Signs Of Left Ventricular Hypertrophy Research Articles

Relationship of chronic kidney disease of the with glycemic status, cardiovascular diseases and laboratory indicators in patients with type 2 diabetes mellitus

Aim. To study the relationship of chronic kidney disease parameters with glycemic control, subclinical and clinical signs of cardiovascular diseases and laboratory parameters.Material and methods. The study included 528 patients with type 2 diabetes mellitus (T2DM) aged 30-69 years. All respondents answered questions from the ARIC questionnaire about T2DM and cardiovascular diseases. We determined the ankle-brachial index, sonographic left ventricular hypertrophy, intima-media thickness and defined hypertensive, diabetic angiopathy and polyneuropathy. The levels of glycemia, lipid spectrum, creatinine, uric acid, glycohemoglobin were evaluted. Glomerular filtration rate (GFR) was calculated using the Cockroft-Gault method, and microalbuminuria (MAU) was determined using Micral tests.Results. Glycohemoglobin did not depend on MAU (p=0,564), a decrease in GFR was accompanied by an improvement in glycemic control (p=0,393). There was a direct association between MAU and the duration of diabetes (p=0,001), in patients with a longer course of the disease GFR was reduced (p=0,001). With increasing of systolic blood pressure, MAU progressed (p=0,016), while GFR decreased (p<0,01). In patients with hypertensive angiopathy, MAU of 100 mg/dl (p=0,001) and stage 2 of chronic kidney disease (p=0,048) occurred with the highest incidence (1/4) (p=0,048). According to the survey, angina was found in patients with MAU of 100 mg/dl (p=0,006). Chronic heart failure led to the progression of albuminuria (p=0,007), in patients with clinical signs of atherosclerosis of the lower extremities, the frequency of MAU was 72-87,5% (p=0,032). The highest intima-media thickness of the right carotid artery in patients with GFR 89-60 ml/min and MAU 100 mg/dL (respectively, 1,77±0,41, 1,33±0,49) were determined. Sonographic signs of left ventricular hypertrophy were observed in 84,6% of patients with an MAU of 300 mg/dL (p=0,022), as the severity of albuminuria increased, the ejection fraction of the left ventricle decreased (p=0,003). Albuminuria increased the level of myocardial remodeling (p<0,05) and this indicator showed a direct relationship with the severity of MAU. With an increase in albuminuria, the degree of triglyceridemia increased. An increase of MAU level and a decrease in GFR was accompanied by an increase in creatininemia (p<0,001). A direct relationship was found between lithemia and MAU. Conversely, a decrease in GFR contributed to the progression of MAU (p<0,001).Conclusion. Reduction of GFR and MAU are the major risk factors for cardiovascular diseases in the Azerbaijani population with T2DM. We suppose that periodic monitoring of these parameters for primary and secondary prevention of diabetic nephropathy plays an important role.

Consistent histologic findings in Brugada syndrome: The stubborn structural substrate

Since the first description of Brugada syndrome (BrS), there has been controversy about his association with structural abnormalities of the myocardium. To identify an invariant histological substrate in patients with a definite BrS. A BrT1 patient who had an autopsy after an episode of VF prompted us to perform a review of published case reports of autopsies and bi-ventricular histological samples to study patients with a spontaneous BrT1 who experienced VF and/or SCD and for whom there was no signs of an associated myocardial disease before the histological examinations. Sixteen studies and cases reports were reviewed that included 127 patients; eight of these cases fulfilled the study criteria. In total, nine patients were evaluated in the present study (mean age 35.3 ± 10.4 years, eight males, four autopsies, five bi-ventricular myocardial biopsies). Eight patients had undergone cardiac imaging and no abnormality was found. None of the four patients in the autopsy series presented with a normal heart and all four had significant left ventricular hypertrophy. Pathological examination was abnormal in all patients. An occult myocarditis was diagnosed histologically in six of the nine patients and seven had criteria for myocardial inflammation. Local myocardial PCR were positive for parvovirus B19 in three patients. Only one patient had criteria consistent with an arrhythmogenic cardiomyopathy. Viral myocarditis and left ventricular hypertrophy appear to be recurrent findings in patients with Brugada syndrome who experience VF and/or SCD. In contrast to the classical definition of this disease, none of the BrS patients with detailed histologic investigations had a normal heart.

