in the frontal plane QRS axis either to the left or right
QRS widening
Changes associated with abnormal repolarisation (ST depression and/or T wave inversion [= strain pattern])
Signs of increased atrial pressure
The QRS amplitude on an ECG recording correlates with the myocardial mass, the sex and ethnic background of the patient and the ”insulating layer” surrounding the heart.
The ECG amplitude is lowered by myocardial damage, obesity, emphysema, pericardial fluid, hypothyroidism and the female gender.
Correspondingly the amplitude may be increased by intense exercise, the male gender, advanced age and a thin subcutaneous tissue layer.
The ECG strain pattern (ST segment depression and asymmetric T wave inversion) does not result from the increased muscle mass but from its slow relaxation. This in turn indicates impaired myocardial function and a worsened prognosis.
Left ventricular hypertrophy
LVH = left ventricular hypertrophy
Causes of LVH
Hypertension (the most important and common cause!)
Significant aortic stenosis
Significant mitral regurgitation
Hypertrophic cardiomyopathy (the thickening affects the entire left ventricle)
Hypertrophic septal cardiomyopathy (the thickening involves the interventricular septum - in the obstructive form the thickening hinders blood flow within the left ventricular outflow tract)
As a result of long-term training at high intensities for competitive sports (part of the athletic heart syndrome)
ECG changes in LVH
The characteristic ECG change in LVH is an increase in the R wave amplitude in the leads that reflect the left ventricle (I, aVL, V5-V6).
The limb lead changes (I, aVL) are more specific.
The chest lead changes (V5-V6) are more sensitive.
The sensitivity and specificity can be improved by comparing the changes in the different leads.
LVH is likely (Sokolow-Lyon criteria), if SV1 + RV5 or V6 ≥ 3.5 mV (over 35 mm)
Other ECG criteria for LVH
Cornell product ("voltage-duration product")
Men (RaVL + SV3) × QRS duration > 2.44 mm × s
Women (RaVL + SV3 + 6 mm) × QRS duration > 2.44 mm × s
Hypertension-induced LVH is a sign of end-organ damage indicating that the drug therapy needs to be intensified to achieve the target blood pressure (under 130/80 mmHg, 3-4 antihypertensive drugs will be needed).
If a heart murmur is heard, a referral to a specialist is indicated (valvular defect, hypertrophic obstructive cardiomyopathy).
The development of LVH worsens the prognosis of a hypertensive patient.
LVH is an independent and high risk factor for coronary heart disease.
LVH diagnosed through ECG changes signifies a 6-8 fold increase in the risk of coronary heart disease or sudden death. A downward ST-T change (”strain”) doubles the risk further.
The thickening of the left ventricle may cause ischaemia even in the absence of an atherosclerotic disease and thus increase the risk of sudden death.
In LVH, the duration of QRS complex has prognostic significance: QRS > 0.1 second increases mortality from a cardiovascular disease as well as the incidence of heart failure.
Regression of the hypertrophic changes is a sign of good management of hypertension and is thought to improve the prognosis of a hypertensive patient. Hypertrophic changes will also regress after successful surgery to correct a faulty aortic or mitral valve.
An echocardiography should be considered at an early stage if LVH is suspected or target blood pressure is not achieved, even if no ECG changes suggestive of LVH were evident as the sensitivity of ECG criteria is not particularly good.
Should LBBB develop, echocardiography should be carried out in order to confirm the possible existence of an underlying disease Bundle Branch Blocks in an ECG or LVH.
Secondary pulmonary hypertension caused by malfunction of the left-sided valves
Congenital heart defects
ECG changes in RVH
The characteristic ECG change in RVH is an increase in the R wave amplitude in the leads that reflect the right ventricle (V1-V2) as well as right axis deviation.
The changes in the right-sided leads are fairly specific but have poor sensitivity.
Sensitivity will improve if the changes in limb leads are also considered, but this will compromise specificity.
RVH is probable if one or more of the following ECG criteria is present:
QRS axis > +100 (in the absence of RBBB); QRS negative in lead I
R/S > 1 in lead V1 (and V2) (no RBBB)
R/S < 1 in leads V5-V6 (in the absence of LAHB and anterior MI)
Additional RVH criteria
right atrial strain ("P pulmonale")
ST-T strain in V1-V2
Incomplete, or sometimes complete, RBBB.
Note
RVH is probable if the patient has, or is suspected to have, a disease capable of leading to RVH.
RVH is not always evident in an ECG due to the greater, more dominating muscle mass of the left ventricle.
Even though emphysema can lead to RVH it reduces sensitivity by lowering QRS amplitudes.
RBBB is often an innocent finding but it can mask an underlying RVH.
An acute extensive pulmonary embolism will temporarily strain the right ventricle but will not cause permanent ECG changes.
Echocardiography is the most reliable way to estimate right-sided strain.
Acute RVH in association with pulmonary embolism
Incomplete RBBB
Septal Q waves in V1-V4 resembling anterior injury
Septal T wave inversion in V1-V4
Right axis deviation (increased S wave in lead I)
Anterior ST segment depression (V1-V4) and/or inferior ST elevation mimicking inferoposterior myocardial injury
Remember: pulmonary embolism does not cause reliable ECG changes (often no ECG abnormalities at all)!
Clinical significance of RVH
RVH indicates severe heart or lung disease and is usually not encountered in asymptomatic patients; investigations and treatment need specialist intervention.
RVH may cause symptoms of right heart failure, including dyspnoea, reduced exercise capacity, ascites and peripheral oedema.
Pulmonary embolism must be suspected from clinical evidence Pulmonary Embolism; it cannot be excluded with a normal ECG.
References
Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990 May 31;322(22):1561-6. [PubMed]
Dahlöf B, Devereux RB, Kjeldsen SE et al; LIFE Study Group. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 2002 Mar 23;359(9311):995-1003. [PubMed]