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Chronic elevation in the systolic blood pressure (SBP) adversely affects the lifespan in the dog by causing injury to the eye, heart, kidney and brain. Understanding the association between SBP and target organ damage (TOD) helps in risk categorization and treatment planning. Therefore, a prospective study was undertaken to find the association between SBP and renal resistive index (RI) in naturally occurring cases of canine systemic hypertension. Based on the ACVIM guidelines 2018, dogs (n=135) were categorized into four risk groups of SBP, viz., A (minimal), B (low), C (moderate), and D (high). Ophthalmoscopy and echocardiography were used to assess ocular and cardiac changes, respectively. Nephrosonography, urinalysis, and RI were used to assess kidney damage. Odds ratio (OR) was used to quantify the risk of TOD for different categories of SBP. One-way Anova with Tukey's post-hoc test was used to test the effect of different SBP risk groups on urine protein creatinine ratio (UPC) and RI as well as the effect of number of TOD on the RI. Pearson's correlation test was done to see the relation of SBP with UPC and RI. Tortuous retinal vessels were common in group B with an OR of 11 (95% CI: 0.59-207). Retinal hemorrhage and left ventricular hypertrophy were common in group D with an OR of 13 (95% CI: 0.67-234) and 11 (95% CI: 0.61-207), respectively. A significant strong positive correlation of SBP with UPC (R 2 =0.65) and RI (R 2 =0.58) was observed. The renal RI significantly increased when the number of TOD was ≥ 2. It was concluded that SBP and RI are associated with the number and severity of TOD and might be valuable in risk classification in hypertensive dogs., Competing Interests: Declaration of Competing Interest The authors declare that they do not have any relevant financial or non-financial interests to disclose., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Left ventricular (LV) morphologic progression in apical hypertrophic cardiomyopathy (AHC) has not been well studied. We evaluated serial echocardiographic changes in LV morphology., Methods: Serial echocardiograms in AHC patients were assessed. LV morphology was categorized according to the presence of an apical pouch or aneurysm, and LV hypertrophic severity and extent; relative, pure, and apical-mid type defined as mild (<15 mm thickness) apical hypertrophy, significant (≥15 mm) apical hypertrophy, and both apical and midventricular hypertrophy, respectively. Adverse clinical events and late gadolinium enhancement (LGE) extent on cardiac magnetic resonance were evaluated for each morphologic type., Results: In 41 patients, 165 echocardiograms (maximal interval: 4.2 [IQR, 2.3-11.8] years) were evaluated. Morphologic changes were observed in 19 (46%) patients. Eleven (27%) patients displayed the progression of LV hypertrophy toward pure or apical-mid type. Five (12%) and 6 (15%) patients developed new pouches and aneurysms. Patients with progression tended to be younger (50 ± 15.6 vs 59 ± 14.4 years, P = 0.058) and had a longer period of follow-up (12 [5-14] vs 3 [2-4] years, P < 0.001). During a follow-up of 7.6 (IQR 3.0-12.1) years, 21 (51%) experienced clinical events. The relative, pure, and apical-mid types showed different LGE extents (2%, 6%, and 19%, P = 0.004). Patients with severe hypertrophic and apical involvement showed higher clinical event rates., Conclusions: About half of AHC patients had a progression of LV morphology to more hypertrophic involvement and/or an apical pouch or aneurysm formation. Advanced AHC morphologic types were associated with higher event rates and scar burdens., Competing Interests: Declaration of Competing Interest The authors report no relationships that could be construed as a conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: The association of lipoprotein(a) [Lp(a)] with echocardiography-estimated left ventricular hypertrophy (LVH) in high-risk population remains uncertain, so we assessed the association between Lp(a) with echocardiography-derived LVH in patients with new-onset acute myocardial infarction (AMI)., Methods: In this large, single-center, cross-sectional observational study, we enrolled 2,096 patients with new-onset AMI. Lp(a) was used as the independent variable and LVH was used as the dependent variable. Logistic regression, subgroup and sensitivity analysis were performed to test the association of Lp(a) with LVH., Results: The concentration of Lp(a) was higher in LVH group compared with the non-LVH group (P < 0.001). Multivariate logistic regression analysis showed that higher Lp(a) was strongly associated with higher risk of LVH, independently of traditional cardiovascular risk factors (Fully adjusted model, Q4 vs Q1, OR: 1.941, 95% CI: 1.343-2.803, P < 0.001). Subgroup analysis showed that the association of Lp(a) with LVH persisted in the subgroups of age (<60 and ≥60 years), sex (male and female), smoking (yes and no), diabetes (yes), hypertension (yes), hyperlipidemia (yes), and chronic kidney diseases (yes and no). Further sensitivity analysis indicated that Lp(a) remained significantly associated with LVH after further adjusting for high-sensitivity C-reactive protein or excluding patients with estimated glomerular filtration rate < 30 ml/min/1.73 m 2 or dividing Lp(a) into multiple dichotomous variables., Conclusion: Lp(a) was closely associated with LVH in patients with new-onset AMI., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Little is known about prevalence and predictors of myocardial infarction with non-obstructive coronary arteries (MINOCA) in Fabry disease (FD) and hypertrophic cardiomyopathy (HCM). We assessed and compared the prevalence and predictors of MINOCA in a large cohort of HCM and FD patients., Methods: In this multicenter, retrospective study we enrolled 2870 adult patients with HCM and 267 with FD. The only exclusion criterion was documented obstructive coronary artery disease. MINOCA was defined according to guidelines. For each patient we collected clinical, ECG and echocardiographic data recorded at initial evaluation., Results: Overall, 36 patients had MINOCA during a follow-up period of 4.5 ± 11.2 years. MINOCA occurred in 16 patients with HCM (0.5%) and 20 patients with FD (7.5%; p &lt; 0.001). The difference between the 2 groups was highly significant, also after adjustment for the main clinical, ECG and echocardiographic variables (OR 6.12; 95%CI 2.80-13.3; p &lt; 0.001). In the FD population MINOCA occurred in 17 out of 96 patients with left ventricle hypertrophy (LVH, 17.7%) and in 3 out of 171 patients without LVH (1.7%; OR 12.0; 95%CI 3.43-42.3; p &lt; 0.001). At multivariable analysis, voltage criteria for LVH at ECG (OR 7.3; 95%CI 1.93-27.7; p = 0.003) and maximal LV wall thickness at echocardiography (OR 1.15; 95%CI 1.05-1.27; p = 0.002) maintained an independent association with MINOCA. No major significant differences were found in clinical, ECG and echocardiographic findings between HCM patients with or without MINOCA., Conclusions: MINOCA was rare in HCM patients, and 6-fold