The diagnostic value of electrocardiographic criteria for left ventricular hypertrophy in essential arterial hypertension alone and in combination with coronary heart disease

Objective: to evaluate the diagnostic significance of the electrocardiographic (ECG) criteria for left ventricular hypertrophy (LVH) in 12 leads in patients with essential arterial hypertension (AH) and in AH in combination with ischemic heart disease (IHD) compared with echocardiography (EchoCG) data. Materials and methods: ECG and EchoCG were carried out in 165 patients with AH (n = 139) and AH with concommitant IHD (n=26). Results: EchoCG signs of LVH ("EchoCG +") were detected in 72 (51,7%) patients with AH and in 12 (46,1 %) patients in AH + IHD. In the EchoCG + group the electrocardiographic signs of LVH (Sokolov-Lyon index, Cornell product, Cornell index) were determined in 37 (30,5 %) hypertensive patients and in no case in the AH + IHD group. In the "EchoCG-" group, electrocardiographic signs of LVH were determined in 8 hypertensive patients and two in the AH + CHD group. The use of additional voltage criteria for LVH in the frontal plane leads (RI > 15 mm, R I + S III > 25 mm, R aVL > 12 mm) increased the detection of LVH from 30,5 % (n=22) to 51,3 % (n=37). The false negative ECG diagnosis of LVH was influenced by: positional features, interventricular conduction defect, metabolic disorders and high index body mass. Conclusion: The Sokolov-Lyon index, the Cornell index, the Cornell product have low sensitivity in the diagnosis of LVH (30,5 %). Adding the frontal plane leads voltage criteria for LVH may contribute to increase in electocardiographic LVH detection (51,3 %). The decrease in the sensitivity of the ECG criteria for LVH is mainly caused by the positional features of the heart, interventricular conduction defect, metabolic disorders and high index body mass.

SRAGE and early signs of cardiac target organ damage in mild hypertensives

BackgroundSoluble Receptor for Advanced Glycation End Products (sRAGE) may be considered a marker inversely related to inflammation and its participation has been established in patients with advanced atherosclerotic vascular diseases. However, it is still unknown whether sRAGE reduction could be early metabolic change in the first stage of hypertension and initial hypertension-associated cardiac damage. We sought to determine the sRAGE values in otherwise healthy, untreated and recently diagnosed mild hypertensives and evaluate their association with blood pressure (BP) values, metabolic parameters, and with subclinical initial signs of cardiac target organ damage (TOD).MethodssRAGE were measured in 100 hypertensive and 100 normotensive subjects matched for age, gender and body mass index (BMI), submitted to a clinic visit and both ambulatory BP monitoring and echocardiography to determine the presence of initial cardiac TOD (presence of signs of left ventricular hypertrophy: left ventricular mass indexed for height2.7 (LVMi) > 48 g/m2.7 for men and > 44 g/m2.7 for women and/or increased left atrial volume 4-chamber indexed for body surface area (LAVi) > 34 ml/m2).ResultssRAGE levels were similar between hypertensive and normotensive subjects and were not significantly correlated with office and 24-h BPs values. However, when subgrouping the hypertensive patients in Hyp-TOD and Hyp-withoutTOD, sRAGE was found to be different among the three groups (p = 0.030), being lower in the Hyp-TOD group than the values of both Hyp-withoutTOD (p = 0.038) and normotensives (p = 0.038). In hypertensive patients sRAGE was negatively related with both LVMi (r = − 0.239, p = 0.034) and LAVi (r = − 0.315, p = 0.005) and was independently related to cardiac TOD also in multivariable analysis.ConclusionsIn this population of mild hypertensives, low circulating sRAGE may be a very early marker of initial TOD, suggesting the possible participation of oxidative stress in initial cardiac changes in human hypertension.

Surgical management of hypertrophic obstructive cardiomyopathy: the role of mitral valve

Hypertrophic obstructive cardiomyopathy (HOCM) is the most frequently inherited cardiovascular disease (prevalence in the general population of 1/500) and is characterized by significant left ventricular hypertrophy, especially in the interventricular septum, combined with small-volume cardiac cavities. Transaortic surgical septal myectomy is the most commonly used technique to treat HOCM, and is associated with low operative morbidity and mortality and a reduction of the outflow gradients. The composite operative mortality of only 0.4% (17/3695 patients) from 5 major high-volume centers in North America highlights the role of dedicated HOCM units. The involvement of the mitral valve in the pathophysiology of HOCM has been addressed as systolic anterior motion (SAM)-related left ventricular outflow tract obstruction. Hypertrophic cardiomyopathy mitral malformations include leaflet elongation and a wide array of malformations of the papillary muscles and chordae that can be detected by transthoracic and transesophageal echocardiography and by cardiac magnetic resonance. Because they participate fundamentally in the predisposition to SAM, they have increasingly been repaired surgically.

Hypertrophic cardiomyopathy – symptomatic atrial fibrillation in a patient at high risk of sudden cardiac death (RCD code: V-2A.2)

We present the case of a young patient with significant left ventricular hypertrophy as a common representation of the hypertrophic cardiomyopathy (HCM) phenotype. The clinical presentation and diagnostic route of the disease (despite negative genotype), which can be found in everyday cardiology practice, are shown. Despite the presence of guidelines on this topic, each clinical case is demanding, especially during qualification for invasive procedures. Limited data about the periprocedural risk of catheter ablation and success rate in HCM makes physician decisions for this type of patient challenging. The importance of informed consent and how the patient’s decisions affet further progress are also shown. JRCD 2018; 4 (1): 18-21.

