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hypertrophy, left ventricular - Top 30 Publications

Ideal cardiovascular health and the subclinical impairments of cardiovascular diseases: a cross-sectional study in central south China.

Ideal cardiovascular health (CVH) is related to a low cardiovascular disease risk profile. This study aimed to investigate CVH metrics with both the biomarkers and markers of subclinical impairments of cardiovascular diseases (CVDs) in subjects from central south China.

Ventricular arrhythmia and sudden cardiac death in Fabry disease: a systematic review of risk factors in clinical practice.

Fabry disease (FD) is an X-linked lysosomal storage disorder caused by deficiency of α-galactosidase A enzyme. Cardiovascular (CV) disease is a common cause of mortality in FD, in particular as a result of heart failure and arrhythmia, with a significant proportion of events categorized as sudden. There are no clear models for risk prediction in FD. This systematic review aims to identify the risk factors for ventricular arrhythmia (VA) and sudden cardiac deaths (SCD) in FD. A systematic search was performed following PRISMA guidelines of EMBASE, Medline, PubMed, Web of Science, and Cochrane from inception to August 2016, focusing on identification of risk factors for the development of VA or SCD. Thirteen studies were included in the review (n = 4185 patients) from 1189 articles, with follow-up of 1.2-10 years. Weighted average age was 37.6 years, and 50% were male. Death from any cause was reported in 8.3%. Of these, 75% was due to CV problems, with the majority being SCD events (62% of reported deaths). Ventricular tachycardia was reported in 7 studies, with an average prevalence of 15.3%. Risk factors associated with SCD events were age, male gender, left ventricular hypertrophy, late gadolinium enhancement on CV magnetic resonance imaging, and non-sustained ventricular tachycardia. Although a multi-system disease, FD is a predominantly cardiac disease from a mortality perspective, with death mainly from SCD events. Limited evidence highlights the importance of clinical and imaging risk factors that could contribute to improved decision-making in the management of FD.

The Prognostic Implications of Two-Dimensional Speckle Tracking Echocardiography in Hypertrophic Cardiomyopathy: Current and Future Perspectives.

Two-dimensional (2D) speckle tracking echocardiography represents a novel, simple and reproducible technique for the estimation of left ventricular myocardial deformation (strain) and the evaluation of left ventricular twist mechanics. During the last few years, its clinical and prognostic implications in cardiomyopathies and hypertrophic cardiomyopathy (HCM) in particular have been rapidly increasing. Reduced global longitudinal strain is associated with more severe disease and confers an increased risk for major cardiac events, independently of other clinical and echocardiographic risk factors. Left ventricular dyssynchrony also seems promising as a risk factor for sudden cardiac events. With respect to left atrial mechanics, left atrial reservoir, conduit and contractile strain may also confer an increased prognostic value for atrial fibrillation, major cardiac events and even sudden death. Although right ventricular global longitudinal strain is impaired in HCM compared with healthy controls and individuals with physiological hypertrophy, its prognostic significance is currently unknown. Conclusively, two-dimensional speckle tracking imaging seems promising for HCM. However, future studies are needed in order to incorporate this new imaging technique in the standard evaluation of an HCM individual.

APOL1 nephropathy risk variants do not associate with subclinical atherosclerosis or left ventricular mass in middle-aged black adults.

