Do we recognize obesity as an important hemodynamic, morphologic and cardiometabolic factor in echocardiographic evaluation?

Obesity has become a global public health issue. Cardiac adaptation to obesity includes structural and functional changes of the heart. Anatomic and biomolecular characteristics of adipose tissue present it as an endocrine organ with neurohumoral adipokines activity. However, fat tissue differs according to embryologic origin, anatomic localization, gender and biomolecular properties. Qualitative and quantitative echocardiographic evaluation in obese patients can be crucial for detecting cardiometabolic risk factors. Increased adipose mass causes functional and morphological changes of the heart. Increased body fat and body surface area are associated with increased blood volume, ventricle preload, resting output and stroke volume; supranormal systolic function and possible aortic root dilatation; abnormal left and right ventricle geometry, as a result of compensatory wall hypertrophy regarding pressure or volume overload; enlarged left and right ventricular end-diastolic diameter and elevated end-diastolic volume; and increased left atrium area and volume. Using indexed parameters in echo analysis in obese patients are recommended. Early detection of obesity related cardiovascular abnormalities may be useful in the future for patient management. Particularly, strain echo acts as a technique for the early detection of subclinical changes of the left ventricle in obese patients, while epicardial adipose tissue is the newest echo detector of cardiac visceral fat as a cardiometabolic and right ventricle remodeling risk factor. Routine clinical echo practice in obese patients can be limited by technical factors, especially right heart morphologic and functional measurements. However, contrast and transesophageal echocardiography offers additional methods for cardiac structure visualization.1-

Obesity related cardiomyopathy

Pretilost predstavlja svjetski epidemijski i veliki zdravstveni problem osobito otkako se povezuje s metaboličkim, kardijalnim i vaskularnim komplikacijama. Prema posljednjim istraživanjima, ektopično visceralno masno tkivo je važan prediktor razvoja kardiovaskularnih bolesti i inzulinske rezistencije, značajnije nego ukupno akumulirano masno tivo. Kardijalno visceralno masno tkivo čine intratorakalne, epikardijalne i intramiokardijalne masne stanice, koje su povezane i s konvencionalni kardiovaskularnim čimbenicima rizika. Adipociti su aktivane endokrine stanice koje produciraju mnogobrojne adipocitokemokine. Leptin i adiponektin su adipokini sa značajnom ulogom u razvoju kardiovaskularnih bolesti, uključujući aterosklerotske procese, hipertrofiju kardiomiocita i remodelaciju miokardnog ekstracelularnog matriksa. U stanju pretilosti koncentracija cirkulirajućeg protektivnog adiponektina je snižena, dok je koncentracija leptina povišena. Zajedno, hipoadiponektinemija i hiperleptinemija imaju proaterosklerotski i proupalni učinak, djelujući na hipertrofični signal u kardiomiocitima putem kompleksnih mehanizama. Može se zaključiti da pretilost, ektopično kardijalno masno tkivo i adipokini utječu na lokalne i sistemske, metaboličke i mehaničke promijene kardiovaskularnog sustava s patohistološkim i patofiziološkim promijenama kardiomiocita i miokarda. Rezultat svih promjena je razvoj debljinom uzrokovane kardiomiopatije s poremećajem miokardijalne relaksacije i dijastoličke funkcije.Obesity is becoming a worldwide epidemic and a major health problem, since its presence is associated with significant adverse effects on health including metabolic, cardiac and vascular complications. According to latest research, ectopic visceral fat accumulation is an important predictor of diseases, particularly of cardiovascular diseases and insulin resistance, carrying more risk than general fat accumulation. Cardiac ectopic fat includes fat deposition around the heart (epicardial and intrathoracic fat) and intra-myocardial fat cells. All ectopic fat depots are related to conventional risk factors for cardiovascular diseases. Adipocytes act as an endocrine organ, producing number of adipocytokemokines. Leptin and adiponectin are adipokines with significant role in development of cardiovascular diseases, including atherosclerosis, cardiac hypertrophy and myocardial extracellular matrix remodeling. The level of circulating protective adiponectin is decreased while leptin level is increased in obese patients. Hypoadiponectinemia and hyperleptinemia have proatherosclerotic and proinflammatory effects inducing hypertrophic signal in cardiomyocytes via complex mechanisms. It can be concluded that obesity, cardiac fat, inflammation and adipokines changes contribute to local and systemic, metabolic and mechanical changes in cardiovascular system, with pathohistological and pathophysiological changes of cardiomyocytes and myocardium. Result of all these changes is obesity related cardiomyopathy with disturbances of myocardium relaxation and diastolic dysfunction

