Left ventricular mass as a modulator of ventricular arrhythmia risk and sex differences after CRT for nonischemic cardiomyopathy and LBBB.

BACKGROUND: The risk of ventricular arrhythmias (VAs) after cardiac resynchronization therapy (CRT) has been associated with ischemic disease/scar, sex, and possibly left ventricular mass (LVM). OBJECTIVE: The purpose of this study was to evaluate sex differences and baseline/postimplant change in LVM on VA risk after CRT implantation in patients with nonischemic cardiomyopathy and left bundle branch block. METHODS: In patients meeting the criteria, baseline and follow-up echocardiographic images were obtained for LVM assessment. VA events were reported from device diagnostics and therapies. VA risk was stratified by receiver operating characteristic (Youden index cutoff point) for baseline LVM and baseline/postimplant change in LVM. Multivariate Cox regression model was also used for VA risk stratification. RESULTS: One hundred eighteen patients (71 female patients [60.2%]; mean age 60.5 ± 11.3 years; left ventricular ejection fraction 19.2% ± 7.0%; QRS duration 165.6 ± 20 ms; LVM 313.9 ± 108.8 g) were enrolled and followed up for a median of 90 months (interquartile range 44-158 months). Thirty-five patients (29.6%) received appropriate shocks or antitachycardia pacing at a median of 73.5 months (interquartile range 25-130 months) postimplantation. Males had a higher VA incidence (male patients 18 of 47 [38.3%] vs female patients 17 of 71 [23.9%]; P = .02). Baseline LVM > 308.9 g separated patients with higher VA risk (P = .001). Less than a 20% decrease in LVM increased VA risk (P < .001). Baseline LVM was the only baseline characteristic predicting VA events in the Cox regression model (hazard ratio 1.01; 95% confidence interval 1.001-1.009; log-rank, P = .003). Sex differences in VA risk were eliminated by the baseline LVM parameters. CONCLUSION: VA risk after CRT implantation in nonischemic cardiomyopathy was associated with baseline LV > 308.9 g and a decrease in LVM ≤ 20%, without sex differences.

Adulthood adiposity affects cardiac structure and function in later life.

BACKGROUND AND AIMS: Excess adiposity is associated with poorer cardiac function and adverse left ventricular (LV) remodelling. However, its importance over the adult life course on future cardiac structure and systolic and diastolic function is unknown. METHODS: A total of 1690 participants in the National Survey of Health and Development birth cohort underwent repeated adiposity [body mass index (BMI)/waist-to-hip ratio (WHR)] measurements over adulthood and investigation, including echocardiography at age 60-64 years. The relationship between LV structure [LV mass (LVM), relative wall thickness, and LV internal diameter in diastole (LVIDd)] and function (diastolic: E/e', e', and left atrial volume indexed to body surface area; systolic: ejection fraction, S', and myocardial contraction fraction) was investigated using multivariable linear regression models. RESULTS: Increased BMI from age 20 years onwards was associated with greater LVM and LVIDd independent of confounders. Associations remained independent of current BMI for LVIDd and at age 26, 43, and 53 years for LVM. Increased BMI from 43 years onwards was associated with greater relative wall thickness, but not when BMI at age 60-64 years was accounted for. Increased BMI at age 26, 36, and 53 years and at 20 years onwards was associated with lower ejection fraction and myocardial contraction fraction, respectively, but not independently of BMI at 60-64 years. Higher BMI from 20 years onwards was associated with poorer diastolic function independent of confounders. Associations between BMI and left atrial volume indexed to body surface area persisted from 26 years onwards after adjustment for BMI at 60-64 years. Similar relationships were observed for WHR from age 43 years onwards. CONCLUSIONS: Higher adiposity (BMI/WHR) over adulthood is associated with evidence of adverse cardiac structure and function. Some of these associations are independent of adiposity in later life.

LBBB and heart failure-Relationships among QRS amplitude, duration, height, LV mass, and sex.

