Although there is a well established link between blood pressure (BP) levels and the severity of hypertension-mediated organ damage (HMOD), some patients with hypertension exhibit a disproportionate degree of HMOD relative to their BP. This study aims to define disproportionate degrees, relative to blood pressure, of left ventricular hypertrophy (LVH) measured by Sokolow-Lyon (SL) index and of arterial stiffness measured by carotid-femoral pulse wave velocity (PWV), and to assess the sex differences and characteristics of individuals with such disproportional SL index and PWV. SL index was analysed in 6487 participants of The Maastricht Study [50.9% men; 23.7% type 2 diabetes mellitus (T2DM)]. PWV was analysed in 6239 participants (51.3% men; 23.5% T2DM). The residuals of linear regression models for the relationship between SL index or PWV and 24 h mean arterial pressure (MAP) was used to define participants with disproportional SL index and PWV, respectively. Individuals with higher-than-expected (>90th percentile of the residuals) and lower-than-expected (<10th percentile) of SL index or PWV were defined as subclinical HMOD. A multinomial regression analysis was conducted to identify the clinical characteristics associated with subclinical HMOD. Males and females with higher SL index than expected based on their 24 h MAP, were older, had a higher BMI and were more often living with type 2 diabetes in comparison to those in the as-expected and lower-than-expected groups. In line, men who are living with diabetes are 34% less likely to be in the group with lower-than-expected SL index while women living with prediabetes and type 2 diabetes are 40% more likely to be in the group with higher-than-expected SL index. Likewise, males and females with higher-than-expected PWV were older and more often living with type 2 diabetes than those in the as-expected and lower-than-expected groups. Persons who are older, or living with obesity and/or T2D are more likely to have subclinical HMOD, than would be expected based on their prevailing level of BP. Therefore, these clinical determinants would result in higher-than-expected HMOD. Treating those with overweight and obesity with prediabetes and diabetes more aggressively will likely reduce subclinical HMOD.

Aortic stenosis (AS) may lead to left ventricular (LV) hypertrophy (LVH). After aortic valve replacement (AVR), LVH often does not regress fully. This has been associated with a worse prognosis. This study aimed at comparing LVH regression between male and female patients and to discover cardiac molecular factors associated with it. Myocardial samples were collected from 18 patients (50% female) who underwent surgical AVR. Preoperative and postoperative LV mass indices (LVMi) were compared between male and female patients. Expression of ADGRL4 and AQP7 was quantified by PCR and assessed with relative regression of LVMi. High-depth RNA-sequencing data from LV free-wall tissues of subjects with heart failure were employed for RNA editing analysis. Male patients had significant LVH regression (P < 0.05) after AVR, while female patients did not (P = 0.116). In male patients, a significant relationship was found between the expression of ADGRL4 (P < 0.05, R2 = 0.497) and AQP7 (P < 0.05, R2 = 0.576) and LVMi regression after AVR. This relationship was insignificant for ADGRL4 (P = 0.704, R2 = 0.0220) and AQP7 (P = 0.860, R2 = 0.00477) in female patients. RNA editing analysis revealed significant sex-biased differences in intronic adenosine-to-inosine (A-to-I) editing of AQP7, with five positions, particularly within Alu elements, along with sex-biased predicted RBP binding motifs. Recognizing patients at risk of defective LVH regression using molecular factors could lead to more intensive postoperative follow-up and earlier treatment, consequently improving reverse remodeling and prognosis. The present findings warrant further research in a larger study.NEW & NOTEWORTHY Regression of left ventricular hypertrophy is associated with better long-term outcome. This study demonstrates a significant relationship between ADGRL4 and AQP7 gene expression in perioperatively collected myocardial tissues and the regression of left ventricular mass postoperatively in male patients with aortic stenosis only. This could contribute to the development of a sex-based tool to predict the extent of postoperative hypertrophy regression.