more frequent in FD patients. MINOCA may be considered a red flag for FD and aid in the differential diagnosis from HCM., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Hypertension Canada's 2020 guidelines for the prevention, diagnosis, risk assessment, and treatment of hypertension in adults and children provide comprehensive, evidence-based guidance for health care professionals and patients. Hypertension Canada develops the guidelines using rigourous methodology, carefully mitigating the risk of bias in our process. All draft recommendations undergo critical review by expert methodologists without conflict to ensure quality. Our guideline panel is diverse, including multiple health professional groups (nurses, pharmacy, academics, and physicians), and worked in concert with experts in primary care and implementation to ensure optimal usability. The 2020 guidelines include new guidance on the management of resistant hypertension and the management of hypertension in women planning pregnancy., (Copyright © 2020 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Background: The underlying mechanisms causing myocardial ischemia in non-obstructive coronary artery disease (CAD) are still unclear. We explored whether left ventricular hypertrophy (LVH) was associated with myocardial ischemia in patients with stable angina and non-obstructive CAD., Methods: 132 patients (mean age 63 ± 8 years, 56% women) with stable angina and non-obstructive CAD diagnosed as <50% stenosis by coronary computed tomography angiography (CCTA) underwent myocardial contrast stress echocardiography. Left ventricular (LV) hypertrophy (LVH) was identified by LV mass index >46.7 g/m 2.7 in women and >49.2 g/m 2.7 in men. Patients were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. The number of LV segments with ischemia at peak stress was taken as a measure of the extent of myocardial ischemia., Results: Myocardial ischemia was found in 52% of patients, with on average 5 ± 3 ischemic LV segments per patient. The group with myocardial ischemia had higher prevalence of LVH (23 vs. 10%, p = 0.035), while age, sex and prevalence of hypertension did not differ between groups (all p > 0.05). In multivariable regression analyses, LVH was associated with presence of myocardial ischemia (odds ratio 3.27, 95% confidence interval [1.11-9.60], p = 0.031), and larger extent of myocardial ischemia (β = 0.22, p = 0.012), independent of confounders including age, hypertension, obesity, hypercholesterolemia, calcium score and segment involvement score by CCTA., Conclusions: LVH was independently associated with both presence and extent of myocardial ischemia in patients with stable angina and non-obstructive CAD by CCTA. These results suggest LVH as an independent contributor to myocardial ischemia in non-obstructive CAD., Clinical Trial Registration Number: ClinicalTrials.gov, identifier NCT018535271., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: The pedicled greater omentum has been shown to offer benefit in ischemic heart disease for both animal models and human patients. The impact of cardio-omentopexy in a pressure overload model of left ventricular hypertrophy (LVH) is unknown., Methods: LVH was created in rats by banding the ascending aorta after right thoracotomy (n = 23). Sham surgery was performed in 12 additional rats. Six weeks after banding, surviving LVH rats were assigned to cardio-omentopexy by left thoracotomy (LVH+Om, n = 8) or sham left thoracotomy (LVH, n = 8). Sham rats also underwent left thoracotomy for cardio-omentopexy (Sham+Om, n = 6); the remaining rats underwent sham left thoracotomy (Sham, n = 6)., Results: Echocardiography 10 weeks after cardio-omentopexy revealed LV end-systolic diameter, cardiomyocyte diamter, and myocardial fibrosis in the LVH group were significantly increased compared with the LVH+Om, Sham+Om, and Sham groups (p < 0.01). LV ejection fraction of the LVH group was lower than the LVH+Om group (p < 0.01). Gene expression analysis revealed significantly lower levels of sarcoendoplasmic reticulum calcium adenosine triphosphatase 2b in LVH rats than in the LVH+Om, Sham+Om, and Sham groups (p < 0.01). In contrast, collagen type 1 α 1 chain, lysyl oxidase-like protein 1, nuclear protein-1, and transforming growth factor- β1 in the LVH group were significantly higher than in the LVH+Om cohort (p < 0.01), consistent with a reduced fibrotic phenotype after omentopexy. Lectin staining showed myocardial capillary density of the LVH group was significantly lower than all other groups (p < 0.01)., Conclusions: Cardio-omentopexy reduced cardiac dilation, contractile dysfunction, cardiomyocyte hypertrophy, and myocardial fibrosis, while maintaining other molecular indicators of contractile function in this LVH model., (Copyright © 2019 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

This report presents the case of an 82-year-old man with known dextrocardia and situs inversus totalis who presented with increasing dyspnea on exertion and was diagnosed with severe aortic stenosis. Transcatheter aortic valve replacement was performed and required deviation from standard techniques for patients with normal anatomy and left-sided aortic arch. We describe two technical differences required for patients with dextrocardia and right-sided aortic arch that facilitate transcatheter aortic valve replacement in this patient group., (Copyright © 2019 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Background: Left ventricular (LV) dysfunction develops during LV hypertrophy and particularly during tachycardia. Thus we investigated the effects of heart rate (HR) reduction with ivabradine, an I f -channel blocker, on LV twist and untwist which represents myocardial deformation occurring during the overall systole and diastole and therefore provide valuable evaluation of global LV systolic and diastolic function., Methods: Eight chronically instrumented pigs receiving continuous angiotensin II infusion during 28days to induce chronic hypertension and LV hypertrophy. Measurements were performed at Days 0 and 28 after stopping angiotensin II infusion in the presence and absence of ivabradine., Results: At Day 0, reducing HR from 75±3 to 55±2beats/min with ivabradine did not affect LV twist but slowed LV untwist along with an increase in LV end-diastolic pressure. At Day 28, LV posterior and septal wall thickness as well as the estimated LV mass increased, indicating LV hypertrophy. LV twist and untwist were significantly reduced by 33±4% from 16±1° and 32±6% from -154±9°/s, respectively, showing global LV systolic and diastolic dysfunction. In this context, ivabradine decreased HR by 25% from 86±5beats/min and significantly improved LV twist from 11±1 to 14±1° and LV untwist from -104±8 to -146±5°/s., Conclusions: Administration of ivabradine during chronic hypertension and LV hypertrophy improved LV twist and untwist. This further supports the beneficial effect of this drug on both LV systolic and diastolic function during the development of LV hypertrophy., (Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.)