BACKGROUND: Height, left ventricular (LV) size, and sex were proposed as additional criteria for patient selection for cardiac resynchronization therapy (CRT) but their connections with the QRS complex in left bundle branch block (LBBB) are little investigated. We evaluated these. METHODS: Among patients with "true" LBBB, QRS duration (QRSd) and amplitude, and LV hypertrophy indices, were correlated with patient's height and LV mass, and compared between sexes. RESULTS: In this study cohort (n = 220; 60 ± 12 years; left ventricular ejection fraction [LVEF] 21 ± 7%; mostly New York Heart Association II-III, QRSd 165 ± 19 ms; 57% female; 70% responders [LVEF increased ≥5%]), LV mass was increased in all patients. QRS amplitude did not correlate with LV mass or height in any individual lead or with Sokolow-Lyon or Cornell-Lyon indices. QRSd did not correlate with height. In contrast, QRSd correlated strongly with LV mass (r = .51). CRT response rate was greater in women versus men (84% vs. 58%, p < .001) despite shorter QRSd [7% shorter (p < .0001)]. QRSd normalized for height resulted in a 2.7% and for LV mass 24% greater index in women. CONCLUSION: True LBBB criteria do not exclude HF patients with increased LV mass. QRS amplitudes do not correlate with height or LV mass. Height does not affect QRSd. However, QRSd correlates with LV size. QRSd normalized for LV mass results in 24% greater value in women in the direction of sex-specific responses. LV mass may be a significant nonelectrical modifier of QRSd for CRT.

Rationale and Design of the SOTA-P-CARDIA Trial (ATRU-V): Sotagliflozin in HFpEF Patients Without Diabetes.

Heart failure with preserved ejection fraction (HFpEF) is now the most common form of heart failure (HF). This syndrome is associated with an elevated morbi-mortality, and effective therapies are urgently needed. Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are the first pharmacological class that has demonstrated to reduce hospitalization and cardiovascular mortality in large clinical trials in HFpEF. Furthermore, the dual SGLT 1/2 inhibitor sotagliflozin has shown a reduction in cardiovascular outcomes in diabetic HF patients, regardless of ejection fraction Sotagliflozin on Cardiovascular Events in Patients with Type 2 Diabetes Post Worsening Heart Failure (SOLOIST-WHF) Trial, and prevents the development of HF in patients with diabetes and chronic kidney disease Sotagliflozin on Cardiovascular and Renal Events in Patients with Type 2 Diabetes and Moderate Renal Impairment Who Are at Cardiovascular Risk (SCORED) trial. The major objective of the Sotagliflozin in Heart Failure With Preserved Ejection Fraction Patients (SOTA-P-CARDIA) trial (NCT05562063) is to investigate whether the observed cardiorenal benefits of sotagliflozin in HF patients with diabetes can be extended to a non-diabetic population. The SOTA-P-CARDIA is a prospective, randomized, double-blinded, placebo-controlled study that will randomize non-diabetic patients with the universal definition of HFpEF (ejection fraction > 50% assessed the day of randomization). Qualifying patients will be randomized, in blocks of 4, to receive either sotagliflozin or placebo for a period of 6 months. The primary outcome is changes in left ventricular mass by cardiac magnetic resonance from randomization to end of the study between the groups. Secondary end points include changes in peak VO2; myocardial mechanics, interstitial myocardial fibrosis, and volume of epicardial adipose tissue; distance in the 6-min walk test; and quality of life. Finally, the authors expect that this trial will help to clarify the potential benefits of the use of sotagliflozin in non-diabetic HFpEF patients.

Relation of the left ventricular geometric patten to coronary artery disease in hypertensive patients using a 320-detector-row CT scanner.

BACKGROUND: It was estimated that about 1.3 billion people were diagnosed to be hypertensive in 2015. All countries consistently show this high prevalence. Ischemic heart disease stands as the most common cause of systolic blood pressure-related deaths per year. Left ventricular hypertrophy determined by echocardiography can predict cardiovascular morbidity and mortality. The question of whether the LV geometric pattern has an additional prognostic value is still not clearly answered. Currently, coronary computed tomography is widely used in clinical practice with a great capability of simultaneous evaluation of the LV mass and the coronary arterial tree. Our study aims to examine the relationship between LV mass and geometry and coronary artery disease using an ECG-gated 320-detector- row CT scanner. RESULTS: Two hundred ninety-eight hypertensive Egyptian individuals were enrolled in our study, the mean age was 57.5 ± 10.5, and males comprised 76.5% of the study population. The mean LV mass and LV mass index were 193 ± 60 gm and 95.2 ± 27.5 g/m2 respectively. One-fifth of the patient had CAD luminal stenosis ≥ 50%. Normal LV geometric pattern was observed in about 37% of the study population. About one-third of the patients showed concentric remodeling. Patients with increased LV mass index represented one-third of the study population with a greater percentage of the concentric hypertrophy pattern than the eccentric hypertrophy pattern. Patients with high CAD-RADS showed statistically significant higher LV mass, LV mass index, and septal wall thickness. Patients with high CAD-RADS showed a greater percentage of concentric and eccentric hypertrophy. The LV geometric pattern was the only independent predictor of the high CAD-RADS. The LV geometric patterns associated with high RADS ordered from the highest to the lowest, were concentric LVH, Eccentric LV, and concentric remodeling. CONCLUSIONS: LV geometric pattern is the only independent predictor of high CAD-RADS after adjustment for LV mass index and septal wall thickness. Among abnormal LV geometric patterns, concentric hypertrophy stands as the most important predictor of high CAD-RADS.