Obstructive Hypertrophic Cardiomyopathy with Concomitant Mitral Regurgitation Treated with a Septal Myectomy and MV Repair: A Case Report

Abstract Case presentation Hypertrophic cardiomyopathy (HCM) is the most common and very heterogeneous genetic cardiac disease with a different clinical presentation and prognosis. The overall prevalence of the disease is estimated between 0.05-0.2% of the population. Left ventricular outflow obstruction at rest is present in about 20% of patients. Most of the patients have a normal life expectancy, however high risk patients might develop heart failure, atrial fibrillation, ventricular arrhythmias and sudden cardiac death. We present the case of 47-year-old Caucasian man who was hospitalized at our clinic with a history of chest pain and shortness of breath on physical activity in the last six months, which caused significant limitations of his life quality. Hypertrophic obstructive cardiomyopathy was diagnosed in 2011, when the patient was put on therapy with beta blocker. Transthoracic echocardiography revealed normal systolic function, presence of systolic anterior mitral valve motion (SAM) with moderate mitral regurgitation (MR). There was a significant concentric left ventricular hypertrophy predominantly located in the ventricular septum. The intraventricular gradient at rest was 77.8 mmHg. MRI of the heart confirmed significant LV hypertrophy with regions of fibrosis at the septum. The patient shortness of breath worsened progressively in the last month (NYHA III) despite optimized medical treatment with maximal beta blocker dose. Surgical approach with septal myectomy was performed with mitral valve repair. There were no operative complications, with excellent postoperative recovery and complete symptoms resolution. Control Doppler echocardiograms revealed LVOT rest gradient reduction to 34 mmHg. The good operative results were still present 9 months after the intervention. Our case confirmed that septal myectomy with MV repair is an excellent treatment approach in young patient with obstructive hypertrophic cardiomyopathy and mitral valve involvement refractory to medical treatment.

Value of the CHA2DS2-VASc score and Fabry-specific score for predicting new-onset or recurrent stroke/TIA in Fabry disease patients without atrial fibrillation

ObjectivesTo evaluate potential risk factors for stroke or transient ischemic attacks (TIA) and to test the feasibility and efficacy of a Fabry-specific stroke risk score in Fabry disease (FD) patients without atrial fibrillation (AF).BackgroundFD patients often experience cerebrovascular events (stroke/TIA) at young age.Methods159 genetically confirmed FD patients without AF (aged 40 ± 14 years, 42.1% male) were included, and risk factors for stroke/TIA events were determined. All patients were followed up over a median period of 60 (quartiles 35–90) months. The pre-defined primary outcomes included new-onset or recurrent stroke/TIA and all-cause death.ResultsPrior stroke/TIA (HR 19.97, P < .001), angiokeratoma (HR 4.06, P = .010), elevated creatinine (HR 3.74, P = .011), significant left ventricular hypertrophy (HR 4.07, P = .017), and reduced global systolic strain (GLS, HR 5.19, P = .002) remained as independent risk predictors of new-onset or recurrent stroke/TIA in FD patients without AF. A Fabry-specific score was established based on above defined risk factors, proving somehow superior to the CHA2DS2-VASc score in predicting new-onset or recurrent stroke/TIA in this cohort (AUC 0.87 vs. 0.75, P = .199).ConclusionsPrior stroke/TIA, angiokeratoma, renal dysfunction, left ventricular hypertrophy, and global systolic dysfunction are independent risk factors for new-onset or recurrent stroke/TIA in FD patients without AF. It is feasible to predict new or recurrent cerebral events with the Fabry-specific score based on the above defined risk factors. Future studies are warranted to test if FD patients with high risk for new-onset or recurrent stroke/TIA, as defined by the Fabry-specific score (≥ 2 points), might benefit from antithrombotic therapy. Clinical trial registration HEAL-FABRY (evaluation of HEArt invoLvement in patients with FABRY disease, NCT03362164).

Arch Augmentation via Median Sternotomy for Coarctation of Aorta With Proximal Arch Hypoplasia

