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Left ventricular hypertrophy: An overlooked cardiovascular risk factor

Cleveland Clinic Journal of Medicine. 2010 June;77(6):381-387 | 10.3949/ccjm.77a.09158
June 1, 2010|Cleveland Clinic Journal of Medicine
Michael A. Bauml, MD;Donald A. Underwood, MD
Author and Disclosure Information

Michael A. Bauml, MD
Department of Internal Medicine, Cleveland Clinic

Donald A. Underwood, MD
Department of Cardiovascular Medicine, Cleveland Clinic

Address: Michael A. Bauml, MD, Department of Internal Medicine, NA10, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195; email: baumlm@ccf.org

ABSTRACTLeft ventricular hypertrophy (LVH) is common in hypertensive patients, and it increases the risk of myocardial infarction, stroke, and death. Recent evidence indicates it is a modifiable risk factor that is not entirely dependent on blood pressure control. The authors review its pathogenesis, diagnosis, and treatment.

KEY POINTS

  • LVH is caused by a chronically increased cardiac workload, most commonly from hypertension.
  • Ideally, all hypertensive patients should undergo echocardiography to screen for LVH, using the calculated left ventricular mass index.
  • Electrocardiography is too insensitive to be used alone to screen for LVH.
  • In hypertensive patients, initial therapy of LVH should consist of an angiotensin II receptor blocker or an angiotensin-converting enzyme inhibitor.
  • Treatment-induced regression of LVH improves cardiovascular outcomes independent of blood pressure.
  • Further study is necessary to examine the utility of following the left ventricular mass index as a treatment goal.

Left ventricular hypertrophy (LVH) strongly predicts cardiovascular morbidity and overall mortality in hypertensive patients. 1–7 Antihypertensive treatment that causes LVH to regress decreases the rates of adverse cardiovascular events and improves survival, independent of how much the blood pressure is lowered.8–11 It is clinically important to recognize that LVH is a modifiable risk factor and that management is more complex than just blood pressure control.

This paper reviews the definition of LVH, compares the diagnostic tests for it, and discusses the current evidence-based approach to managing this dangerous risk factor.

A CHRONICALLY ELEVATED CARDIAC WORKLOAD CAUSES LVH

LVH is an abnormal increase in the mass of the left ventricular myocardium caused by a chronically increased workload on the heart.12 This most commonly results from the heart pumping against an elevated afterload, as in hypertension and aortic stenosis. Another notable cause is increased filling of the left ventricle (ie, diastolic overload), which is the underlying mechanism for LVH in patients with aortic or mitral regurgitation and dilated cardiomyopathy. Coronary artery disease can also play a role in the pathogenesis of LVH, as the normal myocardium attempts to compensate for the ischemic or infarcted tissue.13

Figure 1.
A key component in the development of LVH is myocardial fibrosis (Figure 1), which compromises cardiac function.14 The fibrosis is initially manifested by diastolic dysfunction, although systolic dysfunction also occurs with progressive disease.

The development of myocardial fibrosis appears to be pathophysiologically linked to the renin-angiotensin-aldosterone system. Specifically, there is evidence that angiotensin II has a profibrotic effect on the myocardium of hypertensive patients.15 This may explain why angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are among the most potent agents for treating LVH, as we will discuss later in this review.

Figure 2. This electrocardiogram from a 62-year-old woman shows left ventricular hypertrophy by the Cornell voltage criteria, the Cornell product criteria, the Sokolow-Lyon voltage criteria, and the Romhilt-Estes point score system.
Genetics also play an important role in the pathogenesis of LVH. Mutations in genes encoding sarcomeric proteins have a direct causal relationship in patients with hypertrophic cardiomyopathy.16 In addition, there appears to be a genetic predisposition that causes some patients with mild hypertension to develop LVH while others do not.17,18

DIAGNOSIS BY ELECTROCARDIOGRAPHY, ECHOCARDIOGRAPHY, OR MRI

Figure 3. An echocardiogram performed in a 68-year-old man being evaluated for uncontrolled hypertension and symptoms of congestive heart failure. Left ventricular hypertrophy is diagnosed by an elevated left ventricular mass index, which is calculated from the intraventricular septal thickness (IVSd), posterior wall thickness (PWTd), and left ventricular end-diastolic internal diameter (LVIDd).
LVH can be detected by electrocardiography (Figure 2), echocardiography (Figure 3), or cardiac magnetic resonance imaging (MRI) (Figure 4). Each has unique advantages and disadvantages.

Figure 4. This magnetic resonance image, which also demonstrates concentric left ventricular hypertrophy, was performed in the same 68-year-old man due to suspicion of an infiltrative myocardial disorder.
Electrocardiography is the cheapest and most readily available of the three tests for LVH. While its specificity is acceptably high, its clinical utility is limited by its very low sensitivity.19,20

Many different criteria for electrocardiographic LVH have been proposed over the years. Most use the voltage in one or more leads, with or without additional factors such as QRS duration, secondary ST-T wave abnormalities, or left atrial abnormalities. The most well known electrocardiographic criteria are the Cornell voltage,21 the Cornell product,22 the Sokolow-Lyon index,23 and the Romhilt-Estes point score system (Table 1).24

A systematic review of 21 studies,19 published in 2007, found that all the criteria were less sensitive than specific:

  • Cornell voltage—median sensitivity 15%, median specificity 96%
  • Cornell product—median sensitivity 19.5%, median specificity 91%
  • Sokolow-Lyon voltage—median sensitivity 21%, median specificity 89%
  • Romhilt-Estes point score—median sensitivity 17%, median specificity 95%.

Of note, the ranges of the published values were extremely broad. For example, the ranges in sensitivity were:

  • Cornell voltage—2% to 41%
  • Cornell product—8% to 32%
  • Sokolow-Lyon voltage—4% to 51%
  • Romhilt-Estes point score—0% to 41%.

While the studies with the extreme values may have had issues of small sample size or poor study quality, the wide range in values may primarily be the result of diverse study populations as well as different validation methods and cutoff values to define LVH. Regardless, the overall message of high specificity and low sensitivity is indisputable.

Electrocardiography is insensitive for diagnosing LVH because it relies on measuring the electrical activity of the heart by electrodes on the surface of the skin to predict the left ventricular mass. The intracardiac electrical activity is problematic to measure externally because the measurements are affected by everything between the myocardium and the electrodes, most notably fat, fluid, and air. Because of this effect, electrocardiography underdiagnoses LVH in patients with obesity, pleural effusions, pericardial effusions, anasarca, or chronic obstructive pulmonary disease. In addition, the diagnosis of LVH by electrocardiography is strongly influenced by age and ethnicity.25–26

While electrocardiography is not sensitive and cannot be used to rule out LVH, it still has a role in its diagnosis and management. In the landmark Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study, regression of LVH (diagnosed electrocardiographically by the Sokolow-Lyon index or the Cornell product criteria) in response to losartan (Cozaar) improved cardiovascular outcomes independent of blood pressure.10 Based on this, it is reasonable that all hypertensive patients and other patients at risk of LVH who undergo electrocardiography be screened with these two criteria.

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