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Background: Increased afterload in aortic stenosis (AS) induces left ventricle (LV) remodeling to preserve a normal ejection fraction. This compensatory response can become maladaptive and manifest with motion abnormality. It is a clinical challenge to identify contractile and relaxation dysfunction during early subclinical stage to prevent irreversible deterioration. Purpose: To evaluate the changes of regional wall dynamics in 3D + time domain as remodeling progresses in AS. Study Type: Retrospective. Population: A total of 31 AS patients with reduced and preserved ejection fraction (14 AS_rEF: 7 male, 66.5 [7.8] years old; 17 AS_pEF: 12 male, 67.0 [6.0] years old) and 15 healthy (6 male, 61.0 [7.0] years old). Field Strength/Sequence: 1.5 T Magnetic resonance imaging/steady state free precession and late‐gadolinium enhancement sequences. Assessment: Individual LV models were reconstructed in 3D + time domain and motion metrics including wall thickening (TI), dyssynchrony index (DI), contraction rate (CR), and relaxation rate (RR) were automatically extracted and associated with the presence of scarring and remodeling. Statistical Tests: Shapiro–Wilk: data normality; Kruskal–Wallis: significant difference (P < 0.05); ICC and CV: variability; Mann–Whitney: effect size. Results: AS_rEF group shows distinct deterioration of cardiac motions compared to AS_pEF and healthy groups (TIAS_rEF: 0.92 [0.85] mm, TIAS_pEF: 5.13 [1.99] mm, TIhealthy: 3.61 [1.09] mm, ES: 0.48–0.83; DIAS_rEF: 17.11 [7.89]%, DIAS_pEF: 6.39 [4.04]%, DIhealthy: 5.71 [1.87]%, ES: 0.32–0.85; CRAS_rEF: 8.69 [6.11] mm/second, CRAS_pEF: 16.48 [6.70] mm/second, CRhealthy: 10.82 [4.57] mm/second, ES: 0.29–0.60; RRAS_rEF: 8.45 [4.84] mm/second; RRAS_pEF: 13.49 [8.56] mm/second, RRhealthy: 9.31 [2.48] mm/second, ES: 0.14–0.43). The difference in the motion metrics between healthy and AS_pEF groups were insignificant (P‐value = 0.16–0.72). AS_rEF group was dominated by eccentric hypertrophy (47.1%) with concomitant scarring. Conversely, AS_pEF group was dominated by concentric remodeling and hypertrophy (71.4%), which could demonstrate hyperkinesia with slight wall dyssynchrony than healthy. Dysfunction of LV mechanics corresponded to the presence of myocardial scarring (54.9% in AS), which reverted the compensatory mechanisms initiated and performed by LV remodeling. Data Conclusion: The proposed 3D + time modeling technique may distinguish regional motion abnormalities between AS_pEF, AS_rEF, and healthy cohorts, aiding clinical diagnosis and monitoring of AS progression. Subclinical myocardial dysfunction is evident in early AS despite of normal EF. Level of Evidence: 4 Technical Efficacy: Stage 1 [ABSTRACT FROM AUTHOR]

Background: Fibroblast growth factor 23 (FGF-23) has been associated with left ventricular hypertrophy (LVH) and heart failure. However, its role in right ventricular (RV) remodeling and RV failure is unknown. This study analyzed the utility of FGF-23 as a biomarker of RV function in patients with pulmonary hypertension (PH). Methods: In this observational study, FGF-23 was measured in the plasma of patients with PH (n = 627), dilated cardiomyopathy (DCM, n = 59), or LVH with severe aortic stenosis (n = 35). Participants without LV or RV abnormalities served as controls (n = 36). Results: Median FGF-23 plasma levels were higher in PH patients than in healthy controls (p < 0.001). There were no significant differences between PH, DCM, and LVH patients. Analysis across tertiles of FGF-23 levels in PH patients revealed an association between higher FGF-23 levels and higher levels of NT-proBNP and worse renal function. Furthermore, patients in the high-FGF-23 tertile had a higher pulmonary vascular resistance (PVR), mean pulmonary artery pressure, and right atrial pressure and a lower cardiac index (CI) than patients in the low tertile (p < 0.001 for all comparisons). Higher FGF-23 levels were associated with higher RV end-diastolic diameter and lower tricuspid annular plane systolic excursions (TAPSE) and TAPSE/PASP. Receiver operating characteristic analysis revealed FGF-23 as a good predictor of RV maladaptation, defined as TAPSE < 17 mm and CI < 2.5 L/min/m2. Association of FGF-23 with parameters of RV function was independent of the glomerular filtration rate in regression analysis. Conclusion: FGF-23 may serve as a biomarker for maladaptive RV remodeling in patients with PH. [ABSTRACT FROM AUTHOR]