Nocturnal hypertension is closely associated with left ventricular hypertrophy (LVH) in patients with chronic kidney disease (CKD). Recently, several studies have shown that central pressure reflects the actual load on the cardiovascular system. However, the relationship between nighttime central systolic blood pressure (SBP) and LVH in CKD patients remains unknown. A total of 3198 non-dialysis CKD patients were enrolled in this multicenter retrospective study. Ambulatory blood pressure monitoring was performed using the Mobil-O-Graph PWA device. Applying 120/130 mm Hg as the nighttime brachial SBP (bSBP)/central SBP with c2 calibration (c2SBP) thresholds, patients were classified into 4 nocturnal hypertension patterns. Logistic regression and the net reclassification improvement were used to analyze the associations between nocturnal SBP indices and LVH. There were 989 patients (30.9%) who had nocturnal central hypertension, and 448 patients (15%) had LVH. As renal function declined, the incidence of both LVH and nocturnal hypertension demonstrated a significant ascending trend. In addition, LVH risk increased progressively with higher nighttime c2SBP levels. Multivariate logistic regression and net reclassification improvement analyses suggested that nighttime c2SBP demonstrated superior correlation with LVH compared to nighttime bSBP. With consistent nocturnal normotension as the reference, the adjusted odds ratios were 1.183 (95% CI: 0.816-1.715, P = .377) for isolated nocturnal brachial hypertension and 2.660 (95% CI: 2.051-3.449, P < .001) for consistent nocturnal hypertension, respectively. Nighttime central SBP is more closely associated with LVH in non-dialysis CKD patients, and further prospective studies are needed to validate its prognostic value.

Among patients with acute myocardial infarction undergoing PCI, subsequent structural alterations of the left ventricle, including left ventricular remodeling (LVR) and left ventricular hypertrophy (LVH), may contribute to later heart failure. This study examined whether GLS measured early after reperfusion could help identify patients at increased risk for these post-infarction changes. A total of 131 patients with AMI who underwent primary PCI at our hospital between March 2023 and October 2024 were included. GLS was assessed within 7 days after PCI using two-dimensional speckle-tracking echocardiography. The primary endpoints were LVR and LVH assessed at 6-12 months of follow-up. We used logistic regression to estimate the associations of GLS with the endpoints, applied restricted cubic splines (RCS) to explore possible nonlinear trends, and conducted subgroup analyses to assess the robustness of the results. Logistic regression analyses demonstrated that impaired GLS was independently associated with a higher risk of LVR. In tertile analyses, compared with patients in T1, representing better preserved LV systolic function, those in T3, representing more impaired LV systolic function, had significantly higher risks of LVR (OR = 7.51, 95% CI: 1.41-39.96, p = 0.02) and LVH (OR = 6.15, 95% CI: 1.40-27.04, p = 0.02). RCS analysis indicated linear associations between GLS and the risks of both LVR and LVH. ROC analysis showed that the optimal GLS cut-off values for predicting LVR and LVH were -11.54% and -11.22%, with AUCs of 0.724 and 0.774, respectively. Early impairment of GLS in patients with AMI after PCI was associated with subsequent LVR and LVH, suggesting that GLS may be useful for early risk stratification in this population.

Fluid overload in children undergoing dialysis can lead to serious cardiac complications, i.e., left ventricular hypertrophy (LVH) and cardiac dysfunction. Studies investigating the cardiovascular effects of persistent subclinical hypervolemia-characterized by euvolemia at clinical assessment but hypervolemia at technical evaluation-are lacking. This pilot study explored the combined use of lung ultrasound (LUS), bioimpedance spectroscopy (BIS), and ultrasound assessment of the inferior vena cava collapsibility index (IVC-CI) to identify subclinical hypervolemia and investigated its cardiac impact. In this longitudinal study, we recruited 23 children on chronic dialysis who underwent fluid status evaluation (physical examination, LUS, IVC-CI, BIS) every 2months and echocardiography every 6months. In clinically euvolemic patients, we observed a significant positive correlation between the interdialytic weight gain and the number of B-lines observed by LUS (R = 0.2923, p < 0.001); similar results were obtained for the OH/ECW measured by BIS (R = 0.4144, p < 0.001), while a negative correlation with IVC-CI (R = - 0.2597, p = 0.019) was observed. Moreover, we identified a significant linear correlation between left ventricular mass index values and the average pre-dialysis systolic blood pressure measured over the preceding 6months (R2 = 0.16, p = 0.002). Hospitalizations due to hypertensive crises (67% vs. 0%, p < 0.01) and the occurrence of LVH at the final follow-up (75% vs. 27%, p = 0.04) were notably more frequent in children with subclinical hypervolemia. In clinically euvolemic children on dialysis, the combined use of LUS, BIS, and IVC-CI (multiparametric approach) effectively quantified subclinical hypervolemia, which was correlated with the risk of LVH.

