Forms Of Left Ventricular Hypertrophy Research Articles

Influence of Antihypertensive Drugs on Left Ventricular Hypertrophy Regression in Hypertensive Patients

Background: Hypertension and its effect on heart in the form of left ventricular hypertrophy are the important predictors of heart failure. Hypertension treatment and left ventricular hypertrophy regression is crucial in the prevention of cardiovascular disease. However, the impact of antihypertensive treatment on left ventricular hypertrophy is less studied and which particular class of antihypertensive medicine is more effective is largely unexplored in our population. We designed this study to explore this issue in subjects taking treatment by evaluation initial and after six months echocardiography findings. Methods: One hundred fifty subjects aged 25-75 years, taking antihypertensive medicine were enrolled in the study. Along with basic demographic and epidemiological data, initial and after 6 months echocardiographic findings were analyzed for the presence of LV hypertrophy regression. Choice of medicine and necessary changes for the achievement of blood pressure targets were done on treating physician’s discretion.Results: Out of 150 subjects, data for 130 subjects were available for final analysis. Mean age was 54.4 years with standard deviation of 12.3 years. Apart from age, smoking, overweight and obesity, dyslipidemia, and diabetes were the important risk factors with a prevalence of 28%, 26%, 22% and 20% respectively. Although the decrease in rates of LV hypertrophy over the duration of 6 months were not significant in overall and in subjects treated with various antihypertensive medicines, the reductions in LV mass index (108.76+/-11.3 to 98.46+/-11.23) in overall and in different antihypertensives were significant (p<0.001). The decrease in LV mass index was statistically significant in subjects taking angiotensin converting enzyme inhibitors or angiotensin receptor blockers when compared to subjects taking calcium channel blockers (p<0.05). This decrease in LV mass index was not significant when compared between CCBs and mixed drugs.Conclusion: There was regression in LV hypertrophy among subjects taking antihypertensive treatment. It was more obvious in subjects taking angiotensin converting enzyme inhibitors/angiotensin receptor blockers when compared with subjects taking calcium channel blockers or both.

C-natriuretic peptide – as an indicator of persistent increase in blood pressure in men with hypertension

Annotation. According to multiple studies hypertension (AH) is a multifactorial disease. It is recognized that one of the key mechanisms of persistent increase in blood pressure (BP) is the imbalance between vasoconstriction and vasodilation and endothelial dysfunction (ED) is one of the leading links in the pathogenesis of AH. The consequence of ED is a persistent vasoconstrictor reaction which results in myocardial remodeling in the form of left ventricular hypertrophy (LVH) and the subsequent development of congestive heart failure (CHF). One of the most important representatives of the group of vasoconstrictor peptides is endothelin-1 (ET-1). It has been previously shown that the polymorphism of the gene encoding it (Lys198Asn) is associated with fluctuations in ET-1 plasma concentration. In this regard, the corresponding changes in plasma levels of one of the most powerful vasodilators – C-natriuretic peptide (CNP) – remain poorly understood. CNP is a direct antagonist of ET-1 which increases in the blood in AH and can be used as a screening method to identify patients with high BP. The aim of the study – improving the detection of men with AH who has persistent long-term elevations in BP by using the plasma level of CNP and taking into account the carrier of polymorphic variants of the ET-1 gene. The study involved 191 men aged 40-60 years: 79 men were from control group, 62 patients with AH and LVH and 50 patients with AH complicated by CHF II-III classes for NYHA. Enzyme-linked immunosorbent assay was used to determine the plasma concentration of CNP. Genotyping of the ET-1 gene was performed using the polymerase chain reaction. Mathematical processing was performed on a personal computer using the standard statistical package STATISTICA 6.0. It is established that plasma CNP levels in men with AH and LVH (5.21±0.11) pmol/ml and in patients with AH and CHF (5.22±0.13) pmol/ml are significantly higher than in control patients (2.35±0.06) pmol/ml (p<0.0001) however did not differ in patients with AH from different groups. The obtained results allowed to calculate the limit level of CNP which is ≥3.37 pmol/ml and can be used for screening detection of males with persistently elevated BP in the survey of large populations. It was found that in patients with AH as in the control group the Lys/Lys genotype and the Lys allele of the ET-1 gene predominate. There was no significant difference in the frequency of ET-1 gene between groups (p>0.05). It should be noted that in patients with AH carrying all polymorphic variants of the ET-1 gene the level of CNP in blood was also significantly higher than in the control group, however in carriers of the Asn allele plasma level of CNP is higher than in individuals with the Lys/Lys genotype in all study groups. So it was investigated that the average plasma concentration of CNP in patients with AH is higher than in the control group which made it possible to establish a limit level of peptide for screening of individuals with persistent long-term elevation of BP. In men of the control group and in patients with AH the carrier of the Asn allele of the ET-1 gene is associated with a higher level of CNP but in all study groups the Lys/Lys genotype and the Lys allele of the ET-1 gene were dominant.

