scholarly journals Time of Anderson-Fabry Disease Detection and Cardiovascular Presentation

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
K. Selthofer-Relatic
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Fabry Disease ◽  
Ventricular Hypertrophy ◽  
Heart Surgery ◽  
Late Onset ◽  
Cardiac Pacemaker ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Family Screening

Background. Anderson-Fabry disease is an X-linked inherited disease, which manifests in a different manner depending on gender and genotype. Making a working diagnosis of Anderson-Fabry disease is difficult because of several reasons: (a) that it is a multiorgan disease with wide variety of phenotypes, (b) different timelines of presentation, (c) gender differences, and (d) possible coexistence with other comorbidities. Late-onset/cardiac type of presentation with minimal involvement of other organs can additionally make diagnosis difficult. Aim. To describe different cardiac manifestations at different time points in the course of the disease: (1) 72-year-old female (echocardiography detection), heterozygote, significant left and mild right ventricular hypertrophy; (2) 62-year-old male (echocardiography detection), hemizygote, left ventricular hypertrophy, implanted cardiac pacemaker, a performed percutaneous coronary intervention after myocardial infarction, degenerative medium degree aortic valve stenosis; (3) 45-year-old female (asymptomatic/family screening), heterozygote, thickened mitral papillary muscle, mild left ventricular hypertrophy, first degree diastolic dysfunction; and (4) 75-year-old female (symptomatic/family screening), heterozygote, cardiomyopathy with reduced left ventricular ejection fraction after heart surgery (mitral valve annuloplasty and plastic repair of the tricuspid valve). Conclusion. All patients have Anderson-Fabry disease but with different clinical presentations depending on the gender, the type of mutation, and the time of detection. All these features can make the patients’ profiles unique and delay the time of detection.

Adrenomedullin modulates hemodynamic and cardiac effects of angiotensin II in conscious rats

2004 ◽  
Vol 286 (6) ◽  
pp. R1085-R1092 ◽  
Author(s):  
Marja Luodonpää ◽  
Hanna Leskinen ◽  
Mika Ilves ◽  
Olli Vuolteenaho ◽  
Heikki Ruskoaho
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Systolic Function ◽  
Subcutaneous Administration ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ang Ii ◽  
Ventricular Ejection Fraction ◽  
Systolic And Diastolic Function

We examined whether adrenomedullin, a vasoactive peptide expressed in the heart, modulates the increase in blood pressure, changes in systolic and diastolic function, and left ventricular hypertrophy produced by long-term administration of ANG II or norepinephrine in rats. Subcutaneous administration of adrenomedullin (1.5 μg·kg−1·h−1) for 1 wk inhibited the ANG II-induced (33.3 μg·kg−1·h−1 sc) increase in mean arterial pressure by 67% ( P < 0.001) but had no effect of norepinephrine-induced (300 μg·kg−1·h−1 sc) hypertension. Adrenomedullin enhanced the ANG II-induced improvement in systolic function, resulting in a further 9% increase ( P < 0.01) in the left ventricular ejection fraction and 19% increase ( P < 0.05) in the left ventricular fractional shortening measured by echocardiography, meanwhile norepinephrine-induced changes in systolic function were remained unaffected. Adrenomedullin had no effect on ANG II- or norepinephrine-induced left ventricular hypertrophy or expression of hypertrophy-associated genes, including contractile protein and natriuretic peptide genes. The present study shows that adrenomedullin selectively suppressed the increase in blood pressure and augmented the improvement of systolic function induced by ANG II. Because adrenomedullin had no effects on ANG II- and norepinephrine-induced left ventricular hypertrophy, circulating adrenomedullin appears to act mainly as a regulator of vascular tone and cardiac function.

scholarly journals Transthoracic echocardiography in patients with chronic kidney disease

2019 ◽  
Vol 8 (1) ◽  
pp. 24-31
Author(s):  
Balaram Shrestha ◽  
Dhiraj Gurung ◽  
Sanjib Dhungel
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
College Teaching ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Female Ratio ◽  
Cardiac Lesions

Background: Evaluation of cardiac diseases in chronic kidney disease has been rarely investigated in Nepal. Objectives: Objective of this study is to evaluate cardiac lesions in admitted chronic kidney disease patients. Methodology: It is a prospective observational study of echocardiography of chronic kidney disease patients from April, 2007 to April, 2013 in Nepal Medical College Teaching Hospital. Results: One hundred chronic kidney disease patients were evaluated. Male to Female ratio was 1.8:1 and age ± SD was 46.3 ± 17.2 years. Forty eight percent of the chronic kidney disease patients had left ventricular hypertrophy. Patients with chronic kidney disease with left ventricular hypertrophy group had interventricular septum of 1.5 ± 0.3 cm vs. 1.1 ± 0.1 cm (p<0.0001) and posterior wall of 1.1 ± 0.2cm vs. 1.0 ± 0.1cm (p< 0.01) in comparison to chronic kidney disease without left ventricular hypertrophy. Forty one percent had left ventricular systolic dysfunction with left ventricular ejection fraction of 39 ± 9.9 %. Pulmonary arterial hypertension was noticed in 39% patients. Valvular regurgitant lesions were quite common (24.1%) usually as multivalvular lesions (4.4 lesions per patient). Mitral regurgitation was the commonest regurgitant lesion (81%). Conclusion: Echocardiographic cardiac evaluation is useful to diagnose concomitant cardiac lesions for standard care of chronic kidney disease patients.

scholarly journals Anabolic Androgenic Steroids Induce Reversible Left Ventricular Hypertrophy and Cardiac Dysfunction. Echocardiography Results of the HAARLEM Study