Elevated lipoprotein(a) [Lp(a)] levels have been strongly related to cardiovascular (CV) risk. However, its association with Hypertension Mediated Organ Damage (HMOD) and CV events in the primary prevention setting remains unclear. To evaluate in these patients, the correlation between Lp(a) levels and: (i) heart, vessels and kidney HMOD and; (ii) CV events and all-cause mortality in a primary prevention setting. 747 low CV risk subjects were recruited between 2009 and 2014. HMOD was assessed through Pulse Wave Velocity, carotid Intima-Media Thickness (IMT), presence of carotid plaques, Left Ventricular Hypertrophy (LVH) and Ejection Fraction and glomerular filtration rate. All-cause mortality and CV events up to 2021 were retrieved by electronic health records, for a median follow-up time of 10 years (I-III quartiles 9.6-11.1). Mean age was 50.8 ± 13.0 years and 63.5% of the subjects were men. The prevalence of hypertension was 37.9%, dyslipidemia 67.2%, smoking 17.8%, and diabetes mellitus 8.7%. Median Lp(a) value was 17 mg/dL (5.9-56.0), and 26.5% of patients had values above 50 mg/dL. Regarding HMOD, 10.3% subjects had arterial stiffness, 7.2% increased IMT, 19.8% carotid plaques while only 0.7% had LVH. No significant correlation was found between Lp(a) levels and indices of subclinical HMOD. Furthermore, no relationship was found between CV events and all-cause mortality and Lp(a) levels. In this primary prevention cohort, elevated Lp(a) levels were not associated with significant structural damage to the heart, carotid arteries, or increased aortic stiffness and were not associated with CV events and all-cause mortality.

Screening of Atrial Fibrillation/Arrhythmia Events in Patients With Abnormal ECHOcardiographic Parameters: The Randomized, Prospective SAFE-ECHO Study Design and Rationale.

Blood pressure (BP) is a dynamic trait associated with cardiovascular disease. We aimed to estimate age-specific BP levels and rates of change from childhood to mid-adulthood and to examine their associations with subsequent subclinical target organ damage. We included 2508 participants from the Hanzhong Adolescent Hypertension Study with BP measured ≥4× from 1987 to 2023. Surrogate markers of target organ damage were assessed, including arterial stiffness, left ventricular hypertrophy, and albuminuria. Growth models were used to construct BP trajectories and estimate age-specific BP levels and rates of change (slopes). Rates of change in BP at each age point from childhood to mid-adulthood were positively associated with arterial stiffness and albuminuria in mid-adulthood, independent of corresponding BP levels. The magnitude of the associations rose from childhood, peaked in adolescence, and declined thereafter. For example, odds ratios (95% CIs) per 1 SD increase in systolic BP change rates for arterial stiffness increased from 1.94 (1.69-2.24) at age 6 to 2.11 (1.82-2.44) at age 13, then declined to 1.13 (1.01-1.28) by age 52. Faster BP increases were more strongly associated with arterial stiffness and albuminuria than concurrent BP levels during childhood and adolescence, whereas the opposite trend was observed in young and mid-adulthood. Similar age-dependent trends were identified for left ventricular hypertrophy, with minor variations in the ages at which associations reached statistical significance. Accelerated BP increases during childhood and adolescence show a stronger association with mid-adult subclinical target organ damage than increases occurring in adulthood.

Hypertension-mediated organ damage (HMOD) represents a critical and dynamic stage on the cardiovascular continuum, serving as the primary mechanistic link between sustained arterial pressure elevation and major adverse cardiovascular and renal events. HMOD is often subclinical at first occurrence and is a systemic, cumulative process, representing structural and functional injury of the heart, brain, kidneys, and vasculature. This narrative review synthesises current evidence on the pathogenesis and clinical sequelae of HMOD, specifically focusing on the interplay between chronic haemodynamic load, endothelial dysfunction, oxidative stress, neurohormonal activation, inflammation, and microvascular remodelling. Key manifestations such as left ventricular hypertrophy, hypertensive nephrosclerosis, cerebral small vessel disease, and arterial stiffness can be regarded as dynamic and partly modifiable phenomena of subclinical injury rather than inevitable sequelae of long-standing hypertension. This review aims to summarise contemporary detection and risk stratification approaches, drawing on the 2023 European Society of Hypertension (ESH) and 2024 European Society of Cardiology (ESC) guidelines, combining imaging and biomarker-based assessment. Evidence supporting organ protection as an important therapeutic objective is also reviewed, with particular attention to regression of left ventricular mass and reduction in albuminuria as treatment endpoints associated with improved prognosis beyond blood pressure reduction alone. Finally, unresolved issues such as causal versus associative properties of candidate biomarkers, comparative validity of vascular indices, and heterogeneity in organ-specific response to therapy are critically analysed. The overarching goal of this review is to support a clinically applicable framework for early HMOD detection and organ-protective treatment strategies in routine hypertension care.

