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Introduction Hypertrophic obstructive cardiomyopathy (HOCM) is a hereditary heart muscle disorder characterized by significant myocardial hypertrophy. we assessed perioperative and long-term follow-up data of Iranian HOCM patients who underwent SM in 2 pioneering centers. Methods Clinical data of patients with HOCM septal myectomy are collected. Thirty-day outcome and long-term follow-up data for recurrence of gradient and mortality are reported. Results Ninety-six patients in two different centers enrolled in the study. Most patients of 52 patients in center 1 were male (34/52 [65.3%]).and the mean age was of 36.7 ± 19 years. Syncope before admission was reported in 5.7%, the mean left ventricular ejection fraction on admission was 53 ± 8%, the mean left ventricular outflow tract gradient was 66.3 ± 20.4 mm Hg, and the mean preoperativeseptal thickness was 25.4 ± 6.7 mm. A redo SM was performed in 3 patients (5.8%), mitral valve repair in 5 patients (9.6%), and atrioventricular repair in 5 patients (9.6%). A residual systolic anterior motion was detected in 4 patients (7.7%), the mean postoperative septal thickness was 19 ± 6 mm (25.1% septal thickness reduction), and in-hospital mortality was 5.8% (n = 3). A longer-term follow-up showed death in 3 patients (5.8%) and late recurrent left ventricular outflow tract obstruction in 1 patient. Conclusions Transaortic myectomy is an effective surgery with acceptable early and late mortality rates. Improvements in functional status are seen in almost all patients. Appropriate SM is crucial to a good clinical outcome. Long-term survival is excellent and cardiac sudden death is extremely rare after a good surgical treatment.

Aims This study aimed to elucidate the long‐term effect of cibenzoline therapy on cardiovascular complications and prognosis in patients with hypertrophic obstructive cardiomyopathy (HOCM). Methods and results Eighty‐eight patients with HOCM were treated with cibenzoline (Group A), and 41 patients did not receive cibenzoline (Group B). The changes in left ventricular (LV) remodelling, incidences of cardiovascular complications and deaths, were examined. The mean follow‐up period was 15.8 ± 5.6 years in Group A and 17.8 ± 7.2 years in Group B. In Group A, the LV pressure gradient (LVPG) decreased immediately after treatment, and the reduction was maintained throughout the study. In Group B, the LVPG decreased gradually according to the deterioration of LV function. LV reverse remodelling was confirmed in Group A, and LV remodelling advanced in Group B. In Group A, the incidence of each cardiovascular complication was

Author's summary Hypertrophic cardiomyopathy (HCM) in infancy is rare and many fulminant cases are fatal. Infantile HCM shows a rapid progressive clinical course and different characteristics compared with late-onset HCM presenting during the prepubertal age. There are also spontaneously resolving phenotypes of HCM that are diagnosed in neonates being treated for bronchopulmonary dysplasia with corticosteroids or in those with other problems related to maternal endocrine diseases. The pathophysiology of infantile HCM has not been well described. Therefore, this review updates the pathophysiology of infantile HCM and includes molecular studies on maturation of cardiomyocytes from a clinician's point of view., Hypertrophic cardiomyopathy (HCM) is characterized by ventricular wall hypertrophy with diastolic dysfunction. Pediatric HCM is distinguished from the adult in many aspects. Most children with HCM do not present clinically until the adolescent period, even when they are born with genetic mutations. Some infants with early-onset HCM present with massive progressive myocardial hypertrophy in the first few months of life, which is often fatal. The mortality of pediatric HCM peaks during the infantile and adolescent periods. These periods roughly correlate with children's growth spurt. Non-sarcomeric causes of HCM are more frequent in pediatric HCM, while sarcomeric causes are more common in adults. From the perspective of cardiac development, the fetal heart has immature cardiomyocytes, which are characterized by proliferation and exit their cell cycles with a decreased regenerative property after birth. In the perinatal period, there is a dynamic change in maturation of cardiomyocytes from immature to mature cells. Infants who are treated with steroids or born to mothers with diabetes or hyperthyroidism often show phenotypes of HCM, which gradually resolve. With remarkable advancement of molecular biology, understanding on maturation of cardiomyocytes has increased. Neonates undergo abrupt environmental changes during the transitional circulation, which is affected by oxygen, metabolic and hormonal fluctuations. Derangement in physiological transition to the normal postnatal environment may influence maturation of proliferative immature cardiomyocytes during early infancy. This article reviews updates of infantile HCM and recent molecular studies related to maturation of cardiomyocytes from the clinical point of view of identifying distinct characteristics of infantile HCM.

Background: Differentiation between exercise induced adaptive myocardial hypertrophy (athlete's heart) and hypertrophic cardiomyopathy (HCM) is currently based on echocardiographic and cardiac magnetic resonance (CMR) criteria, but these may be insufficient in patients with subtle phenotype expression. This study aimed to assess whether left ventricular (LV) fractal pattern could permit to differentiate athlete's heart from HCM. Methods: We recruited retrospectively 61 elite marathon runners, 67 patients with HCM, and 33 healthy subjects. A CMR study was performed in all subjects and the LV trabeculae fractal dimension (ED) was measured in end-diastolic frames of each short-axis cine sequence. For group comparison, the ratio of maximal myocardial wall thickness (mMWT)/indexed LV end-diastolic volume (LVED) was determined. Results: As compared with athletes, patients with HCM had significantly (p < 0.001) greater FD in the LV basal (1.30 +/- 0.07 vs. 1.23 +/- 0.05) and apical (1.38 +/- 0.06 vs. 1.30 +/- 0.07) regions and in the whole heart (1.34 +/- 0.05 vs. 127 +/- 0.05). FD increased with age, left atrial area and indexed left ventricular mass (p < 0.05 for all) and correlated negatively with LV and RV end-diastolic volumes (p < 0.05 each). The addition of whole heart FD to the ratio of maximal myocardial wall thickness/indexed LVEDV lead to an improvement in the ability to discriminate HCM with a net reclassification index (NRI) of 71%. Conclusions: The FD regional distribution of the LV trabeculae differentiates patients with athlete's heart from patients with HCM. The addition of whole heart FD to the mMWT/indexed LVEDV ratio improves the predictive capacity of the model to differentiate both entities. (C) 2021 Elsevier B.V. All rights reserved.