Left ventricle myocardium has a complex micro-architecture, which was revealed to consist of myocyte bundles arranged in a series of laminar sheetlets. Recent imaging studies demonstrated that these sheetlets re-orientated and likely slided over each other during the deformations between systole and diastole, and that sheetlet dynamics were altered during cardiomyopathy. However, the biomechanical effect of sheetlet sliding is not well-understood, which is the focus here. We conducted finite element simulations of the left ventricle (LV) coupled with a windkessel lumped parameter model to study sheetlet sliding, based on cardiac MRI of a healthy human subject, and modifications to account for hypertrophic and dilated geometric changes during cardiomyopathy remodeling. We modeled sheetlet sliding as a reduced shear stiffness in the sheet-normal direction and observed that (1) the diastolic sheetlet orientations must depart from alignment with the LV wall plane in order for sheetlet sliding to have an effect on cardiac function, that (2) sheetlet sliding modestly aided cardiac function of the healthy and dilated hearts, in terms of ejection fraction, stroke volume, and systolic pressure generation, but its effects were amplified during hypertrophic cardiomyopathy and diminished during dilated cardiomyopathy due to both sheetlet angle configuration and geometry, and that (3) where sheetlet sliding aided cardiac function, it increased tissue stresses, particularly in the myofibre direction. We speculate that sheetlet sliding is a tissue architectural adaptation to allow easier deformations of the LV walls so that LV wall stiffness will not hinder function, and to provide a balance between function and tissue stresses. A limitation here is that sheetlet sliding is modeled as a simple reduction in shear stiffness, without consideration of micro-scale sheetlet mechanics and dynamics. [ABSTRACT FROM AUTHOR]

Purpose: The geometric patterns of ventricular remodeling are determined using indexed left ventricular mass (LVM), end-diastolic volume (LVEDV) and concentricity, most often measured using the mass-to-volume ratio (MVR). The aims of this study were to validate lean body mass (LBM)-based allometric coefficients for scaling and to determine an index of concentricity that is independent of both volume and LBM. Methods: Participants from the UK Biobank who underwent both CMR and dual-energy X-ray absorptiometry (DXA) during 2014–2015 were considered (n = 5064). We excluded participants aged ≥ 70 years or those with cardiometabolic risk factors. We determined allometric coefficients for scaling using linear regression of the logarithmically transformed ventricular remodeling parameters. We further defined a multiplicative allometric relationship for LV concentricity (LVC) adjusting for both LVEDV and LBM. Results: A total of 1638 individuals (1057 female) were included. In subjects with lower body fat percentage (< 25% in males, < 35% in females, n = 644), the LBM allometric coefficients for scaling LVM and LVEDV were 0.85 ± 0.06 and 0.85 ± 0.03 respectively (R2 = 0.61 and 0.57, P < 0.001), with no evidence of sex–allometry interaction. While the MVR was independent of LBM, it demonstrated a negative association with LVEDV in (females: r = − 0.44, P < 0.001; males: − 0.38, P < 0.001). In contrast, LVC was independent of both LVEDV and LBM [LVC = LVM/(LVEDV0.40 × LBM0.50)] leading to increased overlap between LV hypertrophy and higher concentricity. Conclusions: We validated allometric coefficients for LBM-based scaling for CMR indexed parameters relevant for classifying geometric patterns of ventricular remodeling. [ABSTRACT FROM AUTHOR]

Objective : To study the extent of left ventricular (LV) mass regression in aortic stenosis after aortic valve replacement with the TTK Chitra™ tilting disc valve. Methods and materials: This study included patients with severe isolated aortic stenosis (AS), admitted in our department. They had aortic valve replacement (AVR) with the TTK Chitra™ tilting disc valve, between January 2008 and December 2010. Data were collected from consecutive forty-eight patients. LV mass and diametric and functional parameters were recorded preoperatively and compared with echocardiography after 3 months, 6 months, then yearly, up to 3 years. Results: 70.8% of the patients were males and 29.2% were females. The mean duration of illness was 37.92 ± 25.87 months. The mean LV ejection fraction increased 3 months after surgery (61.56 ± 10.10% to 69.31 ± 9.34%) with a sustained increase for the next 3 years. The mean LV end-diastolic diameter decreased (50.16 ± 6.05 mm to 45.69 ± 5.93 mm) after 3 months of surgery, with a sustained decrease for the next 3 years. The mean LV end-systolic diameter decreased (32.84 ± 6.96 mm to 29.41 ± 5.86 mm) after 3 months of surgery and then showed a sustained decrease for the next 3 years. The LV mass assessed with echocardiography regressed from 324.65 ± 97.77 g before surgery to 252.64 ± 71.12 g after 3 months and then showed a sustained decrease over the next 3 years. Conclusion: Significant LV mass regression occurred after AVR with the TTK Chitra™ valve. The maximum reversal was found to be within the first 3 months after surgery with sustained beneficial improvement for the next 3 years. [ABSTRACT FROM AUTHOR]

