Table of Contents
Year : 2016  |  Volume : 1  |  Issue : 3  |  Page : 37-47

Asian expert consensus for the diagnosis and treatment of hypertension-associated left ventricular hypertrophy

1 Department of Cardiology, People's Hospital of Peking University, Beijing, China
2 Department of Cardiology, Taipei Veterans General Hospital, Taiwan, China
3 Department of Cardiology, Ruijin Hospital of Shanghai Jiaotong University, School of Medicine, Shanghai, China
4 Department of Cardiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China
5 Department of Cardiology, People's Hospital of Guangdong Province, Guangzhou, China
6 Department of Cardiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
7 Department of Cardiology, The General Hospital of Tianjin Medical University, Tianjin, China
8 Department of Cardiology, Prince of Wales Hospital, Hong Kong
9 Department of Cardiology, National University Heart Centre of Singapore, Singapore
10 Department of Cardiology, National Heart Institute of Malaysia, Kuala Lumpur, Malaysia
11 Department of Cardiology, Peking University First Hospital, Beijing, China

Date of Web Publication26-Dec-2018

Correspondence Address:
Prof. Ningling Sun
Department of Cardiology, People's Hospital of Peking University, Beijing
Prof. Yong Huo
Department of Cardiology, Peking University First Hospital, Beijing
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2470-7511.248356

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How to cite this article:
Sun N, Chen JW, Wang J, Xie L, Chen L, Mu J, Sun Y, Chiang CE, Yu CM, Tan HC, Omar R, Huo Y. Asian expert consensus for the diagnosis and treatment of hypertension-associated left ventricular hypertrophy. Cardiol Plus 2016;1:37-47

How to cite this URL:
Sun N, Chen JW, Wang J, Xie L, Chen L, Mu J, Sun Y, Chiang CE, Yu CM, Tan HC, Omar R, Huo Y. Asian expert consensus for the diagnosis and treatment of hypertension-associated left ventricular hypertrophy. Cardiol Plus [serial online] 2016 [cited 2021 Oct 16];1:37-47. Available from:

  Introduction Top

Left ventricular hypertrophy (LVH) is an important manifestation of hypertensive organ damage associated with increased ventricular wall thickness, left ventricle mass, and cardiac remodeling. Neurohumoral and hemodynamic factors play important roles in the development of LVH. The heart is the most vulnerable target organ for hypertension, and >30% of patients with hypertension will undergo LVH. The incidence rate is positively correlated with the severity of hypertension.[1]

LVH is an independent risk factor for a number of cardiovascular disorders such as coronary diseases, congestive heart failure, stroke, temporary ischemic heart disease, and sudden death.[2] LVH accompanied with hypertension can increase and the progression of cardiovascular and cerebrovascular diseases, thus, hypertension associated LVH as a contributor to organ damage, should be paid attention to. Asia is a region with a high prevalence of hypertension (20%–30% of the population). The growth rate of the hypertensive population within Asia is higher than in developed countries.[3],[4] A Chinese cohort study showed that 64.6% of pre-hypertensive patients developed hypertension 17 years later, with a total mortality rate of 27.9/1000 person/year. The main cause of death was stroke,[5] and hypertension-associated LVH is related to stroke. A higher risk of coronary disease and stroke was found in the Asian populations with increased systolic pressure than in Caucasians.[6] With urbanization, day-to-day stress, obesity, and high-salt/high-fat diets are becoming more prevalent in Asia, and thus an unhealthy lifestyle has become an important risk factor for heart diseases, which is the main cause of hypertension-induced LVH. The dysfunction in cardiac diastole, as well as the rate of symptomatic heart failure, is also increased. A study from Japan reported that >50% of people with high blood pressure having LVH combined with obviously increased cardiovascular events.[7] Effective blood pressure control and regression of LVH significantly decreased the risk of cardiovascular events and death.[8],[9],[10]

Taking all these into account, health guidelines for the Asian Region all take LVH as an important index for hypertension-induced heart damage, and by consequence, blood pressure control is an important therapeutic strategy for treatment of LVH.[11],[12],[13]

Because of the importance of LVH in hypertension and cardiovascular diseases, and the insufficient strategy for intervention of LVH, experts in the Asian Region have achieved a consensus regarding diagnosis, classification, and treatment criteria for LVH, as well as clinical guidelines for the diagnosis and management of patients with hypertension combined with LVH (this guideline is only aimed at hypertension-associated hypertension).