Left ventricular (LV) hypertrophy and dysfunction secondary to aortic stenosis (AS) are key components of the disease's underlying pathophysiology. Previous trials suggest that up to 1/3 of patients do not benefit symptomatically after aortic valve replacement (AVR), which could be explained by insufficient LV remodeling. Sodium‒glucose cotransporter-2 (SGLT2) inhibitors are effective in heart failure (HF) and have been shown to improve LV remodeling (change in LV mass). The EMPAVR study is an investigator-initiated, randomized, placebo-controlled, and double-blinded trial comparing the effect of empagliflozin to placebo in patients with severe and symptomatic AS undergoing transcatheter aortic valve implantation (TAVI). The primary outcome for the EMPAVR trial is the difference in LV mass indexed to body surface area (measured by cardiac CT) from pre-AVR to 6 months post-AVR. Patients are randomized in a 1:1 ratio to 180 days of treatment. To the best of our knowledge, the EMPAVR study is the first placebo-controlled trial investigating the effects of SGLT2 inhibition in patients following TAVI because of AS. The EMPAVR study has the potential to pave the way for treatment of the LV in valvular heart disease and may help patients worldwide and expand our understanding of aortic stenosis. The EMPAVR study was registered in December 2024 (Clinical Trial Registration number: NCT06171802) before enrollment of the first patient. All patients will provide oral and written informed consent. The EMPAVR study is approved by the Regional Committee on Health Research Ethics and the Danish Medicines Agency.

We aimed to examine the association between insulin resistance (IR) and target organ damage (TOD) in patients with hypertension. Three indices of IR (Triglyceride-Glucose index: TyG; triglyceride-to-HDL ratio: TG/HDL-C; Metabolic Score for Insulin Resistance: METS-IR) were examined for their association with TOD in 614 newly diagnosed patients with hypertension. Left ventricular mass index (LVMI), the intima-media thickness of the common carotid artery (IMT-CCA) and estimated Glomerular Filtration Rate (eGFR) were used as indices of cardiac, artery and renal damage. Receiver Operating Characteristic (ROC) analysis performed to estimate optimal cut-off for each index, while simple and multiple logistic regression models were applied to examine the indices as binary predictors of organ damage. Linear and non-linear associations were examined with continuous variables using linear regression and restricted cubic splines (RCS) models. After adjusting for confounders, logistic regression showed that high TG/HDL-C (OR:1.50, 95%CI:1.03-2.18) and METS-IR (OR:2.17, 95%CI:1.50-3.13) were associated with increased risk of left ventricular hypertrophy, while only high METS-IR was associated with increased risk of carotid plaque (OR:2.07, 95%CI:1.17-3.68) and only high TG/HDL-C was associated with renal damage (OR:2.33, 95%CI:1.02-5.36). Adjusted linear regression showed that none of the indices were significantly associated with LVMI. However, all indices were associated with CCA-IMT (p<0.05), but none with eGFR (p>0.05). Adjusted RCS models showed a significant non-linear association between TyG and CCA-IMT (p for non-linearity = 0.009). In conclusion, IR biomarkers are of clinical value in newly diagnosed patients with hypertension.