Numerous studies on the effects of antihypertensive treatment in young spontaneously hypertensive rats (SHRs) have shown that early-onset therapy may effectively reduce their blood pressure (BP) even to normotensive values. In contrast, only a few studies investigated the effects of treatment started at an advanced age. These studies revealed that antihypertensive effects are lower in adult or even in senescent SHRs compared with young SHRs. Even more, prevention of cardiac sequelae of hypertension such as hypertrophy and fibrosis is less effective when treatment starts late in life. Because, in patients, combination therapies with calcium antagonists are favored, we studied the efficacy of a combination therapy with captopril and nifedipine in young and old SHRs. We directly compared the treatment effects on BP as well as on cardiac hypertrophy and remodeling between these two animal cohorts. With antihypertensive treatment, significantly lower BP values were achieved in young SHRs despite a shorter treatment period compared with old SHRs. Although treatment effects on cardiac hypertrophy were greater in old than in young SHRs, cardiac fibrosis was significantly attenuated only in young but not in old SHRs. The results emphasize the value of antihypertensive therapy and particularly accentuate the importance of an early-onset therapy. With respect to problems such as late diagnosis and poor therapy adherence, these results may have great importance for the treatment of human hypertension. [ABSTRACT FROM AUTHOR]

Abstract Background There is a lack of clinical data on hypertrophic cardiomyopathy (HCM) in dogs. Hypothesis/Objectives To investigate signalment, clinical signs, diagnostic findings, and survival in dogs with HCM. Animals Sixty‐eight client‐owned dogs. Methods Retrospective multicenter study. Medical records were searched between 2003 and 2015. The diagnosis of left ventricular (LV) hypertrophy was made by echocardiographic examination. Results Three hundred and forty‐five dogs with LV hypertrophy were identified, of which 277 were excluded. The remaining 68 dogs were 0.3 to 14 years old and predominantly

Abstract Aims This study aimed to determine the relationship of low birth weight (LBW) with adult cardiac structure and function and investigate potential causal pathways. Methods and results A population‐based sample of 925 Australians (41.3% male) were followed from childhood (aged 7–15 years) to young adulthood (aged 26–36 years) and mid‐adulthood (aged 36–50 years). Left ventricular (LV) global longitudinal strain (GLS, %), LV mass index (LVMi, g/m2.7), LV filling pressure (E/e′), and left atrial volume index (g/m2) were measured by transthoracic echocardiography in mid‐adulthood. Birth weight category was self‐reported in young adulthood and classified as low (≤5 lb or ≤2270 g), normal (5–8 lb or 2271–3630 g), and high (>8 lb or >3630 g). Of the 925 participants, 7.5% (n = 69) were classified as LBW. Compared with participants with normal birth weight, those with LBW had 2.01‐fold (95% confidence interval: 1.19, 3.41, P = 0.009) higher risks of impaired GLS (GLS > −18%) and 2.63‐fold (95% confidence interval: 0.89, 7.81, P = 0.08) higher risks of LV hypertrophy (LVMi > 48 g/m2.7 in men or >44 g/m2.7 in women) in adulthood, independent of age, sex, and any socio‐economic factors. Participants with LBW significantly increased body fat from childhood to adulthood relative to their peers and had greater levels of triglycerides, fasting glucose, and arterial stiffness in adulthood. These risk factors were the strongest mediators and explained 54% of the LBW effect size on adult GLS and 33% of the LBW effect size on LVMi. The remaining of these associations was independent of any of the measured risk factors. Conclusions Low birth weight was associated with impaired cardiac structure and function in mid‐adulthood. This association was only partially explained by known risk factors.