Coarctation of the aorta can be associated with hypoplasia of the proximal transverse aortic arch. One approach to manage this condition is via left thoracotomy and extended end-to-end anastomosis with the expectation that the proximal arch will grow over time. Our preferred approach is to augment the aorta via midline sternotomy. We hypothesized that this approach is safe, durable, and allows reliable growth of the aorta. We identified the records of patients with biventricular anatomy who had coarctation of the aorta, hypoplasia of the proximal transverse arch, and no other cardiac lesion that would mandate cardiopulmonary bypass use and midline sternotomy. The records of 62 such patients operated on between 2005 and 2016 were retrospectively reviewed. Patient demographics, clinical variables and outcome data were collected and analyzed using SAS 9.4. Data are presented as median (interquartile range [IQR]). Sixty-two patients (23 girls [37%]) underwent repair at 10 (IQR, 5 to 21) days of life. Forty-nine (79%) patients were on prostaglandin infusion to maintain ductal patency. Fifteen (24%) patients presented in shock with end organ dysfunction, 17 (27%) were on inotropes, and 26 (42%) were mechanically ventilated. The proximal transverse arch was 41% (IQR, 34% to 47%) of the size of ascending aorta as measured by echocardiography (z-score, -5 [IQR, -5.8 to -4.3]). Following median sternotomy, repair was carried out on cardiopulmonary bypass (41 [IQR, 37 to 47] minutes). The arch was reconstructed with (n= 26 [42%]) or without (n= 36 [58%]) coarctectomy usually using homograft patch aortoplasty (n= 58 [94%]). In all but 2 patients, repair was undertaken with circulatory arrest (27 [IQR, 22 to 31] minutes). Patients were extubated 4 (IQR, 3 to 5) days later and discharged home in 12 (IQR, 8 to 18) days. There was no mortality, and 8 morbidity events (3 recurrent nerve injury, 2 chylothorax, 1 phrenic nerve injury, 1seizure, and 1 superficial wound infection) in 7 (11%) patients. All patients are alive at 41 (IQR, 11 to 64) months of follow-up. Reintervention was required in 6 (10%) patients (5 catheter based and 3 surgical) for recurrent distal coarctation. Reintervention-free survival at 1, 3, and 5 years was 87%. Only 1 child was currently on antihypertensive therapy, and all were in New York Heart Association functional class I symptoms. At last echocardiogram, the proximal transverse arch was 97% (IQR, 84% to 103%) of the diameter of the ascending aorta (z-score, 0.8 (IQR, 0.3 to 1.3]), ejection fraction was 70% (IQR, 60% to 76%), and only 2 patients had significant left ventricular hypertrophy. Arch augmentation via median sternotomy is a safe and effective procedure that can be accomplished with low morbidity and mortality. The reconstructed arch retains excellent growth potential resulting in a very favorable physiologic outcome.

Inhibition of Lysyl Oxidase Activity Prevents Volume Overload Diastolic and Systolic Dysfunction

The cardiac extracellular matrix (ECM) is a structural framework which bridges cardiomyocytes to the cystoskeletal myofibril, preserving alignment, while providing tensile strength to the myocardium. Abnormalities in the architectural scaffolding of the ECM have been noted during various cardiac pathologies. The major structural components of the cardiac ECM are collagens, which are produced by fibroblasts. The relative expression of collagens and the degree of cross‐linking dictate the passive mechanical properties of the heart. Lysyl oxidase (LOX) is a copper‐dependent amine oxidase that plays a critical role in covalently cross‐linking fibrillar collagens, which determines the insolubility, stiffness and resistance to degradation of the resulting collagen fibrils. In our previous studies we have shown marked increases in LOX expression and activity in failing hearts relative to compensated and unstressed hearts. Our goal of this study was to determine whether LOX inhibition, initiated during the early stages of cardiac remodeling, could attenuate fibrosis and cardiac dysfunction.We used the aortocaval fistula (ACF) surgical model on Sprague‐Dawley rats to induce biventricular volume overload (VO). Two weeks after surgery, both sham‐operated and VO rats were treated with the LOX inhibitor, beta‐aminoproprionitrile (BAPN; 100 mg/kg/d), for 12 weeks. BAPN was administered via an osmotic pump surgically inserted into the abdominal cavity. After a total of 14 weeks of VO, left ventricular (LV) pressure‐volume catheterization was used to assess alterations in cardiac function. Western blot protein analyses were performed to assess alterations in LOX, collagens I and III, matrix metalloproteinases (MMPs), and their inhibitors (TIMPs). Further, LV strain and stiffness were calculated to determine alterations in diastolic function.Our data demonstrate that chronic VO caused a significant increase in LV wall stress at both diastole and systole, and produced significant LV hypertrophy (183%, 60%, and 92% increase, respectively vs. control; p&lt;0.05). Further, VO induced significant increases in LV strain and stiffness (126% and 77% increase, respectively vs. control), as well as significant increases in the expression of fibrotic proteins including LOX, collagen I, collagen III, MMP2, and TIMP1 (135%, 58.4%, 26.7%, 39%, and 63% increase, respectively vs. control; p&lt;0.05). Finally, VO also caused systolic dysfunction, as evident by decreases in cardiac contractility and ejection fraction (51% and 26% decrease, respectively vs. control; p&lt;0.05). Further, our data highlight the cardioprotective role of LOX inhibition against adverse cardiac remodeling due to VO. LOX inhibition completely prevented VO‐induced increases in LV wall stress and ventricular hypertrophy. Further, LOX inhibition prevented VO‐induced fibrosis and diastolic dysfunction, as evident by normalized levels of collagens, LOX, MMPs, TIMPs, and LV stiffness. Finally, LOX inhibition prevented the VO‐induced decline in cardiac contractility. Overall, our data indicate that LOX inhibition prevented adverse ECM remodeling and cardiac dysfunction in the volume overloaded heart.Support or Funding InformationSupport for this project provided by the American Heart Association Southeast Affiliate and the NIH Heart, Lung and Blood Institute: Grant‐in‐Aid (#16GRNT30440008‐JDG), AHA Predoctoral Fellowship (# 16PRE29150010‐EEH), and F31 (#1F31HL134263‐ 01A1‐EEH).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

