Elsevier

Progress in Cardiovascular Diseases

Volume 52, Issue 2, September–October 2009, Pages 153-167
Progress in Cardiovascular Diseases

Clinical Impact of Left Ventricular Hypertrophy and Implications for Regression

https://doi.org/10.1016/j.pcad.2009.05.002Get rights and content

Abstract

Left ventricular hypertrophy (LVH) is an independent risk factor and predictor of cardiovascular (CV) events and all-cause mortality. Patients with LVH are at increased risk for stroke, congestive heart failure, coronary heart disease, and sudden cardiac death. Left ventricular hypertrophy represents both a manifestation of the effects of hypertension and other CV risk factors over time as well as an intrinsic condition causing pathologic changes in the CV structure and function. We review the risk factors for LVH and its consequences, concentric remodeling, and its prognostic significance, clinical benefits and supporting evidence for LVH regression, and its implications for management. We conclude our review summarizing the various pharmacological and nonpharmacological therapeutic options approved for the treatment of hypertension and LVH regression and the supporting clinical trial data for these therapeutic strategies.

Section snippets

Risk Factors

Epidemiologic studies have determined that age is a very important risk factor for the development of LVH.18 Because both elevated blood pressure (BP) and increased body weight, which by themselves are independent risk factors for the development of LVH, increase with age in most populations, it is not surprising that there is a very high prevalence of LVH in the elderly.1, 6, 7, 18 In fact, most studies suggest that age is an independent risk factor for LVH.3, 4, 5

Left ventricular hypertrophy

Consequences of LVH

For decades, it has been known that LVH is not benign but is accompanied by numerous adverse events including myocardial ischemia and MI, ventricular dysrhythmias, ventricular dysfunction, and increased CV and all-cause morbidity and mortality (Fig 2).2, 3, 9, 14, 15,29, 30, 31 More than 3 decades ago, data from the Framingham cohort demonstrated that definite electrocardiographic (ECG) evidence of LVH was associated with an 8-fold increase in CV mortality and a 6-fold increase in CHD mortality.

Concentric Remodeling

HTN induces four distinct patterns of LV geometry based on the relationships between cavity size and wall thickness, including eccentric and concentric LVH as well as CR (Fig 4).62 Concentric remodeling, a subtle abnormal LV geometric pattern associated with increased CV risk, is defined as an increase in RWT with normal LVMI (RWT ≥0.45 and LVMI <125 g/m2, although many studies utilize slightly different cut-points for RWT and LVH).

Alterations in LV geometry in the absence of LVH have not

Determination of LVH

The prevalence of LVH in patients with HTN varies by severity of HTN, age and the methods of detection. Rates of 20% to nearly 50% have been reported in populations with mild-to-moderate HTN.68 Electrocardiogram and echocardiography are the 2 most widely used diagnostic tools for the detection of LVH: ECG is highly specific but not nearly as sensitive when compared with anatomically validated echocardiographic methods.69

Quantitative echocardiography, which accurately estimates LVM, not only is

Impact of Obesity on LVH Determination

As we discussed above, obesity is one of the most powerful predictors of LVH. In fact, we have recently demonstrated that abnormal LV geometry, including CR as well as both eccentric and concentric LVH, occur more commonly in obese than leaner patients.63, 65, 72

Moreover, although we have identified an “obesity paradox” (obese have better prognosis than their leaner counterparts) among our echocardiographic cohorts with preserved LV systolic function, similar to the finding by our group and

Central Aortic Pressure

Findings of the Conduit Artery Function Evaluation study74 showed that central aortic pressure might be a better predictor of CV outcomes compared to peripheral brachial BP. Central aortic BP is measured noninvasively by using applantation tonometer to record radial artery pulse waves, which are then transformed to derive a central arterial wave form and central aortic mean systolic and diastolic pressures. In this particular study, the calcium-channel blocker (CCB) amlodipine was proven to be

Regression of LVH

It is well known from both animal and human studies that antihypertensive therapy could cause regression of LVH.76, 77 In addition, regression of LVH is associated with lower CV risk, independent of BP lowering. As a result, prevention or reversal of hypertensive LVH is widely accepted as a desirable treatment goal.

It is evident from numerous studies that prevention and/or regression of ECG-LVH is associated with a reduced risk of CV morbidity and mortality.78, 79, 80 Fouad et al81 first

Pharmacologic Interventions

The above data suggest that antihypertensive treatment should be directed both towards BP reduction and LVH regression. With the exception of minoxidil and hydralazine, other classes of hypertensive drugs have been shown to produce some reduction in LVH.106 Because of the heterogeneity of the trials and inconsistent data, clear recommendations in favor of one group of medications are not yet available. However, overall evidence is in favor of ACE inhibitors and angiotensin receptor blockers

Conclusions

These results in hypertensive subjects show that a reduction in LVM is associated with a reduction in major CV morbidity and mortality exceeding that achieved by BP control alone, strongly suggesting that emphasis is needed not only on BP lowering but also on reducing LVH. Evidence suggests that RAAS inhibition with either an ACE inhibitor or an ARB should be primary choice, as these agents appear to lower LVM to a greater extent compared to other antihypertensive agents. In view of recent

Statement of Conflict of Interest

All authors declare that there are no conflicts of interest.

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