Prior studies reported associations of APOL1 nephropathy risk variants with subclinical atherosclerosis. However, these findings were limited to older individuals with high comorbidities. To evaluate this in younger individuals, we calculated associations of APOL1 risk variants (high risk [2 risk variants] vs. low risk [0-1 risk variant]) with prevalent, incident, or progressive coronary artery calcification, a carotid intima media thickness over the 90th percentile, and left ventricular hypertrophy in 1315 black participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study. The mean age of this cohort was 44.6 years and their mean estimated glomerular filtration rate was 102.5 ml/min/1.73m(2). High-risk participants were found to be younger and have a higher prevalence of albuminuria than low-risk participants. In Poisson regression models adjusted for comorbidities and kidney function, the risk of prevalent coronary artery calcification (relative risk [95% confidence interval] 1.12 [0.72,1.71]), the incident coronary artery calcification (1.50 [0.87,2.59]), and the progression of coronary artery calcification (1.40 [0.88,2.23]) did not significantly differ in high vs. low-risk participants. Furthermore, the risk of carotid intima media thickness over the 90th percentile (1.28 [0.78,2.10]) and left ventricular hypertrophy (1.02[0.73,1.43]) did not significantly differ in high vs. low-risk participants in fully-adjusted models. Thus, APOL1 risk variants did not associate with subclinical markers of atherosclerosis or left ventricular hypertrophy in middle-aged black adults with preserved kidney function.

Geometric predictors of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy: a 3D computed tomography analysis.

To establish geometric predictors of left ventricular outflow tract obstruction (LVOTO) in hypertrophic cardiomyopathy (HCM) patients by use of cardiac computed tomography (CT).

Isolated heart model demonstrates evidence of contractile and diastolic dysfunction in right ventricles from rats with sugen/hypoxia-induced pulmonary hypertension.

Although extensively used for the study of left ventricular function, limited experience exists with the isolated heart model in the evaluation of right ventricular (RV) function. In particular, no published experience exists with this tool in sugen/hypoxia-induced pulmonary hypertension (SuHx-PH), a frequently used model of severe and progressive PH We sought to characterize markers of RV contractile and diastolic function in SuHx-PH and to establish their relationship with markers of maladaptive RV remodeling. Hearts were excised from anesthetized Sprague Dawley rats with or without SuHx-PH and perfused via the aorta using a Langendorff preparation. We explored the Frank-Starling relationship of RV function (RV developed pressure, dP/dtmax, and dP/dtmin; all normalized to RV mass) by increasing RV end-diastolic pressure (RVEDP) from 0 to 40 mmHg. Functional studies were complemented by quantification of RV pro-apoptotic signaling (bcl2/bax), procontractile signaling (apelin), and stress response signaling (p38MAPK activation). Pearson's correlation analysis was performed for functional and biochemical parameters. SuHx-RVs exhibited severe RV dysfunction with marked hypertrophy and decreased echocardiographic cardiac output. For any given RVEDP, SuHx-RVs demonstrated less developed pressure and lower dP/dtmax, as well as less pronounced dP/dtmin, suggestive of decreased contractile and diastolic function. SuHx-RVs exhibited decreased bcl2/bax ratios, apelin expression, and p38MAPK activation. Bcl2/bax and apelin RNA abundance correlated positively with RV developed pressure and dP/dtmax and negatively with dP/dtmin p38MAPK activation correlated positively with RV developed pressure. We conclude that SuHx-RVs exhibit severe contractile and diastolic dysfunction. Increased pro-apoptotic signaling and attenuated procontractile and stress response signaling may contribute to these functional alterations.

Left ventricular hypertrophy predicts cardiovascular events in hypertensive patients with coronary artery calcifications.

Coronary artery calcification (CAC) is associated with increased cardiovascular (CV) risk. Left ventricular hypertrophy (LVH) is an independent risk factor for CV events. Our aim was to estimate the relative CV risk of LVH in the presence of CAC.

Association between common carotid artery diameter and target organ damage in essential hypertension.

To investigate the relationship between common carotid artery diameter (CCA-D) and target organ damage (TOD) in essential hypertension.

Effects of gallic acid on hemodynamic parameters and infarct size after ischemia-reperfusion in isolated rat hearts with alloxan-induced diabetes.