Transient hypertension precedes sustained hypertension and can arise from reduced aortic compliance with aging. We recently demonstrated that daily hypertension transients in swine rapidly lead to irreversible increases in left ventricular (LV) chamber stiffness without the development of anatomic hypertrophy (LVH). This dissociation was surprising and led us to hypothesize that the transcriptional response to pressure overload was determined by LV diastolic chamber stiffness. Myocardial tissue for RNASeq was obtained 24 h after transient pressure elevation (left ventricular end-diastolic pressure from 12.2 ± 0.8 mmHg to 34.3 ± 2 mmHg and LVSP from 105 ± 3 mmHg to 223 ± 8 mmHg) using phenylephrine. Animals with a single episode [single pressure overload (SPO), n = 6] were compared with those with daily repetitive pressure overload (RPO) for 2 wk (RPO, n = 8). After RPO, LV diastolic chamber stiffness increased fourfold (0.55 ± 0.08 to 2.38 ± 0.50 mmHg/mL/m2 after RPO, P < 0.01) and fibrosis increased (normal 5.7 ± 0.2% to 12.9 ± 1.8% after RPO, P < 0.01) without the development of LVH (128 ± 6.6 g/m2 vs. 129 ± 3.6 g/m2 after RPO, p-ns). There was a robust transcriptional response to SPO, with 5,885 of 12,483 genes (47%) differentially expressed (DEGs). These included potential determinants of chamber stiffness (extracellular matrix, fibrosis, and actin-cytoskeleton), hypertrophy, and inflammation. In contrast, after 2 wk of RPO, the transcriptional response to similar elevations in pressure was markedly attenuated with only 841 DEGs (7%). Our data indicate that LV chamber stiffness is a key determinant of the transcriptional response to pressure overload that attenuates hypertrophic gene expression. This may explain the wide variability of LVH among patients with a similar extent of pressure overload.NEW & NOTEWORTHY Data indicate that left ventricular (LV) chamber stiffness is the key determinant of the myocardial transcriptional response to transient pressure overload. In contrast to sustained pressure overload, repetitive LV pressure overload stimulates fibrosis, increases LV chamber stiffness in the absence of hypertrophy, and attenuates multiple transcriptional pathways. Alterations in chamber stiffness from blood pressure transients may explain the wide variability of LV hypertrophy seen among patients despite similar pressure overload.

Systemic inflammation contributes to hypertension-mediated organ damage. The Systemic Immune-Inflammation Index (SII), derived from peripheral blood counts, has emerged as a potential marker, but data in newly diagnosed, treatment-naïve hypertensive patients in India are limited. To evaluate the association between SII and the presence and severity of asymptomatic organ damage (AOD) in newly diagnosed hypertension. This hospital-based, cross-sectional study was conducted at a tertiary care center over 2 years. Sixty-six adults with newly diagnosed, treatment-naïve hypertension were included. SII was calculated as platelet count × neutrophil count/lymphocyte count. AOD was assessed using urine albumin-to-creatinine ratio, left ventricular mass index, carotid intima-media thickness, and fundus examination. Organ damage severity was graded by the number of organs involved. Correlation and receiver operating characteristic analyses were performed. The mean age was 51.88 ± 12.1 years and 54.5% were male. AOD was present in 90.9% of patients. Median SII values were significantly higher in patients with renal involvement, left ventricular hypertrophy, increased carotid intima-media thickness, and hypertensive retinopathy (all P < 0.0001). SII increased progressively with higher AOD grades (P < 0.0001) and showed significant positive correlations with urine albumin-to-creatinine ratio, left ventricular mass index, and carotid intima-media thickness. The area under the curve for SII in detecting AOD was 0.812. Higher SII was significantly associated with the presence and severity of AOD in newly diagnosed hypertension and may aid early risk stratification.

Icariside Ⅱ alleviates heart failure based on Wnt/β-catenin-mitochondrial apoptotic pathway.

A male in his 50s initially presented with left ventricular hypertrophy (LVH) identified on transthoracic echocardiogram. He was diagnosed with hypertrophic cardiomyopathy without any further investigations. He later presented in his 70s with decompensated heart failure. A cardiac MRI was performed that demonstrated extensive scarring, and the patient was labelled with a presumptive diagnosis of cardiac amyloidosis. An endomyocardial biopsy demonstrated extensive myocyte hypertrophy and fibrosis but was non-diagnostic in identifying a cause of the LVH. Genetic testing revealed that the patient had a genetic variant in the GLA gene, which encodes for the α-galactosidase A enzyme that is known to be associated with adult onset of Fabry disease. This case highlights the importance of early incorporation of genetic screening and advanced imaging modalities in patients presenting with LVH.

Impaired global longitudinal strain predicted cardiovascular outcomes in incident peritoneal dialysis patients: a prospective study

Mitral valve dysplasia is a rare congenital etiology of primary mitral valve regurgitation. It can cause severe chronic mitral regurgitation, which may eventually lead to left atrial and ventricular dilation and dysfunction. Left ventricular non-compaction is a relatively rare cardiomyopathy that overlaps with hypertrophic and dilated cardiomyopathy. It can also lead to left or right ventricular dysfunction and failure. Papillary muscle hypertrophy may be a subtype of, or an early expression of, hypertrophic cardiomyopathy. Herein, we present a 42-year-old woman with a rare coexistence of mitral valve dysplasia, non-compaction left ventricular cardiomyopathy, and papillary muscle hypertrophy.