Obesity related cardiomyopathy

Pretilost predstavlja svjetski epidemijski i veliki zdravstveni problem osobito otkako se povezuje s metaboličkim, kardijalnim i vaskularnim komplikacijama. Prema posljednjim istraživanjima, ektopično visceralno masno tkivo je važan prediktor razvoja kardiovaskularnih bolesti i inzulinske rezistencije, značajnije nego ukupno akumulirano masno tivo. Kardijalno visceralno masno tkivo čine intratorakalne, epikardijalne i intramiokardijalne masne stanice, koje su povezane i s konvencionalni kardiovaskularnim čimbenicima rizika. Adipociti su aktivane endokrine stanice koje produciraju mnogobrojne adipocitokemokine. Leptin i adiponektin su adipokini sa značajnom ulogom u razvoju kardiovaskularnih bolesti, uključujući aterosklerotske procese, hipertrofiju kardiomiocita i remodelaciju miokardnog ekstracelularnog matriksa. U stanju pretilosti koncentracija cirkulirajućeg protektivnog adiponektina je snižena, dok je koncentracija leptina povišena. Zajedno, hipoadiponektinemija i hiperleptinemija imaju proaterosklerotski i proupalni učinak, djelujući na hipertrofični signal u kardiomiocitima putem kompleksnih mehanizama. Može se zaključiti da pretilost, ektopično kardijalno masno tkivo i adipokini utječu na lokalne i sistemske, metaboličke i mehaničke promijene kardiovaskularnog sustava s patohistološkim i patofiziološkim promijenama kardiomiocita i miokarda. Rezultat svih promjena je razvoj debljinom uzrokovane kardiomiopatije s poremećajem miokardijalne relaksacije i dijastoličke funkcije.Obesity is becoming a worldwide epidemic and a major health problem, since its presence is associated with significant adverse effects on health including metabolic, cardiac and vascular complications. According to latest research, ectopic visceral fat accumulation is an important predictor of diseases, particularly of cardiovascular diseases and insulin resistance, carrying more risk than general fat accumulation. Cardiac ectopic fat includes fat deposition around the heart (epicardial and intrathoracic fat) and intra-myocardial fat cells. All ectopic fat depots are related to conventional risk factors for cardiovascular diseases. Adipocytes act as an endocrine organ, producing number of adipocytokemokines. Leptin and adiponectin are adipokines with significant role in development of cardiovascular diseases, including atherosclerosis, cardiac hypertrophy and myocardial extracellular matrix remodeling. The level of circulating protective adiponectin is decreased while leptin level is increased in obese patients. Hypoadiponectinemia and hyperleptinemia have proatherosclerotic and proinflammatory effects inducing hypertrophic signal in cardiomyocytes via complex mechanisms. It can be concluded that obesity, cardiac fat, inflammation and adipokines changes contribute to local and systemic, metabolic and mechanical changes in cardiovascular system, with pathohistological and pathophysiological changes of cardiomyocytes and myocardium. Result of all these changes is obesity related cardiomyopathy with disturbances of myocardium relaxation and diastolic dysfunction

Hyperleptinemia – Non-Haemodynamic Risk Factor for the Left Ventricular Hypertrophy Development in Hypertensive Overweight Females

Obesity is directly and strongly associated with hypertension and left ventricular hypertrophy (LVH). Development of LVH is multifactorial, caused both by haemodynamic and non-haemodynamic factors. Hypertension is the main haemodynamic factor. Humoral mechanisms, as a non-haemodynamic factor for LVH development, have not been completely explained. The aim of this study is to determine whether hyperleptinemia can be one of humoral – non-haemodynamic factor inducing LVH together with haemodynamic factors in overweight females. The study was done on thirty six adult, overweight female patients, body mass index in range 25–30 kg/m2. Patients are nondiabetic with regular renal function. Twenty one female patients were hypertensive with left ventricular hypertrophy. Control group included fifteen hypertensive female patients without left ventricular hypertrophy. In all patients was determined glucose profile and creatinine clearance, cholesterol, triglycerides, LDL, HDL.Weight, high, circumference of the waist and hips was taken. Cardiovascular determination was done applying two-dimensional ultrasound. Serum leptin level was measured using radioimmunoassay method (RIA). Results showed that serum leptin level was significantly higher in hypertensive, overweight females with LVH. This suggests that non-haemodynamic factors, such as hyperleptinemia, participate in left ventricular hypertrophy development together with haemodynamic factors in adult hypertonic, overweight females