Objectives: To assess the prevalence of left ventricular hypertrophy according to electrocardiographic and echocardiographic criteria among hypertensive patients living in semi-rural Senegalese area., Patients and Methods: According to the World Health Organization STEPSwise approach, we conducted, in November 2012, a cross-sectional and exhaustive study in the population aged at least 35 years old and living for at least six months in the semi-rural area of Guéoul. We researched electrocardiographic and echocardiographic left ventricular hypertrophy in hypertensive subjects. Data were analyzed with SPSS 18.0 software version. The significance level was agreed for a value of P<0.05., Results: We examined 1411 subjects aged on average of 48.5±12.7 years. In total, 654 subjects were hypertensive and screening of left ventricular hypertrophy (LVH) was effective in 515 of them. According to Sokolow-Lyon index, 86 subjects (16.7%) presented electrocardiographic LVH, more frequently in men (P=0.002). According to Cornell index and Cornell product, LVH was founded respectively in 66 (12.8%) and 52 subjects (10.1%), more frequently in female (P=0.0001; P=0.004). It was more common in grade 3 of hypertension however criteria. In echocardiography, prevalence of LVH was 2.2% (13 cases) according to the left ventricular mass, 9.3% (48 cases) according to the left ventricular mass indexed to body surface area and 8.2% (42 cases) according to the left ventricular mass indexed to height 2.7 . LVH was significantly correlated with the electrocardiographic LVH according to Sokolow-Lyon index (P<0.0001) and the grade 3 of hypertension (P=0.003)., Conclusion: Although rare in hypertensive Senegalese living in semi-rural area, left ventricular hypertrophy is correlated with severity of grade of hypertension. Screening by electrocardiogram will allow better follow-up of these hypertensive subjects., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)

Background: Left ventricular false tendons (LVFTs) are chord-like structures that traverse the LV cavity and are generally considered to be benign. However, they have been associated with arrhythmias, LV hypertrophy and LV dilation in some small studies. We hypothesize that LVFTs are associated with LV structural and functional changes assessed by echocardiography., Methods: We retrospectively evaluated echocardiographic and clinical parameters of 126 patients identified as having LVFTs within the past 2 years and compared them to 85 age-matched controls without LVFTs., Results: There were no significant differences in age (52 ± 18 versus 54 ± 18 years, P = 0.37), sex (55% versus 59% men, P = 0.49), race (36% versus 23% white, P = 0.07), systolic blood pressure (131 ± 22 versus 132 ± 23mmHg, P = 0.76) or body mass index (BMI, 31 ± 8 versus 29 ± 10kg/m 2 , P = 0.07) between controls and patients with LVFTs, respectively. Patients with LVFTs had more prevalent heart failure (43% versus 21%, P = 0.001). Patients with LVFTs had more LV dilation, were 2.5 times more likely to have moderate-to-severe mitral regurgitation, had more severe diastolic dysfunction and reduced LV systolic function (18% lower) compared with controls (all P < 0.05). After adjustment for covariates, basal and middle LVFT locations were associated with reduced LV systolic function (P < 0.01), and middle LVFTs were associated with LV dilation (P < 0.01)., Conclusions: Our findings suggest that LVFTs may not be benign variants, and basal and middle LVFTs may have more deleterious effects. Further prospective studies should be performed to determine their pathophysiological significance and whether they play a causal role in LV dysfunction., (Copyright © 2017 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Abnormal papillary muscle is a rare cause of midventricular obstruction. In this case report, hypertrophied abnormal papillary muscles and abnormal tissue growth from the septal wall formed an intra-left ventricular septum with a small hole and resulted in severe midventricular obstruction. Radical resection of both papillary muscles and the intra-left ventricular septum was performed along with mitral valve replacement to relieve the obstruction., (Copyright © 2017 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Background: Substantial aortic calcification is known to be associated with aortic stiffening and subsequent left ventricular (LV) hypertrophy. This study examined whether the thoracic aorta calcium score (TACS) is related to LV hypertrophy and whether it leads to an adverse prognosis in patients with severe aortic stenosis (AS) after aortic valve replacement (AVR)., Methods: We retrospectively reviewed 47 patients (mean age, 64 ± 11 years) with isolated severe AS who underwent noncontrast computed tomography of the entire thoracic aorta and who received AVR. TACS was quantified using the volume method with values becoming log transformed ( log [TACS+1]). Transthoracic echocardiography was performed before and 1 year after the operation., Results: Preoperative LV mass index (LVMI) displayed significant positive correlations with male gender (r = 0.430, p = 0.010) and log (TACS+1) (r = 0.556, p = 0.003). In multivariate linear regression analysis, only log (TACS+1) was independently associated with LVMI, even after adjusting for age, gender, transaortic mean pressure gradient, and coronary or valve calcium score. Independent determinants for postoperative LVMI included log (TACS+1) and preoperative LVMI after 1 year of follow-up echocardiography, adjusting for age, gender, indexed effective orifice area, and coronary or valve calcium score. During a median follow-up period of 54 months after AVR, there were 10 events (21%), which included 4 deaths from all-causes, 3 strokes, 2 inpatient admissions for heart failure, and 1 myocardial infarction. The event-free survival rate was significantly lower for patients with TACS of 2,257 mm 3 or higher compared with those whose TACS was lower than 2,257 mm 3 (log-rank p < 0.001)., Conclusions: High TACS was associated with increased LVMI among patients with severe AS. Further, high TACS usefully predicted less regression of LVMI and poor clinical outcomes after AVR. TACS may serve as a useful proxy for predicting LV remodeling and adverse prognosis in patients with severe AS undergoing AVR., (Copyright © 2017 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Aortic root dilatation is associated with increased cardiovascular risk in hypertensive adults. In the young, few data have been published evaluating the cardiovascular organ damage that may be present in patients with aortic dilatation. The objective was to evaluate the prevalence of proximal aorta dilatation, its possible determinants, and its relation with target organ damage in young subjects. The aorta was measured at the level of the sinus of valsalva and at its proximal ascending aorta (pAA) in a total of 177 young subjects (11-35 years). Linear regression analysis was used to assess the association between aortic size, clinical, and hemodynamic parameters. Prevalence of pAA and sinus of valsalva dilatation was 10.2% and 8.7%, respectively. No significant differences in prevalence were found in hypertensive, diabetic and obese subjects; aortic enlargement was less frequent in African-Americans. Age, sex, and central pulse pressure were the most important determinants of aortic size. Left ventricular mass was increased in patients