Introduction: The use of angiotensin II receptor blockers (ARBs) in the treatment of hypertrophic cardiomyopathy (HCM) remains a subject of controversy. Methods: We conducted a comprehensive search of the Cochrane Library, PubMed, EMBASE, ClinicalTrials.gov, and Web of Science databases until October 2023 to identify articles investigating the effects of ARBs in patients diagnosed with HCM. Predefined criteria were utilized for selecting data on study characteristics and results. Results: The study included a total of 387 patients from 6 randomized controlled trials, which were reported in 7 articles. The results of the meta-analysis revealed that the utilization of ARBs did not yield a reduction in left ventricular (LV) mass (p = 0.07) and maximum LV wall thickness (p = 0.25), nor did it demonstrate any improvement in LV fibrosis (p = 0.39). Furthermore, there was no significant impact observed on early diastolic mitral annular velocity (p = 0.19) and LV ejection fraction (p = 0.44). Conclusions: The administration of ARBs does not appear to yield improvements in cardiac structure, function, and myocardial fibrosis in patients with HCM.

Hypertrophic cardiomyopathy (HCM) is an inherited cardiac disorder, typically transmitted in an autosomal dominant pattern [1]. The prevalence of HCM in adults is approximately 0.2% [2]. HCM is characterized by an increase in the thickness of the left ventricular (LV) wall that cannot be fully attributed to loading conditions, and around two-thirds of patients exhibit obstruction in the LV outflow tract [2, 3]. Histologically, HCM is characterized by disarray of myocardial cells, myocardial hypertrophy, and interstitial fibrosis [4]. The majority of patients typically remain asymptomatic, while others may present with dyspnea, chest pain, syncope, and sudden death [5]. Currently, HCM has no known cure. The primary objective of certain medical and surgical interventions is to mitigate obstruction in the LV outflow tract, alleviate symptoms, and effectively manage associated complications [2].

The renin-angiotensin-aldosterone system (RAAS) represents a control system for fluid regulation, governing blood pressure, volume, and electrolyte homeostasis while also contributing to the pathogenesis of cardiac hypertrophy and fibrosis [6, 7]. Angiotensin II receptor blockers (ARBs) primarily inhibit the binding between angiotensin II and the angiotensin II type 1 (AT-1) receptor, acting as inhibitors of the RAAS [8]. The findings from several preliminary small-scale studies have indicated a potential benefit of ARBs in HCM, primarily attributed to an amelioration in LV mass [9‒11]. Nevertheless, recent large-scale randomized controlled trials (RCTs) have failed to replicate these favorable outcomes. The INHERIT study revealed that losartan did not demonstrate efficacy in improving myocardial hypertrophy and fibrosis among patients diagnosed with HCM [12]. In addition, the VANISH trial indicated that valsartan solely exhibited disease progression mitigation effects rather than complete reversal of ventricular remodeling in individuals presenting early sarcomeric HCM [13]. The conclusions of certain pertinent meta-analyses in recent years also exhibit disparities [14‒16]. To further evaluate the effectiveness of ARBs in managing HCM, we conducted an updated meta-analysis.

Our meta-analysis adhered to the guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analyses in order to ensure methodological rigor [17]. This study has been registered on the International Prospective Register of Systematic Reviews, PROSPERO (CRD42023471357). All data were obtained from published articles, thus obviating the need for ethical approval.

Search Strategy and Selection Criteria

We conducted a comprehensive search of PubMed, Web of Science, EMBASE, Cochrane Library, and ClinicalTrials.gov up to October 2023 to retrieve relevant articles. Our search strategy included terms such as “hypertrophic cardiomyopathy,” “HCM,” “ventricular hypertrophy,” “angiotensin II receptor antagonist/blocker/inhibitor,” “ARB,” and the specific names of each angiotensin receptor blocker (azilsartan, candesartan, eprosartan, irbesartan, losartan, olmesartan, valsartan).

The following studies were included: RCTs, trials were conducted in patients with a diagnosis consistent with HCM, the participants were assigned to receive either ARB treatment or non-ARB treatment for any duration of time, and studies that provided sufficient information. The following studies were excluded: those not published in English, articles that did not contain complete results, and articles that did not report any indicators related to the prognosis of HCM.

