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Left ventricular hypertrophy: Clinical findings and ECG diagnosis

Left ventricular hypertrophy: Clinical findings and ECG diagnosis
Literature review current through: Aug 2023.
This topic last updated: Nov 03, 2022.

INTRODUCTION — Left ventricular hypertrophy (LVH) refers to an increase in the size of myocardial fibers in the main cardiac pumping chamber. Such hypertrophy is usually the response to a chronic pressure or volume load.

The two most common pressure overload states are systemic hypertension and aortic stenosis.

The major conditions associated with LV volume overload are aortic or mitral valve regurgitation and dilated cardiomyopathy.

Other causes of LVH include ventricular septal defects, hypertrophic cardiomyopathy, and physiologic changes associated with intense athletic training. (See 'Causes' below.)

The electrocardiogram (ECG) is a useful but imperfect tool for detecting LVH. The utility of the ECG relates to its being relatively inexpensive and widely available. The limitations of the ECG relate to its moderate sensitivity or specificity depending upon which of the many proposed sets of diagnostic criteria are applied [1,2]. Therefore, because of these ECG limitations, LVH is most reliably identified on imaging with either echocardiography or cardiac magnetic resonance imaging. (See 'Electrocardiographic findings: General' below and 'Imaging findings' below.)

This topic will provide a broad overview of LVH, including associated conditions, with a primary focus on ECG findings.

DEFINITION — LVH, defined as an increase in the mass of the LV, can be secondary to an increase in wall thickness, an increase in cavity size, or both. LVH usually presents with an increase in wall thickness, with or without an increase in cavity size, but presentations can vary depending upon the underlying pathology. For the most common causes of LVH (hypertension or aortic stenosis), the increase in mass results from a chronic increase in afterload of the LV, although there may also be a genetic component. A significant increase in the number and/or size of sarcomeres within each myocardial cell is the pathologic mechanism.

The estimation of LV mass is commonly derived from LV measurements obtained by 2D echocardiography. The American Society of Echocardiography, with the European Association of Echocardiography, has issued the following criteria for LVH using wall thickness and cavity dimensions [3]:

Estimated LV mass of 201 to 227 g (103 to 116 g/m2) for males and 151 to 171 g (89 to 100 g/m2) for females is mildly abnormal.

Estimated LV mass of 228 to 254 g (117 to 130 g/m2) for males and 172 to 193 g (101 to 112 g/m2) for females is moderately abnormal.

Estimated LV mass >254 g (>130 g/m2) for males and >193 g (>112 g/m2) for females is severely abnormal.

EPIDEMIOLOGY — LVH is a relatively uncommon ECG finding in unscreened general populations. LVH was reported in approximately 15 percent of the original Framingham Heart Study participants but in only 5.2 percent of those in the more contemporary Atherosclerosis Risk in Communities (ARIC) study [4]. Not unexpectedly (using the ARIC findings as a benchmark) the prevalence of LVH by ECG is higher in populations with high blood pressure, reported in 7.4 percent of hypertensive patients in the SPRINT trial and 13.9 percent of hypertensive patients in an Italian cohort [5,6]. While the ECG finding of LVH is associated with worse long-term outcomes, LVH regression following treatment is associated with improved outcomes. (See 'Treatment and follow-up' below.)

CAUSES — LVH is caused by long-term pressure or volume overload states or by combinations of pressure and volume overload (eg, aortic stenosis and regurgitation). Examples of pathologic conditions that can result in LVH include but are not limited to:

Systemic hypertension

Aortic stenosis (valvular, supravalvular, or subvalvular)

Aortic regurgitation

Mitral regurgitation

Dilated cardiomyopathy

Hypertrophic cardiomyopathy

Ventricular septal defect

Some infiltrative cardiac processes (eg, Fabry disease, Danon disease)

Additionally, some infiltrative cardiac processes can lead to increased LV wall thickness without associated LVH on the ECG:

Amyloidosis

Sarcoidosis

Hemochromatosis

CLINICAL FINDINGS AND EVALUATION

Symptoms and physical examination — LVH is a marker of the pathophysiologic response of the myocardium to the stimulus of chronic pressure overload, chronic volume overload, or both. As such, there are no signs or symptoms that result from LVH itself, but rather signs and symptoms related to the underlying pathologic cause of LVH (eg, elevated blood pressure, abnormal heart sounds including gallops and murmurs, etc).