Supplemental Digital Content is available in the text., Background: Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress. Methods: C57BL/6 mice were submitted to 21 days of swimming training to develop PMH. After termination of exercise, PMH regressed within 1 week. PMH regression mice (exercise hypertrophic preconditioning [EHP] group) and sedentary mice (control group) then underwent transverse aortic constriction or a sham operation for 4 weeks. Cardiac remodeling and function were evaluated with echocardiography, invasive left ventricular hemodynamic measurement, and histological analysis. LncRNA sequencing, chromatin immunoprecipitation assay, and comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot were used to investigate the role of Mhrt779 involved in the antihypertrophic effect induced by EHP. Results: At 1 and 4 weeks after transverse aortic constriction, the EHP group showed less increase in myocardial hypertrophy and lower expression of the Nppa and Myh7 genes than the sedentary group. At 4 weeks after transverse aortic constriction, EHP mice had less pulmonary congestion, smaller left ventricular dimensions and end-diastolic pressure, and a larger left ventricular ejection fraction and maximum pressure change rate than sedentary mice. Quantitative polymerase chain reaction revealed that the long noncoding myosin heavy chain–associated RNA transcript Mhrt779 was one of the markedly upregulated lncRNAs in the EHP group. Silencing of Mhrt779 attenuated the antihypertrophic effect of EHP in mice with transverse aortic constriction and in cultured cardiomyocytes treated with angiotensin II, and overexpression enhanced the antihypertrophic effect. Using chromatin immunoprecipitation assay and quantitative polymerase chain reaction, we found that EHP increased histone 3 trimethylation (H3K4me3 and H3K36me3) at the a4 promoter of Mhrt779. Comprehensive identification of RNA-binding proteins by mass spectrometry and Western blot showed that Mhrt779 can bind SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4 (Brg1) to inhibit the activation of the histone deacetylase 2 (Hdac2)/phosphorylated serine/threonine kinase (Akt)/phosphorylated glycogen synthase kinase 3β(p-GSK3β) pathway induced by pressure overload. Conclusions: Myocardial hypertrophy preconditioning evoked by exercise increases resistance to pathological stress via an antihypertrophic effect mediated by a signal pathway of Mhrt779/Brg1/Hdac2/p-Akt/p-GSK3β

It is known, that diabetes mellitus has a significant impact on the growth and development of the fetus. Hyperglycemia during pregnancy increases significantly the incidence of congenital malformations, perinatal morbidity and neonatal mortality. Over the past decades has been a steady increase in the prevalence of diabetes mellitus both in the general population and among pregnant women. In this regard, the study of the influence of diabetes mellitus in the mother on the condition of the fetus and newborn is today a relevant problem of obstetric-gynecological, neonatological and pediatric services. Hyperglycemia during pregnancy has the greatest effect on the fetal cardiovascular system. Diabetes mellitus of the mother causes an increase in the frequency of congenital heart defects in the newborn, myocardial hypertrophy, as well as various functional disorders of the cardiovascular system.This review mainly discusses the pathogenetic aspects and molecular mechanisms of the effect of hyperglycemia on the development of the fetal heart, provides an assessment of clinical, echocardiographic and some laboratory changes in the functioning of the cardiovascular system in newborns from mothers with diabetes mellitus, and also systematizes data on the relationship between maternal diabetes and the risks of cardiovascular disease in their children in the long term.

Hypertrophic cardiomyopathy (HCM) may be associated with considerable mortality in athletes. However, differentiating myocardial hypertrophy as a physiological adaptation of the heart to exercise can be a clinical challenge. In this context, nuclear magnetic resonance imaging has been shown to be a essential exam for diagnostic elucidation. The case report aimed to depict a young athlete with syncope and an initial investigation suggestive of HCM, which was excluded after deconditioning and serial MRI.

Cardiovascular complications including arrhythmias and cardiac conduction disorders are one of the main reasons of high mortality rate in acromegaly, while they have not been well explored.To estimate arrhythmias frequency in acromegaly, identify risk factors leading to the development of arrhythmia and cardiac conduction disorder, to determine the role of cardiac MRI in detecting structural and functional changes.A single-center prospective cohort study, which included 461 patients (151 men and 310 women) with acromegaly, was conducted. All the patients underwent a standard medical examination, including hormonal blood test, electrocardiogram, echocardiography, electrocardiogram daily monitoring. 18 patients with arrhythmias (11 men and 7 women) had cardiac MRI with gadolinium-based contrast.The results of our research show high frequency of arrhythmias and cardiac conduction disorders in patients with acromegaly 42%. Most frequent kinds of arrhythmias and cardiac conduction disorders were sinus bradycardia 19.1% of the cases and conduction disorders of bundle branch blocks 14.5%. Men were more likely to suffer from arrhythmias and cardiac conduction disorders than women (54.2% and 37.4%, respectively,p=0.0005). Not acromegaly activity but duration of the disease was a main risk factor of arrhythmias and cardiac conduction disorders. Patients with arrhythmias had a long anamnesis of acromegaly (10 and 7 years, respectively, p=0.04). Meanwhile, cardiac conduction disorders were commonly observed in the patients who were treated with somatostatin analogs comparing to the patients who didnt undergo this therapy (50% and 38.6% respectively,p=0.004). We showed that 61% of patients with acromegaly and cardiac conduction disorders who underwent magnetic resonance imaging (MRI) had the signs of myocardial fibrosis. The value of the ejection fraction of the left ventricle according to MRI was higher than with echocardiography (p=0.04).Arrhythmias and cardiac conduction disorders are often observed in patients with acromegaly even with remission of the disease. High risk group need careful diagnostic and monitoring approaches. Cardiac MRI is the gold standard for visualization of structural and morphological changes in the heart. Use of cardiac MRI in acromegalic patients expands our understanding of arrhythmias and cardiac conduction disorders in this disease. There are no specific laboratory markers of diffuse myocardial fibrosis, and the role of myocardial fibrosis in the occurrence of cardiac arrhythmias and conduction disorders needs further studying.Сердечно-сосудистые осложнения, включая нарушение ритма и проводимости сердца (НРПС), являются одной из основных причин высокой летальности при акромегалии, однако в настоящее время недостаточно изучены. Цель.Оценить частоту аритмий у пациентов с акромегалией, выявить факторы риска, способствующие развитию НРПС, определить роль магнитно-резонансной томографии (МРТ) сердца в выявлении структурных и функциональных изменений. Материалы и методы.Проведено одноцентровое проспективное когортное исследование, в которое включен 461 пациент (151 мужчина и 310 женщин) с акромегалией. Всем пациентам проведено стандартное медицинское обследование, включающее гормональное исследование крови, регистрацию электрокардиограммы (ЭКГ), эхокардиографию, холтеровское мониторирование ЭКГ. МРТ сердца с контрастированием гадолинием выполнено 18 пациентам с НРПС (11 мужчин и 7 женщин). Результаты.Результаты нашего исследования демонстрируют высокую встречаемость НРПС среди пациентов с акромегалией 42%. Наиболее частыми видами являлись синусовая брадикардия 19,1% случаев, а также нарушения проводимости по ножкам пучка Гиса 14,5%. Мужчины чаще страдали НРПС, чем женщины (54,2 и 37,4% соответственно,р=0,0005). Мы показали, что развитие НРПС зависит, в первую очередь, от длительности акромегалии, в то время как активность заболевания не оказывает значимого влияния. Анамнез акромегалии у пациентов с НРПС и без них составил 10 и 7 лет соответственно (p=0,04). Кроме того, важным фактором риска оказалась терапия аналогами соматостатина. Доля пациентов, получающих данный вид лечения, составила 50% с НРПС и 38,6% среди пациентов без НРПС (р=0,004). Мы продемонстрировали, что 61% пациентов с акромегалией и НРПС, которым провели МРТ сердца, имели признаки фиброза миокарда. При этом значение фракции выброса левого желудочка по данным МРТ оказалось статистически выше, чем при эхокардиографии (p=0,04). Заключение.НРПС часто встречаются у пациентов с акромегалией, несмотря на достижение ремиссии заболевания. Группа высокого риска требует более тщательной диагностики и мониторинга. МРТ сердца является золотым стандартом визуализации структурно-морфологических изменений сердца. Проведение МРТ сердца у пациентов с акромегалий расширяет наше представление о развитии НРПС при данном заболевании. В настоящее время отсутствуют специфические лабораторные маркеры диффузного миокардиального фиброза, а его роль в возникновении нарушений ритма и проводимости сердца требует дальнейшего изучения.