Data Extraction and Quality Assessment

Two independent reviewers (Y.W. and P.G.) utilized predetermined criteria to conduct a systematic review of eligible studies and extract pertinent data. We gathered the subsequent data: study characteristics, patient numbers, patient profiles, treatment protocols, follow-up periods and outcomes of interest including LV mass, maximum LV wall thickness, LV fibrosis, early diastolic mitral annular velocity (E′), and LV ejection fraction. We used the Cochrane risk of bias tool to analyze the bias risk of enrolled RCTs [18].

Statistical Analysis

Continuous variables were expressed as the mean and standard deviation (SD). The conversion of 95% confidence intervals (CIs) to SDs and the calculation of the mean and SD of the difference were conducted following the guidelines provided by the Cochrane Handbook for Systematic Reviews of Interventions [19]. The LV mass values reported by Yamazaki et al. [9] are expressed in terms of volume (cm3), and the myocardial density is approximately 1.05 g/cm3 [20]; thus, we converted these values into weight units (g). The LV mass index (LV mass index = LV mass/body surface area) was reported by Axelsson et al. [12] and Ho et al. [13], which we recalculated to determine the LV mass using an average body surface area of 1.73 m2. Considering all the standardization measures for evaluating variable units of measurement, we employed the mean difference (MD) and its corresponding 95% CI to assess differences among the evaluation team.

The heterogeneity of the results was evaluated using Cochran’s Q test and quantified by the I2 statistic. High heterogeneity was defined as I2 >50%. In cases of significant heterogeneity, a random-effects model was employed; otherwise, a fixed-effects model was used. Sensitivity analysis was conducted by systematically excluding each study in succession. The presence of publication bias was assessed using Egger’s test. The study results were summarized using Review Manager version 5.4 (The Cochrane Collaboration, Copenhagen, Denmark), while sensitivity analysis and Egger test were conducted using STATA version 14.0 (STATA Corporation, TX, USA).

Search Results

By conducting a thorough search of databases and relevant article references, we identified 1913 eligible articles. After removing duplicates, we screened 895 articles based on their titles and abstracts, resulting in the exclusion of 859 more. Finally, we reviewed the full text of 36 remaining articles according to our inclusion and exclusion criteria, ultimately including 7 articles [9‒13, 21, 22] in our analyses (Fig. 1).

Fig. 1.

Flowchart of the meta-analysis.

Fig. 1.

Flowchart of the meta-analysis.

Close modal

Study Characteristics

Table 1 presents a summary of the clinical characteristics of the studies that were included in this analysis. The study included a total of 7 articles with 387 participants, two of which presented distinct data from the same trial (the INHERIT trial) [12, 22].

Table 1.

Study characteristics

Auther (Year)CountryAge, yearsType of ARBParticipants, nDose of ARBControl groupFollow-upMeasurementOutcome
Kawano et al. [21] (2005) Japan Valsartan 23 80 mg per day Conventional treatment without ARB 12 months ECHO LV ejection fraction 
Yamazaki et al. [9] (2007) Japan Losartan 19 50 mg per day Conventional treatment without ARB 12 months CMR or ECHO LV mass 
Penicka et al. [10] (2009) Czech Republic ≥18 Candesartan 23 32 mg per day Placebo 12 months ECHO LV mass, E′, LV ejection fraction 
Shimada et al. [11] (2013) USA ≥18 Losartan 20 100 mg per day Placebo 12 months CMR or ECHO LV mass, LV fibrosis 
Axelsson et al. [12] (2015) Denmark ≥18 Losartan 124 100 mg per day Placebo 12 months CMR, CT, or ECHO LV mass, maximum LV wall thickness, LV fibrosis 
Axelsson et al. [22] (2016) Denmark ≥18 Losartan 124 100 mg per day Placebo 12 months CMR, CT, or ECHO E′, LV ejection fraction 
Ho et al. [13] (2021) 4 countries Primary 8–45 Valsartan 188 Adults 320 mg/d, children ≥35 kg: 160 mg/d; children <35 kg: 80 mg/d Placebo 24 months CMR or ECHO LV mass, maximum LV wall thickness, E′ 
Auther (Year)CountryAge, yearsType of ARBParticipants, nDose of ARBControl groupFollow-upMeasurementOutcome
Kawano et al. [21] (2005) Japan Valsartan 23 80 mg per day Conventional treatment without ARB 12 months ECHO LV ejection fraction 
Yamazaki et al. [9] (2007) Japan Losartan 19 50 mg per day Conventional treatment without ARB 12 months CMR or ECHO LV mass 
Penicka et al. [10] (2009) Czech Republic ≥18 Candesartan 23 32 mg per day Placebo 12 months ECHO LV mass, E′, LV ejection fraction 
Shimada et al. [11] (2013) USA ≥18 Losartan 20 100 mg per day Placebo 12 months CMR or ECHO LV mass, LV fibrosis 
Axelsson et al. [12] (2015) Denmark ≥18 Losartan 124 100 mg per day Placebo 12 months CMR, CT, or ECHO LV mass, maximum LV wall thickness, LV fibrosis 
Axelsson et al. [22] (2016) Denmark ≥18 Losartan 124 100 mg per day Placebo 12 months CMR, CT, or ECHO E′, LV ejection fraction 
Ho et al. [13] (2021) 4 countries Primary 8–45 Valsartan 188 Adults 320 mg/d, children ≥35 kg: 160 mg/d; children <35 kg: 80 mg/d Placebo 24 months CMR or ECHO LV mass, maximum LV wall thickness, E′ 