Electrocardiographic findings: General — LVH and related changes can produce five major ECG findings: increased QRS voltage, increased QRS duration, left axis deviation, repolarization (ST-T) changes, and left atrial abnormality [1,7]. However, in some cases, diagnostic changes are not seen, and in others, false positives appear. Thus, clinicians should distinguish between ECG diagnosis of LVH or its absence and anatomic/imaging evidence. (See 'Electrocardiographic criteria for diagnosing LVH' below.)

Increased QRS voltage – An increase in LV mass may augment the amplitude of voltage generated by myocardial fibers. This effect will, in turn, increase the amplitude of positive forces (R waves) recorded over the left chest leads and negative forces (S waves) recorded over the right chest leads. LVH will also increase the amplitude of R waves in those limb leads that record the projection of these positive forces (typically I and aVL with a horizontal or leftward QRS axis) (waveform 1). However, the sensitivity of voltage criteria in adults is only modest. (See 'Electrocardiographic criteria for diagnosing LVH' below.)

Increased QRS duration – An increase in LV mass is often associated with widening of the QRS duration. This change is usually subtle or may be associated with incomplete, or rarely complete, left bundle branch block (LBBB). On the other hand, most patients with LBBB have underlying LVH. In addition, some causes of LVH can lead to LBBB by other mechanisms such as calcification or fibrosis of the proximal ventricular conduction system, which lies close to the valve ring, in calcific aortic stenosis.

Left axis deviation – LVH is usually associated with a horizontal or frankly leftward (≥-30º) QRS axis in the frontal plane leads. However, LVH may occur with any QRS axis (normal/vertical or even rightward axis), especially in young adults or patients with biventricular hypertrophy. (See "Left anterior fascicular block".)

Repolarization abnormalities – LVH, especially due to a severe, chronic pressure load (eg, pronounced and sustained systolic hypertension or severe aortic stenosis), is often associated with ST depressions and T wave inversions in leads with relatively tall R waves (waveform 2). This pattern, formerly referred to as LV "strain" (but best termed "LVH with associated ST-T wave abnormalities"), may be due to primary alteration in repolarization of hypertrophied muscle or to relative subendocardial ischemia. By comparison, LVH with a volume load state, particularly due to mitral or aortic regurgitation, is sometimes associated with prominent positive T waves in the lateral chest leads. However, the classic distinction between "systolic" (ie, pressure overload) and "diastolic" (ie, volume overload) variants of hypertrophy is not reliable, and most references using this terminology are from the early literature on this subject [8].

In a review of 886 hypertensive patients with LVH, ST-T wave changes consistent with "strain" were present in 15 percent, were more common in those with coronary heart disease (29 versus 11 percent without coronary disease), and were associated with a greater LV mass [9]. In another report of patients without evidence of coronary disease, increasing magnitude of ST depression correlated with increasing LV mass and with increasing prevalence of LVH [10]. In the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, the presence of repolarization abnormalities with LVH voltage criteria increased the five-year risk of chronic heart failure (HF) by more than threefold and the risk of HF-related mortality by more than fourfold [9]. Furthermore, the appearance of repolarization abnormalities during the first year of follow-up was associated with a three- to fivefold increase in adverse clinical events. LVH with ST-T changes in patients with valvular aortic stenosis was also associated with more severe hypertrophy with fibrosis by magnetic resonance imaging and with more severe aortic stenosis [11].

Left atrial abnormality – Most patients with LVH develop abnormalities in left atrial depolarization due to conduction delay or actual atrial enlargement. The two major markers of left atrial abnormality are increased duration of P waves (≥120 milliseconds) in the limb leads and/or biphasic P waves with a prominent negative (terminal) component (≥40 milliseconds in duration and/or ≥1 mV in depth) in V1. Biphasic P waves with a very prolonged but low amplitude negative component may be a subtle but important clue to major abnormalities such as severe mitral regurgitation or dilated cardiomyopathy. This finding of a very broad P wave may indicate an intra-atrial conduction delay. The presence of a left atrial abnormality may be particularly helpful for electrocardiographically detecting LVH in the setting of an LBBB [12].

ELECTROCARDIOGRAPHIC CRITERIA FOR DIAGNOSING LVH — The ECG diagnosis of LVH is quite reliable when very prominent voltage is seen in conjunction with left atrial and ST-T abnormalities, leftward axis, or widening of the QRS. Generally, however, only some of the many ECG findings will be present. Several different ECG criteria for the diagnosis of LVH have been developed. Given the intrinsic limitations of the ECG and the many extracardiac factors that affect QRS voltage (eg, body habitus, pulmonary status, age, etc), most of the ECG criteria are insensitive but fairly specific for LVH in middle-aged or older adults [7].