Diabetic rats are more susceptible to myocardial ischemia-reperfusion injury than control rats. The aim of the present study was to evaluate the cardioprotective effect of gallic acid (GA) on isolated rat hearts with alloxan-induced diabetes mellitus. Adult male Sprague-Dawley rats were divided randomly into three groups: control, untreated diabetic and diabetic animals treated with (GA, 25mg/kg). Diabetes was induced by 120mg/kg alloxan injection. Eight weeks after GA administration, the hearts were isolated and exposed to myocardial ischemia-reperfusion. The body weight, blood glucose, hypertrophy index, left ventricular function, infarct size, cardiac markers and oxidative stress were measured. In the diabetic group, body weight, cardiac contractility (±dp/dt), glutathione peroxidase (GPx) level (p<0.001), left ventricular developed pressure (LVDP), rate pressure product (RPP), superoxide dismutase (SOD) and catalase (CAT) levels (p<0.01) as well as the heart weight (p<0.05) significantly reduced. However, blood glucose, infarct size, hypertrophy index, lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB, p<0.001) and troponin-I (cTnI) levels (p<0.05) significantly increased in the diabetic rats compared with the control group. Nevertheless, administration of GA improved significantly LVDP, ±dp/dt, infarct size, LDH, CK-MB (p<0.001), blood glucose, the heart weight (p<0.01), body weight, RPP, hypertrophy index, antioxidant enzyme and cTnI levels (p<0.05) in the diabetic rats. The results of this study indicated that in the diabetic rats, left ventricular dysfunction and hypertrophy significantly induced possibly by oxidative stress. Moreover, GA as a potent antioxidant improved both left ventricular dysfunction and hypertrophy.

Prognostic Application of Thoracic Aortic Calcium Scoring for Adverse Clinical Outcome Risk in Elderly Patients with Left Ventricular Hypertrophy.

Left ventricular hypertrophy (LVH) is associated with poor cardiovascular outcomes. Heavy aortic calcification exacerbates arterial stiffness, which consequently heightens left ventricular (LV) afterload. We assessed the usefulness of aortic calcification for predicting adverse cardiovascular outcomes and to determine whether the relationship, if any, differed as a function of LVH.

Association between growth differentiation factor 15 and left ventricular hypertrophy in hypertensive patients and healthy adults.

Growth differentiation factor 15 (GDF-15) as an independent biomarker of cardiovascular diseases merits further evaluation. We studied the association between plasma GDF-15 levels and left ventricular hypertrophy (LVH) in hypertensive patients and healthy adults. Hypertensive LVH measurements were performed via echocardiography and analyzed using the cube formula, and human GDF-15 together with interleukin-6 (IL-6) and matrix metalloproteinase-9 (MMP-9) concentrations were determined via enzyme-linked immunosorbent assay (ELISA). All data were analyzed using SPSS 13.0 software. A total of 302 participants were recruited for this clinical study. Circulating GDF-15, IL-6 and MMP-9 levels were significantly higher in LVH patients (n = 67) than in non-LVH patients (n = 172) and healthy controls (n = 63) (p < 0.001). After adjustment for confounders via multivariate logistic regression, elevated plasma GDF-15 concentrations remained independently associated with LVH in hypertensive patients. In addition, GDF-15 was positively correlated with IL-6 and MMP-9 levels in human plasma, respectively, suggesting that a link exists between GDF-15 expression and inflammation. We also calculated an optimal GDF-15 cut-off point with which LVH severity can be predicted in the current study. In conclusion, GDF-15 is associated with hypertensive LVH and may be a powerful biomarker with which LVH risk can be predicted in patients with hypertension.

A Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial of the Efficacy and Safety of the Oral Soluble Guanylate Cyclase Stimulator: The VICTORIA Trial.