Determinants of LV mass in athletes: the impact of sport, constitutional traits and cardiovascular risk factors.

BACKGROUND: Whether cardiovascular (CV) risk factors might impact Left Ventricular (LV) mass in athletes is unknown. METHODS: The impact of CV risk factors (Total/LDL cholesterol, triglycerides, positive family history, smoking, body fat, blood pressure), constitutional characteristics (age, sex, body mass index) and type of sport was assessed in 1111 Olympic athletes. RESULTS: Multivariate logistic regression analysis demonstrated a significant impact: BMI ≥ 30 kg/m2 (odds ratio [OR] = 2.8. 95° Confidence Interval [CI] 0.9-13.7; < 0.001; in males); age ≥ 20-year (OR = 2.1, CI 1.4-3.3; p < 0.001) in males; (OR = 2.3; CI 1.4-3.7) in females; systolic blood pressure ≥ 130 mmHg (OR = 1.1, CI 1.01-1.16; p < 0.001) in males; (OR = 1.03; CI 1.01-1.06; p < 0.03) in females; diastolic ≥ 85 mmHg (OR = 1.1, CI 1.03-1.2; p = 0.003) in males; (OR = 1.05, CI 1.02-1.08, p < 0.001) in females. No association was found for family history, smoking, body fat, LDL, total cholesterol, triglycerides. Overall, constitutional traits explain > 60% of the LV mass. Sport explains on average 14%, but large differences existed among disciplines, i.e., endurance showed the highest impact (55%, mixed: 20%, power: 17%, skill: 8%; p < 0.001). CONCLUSION: LV mass in athletes is largely governed by constitutional traits and type of sport, and independent from CV risk factors, except for systolic and diastolic blood pressure. Overall, constitutional traits explain more than 60% of LV mass. The impact of sport is largely different in relation to the discipline, and highest in endurance, moderate mixed and power and mild in skill disciplines.

Left ventricular function and mechanics in backs and forwards elite rugby union players.

ABSTRACTPurpose: The aim of the present study was to assess left ventricular (LV) morphological and regional functional adaptations in backs and forwards elite rugby union (RU) players. METHODS: Thirty-nine elite male RU players and twenty sedentary controls have been examined using resting echocardiography. RU players were divided into two groups, forwards (n = 22) and backs (n = 17). Evaluations included tissue Doppler and 2D speckle-tracking analysis to assess LV strains and twisting mechanics. RESULTS: The elite RU players exhibited an LV remodelling characterized by an increase in LV mass indexed to body surface area (82.2 ± 13.2 vs. 99.9 ± 16.1 and 119.7 ± 13.4 g.m-2, in controls, backs and forwards; P < .001). Compared to backs, forwards exhibited lower global longitudinal strain (19.9 ± 2.5 vs. 18.0 ± 1.6%; P < .05), lower early diastolic velocity (16.5 ± 1.8 vs. 15.0 ± 2.3 cm.s-1; P < .05) and lower diastolic longitudinal strain rate (1.80 ± 0.34 vs. 1.54 ± 0.26 s-1; P < .01), especially at the apex. LV twist and untwisting velocities were similar in RU players compared to controls, but with lower apical (-46.2 ± 22.1 vs. -28.2 ± 21.7 deg.s-1; P < .01) and higher basal rotational velocities (33.9 ± 20.9 vs. 48.4 ± 20.7 deg.s-1; P < .05). CONCLUSION: RU players exhibited an increase in LV mass which was more pronounced in forwards. In forwards, LV global longitudinal strain was depressed, LV filling pressures were decreased, and LV relaxation depressed at the apex.Highlights Elite RU players exhibited LV hypertrophy, especially in forwards players.LV regional function suggested a drop in LV relaxation and an increase in LV filling pressures in RU players, with higher alterations in forwards.LV remodelling was associated with regional alterations in torsional mechanics: higher rotations and rotational diastolic velocities at the basal level of LV but lower rotation and rotational diastolic velocities at the apex were observed in RU players.