Cardiac Magnetic Resonance Features of Fabry Disease: From Early Diagnosis to Prognostic Stratification

In the past few years, the wide application of cardiac magnetic resonance (CMR) significantly changed the approach to the study of cardiac involvement in Fabry Disease (FD). The possibility to perform non-invasive tissue characterization, including new sequences such as T1/T2 mapping, offered a powerful tool for differential diagnosis with other forms of left ventricular hypertrophy. In patients with confirmed diagnosis of FD, CMR is the most sensitive non-invasive technique for early detection of cardiac involvement and it provides new insight into the evolution of cardiac damage, including gender-specific features. Finally, CMR multiparametric detection of subtle changes in cardiac morphology, function and tissue composition is potentially useful for monitoring the efficacy of specific treatment over time. This paper aims to provide a comprehensive review of current knowledge regarding the application of CMR in FD cardiac involvement and its clinical implication.

Role of global longitudinal strain in discriminating variant forms of left ventricular hypertrophy and predicting mortality.

In this study, we aimed to compare the functional adaptations of the left ventricle in variant forms of left ventricular hypertrophy (LVH) and to evaluate the use of two-dimensional speckle tracking echocardiography (2D-STE) in differential diagnosis and prognosis. This was a prospective cohort study of 68 patients with LVH, including 20 patients with non-obstructive hypertrophic cardiomyopathy (HCM), 23 competitive top-level athletes free of cardiovascular disease, and 25 patients with hypertensive heart disease (HHD). All the subjects underwent 2D transthoracic echocardiography (TTE) and 2D-STE. The primary endpoint was all-cause mortality. Global longitudinal strain (GLS) below -12.5% was defined as severely reduced strain, -12.5% to -17.9% as mildly reduced strain, and above -18% as normal strain. The mean LV-GLS value was higher in athletes than in patients with HCM and HHD with the lowest value being in the HCM group (HCM: -11.4±2.2%; HHD: -13.6±2.6%; and athletes: -15.5±2.1%; p<0.001 among groups). LV-GLS below -12.5% distinguished HCM from others with 65% sensitivity and 77% specificity [area under curve (AUC)=0.808, 95% confidence interval (CI): 0.699-0.917, p<0.001]. The median follow-up duration was 6.4±1.1 years. Overall, 11 patients (16%) died. Seven of these were in the HHD group, and four were in the HCM group. The mean GLS value in patients who died was -11.8±1.5%. LV-GLS was significantly associated with mortality after adjusting age and sex via multiple analysis (RR=0.723, 95% CI: 0.537-0.974, p=0.033). Patients with GLS below -12.5% had a higher risk of all-cause mortality compared with that of patients with GLS above -12.5% according to Kaplan-Meier survival analysis for 7 years (29% vs. 9%; p=0.032). The LV-GLS value predicts mortality with 64% sensitivity and 70% specificity with a cut-off value of -12.5 (AUC=0.740, 95% CI: 0.617-0.863, p=0.012). The 2D-STE provides important information about the longitudinal systolic function of the myocardium. It may enable differentiation variable forms of LVH and predict prognosis.

Comparative analysis of phasic left atrial strain and left ventricular posterolateral strain pattern to discriminate Fabry cardiomyopathy from other forms of left ventricular hypertrophy.

"Classical" echocardiographic signs of Fabry cardiomyopathy (FC), such as left ventricular hypertrophy (LVH), posterolateral strain impairment (PLSI), and papillary muscle hypertrophy may be of limited diagnostic accuracy in clinical practice. Our aim was to evaluate the diagnostic value of left atrial (LA) strain impairment compared to "classical" echocardiographic findings to discriminate FC. In standard echocardiographic assessments, we retrospectively analyzed the diagnostic value of the "classical" red flags of FC as well as LA strain in 20 FC patients and in 20 subjects with other causes of LVH. Receiver operating characteristic (ROC) curve analysis was performed to assess the respective diagnostic accuracy. FC was confirmed in 20 patients by genetic testing. In the LVH group, 12 patients were classified by biopsy to have hypertrophic cardiomyopathy, two had hypertensive heart disease, and six LVH combined with borderline myocarditis. Global and regional left ventricular (LV) strain was not significantly different between groups while LA strain was significantly impaired in FC (Left atrial reservoir strain (LASr) 19.1%±8.4 in FC and 25.6%±8.9 in LVH, p=0.009; left atrial conduction strain (LAScd) -8.4%±4.9 in FC and -15.9%±8.4 in LVH, p<0.01). LAScd, with an area under the curve (AUC) of .81 (95% confidence interval [CI] .66-.96) showed the highest diagnostic accuracy to discriminate FC. The PLSI pattern showed an AUC of .49, quantification of papillary muscle hypertrophy an AUC of .47. Adding LA strain analysis to a comprehensive echocardiographic work-up of unclear LVH may be helpful to identify FC as a possible cause.