Based on scientific literature and own data, the article discusses the problem of hypertensive heart disease in real outpatient practice and especially in conducting preventive examinations in the working population. It is shown that the use of modern diagnostic methods, in particular electrocardiography with dopplerography, including pulse-wave tissue mode, should be an integral study included in the professional examination, as well as medical examination, which covers an increasing number of the population of our country. Echocardiography should be performed to clarify the cardiovascular risk and confirm the electrocardiographic diagnosis of left ventricular hypertrophy (LVH), left atrial dilatation, or suspected heart diseases (coronary heart disease, atrial fibrillation, other rhythm disorders). It has been shown that concentric LVH is the strongest predictor of an increased risk of heart failure, although the degree of LVH is not always directly related to the degree of hypertension and the duration of the disease.

Aim. To conduct a comparative analysis of the geometry of the left ventricle (LV) at sportsmen heavyweight power sports with hypertension. Material and methods. We examined 238 representatives of power sports (weightlifting, powerlifting, bodybuilding) with an average body weight of 102.7±6.4 kg and arterial blood pressure at rest: systolic blood pressure – 157.4±5,6, diastolic blood pressure – 91.2±5.3. Along with the examination, all examined athletes underwent: bioimpedansometry, standard resting electrocardiogram, two-fold measurement of blood pressure, transthoracic echocardiography. Results. A survey of 238 weightlifting athletes of heavy weight categories with arterial hypertension showed an increased fat component in powerlifters (SAT 31.8±3.3%; BMI 34.4±1.3 kg/m 2 ; Fat Mass Index 10.9±1,1 kg/m 2 ; Fat-to-Muscle Ratio 0.5±0.1) and a sufficiently large muscle component: bodybuilding Fat Free Mass Index (FFMI) 26.9±2.1 kg/m 2 ; powerlifting FFMI 23.5±1.6 kg/m 2 and weightlifting FFMI 23.7±1.8 kg/m 2 . The examination also showed a violation of the geometry of the LV. For athlete powerlifters, the following LV parameters were noted: LVMM 270.2±28.7 g; LVMI 123.7±7.9 g/m 2 ; RWTLV 0.46±0.03 sm. For representatives of weightlifting; LVMM 267.8±32.3 g; LVMI 121.4±8.6 g/m 2 ; RWTLV 0.45±0.02 sm. For bodybuilder athletes: LVMM 271.4±18.9 g; LVMI 120.1±6.3 g/m 2 ; RWTLV 0.30±0.01 sm. Conclusion. Thus, the patterns obtained in relation to the geometry of the heart of athletes of power sports, heavy weight categories with arterial hypertension, can serve as a scientific basis for the formation of some aspects of the preventive program of physical rehabilitation with a priority focus on “risk groups” in such men.

Aim . To identify genetic predictors of diastolic dysfunction and signs of endothelial dysfunction in relation to indicators of left ventricular myocardial deformity in patients with hypertension. Material and methods . The study included 74 patients (38 women and 36 men) with hypertension 1-2 stages observed in the cardiology department of the Road clinical hospital at Chita II station. The mean age of patients was 32±9.4 years. Circulating endothelial cells (CEC) were determined by flow cytometry with BT 5000 device and antibodies to CD146+, CD45. Besides, 7AAD ion dye was used to detect living and dead endothelial cells. The number of CD146+, CD45 cells per 500000 blood cells was determined. Changes in CEC, Living/Dead CEC were studied. The data was processed using CXP Cytometer and Kaluza programs. The standard echocardiography, Doppler echocardiography and tissue Doppler echocardiography were used. Frequency distribution of alleles and genotypes: 1 mutation nitric oxide synthase 3 gene NOS3 -786 T>C; ( С -786 Т ) in relation to indicators of left ventricular myocardial deformity was analyzed in hypertensive patients with or without diastolic dysfunction as well as in the control group. Polymerase chain reaction with detection of amplification product in real time (RCR-rt) or electrophoresis in agarose gel on genomic DNA of peripheral blood leukocytes were used for studying gene mutations. Results . Development of diastolic dysfunction in hypertensive patients enhanced with the carrier of the genotype NOS3 -786 CC ( р =0.01 2, x 2 =1 2.53), endothelial dysfunction was manifested by an increase in the number of circulating endotheliocytes and was associated with a decrease in global longitudinal deformation of the left ventricle. Conclusion . Endothelial dysfunction in patients with hypertension is associated with a violation of global longitudinal deformation; and in patients with diastolic dysfunction these abnormalities are more pronounced than in patients without diastolic dysfunction.

A steady increase in the number of young sportsmen predetermines the relevance of studying the nature and severity of cardiovascular system remodeling in young athletes, including the development of arterial hypertension (AH) and left ventricular myocardial hypertrophy (LVHM).Objective. To study the prevalence and nature of arterial hypertension (AH) and its associations with signs of cardiovascular remodeling in young athletes taking into account pathogenetic relationship and genetic determination.Characteristics of children and methods. The study included 80 young athletes (including 42 boys, average age 14,5±1,54 years), divided into 4 groups depending on the kind of sports (1 – cyclic, 2 – game, 3 – complex coordination, 4 – power). We used the following research methods: “office” (i.e. during visit to the doctor) measurement of blood pressure, electrocardiography, echocardiography, color Doppler scanning of the neck vessels, daily monitoring of blood pressure, bicycle ergometry, genetic testing using the original panel with 448 markers.Results. An increase in blood pressure at rest was detected in 2,5% of children engaged in power sports, an insufficient decrease at night – in 16,3% of children, and an excessive reaction of blood pressure to dosed physical activity – in 25% of children. These changes correlated with signs of sports remodeling, in particular with the formation of left ventricular myocardial hypertrophy, which was diagnosed in 7–12,5% of athletes. According to the results of genetic testing, pronounced polymorphism in the NO synthase gene at three loci (rs10918594, rs12143842, rs16847548) was associated with a reorganization of the cardiovascular system in 45% of athletes.Conclusion. Violation of the circadian profile of blood pressure and excessive reaction to physical activity demonstrate 7,5–25% of young athletes, especially those involved in complex coordination and power sports. These changes were associated with the severity of sports remodeling and determined by a genetic predisposition.