ARB, angiotensin II receptor blocker; CMR, cardiac magnetic resonance imaging; CT, computed tomography; E′, early diastolic mitral annular velocity; ECHO, echocardiography; LV, left ventricular.

Quality Assessment

The risk of bias assessment is depicted in Figure 2. The risk of selection and detection bias was assessed as low in all the studies. The implementation of patient blinding was not explicitly disclosed by Yamazaki et al. [9] and Penicka et al. [10], thus making it impossible to assess the presence of performance bias. Kawano et al. [21] and Yamazaki et al. [9] did not provide information on whether any patients dropped out, thus making it impossible to determine the completeness of the outcome data. Considering the need for meta-analysis, 4 studies [9, 11‒13] may have imperfect outcomes. Other biases were indeterminate in 4 studies [9‒11, 21] owing to small sample sizes.

Fig. 2.

Quality evaluations of RCTs. RCT, randomized controlled trial.

Fig. 2.

Quality evaluations of RCTs. RCT, randomized controlled trial.

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Study Outcomes

Five studies [9‒13] reported LV mass, and the pooled results showed that the use of ARBs could reduce LV mass by 11.77 g. However, the effect was not statistically significant, and there was substantial heterogeneity (95% CI: −24.51 g, 0.97 g; p = 0.07; I2 = 72%; Fig. 3a).

Fig. 3.

The forest plots provide a comprehensive summary of the correlation between ARBs and changes in indicators related to HCM. a LV mass. b Maximum LV wall thickness. c LV fibrosis. d E’. e LV ejection fraction. ARB, angiotensin II receptor blocker; CI, confidence interval; E’, early diastolic mitral annular velocity; HCM, hypertrophic cardiomyopathy; LV, left ventricular; MD, mean difference.

Fig. 3.

The forest plots provide a comprehensive summary of the correlation between ARBs and changes in indicators related to HCM. a LV mass. b Maximum LV wall thickness. c LV fibrosis. d E’. e LV ejection fraction. ARB, angiotensin II receptor blocker; CI, confidence interval; E’, early diastolic mitral annular velocity; HCM, hypertrophic cardiomyopathy; LV, left ventricular; MD, mean difference.

Close modal

Two studies [12, 13] reported the maximum LV wall thickness, and the pooled results demonstrated a non-statistically significant reduction of 0.67 mm in myocardial thickness with the use of ARBs, accompanied by substantial heterogeneity (95% CI: −1.79 mm, 0.46 mm; p = 0.25; I2 = 53%; Fig. 3b). The extent of LV fibrosis was evaluated in two studies [11, 12], and the combined findings revealed that the utilization of ARBs did not yield a significant improvement in LV fibrosis and exhibited a high degree of heterogeneity (MD = −23.84%; 95% CI: −78.25%, 30.57%; p = 0.39; I2 = 92%; Fig. 3c). The combined findings from the three studies [10, 13, 22] indicated that there was no significant improvement in E′ observed in the ARB group compared to the control group, and a high level of heterogeneity was noted (MD = 1.02 cm/s; 95% CI: −0.49 cm/s, 2.53 cm/s; p = 0.19; I2 = 84%; Fig. 3d). The LV ejection fraction was reported in three studies [10, 21, 22], and the comprehensive results indicate that there is no significant difference in the degree of change between patients treated with ARBs and those in the control group, with low heterogeneity observed (MD = 0.73%; 95% CI: −1.12%, 2.57%; p = 0.44; I2 = 12%; Fig. 3e).

Sensitivity Analysis and Publication Bias

As the number of included articles was limited, we did not perform sensitivity analysis or publication bias detection for results based on less than 3 studies. Sensitivity analysis is shown in Figure 4.