Myocardial performance is impaired in cardiac amyloidosis: role of myocardial work-derived parameter in differential diagnosis with phenocopies and prognostic implications

Abstract Background Cardiac amyloidosis (CA) is an infiltrative disorder characterized by left ventricular (LV) thickening and dysfunction. Due to it poor prognosis its early detection and differential diagnosis among other forms of cardiomyopathies is fundamental. Purpose This study aimed to compare the diagnostic accuracy of LV classical and and novel echocardiographic parameters in differentiating CA from other forms of genetic and non-genetic cardiomyopathies with hypertrophic phenotype. Methods We included 50 patients with CA (26 pts with AL and 24 pts with wild type ATTR form) and 75 patients with LV hypertrophy (LVH) [25 patients with hypertrophic cardiomyopathy (HCM), 25 with hypertensive cardiomyopathy (HypCM), and 25 with aortic stenosis (AS)]. Besides routine echocardiographic measurements, we analysed standard and novel echo parameters implied in LV assessment [LV ejection fraction (LVEF), myocardial contraction fraction (MCF), global longitudinal strain (GLS), relative regional strain ratio (RRSR), ejection fraction on strain ratio (EFSR)], included novel Myocardial Work (MW) parameters [Global Work Index (GWI), Global Constructive Work (GCW), Global Wasted Work (GWW), Global Work Efficiency (GWE)]. Results Patients in CA group showed a smallest LV cavity size, higher LV mass and, consequently, a more pronounced concentric hypertrophy compared to LVH group. All LV systolic parameters where more impaired in CA than in LVH group. At ROC curve analysis, among all others, GCW showed the best performance in discriminating CA from LVH (AUC 0.886; 95% CI: 0.819–0.954; P&amp;lt;0,0001), with a cut-off value &amp;lt;1473 mmHg% showing good sensitivity and specificity (90% and 82%, respectively). At linear regression analysis GCW correlated with IVSD (P&amp;lt;0,0001), PWD (p&amp;lt;0,0001), RWT ratio (p&amp;lt;0,0001), LVMi (p&amp;lt;0,0001), MCF (P&amp;lt;0,0001), LVESV (p&amp;lt;0,002), LVEF (P&amp;lt;0,0001), EFSR (p&amp;lt;0,0001) and RRSR (p&amp;lt;0,0001). At multivariate analysis, PWD (P&amp;lt;0,029) and RWT ratio (p&amp;lt;0,014) were the only parameters associated. At 24 months follow-up there were 15 deaths in the CA group and 4 in LVH group. At Kaplan-Meier analysis the overall survival free of cardiovascular death was reduced in the lowest GCW interquartile ranges (log-rank χ2 21,5; p&amp;lt;0,0001). At Cox hazard ratio analysis GCW (β 1,233; 95% CI: 1,201–1,246; P&amp;lt;0,0001) was the only prognostic parameter associated with cardiovascular mortality. Discussion Although CA and and LVH have with similar phenotype, they differ greatly in terms of systolic function. The MW, estimated by non-invasive pressure-strain loops, is a novel method for a load-independent LV systolic function assessment. In the present study the GCW showed the best ability in detecting CA in comparison to other parameters usually implied in clinical practice. Conclusion Myocardial performance is significantly reduced in CA compared to other forms of LVH. GCW showed to be a promising novel diagnostic and prognostic factor in this setting. Funding Acknowledgement Type of funding sources: None. Table 1Figure 1

Comparative analysis of phasic left atrial strain and left ventricular posterolateral strain to discriminate Fabry cardiomyopathy from other forms of left ventricular hypertrophy

Abstract Background “Classic” echocardiographic signs of Fabry cardiomyopathy (FC), such as left ventricular hypertrophy (LVH) and posterolateral strain deficiency (PLSD) have a low diagnostic accuracy in clinical practice. Purpose Our aim was to evaluate the diagnostic accuracy of phasic left atrial strain impairment compared to PLSD to discriminate FC from other forms of LVH. Methods 40 patients with LVH due to bioptically and genetically confirmed FC or with LVH due to other causes, defined by exclusion of storage diseases, such as Amyloidosis or FC, by myocardial biopsy, were retrospectively analysed. Standard echocardiographic views (Vivid E9, GE, Vingmed, Horton) were used to analyse left atrial (LA) reservoir, conduit, and contraction strain using 2D speckle tracking echocardiography (2DSTE; EchoPAC software, GE) as well as the PLSD, obtained by the mean of deformation values in basal posterior and lateral segments in a 17-segment model. Receiver operating characteristic (ROC) curve analysis and a logistic regression model were performed to assess the diagnostic accuracy of LA and LV strain impairment. Results FC was confirmed in 20 patients by genetic testing and myocardial biopsy. In the LVH group, 12 patients were classified to have hypertrophic cardiomyopathy, two had hypertensive heart disease, and six expressed the pattern of LV hypertrophy combined with borderline myocarditis. LV septum thickness (15.8mm±3.4 in FC; 17.9mm±4.3 in LVH) and left atrial volume index (LAVI) (36.7ml/m2±11.3 in FC; 45.7ml/m2±16.3 in LVH) as well as LVEF (54.2%± 9.8 in FC; 52.5%±7.7 in LVH,) were not statistically different between groups. LV filling parameters such as E/A (1.2±0.5 in FC; 1.2±0.7 in LVH) and E/e' (11.0±4.9 in FC; 13.2±5.3 in LVH) showed a slightly more advanced impairment in the LVH group. Global and regional LV function was not different between groups (LVGLS −13.8±3.7% in FC and −12.8±3.7% in LVH; PLSD −10.7±5.2% in FC and −8.85±3.9% in LVH; p-value?). LA reservoir strain (LASr) and LA conduit strain (LAScd) were significantly impaired in FC compared to the LVH group (LASr 14,6±2.5% in FC and 26.3±8.5% in LVH, p&amp;lt;0.01; LAScd −5.9±2.6% in FC and −15.8±4.7% in LVH, p&amp;lt;0.01). In ROC analysis, LASr, with an area under the curve (AUC) of 0.81 (95% CI 0.64–0.97) and LAScd with an AUC of 0.85 (95% CI 0.71–0.99), respectively, showed the highest diagnostic accuracy to discriminate FC. PLSD, in contrast, held a low diagnostic accuracy with an AUC of only 0.47 (95% CI 0.27–0.68). Conclusion A substantially higher diagnostic accuracy could be shown for LASr and LAScd impairment in discriminating FD and other forms of LVH compared to PLSD. The echocardiographic assessment of phasic LA strain may help to identify FC in patients with unclear LVH. Funding Acknowledgement Type of funding sources: None. ROC analysisRepresentative examples