The aim: to study the peculiarities of structural and functional remodeling of the heart in arterial hypertension patients depending on the degree of thyrotoxicosis compensation. Materials and methods.The study included 80 patients with AH, 50 patients per AH with concomitant TT (mean age 52.6±12.7 years, mean duration of AG – 6.5±4.0 years, duration of TT 3.9±2.5), depending on the degree of compensation for TT the patients were divided into 2 groups (group 1 – compensated TT, group 2 – decompensated TT). The control group consisted of 30 patients from AH (mean age – 56.2±7.6 years, mean duration of AG – 8.8±4.4 years), who had excluded thyroid dysfunction during the examination. Results and discussion. According to the results of echocardiography, types of myocardial hypertrophy of the left ventricle were studied. Correlation and regression analyses were performed concerning the influence of thyroid hormone on the systolic blood pressure level according to the data of the outpatient blood pressure monitor. Conclusions.It was proved that the absence of thyrotoxicosis compensation in patients with arterial hypertension is accompanied by an increased level of systolic blood pressure, both during the whole day and during the day and night periods as compared to the control group and the group of patients with compensated thyrotoxicosis. Feedback between the systolic blood pressure level and the thyroid hormone has been proved. Based on correlation and regression analyses, it was established that heart remodeling in patients with arterial hypertension and thyrotoxicosis depends both on the level of systolic blood pressure (according to outpatient blood pressure monitoring) and the level of thyroid hormone

The introduction gives the morphological characteristics of myocardial hypertrophy, hy-pertrophic cardiomyopathy, as a subject of differential diagnosis. In the description of clinical cases of diagnostics of transient myocardial hypertrophy by echocardiographic method, the aim was to show the possibilities of such diagnostics in newborns

A comparative analysis of the clinical and functional state of patients suffering from arterial hypertension is given, depending on the localization of vascular stenosis of atherosclerotic origin. It is shown that stenosing atherosclerosis often affects men with hypertension. Lesions of the brachiocephalic arteries and renal arteries in patients suffering from arterial hypertension are detected at a younger age than with other localizations. Patients suffering from lesions of the coronary and brachiocephalic arteries are characterized by the presence of concentric left ventricular myocardial hypertrophy and hyperlipidemia. In patients suffering from damage to the renal arteries, leg arteries, and multivascular pathology, myocardial hypertrophy is eccentric, in addition, they have atherogenic dyslipidemia and significant signs of renal dysfunction. An excessive decrease in blood pressure at night is most often recorded in people suffering from coronary atherosclerosis, and its excessive increase in patients suffering from damage to the arteries of the legs. Arterial hypertension in patients with stenosing atherosclerosis in most cases is well-mediated, however, with stenosis of the renal arteries and with multivascular lesions, it is less likely to achieve a level of «normal» or «high normal» systolic blood pressure than with damage to other vascular pools. Significant differences in the levels of both systolic and diastolic blood pressure in all comparison groups indicate a different effect of local hemodynamic disturbances on systemic blood pressure.

Left ventricular hypertrophy - is one of the most frequent structural changes in the heart. This article is devoted to the assessment of modern views on the causes of myocardial hypertrophy of the donor heart, indications and contraindications for the heart trans‑ plantation, the outlook of expanding the pool of effective donors through the use of these hearts. Here are considered the issues of post-transplantation remodeling of the donor heart myocardium, The pathogenesis features, the nascence risk and possibilities of drug regulation of the transplanted heart's myocardial hypertrophy of the left ventricle.

Rationale and Objectives Diagnosis of cardiac amyloidosis (CA) on cardiac magnetic resonance (CMR) can be challenging and quantitative indexes are relevant to further characterize the myocardium. We hypothesize that the relative myocardial enhancement measured from pre and post contrast cine imaging provides diagnostic information for CA in the setting of left ventricular hypertrophy (LVH). Materials and Methods Patients with LVH referred to our center and control subjects with normal CMR were retrospectively included. Percentage of myocardial enhancement (percentage ME) was obtained from pre and post contrast (5 minutes) cine sequences. Post contrast myocardial T1 and LGE extent were also recorded. Results Twenty-one patients with CA, 25 patients with non-amyloid left ventricular myocardial hypertrophy (CH) and 20 controls with normal CMR were analyzed. Percentage ME was significantly higher in CA patients (200% (174–238)) than in CH patients (122% (88–151); p = 0.0001) and control patients (104% (90–149); p = 0.0001). Percentage ME was significantly correlated with the LGE extent (Rho Spearman coefficient = 0.66; p = 0.0001) and with the post contrast myocardial T1 (Rho Spearman coefficient = −0.61; p = 0.0001). With a cutoff value of 152%, the sensitivity and specificity of percentage ME for detection of CA were 90% and 80%, respectively. Conclusion Percentage ME obtained from pre and post contrast cine imaging is correlated to LGE extent and myocardial T1 and may represent an additional diagnostic parameter to consider CA in patients with LVH.

Objective: To study the effect of intense physical exertion on the normal physiology of the left ventricle (LV).Material and Methods. 146 professional athletes underwent a non-invasive assessment of LV systolic deformity in various directions. As a control group, 22 bowling athletes were surveyed.Results. In cyclists, eccentric hypertrophy of the LV myocardium was detected in 31.7% of men and in 29.5% of women. The values of global longitudinal strain were below 18% in male athletes from the cycling-BMX and cycling-highway groups (17.70±2.40% and 17.50±2.39%, respectively). Indicators of circular apical and circular global deformation were significantly lower in the group of cycling-BMX (men) compared with the corresponding values in the bowling group (14.50±6.23% and 14.70±6.42%; 18.40±6.32% and 16.90±6.43%, respectively, p

Introduction Improved myocardial contractility is a critical circulatory adaptation to exercise training. However, the types of exercise that enhance left ventricular (LV) contractile and diastolic functions have not yet been established. This study investigated how high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) influence LV mechanics during exercise. Methods Fifty-four healthy sedentary men were randomized to engage in either HIIT (3-min intervals at 40% and 80% of V˙O2max, n = 18) or MICT (sustained 60% of V˙O2max, n = 18) for 30 min·d, 5 d·wk for 6 wk or to a control group (n = 18) that did not engage in exercise intervention. LV mechanics during semiupright bicycle exercise tests were measured by two-dimensional speckle-tracking echocardiography. Results Before the interventions, acute bicycle exercise increased (i) peak basal/apical radial and circumferential and peak longitudinal strains and strain rates, (ii) peak basal/apical rotations and torsion, and (iii) peak systolic twisting and early diastolic untwisting velocities in the LV. After the interventions, the HIIT group exhibited greater LV mass and diastolic internal diameter as well as higher ratio of E wave to A wave and early diastolic propagation velocity than did the MICT group. Despite decreased peak apical rotation and torsion, HIIT enhanced peak apical radial strain and strain rate as well as shortened the time to reach peak untwisting velocity in the LV during exercise. However, the LV mechanics during exercise were unchanged in the control group. Conclusion HIIT but not MICT induces eccentric myocardial hypertrophy. Moreover, HIIT effectively improves the LV mechanics during exercise by increasing contractile and diastolic functions.