  Epidemiology of Hypertension-Associated Left Ventricular Hypertrophy Top

At present, the diagnosis of LVH for patients with hypertension relies on electrocardiogram (ECG) and echocardiogram (ECHO) readouts. The detectable rate relying on adopted method and the differences are non-ignorable [Table 1].
Table 1: Summaries the predictive value, practicability, repeatability and cost effectiveness of electrocardiogram, echocardiogram, and cardiac magnetic resonance

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A retrospective analysis of 26 studies shows that the prevalence of ECG-diagnosed LVH (ECG-LVH) is 18.1%–18.9% within hypertensive patients. A sex-based analysis shows that the average prevalence of LVH is 24.2%–24.4% in men and 16.6%–16.8% in women.[14] Under the same diagnostic criteria (Sokolow–Lyon voltage: SV1 + RV5/RV6 ≥3.5 mV), the prevalence of ECG-LVH in Caucasian hypertensives is 8.6%–26.4%.[14] LVH prevalence in Asian hypertensives is also very high. In a Japanese study, the prevalence of ECHO-diagnosed LVH (ECHO-LVH) is as high as 40%.[15] Prevalence of ECHO-LVH in Chinese hypertensive patients varies from 19.2% to 34.3%,[16],[17],[18] and a Taiwan study shows that the prevalence of ECHO-LVH is 13%.[19]

A retrospective analysis including 30 studies shows that the prevalence of ECG-LVH is 35.6%–40.9% in the hypertensive patients. A sex-based analysis shows that the average prevalence of LVH is 36.3%–43.5% in men and 37.9%–46.2% in women.[1] Under the same diagnostic criteria (Sokolow–Lyon voltage: SV1 + RV5/RV6 ≥3.5 mV), ECG-LVH patients with hypertension Caucasian detection rate is 14.5%–44.8%.[1] In a Japanese study, the prevalence of ECHO-LVH is as high as 58.3%;[7] an Indian study shows that ECHO-LVH is 24.4%.[20] Prevalence of ECHO-LVH in Chinese hypertensive patients varies from 26% to 73.2%,[17],[21],[22],[23] and women show an obviously higher prevalence of LVH than that of men.[22],[23],[24]

  Mechanisms Driving Hypertension Combined Left Ventricular Hypertrophy and the Harm Top

Mechanisms of hypertension combined left ventricular hypertrophy

The development of cardiac hypotrophy can be divided into three stages as follows: progressing period, compensatory stage, and decompensatory stage. Pathological hypotrophy includes eccentric hypotrophy and concentric hypotrophy. In some conditions, eccentric hypotrophy can also be derived from concentric hypotrophy.

The mechanisms of hypertension-related LVH have not been completely elucidated; the pathogenic process is related to factors such as (a) hemodynamics, (b) neurohumoral, paracrine, and autocrine secretions in cardiovascular tissue, and (c) genetic background of patients. Both hemodynamic and neurohumoral factors play major roles in the progression of hypertension-related LVH.

Hemodynamics factors

Systolic phase overload is pressure overload, and diastolic phase overload is volume overload. Hypertensive patients suffer both pressure overload and volume overload. Both of these overloads can increase the volume of cardiac myocytes, enlarge the size of cardiac myocytes and change components of collagen proteins in the extracellular matrix, all of which can finally induce cardiac hypotrophy.[25]

Blood pressure is the most important factor for LVH. The Framingham study revealed that left ventricular mass increased by 10.6 g/m2 for male patient and 3.0 g/m2 for female patient per 20 mmHg increases in systolic pressure. The PALEMA study of 2002 enrolled 2050 patients, in which the left ventricular mass is the highest in hypertensive patients without treatment.[26]

Neurohumoral factors

Neurohumoral factors are the renin–angiotensin–aldosterone system (RAAS), sympathetic nervous, and adrenal system and the endothelin system.[27]

In hypertensive patients, the RAAS activity and synthesis of angiotensin II (AngII) and aldosterone are increased. Circulating AngII can efficiently increase blood pressure through vigorously shrinking arterioles, stimulating secretion of aldosterone to increase circulating blood volume, and promoting the release of catecholamine. AngII in local tissue tends to play long term, therapeutic roles. AngII binds with type I receptor, and regulates expression of proto-oncogene and related protein, causing hypotrophy of cardiac myocytes and overexpression of collagen proteins.[28],[29]