Background: A major problem in the treatment of human hypertension is the late diagnosis of hypertension and, hence, the delayed start of treatment. Very often, hypertension has existed for a long time and cardiac damage has already developed. Therefore, we tested whether late-onset antihypertensive treatment is effective in lowering blood pressure (BP) and in reducing or even preventing left ventricular hypertrophy and fibrosis. Methods: Twenty-one male 60-week-old spontaneously hypertensive rats (SHR) were included. Fourteen rats received oral treatment with captopril (CAP) either as monotherapy or combined with nifedipine (CAP + NIF) over 22 weeks. Seven untreated SHR served as controls. We examined the therapeutic effects on BP, heart weight and histological and biochemical markers of left ventricular remodeling and fibrosis. Results: At 82 weeks of age, BP was reduced in the CAP and CAP + NIF groups by 44 and 51 mmHg, respectively (p < 0.001), but not in untreated controls. Despite the late therapy start, cardiac hypertrophy and fibrosis were attenuated compared to controls. Both treatments reduced heart weight by 1.2 mg/g (25%, p = 0.001) and collagens I and III by 66% and 60%, respectively (p < 0.001), thus proving nearly equivalent cardioprotective efficacy. Conclusion: These data clearly emphasize the benefit of antihypertensive treatment in reducing BP and mitigating the development of cardiac damage even when treatment is started late in life. [ABSTRACT FROM AUTHOR]

Background: There is a lack of clinical data on hypertrophic cardiomyopathy (HCM) in dogs. Hypothesis/Objectives: To investigate signalment, clinical signs, diagnostic findings, and survival in dogs with HCM. Animals: Sixty‐eight client‐owned dogs. Methods: Retrospective multicenter study. Medical records were searched between 2003 and 2015. The diagnosis of left ventricular (LV) hypertrophy was made by echocardiographic examination. Results: Three hundred and forty‐five dogs with LV hypertrophy were identified, of which 277 were excluded. The remaining 68 dogs were 0.3 to 14 years old and predominantly <10 kg (85%), and without a sex predilection. Twenty‐four % were Shih Tzu and 24% terrier breeds. Most (80%) had a systolic heart murmur. Owner‐determined exercise intolerance (37%) and syncope (18%) were most commonly reported signs. The majority (84%) of dogs had symmetrical LV hypertrophy, whereas asymmetrical septal and LV free wall hypertrophy was observed in 9% and 6% of dogs, respectively. Isolated basal interventricular septal hypertrophy was not observed. Commonly recorded were systolic anterior motion of the mitral valve (60%) and LV diastolic dysfunction (89% of dogs where diastolic function was evaluated). Six dogs died unexpectedly, and 3 developed congestive heart failure. Known survival times were between 1 day and 114 months after diagnosis. Conclusions and Clinical Importance: Hypertrophic cardiomyopathy in dogs should be considered as a differential diagnosis if LV hypertrophy is identified. Small breed dogs are overrepresented, and it is uncommon for dogs with HCM to develop CHF although sudden death can occur. [ABSTRACT FROM AUTHOR]

Purpose: Left ventricular hypertrophy (LVH) is a well-known risk factor for poor clinical outcomes in patients undergoing dialysis. However, little evidence supports the above notion in Japan, and the influence of subtypes of LVH on prognosis. Methods: We investigated 367 patients undergoing dialysis who underwent routine echocardiographic examinations between April and September 2018. LVH was defined as any LV mass ≥ 115 g/m2 in men and ≥ 95 g/m2 in women obtained by echocardiography. The primary endpoint was a composite outcome including all-cause death, admission due to heart failure, and ischemic heart event or stroke. LVH was divided into subtype-groups according to eccentric hypertrophy or concentric hypertrophy, and with and without hypertension. Results: LVH was observed in 171 (47%) patients. The primary endpoint was observed in 58 patients (16%) during the median follow-up period of 500 days. Multivariable Cox regression analyses identified four independent risk factors for the primary endpoint: age, pulse rate, serum albumin level, and LV mass index (per 10-g/m2 increase; hazard ratio: 1.12, 95% confidence interval: 1.06–1.18, P < 0.001). Kaplan–Meier analyses demonstrated that patients with LVH had a worse prognosis than those without LVH in terms of the primary endpoint (log-rank P < 0.001). The incidence of the primary outcome was not significantly different between patients with eccentric or concentric hypertrophy, and between LVH patients with and without hypertension. Conclusion: Japanese patients with LVH undergoing dialysis had a worse prognosis than those without LVH in terms of the composite clinical endpoint. [ABSTRACT FROM AUTHOR]