Shear wave (SW) imaging is a novel ultrasound-based technique for assessing tissue characteristics. SW elasticity may be useful to assess the severity of hypertensive left ventricular (LV) hypertrophy. This study aimed to evaluate the efficacy of SW elasticity for assessing the degree of myocardial hypertrophy using hypertensive rats. Rats were divided into hypertension group and control group. SW elasticity was measured on the excised heart. Myocardial hypertrophy was assessed histologically. LV weight was greater in hypertension group. An increase in interventricular septum and LV free wall thicknesses was observed in hypertension group. SW elasticity was significantly higher in hypertension group than in control group (14.6 ± 4.3 kPa vs. 6.5 ± 1.1 kPa, P 2 vs. 243 ± 14 µm2, P

AimTo evaluate the ability of single heartbeat fast-strain encoded (SENC) cardiovascular magnetic resonance (CMR) derived myocardial strain to discriminate between different forms of left ventricular (LV) hypertrophy (LVH).Methods314 patients (228 with hypertensive heart disease (HHD), 45 with hypertrophic cardiomyopathy (HCM), 41 with amyloidosis, 22 competitive athletes, and 33 healthy controls) were systematically analysed. LV ejection fraction (LVEF), LV mass index and interventricular septal (IVS) thickness, T1 mapping and atypical late gadolinium enhancement (LGE) were assessed. In addition, the percentage of LV myocardial segments with strain ≤ − 17% (%normal myocardium) was determined.ResultsPatients with amyloidosis and HCM exhibited the highest IVS thickness (17.4 ± 3.3 mm and 17.4 ± 6 mm, respectively, p 2, p %normalmyocardium = 1.0, 95%CI = 0.85–1.0) and athletes vs. HHD (sensitivity = 83%, specificity = 75%, AUC%normalmyocardium = 0.85, 95%CI = 0.78–0.90). Combining %normal myocardial strain with atypical LGE provided high accuracy also for the differentiation of HHD vs. HCM (sensitivity = 82%, specificity = 100%, AUCcombination = 0.92, 95%CI = 0.88–0.95) and HCM vs. amyloidosis (sensitivity = 83%, specificity = 100%, AUCcombination = 0.83, 95%CI = 0.60–0.96).ConclusionFast-SENC derived myocardial strain is a valuable tool for differentiating between athletes vs. HCM and athletes vs. HHD. Combining strain and LGE data is useful for differentiating between HHD vs. HCM and HCM vs. cardiac amyloidosis.

The heart regeneration after apical resection and myocardial infarction in neonatal mice has been studied for years. However, the response of neonatal mouse heart under pressure overload is seldom explored. This study aimed to induce pressure overload in neonatal mice through a transverse aortic constriction (TAC) with different-gauge needles so as to investigate the effect of pressure overload on cardiomyocyte proliferation and hypertrophy in these mice. Myocardial hypertrophy was evaluated by echocardiographic, pathological, and molecular analyses. Cardiomyocyte proliferation was detected by immune-staining of phospho-histone H3, Ki67, and 5-bromo-2-deoxyuridine. Mild pressure overload induced with a 30-gauge needle stimulated cardiomyocyte proliferation, adaptive hypertrophy, and angiogenesis. The heart function was not hampered even 21 days after the surgery. Moderate pressure overload induced with a 32-gauge needle led to pathological myocardial hypertrophy, fibrosis, and heart failure 7 days after the surgery. The gene and protein expression levels of markers of hypertrophy and fibrosis increased in 32-gauge TAC group compared with that in sham and 30-gauge TAC groups. The mice barely survived after severe pressure overload induced with a 34-gauge needle. The findings of this study might provide new insights into cardiomyocyte proliferation and hypertrophy in neonatal mice under pressure overload.

The QRS-T angle, as an index of non-invasive cardioelectric vector, is closely related to the change of heart structure and function. There are different methedologies to measure the QRS-T angle, which can be roughly dividedinto two types: plane angle and space angle. Studies show that the influence factors include two aspects of physiology and pathology of the angle, in pathological ways, the disease such as myocardial hypertrophy, myocardial ischemia, hypertension, ventricular arrhythmia has larger clinical significance. In recent years, the research on the risk stratification of the QRS-T angle on sudden death has made great progress, but there are still some disputes about whether the space angle can be replaced by the plane angle and the range of normal value and so on.

Based on twice transverse aortic constrictions (TACs) in mice, it is proved that myocardial hypertrophic preconditioning (MHP) could attenuate cardiomyocyte hypertrophy and slow down progression to heart failure. For novices, however, the MHP model is usually quite difficult to establish because of the technical obstacles in ventilator operation, opening the chest repeatedly, and bleeding caused by debanding. To facilitate this model, to increase the surgical success rate and to reduce the incidence of bleeding, we switched to absorbable sutures for the first TAC combing with a ventilator-free technique. Using a 2-week absorbable suture, we demonstrated that this procedure could cause significant myocardial hypertrophy in 2 weeks; and 4 weeks after surgery, myocardial hypertrophy was almost completely regressed to the baseline. Using this protocol, the operators could master the MHP model easily with a lower operation mortality.

AimTo study the association between the life-course accumulation of health deficits and later-life heart size and function using data from the 1946 National Survey of Heath and Development (NSHD) British birth cohort, the world’s longest running birth cohort with continuous follow-up.Methods and ResultsA multidimensional health deficit index (DI) looking at 45-health deficits was serially calculated at 4 time periods of the life-course in NSHD participants (0-16, 19-44, 45-54 and 60 to 64 years), and from these the mean and total DI for the life-course was derived (DImean, DIsum). The step change in deficit accumulation from one time period to another was also calculated. Echocardiographic data at 60-64 years provided: ejection fraction (EF), left ventricular mass indexed to body surface area (LVmassi, BSA), myocardial contraction fraction indexed to BSA (MCFi) and E/e’. Generalized linear models assessed the association between DIs and echocardiographic parameters after adjustment for sex, socio-economic position and body mass index.1,375 NSHD participants were included (46.47% male). For each single new deficit accumulated at any one of the 4 time periods of the life-course, LVmassi increased by 0.91-1.44% (pi decreased by 0.6-1.02% (ppp13.ConclusionThe accumulation of health deficits at any time period of the life-course associates with a maladaptive cardiac phenotype in older age, dominated by myocardial hypertrophy and poorer function. The burden of health deficits appears to strain the myocardium potentially leading to future cardiac dysfunction.

Funding Acknowledgements Sigrid Juselius Foundation, Finnish Foundation for Cardiovascular Research, Aarne Koskelo Foundation, The Finnish Medical Foundation Background Coronary artery disease (CAD) is the most common underlying cause of sudden cardiac death (SCD). Cardiac hypertrophy with varying amount of myocardial fibrosis is a common risk factor for CAD related SCD especially in young SCD victims where severity of CAD seems not to entirely explain the cause of SCD. Purpose The aim was to study the genetic background of hypertrophy and fibrosis among young, ischemic SCD victims with single vessel CAD. Methods The study population was derived from the Fingesture study consisting of all autopsy-verified sudden cardiac deaths in Northern Finland between years 1998-2017 (n = 5,869). CAD was determined to be the cause of SCD in 4,392 victims (74.8%). We carried out targeted next-generation sequencing using a panel of 174 genes associated with myocardial structure and ion channel function in 95 ischemic-SCD victims (mean [standard error] age, 63.6 [1.06] years; 88.4% males) with single-vessel CAD and cardiac hypertrophy in the absence of previously diagnosed CAD, and whose DNA passed the quality control for further analysis. Assessment for pathogenicity of detected variants was based on American College of Medical Genetics consensus guidelines. Results A total of 43 variants were detected in 43 of the study subjects (45.3 %). Five variants in eight subjects (8.4%) were classified as pathogenic or likely pathogenic. We observed 38 variants of uncertain significance in 39 victims (40.6 %). Variants were detected in myocardial structure protein coding genes, associated with arrhythmogenic right ventricular cardiomyopathy (13 variants), dilated cardiomyopathy (16 variants), hypertrophic cardiomyopathy (6 variants) and left ventricular non-compaction cardiomyopathy (3 variants). Five variants were detected in RYR2 associated with both cardiomyopathies and catecholaminergic polymorphic ventricular tachycardias. Seven variants were detected in multiple unrelated subjects. None of the subjects presented characteristic autopsy findings related to cardiomyopathies. Conclusions Variants associated with cardiomyopathies were common findings among CAD related SCD victims with single vessel disease and myocardial hypertrophy found at autopsies, suggesting that these variants may modulate the risk for fatal arrhythmias and sudden death in ischemic disease.