EVALUATION OF LEPTIN SERUM LEVELS IN PATIENTS WITH METABOLIC SYNDROME AND LEFT VENTRICULAR MYOCARDIAL HYPERTROPHY

Aim. To study serum level of leptin in patients with the metabolic syndrome (MS), including in patients with MS in combination with left ventricular hypertrophy (LVH) to determine the diagnostic significance of this marker in MS. Material and methods . The study involved 43 patients with MS, 33 of them with signs of LVH, and 33 patients without MS comparable age, including 10 patients with LVH. The average age of patients in the MS group at the time of inclusion into the study was 62.7±10.3 years, in the control group (without MS) – 60±14.7 years. All patients underwent a comprehensive examination that included the collection of complaints, study of history, physical examination, anthropometric measurements, laboratory and instrumental examination, including study of the serum level of leptin. Results. Patients of both groups had statistically significant differences in the size of the heart chambers, the presence of LVH signs, left ventricle contractile function, the thickness of the epicardial fat layer. Thus, enlargement of the heart, thickness of the interventricular septum, posterior wall of the left ventricle, thickness of epicardial fat, reduction of ejection fraction of the left ventricle and characteristics of aortic atherosclerosis were observed significantly more often in patients with MS compared with the group without MS (p<0.05).The average serum level of leptin in the MS group (41.89±33.28 ng/ml) was significantly higher compared to the group without MS (17.64±16.87 ng/ml), p<0.001. At that women had significantly higher levels of serum leptin (38.65±29.23 ng/ml) compared to males (19.54±27.23 ng/ml), p=0.006. A positive correlation between leptin levels and symptoms of LVH (r=0.294, p<0.001) was revealed: in the absence of LVH average level of leptin was 21.7±4.1 ng/ml, in the presence of signs of LVH – 39.2±4.95 ng/ml. Conclusions . Leptin levels in MS patients is higher than in patients without MS, and in patients with MS associated with LVH is higher than in MS patients without LVH. As the leptin level increases, the risk of LVH increases.

Cold crystalloid versus warm blood cardioplegia in patients undergoing aortic valve replacement.

Myocardial protection techniques during cardiac arrest have been extensively investigated in the clinical setting of coronary revascularization. Fewer studies have been carried out of patients affected by left ventricular hypertrophy, where the choice of type and temperature of cardioplegia remain controversial. We have retrospectively investigated myocardial injury and short-term outcome in patients undergoing aortic valve replacement plus or minus coronary artery bypass grafting with using cold crystalloid cardioplegia (CCC) or warm blood cardioplegia (WBC). From January 2015 to October 2016, 191 consecutive patients underwent aortic valve replacement plus or minus coronary artery bypass grafting in normothermic cardiopulmonary bypass. Cardiac arrest was obtained with use of intermittent antegrade CCC group (n=32) or WBC group (n=159), according with the choice of the surgeon. As compared with WBC group, in CCC group creatine-kinase-MB (CK-MB), cardiac troponin I (cTnI), aspartate aminotransferase (AST) release, and their peak levels, were lower during each time points of evaluation, with the greater statistically significant difference at time 0 (P<0.05, for all comparisons). A time 0, CK-MB/CK ratio >10% was 5.9% in CCC group versus 7.8% in WBC group (P<0.0001). At time 0 CK-MB/CK ratio >10% in patients undergoing isolated aortic valve replacement was 6.0% in CCC group versus 8.0% in WBC group (P<0.01). No any difference was found in perioperative myocardial infarction (0% versus 3.8%), postoperative (PO) major complications (15.6% versus 16.4%), in-hospital mortality (3.1% versus 1.3%). In aortic valve surgery a significant decrease of myocardial enzymes release is observed in favor of CCC, but this difference does not translate into different clinical outcome. However, this study suggests that in presence of cardiac surgical conditions associated with significant left ventricular hypertrophy, i.e., the aortic valve disease, a better myocardial protection can be achieved with the use of a cold rather than a warm cardioplegia. Therefore, CCC can be still safely used.

Cardiac function in paediatric patients with congenital adrenal hyperplasia due to 21 hydroxylase deficiency.