Study on microalbuminuria as predictor factor for target organ damage in essential hypertension in a teaching hospital, Telangana

Background: Microalbuminuria in hypertensives is related to future development of cardiovascular morbidity. It is a simple test which is easily available. In the present study we attempted to look at the prevalence of microalbuminuria in cases of essential hypertension and also to determine its association with left ventricular hypertrophy and carotid intima-media thickness and retinopathy. Aim of the study: To study microalbuminuria as a predictor factor for target organ damage in essential hypertension. Materials and Methods: Hospital based prospective observational study done on 45 cases for duration of one year. Cases of essential hypertension were studied for microalbuminuria, for changes of left ventricular hypertrophy, left ventricular mass index distribution and for retinopathy. Results: There was a slight male predominance and the M:F ratio was 2.7:1. Majority of cases were among 40-50 years age group ie, 62.2% cases. Microalbuminuria was present in 77.7% cases. ECG changes of left ventricular hypertrophy were present in 77.7% cases. Obesity and over weight were present in 15 (33.3%) subjects. Among 35 cases with microalbuminuria, 19 patients had hypertensive retinopathy changes. Among these 19 patients, Grade II retinopathy was most common and was diagnosed in 68.4% cases. Conclusion: Microalbuminuria is common in patients with essential hypertension. Microalbuminuria can predict cardiovascular and ocular morbidity in the form of left ventricular hypertrophy, increased carotid intima-media thickness; and ocular morbidity respectively. Screening of all patients with essential hypertension will help to predict the future risk for target organ damage. Keywords: Microalbuminuria, Essential Hypertension, Left ventricular hypertrophy.

Myocardial constructive work is impaired in cardiac amyloidosis, eases the differential diagnosis and predicts the prognosis among patients with left ventricular hypertrophy

Abstract Background Myocardial Work (MW) is a novel non-invasive echocardiographic method for myocardial performance assessment. MW is abnormal in patients with many forms of left ventricular hypertrophy [hypertrophic cardiomyopathy (HCM), hypertensive cardiomyopathy (HypCM), aortic stenosis (AS)] while little is known about cardiac amyloidosis (CA). Purpose We aimed to evaluate the role of MW in myocardial performance assessment, diagnostic significance and prognostic relevance in CA patients. Methods 25 patients with CA (10 AL pts and 15 ATTRwt pts) and 75 patients with LVH (25 HCM pts, 25 HypCMP pts, 25 pts mild AS pts) were enrolled. Beside routine measurements, deformation parameters [GLS (Global Longitudinal Strain), EFSR (Ejection Fraction on Strain Ratio), RRSR (Relative Regional Strain Ratio)], and MW parameters [MWI (Myocardial Work Index), GCW (Global Constructive Work), GWW (Global Wasted Work), GWE (Global Work Efficiency)] for LV function evaluation were analysed. Results LV and RV function evaluated with classical and novel parameters were significantly impaired in CA group (see table). Among all these parameters, GCW showed the best performance to discriminate CA from other forms of LVH (AUC 0.90; 95% CI: 0.80–0.99; P&amp;lt;0,0001), with a cut-off value &amp;lt;1141 mmHg% showing good sensitivity and specificity (90% and 82%, respectively). At Kaplan-Meier estimation of cardiovascular mortality there were 9 deaths in the CA group and none in LVH group, showed significantly higher mortality at follow-up (p=0,0001). At multivariate analysis GCW (β=1,006; 95% CI: 1,003–1,009; P&amp;lt;0,0001) was the only prognostic parameter associated with cardiovascular mortality. Discussion Myocardial performance was reduced in CA group. GCW was able to discriminate CA from other forms of LVH and showed to be an independent prognostic factor. In our pilot study GCW seems a promising novel diagnostic and prognostic factor in CA. Kaplan-Meier curve Funding Acknowledgement Type of funding source: None

Left ventricular longitudinal strain in professional athletes, a useful tool to detect an athletes hearts?