ObjectiveWith increasing age, the prevalence of aortic stenosis grows exponentially, increasing left heart pressures and potentially leading to myocardial hypertrophy, myocardial fibrosis and adverse outcomes. To identify patients who are at greatest risk, an outpatient model for risk stratification would be of value to better direct patient imaging, frequency of monitoring and expeditious management of aortic stenosis with possible earlier surgical intervention. In this study, a relatively simple model is proposed to identify myocardial fibrosis in patients with a diagnosis of moderate or severe aortic stenosis.DesignPatients with moderate to severe aortic stenosis were enrolled into the study; patient characteristics, blood work, medications as well as transthoracic echocardiography and cardiovascular magnetic resonance were used to determine potential identifiers of myocardial fibrosis.SettingThe Royal Brompton Hospital, London, UKParticipantsOne hundred and thirteen patients in derivation cohort and 26 patients in validation cohort.Main outcome measuresIdentification of myocardial fibrosis.ResultsThree blood biomarkers (serum platelets, serum urea, N-terminal pro-B-type natriuretic peptide) and left ventricular ejection fraction were shown to be capable of identifying myocardial fibrosis. The model was validated in a separate cohort of 26 patients.ConclusionsAlthough further external validation of the model is necessary prior to its use in clinical practice, the proposed clinical model may direct patient care with respect to earlier magnetic resonance imagining, frequency of monitoring and may help in risk stratification for surgical intervention for myocardial fibrosis in patients with aortic stenosis.

Hypertension is a major risk factor for the development of atherosclerosis. Cardiovascular risk has been reported to be significantly increased in hyperlipidemic patients with hypertension. However, it is not clear whether hypertension can directly destabilize plaques, thereby enhancing cardiovascular events. To examine whether hypertension enhances the development of atherosclerosis and increases plaque vulnerability, we generated hypertensive Watanabe heritable hyperlipidemic (WHHL) rabbits by surgical removal of one kidney and partial ligation of the other renal artery and compared the nature of aortic and coronary atherosclerosis in hypertensive WHHL rabbits with normotensive WHHL rabbits. All hypertensive WHHL rabbits died from 34 to 56 weeks after surgery, whereas no normotensive WHHL rabbits died. Pathologic examinations revealed that hypertensive WHHL rabbits showed different degrees of myocardial infarction caused by severe coronary stenosis along with myocardial hypertrophy. Furthermore, aortic lesions in hypertensive WHHL rabbits exhibited a higher frequency of intraplaque hemorrhage and vulnerable plaques than those in normotensive WHHL rabbits. These results indicate that hypertension induced by the surgical removal of one kidney and partial ligation of the other renal artery method in WHHL rabbits may not only enhance the development of atherosclerosis but also destabilize the plaques, increasing cardiac death.

Objective The purpose of this article is to review how cardiac MRI provides the clinician with detailed information about the hypertrophic cardiomyopathy (HCM) phenotypes, assessing its morphological and functional consequences. Conclusion An understanding of cardiac MRI manifestations of HCM phenotypes will aid early diagnosis recognition and its functional consequences. Teaching Points • The phenotypic variability of HCM expands beyond myocardial hypertrophy, to include morphological and functional manifestations, ranging from subtle anomalies to remodelling of the LV with progressive dilatation and thinning of its wall. • The stages of HCM, which are based on the clinical evidence of disease progression, include subclinical HCM, the classic HCM phenothype, adverse remodelling and overt dysfunction, or end-stage HCM. • Cardiac MRI provides the clinician with detailed information regarding the HCM phenotypes and enables the assessment of its functional consequences.

Objectives The purpose of this article is to describe the key cardiac magnetic resonance imaging (MRI) features to differentiate hypertrophic cardiomyopathy (HCM) phenotypes from other causes of myocardial thickening that may mimic them. Conclusions Many causes of myocardial thickening may mimic different HCM phenotypes. The unique ability of cardiac MRI to facilitate tissue characterisation may help to establish the aetiology of myocardial thickening, which is essential to differentiate it from HCM phenotypes and for appropriate management. Teaching points • Many causes of myocardial thickening may mimic different HCM phenotypes. • Differential diagnosis between myocardial thickening aetiology and HCM phenotypes may be challenging. • Cardiac MRI is essential to differentiate the aetiology of myocardial thickening from HCM phenotypes.

The article presents current knowledge of рro- and antihypertensive mechanisms involved in the development of hypertension (HTN), and antihypertensive management strategies. Particular attention is paid to the angiotensin converting enzyme inhibitor lisinopril and thiazide-like diuretic indapamide. The mechanisms and effects are described. The paper discusses the results of multicenter randomized clinical trials, and the antihypertensive effects of lisinopril and indapamide and their impact on myocardial hypertrophy in hypertensive patients. The potential advantages of fixed combination of lisinopril and indapamide in the treatment of patients with HTN are also discussed.

The aim of the study is to assess the compliance of the results of electrocardiographic (ECG) and echocardiographic diagnostic methods of hypertrophy of left ventricular myocardium (LVH) with the postmortem finding of measurement of left ventricular myocardium mass (LVM). Materials and methods. We examined the data of intravital study of anthropometric measurements [age, height, weight, body mass index (BMI)], instrumental results [12-lead ECG, EchoCG], as well as the postmortem finding (direct measurement of LVM at autopsy) in 15 patients of general therapy department. While analyzing ECG we studied as conventional ECG criteria for the detection of LVH as well as the author's own criteria based on two models (regression and discriminant analyses), including voltage, sex and age criteria. Echocardiographic diagnostic method used to calculate LVM (according to ASE formula) and left ventricular mass index (LVMI). Postmortem finding of LVM was carried out according to the standard measurement method. According to the absence of the single conventional postmortem finding of measurement of LVH, we considered three different variants of the postmortem finding of LVH: the criterion of K. Bove et al. (CB); the criterion of A.M. Lifshitz, also called ventricular index (VI) and the criterion of P. Casale - the left ventricular mass index at autopsy (LVMI). Results and discussion. Conventional ECG criteria for the detection of LVH showed high specificity (71-100%) using any method of the postmortem finding of measurement, but were characterized by extremely low sensitivity (0-37.5%). Their overall diagnostic accuracy was higher on using K. Bove or A.M. Lifshitz criteria (40-66.7%) and low - on using the criterion of P. Casale (13.3-40%). The author's ECG criteria were less specificity (50-100%) and had higher sensitivity (54-75%), and their diagnostic accuracy remained higher and showed small dependence on the method of the postmortem finding of measurement of LVH (60-66.7%). Conclusion. Usually the ECG criteria to diagnose left ventricular hypertrophy were expectedly showed low sensitivity using any method of the postmortem finding of measurement. Meanwhile, the author's own ECG criteria associated with the most sensitive electrocardiographic characteristics to LVH and sex and age-specific indexes of the examined patients exceeded the conventional ECG criteria in sensitivity and diagnostic accuracy.