Increasing myocardial edema is associated with greater microvascular obstruction in ST-segment elevation myocardial infarction.

Microvascular obstruction (MVO) frequently develops after ST-elevation myocardial infarction (STEMI) and is associated with increased mortality and adverse left ventricular remodeling. We hypothesized that increased extravascular compressive forces in the myocardium that arise from the development of myocardial edema because of ischemia-reperfusion injury would contribute to the development of MVO. We measured MVO, infarct size, and left ventricular mass in patients with STEMI (n = 385) using cardiac MRI 2 to 3 days following successful percutaneous coronary intervention and stenting. MVO was found in 57% of patients with STEMI. The average infarct size was 45 ± 29 g. Patients with MVO had significantly greater infarct size and reduced left ventricular (LV) function (P < 0.01) compared with patients without MVO. Patients with MVO had significantly greater LV mass than patients without MVO and there was a linear increase in MVO with increasing LV mass (P < 0.001). Myocardial edema by T2-weighted imaging increased with increasing LV mass and patients with MVO had significantly greater myocardial edema than patients without MVO (P < 0.01). Patients with MVO had significantly greater left ventricular end-diastolic pressure (LVEDP) than patients without MVO (P < 0.05). In a cohort of patients with STEMI who underwent primary percutaneous intervention, we observed that MVO increased linearly with increasing LV mass and was associated with increased myocardial edema and higher LVEDP. These observations support the concept that extravascular compressive forces in the left ventricle may increase with increasing ischemic injury and contribute to the development of MVO.NEW & NOTEWORTHY Patients with STEMI (n = 385) had cardiac MRIs 2 to 3 days following reperfusion with primary PCI to determine the relationship between myocardial edema, LV mass, and MVO. We observed that MVO increased linearly with LV mass and that myocardial edema measured by T2-imaging also increased linearly with LV mass. Patients with MVO had greater edema and LVEDP than subjects without MVO. These findings suggest that myocardial edema which arises from ischemia-reperfusion injury may result in extravascular compression of the microcirculation manifested as MVO on cardiac MRI.

Left ventricular geometry and electrocardiographic criteria in assessing left ventricular hypertrophy in sickle cell anemia patients.

BACKGROUND: Left ventricular hypertrophy (LVH) is recognized as a cardiovascular risk factor and is a known consequence of sickle cell anemia (SCA). Abnormal left ventricular geometric patterns have been described but the determinants have not been well elucidated. METHOD: Electrocardiography (ECG) and Echocardiography (ECHO) was done on subjects with SCA and hemoglobin A(HBA). Those with systemic hypertension were excluded. Voltages, durations, and intervals were measured as appropriate and recorded in a standard proforma. Analysis was made using a standard statistical software. RESULTS: Eighty four people with SCA and 91 with HBA were recruited as cases and controls respectively. Subjects with SCA have more abnormal LV geometric patterns than those with HBA(p=0.000). Eccentric LVH(p=0.000) was more in SCA subjects while concentric LVH(p=0.054) and concentric remodeling(p=0.319) were not. Forty-one and fifty-two subjects with SCA and HBA respectively did ECGs. . Subjects with eccentric LVH had lower hip circumference, higher left atrial diameter, right atrial area, higher sokolow-lyon voltage sum, stroke volume and cardiac output. The Sokolow-Lyon voltage criteria at the traditional cut off point was not different between those with and without eccentric LVH. However, Sokolow-Lyon voltage criteria at a cut-off of ≥4.7mV detected eccentric LVH with a sensitivity of 60% and specificity of 83.3%.While Sokolow-Lyon voltage sum, stroke volume, right atrial area, and left atrial diameter correlated positively, pulse rate and hip circumference correlated inversely with eccentric LVH. Sokolow Lyon voltage sum was the independent determinant of eccentric LVH in this study. CONCLUSION: Sickle cell anemia predisposes to abnormal LV geometric patterns, especially eccentric LVH. There may be a need to review the electrocardiographic cut off points for defining eccentric LVH in the SCA populace.

The Impact of Uncontrolled Hypertension on the Longitudinal Systolic Function of the Left Ventricle.