Abstract Background Professional cyclists frequently present with physiological adaptations to endurance exercise with an increase in left ventricular wall thickness and mass. Global longitudinal strain (GLS) is an early and sensitive echocardiographic method to detect left ventricular dysfunction. However, it is unclear whether GLS is able to differentiate between athlete's hearts or different pathological conditions of left ventricular hypertrophy. Methods A total of 87 professional athletes (37 professional cyclists, 29 professional soccer players, and 21 professional handball players) were compared to 125 patients with different forms of left ventricular hypertrophy (17 hypertrophic obstructive cardiomyopathy (HOCM), 36 hypertensive heart disease (HHD), 35 severe aortic valve stenosis (AVS); 37 untrained individuals served as controls. Examinations were performed between October 2018 to October 2019. All subjects underwent echocardiographic examination, including GLS. Results In all 212 participants/patients included a preserved ejection fraction &amp;gt;50% (mean 61±7%) was detected. Left ventricular mass index (LVMI) in professional cyclists (165.5±37.1 g/m2) was increased when compared to professional soccer players (97.3±12.4 g/m2, p&amp;lt;0.001), professional handball players (92.2±15.8 g/m2, p&amp;lt;0.001) and healthy controls (94.3±20.7 g/m2, p&amp;lt;0.001), as well as to patients with HHD (129.2±30.0 g/m2, p&amp;lt;0.001), or AVS (140.1±35.4 g/m2, p=0.064), but not to patients with HOCM (159.7±39.4 g/m2, p=0.64). Professional cyclists (−21.0±3.5%) achieved higher average GLS values than professional soccer (−18.4 ± %, p=0.004) or handball players (−18.4 ± %, p=0.021), healthy controls (−19.0±3.0%, p=0.008), HOCM (−15.0±6.5%, p&amp;lt;0.001), HHD (−13.8±5.9%, p&amp;lt;0.001), and AVS (−16.0±7.0%, p&amp;lt;0.001) (Figure 1). Conclusion In professional cyclists, higher LVMI and average GLS values were detected compared to professional soccer and handball players with lower excessive endurance exercise, as well as untrained healthy controls. Average GLS can help to differentiate between athletes' hearts in professional cyclists compared to pathologic patterns in different diseases characterized by left ventricular hypertrophy with elevated LVMI. Figure 1 Funding Acknowledgement Type of funding source: None

The Possibilities of Single-Pill Combinations of Antihypertensive Drugs in Cerebroprotection: Focus on the Combination of Amlodipine with Ramipril

Stroke remains one of the leading causes of death and disability both worldwide and in Russia. Acute cerebrovascular events have many risk factors, among them the most important is arterial hypertension (AH), which predisposes to the stroke development through the direct effect of increased hydrostatic blood pressure on the brain vascular system, followed by arterial remodeling and an increase in their stiffness. In addition, excessive blood pressure variability, activation of the tissue renin-angiotensin-aldosterone system, as well as target-organ damage - primarily the heart in the form of left ventricular hypertrophy, kidneys in the form of microalbuminuria and decrease in glomerular filtration rates. An additional risk factor for stroke is hyperuricemia, which is included in the current European and Russian guidelines for the management of AH as one of the new risk factors in patients with this disease. The state-of-the-art approach to antihypertensive therapy is the using of antihypertensive single-pill combinations, one of the frontline combinations in the absence of special clinical conditions is a combination of an angiotensin converting enzyme inhibitor and a calcium channel blocker. The reference drugs in both classes due to large body of evidence are ramipril and amlodipine, respectively. These drugs provide a high level of brain protection, not only due to the ultra-long and powerful antihypertensive action, but also through a unique potential in target-organ protection via left ventricular hypertrophy regression, antiatherosclerotic effects and improved endothelial function, renal protection, as well as the ability to decrease uric acid in the blood.

P311Hypertrophic cardiomyopathy and other forms of left ventricular hypertrophy. The P wave can make the difference