BOLD (blood oxygen level dependent) MRI can detect regional condition of myocardial oxygen supply and demand by means of paramagnetic properties.Noninvasive assessment of myocardial oxygenation by BOLD MRI in hypertensive patients with hypertension (HTN) left ventricular myocardial hypertrophy (LVMH) and HTN non-LVMH and its correlation with myocardial mechanics were performed.Prospective.Twenty patients with HTN LVMH, 21 patients with HTN non-LVMH, and 23 normotensive controls were enrolled.Cine imaging, T2* and T1 mapping sequences were achieved at 3.0T.Dedicated T1 mapping, T2*, and cine imaging analysis were performed by two radiologists using cvi42.One-way analysis of variance, Kruskal-Wallis test, Bland-Altman analysis, Pearson's correlation coefficient, Spearman's rank correlation.T2* values of HTN LVMH group were significantly lower versus the controls (23.78 ± 3.09 versus 30.77 ± 2.71; P 0.001) and HTN non-LVMH group (23.78 ± 3.09 versus 28.64 ± 4.23; P 0.001). Left ventricular peak circumferential strain were reduced in HTN LVMH patients compared with other two groups (-11.32 [-15.64, -10.3], -16.78 [-19.35, -15.34], and -19.73 [-20.57, -18.73]; P 0.05); and longitudinal strain of HTN LVMH patients were lower than other two groups (-11.31 ± 2.91, -15.1 ± 3.06, and -18.85 ± 1.85; P 0.05); radial strain of HTN LVMH patients were also lower than other two groups (25.03 ± 16, 40.95 ± 17.5 and 47.9 ± 10.23; P 0.05). Extracellular volume correlated with peak circumferential, longitudinal, and radial strain (spearman rho = 0.6, 0.64, and -0.69; P 0.05), respectively; T2* negatively correlated with peak circumferential and longitudinal strain (spearman rho = -0.43 and -0.49; P 0.05), respectively. Patients with lower T2* values had significant decreases in myocardial mechanics (P 0.05).HTN LVMH patients have both impaired myocardial mechanics and decreased T2* values compared with HTN non-LVMH and normotensive groups. BOLD MRI could provide a feasible assessment modality for detecting altered T2* due to the change of de-oxygenated hemoglobin and hence to the change of signal intensity in oxygenation-sensitive images.1 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2018;47:1297-1306.

The article is focused on the data concerning the influence of ivabradine on myocardial electrophysiology in experimental and clinical studies. It is shown that ivabradine decreases ventricular rate in chronic atrial fibrillation, and prevents the paroxysms of atrial fibrillation. In myocardial hypertrophy patients or in serious chamber dilation, ivabradine shows moderate antiarrhythmic effect on ventricular arrhythmias.

Although the prevalence of arterial hypertension (AH) in athletes is significantly lower than that in the general population, the prevalence of high blood pressure (BP) and increased left ventricular mass in a number of sports with high isometric loads (speed and strength sports) is higher than that in cyclic sports with high aerobic load. Specific risk factors of hypertension in athletes include high intake of sodium, alcohol, caffeine, and a number of illicit drugs, such as erythropoietin, growth hormone, and oral contraceptives in women. The development of athletic heart is determined by training and competitive activity and generally does not lead to the disorders of systolic and diastolic function. However, elevated BP in athletes increases the risk of myocardial hypertrophy and remodeling, which is one of the possible contraindications for sports with high static loads.

// Qiancheng Wang 1, 2 , Zhenhuan Chen 1 , Xiaobo Huang 1 , Lin Chen 1 , Baihe Chen 1 , Yingqi Zhu 1 , Shiping Cao 1 , Wangjun Liao 3 , Jianping Bin 1 , Masafumi Kitakaze 1, 4 and Yulin Liao 1 1 State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China 2 Department of Cardiology, Jiaozuo People's Hospital of Henan Province, Jiaozuo 454000, China 3 Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China 4 Cardiovascular Division of the Department of Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka 565-8565, Japan Correspondence to: Yulin Liao, email: liao18@msn.com Xiaobo Huang, email: chw47922@163.com Keywords: periostin; olmesartan; myocardial hypertrophy; myocardial infarction; fibrosis Received: April 07, 2017 Accepted: December 11, 2017 Epub: December 23, 2017 Published: May 15, 2018 ABSTRACT Either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor 1 blocker (ARB) attenuates cardiac remodeling. However, the overall molecular modulation of the reversing remodeling process in response to the ACEI or ARB treatment is not yet well determined. In this study, we examined whether gene expressions are modulated by ACEI (temocapril), ARB (olmesartan) or both in a murine model with transverse aortic constriction (TAC) and confirm whether periostin is a target gene of olmesartan in mice with myocardial infarction (MI). We detected 109 genes that were significantly up-regulated in TAC mice and a majority of these were down-regulated in response to temocapril, olmesartan or their combination which significantly attenuated cardiac remodeling at one or four weeks. Real-time RT-PCR demonstrated that olmesartan, temocapril or their combination down-regulated the expression of periostin. In MI mice treated with olmesartan for 4 weeks, the left ventricular end-diastolic and systolic dimensions measured with echocardiography were lower, whereas maximum rate of rise and fall rate of LV pressure (±dp/dt max) were greater, and Azan-staining cardiac fibrotic area was smaller. Furthermore, periostin was upregulated in response to MI, whereas olmesartan blocked this upregulation. Post-MI fibrosis was smaller in periostin knockout adult mice than in wildtype mice, while glycogen synthase kinase 3β was increased and cyclin D1 was decreased in periostin knockout mice. These findings indicate that periostin is a target gene of ARB and olmesartan reverses cardiac remodeling at least partially through the downregulation of periostin.

Purpose: To explore the association between the sympathetic system activity and myocardial hypertrophy in patients with essential hypertension. Methods: A total of 84 essential hypertension inpatients were recruited from China-Japan Friendship Hospital between January 2019 and September 2019. Activity of sympathetic system was quantified by plasma metanephrines (MNs) levels. All subjects received an echocardiographic test. Results: The interventricular septum thickness (diastolic), left ventricular mass and left ventricular mass index increased significantly with plasma MNs quartiles, and plasma MNs were positively and significantly correlated with early diastolic transmitral flow velocity to early diastolic mitral annular tissue velocity. Conclusions: In patients with essential hypertension, high level of plasma MNs associates with left ventricular hypertrophy and impaired diastolic function.