with aortic enlargement, and aortic size showed an inverse relation with indices of local distensibility. The prevalence of aortic dilatation among young patients is high (10%). As in adults, age and body surface area are the main determinants of aortic size. Dilatation of the ascending aorta is associated with an increased left ventricular mass, as in adults, but not with increased arterial stiffness. Local distensibility is reduced in patients with pAA enlargement., (Copyright © 2016 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Background: Presence of pulmonary hypertension (PH) and right ventricular dysfunction worsens prognosis in patients with chronic heart failure (CHF). Preclinical and clinical studies suggest a role for the impaired nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) signaling pathway in both PH and CHF. Hence, we examined the effects of the NO-sGC-cGMP pathway modulation by the PDE5 inhibitor sildenafil or sGC stimulator riociguat on pulmonary hemodynamics and heart function in a murine model of secondary PH induced by transverse aortic constriction., Methods: C57Bl/6N mice were subjected to transverse aortic constriction (TAC) for 6weeks to induce left heart failure and secondary PH and were subsequently treated with either sildenafil (100mg/kg/day) or riociguat (10mg/kg/day) or placebo for 2weeks., Results: Six weeks after surgery, TAC induced significant left ventricular hypertrophy and dysfunction associated with development of PH. Treatment with riociguat and sildenafil neither reduced left ventricular hypertrophy nor improved its function. However, both sildenafil and riociguat ameliorated PH, reduced pulmonary vascular remodeling and improved right ventricular function., Conclusions: Thus, modulation of the NO-sGC-cGMP pathway by the PDE5 inhibitor sildenafil or sGC stimulator riociguat exerts direct beneficial effects on pulmonary hemodynamics and right ventricular function in the experimental model of secondary PH due to left heart disease and these drugs may offer a new therapeutic option for therapy of this condition., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

AVE 0991, the nonpeptide angiotensin-(1-7) (Ang-(1-7)) analog, is recognized as having beneficial cardiovascular effects. However, the mechanisms have not been fully elucidated. This study was designed to investigate the effects of AVE 0991 on cardiac hypertrophy and the mechanisms involved. Mice were underwent aortic banding to induce cardiac hypertrophy followed by the administration of AVE 0991 (20 mg kg·day (-1)) for 4 weeks. It was shown that AVE 0991 reduced left ventricular hypertrophy and improved heart function, characterized by decreases in left ventricular weight and left ventricular end-diastolic diameter, and increases in ejection fraction. Moreover, AVE 0991 significantly down-regulated mean myocyte diameter and attenuate the gene expression of the hypertrophic markers. Furthermore, AVE 0991 inhibited the expression of NOX 2 and NOX 4, meaning that AVE 0991 reduced oxidative stress of cardiac hypertrophy mice. Our data showed that AVE 0991 treatment could attenuate cardiac hypertrophy and improve heart function, which may be due to reduce oxidative stress., (Copyright © 2016. Published by Elsevier Inc.)

Background: Prolongation of initial ventricular depolarization on the 12-lead electrocardiogram (ECG), or delayed intrinsicoid deflection (DID), can indicate left ventricular hypertrophy (LVH). The possibility that this marker could convey distinct risk of sudden cardiac arrest (SCA) has not been evaluated., Objective: To evaluate the association of DID and SCA in the community., Methods: In the ongoing prospective, population-based Oregon Sudden Unexpected Death Study (Oregon SUDS; catchment area approximately 1 million), SCA cases were compared to geographic controls with no SCA. Archived ECGs (closest and unrelated to SCA event for cases) were evaluated for the presence of DID, defined as ≥0.05 second in leads V5 or V6. Left ventricular (LV) mass and function were evaluated from archived echocardiograms., Results: SCA cases (n = 272, 68.7 ± 14.6 years, 63.6% male) as compared to controls (n = 351, 67.6 ± 11.4 years, 63.3% male) were more likely to have DID on ECG (28.3% vs. 17.1%, P = .001). DID was associated with increased SCA odds (odds ratio [OR] 1.92; 95% confidence interval [CI] 1.31-2.81; P = .001), but showed poor correlation with LV mass and echocardiographic LVH (kappa 0.13). In multivariate analysis adjusted for clinical and ECG markers, reduced LV ejection fraction, and echocardiographic LVH, DID remained an independent predictor of SCA (OR 1.82; 95% CI 1.12-2.97; P = .016). Additionally, in a sensitivity analysis restricted to narrow QRS, DID and ECG LVH by voltage were each independently associated with SCA risk., Conclusion: DID was associated with increased SCA risk independent of echocardiographic LVH, ECG LVH, and reduced LV ejection fraction, potentially reflecting unique electrical remodeling that warrants further investigation., (Copyright © 2016 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Serum parathyroid hormone (PTH) has been found to be associated with cardiovascular mortality in the elderly, but little is known about the mechanisms underlying this association. This study investigated the association between PTH and structural and functional changes of the heart and arterial wall in a cohort of very elderly individuals. Healthy individuals aged 80 years or more (n = 90) underwent evaluation of serum PTH, cardiac morphology and function by Doppler echocardiography, endothelium dependent and independent vasodilatation by brachial reactivity, carotid stiffness and intima-media thickness by ultrasound, and coronary calcification by computed tomography. Participants with PTH levels above the median 5.8 pmol/L had higher left ventricular mass index (P = .02), relative wall thickness (P = .02), left atrial volume index (P = .03), and shorter deceleration time of E mitral wave (P = .04). Serum PTH levels (odds ratio, 1.027; P = .032) and systolic blood pressure (odds ratio, 1.032; P = .008) were independently associated with left ventricular hypertrophy. No difference was found between PTH groups in flow- or nitrate-mediated brachial artery dilatation, coronary artery calcification, intima-media thickness, or arterial stiffness. Elevation of serum PTH in the very elderly is associated with concentric left ventricular hypertrophy, but no association with arterial wall structure or function was found in this study., (Copyright © 2015 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Background: To (1) determine the prevalence of hypertension late after coarctation repair in patients with normal-sized transverse arches, and (2) evaluate the potential for end-organ damage related to hypertension after coarctation repair. There are no studies specifically investigating end-organ damage and hypertension after coarctation repair using noninvasive techniques., Methods: Eighty-two patients aged 10 years or greater with a coarctation repair and a normal-sized arch operated on between 1978 and 2010, underwent a transthoracic echocardiogram, 24-hour blood pressure (BP) monitoring, and retinal imaging. Median age at repair was 1 year (interquartile range, 0 to 6); 45% (37 of 82) were operated in the first year of life., Results: After a follow-up of 24 ± 7 years, 27% (22 of 82) and 50% (41 of 