Commonly used ECG criteria for diagnosing LVH include the follow:

Sokolow-Lyon criteria — For the Sokolow-Lyon criteria, LVH is diagnosed if either of the two criteria is satisfied:

Sum of S wave in V1 and R wave in V5 or V6 ≥3.5 mV (35 mm)

OR

R wave in aVL ≥1.1 mV (11 mm; or sometimes ≥1.3 mV [13 mm] is used primarily in the setting of concurrent left anterior fascicular block)

Romhilt-Estes point score system — This index gives different weights to specific findings (table 1). A score of 5 or more indicates "definite" LVH; a score of 4 indicates "probable" LVH. The upper limits of the QRS duration used in this system (90 milliseconds) was from the pre-computerized measurement era. The upper limits of QRS duration by computerized measurements in adults is 100 to 110 milliseconds.

Cornell voltage criteria — These criteria are based upon echocardiographic correlative studies designed to detect an LV mass index >132 g/m2 in males and >109 g/m2 in females.

For males – S in V3 plus R in aVL >2.8 mV (28 mm)

For females – S in V3 plus R in aVL >2.0 mV (20 mm)

Accuracy — The ECG is relatively specific but lacks sensitivity in diagnosing LVH in middle-aged to older individuals. False positives are more common in young or thin individuals, whose voltage may exceed conventional thresholds. False negatives may occur with right bundle branch block (RBBB), obesity, or chronic obstructive pulmonary disease. Conversely, increased voltage is a common normal variant, particularly in young adult males and in athletes [1,13]. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Athlete's heart'.)

The sensitivity is also reduced in females and in subjects with obesity. RBBB, when associated with decreased S waves in leads V1 and V2, may decrease the sensitivity of some voltage criteria for LVH. On the other hand, increased voltage is a common normal variant, particularly in young adult males and in athletes [1,13]. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Athlete's heart'.)

The sensitivity and specificity also vary widely depending upon the populations studied, the "gold standard" employed (LV mass or chamber dimension by echocardiographic or magnetic resonance imaging [MRI] versus necropsy measurements), and the severity of LVH. Conservative estimates of the sensitivity of the various criteria for moderate to severe LVH have been in the 30 to 60 percent or lower range, with specificities in the 80 to 90 percent range [7].

This wide range of sensitivity and specificity is supported by data from the Multi-Ethnic Study of Atherosclerosis (MESA) in middle-aged to older males and females [14]. Traditional ECG-LVH criteria were reassessed and showed overall and ethnicity-specific low sensitivity (10 to 26 percent) and high specificity (88 to 99 percent) in diagnosing MRI-defined LVH. The Cornell criteria provided moderate sensitivity (40 percent) while maintaining good specificity (90 percent). The highest accuracy of various criteria was noted in African Americans.

A preliminary study utilizing artificial intelligence (AI) networks suggested that AI methods show promise in identifying LVH from the ECG more accurately than cardiologists using a variety of conventional ECG criteria [15]. The study was based on hospitalized patients, primarily middle aged to older, using transthoracic echocardiogram as the "gold standard." Additional studies are required to determine the optimal approach to utilizing this (or a similar) technology in clinical practice [15,16]. Further analysis may help determine if AI "black-box" methods can be used to identify ECG or demographic features that can enhance the accuracy of conventional interpretative methods.

Imaging findings — Echocardiography is the procedure of choice for identifying LVH, given its widespread availability, ease of use, and lack of associated radiation or nephrotoxic contrast administration (movie 1 and movie 2). Echocardiography can also permit quantitation of LV mass, including the severity of LVH, and give important information about the etiology of LVH (such as aortic or mitral valve disease, or hypertrophic cardiomyopathy). (See 'Definition' above and "Transthoracic echocardiography: Normal cardiac anatomy and tomographic views".)

However, echocardiography may be nondiagnostic in patients with suboptimal acoustic windows. In such instances, cardiac magnetic resonance (CMR) imaging is a reasonable alternative, although CMR is not universally available. (See "Clinical utility of cardiovascular magnetic resonance imaging".)