BACKGROUND: The assessment of the longitudinal component of left ventricular (LV) function is of major clinical importance for the early detection of LV contractile impairment. The aim of this study was to determine the impact of uncontrolled hypertension, on LV longitudinal systolic performance. METHODS: The study population included 400 hypertensive patients: 271 patients with uncontrolled blood pressure (BP) and 112 without controlled BP, all patients underwent a complete ultrasound evaluation with the calculation of the LV mass, evaluation of diastolic function as well as longitudinal systolic function. RESULTS: Conventional echo demonstrated that uncontrolled patients had increased LV mass (P 0.007), LA (left auricular) dimension (P 0.004), left ventricular wall thickness and impairment of diastolic function (E/E'6 ± 2.1 vs 7.4 ±3.0 P=0.001) while no affection of systolic function could be detected. By deformation imaging, there was a reduction in longitudinal strain (apical 4 view -16.2 ±2.9 vs -18.2± 2.6 P 0.02, apical 3 view -17.3 ± 3.3 vs. -18.9 ± 4.1 P 0.01). Similarly, systolic strain rate (SRsys) and early diastolic SR (SRe) reduced significantly in longitudinal direction. CONCLUSION: Although EF was not different between uncontrolled patients and controls, LV longitudinal strain and strain rate by 2D speckle tracking were lower in the uncontrolled group.

Left ventricular remodelling in bicuspid aortic valve disease.

AIMS: Characterization of left ventricular (LV) geometric pattern and LV mass could provide an important insight into the pathophysiological adaptations of the LV to pressure and/or volume overload in patients with bicuspid aortic valve (BAV) and significant (≥moderate) aortic valve (AV) disease. This study aimed to characterize LV remodelling and its prognostic impact in patients with BAV according to the predominant type of valvular dysfunction. METHODS AND RESULTS: In this international, multicentre BAV registry, 1345 patients [51.0 (37.0-63.0) years, 71% male] with significant AV disease were identified. Patients were classified as having isolated aortic stenosis (AS) (n = 669), isolated aortic regurgitation (AR) (n = 499) or mixed aortic valve disease (MAVD) (n = 177). LV hypertrophy was defined as a LV mass index >115 g/m2 in males and >95 g/m2 in females. LV geometric pattern was classified as (i) normal geometry: no LV hypertrophy, relative wall thickness (RWT) ≤0.42, (ii) concentric remodelling: no LV hypertrophy, RWT >0.42, (iii) concentric hypertrophy: LV hypertrophy, RWT >0.42, and (iv) eccentric hypertrophy: LV hypertrophy, RWT ≤0.42. Patients were followed-up for the endpoints of event-free survival (defined as a composite of AV repair/replacement and all-cause mortality) and all-cause mortality. Type of AV dysfunction was related to significant variations in LV remodelling. Higher LV mass index, i.e. LV hypertrophy, was independently associated with the composite endpoint for patients with isolated AS [hazard ratio (HR) 1.08 per 25 g/m2, 95% confidence interval (CI) 1.00-1.17, P = 0.046] and AR (HR 1.19 per 25 g/m2, 95% CI 1.11-1.29, P < 0.001), but not for those with MAVD. The presence of concentric remodelling, concentric hypertrophy and eccentric hypertrophy were independently related to the composite endpoint in patients with isolated AS (HR 1.54, 95% CI 1.06-2.23, P = 0.024; HR 1.68, 95% CI 1.17-2.42, P = 0.005; HR 1.59, 95% CI 1.03-2.45, P = 0.038, respectively), while concentric hypertrophy and eccentric hypertrophy were independently associated with the combined endpoint for those with isolated AR (HR 2.49, 95% CI 1.35-4.60, P = 0.004 and HR 3.05, 95% CI 1.71-5.45, P < 0.001, respectively). There was no independent association observed between LV remodelling and the combined endpoint for patients with MAVD. CONCLUSIONS: LV hypertrophy or remodelling were independently associated with the composite endpoint of AV repair/replacement and all-cause mortality for patients with isolated AS and isolated AR, although not for patients with MAVD.

Normalization of left ventricular filling pressure after cardiac surgery for the Loeffler's endocarditis: a case report.