82) suffered resting hypertension and resting prehypertension, respectively. On 24-hour BP monitoring, 61% (49 of 80) and 21% (17 of 80) suffered hypertension and prehypertension, respectively. Arch reobstruction (echo gradient > 25 mm Hg) was present in only 15% (12 of 82), and in only 15% (7 of 47) with 24-hour hypertension. Resting hypertension was associated with a smaller central retinal artery equivalent (average width of arterioles) and central retinal vein equivalent (average width of venules) (p = 0.0006 and p = 0.003, respectively). Left ventricular hypertrophy on echocardiography was present in 63% (31 of 49) with 24-hour hypertension compared with only 42% (13 of 31) with normal 24-hour BP (p = 0.06)., Conclusions: There is a high rate of hypertension late after coarctation repair, even in patients with unobstructed arches. The presence of retinal imaging abnormalities and left ventricular hypertrophy signals the presence of end-organ damage in this young adult population. Regular follow-up with 24-hour BP monitoring is warranted., (Copyright © 2015 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Objectives: The receiver operating characteristic curves (ROC curves) are often used to compare continuous diagnostic tests or determine the optimal threshold of a test; however, they do not consider the costs of misclassifications or the disease prevalence. The ROC graph was extended to allow for these aspects., Study Design and Setting: Two new lines are added to the ROC graph: a sensitivity line and a specificity line. Their slopes depend on the disease prevalence and on the ratio of the net benefit of treating a diseased subject to the net cost of treating a nondiseased one. First, these lines help researchers determine the range of specificities within which test comparisons of partial areas under the curves is clinically relevant. Second, the ROC curve point the farthest from the specificity line is shown to be the optimal threshold in terms of expected utility., Results: This method was applied: (1) to determine the optimal threshold of ratio specific immunoglobulin G (IgG)/total IgG for the diagnosis of congenital toxoplasmosis and (2) to select, among two markers, the most accurate for the diagnosis of left ventricular hypertrophy in hypertensive subjects., Conclusion: The two additional lines transform the statistically valid ROC graph into a clinically relevant tool for test selection and threshold determination., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background and Purpose: Approximately 20-25% of the patients with hypertrophic cardiomyopathy (HCM) develop atrial fibrillation (AF) during the clinical course of the disease, a percentage significantly larger than that of the general population. The purpose of the present study was to report on the procedural results of patients with AF and either primary or secondary left ventricular hypertrophy (LVH)., Methods and Subjects: Twenty-two consecutive HCM patients (55% male, mean age 57±8 years) with symptomatic AF, having undergone AF ablation procedures between September 2009 and July 2012 were compared with respect to procedural outcome and follow-up characteristics with 22 matched controls with secondary cardiac hypertrophy (64% male, 63±10 years) from our prospective AF catheter ablation registry., Results and Conclusion: Radiofrequency catheter ablation (RFCA) was successful in restoring long-term sinus rhythm in patients with LVH due to HCM and due to secondary etiology. However, patients with HCM needed more RFCA procedures and frequently additional antiarrhythmic drug therapy in order to maintain sinus rhythm., (Copyright © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Objectives: This study hypothesized that biomarkers of subclinical myocardial injury (high-sensitivity cardiac troponin T [hs-cTnT]) and hemodynamic stress (N-terminal pro-B-type natriuretic peptide [NT-proBNP]) would differentiate heart failure (HF) risk among older adults with left ventricular hypertrophy (LVH)., Background: The natural history of LVH, an important risk factor for HF, is heterogeneous., Methods: NT-proBNP and hs-cTnT were measured at baseline and after 2 to 3 years in older adults without prior HF or myocardial infarction in the CHS (Cardiovascular Health Study). LVH and left ventricular ejection fraction were determined by echocardiography. HF events were adjudicated over a median of 13.1 years and classified as preserved or reduced left ventricular ejection fraction (heart failure with preserved ejection fraction or heart failure with reduced ejection fraction [HFrEF]). Adjusted risk of HF by LVH and biomarker tertiles, and by LVH and longitudinal increase in each biomarker was estimated using Cox regression., Results: Prevalence of LVH was 12.5% among 2,347 participants with complete measures. Adjusted risk of HF (N = 643 events) was approximately 3.8-fold higher among participants with LVH and in the highest biomarker tertile, compared with those with low biomarker levels without LVH (NT-proBNP, hazard ratio [HR]: 3.78; 95% confidence interval [CI]: 2.78 to 5.15 and hs-cTnT, HR: 3.86; 95% CI: 2.84 to 5.26). The adjusted risk of HFrEF was 7.8 times higher among those with the highest tertile of hs-cTnT and LVH (HR: 7.83; 95% CI: 4.43 to 13.83). Those with LVH and longitudinal increases in hs-cTnT or NT-proBNP were approximately 3-fold more likely to develop HF, primarily HFrEF, compared with those without LVH and with stable biomarkers., Conclusions: The combination of LVH with greater hs-cTnT or NT-proBNP levels, and their longitudinal increase, identifies older adults at highest risk for symptomatic HF, especially HFrEF. These biomarkers may characterize sub-phenotypes in the transition from LVH to HF and suggest modifiable targets for prevention., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Resistant hypertension (RH) is defined as uncontrolled blood pressure (BP) despite the use of ≥3 anti-hypertensive drugs, or controlled requiring use of ≥4 drugs. Recently, a new definition for an extreme phenotype of RH (uncontrolled BP using at least five drugs) has emerged-the refractory hypertension (RfH). Although characteristics of RH are well established, little is known about this newly described subgroup. For this work, 116 subjects with RH were enrolled from a specialized clinic and divided into RH (n = 80) and RfH (n = 36). Subjects were submitted to echocardiography, 24-hour ambulatory BP measurement and biochemical analyses. Logistic regression analysis demonstrated that: (1) white-coat effect (odds ratio [OR], 3.23; 95% confidence interval [CI], 1.12-9.27; P = .03), (2) black race (OR, 6.67; 95% CI, 1.99-16.16; P < .001), and (3) left ventricular mass index (OR, 1.02; 95% CI, 1.01-1.03; P = .04) were independent predictors of refractoriness. In conclusion, RfH and RH present different patient characteristics, and these phenotypic aspects can be useful for better understanding this harder-to-treat subgroup., (Copyright © 2015 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Background: Fibroblast growth factor 23 (FGF-23) is a phosphorus-regulating hormone. In chronic kidney disease (CKD), circulating FGF-23 levels are markedly elevated and independently associated with mortality. Left ventricular hypertrophy (LVH) is a potent risk factor for mortality in CKD, and FGFs have been implicated in the pathogenesis of myocardial hypertrophy. In addition, the