Abstract Background Structural disarray of hypertrophied myocytes and interstitial fibrosis characterize hypertrophic cardiomyopathy (HCM). These morphological changes also affect atrial myocytes and, together with hemodynamic alterations because of HCM, may lead to atrial cardiomyopathy. Purpose To investigate the incremental value of P-wave parameters to differentiate left ventricular hypertrophy (LVH) because of HCM from LVH in hypertensive heart disease (HHD) and athletes heart. Methods In a prospective study, we compared electrocardiographic (including signal-averaged ECG of the P wave) and echocardiographic data of patients with HCM, HHD and athletes heart. We developed a predictive model with a simple scoring system to identify HCM. Results We compared data of 27 patients with HCM (70% males, 49.8 ± 14.5 years), 324 patients with HHD (52% males, 74.8 ± 5.5 years), and 215 subjects with athletes heart (72% males, 42.3 ± 7.5). The table shows the significant differences among the 3 groups. We included the following parameters into a predictive score to differentiate HCM from other forms of LVH: QRS width (&amp;gt;88ms = 1 point), P-wave integral (&amp;gt;688µVs = 1 point) and septum thickness (&amp;gt;12mm = 2 points). A score &amp;gt;2 (Youden index 0.626) correctly classified HCM in 81% of the cases with a sensitivity and specificity of 82% an 81%, respectively. Conclusion Differentiation of HCM from other forms of LVH is improved by including atrial parameters. A simple scoring system including septum thickness, QRS width and P wave integral allowed identification of patients with HCM with a sensitivity and specificity of &amp;gt;80%. This score needs to be validated prospectively. Table 1 HCM HHD Athletes P-value HCM vs HHD* HCM vs Athletes* 95%-CI P-value 95%-CI P-value P-wave duration [ms] 152.7 ± 25.8 143.9 ± 16.5 133.5 ± 14.2 &amp;lt;0.001 -16.9 -24.6 to -9.1 &amp;lt;0.001 -16.3 -22.7 to -9.9 &amp;lt;0.001 P-wave integral [µVs] 850.4 ± 272.4 672.0 ± 235.4 773.1 ± 260.1 &amp;lt;0.001 -198.6 -320.8 to -76.3 0.002 -68.2 -169.7 to 33.2 0.187 QRS [ms] 110.3 ± 27.3 96.9 ± 20.3 95.1 ± 9.8 &amp;lt;0.001 -16.4 -24.7 to -8.1 &amp;lt;0.001 -13.8 -20.8 to -6.9 &amp;lt;0.001 QTc [ms] 447.9 ± 27.2 438.6 ± 24.5 414.0 ± 22.9 &amp;lt;0.001 -21.1 -32.7 to -9.5 &amp;lt;0.001 -30.8 -40.5 to -21.2 &amp;lt;0.001 LVMMI [g/m2] 153.6 ± 55.5 133.5 ± 30.3 98.6 ± 19.7 &amp;lt;0.001 -15.3 -29.7 to -0.9 0.038 -56.1 -67.7 to -44.6 &amp;lt;0.001 IVS [ms] 16.8 ± 4.2 11.8 ± 2.2 10.3 ± 1.5 &amp;lt;0.001 -5.2 -6.3 to -4.1 &amp;lt;0.001 -6.4 -7.3 to -5.6 &amp;lt;0.001 LAVI [ml/m2] 43.2 ± 13.9 30.5 ± 9.7 30.8 ± 9.5 &amp;lt;0.001 -14.6 -20.0 to -9.3 &amp;lt;0.001 -12.2 -16.6 to -7.9 &amp;lt;0.001 The table shows the study result after univariate and multivariate (*; adjusting for age and sex) analysis. Abstract Figure 1

Clinical and diagnostic key points of left ventricular hypertrophy in adults: insights from the ANMCO Lombardy experience

Left ventricular hypertrophy is a common complication of different diseases. Among these, cardiac involvement of amyloidosis or Anderson-Fabry disease are often unrecognized. Early diagnosis is therefore crucial because new therapies can impact the progression of these diseases. Different specific signs unmasked by clinical, laboratory, and non-invasive diagnostic tests such as echocardiography or cardiac magnetic resonance could guide clinicians towards an appropriate diagnosis. The aim of this review is to underline the major diagnostic clues of different forms of left ventricular hypertrophy in adult patients, guiding clinicians towards a more appropriate diagnosis.

A clinical and echocardiographic study in elderly hypertensive patients

Introduction: Isolated systolic hypertension is the commonest cause of raised blood pressure in the older population. As the age progresses more and more persons will be hypertensive. It is a disease, which is definitely the most prevalent, remediable risk factor for cardiovascular diseases and cerebrovascular diseases. Objective: To study the clinical profile of hypertension in elderly, to find out associated risk factors, especially on cardiac through echocardiography. Materials and Methods: A total number of sixty elderly hypertensive patients of ?60 years with systolic blood pressure ? 140 and diastolic blood pressure ? 90 mm of Hg were included in this study. A detailed history with general and systemic examination with fundus examination was carried out. Complete blood count, urine analysis, blood sugar, renal profile, lipid profile, chest x-ray, electrocardiogram, and echocardiogram were done in all patients. Results: Sixty patients were evaluated, and the mean age was 67.72±7.004 years of which 35 (58.33%) were males and 25 (41.67%) females and the common age group was 60-65 years. Chest pain in 45% and breathlessness in 38.33% were commonest clinical presentation. Family history, smoking history and total cholesterol were associated risk factors of hypertension. Hypertensive retinopathy was observed in 38.33% patients. Ischemic changes in 31.67% followed by left ventricular hypertrophy in 20% were most common electrocardiographic findings. The echocardiographic evaluation showed left ventricular dysfunction in 63.33% was common entity in the form of left ventricular hypertrophy in 30%, left ventricular dilatation in 15% and left ventricular diastolic dysfunction in 48.33%. Ischemic heart disease was diagnosed in 55% patients. Out of these 18 (54.55%) had anterior, 4 (12.12%) lateral, 3 (9.09%) inferior and 4 (12.12%) septal infarcts. One patient had global hypokinesia, and three patients had more than one segment involvement. There was strong co relation b