A variability in cardiac remodeling is observed in athletes regardless of age, sex, body size and sport participated. We sought to investigate whether other individual characteristics could affect the extent of Left ventricular hypertrophy (LVH). From 2120 consecutive Olympic athletes, those with LVH (defined as LV Wall thickness ≥ 13 mm) were matched 1:1 by age, gender, body surface area and type of sport with non-LVH Athletes. Clinical and Echocardiographic variables were compared. 48 athletes with LVH (2.3%) and 48 matched non-LVH athletes were identified. LVH Athletes had higher body weight (90 ± 18 vs 81 ± 11Kg; p = 0.006) body mass index (26 ± 2 vs 24 ± 2 Kg/m2; p < 0.001) and body fat percentage (15 ± 7% vs 12 ± 4%; p = 0.016) compared to non-LVH Athletes. They also had higher systolic (123 ± 1 vs 116 ± 11 mmHg; p = 0.002) and diastolic blood pressure (76 ± 8 vs 71 ± 9 mmHg; p = 0.002). On exercise testing, LVH Athletes reached a lower index workload (3.7 ± 0.9 vs 4.1 ± 0.8 W/Kg; p = 0.013) and a higher peak diastolic blood pressure (79 ± 10 vs 74 ± 11 mmHg; p = 0.012) than those without LVH. Binary logistic regression analysis showed that diastolic blood pressure (OR 1.052; 95% CI from 1.011 to 1.130; p = 0.020) and BMI (OR 1.220; 95% CI from 1.016 to 1.465; p = 0.033) had the strongest association with LVH as categorical variable. Our study showed that increased blood pressure at rest and during exercise, together with larger body weight, body mass and fat percentage are associated with a higher degree of LVH, which is not associated with a greater physical performance and therefore possibly disproportionate to the sport activity. • Cardiac remodeling in athletes may vary despite similar body characteristics and training protocols • Blood pressure, body fat and weight may be additional determinants of left ventricular hypertrophy. • Left ventricular hypertrophy may be in some cases disproportionate to the sport activity. • Greater left ventricular hypertrophy doesn't imply better physical performance. [ABSTRACT FROM AUTHOR]

Aims: This study aimed to determine the relationship of low birth weight (LBW) with adult cardiac structure and function and investigate potential causal pathways. Methods and results: A population‐based sample of 925 Australians (41.3% male) were followed from childhood (aged 7–15 years) to young adulthood (aged 26–36 years) and mid‐adulthood (aged 36–50 years). Left ventricular (LV) global longitudinal strain (GLS, %), LV mass index (LVMi, g/m2.7), LV filling pressure (E/e′), and left atrial volume index (g/m2) were measured by transthoracic echocardiography in mid‐adulthood. Birth weight category was self‐reported in young adulthood and classified as low (≤5 lb or ≤2270 g), normal (5–8 lb or 2271–3630 g), and high (>8 lb or >3630 g). Of the 925 participants, 7.5% (n = 69) were classified as LBW. Compared with participants with normal birth weight, those with LBW had 2.01‐fold (95% confidence interval: 1.19, 3.41, P = 0.009) higher risks of impaired GLS (GLS > −18%) and 2.63‐fold (95% confidence interval: 0.89, 7.81, P = 0.08) higher risks of LV hypertrophy (LVMi > 48 g/m2.7 in men or >44 g/m2.7 in women) in adulthood, independent of age, sex, and any socio‐economic factors. Participants with LBW significantly increased body fat from childhood to adulthood relative to their peers and had greater levels of triglycerides, fasting glucose, and arterial stiffness in adulthood. These risk factors were the strongest mediators and explained 54% of the LBW effect size on adult GLS and 33% of the LBW effect size on LVMi. The remaining of these associations was independent of any of the measured risk factors. Conclusions: Low birth weight was associated with impaired cardiac structure and function in mid‐adulthood. This association was only partially explained by known risk factors. [ABSTRACT FROM AUTHOR]

Congestive Heart failure (CHF) is a severe pathology representing a major public health problem in industrialized nations which is increasing in prevalence and incidence. The aortic banding rat model provides steady progression of cardiac dysfunction under chronic pressure overload. Present study evaluated two abdominal aortic constriction techniques including constriction of aorta above renal arteries and between renal arteries. The extent of constriction was varied with 22 G and 24 G needles and the duration for evaluation of CHF was also varied by terminating the banded animals after 6 and 8 weeks of banding. Various hemodynamic, ECG and tissue parameters were evaluated after banding to see the progression of CHF. The findings revealed that the constriction of the aorta above both renal arteries with 24 G needle is a better technique amongst other tested banding techniques as the rate of progression of CHF was found to be maximum with it. On the basis of above study, it was concluded that, aortic banding above both renal arteries with 24 G needle is a better technique for induction of pressure overload and for further observation in transition of the cardiac compensatory to decompensatory phase, the duration of the model needs to be prolonged.