This trial sought to evaluate whether vericiguat, a novel oral soluble guanylate cyclase (sGC) stimulator, was superior to placebo, on a background of standard of care, in increasing the time to the first occurrence of the composite endpoints of cardiovascular (CV) death and heart failure (HF) hospitalization in patients with HF with reduced ejection fraction (HFrEF). Deficiency in sGC-derived cyclic guanosine monophosphate (cGMP) causes both myocardial dysfunction and impaired endothelium-dependent vasomotor regulation that includes the myocardial microcirculation. Experimental studies have suggested multiple potential benefits of sGC stimulators including prevention, or even reversal, of left ventricular hypertrophy and fibrosis, as well as reduction of ventricular afterload through both systemic and pulmonary vasodilation. Hence, restoration of sufficient nitric oxide (NO)-sGC-cGMP signaling has been proposed as an important treatment target in HF. Vericiguat has been shown to directly stimulate sGC and enhance sGC sensitivity to endogenous NO. Available phase IIb data in HFrEF patients indicate vericiguat is safe and well-tolerated, and exploratory analyses indicate that it results in a dose-dependent, clinically significant reduction in N-terminal pro-B-type natriuretic peptide (NT-proBNP) at the highest tested dose. VICTORIA (Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction) is a randomized, placebo-controlled, parallel group, multicenter, double-blind, event-driven phase 3 trial of vericiguat in subjects with HFrEF. Approximately 4,872 subjects will be randomized to evaluate the efficacy and safety of vericiguat compared with placebo on a background of standard of care. After a screening phase of up to 30 days, eligible subjects will be treated until the required number of cardiovascular deaths is observed. The estimated median follow-up duration is approximately 18 months. All subjects will be followed until study completion to assess for the occurrence of endpoint events. VICTORIA will establish the efficacy and safety of vericiguat on cardiovascular death and HF hospitalization in patients with HFrEF. (A Randomized Parallel-Group, Placebo-Controlled, Double-Blind, Event-Driven, Multi-Center Pivotal Phase III Clinical Outcome Trial of Efficacy and Safety of the Oral sGC Stimulator Vericiguat in Subjects With Heart Failure With Reduced Ejection Fraction [HFrEF]-VerICiguaT Global Study in Subjects With Heart Failure With Reduced Ejection Fraction [VICTORIA]; NCT02861534).

Detection of concentric left ventricular wall hypertrophy by contrast-enhanced non-electrocardiogram-gated chest computed tomography.

No established measure of concentric left ventricular wall hypertrophy (cLVH) on routine computed tomography (CT) of the adult chest currently exists. The objective of this study was to identify and test linear measures for the detection of cLVH using transthoracic echocardiography (TTE) as the reference standard.

Rho-kinase inhibition reverses impaired Ca(2+) handling and associated left ventricular dysfunction in pressure overload-induced cardiac hypertrophy.

Recent studies have implicated a relationship between RhoA/ROCK activity and defective Ca(2+) homeostasis in hypertrophic hearts. This study investigated molecular mechanism underlying ROCK inhibition-mediated cardioprotection against pressure overload-induced cardiac hypertrophy, with a focus on Ca(2+) homeostasis. Cardiac hypertrophy model was established by performing transverse aortic constriction (TAC) in 8-week-old male rats. Groups were assigned as SHAM, TAC and TAC+Fas (rats undergoing TAC and treated with fasudil). Rats in the TAC+Fas group were administered fasudil (5mg/kg/day), and rats in the SHAM and TAC groups were treated with vehicle for 10 weeks. Electrophysiological recordings were obtained from isolated left ventricular myocytes and expression levels of proteins were determined using western blotting. Rats in the TAC group showed remarkable cardiac hypertrophy, and fasudil treatment significantly reversed this alteration. TAC+Fas myocytes showed significant improvement in reduced contractility and Ca(2+) transients. Moreover, these myocytes showed restoration of slow relaxation rate and Ca(2+) reuptake. Although L-type Ca(2+) currents did not change in TAC group, there was a significant reduction in the triggered Ca(2+) transients which was reversed either by long-term fasudil treatment or incubation of TAC myocytes with fasudil. The hearts of rats in the TAC group showed a significant decrease in ROCK1, ROCK2, RyR2 protein levels and p-PLB(S16/T17)/SERCA2 ratio and increase in RhoA expression and MLC phosphorylation. However, fasudil treatment largely reversed TAC-induced alterations in protein expression. Thus, our findings indicate that upregulation of the RhoA/ROCK pathway is significantly associated with cardiac hypertrophy-related Ca(2+) dysregulation and suggest that ROCK inhibition prevents hypertrophic heart failure.