Fig. 4.

The sensitivity analysis of ARBs on the impact of related parameters in HCM. a LV mass. b E’. c LV ejection fraction. ARB, angiotensin II receptor blocker; E’, early diastolic mitral annular velocity; HCM, hypertrophic cardiomyopathy; LV, left ventricular.

Fig. 4.

The sensitivity analysis of ARBs on the impact of related parameters in HCM. a LV mass. b E’. c LV ejection fraction. ARB, angiotensin II receptor blocker; E’, early diastolic mitral annular velocity; HCM, hypertrophic cardiomyopathy; LV, left ventricular.

Close modal

When assessing the effect of ARBs on LV mass, no significant decrease in heterogeneity was observed upon exclusion of each individual study; however, after excluding the study conducted by Axelsson et al. [12], the pooled results became statistically significant (MD = −21.38 g; 95% CI: −41.91 g, −0.84 g; p = 0.04; I2 = 68.1%). As for the effect of ARBs on E′, after excluding the study conducted by Penicka et al. [10], a significant reduction in heterogeneity was observed, and the pooled results demonstrated that ARBs exhibited improvement in E' (MD = 0.311 cm/s; 95% CI: 0.039 cm/s, 0.584 cm/s; p = 0.025; I2 = 0%). The exclusion of each individual study did not yield a reduction in heterogeneity when evaluating the impact of ARBs on LV ejection fraction, and every outcome consistently indicated that ARBs failed to elicit improvement in LV ejection fraction. The Egger test did not show any publication bias related to these results (LV mass: p = 0.12; E′: p = 0.67; LVEF: p = 0.44).

We conducted a meta-analysis by synthesizing data from 7 articles derived from 6 RCTs involving 387 participants, aiming to evaluate the impact of ARBs on patients with HCM. The findings revealed no significant association between ARB treatment and alterations in LV mass, maximum LV wall thickness, LV fibrosis, E′, or LV ejection fraction.

The pathogenesis of HCM is still under investigation, with several studies indicating that the relationship between mutations in genes associated with HCM and clinical phenotypes encompasses a diverse range of factors [23]. Additionally, there exists a correlation between the RAAS and HCM. Numerous studies have indicated that genetic variations in RAAS components (such as angiotensin-converting enzyme [ACE], angiotensinogen, AT-1 receptor, AT-2 receptor) may impact the phenotypic alterations observed in HCM [24]. As blockers of the RAAS, ARBs effectively inhibit transforming growth factor-beta (TGF-β) [25]. Several animal models of HCM have demonstrated the significant role played by TGF-β activation in triggering the development of cardiac hypertrophy and fibrosis [25, 26]. The use of ARBs as a vasodilator carries a certain risk of exacerbating outflow obstruction in patients with obstructive HCM. Current guidelines only recommend its use in patients with non-obstructive HCM and heart failure with an ejection fraction below 50% [2]. However, several studies have demonstrated the safety profile of ARBs in patients with obstructive HCM [12, 27].

The presence of LV hypertrophy is a characteristic pathological manifestation observed in cases of HCM. In contrast to the uniform myocardial hypertrophy associated with hypertension, individuals with HCM often exhibit irregular focal areas of myocardial hypertrophy [28]. Some studies have indicated that muscle fiber contractile dysfunction, impaired calcium sensitivity, and impaired mitochondrial energy production may play significant roles in the development of compensatory myocardial hypertrophy among patients with HCM [23]. Vignier et al. [29] demonstrated that treatment with irbesartan effectively reversed cardiac hypertrophy in mutant knockout mice with HCM. An increase in LV mass is considered one of the hallmarks of cardiac hypertrophy. Previous studies have produced conflicting results regarding the efficacy of ARBs in reducing LV mass in patients with HCM. The meta-analysis conducted by Liu et al. [15] revealed that the use of ARBs did not yield significant improvements in LV mass among patients diagnosed with HCM. The results of a recent study on patients with early stage sarcomeric HCM who received valsartan treatment for 2 years indicated that while there was no improvement in LV mass, the use of valsartan still demonstrated beneficial effects as assessed by a composite score comprising 9 indicators related to cardiac structure/function and remodeling [13]. Our comprehensive meta-analysis of all available RCTs revealed that ARBs not only failed to demonstrate any improvement in LV mass but also exhibited no significant impact on maximum LV wall thickness in patients with HCM. These findings seem to suggest that ARBs do not effectively enhance cardiac structure among individuals suffering from HCM.