The activity of the sympathetic nervous system for patients with hypertension-related LVH is much higher than that of primary hypertension without LVH.[30] In patients with the active sympathetic system, the concentration of norepinephrine (NE) in circulation is also higher. NE can promote protein expression in cardiac myocytes through activating α1-adrenergic receptor; it can also activate β-adrenergic receptors to enhance the systolic ability of cardiac muscle, increase heart rate as well as the synthesis of glycogen and adenosine phosphate. The increased content of total protein and un-contractile protein in cardiac myocytes leads to cardiac hypotrophy.[31],[32] Meanwhile, increased activity of the sympathetic nervous system enhances invasion of inflammatory mediators into the heart, causing cardiac fibrosis, and aggravating cardiac hypotrophy.[33]

In summary, neurohumoral factors participate in the formation of hypertension-induced LVH, induce abnormalities in the signaling transduction system of cardiac myocytes (beta-receptor, G-protein, cyclases, calcium channel, phosphokinase, etc.), and influence protein expression of cardiac myocytes. The increased expression of structural proteins will gradually enhance cardiac contractility, but uncontrolled expression of cardiac fibrils will result in cardiac hypotrophy and enlargement of the ventricular chamber.

Risk factors

Prevalence of LVH and ventricle remodeling in hypertensive patients is influenced by age, body fat, and genetic factors. The prevalence of LVH is correlated with patient age, i.e., older age means a higher risk of LVH.[34] The left ventricular mass index (LVMI) is distinctly higher in obese patients; and like high systolic and diastolic pressure, obesity (high body mass index) during childhood and adult is distinctly related with eccentric and concentric hypotrophy.[35] Moreover, the left ventricle mass (LVM) displays the obvious difference in patients with a similarly increased segment of blood pressure, suggesting that genetic factors are involved in the development of LVH. Gene polymorphisms associated with both the sympathetic nervous system and RAAS system is correlated with the prevalence of LVH and the impairment of cardiac functions. Gene polymorphism in the sympathetic nervous system and RAAS is related with LVH, yet it has not been identified as the cause or consequence of LVH.[27],[36] High-salt diet is also involved in LVH; there have been animal experiments which showed that high-salt diets could induce LVH.[37],[38]

The damage of hypertension-related left ventricular hypertrophy

Reducing coronary flow reserve

Because the myocardium is totally dependent on aerobic metabolism, an increase in myocardial oxygen consumption requires an increased coronary blood flow, and this is achieved by dilatation. The ability of the heart to autoregulate coronary perfusion in response to metabolic demands is called coronary flow reserve. Some studies find that in hypertension patients with LVH, the CRF is significantly reduced and the risk of ischemic heart diseases is increased. This can easily induce ischemic disease and increase the risk of death.[39],[40],[41]

Impairing left ventricle functions

In hypertensive patients with LVH, left ventricle hypotrophy will further impair left ventricle functions and finally induce development of heart failure regardless of the contractile status with the left ventricle. Compared with patients suffering from left ventricle systolic dysfunction, LVH patients are more inclined to suffer from left ventricular diastolic dysfunction. Studies show that both the increase in LVM and relative wall thickness (RWT) significantly increase the risk of left ventricle diastolic dysfunction in hypertensive patients.[39],[42],[43] However, about 13% of concentric LVH patients with normal left ventricle systolic function progress to left ventricle systolic dysfunction within 3 years post-follow-up.[44]

Increasing risk of arrhythmia

A meta-analysis including 12 studies reveals that risk of arrhythmia in patients with hypertensive-induced LVH is 3 times higher than hypertensive patients without LVH.[45] LVH diagnosed by ECG suggests an obvious increase in SCD risk,[46],[47] and reversing LVH can prominently reduce the prevalence of SCD.[48] LVH is also a major risk factor for arterial fibrillation (AF).[49],[50] For every 1, standard deviation increase in left ventricular mass, the risk of AF was increased by 1.20 times.[51],[52]