effect of anemia on CV disease and LVH is well known in CKD. A relation between iron and FGF-23 metabolism is mentioned in a few studies. The aim of this study was to test the association of FGF-23 levels with echocardiographic (ECHO) and iron parameters in peritoneal dialysis patients (PD)., Methods: In this cross-sectional study, 61 subjects with PD (29 women and 32 men, mean age: 46.9±13.3 years, mean PD vintage: 69.5±39 months) underwent echocardiograms to assess left ventricular mass index (LVMI). Medical treatments and average values of the basic laboratory results of the last 6 months for all patients were recorded. Serum FGF-23 concentrations were measured using intact FGF-23 (iFGF-23) human enzyme-linked immunosorbent assay (ELİSA) kit. According to the median levels of serum FGF-23 the patients were grouped into two (FGF-23 high and low groups)., Results: Significant positive correlation was recorded between serum FGF-23 levels and LVMI (P=0.023). There was also significant difference in terms of hemoglobin (12.1±2 versus 11.0±2, P=0.017), transferrin saturation (TSAT) (24.9±16.8 versus 19.5±10.8, P=0.042) between low and high FGF-23 group. Also in linear regression analysis the negative relation between FGF-23 and hemoglobin is persisted (r=0.199, P=0.045)., Conclusions: FGF-23 is associated with LVMI, anemia and low TSAT in patients with PD. Whether increased FGF-23 is a marker or a potential mechanism of myocardial hypertrophy and anemia in patients with end-stage renal disease (ESRD) requires further study., (Copyright © 2015 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Background: Atrial fibrillation (AF) patients with left ventricular hypertrophy (LVH) and diastolic dysfunction may derive benefit from being in sinus rhythm but no data are available to support this strategy in them. We sought to investigate effect of left ventricular remodeling on cardiovascular outcomes in AF patients undergoing rhythm control strategy., Methods: We identified 1088 patients with echocardiographic data on left ventricular mass (LVM) enrolled in the AFFIRM trial. Using the American Society of Echocardiography (ASE) criteria, patients were divided into 4 categories: 1) normal geometry, 2) concentric remodeling, 3) eccentric hypertrophy, and 4) concentric hypertrophy. The primary endpoint was AF recurrence and the secondary endpoint was cardiovascular hospitalization (CVH)., Results: In rhythm control arm, median time to recurrence in patients with concentric LVH was 13.3 months (95% CI 8.2-24.5) vs. 28.3 months (95% CI 20.2-48.6) in patients without LVH. Concentric left ventricular hypertrophy (LVH) was independently predictive of AF recurrence (HR 1.49, 95% CI 1.10-2.01, p=0.01) in rhythm control arm, but not in overall population or rate control arm. Both concentric and eccentric LVH were independently predictive of cardiovascular hospitalization (CVH) in the overall population, with respective HRs of 1.36 (1.04-1.78, p=0.03) and 1.38 (1.02-1.85, p=0.04)., Conclusion: Concentric LVH is predictive of AF recurrences when a predominantly pharmacologic rhythm-control strategy is employed. Different patterns of LVH seem to be important determinants of outcomes (AF recurrence and CVH). These findings may have important clinical implications for the management of patients with AF and LVH. Further studies are warranted to confirm our findings., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Background: Framingham risk score (FRS) underestimates risk in young adults. Left ventricular mass (LVM) relates to cardiovascular disease (CVD), with unclear value in youth. In a young biracial cohort, we investigate how FRS predicts CVD over 20 years and the incremental value of LVM. We also explore the predictive ability of different cut-points for hypertrophy., Methods: We assessed FRS and echocardiography-derived LVM (indexed by body surface area or height2.7) from 3980 African-American and white Coronary Artery Risk Development in Young Adults (CARDIA) participants (1990-1991); and followed over 20 years for a combined endpoint: cardiovascular death; nonfatal myocardial infarction, heart failure, cerebrovascular disease, and peripheral artery disease. We assessed the predictive ability of FRS for CVD and also calibration, discrimination, and net reclassification improvement for adding LVM to FRS., Results: Mean age was 30±4 years, 46% males, and 52% white. Event incidence (n=118) across FRS groups was, respectively, 1.3%, 5.4%, and 23.1% (p<0.001); and was 1.4%, 1.3%, 3.7%, and 5.4% (p<0.001) across quartiles of LVM (cut-points 117 g, 144 g, and 176 g). LVM predicted CVD independently of FRS, with the best performance in normal weight participants. Adding LVM to FRS modestly increased discrimination and had a statistically significant reclassification. The 85th percentile (≥116 g/m2 for men; ≥96 g/m2 for women) showed event prediction more robust than currently recommended cut-points for hypertrophy., Conclusion: In a biracial cohort of young adults, FRS and LVM are helpful independent predictors of CVD. LVM can modestly improve discrimination and reclassify participants beyond FRS. Currently recommended cut-points for hypertrophy may be too high for young adults., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Objectives: The aim of this study was to evaluate the effects of losartan on left ventricular (LV) hypertrophy and fibrosis in patients with nonobstructive hypertrophic cardiomyopathy (HCM)., Background: Despite evidence that myocardial hypertrophy and fibrosis are mediated by angiotensin II and are important determinants of morbidity and mortality in patients with HCM, no prior studies have evaluated the effects of angiotensin receptor blockers on LV hypertrophy and fibrosis with cardiac magnetic resonance imaging., Methods: In double-blind fashion, 20 patients (3 women, 17 men; age: 51 ± 13 years) with HCM were randomly assigned to receive placebo (n = 9) or losartan 50 mg twice a day (n = 11) for 1 year. Cardiac magnetic resonance imaging was performed at baseline and 1 year to measure LV mass and extent of fibrosis as assessed by late gadolinium enhancement., Results: There was a trend toward a significant difference in the percent change in LV mass (median [interquartile range]: +5% [-4% to +21%] with placebo vs. -5% [-11% to -0.9%] with losartan; p = 0.06). There was a significant difference in the percent change in extent of late gadolinium enhancement, with the placebo group experiencing a larger increase (+31% ± 26% with placebo vs. -23% ± 45% with losartan; p = 0.03)., Conclusions: This pilot study suggests attenuation of progression of myocardial hypertrophy and fibrosis with losartan in patients with nonobstructive HCM. Confirmation of these results in a larger trial is required to confirm a place for angiotensin receptor blockers in the management of patients with HCM. (Effect of Losartan in Patients With Nonobstructive Hypertrophic Cardiomyopathy; NCT01150461)., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Diastolic dysfunction often precedes the onset of diastolic heart failure. We previously demonstrated that diastolic dysfunction and left ventricular hypertrophy (LVH) in Dahl salt-sensitive rats can be ameliorated by quantitative trait loci (QTLs)., Methods: We analyzed cardiac phenotypes of 2 "single" congenic strains, C10S.L33 and C10S.L28, by echocardiography, in which a specific Dahl salt-sensitive rat chromosome