The effect of sacubitril/valsartan compared to olmesartan on cardiovascular remodelling in subjects with essential hypertension: the results of a randomized, double-blind, active-controlled study.

Progressive aortic stiffening eventually leads to left ventricular (LV) hypertrophy and heart failure if left untreated. Anti-hypertensive agents have been shown to reverse this to some extent. The effects of sacubitril/valsartan (LCZ696), a dual-action angiotensin receptor blocker (ARB), and neprilysin inhibitor, on arterial stiffness and LV remodelling have not been investigated.

Epigenome alterations in aortic valve stenosis and its related left ventricular hypertrophy.

Aortic valve stenosis is the most common cardiac valve disease, and with current trends in the population demographics, its prevalence is likely to rise, thus posing a major health and economic burden facing the worldwide societies. Over the past decade, it has become more than clear that our traditional genetic views do not sufficiently explain the well-known link between AS, proatherogenic risk factors, flow-induced mechanical forces, and disease-prone environmental influences. Recent breakthroughs in the field of epigenetics offer us a new perspective on gene regulation, which has broadened our perspective on etiology of aortic stenosis and other aortic valve diseases. Since all known epigenetic marks are potentially reversible this perspective is especially exciting given the potential for development of successful and non-invasive therapeutic intervention and reprogramming of cells at the epigenetic level even in the early stages of disease progression. This review will examine the known relationships between four major epigenetic mechanisms: DNA methylation, posttranslational histone modification, ATP-dependent chromatin remodeling, and non-coding regulatory RNAs, and initiation and progression of AS. Numerous profiling and functional studies indicate that they could contribute to endothelial dysfunctions, disease-prone activation of monocyte-macrophage and circulatory osteoprogenitor cells and activation and osteogenic transdifferentiation of aortic valve interstitial cells, thus leading to valvular inflammation, fibrosis, and calcification, and to pressure overload-induced maladaptive myocardial remodeling and left ventricular hypertrophy. This is especcialy the case for small non-coding microRNAs but was also, although in a smaller scale, convincingly demonstrated for other members of cellular epigenome landscape. Equally important, and clinically most relevant, the reported data indicate that epigenetic marks, particularly certain microRNA signatures, could represent useful non-invasive biomarkers that reflect the disease progression and patients prognosis for recovery after the valve replacement surgery.

FGF23 and Left Ventricular Hypertrophy in Children with CKD.

High plasma concentration of fibroblast growth factor 23 (FGF23) is a risk factor for left ventricular hypertrophy (LVH) in adults with CKD, and induces myocardial hypertrophy in experimental CKD. We hypothesized that high FGF23 levels associate with a higher prevalence of LVH in children with CKD.

Acute and Chronic Response to Exercise in Athletes: The "Supernormal Heart".

During last decades, most studies have examined the exercise-induced remodeling defined as "athlete's heart". During exercise, there is an increased cardiac output that causes morphological, functional, and electrical modification of the cardiac chambers. The cardiac remodeling depends also on the type of training, age, sex, ethnicity, genetic factors, and body size. The two main categories of exercise, endurance and strength, determine different effects on the cardiac remodeling. Even if most sport comprise both strength and endurance exercise, determining different scenarios of cardiac adaptation to the exercise. The aim of this paper is to assemble the current knowledge about physiologic and pathophysiologic response of both the left and the right heart in highly trained athletes.

Prevalence and predictive value of electrocardiographic abnormalities in pulmonary hypertension: evidence from the Pan-African Pulmonary Hypertension Cohort (PAPUCO) study.

Pulmonary hypertension (PH) is prevalent in Africa and is still often diagnosed only at an advanced stage, therefore it is associated with poor quality of life and survival rates. In resource-limited settings, we assessed the diagnostic utility of standard 12-lead electrocardiograms (ECG) to detect abnormalities indicating PH.

α-Galactosidase A Genotype N215S Induces a Specific Cardiac Variant of Fabry Disease.