Hyperandrogenism and exogenous glucocorticoid excess may cause unfavourable changes in the cardiovascular risk profile of patients with congenital adrenal hyperplasia (CAH). To evaluate the cardiac function in paediatric patients with CAH. Twenty-seven paediatric patients with CAH, aged 8-16years, were evaluated by physical examination, electrocardiogram (ECG), conventional echocardiography, tissue Doppler imaging and two-dimensional (2D) myocardial strain (rate) imaging. Results were compared to 27 age- and gender- matched healthy controls. No signs of left ventricular hypertrophy or dilatation were detected on echocardiography. ECG revealed a high prevalence (25.9%) of incomplete right bundle branch block. Left ventricular posterior wall thickness in diastole (LVPWd) was significantly lower in patients with CAH compared to controls (5.55 vs 6.53mm; P=.009). The LVPWd Z-score was significantly lower in patients with CAH yet within the normal range (-1.12 vs -0.35; P=.002). Isovolumetric relaxation time was significantly lower in patients with CAH (49 vs 62ms; P=.003). Global longitudinal, radial and circumferential strain was not significantly different compared to controls. Global radial strain rate was significantly higher compared to healthy controls (2.58 vs 2.06 1/s; P=.046). Global longitudinal strain was negatively correlated with 24-hour blood pressure parameters. Cardiac evaluation of paediatric patients with CAH showed no signs of left ventricular hypertrophy or ventricular dilatation. LVPWd was lower in patients with CAH than in controls but within the normal range. A shorter isovolumetric relaxation time in patients with CAH may be a sign of mild left ventricular diastolic dysfunction.

Дополнительные критерии стратификации риска ишемического инсульта у пациентов с фибрилляцией предсердий и одним не связанным с полом баллом по шкале CHA2DS2-VASс обусловленным артеиальной гипертонией

Purpose. Identification of characteristics, not included in the CHA2DS2-VASc scale, affecting the risk of ischemic stroke in patients with atrial fibrillation (AF) and one non-sex-related risk factor (RF), due to arterial hypertension (AH), of thromboembolic events on this scale. Methods. A “case-control” study was conducted according to retrospective analysis of medical records of patients with AF. The main group included hospitalized due to development of ischemic stroke patients with non-valvular AF and single additional to gender RF on the CHA2DS2-VASc scale due to AH in the period prior to the stroke development. As a comparison group, patients with comparable demographic characteristics, having non-valvular AF with single additional to gender RF on the CHA2DS2-VASc scale due to AH and no history of stroke or systemic embolism, were selected. Anamnesis data and the results of electrocardiography, echocardiography and ultrasonic duplex scanning of brachiocephalic arteries were analyzed. Results. The main group included 37 patients, age 60.15 (±6,21) years, 27% women. The control group included 88 patients, age 60.13 (±4,85) years, 37.58% women. Patients of the main group, compared to the control group patients, significantly more often showed permanent AF (48.7% and 14.3%, p = 0.01), signs of left ventricular hypertrophy (LVH) according to echocardiography (67.6% and 43.6% , p = 0.026), and thickening of the intima-media complex (cIMT) > 0.9 mm (73% and 25%, p <0.0001) according to ultrasonic duplex brachiocephalic arteries scanning. The univariate analysis showed a significant increase of ischemic stroke risk in the presence of a permanent AF (odds ratio (OR) 5.28; 95% confidence interval (CI) 1,15 - 6,94), LVH according to echocardiography (OR 2.81, 95% CI 1.15 - 6.91) and cIMT thickening (OR 7.88, 95% CI 2.96 - 20.94). Conclusion. When assessing the risk of ischemic stroke and making the decision on the oral anticoagulants appointment in patients with atrial fibrillation and single additional to gender risk factor on the CHA2DS2-VASc scale due to AH, in which the indications for anticoagulant therapy are not absolute, it is advisable to consider the data of echocardiography, ultrasonic duplex scanning of brachiocephalic arteries and the form of AF.

Subclinical target organ damage in subjects with different components of metabolic syndrome

ABSTRACTBackground: To assess the association of metabolic syndrome (MS) and its components with target organ damage in a follow-up study of relatively healthy bank employers.Methods: Out of 1600 random samples of office workers in Saint Petersburg (Russia), a group of 383 participants with at least one component of MS and without cardiovascular complications was selected (mean age 46.6 ± 9.0 years, 214 females (64.6%)). Follow-up visit was performed in 331 subjects. Target organ damage (TOD) was assessed by echocardiography, carotid ultrasound, applanational tonometry, brachial–ankle index, and urine albumin excretion measurements. Anthropometry, vital signs, and biochemistry were performed according to standard protocols.Results: Presence of MS was not associated with higher probability of TOD. Multiple linear regression revealed significant association of all markers of TOD with older age. Hypertension was a significant predictor of left ventricular hypertrophy (LVH), increased arterial stiffness, and early signs of carotid atherosclerosis in logistic regression adjusted for age and gender. During follow-up, proportion of patients with LVH significantly decreased (from 46.7% to 32.9%, р = 0.003) and prevalence of patients with IMT > 0.09 сm increased (from 24.5% to 44.1%, p < 0.001) accompanying by significant declining of office blood pressure (BP) and total cholesterol.Conclusions: MS per se is not related to increased probability to TOD. Hypertension, female gender, and older age are main determinants of subclinical changes. After 2-years follow-up, significant LVH and renal damage regression was observed probably owing to BP reduction. Alternatively, early signs of carotid atherosclerosis increase with aging despite decreasing of the prevalence of hypercholesterolemia.