Chronic kidney disease induces left ventricular overexpression of the pro-hypertrophic microRNA-212

Chronic kidney disease (CKD) is a public health problem that increases the risk of cardiovascular morbidity and mortality. Heart failure with preserved ejection fraction (HFpEF) characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction is a common cardiovascular complication of CKD. MicroRNA-212 (miR-212) has been demonstrated previously to be a crucial regulator of pathologic LVH in pressure-overload-induced heart failure via regulating the forkhead box O3 (FOXO3)/calcineurin/nuclear factor of activated T-cells (NFAT) pathway. Here we aimed to investigate whether miR-212 and its hypertrophy-associated targets including FOXO3, extracellular signal-regulated kinase 2 (ERK2), and AMP-activated protein kinase (AMPK) play a role in the development of HFpEF in CKD. CKD was induced by 5/6 nephrectomy in male Wistar rats. Echocardiography and histology revealed LVH, fibrosis, preserved systolic function, and diastolic dysfunction in the CKD group as compared to sham-operated animals eight and/or nine weeks later. Left ventricular miR-212 was significantly overexpressed in CKD. However, expressions of FOXO3, AMPK, and ERK2 failed to change significantly at the mRNA or protein level. The protein kinase B (AKT)/FOXO3 and AKT/mammalian target of rapamycin (mTOR) pathways are also proposed regulators of LVH induced by pressure-overload. Interestingly, phospho-AKT/total-AKT ratio was increased in CKD without significantly affecting phosphorylation of FOXO3 or mTOR. In summary, cardiac overexpression of miR-212 in CKD failed to affect its previously implicated hypertrophy-associated downstream targets. Thus, the molecular mechanism of the development of LVH in CKD seems to be independent of the FOXO3, ERK1/2, AMPK, and AKT/mTOR-mediated pathways indicating unique features in this form of LVH.

The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM.

Hypertrophic cardiomyopathy (HCM) is a genetic form of left ventricular hypertrophy, primarily caused by mutations in sarcomere proteins. The cardiac remodeling that occurs as the disease develops can mask the pathogenic impact of the mutation. Here, to discriminate between mutation-induced and disease-related changes in myofilament function, we investigate the pathogenic mechanisms underlying HCM in a patient carrying a homozygous mutation (K280N) in the cardiac troponin T gene (TNNT2), which results in 100% mutant cardiac troponin T. We examine sarcomere mechanics and energetics in K280N-isolated myofibrils and demembranated muscle strips, before and after replacement of the endogenous troponin. We also compare these data to those of control preparations from donor hearts, aortic stenosis patients (LVHao), and HCM patients negative for sarcomeric protein mutations (HCMsmn). The rate constant of tension generation following maximal Ca2+ activation (k ACT) and the rate constant of isometric relaxation (slow k REL) are markedly faster in K280N myofibrils than in all control groups. Simultaneous measurements of maximal isometric ATPase activity and Ca2+-activated tension in demembranated muscle strips also demonstrate that the energy cost of tension generation is higher in the K280N than in all controls. Replacement of mutant protein by exchange with wild-type troponin in the K280N preparations reduces k ACT, slow k REL, and tension cost close to control values. In donor myofibrils and HCMsmn demembranated strips, replacement of endogenous troponin with troponin containing the K280N mutant increases k ACT, slow k REL, and tension cost. The K280N TNNT2 mutation directly alters the apparent cross-bridge kinetics and impairs sarcomere energetics. This result supports the hypothesis that inefficient ATP utilization by myofilaments plays a central role in the pathogenesis of the disease.

Cellular interplay via cytokine hierarchy causes pathological cardiac hypertrophy in RAF1-mutant Noonan syndrome

Noonan syndrome (NS) is caused by mutations in RAS/ERK pathway genes, and is characterized by craniofacial, growth, cognitive and cardiac defects. NS patients with kinase-activating RAF1 alleles typically develop pathological left ventricular hypertrophy (LVH), which is reproduced in Raf1L613V/+ knock-in mice. Here, using inducible Raf1L613V expression, we show that LVH results from the interplay of cardiac cell types. Cardiomyocyte Raf1L613V enhances Ca2+ sensitivity and cardiac contractility without causing hypertrophy. Raf1L613V expression in cardiomyocytes or activated fibroblasts exacerbates pressure overload-evoked fibrosis. Endothelial/endocardial (EC) Raf1L613V causes cardiac hypertrophy without affecting contractility. Co-culture and neutralizing antibody experiments reveal a cytokine (TNF/IL6) hierarchy in Raf1L613V-expressing ECs that drives cardiomyocyte hypertrophy in vitro. Furthermore, postnatal TNF inhibition normalizes the increased wall thickness and cardiomyocyte hypertrophy in vivo. We conclude that NS-cardiomyopathy involves cardiomyocytes, ECs and fibroblasts, TNF/IL6 signalling components represent potential therapeutic targets, and abnormal EC signalling might contribute to other forms of LVH.