BACKGROUND: Loeffler endocarditis is a rare restrictive cardiomyopathy, characterized by hypereosinophilia and fibrous thickening of the endocardium causing progressive onset of heart failure and appearance of thrombi on the walls of the heart chambers. CASE SUMMARY: A 72-year-old man known for hypertension and dyslipidaemia consults for progressive dyspnoea up to New York Heart Association (NYHA) Classes 2-3 over 3 weeks. The biological balance sheet shows a high eosinophil level and an echocardiography shows a mild echodensity fixed to the left apex. After exclusion of a secondary cause of hypereosinophilia, diagnosis of endomyocardial fibrosis in the context of a hypereosinophilic syndrome (HES) is therefore retained. The patient's clinical presentation with cardiac involvement leads us to start a treatment with corticosteroids. The patient is then regularly followed every 6 months with an initially stable course without complications. Two years later, he develops progressive signs of heart failure. Transthoracic echocardiography shows a left ventricular (LV) dilatation with a normal ejection fraction, but decreased volume due to a large echodense mass in the apex, and moderate aortic regurgitation caused by myocardial infiltration. In view of this rapid evolution, resection of the LV mass with concomitant aortic valve replacement is performed. Pathology confirms eosinophilic infiltration. The clinical course is very good with a patient who remains stable with dyspnoea NYHA Classes 1-2, and echocardiography at 1 year shows a normalization of LV filling pressure. DISCUSSION: HES represents a heterogeneous group of disorders characterized by overproduction of eosinophils. One of the major causes of mortality is associated cardiac involvement. Endocardial fibrosis and mural thrombosis are frequent cardiac findings. Echocardiography plays a crucial role in initial diagnosis of endomyocardial fibrosis, and for regular follow-up in order to adapt medical treatment and monitor haemodynamic evolution of the restrictive physiology and of valvular damage caused by the disease's evolution. This case also shows that surgery can normalize filling pressure and allow a clear improvement on the clinical condition even at the terminal fibrotic state.

Spotlights on some electrocardiographic paradigms: How should we evaluate normal reference values of Tp-Te interval, Tp-Te dispersion and Tp-Te/QT ratio?

BACKGROUND: Experimental and clinical studies evaluating the Tp-Te interval and Tp-Te/QT ratio have reported conflicting data. The overlap between normal Tp-Te/QT ratios (0.17 ±0.02-0.27 ±0.06 ms) and pathological values (0.20 ±0.03-0.30 ±0.06 ms) measured in earlier studies has raised questions about this ECG measurement technique. OBJECTIVES: To analyze normal values of the Tp-Te interval, Tp-Te dispersion Tp-Te(d) and the Tp-Te/QT ratio based on electrocardiographic (ECG) assessment across sex and age groups in a healthy Turkish population. MATERIAL AND METHODS: A total of 1,485 healthy participants (723 men) were enrolled into the study. The age of the participants ranged 17-75 years and they did not have either any cardiovascular/systemic disorders or risk factors for atherosclerosis which were detected with physical examination and laboratory tests. The Tp-Te interval, Tp-Te(d) and Tp-Te/QT ratio were determined from V1-V6 derivations. RESULTS: For the entire study, the median Tp-Te interval was 66.0 (64.0-70.0) ms, the Tp-Te(d) was 15.0 (10.0-20.0) ms, and the Tp-Te/QT ratio was 0.18 (0.17-0.19). The Pearson's correlation test demonstrated that the Tp-Te/QT ratio significantly correlated with older age (r = 0.297; p < 0.0001), left ventricular (LV) end-diastolic diameter (LVEDD; r = 0.481; p < 0.0001), body mass index (BMI; r = 0.421; p < 0.0001), body surface area (BSA; r = 0.191; p < 0.0001), LV end-diastolic volume (LVEDV; r = 0.484; p < 0.0001), LVEDV index (r = 0.450; p < 0.0001), LV mass (r = 0.548; p < 0.0001), and LV mass index (r = 0.539; p < 0.0001). CONCLUSIONS: The reference values for Tp-Te interval, Tp-Te(d) and Tp-Te/QT ratio are associated with age, BMI, BSA, LVEDV, LVEDV index, LV mass, and LV mass index. These structural elements should be considered when using these ECG parameters for assessing repolarization inhomogeneity. These findings may guide further studies assessing healthy and diseased populations.

Time course of left ventricular remodelling and mechanics after aortic valve surgery: aortic stenosis vs. aortic regurgitation.

AIMS: Pressure overload in aortic stenosis (AS) and both pressure and volume overload in aortic regurgitation (AR) induce concentric and eccentric hypertrophy, respectively. These structural changes influence left ventricular (LV) mechanics, but little is known about the time course of LV remodelling and mechanics after aortic valve surgery (AVR) and its differences in AS vs. AR. The present study aimed to characterize the time course of LV mass index (LVMI) and LV mechanics [by LV global longitudinal strain (LV GLS)] after AVR in AS vs. AR. METHODS AND RESULTS: Two hundred and eleven (61 ± 14 years, 61% male) patients with severe AS (63%) or AR (37%) undergoing surgical AVR with routine echocardiographic follow-up at 1, 2, and/or 5 years were evaluated. Before AVR, LVMI was larger in AR patients compared with AS. Both groups showed moderately impaired LV GLS, but preserved LV ejection fraction. After surgery, both groups showed LV mass regression, although a more pronounced decline was seen in AR patients. Improvement in LV GLS was observed in both groups, but characterized by an initial decline in AR patients while LV GLS in AS patients remained initially stable. CONCLUSION: In severe AS and AR patients undergoing AVR, LV mass regression and changes in LV GLS are similar despite different LV remodelling before AVR. In AR, relief of volume overload led to reduction in LVMI and an initial decline in LV GLS. In contrast, relief of pressure overload in AS was characterized by a stable LV GLS and more sustained LV mass regression.