Increasing major cardiovascular events and risk of death

The reduction of endpoints in NIDDM with the angiotensin II antagonist losartan study showed thatchronic kidney disease combined with LVH is an predictor of increased CK level in plasma/end-stage renal disease (Hazard Ratio (HR) = 1.42; P = 0.03) and cardiovascular event (HR = 1.68; P = 0.001).[53]

The Framingham study shows that persons who acquire ECG-LVH have an eightfold increased risk of CVD death and a six-fold increased risk of CHD death.[54] The following studies coherently verify that ECG-LVH is associated with the incidence of cardiovascular diseases, death from cardiovascular disease, and death from all causes.[55],[56],[57],[58],[59],[60] Furthermore, there is a continuous relation between LVH severity and CVD risks.[61]

Significance of reversing left ventricular hypertrophy

Preclinical and clinical researches have verified that blood pressure control can effectively reverse LVH.[62],[63] Regression of LVH can decrease the risk of cardiovascular events, regardless of endpoint reduction of blood pressure.[64],[65] Therefore, more attention should be paid to patients with hypertension-induced LVH, and early prevention and/or regression of LVH should be one of the therapeutic targets for clinical hypertension treatment.

Reducing risk of cardiovascular events

Some studies revealed that prevention/regression of ECG-LVH could significantly reduce morbidity and mortality from cardiovascular events. A meta-analysis including five studies and comprising 2449 patients found that compared with patients of LVH persistence/LVH development, the total risk of cardiovascular events was reduced by 46% in patients of LVH regression/persistent normal.[66] Mathew et al.[8] found that prevention and regression of ECG-LVH are associated with reduced clinical endpoints including the risk of death, myocardial infarction, stroke, and congestive heart failure.[7] A total of 941 prospectively identified patients aged 55–80 years with essential hypertension and electrocardiographic LV hypertrophy had LV mass measured by echocardiography at enrolment in the The Losartan Intervention For Endpoint reduction (LIFE) trial and thereafter are followed up annually for a mean (standard deviation of 4.8 (1.0) years for CV events. The LIFE study used a composite endpoint of CV death, myocardial infarction, or stroke. The multivariable Cox regression model showed a strong association between lower LV mass index and reduced rate of the composite cardiovascular end point. Risk of cardiovascular event declined 22% (P = 0.009) for 1 reduction of LVMI standard deviation (25.3 g/m2). Reduction of LVMI was proved to be a more suitable predictor for reduced risk of cardiovascular events than the decrease of blood pressure. Lower LVMI is associated with lower rates of all clinical endpoints, including CV death (HR = 0.62; P = 0.0001), stroke (HR = 0.76; P = 0.02), myocardial infarction (HR = 0.85; P = 0.33) and all-cause mortality (HR = 0.72; P = 0.002).[64],[65]

Other benefits

In addition to reducing the risk of cardiovascular events, Okin et al.[67] found new benefits of antihypertensive therapy. Electrocardiographic hypertrophy was evaluated over time in 7998 hypertensive patients without diabetes at baseline in the Losartan Intervention for endpoint reduction in hypertension (LIFE) study. During a mean follow-up of 4.6 ± 1.2 years, resolution or continued absence of LVH during antihypertensive therapy is associated with a lower likelihood of new-onset diabetes.

  Diagnosis and Differential Diagnosis of Hypertension-Associated Left Ventricular Hypertrophy Top

The diagnostic criteria for hypertensive-associated LVH include three aspects as follows: (1) the definitive diagnosis of hypertension; (2) the definitive diagnosis of LVH; and (3) elimination of other causes of LVH.

The clinical diagnosis methods for left ventricular hypertrophy

The diagnostic approaches include ECG, ECHO, and cardiac magnetic resonance (CMR). These methods have different sensitivity, specificity, costs and feasibility, as shown in [Figure 1]. When it comes to clinical use, the individualized diagnostic method should be considered.
Figure 1: Diagnostic pathway for hypertension-associated left ventricular hypertrophy

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ECG is simple and practical. It is recommended by a majority of guidelines as the most optical method for LVH diagnosis. The sensitivity of ECG to LVH is relatively lower than other approaches, and its diagnostic sensitivity for mild and modest/severe LVH is 7%–35% and 30%–60%, respectively.[68] The specificity of ECG is much higher than its sensitivity, especially for severely hypertensive patients, the specificity is as high as 80%–90%. Obesity markedly attenuates the validity and performance of ECG criteria for LVH detection.[69] There are ethnic differences in ECG criteria for LVH and the African heritage strongest independent predictor of decreased ECG specificity.[70],[71]