TREATMENT AND FOLLOW-UP — LVH itself is not a direct target of therapy. Treatment of patients with LVH is directed at the relevant underlying pathology (eg, antihypertensive medications, aortic valve replacement, etc) and is discussed in detail separately in relevant sections. (See "Overview of hypertension in adults" and "Indications for valve replacement for high gradient aortic stenosis in adults".)

Serial monitoring of ECG voltage also may be helpful. In particular, changes in ECG voltage and repolarization abnormalities over time may reflect changes in LV mass and correlate with cardiovascular risk (eg, regression of LVH with effective antihypertensive therapy) [17,18]. However, "loss" of LVH voltage criteria may also be due to alterations in lead placement or to factors that may be associated with decreased QRS voltage such as anasarca, pleural or pericardial effusion, weight gain, and increased severity of chronic obstructive pulmonary disease. Thus, regression of LVH is most accurately determined by echocardiography [19]. (See 'Definition' above.)

PROGNOSIS — Although it is relatively insensitive, the ECG does have prognostic significance [7,20-24]. Hypertensive patients with echocardiographically-proven LVH who also meet ECG criteria have a greater LV mass than those without the expected ECG changes. The LV mass is highest in those with associated ST-T abnormalities (formerly termed the "strain" pattern).

Patients with LVH from any cause are at increased risk for mortality and major cardiovascular complications, including chronic HF (HF) and cardiac arrhythmias, including sudden cardiac arrest/death [6,20-22,25-27]. ECG markers of LVH were also associated with a significant increase in all-cause mortality in a large prospective study (ARIC) of the general, middle-aged population [22]. Similarly, among 4988 participants in the MESA trial without baseline CVD who were followed for 15 years, patients with increased LV mass and LVH on baseline CMR had significantly higher rates of major adverse cardiac events (HR 2.7; 95% CI 1.9-3.8), death due to coronary heart disease (HR 4.3; 95% CI 2.5-7.3) and HF (HR 5.4; 95% CXI 3.8-7.5) compared to those with normal LV mass at baseline [25].

The presence of ST-T wave abnormalities with LVH has adverse prognostic implications. In the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, ST-T changes in lateral leads ("strain") on the baseline ECG in concert with voltage criteria for LVH increased the five-year risk of HF by more than threefold and the risk of HF-related mortality by fourfold [23].

Finally, emerging evidence from cohort studies suggests that the "electrical" (ECG) LVH observed on the 12-lead ECG and "anatomic" (echocardiographic) LVH may provide complementary information about the increased risk of atrial and ventricular arrhythmias [7,24]. (See "Left ventricular hypertrophy and arrhythmia".)

SUMMARY AND RECOMMENDATIONS

Left ventricular hypertrophy (LVH), defined as an increase in the mass of the LV, can be secondary to an increase in wall thickness, an increase in cavity size, or both. LVH usually presents with an increase in wall thickness, with or without an increase in cavity size, but presentations can vary depending upon the underlying pathology. For the most common causes of LVH (hypertension or aortic stenosis), the increase in mass results from a chronic increase in afterload of the LV. (See 'Definition' above.)

LVH and related changes can produce five major electrocardiographic (ECG) findings (waveform 1 and waveform 2): increased QRS voltage, increased QRS duration, left axis deviation, repolarization (ST-T) changes, and left atrial abnormality. (See 'Electrocardiographic findings: General' above.)

The ECG diagnosis of LVH is quite reliable when very prominent voltage is seen in conjunction with left atrial and ST-T abnormalities, leftward axis, or widening of the QRS. Generally, however, only some of the many ECG findings will be present. Several different ECG criteria for the diagnosis of LVH have been developed, all with advantages and disadvantages. None are ideal. (See 'Electrocardiographic criteria for diagnosing LVH' above.)

Patients with LVH may fail to show voltage criteria, especially if they have only mild hypertrophy or underlying obstructive lung disease. The sensitivity is also reduced in females and in subjects with obesity. Right bundle branch block (RBBB), when associated with decreased S waves in leads V1 and V2, may decrease the sensitivity of some voltage criteria for LVH. On the other hand, increased voltage is a common normal variant, particularly in young adult males and in athletes. (See 'Accuracy' above.)

LVH itself is not a target of therapy. Treatment of patients with LVH is directed at the relevant underlying pathology (eg, antihypertensive medications, valve replacement or repair, etc). Patients with LVH from any cause are at increased risk for major cardiovascular complications. (See 'Treatment and follow-up' above and 'Prognosis' above.)

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