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Left ventricular hypertrophy: An overlooked cardiovascular risk factor

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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.


 

References

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

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