Can the echocardiographic LV mass equation reliably demonstrate stable LV mass following acute change in LV load?

BACKGROUND: Limited data are available on performance of the left ventricular (LV) mass equation when there is a dynamic change to LV load. We aimed to test this equation in the immediate post-operative period following aortic valve replacement (AVR) for aortic regurgitation (AR) to see if it would reliably demonstrate stable LV mass before and after surgery. Since LV mass would be unlikely to change in the immediate postoperative period, we hypothesized that a decrease in LV diameter postoperatively would be accompanied by concomitant increases in LV wall thickness as predicted by the LV mass equation. METHODS: We reviewed echocardiograms of adult patients with AR who underwent AVR from 2007-2017 at Montefiore Medical Center (n=28). Three independent readers performed septal wall thickness (SWT), posterior wall thickness (PWT) and left ventricular internal diameter (LVID) measurements on pre-operative and post-operative echocardiograms. LV masses were calculated using the American Society of Echocardiography (ASE) equation. RESULTS: Post-operatively, LVID decreased from 5.7±1.2 to 4.9±1.0 cm, P<0.001. SWT was noted to increase from 1.08±0.20 to 1.18±0.27 cm, P=0.03, but PWT was unchanged, 1.11±0.21 to 1.16±0.27 cm, P=0.21. Accordingly, the LV mass equation calculated a decrease in LV mass from 266±126 to 232±99 gm, P=0.01. A control group of coronary artery bypass grafting alone (n=14) did not demonstrate any significant change in SWT, LVID, PWT and LV mass measurements. Similar findings were found for all three readers. CONCLUSIONS: Following aortic valve replacement for regurgitation, the LV mass equation calculated a reduction in LV mass in the immediate postoperative period. Since an immediate change in LV mass after AVR is unlikely, we feel that these results highlight an important limitation of the mass equation, when used with acutely changing loading conditions.

Impact of glycemic control on aortic stiffness, left ventricular mass and diastolic longitudinal function in type 2 diabetes mellitus.

BACKGROUND: Poor glycemic control is associated with impaired left ventricular (LV) diastolic function in patients with type 2 diabetes mellitus (T2DM). Inappropriate LV mass increase and accelerated aortic stiffening were suggested to participate on deterioration of diastolic function. The present study investigated the inter-relationships between glycemic control, early diastolic and systolic longitudinal velocity of mitral annulus, LV mass and aortic stiffness in T2DM patients free of cardiovascular disease and with preserved LV ejection fraction, and compared them with those observed in healthy volunteers of similar age and sex distribution. METHODS: 125 T2DM patients and 101 healthy volunteers underwent noninvasive measurement of systolic (s') and early diastolic (e') velocities of mitral annulus, LV mass, carotid-femoral pulse wave velocity (cfPWV) and local carotid blood pressure (BP). RESULTS: Forty-four (35.2%) T2DM patients had e' velocity lower than that expected for age (against 7.9% in healthy volunteers; P < 0.0001), 34 (27.2%) had cfPWV higher than that expected for age and mean BP (against 5.9% in healthy volunteers; P < 0.0001), and 71 (56.8%) had LV mass higher than that expected for body size and stroke work (against 17.6% in healthy volunteers; P < 0.0001). Carotid systolic BP was higher in T2DM patients (124 ± 14 vs 111 ± 11 mmHg; P < 0.0001). In multivariate analysis, e' velocity was independently related to age, carotid BP and s' velocity in healthy volunteers, and to male sex, age, carotid BP, heart rate and LV mass in T2DM. Glycosylated hemoglobin (HbA1c) was independently related to cfPWV and LV mass in T2DM patients. T2DM patients with HbA1c ≥6.5% (N = 85) had higher cfPWV (P < 0.05), central BP (P = 0.01), prevalence of LV hypertrophy (P = 0.01) and lower e' and s' velocity (P = 0.001 and <0.05, respectively) as compared to those with HbA1c <6.5%. CONCLUSIONS: One-third of T2DM patients with preserved LV ejection fraction has sign of subclinical LV diastolic dysfunction. HbA1c levels are positively associated with LV mass and aortic stiffness, both of which show a negative independent impact on early diastolic velocity e', the latter through an increase in afterload. T2DM patients with suboptimal glycemic control (HbA1c ≥ 6.5%) have lower diastolic and systolic LV longitudinal performance, together with increased aortic stiffness and a higher prevalence of LV hypertrophy.