Although we included the same number of studies as Abdelazeem et al. [16] in the assessment of LV mass, different results were obtained. Abdelazeem et al. [16] incorporated LV myocardial volume and LV mass index into their evaluation of the impact of ARBs on LV mass and analyzed the combined outcomes using standardized MD. However, considering that these data can be transformed, our meta-analysis using MD provides a more accurate reflection of the trial effect associated with this measure [19]. Additionally, the LV mass data we collected from Shimada et al. [11] differed from that obtained by Abdelazeem et al. [16] By utilizing the unprocessed values of LV mass provided by Shimada et al. [11] in their supplementary material, we calculated the mean and SD for each group, indicating a higher level of accuracy in our results.

Myocardial fibrosis is also a significant pathological manifestation of HCM, and several studies suggest that myocardial fibrosis may serve as an early indicator of HCM [23, 30]. Myocardial fibrosis can be attributed to premature apoptosis of myocytes and subsequent expansion of the interstitial matrix, as well as potential causes such as microvascular ischemia and cardiomyocyte hypertrophy [23, 31]. Additionally, the activation of TGF-β signaling by non-muscle cells, such as fibroblasts, also plays a crucial role in the pathogenesis of increased fibrosis associated with HCM [25]. Lim et al. [26] discovered that losartan treatment effectively reversed cardiac interstitial fibrosis and suppressed the expression of collagen 1α and TGF-β1 in HCM mice. Teekakirikul et al. [25] found that the administration of losartan effectively inhibited the development of cardiac hypertrophy and fibrosis in mice carrying the mutant gene. However, no inhibitory effects were observed in mice with hypertrophic formation; they only exhibited a reduction in the proliferation of nonmuscle cells [25]. The current clinical trials investigating the effects of ARBs on myocardial fibrosis in patients with HCM are limited. The study conducted by Kawano et al. [21] demonstrated the efficacy of valsartan in reducing type I collagen synthesis in patients with HCM, suggesting its potential for improving myocardial fibrosis. Axelsson et al. [12] and Shimada et al. [11] both employed losartan for the treatment of HCM, utilizing cardiac magnetic resonance imaging to quantify late gadolinium enhancement as a means of evaluating the extent of myocardial fibrosis; however, their findings diverged. The pooled results of these two studies indicated that the use of ARBs did not lead to any significant improvement in myocardial fibrosis.

Furthermore, the analysis results of both E′ and LV ejection fractions indicate that ARBs do not appear to enhance cardiac function in patients with HCM. In the early stage of HCM, diastolic function is often impaired due to myocardial hypertrophy and inadequate ventricular filling, while systolic function remains unaffected [32]. A decline in LV ejection fraction may serve as an indicator of advanced disease progression [22]. The findings of a recent study suggest that reduced LV ejection fraction can serve as an independent indicator for hospitalization due to heart failure and cardiovascular mortality in patients with HCM [33].

HCM, being a genetic disorder, is primarily attributed to gene dysregulation. The animal study demonstrated that the administration of ARB effectively reversed cardiac hypertrophy following the knockout of the mutant gene (eliminating the cause) [25]. However, our findings suggest that the utilization of ARBs as a standalone intervention remains insufficient to counteract genetic mechanisms in cases where the underlying cause cannot be eradicated.

In addition, HCM is a progressive disease [34]. In the VANISH trial, patients with early HCM and subclinical HCM who received treatment with valsartan demonstrated comparable outcomes, while in the placebo group, patients with early HCM exhibited greater ventricular remodeling compared to those with subclinical HCM [13, 35]. These findings suggest that valsartan may potentially attenuate the phenotypic progression of early stage HCM. Therefore, we speculate that ARBs may not be effective in reversing ventricular remodeling in HCM patients; however, they might play a role in attenuating phenotypic progression, which necessitates further investigation.