Clinical efficacy and cardioprotective capabilities of olmesartan and lercanidipine in the form of monotherapy and with their combined use in patients with arterial hypertension 1-2 degree

The aim of the study was to evaluate the clinical efficacy and cardioprotective effects of olmesartan and lercanidipine in the form of monotherapy and combined use in patients with arterial hypertension (AH) 1-2 degree and the presence of target organ damage in the form of left ventricular hypertrophy (LVH) and microalbuminuria UIA). Materials and methods. 90 patients with AH of 1-2 degree were examined and presence of LVH according to echocardiography (EchoCG) data, middle age 50.3±4.3 years, 42 of them men and 48 women, with AH of 1st degree - 44 (48.9%) people, with AH of the 2nd degree - 46 (51.1%) people. The mean duration of hypertension was 6.8±1.5 years. Methods included daily monitoring of blood pressure (cardiovascular system): CardioTens (Meditech, Hungary), transthoracic EchoCG: Voluson 730 Expert (General Electric, USA). One of the inclusion criteria was the presence of LVH according to EchoCG data: more than 95 g/m2 in women and more than 115 g/m2 in men. Depending on the initial degree of hypertension patients were divided into 3 groups. Patients with the 1st degree of AH were randomized to olmesartan monotherapy with 10-40 mg/day (group 1) and lercanidipine 10-20 mg/day (group 2), with grade 2 AH included in the combination therapy group Studied drugs (3rd group). Doses of drugs were titrated until the target blood pressure levels were reached. Initially and after 6 months of therapy, the results of SMAD, EchoCG were evaluated, the quality of life of patients was assessed using the visual-analogue scale "Health thermometer". The statistical analysis was carried out using the program Statistica 7.0. Results of the study. The degree of significant decrease in blood pressure in comparison with the baseline values and the corrective effect on the daily profile of blood pressure were comparable in the monotherapy groups with olmesartan and lercanidipine. In the group of combined use of target drugs of target levels, blood pressure was achieved in a larger percentage of cases than in the monotherapy groups. A reliable cardioprotective effect of olmesartan and lercanidipine was revealed both in monotherapy and in combination in patients with AH of 1-2 degree with LVH and MAU, manifested by a decrease in LV mass index (LVMI). The greatest cardioprotective effect in LVH regression was achieved in the combination therapy group. Conclusion. Olmesartan and lercanidipine when used in monotherapy have a cardioprotective effect in the form of a reliable and comparable decrease in LVMI, and their use in combination has a more pronounced effect on LVH regression.

Speckle Tracking as an Adjunctive Echocardiographic Technique for Differentiating Cardiac Amyloidosis from Hypertrophic Cardiomyopathy: A Case Study

Cardiac Amyloidosis (CA) often requires multiple diagnostic modalities with echocardiogram being the most important non-invasive method. Echocardiographic findings of left ventricular hypertrophy (LVH), impaired relaxation and dilated atrias can be seen in others forms of LVH like hypertrophic cardiomyopathy (HCM). Speckle tracking echocardiography (STE), is a relatively new advancement in echocardiography which makes it possible to assess the deformation of the left ventricle and can be utilized for differentiating CA from other forms of LVH. We demonstrate the incremental value provided by STE in distinguishing CA from HCM.

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs.

Left ventricular (LV) hypertrophy is an important physiological compensatory mechanism in response to chronic increase in hemodynamic overload. There are two different forms of LV hypertrophy, one physiological and another pathological. Aerobic exercise induces beneficial physiological LV remodeling. The molecular/cellular mechanisms for this effect are not totally known, and here we review various mechanisms including the role of microRNA (miRNA). Studies in the heart, have identified antihypertrophic miRNA-1, -133, -26, -9, -98, -29, -378, and -145 and prohypertrophic miRNA-143, -103, -130a, -146a, -21, -210, -221, -222, -27a/b, -199a/b, -208, -195, -499, -34a/b/c, -497, -23a, and -15a/b. Four miRNAs are recognized as cardiac-specific: miRNA-1, -133a/b, -208a/b, and -499 and called myomiRs. In our studies we have shown that miRNAs respond to swimming aerobic exercise by 1) decreasing cardiac fibrosis through miRNA-29 increasing and inhibiting collagen, 2) increasing angiogenesis through miRNA-126 by inhibiting negative regulators of the VEGF pathway, and 3) modulating the renin-angiotensin system through the miRNAs-27a/b and -143. Exercise training also increases cardiomyocyte growth and survival by swimming-regulated miRNA-1, -21, -27a/b, -29a/c, -30e, -99b, -100, -124, -126, -133a/b, -143, -144, -145, -208a, and -222 and running-regulated miRNA-1, -26, -27a, -133, -143, -150, and -222, which influence genes associated with the heart remodeling and angiogenesis. We conclude that there is a potential role of these miRNAs in promoting cardioprotective effects on physiological growth.