Background: Hypertrophic cardiomyopathy is characterized by intrinsic myocardial hypertrophy that is not consequent to hemodynamic stimuli. Infantile hypertrophic cardiomyopathy (

Aim: Circulating microRNA expression has become a biomarker of cardiovascular disease; however, the association of microRNA expression between circulation and myocardium in hypertrophic cardiomyopathy remains unclear. The present study aimed to find a circulating biomarker correlated not only to myocardial expression, but also to cardiac hypertrophy and fibrosis. Method: Forty-two cases of hypertrophic obstructive cardiomyopathy (HOCM) diagnosed by echocardiography and magnetic resonance were analysed for microRNA expression in plasma and myocardial tissue. Results: The results showed that myocardial miR-221 was significantly increased (z = −2.249, P = 0.024) and significantly correlated with collagen volume fraction (CVF) (r = 0.516, P < 0.001), late gadolinium enhancement (LGE) (r = 0.307, P = 0.048), and peripheral circulation (r = 0.434, P = 0.004). Moreover, circulating miR-221 expression was significantly correlated with CVF (r = 0.454, P = 0.002), LGE (r = 0.630, P = 0.004), maximum interventricular septal thickness (MIVST) of echocardiography (r = 0.318, P = 0.042), and MIVST of magnetic resonance (r = 0.342, P = 0.027). The area under the receiver operating characteristic curve of miR-221 was 0.764. Conclusions: Circulating miR-221 is consistent with that in myocardial tissue, and correlated with myocardial fibrosis and hypertrophy. It can be used as a biomarker for evaluating myocardial hypertrophy and fibrosis in HOCM.

Left ventricular hypertrophy is a common adaptive response to increased cardiac workload. Cardiomyocytes growth and increase in contractile force are conditioned by sufficient energy production, which implies appropriate mitochondrial function. The 60kDa heat shock protein (HSP60) is a chaperone essential for mitochondrial proteostasis, but when translocates from mitochondria, it can also act as a potent inflammatory mediator binding to toll-like receptors (TLRs). In this study, we aimed to compare the expression pattern of HSP60, TLR2, and TLR4 in hypertrophic vs non-hypertrophic, normal human myocardium. We further examined whether HSP60 in situ binds to TLRs in hypertrophic myocardial tissue. In addition, expression of activated downstream targets of TLR 2/4 pathways was also evaluated. For this purpose, immunohistochemical expression analyses were performed on myocardial tissue samples obtained during the autopsy of human subjects in which left ventricular hypertrophy was the only cardiopathological finding and had died from sudden cardiac death, as well as from the subjects without any cardiac pathology, that died by unnatural death (accident or suicide). Double immunofluorescence was used to examine HSP60 translocation, while proximity ligation assay (PLA) was performed to assess HSP60 and TLRs interactions. Hypertrophic myocardium showed significantly higher expression of HSP60, TLR2, and TLR4 compared to normal myocardium. Furthermore, in hypertrophic cardiomyocytes, we found membrane translocation of HSP60 and signs of HSP60/TLR interactions. Conclusion: The obtained data point to an important supportive role of HSP60 in adaptive cardiomyocytes growth, while concomitant induction of TLR2 and TLR4 candidates HSP60-TLRs interactions as an early events duriing pathogenesis of secondary complications consequently to the left ventricular hypertrophy.

Introduction Degenerative aortic valve presents distinct patterns according to gender. Inappropriate myocardial hypertrophy in response to severe aortic stenosis (AS) and their clinical repercussions is of recent interest. Purpose To evaluate the influence of gender on the pattern of ventricular remodelling in patients with AS and inappropriate ventricular hypertrophy. Methods Retrospective study, analysing clinical and echocardiographic characteristics of 145 patients, between 2008 and 2018, with severe aortic stenosis and inappropriate ventricular hypertrophy, defined as septal wall thickness greater than 14 mm. Results Women were 42% of the patients, with higher mean age compared to men (75.23±12.78 vs 70.01±12.59 years, p=0.01), lower body surface (1.68±0.17 vs 1.94±0.68 m2, p=0.004), lower ventricular volumes (94.33±32.88x3856±23.81 vs 122.68±43.24x50.34±28.10 ml/m2, p Conclusions Septal wall thickness indexed by body surface and difference between septum and the posterior wall in ventricles with smaller volumes suggest that myocardial hypertrophy in response to severe AS is more severe in women than in men. Since inappropriate myocardial hypertrophy is a predictor of outcomes in AS, it is possible that the optimal timing for valve replacement should be earlier in women.

Introduction Myocardial creatine kinase (CK) activity represents an important metabolic reserve: it correlates closely with contractile reserve and post-ischaemic function, keeps cytosolic [ADP] low, and optimises the free energy for ATP hydrolysis. It may also contribute to the transition to failure in the heart hypertrophied by chronic haemodynamic overload; modest up-regulation has been shown to be cardio-protective. Total CK activity measurement requires chemical freeze-and-extract methods, which destroy tissue, precluding repeated measures. To date, non-invasive assessments of human myocardial CK flux (calculated as kf × [PCr], where kf is the pseudo-first-order forward rate constant measured by 31P-magnetic resonance spectroscopy (MRS) have not assessed creatine content or total CK activity. Thus we aimed to validate kf measurement against total CK activity and investigate predictors of CK activity. Methods 39 subjects (median age 71, range 43–84) undergoing clinically indicated cardiac surgery had CK total activity measured from LV biopsy. 31 had severe AS (10 with impaired LVEF); 2 had severe primary MR; 5 had severe mitral stenosis (2 with impaired LVEF) and 1 had an LA mass. 35 of 39 contributed triplicate datasets: CK total activity, kf (31P-MRS TRiST sequence at 3T) and LV volumes (cine-MRI, 3T Siemens). 27 had severe AS (8 with impaired LVEF); other groups were the same. Exclusion criteria were prior myocardial infarction and flow-limiting coronary disease. Flash-frozen LV biopsies obtained within 15 min of cardiopulmonary bypass were analysed for CK total activity, total creatine, and citrate synthase (CS) activity (a marker of oxidative phosphorylation capacity). Results Multiple, novel correlations were observed between CK total activity (IU/mg protein) and CS activity (r=0.87, p=9e-13), total creatine (r=0.59, p=8e-5), kf (r=0.42, p=0.013), total creatine × kf (r=0.64, p=4e-5), LVESVi (r=−0.52, p=8e-4), LVEF (r=0.48, p=0.002) and LVMi (r=−0.42, p=0.009) (Panels A-E) (LVEDVi and non-indexed counterparts were also significant correlates.) The most predictive linear regression model incorporating elements of the CK rate equation included total creatine (nmol/mg protein), kf (/s), and kf × LVESVi (ml/m2) (adjusted R2=0.56, beta=0.426, 0.618, −1.968 and p=0.001, 5e-5, 0.003 respectively, Panel F). Figure 1 Conclusions These results are the first evidence of agreement between non-invasive estimates of human cardiac CK activity (kf) and freeze-extracted chemical methods. The key original finding is that it is feasible to attempt to predict CK capacity in vivo by using a combination of techniques (creatine by 1H MRS, CK kf by 31P-MRS and LVESVi by cine imaging). The key insight is that CK capacity is best estimated not simply from what the rate equation would predict (creatine and kf), but that other factors relating to failing contractility reduce CK activity independently from creatine content and enzyme kf. Acknowledgement/Funding British Heart Foundation Clinical Research Training Fellowship (FS/15/80/31803) and Programme Grant (RG/18/12/34040).