There are a variety of ECG-LVH criteria in the guidelines and in the scientific and medical literature. Each method has advantages and disadvantages. The most prevalent criteria are listed:

  1. Sokolow-Lyon voltage >3.5 mV (2013 ESH/ESC guidelines for hypertension, 2014 Japanese guidelines for hypertension) or Sokolow-Lyon voltage >3.5 mV (2010 Chinese guidelines for prevention and treatment of hypertension)
  2. Cornell product >224 mV·ms (2013 ESH/ESC guidelines for hypertension)
  3. R aVL >1.1 mV (2013 ESH/ESC guidelines for hypertension)
  4. Left ventricular voltage (such as RV5 >2.5 mV) can be used as a simple criterion for primary diagnosis.[72]

It was reported that ECG-LVH was associated with an increased risk of overall mortality, cardiovascular events, and stroke mortality.[73] Another study revealed that in addition to ECG-LVH, various electrocardiographic abnormalities, such as asymmetric inverted T-wave and ST-segment depression, were independent risk factors for cardio-cerebral vascular diseases.[74]


ECHO is more sensitive than ECG in the diagnosis of LVH, and the LVMI normalized by body surface area (BSA) or height is utilized for detection of LVH; the former method is more widely used than the latter one. The generally accepted method for LVMI calculation is the “cube” method.

The criteria for the diagnosis of LVH recommended by “The 2013 ESH/ESC Guidelines for Hypertension Treatment,” ‘2015 Taiwan Hypertension Guidelines’ and ‘The 2014 Japanese Guidelines for Hypertension are listed as follows:

LVMI ≥115 g·m−2 (male), LVMI ≥95 g·m−2 (female).

Computational formula: LVM (g) = 0.8 × 1.04 × ([LVDd + IVST + LVPWT]3-LVDd3) + 0.6

LVDd: Left ventricle diastolic diameter; IVST: Interventricular septum thickness; LVPWT: Left ventricular posterior wall thickness.

LVMI (g·m−2) = LVM (g)/BSA (m2)

Body surface area: Male (m2) = (m2) = 0.0057 × height (cm) + 0.0121 × body weight (kg) + 0.0882

Female (m2) = 0.0073 × height (cm) + 0.0127 × body weight (kg)-0.2106.

According to RWT (RWT, RWT = (2 × LVPWT)/LVDd) and the geometrical configuration of left ventricular hypotrophy/remodeling in LVH, the guidelines also clarifies LVH into three subtypes, as shown in chart 2 [Table 2].[75]
Table 2: Classification of geometrical configuration of left ventricular hypertrophy/remodeling

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The recommended abnormal criteria in 2015 EACVI/ASE adult hypertension echocardiographic examination are IVST and/or PWT >11 mm (male) and IVST and/or PWT >10 mm (female).[76] This is a more sensitive approach for diagnosis of concentric hypotrophy/remodeling, and LVH with concentric hypotrophy is the most reliable criteria for prediction of cardiovascular diseases,[75] therefore, except for LVMI, using IVST and PWT as prognostic criteria for LVH is reasonable.

In clinical practice, IVST or PWT usually be used to diagnose LVH when LVMI is not available.[18],[77] IVST or PWT ≥11 mm is used as earlier diagnostic criteria of LVH. However, the sensitivity, specificity, and universality of this method need further study.

ECHO examination should be conducted individually: in patients with a moderate risk of cardiovascular events, ECHO may checkout LVH which cannot be determined by ECG. In ECG-LVH patients, ECHO can quantitatively evaluate hypertrophic condition with much higher accuracy and to define its geometric construction and dangerous level. In hypertensive patients with symptoms of heart failure, ECHO can help to diagnose the underlying disease.

Cardiac magnetic resonance

Among all kinds of noninvasive diagnostic approaches for LVH, CMR is the most reproducible. There is research showing that the LV volume and function determined by CMR can be repeated at the percentage of 98% and 99%, whereas the percentage of repeatability of two-dimensional ECHO is as low as 65% and 94%.[78] There are limitations for CMR too, such as arrhythmia, artifacts caused by body motion and higher cost. Therefore, ECHO is a differential diagnosis method rather than a conventional detection method for LVH.