Similarities and Differences in Epidemiology and Risk Factors of Cerebral and Myocardial Ischemic Disease

AbstractIschemic heart disease and cerebral ischemia represent the leading causes of mortality worldwide. Both entities share risk factors, pathophisiology and etiologic aspects by means of a main common mechanism, atherosclerosis. The autors aimed to investigate differences and similarities in epidemiology and risk factors that could be found between both entities. In a retrospective sudy 403 patients were included and divided into two groups: group of 289 patients with history of myocardial infarction (AMI), and group of 114 patients with history of ischemic stroke (IS). All patients were evaluated for nonmodifiable risk faktors, which included age and sex, and modifiable, such as hypertension, dyslipidemia, diabetes, obesity, physical activity and smoking. Diff erences in some epidemiological aspects were also considered: occupation, marital status, alcohol consumption, exposure to stress. Patients with history of IS were significantly older then AMI patients (64.0 ± 9.9 vs 64.0 ± 9.9, p=0,028), with higher diastolic blood pressure (87,1 ± 10,2 vs 83,6 ± 10,4, p=0,003) and higher Sokolow-Lyon index in ECG, an also index of left ventricular hypertrophy (19,2 ± 9,1 vs 14,7 ± 6,5). Th ere were no significant differences between groups in the estimated body mass index and waist circumference. Differences between groups in stress exposure, occupation, alcohol consumption or physical activity were no significant. Patients in AMI group were more frequently male (199 (69%) vs 59 (52%), p=0,001), married (252 (87%) vs 88 (77%), p=0,037), smokers (162 (56%) vs 50 (44%), p=0,018) and with higher incidence od dyslipidemia (217 (75%) vs 73 (64%), p=0,019) compared with IS group. Incidence of arterial hypertension and diabetes was similar in both groups. Both entities share similar pathophysiological mechanisms and, consequently, main traditional risk factors. However, incidence of myocardial infarction increases with male sex, dyslipidemia, smoking and marital status, while incidense of ischemic stroke increases with age, higher diastolic blood pressure and also with ECG signs of left ventricular hypertrophy.

PP.29.17] HYPERTENSIVE ENCEPHALOPATHY IN A TERIFLUNOMIDE TREATED PATIENT

Objective: One of the challenges of the last years is to take care of patients with complex treatments, including new drugs. Teriflunomide is a pyrimidine synthesis inhibitor, for the tratament of multiple sclerosis. Hypertension is, according to clinical trials, a rare adverse reaction- 4% for the 14 mg/day. Design and method: Case report: We present the case of a 56 years old women with multiple sclerosis- who begun a treatment with teriflunomide (14 mg/day). She was known as having a grade 2 HTA, obesity and hypercholesterolemia and her treatment consisted in telmisartanum, indapamide and atorvastatine. With this treatment the blood pressure was under 130/ 85 mmHg and she was considered with controlled hypertension when the new drug was introduced. After the second dose- the patient experienced, during nighttime, headache and in the third day of treatment she developed a severe headache, with photophobia and vomitig, and in the Emergency Room the blood pressure was 260/130 mmHg. The rest of clinical examination showed: normal pulmonary auscultation and no signs of systemic congestion, a regular cardiac rhytm and tachycardia (120 beats/min), no focal neurological signs or meningeal irritation. She was admitted to the hospital as hypertensive encefalopathy. The blood tests were normal, excepting a total cholesterol above the recommended limits; the ECG- without changes and an echocardiogram - no signs of left ventricular hypertrophy, a normal kinetic and valves, with a mild dyastolic dysfunction. Results: Under treatment with i.v. vasodilatators and supplementation of the oral treatment with a calcium blocker, the patient become asymptomatic and the blood pressure values return to the recommended limits. She was discharged with a new treatment scheme (adding amlodipine 5 mg/day to the previous drugs), and the ambulatory blood pressure measurement, performed 14 days after that, showed a good control of hypertension. Conclusions: New therapies come with new adverse reactions and in everyday patients, which are rather complex, the close followup is mandatory. The useful tratment for Multiple Sclerosis was, in this patient, followed by a rise of the antihypertensive treatment.

The valosin-containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload.

SummaryHypertension‐induced left ventricular hypertrophy (LVH) is an independent risk factor for heart failure. Regression of LVH has emerged as a major goal in the treatment of hypertensive patients. Here, we tested our hypothesis that the valosin‐containing protein (VCP), an ATPase associate protein, is a novel repressor of cardiomyocyte hypertrophy under the pressure overload stress. Left ventricular hypertrophy (LVH) was determined by echocardiography in 4‐month male spontaneously hypertensive rats (SHRs) vs. age‐matched normotensive Wistar Kyoto (WKY) rats. VCP expression was found to be significantly downregulated in the left ventricle (LV) tissues from SHRs vs. WKY rats. Pressure overload was induced by transverse aortic constriction (TAC) in wild‐type (WT) mice. At the end of 2 weeks, mice with TAC developed significant LVH whereas the cardiac function remained unchanged. A significant reduction of VCP at both the mRNA and protein levels in hypertrophic LV tissue was found in TAC WT mice compared to sham controls. Valosin‐containing protein VCP expression was also observed to be time‐ and dose‐dependently reduced in vitro in isolated neonatal rat cardiomyocytes upon the treatment of angiotensin II. Conversely, transgenic (TG) mice with cardiac‐specific overexpression of VCP showed a significant repression in TAC‐induced LVH vs. litter‐matched WT controls upon 2‐week TAC. TAC‐induced activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling observed in WT mice LVs was also significantly blunted in VCP TG mice. In conclusion, VCP acts as a novel repressor that is able to prevent cardiomyocyte hypertrophy from pressure overload by modulating the mTORC1 signaling pathway.