segment was replaced by its Lewis homologue. C10S.L33 improves diastolic function (DF) and LVH only in rats aged 10 weeks, not aged 15 weeks. C10S.L28 alleviated LVH, but not diastolic dysfunction. Thus, the QTLs captured by C10S.L33 and C10S.L28 are designated as DF/LVH C10QTL7 and LVH C10QTL4, respectively. We then combined multiple single strains to form 2 congenic combinations. One of the 2 congenic combinations included the chromosome segments covered by C10S.L33 and C10S.L28., Results: Diastolic dysfunction was either completely or partially reversed by 15 weeks in the 2 congenic combinations. LVH was permanently improved from 10 to 15 weeks., Conclusions: Distinct QTLs exist that regulate diastolic function and/or LVH in the short term when acting alone, but durably when combined. The Ccl2 chemokine (C-C motif) ligand 1 (Ccl2) gene is the prime candidate for DF/LVH C10QTL7, owing to a nonconserved coding mutation. Schlafen genes are candidates for LVH C10QTL4. Since CCL2 and Schlafens are not known for influencing diastolic function and left ventricular mass, novel long-term strategies of prognosis, diagnosis, and therapy for diastolic heart failure and LVH appear from this work., (Copyright © 2013 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Aims: The aim of this study is to investigate the protective effects of cystamine on lupus-associated cardiac hypertrophy., Main Methods: Balb/c and lupus-prone NZB/W-F1 mice were individually randomized into sham group (saline, n=16) and cystamine group (n=16). Mice received saline or cystamine (100 mmol in 100 μL saline) by daily intraperitoneal injection for 2 consecutive weeks. Morphological, histological, and biochemical alterations were investigated., Key Findings: Cystamine decreased both left ventricular (LV) mass and LV mass/tissue-to-blood ratio (TBR) in NZB/W-F1 mice (p<0.05), whereas slight effects were observed in Balb/c mice. Moreover, cystamine reduced levels of atrial natriuretic peptide (ANP), C-reactive protein (CRP), heart type-fatty acid binding protein (h-FABP), creatine kinase-MB (CK-MB) and IL-6 in LV tissues of NZB/W-F1 mice (p<0.05). Additionally, in LV tissues of NZB/W-F1 mice, suppression of hypertrophic signaling mediated by IL-6 in response to administration of cystamine was revealed, including phosphorylation of MEK5, ERK5, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38) (p<0.05)., Significance: Cystamine alleviated LV hypertrophy in NZB/W-F1 mice as a result of decrease in hypertrophic mediators and suppression of IL-6 mediated hypertrophic signaling., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background and Aims: Increased body mass index (BMI) has been associated with increased cardiovascular morbidity and mortality in hypertension. Less is known about the impact of BMI on improvement in left ventricular (LV) structure and function during antihypertensive treatment., Methods and Results: Annual BMI, echocardiograms and cardiovascular events were recorded in 875 hypertensive patients with LV hypertrophy during 4.8 years randomized treatment in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy. Patients were grouped by baseline BMI into normal (n = 282), overweight (n = 405), obese (n = 150) and severely obese groups (n = 38) (BMI ≤24.9, 25.0-29.9, 30.0-34.9, and ≥35.0 kg/m(2), respectively). At study end, residual LV hypertrophy was present in 54% of obese and 79% of severely obese patients compared to 31% of normal weight patients (both p < 0.01). In regression analyses, adjusting for initial LV mass/height(2.7), higher BMI predicted less LV hypertrophy reduction and more reduction in LV ejection fraction (both p < 0.05), independent of blood pressure reduction, diabetes and in-study weight change. During follow-up, 91 patients suffered cardiovascular death, myocardial infarction or stroke. In Cox regression analysis 1 kg/m(2) higher baseline BMI predicted a 5% higher rate of cardiovascular events and 10% higher cardiovascular mortality over 4.8 years (both p < 0.05)., Conclusions: In hypertensive patients in the LIFE study, increased BMI was associated with less reduction of LV hypertrophy and less improvement in LV systolic function which may contribute to the observed higher cardiovascular event rate of treated hypertensive patients., (Copyright © 2011 Elsevier B.V. All rights reserved.)

The beneficial effects of N-(2-mercaptopropionyl)-glycine (MPG) against ischemia-reperfusion injury in normotensive animals have been previously studied. Our objective was to test the action of MPG during ischemia and reperfusion in hearts from spontaneously hypertensive rats (SHR). Isolated hearts from SHR and age-matched normotensive rats Wistar Kyoto (WKY) were subjected to 50-min global ischemia (GI) and 2-hour reperfusion (R). In other hearts MPG 2mM was administered during 10 min before GI and the first 10 min of R. Infarct size (IS) was assessed by TTC staining technique and expressed as percentage of risk area. Postischemic recovery of myocardial function was assessed. Reduced glutathione (GSH), thiobarbituric acid reactive substances (TBARS) and SOD cytosolic activity - as estimators of oxidative stress and MnSOD cytosolic activity - as an index of (mPTP) opening were determined. In isolated mitochondria H(2)O(2)-induced mPTP opening was also measured. The treatment with MPG decreased infarct size, preserved GSH levels and decreased SOD and MnSOD cytosolic activities, TBARS concentration, and H(2)O(2) induced-mPTP opening in both rat strains. Our results show that in both hypertrophied and normal hearts an attenuation of mPTP opening via reduction of oxidative stress appears to be the predominant mechanism involved in the cardioprotection against reperfusion injury MPG-mediated., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Introduction: Left ventricular hypertrophy (LVH) is a major cardiovascular complication and an important predictor of mortality in patients with end-stage renal disease. Angiotensin II blockades have been widely used in the treatment of hypertension; however, the influence of angiotensin receptor blockers (ARBs) on LVH in dialysis patients has not been thoroughly studied. In this meta-analysis, the authors analyzed the effect of ARBs on LVH and left ventricular function in patients on maintenance dialysis., Methods: The authors did systematic search of PubMed, Embase and Cochrane Central Register of Controlled Trials, until November 2010. Data extracted from the literature were analyzed with the Review Manager., Results: The results of 6 randomized controlled trials (207 participants) reveal that ARB group had a greater regression of left ventricular mass index (LVMi) when compared with non-ARB group (P = 0.002) in dialysis patients while no significant difference for left ventricular ejection fraction (LVEF; P = 0.30). The ARB group had a nonsignificantly greater therapeutic value of LVMi or LVEF when compared with angiotensin-converting enzyme inhibitor (ACEI; P = 0.74 and 0.49, respectively). No significant alterations were observed in LVMi and LVEF between the combination of ARBs and ACEIs and ARBs group (P = 0.43 and 0.24, respectively)., Conclusions: ARBs are associated with a greater reduction in LVH in patients on dialysis. The ARB therapy tends to have a similar favorable effectiveness as ACEI; however, the combination of ARBs with ACEIs did not show additional benefit to LVH in patients on hemodialysis.