Arterial stiffness has gained recognition as a stand-alone risk factor for cardiovascular disease (CVD). Obesity is intricately linked to elevated arterial stiffness, the development of left ventricular (LV) hypertrophy, and the emergence of diastolic dysfunction, all of which collectively contribute substantially to an unfavorable prognosis. Weight loss has become a standard recommendation for all patients with CVD concurrent with morbid obesity; however, randomized evidence to support this recommendation was limited earlier. The latest scientific studies revealed dynamic changes in aortic stiffness after substantial weight loss by bariatric surgery, also known as metabolic surgery, in patients with obesity. There is also a favorable evolution in LV hypertrophy and a significant impact on arterial hypertension and other promising cardiovascular outcomes in obese people after bariatric surgery. We aimed to examine the cardiovascular effects of various metabolic surgeries in morbidly obese individuals, especially their role in improving arterial health, the potential impact on surrogate markers of atherosclerotic vascular disease, and consequently reducing the likelihood of cardiovascular events. In conclusion, metabolic surgery is associated with a significant decrease in the occurrence of major adverse cardiovascular events (MACE) and all-cause mortality among obese individuals, alongside remarkable enhancement of arterial health. These findings underscore the critical importance of implementing strategies to combat obesity and reduce adiposity within the general population. Created with BioRender.com [Display omitted] [ABSTRACT FROM AUTHOR]

Background: A major problem in the treatment of human hypertension is the late diagnosis of hypertension and, hence, the delayed start of treatment. Very often, hypertension has existed for a long time and cardiac damage has already developed. Therefore, we tested whether late-onset antihypertensive treatment is effective in lowering blood pressure (BP) and in reducing or even preventing left ventricular hypertrophy and fibrosis. Methods: Twenty-one male 60-week-old spontaneously hypertensive rats (SHR) were included. Fourteen rats received oral treatment with captopril (CAP) either as monotherapy or combined with nifedipine (CAP + NIF) over 22 weeks. Seven untreated SHR served as controls. We examined the therapeutic effects on BP, heart weight and histological and biochemical markers of left ventricular remodeling and fibrosis. Results: At 82 weeks of age, BP was reduced in the CAP and CAP + NIF groups by 44 and 51 mmHg, respectively (p < 0.001), but not in untreated controls. Despite the late therapy start, cardiac hypertrophy and fibrosis were attenuated compared to controls. Both treatments reduced heart weight by 1.2 mg/g (25%, p = 0.001) and collagens I and III by 66% and 60%, respectively (p < 0.001), thus proving nearly equivalent cardioprotective efficacy. Conclusion: These data clearly emphasize the benefit of antihypertensive treatment in reducing BP and mitigating the development of cardiac damage even when treatment is started late in life.

Fabry disease (FD) is an X-linked disorder with α-galactosidase A deficiency. Males (>30 years) and females (>40 years) often present with cardiac manifestations, predominantly left ventricular hypertrophy (LVH). The aim of this study was to evaluate electrocardiographic (ECG) characteristics within FD patients to identify gender related differences, and to additionally explore the association of ECG parameters with structural and functional alterations on transthoracic echocardiography (TTE). Retrospective cross-sectional analysis of 45 FD patients with contemporaneous ECG and TTE was performed and compared to age and gender matched healthy controls. FD patients demonstrated alterations in several ECG parameters particularly in males, including prolonged P-wave duration (91 vs. 81 ms, p = 0.022), prolonged QRS duration (96 vs. 84 ms, p < 0.001), increased R-wave amplitude in lead I (8.1 vs. 5.7 mV, p = 0.047), increased Sokolow–Lyon index (25 vs. 19 mV, p = 0.002) and were more likely to meet LVH criteria (31% vs. 7%, p = 0.006). FD patients with impaired basal longitudinal strain (LS) on TTE were more likely to meet LVH criteria (41% vs. 0%, p = 0.018). Those with more advanced FD (increased LV wall thickness on TTE) were more likely to meet LVH criteria but additionally demonstrated prolonged ventricular depolarization (QRS duration 101 vs. 88 ms, p = 0.044). Therefore, alterations on ECG demonstrating delayed atrial activation, delayed ventricular depolarization and evidence of LVH were more often seen in male FD patients. Impaired basal LS, a TTE marker of early cardiac involvement, correlated with ECG abnormalities. Increased LV wall thickness on TTE, a marker of more advanced FD, was associated with more severe ECG abnormalities.