Prognostic Indicators for First and Repeated Hospitalizations in Heart Failure Patients with Reduced Left Ventricular Ejection Fraction

Heart failure with reduced ejection fraction (HFrEF) is a progressive clinical syndrome defined by changes in the myocardial structure, which lead to predominant systolic myocardial function impairment, with a left ventricle ejection of fraction ≤40%. The rehospitalization burden in HFrEF patients (pts) remains very high, with poor quality of life, increased mortality and large healthcare expenditures. In this research project, we investigated the risk factors for first and repeated hospitalization in pts with HFrEF. This retrospective study included 50 adult pts with a diagnosis of HFrEF and who were within the age range of 55 to 89 years old and of both sexes. Demographic and clinical data (HFrEF etiology, renal function parameters, complete blood count, markers of inflammation, electrocardiogram, troponin I, NTproBNP, echocardiographic parameters and comorbidities data) were collected from the pts’ medical histories. Statistical analysis was performed via Fischer’s exact test, the Shapiro-Wilk test and the Spearman correlation coefficient. This study included 70% male and 30% female HFrEF pts. Males were younger in both group of pts and had a higher incidence of rehospitalization. The most important HFrEF etiologic risk factors are arterial hypertension (82%), coronary heart disease (54%), atrial fibrillation (52%) and diabetes mellitus (40%). The most important noncardiac comorbidity related with the first HFrEF hospitalization is pneumonia (P=0.03), while progression of left ventricle systolic and diastolic dysfunction is related to rehospitalization risk (left ventricle end systolic diameter, P=0.003; diastolic dysfunction degree, P=0.04). The troponin level was associated with an increased risk of rehospitalization, but this was not statistically significant at this sample size (troponin I, p=0.10). Following the first and repeated hospitalizations of HFrEF pts, comorbidities, ageing and gender difference are crucial to HFrEF development, while echocardiographic parameters and biomarkers critically affect HFrEF rehospitalization risk

Pojavnost intramiokardijalnih masnih stanica u stijenci desne pretklijetke i desne klijetke – postmortalna humana analiza

Histologic and radiologic studies describe intramyocardial fat tissue as a normal finding or as part of cardiac pathology. The role of fat cells within the myocardium is not fully understood. The aim of this study was to assess fat tissue distribution in the myocardium of right atrium (RA) and right ventricle (RV) and age differences in subjects free from cardiac disease. The study included 10 males without cardiac disease divided into two groups according to age (below/above 50 years). Three cross sections were performed (RV free wall and apex and RA free wall) with histomorphological analysis on digital photographs. The shares of total myocardial fat (TMF), perivascular fat (PVF) and non-perivascular (nPVF) fat were calculated. Samples from the older group had larger amounts of fat in the epicardium and myocardium, without statistically significant difference (TMF p=0.847, PVF p=0.4 and nPVF p=0.4). The largest quantities of fat tissue were found in the RV apex samples (14.9%), followed by RV free wall (7.5%) and RA (4.5%), where total apical RV fat share was significantly larger than in RA sample (p=0.044). Intramyocardial fat cells were present within the non-diseased RA and RV in all samples, mostly in the apex. Further investigations on age difference, effect of visceral obesity and sex differences are needed.Dosadašnja histološka i radiološka istraživanja opisuju pojavnost intramiokardijalnog masnog tkiva kao dio normalnog nalaza ili kao dio patološkog nalaza srca. Uloga intramiokardijalnih masnih stanica nije još razjašnjena. Cilj ovoga istraživanja bio je utvrditi raspodjelu masnog tkiva u miokardu desne pretklijetke (DP) i desne klijetke (DK) ovisno o dobi i lokalizaciji kod ispitanika bez kardijalnog morbiditeta. Patohistološka postmortalna studija uključila je 10 muškaraca bez kardijalnih bolesti podijeljenih u dvije skupine prema dobi (ispod/iznad 50 godina). Uzorci su uzeti u tri presjeka (projekcija slobodnog zida DK, slobodni zid vrha DK te stijenka DP) s histomorfološkom analizom na digitalnim fotografijama. Izračunati su udjeli ukupnog masnog tkiva unutar srčanog mišića (UMT), perivaskularnog masnog tkiva (PMT) i ne-perivaskularnog masnog tkiva (nPMT). U uzorcima starijih ispitanika prisutna je veća količina masnog tkiva u epikardu i miokardu, bez statistički značajne razlike (UMT p=0,847, PMT p=0,4, nPMT p=0,4). Najveće količine masnog tkiva pronađene su u uzorcima vrha DK (14,9%), nakon čega slijedi stijenka slobodnog zida DK (7,5%) i DP (4,5%), gdje je ukupni udio masnog tkiva DK bio znatno veći nego kod uzorka DP (p=0,044). Intramiokardijalne masne stanice sastavni su dio histološkog nalaza DP i DK u svim uzorcima bez prisutnih kardijalnih bolesti, dominantno u vrhu DK. Neophodna su daljnja istraživanja utjecaja dobi, spola i visceralne pretilosti na pojavnost intramiokardijalnih masnih stanica unutar stijenke desnog srca

