ECG-LVH is common in young athletes. Aerobically trained athletes usually will develop increased end diastolic LV volumes while isometrically trained athletes (weight lifters) will develop concentric hypertrophy. Unfortunately, the ECG cannot separate left ventricular dilation from hypertrophy. However, intrinsicoid deflection (time of ascent of the R wave) may be lengthened with hypertrophy. The Goldberg sign (the limb leads are less than 10 mm while the precordial leads are large) appears to be associated with left ventricular dilation. The thinned heart wall does not generate much electromotive energy, but the proximity to the chest wall results in increased voltage in the precordial leads.

The following add to the probability of LVH:

• Sum of the largest S wave in V1-3 and the largest R wave in V4-6 exceeds 35mm
• AVL greater than 11 mm
• Any other limb lead exceeds 15 mm
• Left atrial abnormality
• Left axis deviation
• ST depression ("strain")

Particularly when accompanied by ST depression, ECG-LVH is associated with hypertension, diastolic and systolic LV dysfunction, CHF, stroke and cardiac death. When the ECG-LVH is associated with hypertension that has caused actual LV hypertrophy, treatment of the hypertension can cause regression of the hypertrophy and normalization of the ECG. ECG-LVH is an important part of the Framingham risk equation (along with age, cholesterol, BP, gender, diabetes, and smoking) which accurately predicts future cardiac events. In patients with aortic stenosis, the gradient is usually not significant if LVH is not present.

The Cornell-Framingham left ventricular mass equation: The Cornell ECG voltage, defined as the sum of voltages for the R wave of lead AVL and S wave of lead V3, has been shown to correlate strongly with echocardiographically estimated left ventricular mass. Because the magnitude of this voltage varies with both age and obesity, an adjustment formula was estimated from the Framingham Heart Study cohort who were free of myocardial infarction and who had both an ECG and an echocardiogram recorded during the same clinic examination.

Clinical correlation is necessary beginning with BP measurement, physical exam for cardiac size and murmurs and medical history particularly for symptoms of aortic valve disease (angina, syncope) and CHF. If this suggests aortic stenosis, an echocardiogram is indicated. In patients without known heart disease, a lipid panel should be obtained so that the Framingham point system can be used to predict the risk of cardiac events. If the BP is elevated, therapy should be begun with diuretics, then a beta-blocker added if the blood pressure does not normalize. If there is a history of CHF or an abnormal cardiac exam then an echocardiogram is indicated. If systolic dysfunction is demonstrated, an ACE inhibitor should be given to lessen the possibility of CHF exacerbation and other complications including death and stroke. ACE inhibitors can cause a cough, hyperkalemia and renal dysfunction requiring a switch to a long acting nitrate and hydralazine.