Hypertrophic cardiomyopathy is the most common type of cardiomyopathy, but many patients lack sarcomeric/myofilament mutations. We studied whether cardio-specific α-galactosidase A gene variants are misinterpreted as hypertrophic cardiomyopathy because of the lack of extracardiac organ involvement.

KCNJ5 mutation as a predictor for resolution of hypertension after surgical treatment of aldosterone-producing adenoma.

To investigate the effect of KCNJ5 mutations on the cure of hypertension in patients with aldosterone-producing adenoma (APA) after unilateral adrenalectomy.

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy.

Transverse aortic constriction (TAC) in mice is one of the most commonly used surgical techniques for experimental investigation of pressure overload-induced left ventricular hypertrophy (LVH) and its progression to heart failure. In the majority of the reported investigations, this procedure is performed with intubation and ventilation of the animal which renders it demanding and time-consuming and adds to the surgical burden to the animal. The aim of this protocol is to describe a simplified technique of minimally invasive TAC without intubation and ventilation of mice. Critical steps of the technique are emphasized in order to achieve low mortality and high efficiency in inducing LVH. Male C57BL/6 mice (10-week-old, 25-30 g, n=60) were anesthetized with a single intraperitoneal injection of a mixture of ketamine and xylazine. In a spontaneously breathing animal following a 3-4 mm upper partial sternotomy, a segment of 6/0 silk suture threaded through the eye of a ligation aid was passed under the aortic arch and tied over a blunted 27-gauge needle. Sham-operated animals underwent the same surgical preparation but without aortic constriction. The efficacy of the procedure in inducing LVH is attested by a significant increase in the heart/body weight ratio. This ratio is obtained at days 3, 7, 14 and 28 after surgery (n = 6 - 10 in each group and each time point). Using our technique, LVH is observed in TAC compared to sham animals from day 7 through day 28. Operative and late (over 28 days) mortalities are both very low at 1.7%. In conclusion, our cost-effective technique of minimally invasive TAC in mice carries very low operative and post-operative mortalities and is highly efficient in inducing LVH. It simplifies the operative procedure and reduces the strain put on the animal. It can be easily performed by following the critical steps described in this protocol.

Cardiovascular Effects of Renal Distal Tubule Deletion of the FGF Receptor 1 Gene.

The bone-derived hormone fibroblast growth factor-23 (FGF-23) activates complexes composed of FGF receptors (FGFRs), including FGFR1, and α-Klotho in the kidney distal tubule (DT), leading to increased sodium retention and hypertension. However, the role of FGFR1 in regulating renal processes linked to hypertension is unclear. Here, we investigated the effects of selective FGFR1 loss in the DT. Conditional knockout (cKO) of FGFR1 in the DT (FGFR1(DT-cKO) mice) resulted in left ventricular hypertrophy (LVH) and decreased kidney expression of α-Klotho in association with enhanced BP, decreased expression of angiotensin converting enzyme 2, and increased expression of the Na(+)-K(+)-2Cl(-) cotransporter. Notably, recombinant FGF-23 administration similarly decreased the kidney expression of α-Klotho and induced LVH in mice. Pharmacologic activation of FGFR1 with a monoclonal anti-FGFR1 antibody (R1MAb1) normalized BP and significantly attenuated LVH in the Hyp mouse model of excess FGF-23, but did not induce a response in FGFR1(DT-cKO) mice. The hearts of FGFR1(DT-cKO) mice showed increased expression of the transient receptor potential cation channel, subfamily C, member 6 (TRPC6), consistent with cardiac effects of soluble Klotho deficiency. Moreover, administration of recombinant soluble Klotho lowered BP in the Hyp mice. Thus, FGFR1 in the DT regulates systemic hemodynamic responses opposite to those predicted by the actions of FGF-23. These cardiovascular effects appear to be mediated by paracrine FGF control of kidney FGFR1 and subsequent regulation of soluble Klotho and TRPC6. FGFR1 in the kidney may provide a new molecular target for treating hypertension.

Antimalarial-induced cardiomyopathy: a systematic review of the literature.