Diagnostic pathway for hypertension-associated left ventricular hypertrophy

A representative diagnostic pathway is shown in [Figure 1]. Different methods have different applications [Table 3]. For hypertensive patients, the methods adopted should be according to specific conditions. Accurate diagnosis of LVH, and specifying the cause of disease are important for a correct prognosis in the clinic. The appropriate diagnostic method should be made according to disease history, figure examination, and laboratory experiments. To distinguish hypertension-associated LVH from LVH caused by other disease is also required [Figure 2].[79]
Table 3: Clinical significance of electrocardiogram, echocardiogram, and cardiac magnetic resonance in diagnosis of left ventricular hypertrophy

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Figure 2: Diagnostic pathway for left ventricular hypertrophy with different pathogenesis

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  Treatment Strategies For Hypertension-Associated Left Ventricular Hypertrophy Top

Lowering blood pressure is the therapeutic cornerstone of LVH regression. Hypertension-associated LVH patients should receive drug treatment as early as possible to lower blood pressure, effectively reverse LVH, and reduce the occurrence of cerebrovascular and cardiovascular diseases.

Blood pressure treatment targets for hypertension-associated left ventricular hypertrophy patients

LVH is an independent and dangerous factor for cardiovascular events. Treatments to lower blood pressure can effectively reverse LVH and reduce the risk of CV.[8],[10] Authorities of international guidelines for management of hypertension definitely point out that all LVH patients should receive treatments to reduce blood pressure.[12],[13],[75] The 2010 Chinese guidelines for hypertension recommended the blood pressure lowing target is <130/80 mmHg.[11] The 2015 Taiwan guidelines for hypertension and the 2014 Japanese guidelines for hypertension did not have a special target recommendation for blood pressure. In general, the goal is to reduce the blood pressure of hypertensive patients to <140/90 mmHg.[12],[13]

Treatment strategies and choice of drugs for hypertension-associated left ventricular hypertrophy

The conventionally used drugs for lowering of blood pressure include Angiotensin-Converting Enzyme Inhibitors (ACEI), angiotensin receptor blockers (ARB), calcium channel blockers (CCB), Diuretics (thiazides, chlorthalidone, and indapamide) and beta-blockers, either as monotherapy or in some combination with each other. Most classes of antihypertensive agents can improve the clinical symptoms of LVH through a decrease in blood pressure, but these antihypertensive drugs act by different mechanisms and show different effects on LVH. A meta-analysis shows that there is a significant difference (P = 0.004) among five antihypertensive medication classes in their ability to reverse LVH. LVMI decreased by 13% with AngII receptor antagonists, with 11% with calcium antagonists, with 10% with ACE inhibitors, by 8% with diuretics, and by 6% with beta-blockers.[80] For hypertensive-associated LVH patients, the primary goal is blood control; when it comes to the choice of drug, evidence-based drugs are preferable. At present, most evidence comes from renin-angiotensin system inhibitors (RASI).

Choice and application of drugs

Activation of the RAAS can increase blood pressure, induce cardiomyocytes hypotrophy and augment cardiac fibrosis directly, something which plays a key role in the initiation and maintenance of LVH. Direct RASI inhibitors (ACEI or ARB classes of drugs) are often more effective in reducing the LVMI than that of other antihypertensive drugs.[81]

Angiotensin-converting enzyme inhibitors

ACEIs with approved intervening evidence include Captopril, Enalapril, and Ramipril, etc.[82],[83],[84]

Earlier clinical research generally regarded ACEI as a better anti-LVH category than CCB, DIU or beta receptor blockers (BB).[85],[86] However, recently published meta-analyses have shown that there is no significant difference between ACEI and other antihypertensive drugs in reversing LVH (P < 0.30).[87] Moreover, patients treated with ACEI have aggregative bradykinin which will arouse some side effects like a cough and angioneurotic edema, thus reducing their compliance with ACEI treatment. This phenomenon is more prevalent in Asia. What should be kept in mind is that the above researches are all aimed to reverse LVH, rather than clinical endpoint events.