Background: COPD is associated with significant cardiovascular mortality. Left ventricular hypertrophy (LVH) is a pivotal cardiovascular risk factor. The prevalence of LVH in COPD is currently unknown., Methods: We performed a pilot study of 93 normoxemic patients with COPD and 34 control subjects. Patients underwent echocardiography to measure left ventricular (LV) dimensions, ECG, measurement of serum B-type natriuretic peptide (BNP) levels, and 24-h BP recording. Spirometry and oxygen saturations were also recorded., Results: The oxygen saturations of patients with COPD were normal, at 96.5% (95% CI, 96.1%-97.0%), with a mean FEV(1) of 70.0% predicted (95% CI, 65.2%-74.8%). A total of 30.1% of patients with COPD met the echocardiographic criteria for LVH based on LV mass index, with more LVH in female patients than in male patients (43.2% vs 21.4%, P = .02). The LV mass index in patients with COPD was 96.2 g/m(2) (95% CI, 90.1-102.7 g/m(2)) vs 82.9 g/m(2) (95% CI, 75.8-90.6 g/m(2)) in control subjects ( P = .017). The LV mass index remained high in patients with COPD in the absence of a hypertension history (94.5 g/m(2) vs 79.9 g/m(2), P = .015) and with 24-h systolic BP <135 mm Hg (96.7 g/m(2) vs 82.5 g/m(2), P = .024). The LV ejection fraction (mean = 63.4%) and BNP (mean = 28.7 pg/mL) were normal in patients with COPD. The mean 24-h BP was normal in patients with COPD, at 125/72 mm Hg. ECG was less sensitive for detecting LVH than was echocardiography., Conclusion: LVH with normal LV ejection fraction and BNP levels was present in a significant proportion of normotensive, normoxemic patients with COPD, especially female patients. Clinical trials are, therefore, indicated to evaluate treatments to regress LVH in patients with COPD.

Background and Aim: Low serum 25-hydroxyvitamin D [25(OH)D] levels may have an important role in predisposing to hypertension and myocardial disease. We investigated the relationship between 25(OH)D and left ventricular (LV) structure and function, assessed by echocardiography, in a series of patients with essential hypertension (EH)., Methods and Results: Sixty-two newly diagnosed never-treated patients (32 male/30 female), aged 18-65 years, with grade 1-2 hypertension, no diabetes, no obesity, no hyperlipidemia, and no cardiopulmonary, renal, or hepatic disease, were studied. Twenty-four healthy normotensive sex-, age-, BMI-matched subjects served as controls. Hypertensive patients with 25(OH)D deficiency, defined as serum 25(OH)D levels <50 nmol/L, had higher prevalence of LV hypertrophy (LVH) than their 25(OH)D-sufficient counterparts (57.1 vs 17.6%, P = 0.02); no differences between the two groups were found in blood pressure levels as well as in other biochemical and hormone parameters. There was an inverse correlation between LV mass index and 25(OH)D levels (r = -0.366, P < 0.003) and a direct correlation between LV mass index and BMI (r = 0.333, P < 0.006) in the entire hypertensive population. The two variables remained independently associated with LVH at multivariable logistic regression analysis (OR 1.05, P < 0.005 and OR 1.25, P = 0.03, respectively). Prevalence of 25(OH)D deficiency was similar in EH patients and controls (45.1 vs 41.6%, P = 0.89), whereas no correlation between echocardiographic parameters and hormone levels was found., Conclusions: In the absence of major cardiovascular risk factors, 25(OH)D deficiency is a frequent finding in EH patients and is independently associated with LVH., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Background: Fabry cardiomyopathy is characterized by left ventricular (LV) hypertrophy and regional fibrosis. Recent high-end echocardiography studies of selected LV sections suggest an interrelation between regional fibrosis, impaired function, and hypertrophy possibly changing under specific enzyme replacement therapy (ERT)., Methods: Magnetic resonance imaging (MRI) was used for a region dependent study of cardiac function, morphology and late enhancement (LE) in 25 Fabry patients before and after 12 months of ERT in comparison to 43 healthy volunteers., Results: Fabry patients presented with LV increased wall thickness (EDWT) and reduced wall thickening (WT) with a focus on basal and midventricular regions corresponding to areas of LE. The degree of hypertrophy and hypokinesia were the highest if LE was detectable. A significant decrease of the EDWT under ERT was observed in LE negative patients accompanied by a decline of hypokinesia with regional differences., Conclusions: Regional differences of LV hypertrophy and wall motion were detected corresponding to the distribution of myocardial fibrosis (LE). Functional impairment was closely restricted to fibrotic regions while morphologic changes slightly exceeded the areas of fibrosis. ERT resulted in regional improvements whereby absence of fibrosis was connected to a better outcome., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Background and Aim: A decoy receptor for advanced glycation end product (soluble RAGE or sRAGE) is involved in left ventricular hypertrophy (LVH), and cardiomyopathy myocardial damage in experimental models and observational studies in patients with heart failure support the hypothesis that sRAGE attenuates the progression of heart disease and prevents death. Since sRAGE accumulates in patients with chronic kidney disease (CKD) we studied the relationship between plasma sRAGE with LVH in CKD patients., Methods and Results: We enrolled 142 patients with an average estimated glomerular filtration rate (eGFR) of 32 ml/min/1.73 m(2) and 49 healthy control individuals matched for age and gender. Plasma sRAGE was significantly higher in CKD patients than in healthy controls. Significant inverse relationships were found between sRAGE with left ventricular mass index (LVMI) and mean wall thickness (MWT) but no such associations were found in controls. A bootstrap re-sampling validation study confirmed the estimates of the link between sRAGE and these variables. On covariance analysis, the slopes of LVMI and MWT to sRAGE were significantly steeper in CKD patients than in the controls. On logistic regression analysis 1 log unit increase in sRAGE was associated with a 82% decrease in the odds for LVH in CKD patients., Conclusions: sRAGE is an inverse marker of LVH in CKD patients. This association generates the hypothesis that the RAGE pathway could be a causal risk factor for LVH in this population and that blockade of this pathway by the endogenous decoy receptor sRAGE could attenuate LVH in the same population., (Copyright © 2010 Elsevier B.V. All rights reserved.)

'Cardiomyopathy' (CM) is defined by the World Health Organization as 'a disease of the myocardium associated with cardiac dysfunction'. In a child, it is associated with a significant risk for anaesthesia. In addition, cardiac arrest under anaesthesia has been attributed to an undiagnosed CM. Care of these patients is complicated by the fact that there are several different forms of CM that have differing anaesthesia management goals, aimed at maintaining the patient's baseline haemodynamic variables of preload, heart rate, contractility, and afterload. With the emergence of new diagnostic tools, together with advances in cardiac imaging and improved treatment modalities (such as ventricular assist devices), the anaesthetic management of a child with a CM is evolving. This review describes the different forms of the disease in terms of pathology, aetiology, and clinical presentation. Dilated, hypertrophic, and restrictive CM are the most common forms. We examine recent advances in therapy, including the management of severe end-stage disease, while highlighting the specific anaesthetic considerations for children with each type of CM.