In vivo efficacy of the AKT inhibitor ARQ 092 in Noonan Syndrome with multiple lentigines-associated hypertrophic cardiomyopathy.

Noonan Syndrome with Multiple Lentigines (NSML, formerly LEOPARD syndrome) is an autosomal dominant "RASopathy" disorder manifesting in congenital heart disease. Most cases of NSML are caused by catalytically inactivating mutations in the protein tyrosine phosphatase (PTP), non-receptor type 11 (PTPN11), encoding the SH2 domain-containing PTP-2 (SHP2) protein. We previously generated knock-in mice harboring the PTPN11 mutation Y279C, one of the most common NSML alleles; these now-termed SHP2Y279C/+ mice recapitulate the human disorder and develop hypertrophic cardiomyopathy (HCM) by 12 weeks of age. Functionally, heart and/or cardiomyocyte lysates from SHP2Y279C/+ mice exhibit increased basal and agonist-induced AKT and mTOR activities. Here, we sought to determine whether we could reverse the hypertrophy in SHP2Y279C/+ mice using ARQ 092, an oral and selective allosteric AKT inhibitor currently in clinical trials for patients with PI3K/AKT-driven tumors or Proteus syndrome. We obtained echocardiographs of SHP2Y279C/+ and wildtype (SHP2+/+) littermates, either in the presence or absence of ARQ 092 at 12, 14, and 16 weeks of age. While SHP2Y279C/+ mice developed significant left ventricular hypertrophy by 12 weeks, as indicated by decreased chamber dimension and increased posterior wall thickness, treatment of SHP2Y279C/+ mice with ARQ 092 normalized the hypertrophy in as early as 2 weeks following treatment, with hearts comparable in size to those in wildtype (SHP2+/+) mice. In addition, we observed an increase in fractional shortening (FS%) in SHP2Y279C/+ mice, an effect of increased compensatory hypertrophy, which was not apparent in SHP2Y279C/+ mice treated with ARQ 092, suggesting functional improvement of HCM upon treatment with the AKT inhibitor. Finally, we found that ARQ 092 specifically inhibited AKT activity, as well as its downstream effectors, PRAS and S6RP in NSML mice. Taken together, these data suggest ARQ 092 may be a promising novel therapy for treatment of hypertrophy in NSML patients.

A Case of Symptomatic Hypertrophic Cardiomyopathy with Severe Dynamic Gradient

Hypertrophic cardiomyopathy is a disease of the myocardium characterized by the thickening of the heart walls. It is a genetic disorder transmitted by first-degree relatives, caused by mutations in genes that code for sarcomere protein. A 77-year-old woman presented to the emergency department and complained of continuous vertigos and presyncope with subsequent fall to the floor with a concussive traumatic brain injury. The ECG observed signs of left ventricular hypertrophy. Blood exams highlighted a slight increase of troponin T (25 ng/L). The ultrosonography instead demonstrated a pronounced left ventricular hypertrophy with a 240 mmHg dynamic gradient, a moderate mitral regurgitation secondary to SAM. Lastly, ECG Holter excluded significant arrhythmias (1 couple of ventricular contractions). In the ward, the echocardiographic pattern was repeated and confirmed the clinical picture of a pronounced ventricular hypertrophy at the expense of the IVS (VTD 45 ml), a diastolic dysfunction Grade I with anterior systolic movement of the mitral flap valves with a dynamic obstruction to the left ventricular outflow (DP max 260 mmHg). Moreover, a moderatesevere mitral insufficiency was reported. Vital signs were stable. The antihypertensive therapy was enhanced with added ACE inhibitors, loop diuretics, beta blockers and the disopyramide administration started. The patient was discharged from the hospital and was scheduled a cardiologic echocardiographic follow up in order to evaluate the effectiveness of the therapy. This study has demonstrated the association between the clinical symptom, the clinical objectivity and the echocardiographic anomalies typical of the obstructive hypertrophic cardiomyopathy. Severe blood pressure values of dynamic obstruction to the left ventricular outflow have been recorded and which are not currently known by the scientific literature. Our purpose will be to evaluate the clinical and echocardiographic follow up and the potential response to the pharmacological therapy prescribed.