Angiotensin receptor blocker

Extensive clinical studies, as well as comprehensive m-analyses from the medical literature, have confirmed that ARB treatment can reverse LVH. A meta-analysis enrolling 6001 hypertensive patients compares the effects of long-term treatment with five kinds of antihypertensive drugs (ACEI, DIU, BB, CCB, ARB) on left ventricular (LV) hypertrophy. The percentage decline of LVMI significantly increases 3.2% (P = 0.002), but there is no significant difference in SBP among different treatments (P = 0.07).[87] Losartan is the only ARB which has evidence for reversing LVH and improving cardiovascular endpoint events.

LIFE study is the first and the only global prospective cardiovascular endpoint research into hypertension-associated LVH population. The study is conducted among 9193 hypertensive patients with electrocardiographic LVH, who randomly received either losartan- or atenolol-based antihypertensive treatment. After follow-up visits or primary endpoints, 50% of patients had used 100 mg of losartan (average dose: 82 mg). Hydrochlorothiazide was used if blood pressure could not reach standards. Results reveal that with comparable antihypertensive therapeutic effects, losartan treatment is associated with 13% (P = 0.021) lower risks of the composite CV endpoints (nonfatal MI, CV mortality and nonfatal stroke), 25% lower risk of stroke (P = 0.001), 33% lower risk of new-onset arrhythmia and 25% lower risk of new-onset diabetes mellitus. Meanwhile, losartan is more effective in reversing LVH.[9],[52] At the terminal point, reversing was found in 82% of concentric remodeling and 84% of concentric hypotrophy patients, and it is well known that both concentric remodeling and hypotrophy are independent risk factors of the composite CV endpoint.[88] In postmortem analysis, about one-third of the beneficial effects of losartan are ascribed to reversing of LVH. LIFE subsection research shows that compared with reversing of LVH, progression and sustenance of LVH are related with a higher risk of cardiovascular events.[8] Based on this research, ARB is recommended as the first class drug for treatment of patients with hypertension-associated LVH in different countries' guidelines for management of hypertension.

Beta-receptor blockers

BBs combine with the β epinephrine receptor and blocks activation of β receptor induced by cardiac neurotransmitter and catecholamine, thereby improving LVH. Nonselective and hydrophilic BB show weaker LVH reversing effects in clinical application, whereas high β-1 selective and lipophilic BB may have advantages in reversing LVH, but the evidence-based clinical research is not sufficient presently.

Aldosterone blockers

Aldosterone blockers can inhibit effects of aldosterone, as well as reverse perivascular matrix fibrosis and LVH. A randomized, parallel-group study conducted among 202 patients with hypertensive-associated LVH shows that Eplerenone was as effective as enalapril in LVH regression and blood pressure control (reduction of LVM: Eplerenone-14.5 g, enalapril-19.7 g, P = 0.258).[83] However, the compliance of long-term use of spironolactone should be considered and there is a lack of endpoint research showing that it can reverse LVH and reduce cardiovascular events.

Because reaching blood pressure target and LVH regression are equally important, these guidelines present the following recommendation: if RASI fails to achieve targeted goals, RASI combined with highly selective, highly lipophilic BB, low dose of diuretic or CCB should be adopted to lower the blood pressure. Fixed-dose combinations in a single tablet are also recommended to improve compliance and obtain better therapeutic effects.

  Clinical Management of Hypertension-Associated Left Ventricular Hypertrophy Top

Goal of blood pressure control

Goal of blood pressure control <140/90 mmHg.

Diagnosis and screening of hypertension-associated left ventricular hypertrophy


  1. Screening of hypertension-associated LVH by ECG is recommended in all patients with hypertension
  2. Screening of hypertensive patients by ECHO in qualified medical institutes, and LVMI is recommended as a routine item; The principle criteria are: LVMI ≥ 115 g·m−2 (male), LVMI ≥95 g·m−2 (female); the simple surrogate marker is: Thickness of interventricular septum or posterior wall of left ventricle (≥11 mm [male], ≥10 mm [female])
  3. For basic medical institutions where ECHO examination is not available, patients with positive ECG should be transferred to superior hospitals that are enabled for ECHO examinations
  4. For LVH that cannot be clearly explained in the clinic, CMR should be adopted for differential diagnosis.