Hypertrophic cardiomyopathy – screening and etiology detection

Left ventricular hypertrophy is an adopted response to physiological and pathological stress, while hypertrophic cardiomyopathy (HCM) is defined by the presence of increased left ventricular wall thickness that is not solely explained by abnormal loading conditions. Determination of the etiology, pathophysiology and disease severity is important for the management of patients with HCM.1-4 According to latest European Cardiology Society Guidelines for HCM2, etiology in adults are 60% an autosomal dominant trait caused by mutations in cardiac sarcomere protein genes, 5-10% caused by other genetic disorders including inherited metabolic and neuromuscular diseases, chromosome abnormalities and genetic syndromes, malformation syndromes, non-genetic disorders that mimic genetic forms of the disease like amyloidosis and infiltrative diseases. In about 25-30% of HCM etiology is still unknown. In adults, HCM is defined by a wall thickness ≥15 mm in one or more LV myocardial segments as measured by any imaging technique. Transthoracic 2D and tissue doppler echocardiography presents tool for morphologic and hemodynamic evaluation (with additional strain analysis, contrast and transesophageal echocardiography), and cardiac MRI for assessment of cardiac morphology and myocardial tissue characteristics. Routine laboratory tests and specific testing aids the detection of HCM etiology. The majority of HCM cases are inherited autosomal dominant genetic trait with a 50% risk of transmission to offspring. Some cases are explained by de novo mutations, sporadic cases can arise because of incomplete penetrance in a parent and by autosomal recessive inheritance. Regular genetic analysis should include the most commonly implicated sarcomere protein genes, and pedigree analysis should be provided. Annual incidence of cardiovascular death is 1–2% caused by sudden cardiac death, heart failure or thromboembolism. HCM etiology detection is necessary because of treatment possibilities (like Anderson-Fabry disease or ATTR amyloidosis), detection of secondary causes of disease, the need for family screening and differentiating pathogenic from non-pathogenic mutations. Routine clinical practice is challenging, left ventricular hypertrophy and HCM can be presented in different forms and different stages

Serum visfatin concentration in eutrophic and overweight/obese male children in early childhood

Background and Purpose: Childhood overweight/obesity is considered a global epidemic, which began earlier in pediatric patients and presents a major health risk in adulthood. It is well known that adipose tissue is an active endocrine inflammatory organ in obese adults, but its neurohormone activity in the childhood is not yet clarified. Visfatin is one of adipokines with insulin-mimetic and proinflammatory-atherosclerotic effect, whose role in the child’s age is still unknown as well as its physiological concentrations in serum of prepubertal children. The aim of this study was to determine visfatin serum concentration at the early age in eutrophic and overweight/obese male children and its association with arterial blood pressure. Materials and Methods: Healthy boys, 2-14 years old, hospitalized for elective inguinal hernia surgery has been included in the study (N=31) and were divided into two groups according to percentile curve: a) overweight/obese (O/O:above the 85th percentile) and b) eutrophic (E:5th-85th percentile). Anthropometric and biochemical measurements and specific serum levels of visfatin by enzyme immunoassay were determined. Results and Conclusion: Both groups of examinees, eutrophic and overweight/obese, had a normal metabolic profile band on percentile ranks (fasting glucose values and all fractions of lipid profile) and values of blood pressure. However overweight/obese boys had significant higher systolic blood pressure than eutrophic boys, p=0,028. Serum visfatin were 6.90±3.97 ng/ml in eutrophic boys, while in overweight/obese were 7.82±3.75 ng/ml, p=0,57. There is a tendency of visfatin serum concentration to increase with increase of body weight and growing. This suggests possible role of visfatin in future metabolic and cardiovascular processes related to increase in body mass