Background/Aims: Cardiac changes observed in chronic kidney disease patients are of multifactorial origin including chronic uremia, hemodynamics or inflammation. Restoration of renal function by kidney transplantation (KTX) may reverse cardiac changes. Novel echocardiographic methods such as speckle tracking echocardiography (STE) allow early and sensitive detection of subtle changes of cardiac parameters. We evaluated changes of cardiac structure and function after KTX by advanced echocardiographic modalities. Methods: Thirty-one KTX recipients (female n=11) were evaluated by medical examination, laboratory testing and echocardiography before and after KTX (median follow-up 19 months). Left ventricular (LV) and right ventricular (RV) diameters and function were assessed by echocardiographic standard parameters. Longitudinal 2D strain of the LV (GLPS) and left atrium (LA) was determined by 2D STE. Results: After KTX, median serum creatinine level was 1.3 mg/dl (IQR, 1.2-1.5). Systolic blood pressure decreased significantly after KTX. Echocardiography showed a significant reduction in LV end-diastolic septal and posterior wall thickness and LV mass index after KTX, which was accompanied by an improvement of GLPS. There were no relevant changes in parameters of LA (reservoir, conduit or contractile) function, LV diastolic or RV function after KTX. Conclusion: LV hypertrophy reversed after successful KTX and was accompanied by an improvement in longitudinal LV function as assessed by STE. Diastolic function and STE-derived LA function parameters did not change significantly after KTX.

Background: The association of metabolic syndrome (MS) with left ventricular (LV) hypertrophy is controversial. The objective of our study was to investigate the influence of MS on LV mass and geometry in community-based hypertensive patients among Han Chinese. Materials and Methods: This study included 1733 metabolic syndrome patients according to the International Diabetes Federation (IDF) definition and 2373 non-MS hypertension patients. LV hypertrophy was diagnosed by the criteria of LV mass ≥49.2 g/m 2.7 for men and 46.7 g/m 2.7 for women. LV geometric patterns (normal, concentric remodeling, concentric or eccentric hypertrophy) were calculated according to LV hypertrophy and relative wall thickness. Logistic regression analysis was used to determine odds ratio (OR) and 95% confidence interval (CI) of MS for LV hypertrophy and LV geometry abnormality. Results: The LV mass and LV mass index were higher in the MS group than in the non-MS group. In multiple adjusted models. LV mass index, LV mass, interventricular septum, and post wall were raised with the increased number of MS disorders. MS was associated with increased LV hypertrophy risk (unadjusted OR 1.38; 95% CI 1.21-1.57); age, sex, and blood pressure (BP; adjusted OR 1.39; 95% CI 1.22-1.59). MS was also associated with increased risk of eccentric hypertrophy in male and female patients. MS was only associated with increased risk of concentric hypertrophy in female patients; and MS was not associated with concentric remodeling. Conclusion: LV mass and LV mass index were associated with the increased number of MS disorders in the Chinese community-based hypertensive population. MS was not only associated with increased LV hypertrophy risk, but also associated with concentric and eccentric LV geometry abnormality, especially in females.

Objectives This study analyzed the presence of myocardial fibrosis detected by late gadolinium-enhancement (LGE) cardiac magnetic resonance (CMR) in correlation with the performance of competitive triathletes objectified by an exercise test and individual competition history. Background Myocardial fibrosis detected by LGE CMR has been reported to occur in 0% to 50% of asymptomatic athletes. However, the cause and mechanisms of myocardial fibrosis are unclear. Methods Eighty-three asymptomatic triathletes undergoing >10 training h per week (43 ± 10 years of age; 65% male) and 36 sedentary controls were studied by using LGE and extracellular volume (ECV) CMR. Parameters of physical fitness were measured by spiroergometry. Triathletes reported their lifetime competition results. Results LGE CMR revealed focal nonischemic myocardial fibrosis in 9 of 54 (17%) male triathletes (LGE + ) but in none of the female triathletes (p < 0.05). LGE + triathletes had higher peak exercise systolic blood pressure (213 ± 24 mm Hg) than LGE − triathletes (194 ± 26 mm Hg; p < 0.05). Furthermore, left ventricular mass index was higher in LGE + triathletes (93 ± 7 g/m 2 ) than in LGE − triathletes (84 ± 11 g/m 2 ; p < 0.05). ECV in LGE − myocardium was higher in LGE + triathletes (26.3 ± 1.8%) than in LGE − triathletes (24.4 ± 2.2%; p < 0.05). LGE + triathletes completed longer cumulative distances in swimming and cycling races and participated more often in middle and Iron Man distances than LGE − triathletes. A cycling race distance of >1,880 km completed during competition had the highest accuracy to predict LGE, with an area under the curve value of 0.876 (p < 0.0001), resulting in high sensitivity (89%) and specificity (79%). Multivariate analysis identified peak exercise systolic blood pressure (p < 0.05) and the swimming race distance (p < 0.01) as independent predictors of LGE presence. Conclusions Myocardial fibrosis in asymptomatic triathletes seems to be associated with exercise-induced hypertension and the race distances. There appears to be a safe upper limit, beyond which exercise may result in myocardial fibrosis. [ABSTRACT FROM AUTHOR]