These findings provide aggregated estimates from high-quality studies to inform clinical decision-making. We incorporated 6 RCTs into our analysis. By standardizing the unit of relevant data and adopting a different approach to data analysis, we arrived at distinct conclusions compared to the previous meta-analysis [16] for certain outcomes (e.g., LV mass). Relevant beneficial effects of ARB on HCM were not observed in our study. A recent review evaluating the impact of RAAS inhibitors on HCM observed that certain RAAS inhibitors, such as losartan or candesartan, exhibited significant improvements in myocardial hypertrophy and fibrosis, while valsartan did not demonstrate similar effects [36]. Conversely, aldosterone receptor blockers were found to lack a substantial beneficial influence [36]. It is important to note that the inclusion of studies in this review is limited. For instance, a meta-analysis comprising 3 studies investigating the impact of losartan on myocardial hypertrophy in HCM revealed no significant improvement in LV hypertrophy with losartan treatment [15]. Our research primarily focused on ARBs and comprehensively incorporated RCTs to analyze indicators such as myocardial hypertrophy, fibrosis, and cardiac function in order to further elucidate the relationship with HCM.

In addition, ACE inhibitors, as a type of RAAS inhibitor, primarily function by inhibiting the ACE, thereby reducing the production of angiotensin II from angiotensin I. Although they have different target sites compared to ARBs, both can effectively suppress the excessive activation of the RAAS. The clinical trials of ACE inhibitors in HCM are still insufficient. A previous study revealed that sublingual administration of captopril may exacerbate LV diastolic dysfunction in patients with obstructive HCM [37]. A recent trial demonstrated that treatment with RAAS inhibitors (valsartan or enalapril), although deemed safe, did not result in improved all-cause mortality among patients with HCM [27]. Therefore, the current evidence does not support the efficacy of other RAAS inhibitors in HCM.

However, various gene mutations have been identified in association with HCM, and distinct mutated genes may result in diverse clinical phenotypes [38]. For example, the severity of LV hypertrophy and fibrosis may be more pronounced in cases where mutations occur in MYH7, which encodes β-myosin heavy chain, compared to cases with mutations in MYBPC3, which encodes cardiac myosin binding protein c (cMYBPC) [30, 39, 40]. Penicka et al. [10] demonstrated that candesartan exhibited a more pronounced reduction in LV mass in patients with HCM carrying β-myosin heavy chain mutations compared to those with cMYBPC mutations. Since the majority of existing studies have not compared the therapeutic efficacy differences among different genotypes, it is also imperative to further assess the impact of ARB treatment on patients with distinct genotypes of HCM in future studies.

The limitations of our study need to be acknowledged. First, the number of included studies was limited, and some studies had a small sample size. Second, there is high heterogeneity in the analysis of each index in this study. The heterogeneity observed may be attributed to the following factors: (1) variations exist in the baseline conditions selected by different studies. For instance, the majority of patients enrolled in the study conducted by Axelsson et al. [12, 22] exhibited an advanced stage of HCM. In contrast, Ho et al. investigated patients with early stage sarcomeric HCM. (2) The treatment measures employed in the control group varied; Kawano et al. [21] and Yamazaki et al. [9] utilized conventional medical treatment, while the other studies administered a placebo. It is worth noting that Kawano et al. [21] primarily administered calcium channel antagonists and bata-blockers to the control group, whereas Yamazaki et al. [9] treated the control group with calcium channel antagonists, beta-blockers, and diuretics. Although calcium channel antagonists and beta-blockers do not improve myocardial hypertrophy in patients with HCM, they have been demonstrated to effectively enhance LV end-diastolic volume [41, 42]. Additionally, beta-blockers may also augment the global systolic function of the myocardium following exercise [43]. These drugs seem to be more beneficial for patients with HCM compared to placebos. (3) The measurement of LV mass differed between studies: Kawano et al. [21] and Penicka et al. [10] utilized echocardiography, while other investigations predominantly employed cardiac magnetic resonance imaging. The aforementioned factors may have exerted an inevitable impact on our findings. Finally, the sensitivity analysis revealed that the findings of our meta-analysis regarding the impact of ARBs on LV mass and E′ were unstable. Considering the limited number of included studies, however, there may be a deviation in these results.

This study analyzed 7 articles from 6 RCTs and determined that ARBs do not improve cardiac structure, function, or myocardial fibrosis in patients with HCM. Collectively, our findings do not support the effectiveness of angiotensin-receptor blockade in reversing ventricular remodeling in patients with HCM. Further trials are necessary to establish the role of angiotensin in treating patients with HCM.

Ethical approval and consent were not required as this study was based on publicly available data.

The authors have no conflicts of interest to declare.

This study was not supported by any sponsor or funder.

Y.W. and P.G. designed the research study, conducted literature screening, and extracted important information. S.H. and T.X. analyzed the data. S.W. and M.Q. wrote the manuscript.

Additional Information

Yong Wan, Shuai He, Tingli Xu, and Shuwei Wang contributed equally to this work.

All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author.

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