Physical Activity Is Associated With Reduced Left Ventricular Mass in Obese and Hypertensive African Americans.

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.

Sex-Specific Response to Cardiac Resynchronization Therapy: Effect of Left Ventricular Size and QRS Duration in Left Bundle Branch Block.

OBJECTIVES: In this study, the authors sought to assess the impact of body and heart size on sex-specific cardiac resynchronization therapy (CRT) response rate, according to QRS duration (QRSd) as a continuum. BACKGROUND: Effects of CRT differ between sexes for any given QRSd. METHODS: New York Heart Association functional class III/IV patients with nonischemic cardiomyopathy and "true" left bundle branch block (LBBB) were evaluated. Left ventricular mass (LVM) and end-diastolic volume were measured echocardiographically. Positive response was defined by left ventricular ejection fraction (LVEF) improvement post-CRT. RESULTS: Among 130 patients (LVEF 19 ± 7.1%; QRSd 165 ± 20 ms; 55% female), CRT improved LVEF to 32 ± 14% (p < 0.001) during a median 2 years follow-up. Positive responses occurred in 103 of 130 (79%) (78% when QRSd <150 ms vs. 80% when QRSd ≥150 ms; p = 0.8). Body surface area (BSA), QRSd, and LVM were lower in women, but QRSd/LVM ratio greater (p < 0.0001). Sexes did not differ for pharmacotherapy and comorbidities, but female CRT response was greater: 90% (65 of 72) versus 66% (38 of 58) in males (p < 0.001). With QRSd as a continuum, the overall CRT-response relationship showed a progressive increase to plateau between 150 and 170 ms, then a decrease. Sex-specific differences were conspicuous: among females, a peak effect was observed between 135 and 150 ms, thereafter a decline, with the male response rate lower, but with a gradual increase as QRSd lengthened. Sex-specific differences were unaltered by BSA, but resolved with integration of LVM or end-diastolic volume. CONCLUSIONS: Sex differences in the QRSd-response relationship among CRT patients with LBBB were unexplained by application of strict LBBB criteria or by BSA, but resolved by QRSd normalization for heart size using LV mass or volume.

Cardiac CT assessment of left ventricular mass in mid-diastasis and its prognostic value.

AIMS: To determine the influence of cardiac motion on measurements of left ventricular (LV) mass obtained with 64-slice computed tomography (CT) and to elucidate the prognostic value of LV mass on major adverse cardiac events (MACE) and all-cause mortality. Increased LV mass has been linked with MACE. Although Cardiac CT allows measurement of LV anatomy, it is susceptible to motion artefacts often requiring image acquisition during diastasis. There is a need to understand variability in LV mass measurements across phases of the cardiac cycle, and whether mid-diastolic measurements have prognostic value. METHODS AND RESULTS: The study comprised two equally sized cohorts of patients that had undergone retrospectively gated cardiac CT: patients who had MACE and/or all-cause death at follow-up and a matched (age, sex, and risk factors) event-free cohort. LV mass was measured at mid-diastole, end-diastole, and end-systole. Correlation and agreement between phases were determined. The incremental value of mid-diastolic hypertrophy (LVH) over the National Cholesterol Education Programme (NCEP) risk was performed for LV mass indices normalized to body surface area (LVMIBSA) or weight (LVMIWeight). Of 166 patients, 31.3% experienced MACE and 28.9% died of any cause (follow-up 22.9 ± 13.4 months). LV mass at all cardiac phases were strongly correlated (r > 0.94). Mean mid-diastolic LVMIBSA was higher in the cohort with events (93.7 vs. 80.7 g/m2, P= 0.008) as was LVMIWeight (2.26 vs. 1.88 g/kg, P = 0.001). LVMIBSA and LVMIWeight had prognostic value incremental to NCEP with 1.85 and 2.47 hazard ratios, respectively. CONCLUSIONS: Measurement of LV mass can be obtained by cardiac CT images obtained at mid-diastasis. LV mass measurements obtained at mid-diastasis have prognostic value.