Background. Hypertension is a leading cause of chronic kidney disease (CKD) and a decrease in glomerular filtration rate (GFR) is associated with a higher prevalence of hypertension and an increased proportion of suboptimal blood pressure (BP) control. Methods. To investigate characteristics associated with GFR decline, we selected 4539 hypertensive patients from the Campania Salute Network (mean age 53611 years) with at least 3 years of follow-up (FU) and no more than Stage III CKD. GFR was calculated at baseline and at the last available visit using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. GFR decline was defined as a≤30% decrease frominitial GFR for patients in Stage III CKD or by a composite ≥30% decrease from baseline and a final value of<60 for those< with Stage III or higher CKD. Results. At amean FU of 7.5 years, 432 patients (10%) presented with GFR decline. Those patients were older, more likely to be diabetic, with lower GFR and ejection fraction, higher systolic and lower diastolic BP and higher left ventricular (LV) mass and relative wall thickness at baseline; during FU, patients with GFR decline exhibited higher systolic BP, took more drugs and developed more atrial fibrillation (all P<0.02). The probability of GFR decline was independently associated with older age, prevalent diabetes, baseline lower GFR, higher systolic BP during FU, FU duration, increased LVmass and incident AF with no impact from antihypertensive and antiplateletmedications. Conclusions. During antihypertensive therapy, kidney function declines in patients with initially lower GFR, increased LV mass and suboptimal BP control during FU. [ABSTRACT FROM AUTHOR]

Aims The objective of this study was to examine the association between the different patterns of left ventricular (LV) remodelling/hypertrophy on all-cause and cardiovascular mortality in patients with aortic stenosis (AS). Methods and results In total, 747 consecutive patients (69 ± 14 years, 57% men) with AS and preserved LV ejection fraction were included in this study. According to LV mass index and relative wall thickness, patients were classified into four LV patterns: normal, concentric remodelling (CR), concentric hypertrophy (CH), and eccentric hypertrophy (EH). One hundred and sixteen patients (15%) had normal pattern, 66 (9%) had EH, 169 (23%) had CR, and 396 (53%) had CH. During a median follow-up of 6.4 years, 339 patients died (242 from cardiovascular causes). CH was associated with higher risk of all-cause mortality compared with the three other LV patterns (all P < 0.05). After multivariable adjustment, CH remained associated with higher risk of mortality (HR = 1.27, 95% CI 1.01-1.61, P = 0.046). There was a significant interaction (P < 0.05) between sex and CH with regards to the impact on mortality: CH was associated with worse outcome in women (P = 0.0001) but not in men (P = 0.22). In multivariable analysis, CH remained associated with higher risk of worse outcome in women (HR = 1.56, 95% CI 1.08-2.24, P = 0.018). Conclusions This study shows that CH was independently associated with increased risk of mortality in AS patients with preserved ejection fraction. This association was observed in women but not in men. The pattern of LV remodelling/hypertrophy should be integrated in the risk stratification process in patients with AS. [ABSTRACT FROM AUTHOR]

BACKGROUND: Physical activity (PA) has been associated with decreased left ventricular (LV) hypertrophy in previous studies. However, little is known about the relationship between PA and LV structure and factors which influence this relationship among African Americans. METHODS: We evaluated 1,300 African Americans with preserved LV ejection fraction (EF > 50%) from the Genetic Epidemiology Network of Arteriopathy (GENOA) Study (mean age 62.4 years, 73% women). PA index was calculated as 3 * heavy activity hours + 2 * moderate activity hours + slight activity hours/day. The relationship between PA index and LV structure was evaluated using generalized estimating equation. The association between PA index and LV mass index by age group, sex, body mass index (BMI), history of hypertension, diabetes or coronary heart disease, estimated glomerular filtration rate, and current smoking status were plotted. RESULTS: After adjustment for these factors, higher PA index was independently associated with lower LV mass index (P < 0.05). There were significant interactions between PA index and obesity (BMI = 30) and history of hypertension on LV mass index (P for interaction <0.05, for both). Higher PA index was associated with lower LV mass index more in obese or hypertensive participants compared with nonobese or nonhypertensive participants. CONCLUSIONS: Higher PA index was associated with reduced LV hypertrophy in obese and hypertensive African Americans. Prospective studies aimed at assessing whether increasing PA prevents LV hypertrophy and potentially reduces the risk of heart failure in these at risk groups are warranted. [ABSTRACT FROM AUTHOR]