Background Antimalarials (AMs) are widely used in the treatment of connective tissue diseases. Their main side effect is retinal damage, while heart disease has been described in isolated cases. The aim of this study is to systematically review the existing literature on AM-induced cardiomyopathy (AMIC). Methods The PubMed database was searched for heart biopsy-confirmed AMIC cases. Information on demographics, clinical presentation, concomitant AM-related toxicity, cardiological investigations, treatment and outcome were collected. Descriptive statistics were used. Results Forty-seven cases (42 females) were identified with a mean age at diagnosis 56.4 ± 12.6 and mean AM treatment duration 12.7 ± 8.2 years. Systemic lupus erythematosus ( n = 19) and rheumatoid arthritis ( n = 18) were the most common primary diseases. Clinical presentation was that of congestive heart failure in 77%, while eight patients presented with syncope (17%). Complete atrioventricular block was reported in 17 patients; 24 received a permanent pacemaker (51%). Impaired systolic function was detected in 52.8%, bi-ventricular hypertrophy in 51.4% and restrictive filling pattern of the left ventricle in 18 patients. Cardiac magnetic resonance showed late gadolinium enhancement in seven cases, with a non-vascular pattern in the interventricular septum. Cardiomyocyte vacuolation was reported in all cases; intravacuolar lamellar and curvilinear bodies were observed in 46 (98%) and 42 (89.4%) respectively. Mortality rate was 45% (18/40). Conclusion AMIC is a rare, probably under-recognized, complication of prolonged AM treatment. It presents as a hypertrophic, restrictive cardiomyopathy with or without conduction abnormalities. Early recognition and drug withdrawal are critical with a survival rate of almost 55%.

Biomarkers of atrial fibrillation in hypertension.

It is well known that atrial fibrillation (AF) is the most frequent cardiac arrhythmia worldwide and substantially increases the risk for thromboembolic disease. One of the main problems is that it remains undiagnosed (about 20% of all cases of AF). On the other hand, hypertension amplifies the risk for both AF occurrences through hemodynamic and non-hemodynamic mechanisms and cerebrovascular ischemia. Under this prism, prompt diagnosis of undetected AF in hypertensive patients is of pivotal importance. Biomarkers could be used in AF diagnosis as well as in predicting the transition of paroxysmal AF to sustained AF. Last year's many biomarkers has been developed and they can categorized into electrophysiological, morphological, and molecular markers that reflect the underlying mechanisms of adverse atrial remodeling that constitutes the hallmark of this arrhythmia. In this review study, we focused on P-wave duration and dispersion as electrophysiological markers of AF and left atrial (LA) and LA appendage size, atrial fibrosis, left ventricular hypertrophy, aortic stiffness and connexins as structural biomarkers, respectively. The heterogeneous group of molecular biomarkers of AF encompasses products of the neurohormonal cascade, including. NT-pro BNP, BNP, MR-pro ANP, polymorphisms of the ACE and convertases such as corin and furin that are implemented in BNP modulation. In addition, soluble biomarkers of inflammation (i.e. CRP, IL-6) and fibrosis (i.e. TGF-1 and matrix metalloproteinases) were assessed for predicting AF. The reviewed individual biomarkers should add to current diagnostic tools but the ideal candidate is expected to combine multiple indices of atrial remodeling in order to effectively detect both AF and adverse characteristics of high risk hypertensive patients.

Correlations of FGF23 and Klotho with cardiovascular injury in chronic kidney disease patients.