2021 ◽  
Vol 3 ◽  
Author(s):  
Diederik L. Smit ◽  
A. J. Voogel ◽  
Martin den Heijer ◽  
Willem de Ronde
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Recovery Period ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Anabolic Androgenic Steroids ◽  
Cycle Duration ◽  
Weekly Dose ◽  
Ventricular Ejection Fraction ◽  
Androgenic Steroids

Background: The use of anabolic androgenic steroids (AAS) is not uncommon among strength athletes. Several cross-sectional studies have linked AAS use to heart disease, but a causal role for AAS is not certain and it is unknown whether cardiac changes are reversible.Methods: Men of at least 18 years old intending to start an AAS cycle on short notice were included for comprehensive 3D echocardiographic examination before (T0), at the end of the cycle (T1), and 1 year after inclusion (T2) after a recovery period. Details of the AAS cycle performed and the use of other performance and image-enhancing drugs (PIEDs) as well as illicit drug use were recorded. Trend analysis and multivariable regression analysis were performed with mixed effects linear models.Results: Thirty-one subjects were included. Between start (T0) and end of the cycle (T1), after a median AAS cycle duration of 16 weeks, 3D left ventricular ejection fraction declined with 4.9% (CI −7.2 to −2.5, P &lt; 0.001), E/A-ratio declined with−0.45 (CI −0.69 to −0.21, P &lt; 0.001), and 3D left atrial volume increased with 9.2 ml (CI 2.9–15.4, P = 0.004). Left ventricular mass increased with 28.3 g (CI 14.2–42.4, P &lt; 0.001) and was positively correlated with AAS average weekly dose. After a median recovery time of 8 months (T2), all parameters returned to baseline.Conclusion: AAS induce left ventricular hypertrophy and impaired systolic and diastolic function in amateur strength athletes. The structural cardiac changes are positively associated with AAS dose and complete recovery occurred after AAS were discontinued.

scholarly journals Dysregulation of proangiogeneic factors in pressure-overload left-ventricular hypertrophy results in inadequate capillary growth

2019 ◽  
Vol 13 ◽  
pp. 175394471984179 ◽  
Author(s):  
Mohamed Zeriouh ◽  
Anton Sabashnikov ◽  
Arne Tenbrock ◽  
Klaus Neef ◽  
Julia Merkle ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Quantitative Polymerase Chain Reaction ◽  
Pressure Overload ◽  
Capillary Density ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Heart Weight ◽  
Ventricular Ejection Fraction ◽  
Expression Levels

Background: Pressure-overload left-ventricular hypertrophy (LVH) is an increasingly prevalent pathological condition of the myocardial muscle and an independent risk factor for a variety of cardiac diseases. We investigated changes in expression levels of proangiogeneic genes in a small animal model of LVH. Methods: Myocardial hypertrophy was induced by transaortic constriction (TAC) in C57BL/6 mice and compared with sham-operated controls. The myocardial expression levels of vascular endothelial growth factor (VEGF), its receptors (KDR and FLT-1), stromal-cell-derived factor 1 (SDF1) and the transcription factors hypoxia-inducible factor-1 and 2 (HIF1 and HIF2) were analyzed by quantitative polymerase chain reaction over the course of 25 weeks. Histological sections were stained for caveolin-1 to visualize endothelial cells and determine the capillary density. The left-ventricular morphology and function were assessed weekly by electrocardiogram-gated magnetic resonance imaging. Results: The heart weight of TAC animals increased significantly from week 4 to 25 ( p = 0.005) compared with sham-treated animals. At 1 day after TAC, the expression of VEGF and SDF1 also increased, but was downregulated again after 1 week. The expression of HIF2 was significantly downregulated after 1 week and remained at a lower level in the subsequent weeks. The expression level of FLT-1 was also significantly decreased 1 week after TAC. HIF-1 and KDR showed similar changes compared with sham-operated animals. However, the expression levels of HIF1 after 4 and 8 weeks were significantly decreased compared with day 1. KDR changes were significantly decreased after 1, 2, 4, 8 and 25 weeks compared with week 3. After 4 weeks post-TAC, the size of the capillary vessels increased ( p = 0.005) while the capillary density itself decreased (TAC: 2143 ± 293 /mm2 versus sham: 2531 ± 321 /mm2; p = 0.021). Starting from week 4, the left-ventricular ejection fraction decreased compared with controls ( p = 0.049). Conclusions: The decrease in capillary density in the hypertrophic myocardium appears to be linked to the dysregulation in the expression of proangiogeneic factors. The results suggest that overcoming this dysregulation may lead to reconstitution of capillary density in the hypertrophic heart, and thus be beneficial for cardiac function and survival.

scholarly journals Prognostic value of the left ventricular hypertrophy for sudden cardiac death in patients with myocardial infarction

2009 ◽  
Vol 15 (3) ◽  
pp. 325-329
Author(s):  
S. Boldueva ◽  
I. A. Leonova ◽  
E. G. Bykova ◽  
N. A. Trostyanetskaya
Keyword(s):  
Myocardial Infarction ◽  
Sudden Cardiac Death ◽  
Left Ventricular Hypertrophy ◽  
Cardiac Death ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Arrhythmogenic Substrate ◽  
Characteristic Features

Aim. The study addresses the role of left ventricular hypertrophy (LVH) in development of sudden cardiac death (SCD) in patients with myocardial infarction (MI). The incidence of characteristic features of arrhythmogenic substrate in myocardium (late ventricular potentials, left ventricular ejection fraction) and trigger factors of fatal arrhythmias (decreased heart rate variability, ventricular arrhythmias) was higher in patients with MI and LVH. The level of leukocytes, monocytes and eosinophils, CD-95 lymphocytes was significantly higher in patients with LVH. The incidence of general mortality and of SCD was also higher in group with LVH.

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