Summary of recommendations:

  1. ECG is the preferable method for screening of hypertension-associated LVH
  2. ECHO is the main method for diagnosis of hypertension-associated LVH
  3. CMR is the differential diagnostic method for LVH
  4. Hospital equipped with ECHO should take LVMI as a routine examination item.

Treatment of hypertension-associated left ventricular hypertrophy


  1. Controlled salt intake, weight loss, improved mental conditions are important behavioral and lifestyle interventions for hypertensive-associated LVH
  2. For patients with explicit hypertension-associated LVH, ARB (Losartan) 50-100 mg/day is preferable; if the patient fails to achieve target blood pressure, a doubling of dosage for ARB with low dose of diuretic is recommended, and fixed-dose combinations is optional; medical institutes without Lorsartan may choose other ARB or ACEI, but there are less clinical evidence
  3. For hypertension-associated LVH patients with systolic or diastolic dysfunction, higher heart rate (HR >75 bpm) or arterial fibrillation, combination of highly heart selective, highly lipophilic BB is recommended
  4. For patients who cannot reach target blood pressure, the combined use of long-term CCB is recommended
  5. For hypertension-associated LVH patient, cautious use of direct vasodilator substances (hydralazine) and short-term α-blocker (prazosin) is recommended.

  Follow-Up Visits Top

Follow-up visit items include BP and LVH (cardiac structure and function).

Blood pressure follow-up visit


To achieve BP target, clinical BP, family BP, and dynamic BP should be monitored in patients with an explicit diagnosis of hypertension-associated LVH, and the dose of pressure lowering drugs should be adjusted accordingly. In the earlier phase, the follow-up visits of hypertension-associated LVH can be at intervals of 1-3 months. If the blood pressure does not reach the target after six-month treatment with at least 3 kinds of antihypertensive drugs, it is recommended to transfer the patient to a hypertensive specialist clinic or superior hospital for further treatment.

Left ventricular hypertrophy follow-up visits

ECHO is commonly used for the follow-up evaluation of the regression of LVH. The first follow-up visit in early intervention can be conducted at 6 months, after which once a year is sufficient. There is a study showing that LVH regression can be observed 6 months after BP lowering treatment, and the regression of LVH has prognostic value for cardiovascular disease.[75]

For hypertensive patients with arterial fibrillation, a 1–3 month's interval for follow-up visits is recommended, which include ECG examinations of heart rate, cardiac rhythm, and LVH-related indexes.

In addition, tests of serum total cholesterol, plasma glucose, serum creatinine, serum potassium and other indexes for organ damage should be included in the follow-up visits to supply comprehensive information for the assessment of hypertension-associated LVH patients.

Expert board (in alphabetical order of family name)

Luyuan Chen (People's Hospital of Guangdong Province), Chern-En Chiang (Taipei Veterans General Hospital), Cheuk-Man Yu (Prince of Wales Hospital, Hong Kong), Xiaoping Chen (Sichuan University, Huaxi Hospital), Yugang Dong (The First Affiliated Hospital of Sun yat-sen university), Aimin Dang (Chinese Academy of Medical Sciences, Fuwai Hospital), Huay Cheem Tan (National University Heart Centre, Singapore), Yong Huo (Peking University First Hospital), Jaw-Wen Chen (Taipei Veterans General Hospital), Razali Omar (National Heart Institute of Malaysia), Xiangqing Kong (Jiangsu Province Hospital), Jianping Li (Peking University First hospital), Yuhua Liao (Union Hospital of Tongji Medical College and Huazhong University of Science and Technology), Jianjun Mu (The First Affiliated Hospital of Xi' An Jiaotong University), Ningling Sun (People's Hospital of Peking University), Yingxian Sun (The First Hospital of China Medical University), Yuemin Sun (The General Hospital of Tian jin Medical University), Jiguang Wang (Ruijin Hospital of Shanghai Jiaotong University, School of Medicine), Liangdi Xie (The First Affiliated Hospital of Fujian Medical University), Biao Xu (Nanjing Drum Tower Hospital), Xinchun Yang (Beijing Chao-Yang Hospital), Yuqing Zhang (Chinese Academy of Medical Sciences, Fuwai Hospital), Yuanming Zhang (The First Affiliated Hospital of Xinjiang Medical University), Jianhua Zhu (The First Affiliation Hospital of Zhejiang University), Tiangang Zhu (People's Hospital of Peking University).

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2], [Table 3]


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