To analyze the levels of serum calcium, phosphate, fibroblast growth factor 23 (FGF23), and Klotho proteins in patients with chronic kidney disease (CKD), and to investigate the correlations of FGF23 and Klotho proteins with cardiac complicates in patients with chronic kidney disease-mineral and bone disorder (CKD-MBD).
 Methods: A total of 180 CKD-MBD patients were enrolled for this study. Among them, 60 patients underwent regular hemodialysis, 60 patients did not undergo renal replacement therapy and 60 patients were diagnosed as second hyperparathyroidism (SHPT). Thirty age and gender-matched health volunteers served as controls. Serum samples were collected and tested, and the demographical, clinical and biochemical data were all recorded. FGF23 and Klotho levels in serum samples were analyzed by enzyme-linked immunosorbent assay. Data of echocardiography and plain abdominal X rays were collected as well. The influential factors for cardiovascular injury, the relationship between biochemical indexes and ectopic calcification, and the correlations of FGF23 and Klotho with cardiac complicates were analyzed
 Results: Patients, who kept hemodialysis, especially those with SHPT, exhibited an increase in serum FGF23 level while a decrease in serum Klotho protein levels (P<0.01). Patients with higher levels of serum FGF23 were more likely to have ectopic calcification (OR=4.667), while patients with lower levels of serum Klotho had high risks to get myocardial hypertrophy (OR=3.496). Receiver operator characteristic (ROC) curve analysis showed that the area under the curve (AUC) for FGF23 was 0.778 (P<0.01) while for Klotho was 0.715 (P<0.01).
 Conclusion: Patients, who kept hemodialysis, especially those with SHPT, have a significant increase in serum FGF23 protein levels and a significant decrease in serum Klotho protein levels. Serum FGF23 and Klotho protein levels are closely correlated with left ventricular enlargement and hypertrophy. Serum FGF23 and Klotho protein are risk factors for heart.

Acute Myocarditis with Infarct-like Presentation in a Pediatric Population: Role of Cardiovascular Magnetic Resonance.

Chest pain is a typical symptom of acute myocarditis in adolescents. It may be indistinguishable from myocardial ischemia so it is called "infarct-like pattern." Cardiovascular magnetic resonance has an important role as a non-invasive diagnostic tool. The aim of our study is to provide a description of an acute myocarditis series with infarct-like pattern and to evaluate the cardiovascular magnetic resonance role in a pediatric population. We included all pediatric patients (0-16 years) admitted to our hospital (May 2007-May 2016) with clinical diagnosis of acute myocarditis and infarct-like presentation (chest pain, EKG alterations, and released cardiac biomarkers). Diagnosis was confirmed with cardiovascular magnetic resonance using Lake Louise criteria. Seven patients (five males, two females) with a median age of 14 years (12.5-15.2) were included. All patients showed ST-segment changes and released cardiac biomarkers. Three patients had left ventricular hypertrophy and two presented mild systolic left ventricular dysfunction. All patients had at least two positive Lake Louise criteria. Late gadolinium enhancement was positive in all of them. With a median follow-up of 23 months (8-47), all of them are alive, with no cardiac symptoms and normal ventricular function. Infarct-like pattern is a typical presentation of acute myocarditis in adolescents. CMR should be performed in this population and may be considered as a first-line diagnostic tool. Its high sensitivity in infarct-like acute myocarditis may allow us to avoid endomyocardial biopsy. Unlike what was described in adults, late gadolinium enhancement does not imply worse outcome in our series.

Renin-angiotensin system blockade therapy after transcatheter aortic valve implantation.

The persistence of left ventricular (LV) hypertrophy is associated with poor clinical outcomes after transcatheter aortic valve implantation (TAVI) for aortic stenosis. However, the optimal medical therapy after TAVI remains unknown. We investigated the effect of renin-angiotensin system (RAS) blockade therapy on LV hypertrophy and mortality in patients undergoing TAVI.

The Subclinical Cardiomyopathy of Friedreich's Ataxia in a Pediatric Population.

Identification of a subclinical cardiomyopathy in a pediatric patients with Friedreich's ataxia (FA) has not been well-described.

Hypertension and Cardiovascular Risk Profile in a Middle-Income Setting: The HELISUR Study.

Hypertension is the leading risk factor responsible for premature death worldwide, but its burden has shifted to low- and middle-income countries. Therefore, we studied hypertension and cardiovascular risk in the population of Suriname, a middle-income country with a predominantly urban population of African and Asian ancestry.