This study aimed to investigate the relationship between left ventricular (LV) remodelling and systolic function in high-gradient severe aortic stenosis (AS) using cardiovascular magnetic resonance (CMR) imaging. Patients with low ejection fraction (left ventricular ejection fraction (LVEF) <50%) high-gradient severe AS (low ejection fraction high-gradient (LEF-HG)), that is, afterload mismatch, were compared with patients with normal ejection fraction high-gradient (NEF-HG) severe AS. The hypothesis of insufficient left ventricular hypertrophy (LVH) leading to high wall stress as the mechanism of systolic dysfunction in afterload mismatch was tested. This was a cross-sectional study design. The study was performed at a single tertiary academic hospital in the Western Cape, South Africa. A total of 48 participants with high-gradient (mean gradient ≥40 mm Hg) severe AS (aortic valve area (AVA) <1.0 cm2) were consecutively recruited. Of 48 participants, 24 (50%) had LEF-HG AS (mean AVA 0.52±0.18 cm2, mean gradient 54 (21) mm Hg, mean LVEF 29±11%). The remainder of the cohort had NEF-HG AS (mean AVA 0.70±0.17 cm2, mean gradient 53 (25) mm Hg, LVEF 64±14%). End-systolic wall stress (ESWS) was higher in the LEF-HG group (265.3±83.5 vs 122.8±54.7×103 dynes/cm2; p<0.0001) and associated significantly with LVEF. The degree of LVH measured by wall thickness (13.0 vs 13.0 mm, p>0.99) was identical between the groups. The LV mass index was numerically higher in the LEF-HG group (101.9±37.2 vs 77.6±22.2 g/m2) but this was not statistically significant (p=0.91). The LEF-HG AS group demonstrated significant LV cavity dilation (LV End-Diastolic Volume Index 124.9±29.9 vs 78.4±16.0 mL/m2, p<0.0001). Elevated ESWS was associated with smaller valve areas and cavity dilation but not with LVH. The reduced LVEF in afterload mismatch was associated with high ESWS as previously suggested. However, insufficient concentric LVH was not observed in LEF-HG AS and therefore not associated with high ESWS. LV cavity dilation and smaller valve areas were instead associated with the elevated ESWS in afterload mismatch, which may represent the decompensated stage of high-gradient severe AS.

ABSTRACT Background Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor associated with inflammation, endothelial dysfunction, oxidative stress, and arterial stiffness. Although elevated Lp(a) levels have been linked to cardiovascular disease, their relationship with left ventricular (LV) geometric remodeling in hypertension remains insufficiently characterized. This study aimed to investigate the association between serum Lp(a) levels and LV geometry in non-diabetic patients with essential hypertension. Methods This cross-sectional observational study included 110 non-diabetic patients with essential hypertension. Patients were categorized into low Lp(a) (<50 mg/dL, n = 70) and elevated Lp(a) (≥50 mg/dL, n = 40) groups. Comprehensive transthoracic echocardiography was performed to evaluate LV mass index (LVMI), relative wall thickness, and LV geometric patterns. Correlation, multivariate linear regression, and multinomial logistic regression analyses were used to determine independent associations between Lp(a) levels and LV remodeling parameters. Results Patients with elevated Lp(a) levels had significantly greater LVMI values compared with those with lower Lp(a) levels (139.6 ± 28.5 vs. 117.6 ± 24.2 g/m2, p < 0.001). Concentric LV hypertrophy was substantially more prevalent in the elevated Lp(a) group (55.0% vs. 20.0%, p = 0.001), whereas normal LV geometry was more frequently observed in patients with lower Lp(a) concentrations. Serum Lp(a) levels demonstrated a moderate positive correlation with LVMI (r = 0.357, p < 0.001). In multivariate linear regression analysis, Lp(a) remained independently associated with LVMI after adjustment for major clinical confounders (standardized β = 0.363, p < 0.001). Multinomial logistic regression analysis demonstrated that elevated Lp(a) levels were independently associated with markedly greater odds of concentric LV hypertrophy. Conclusions Elevated serum Lp(a) levels were independently associated with adverse LV geometric remodeling and concentric hypertrophy in non-diabetic patients with essential hypertension. Assessment of Lp(a) levels may provide additional value for cardiovascular risk stratification and identification of hypertensive patients at increased risk for hypertensive target organ damage.

Correction to: The Natural History of Massive Left Ventricular Hypertrophy in Pediatric Hypertrophic Cardiomyopathy: A Multiregistry Analysis.