Obesity and hypertension independently promote pathological left ventricular remodelling (LVR) and left ventricular hypertrophy (LVH), but to what extent they do so when they do not coexist is unclear. We used data from the Cardiovision Brno 2030 study to assess-for the first time in a region where no investigations have been previously carried out-the independent association of obesity and hypertension with LV geometry, and to evaluate the effects of hypertension in normal weight patients and the effects of obesity in normotensive patients. Overall, 433 individuals, aged 25⁻65 years, with no history of cardiovascular disease and/or antihypertensive treatment, were stratified into four groups according to BMI and hypertension: normal weight non-hypertensive (NWNH), normal weight hypertensive (NWH), overweight/obese non-hypertensive (ONH) and overweight/obese hypertensive (OH). LVR was classified as normal, concentric LVR (cLVR), concentric LVH (cLVH) or eccentric LVH (eLVH). Linear regression analysis demonstrated that body mass index (BMI) and systolic blood pressure (SBP) are the main predictors of LV mass and that they interact: SBP had a stronger effect in overweight/obese (β = 0.195; p = 0.033) compared to normal weight patients (β = 0.134; p = 0.048). Hypertension increased the odds of cLVR (OR = 1.78; 95%CI = 1.04⁻3.06; p = 0.037) and cLVH (OR = 8.20; 95% CI = 2.35⁻28.66; p = 0.001), independent of age, sex and BMI. Stratified analyses showed that NWH had a greater odd of cLVH (OR = 7.96; 95%CI = 1.70⁻37.08; p = 0.008) and cLVR (OR = 1.62; 95%CI = 1.02⁻3.34; p = 0.047) than NWNH. In the absence of hypertension, obesity was not associated with LVM and abnormal LV geometry, suggesting that it is not per se a determinant of LVR. Thus, antihypertensive therapy still remains the first-line approach against LVH in hypertensive patients, though weight loss interventions might be helpful in those who are obese.

• Klíčová slova
• blood pressure, cardiac hypertrophy, epidemiology, left ventricular remodelling, obesity,
• Publikační typ
• časopisecké články MeSH

BACKGROUND: Enzyme replacement therapy (ERT) with recombinant human α-galactosidase has been available for the treatment of Fabry disease since 2001 in Europe and 2003 in the USA. Treatment outcomes with ERT are dependent on baseline patient characteristics, and published data are derived from heterogeneous study populations. METHODS: We conducted a comprehensive systematic literature review of all original articles on ERT in the treatment of Fabry disease published up until January 2017. This article presents the findings in adult male patients. RESULTS: Clinical evidence for the efficacy of ERT in adult male patients was available from 166 publications including 36 clinical trial publications. ERT significantly decreases globotriaosylceramide levels in plasma, urine, and in different kidney, heart, and skin cell types, slows the decline in estimated glomerular filtration rate, and reduces/stabilizes left ventricular mass and cardiac wall thickness. ERT also improves nervous system, gastrointestinal, pain, and quality of life outcomes. CONCLUSIONS: ERT is a disease-specific treatment for patients with Fabry disease that may provide clinical benefits on several outcomes and organ systems. Better outcomes may be observed when treatment is started at an early age prior to the development of organ damage such as chronic kidney disease or cardiac fibrosis. Consolidated evidence suggests a dose effect. Data described in male patients, together with female and paediatric data, informs clinical practice and therapeutic goals for individualized treatment.

• Klíčová slova
• ACEi, angiotensin-converting enzyme inhibitor, ANS, autonomic nervous system, ARB, angiotensin receptor blocker, BPI, Brief Pain Inventory, CES-D, Center for Epidemiologic Studies Depression Scale, CNS, central nervous system, CR, case report, CT, clinical trial, ECG, electrocardiogram/electrocardiography, EOW, every other week, ERT, enzyme replacement therapy, Fabry disease, GFR, glomerular filtration rate, GI, gastrointestinal, GL-3, globotriaosylceramide, IENFD, intra-epidermal nerve fibre density, IVST, intraventricular septum thickness, LPWT, left posterior wall thickness, LVEDD, left ventricular end-diastolic diameter, LVEF, left ventricular ejection fraction, LVH, left ventricular hypertrophy, LVM, left ventricular mass, LVMi, left ventricular mass index, LVWT, left ventricular wall thickness, MG, mixed gender, MRI, magnetic resonance imaging, MWT, maximal wall thickness, NYHA, New York Heart Association, OS, observational study, PNS, peripheral nervous system, QoL, quality of life, RCT, randomized controlled trial, SF-36, 36-item Short Form Health Survey, TIA, transient ischaemic attack, WMH, white matter hyperintensities., adult male patients, agalsidase alfa, agalsidase beta, eGFR, estimated glomerular filtration rate, enzyme replacement therapy, lyso-GL-3, globotriaosylsphingosine, systematic literature review,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

M-mode echocardiography was used to study cardiac involvement in 78 patients with acromegaly. Proportionate concentric or eccentric left ventricular hypertrophy (LVH) was a common finding. Calculated left ventricular mass (LVM) was increased significantly in a hormonally active disease group compared to an inactive disease group or a control group (153 +/- 7 vs. 96 +/- 8 and 89 +/- 3 g/m2 resp.; p less than 0.001 for both). The increase of LVM in hormonally active disease is due to predominantly LV dilatation, whereas associated hypertension, if present, aggravates the LVH exclusively due to thickening of the LV wall. Hypocorticalism, if present, does not influence the degree of LVH. Asymmetric septal hypertrophy was not found to be specific for acromegaly and was seen in only 7.7% of patients. There was no correlation between LVM and both the plasma levels of growth hormone and duration of disease. On the basis of a retrospective analysis of LVM in successfully treated patients the authors conclude that specific heart muscle disease in acromegaly, manifesting itself as LVH, is slowly reversible after cessation of the growth hormone hyperproduction.

• MeSH
• akromegalie patologie   MeSH
• dospělí MeSH
• echokardiografie * MeSH
• hypertenze patologie   MeSH
• hypertrofická kardiomyopatie patologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• myokard patologie   MeSH
• prognóza MeSH
• růstový hormon krev   MeSH
• senioři MeSH
• srdeční komory patologie   MeSH
• srdeční septum patologie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• růstový hormon MeSH