Abstract 2113: Early End-organ Alterations Due To High Blood Pressure In Children

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Reinhard G Ketelhut ◽  
Ulrich Rode ◽  
Jörg Schröter
Keyword(s):  
Blood Pressure ◽  
Diastolic Function ◽  
High Blood Pressure ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Lv Function ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass

Introduction : Increased left ventricular (LV) mass is known to be an important risk for future cardiovascular morbidity and mortality. Since high blood pressure can be observed more often in early childhood a study was designed to evaluate the influence of blood pressure (BP) on LV mass and function in children. Methods: 2-D-guided-echocardiography and Doppler-echocardiography were performed in 103 children (aged 14.1±0.9 years, 58 girls). BP, LV-mass-index (LVMI) and diastolic function (E/A ratio) were measured and calculated by standardized formula and procedure. Results: Systolic BP (SBP) was significantly higher in boys (124.8±10.6 mmHg) when compared with girls (120.5±8.4 mmHg) (p<0.01). There were no significant differences in diastolic pressure. LVMI was significantly lower in girls (57.6±8.9 g/m 2 ) than in boys (68.3±11.2 g/m 2 ) (p<0.01). There was a negative correlation between SBP and E/A ratio as a measure of LV diastolic function (p<0.01). Hypertensives had a 17% higher LVMI (78±11g/m 2 versus 67±11g/m 2 ; p<0.05), and a 20% lower E/A ratio (1.58±0.3 versus 1.97±0.42) than their normotensive counterparts (p<0.01). Conclusion: Despite the young age of participants with higher blood pressure they had prognostically adverse preclinical cardiovascular disease, including LV hypertrophy and evidence of impaired LV function. Therefore children should be encouraged to enter preventive programs as a primary and early strategy against future cardiovascular morbidity and mortality.

Hypertensive Heart Disease – Diagnosis, Prognostic Value and Changes During Antihypertensive Treatment, Left Ventricular Structure and Function

2010 ◽  
Vol 6 (2) ◽  
pp. 23 ◽  
Author(s):  
Kristian Wachtell ◽  
Keyword(s):  
Diastolic Function ◽  
Antihypertensive Treatment ◽  
Systolic Function ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass ◽  
Lv Systolic Function

Hypertensive heart disease is prevalent and during the last decade it has been determined that patients with left ventricular (LV) hypertrophy have increased cardiovascular morbidity and mortality. However, many have doubted the effectiveness of LV mass assessment because it is difficult to measure, and there were no data showing a relation between reduced LV mass and improvement in LV systolic and diastolic function and improved cardiovascular outcome. However, improvements to echocardiographic equipment have made it possible to measure LV mass with the same precision as for aortic valve replacement. Reduction of LV hypertrophy, independent of the simultaneous blood pressure reduction, is associated with large improvements in cardiovascular morbidity and mortality. A reduction in LV mass by 25g/m² leads to a 34% reduction in cardiovascular mortality. Time-varying analyses showed 66% associated risk reduction in cardiovascular mortality if patients with LV hypertrophy were treated to limits of LV mass. Hypertension causes impaired LV systolic function by increased afterload and LV hypertrophy. Normal estimations of LV ejection fraction tend to overestimate LV systolic function; however, improvement of LV systolic function by antihypertensive treatment leads to an improvement of cardiovascular morbidity and mortality. Furthermore, even though there is significant improvement in LV diastolic function during antihypertensive treatment, this occurs more slowly compared with the treatment effects on LV systolic function, and diastolic function does not, compared with LV systolic function, translate into improvement in cardiovascular morbidity and mortality. The perspective of finding cardiac target organ damage is used not only to classify the cardiovascular risk of patients, but also to indicate to the treating physician that specific treatment is needed.

scholarly journals Cardiovascular morbidity and mortality in patients treated with hemodialysis: Epidemiological analysis

2008 ◽  
Vol 65 (12) ◽  
pp. 893-900 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Mortality Rate ◽  
Cardiovascular Mortality ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass

Background/Aim. Cardiovascular diseases are the leading cause of death in patients treated with hemodialysis (HD). The annual cardiovascular mortality rate in these patients is 9%. Left ventricular (LV) hypertrophy, ischemic heart disease and heart failure are the most prevalent cardiovascular causes of death. The aim of this study was to assess the prevalence of traditional and nontraditional risk factors for cardiovascular complications, to assess the prevalence of cardiovascular complications and overall and cardiovascular mortality rate in patients on HD. Methods. We investigated a total of 115 patients undergoing HD for at least 6 months. First, a cross-sectional study was performed, followed by a two-year follow-up study. Beside standard biochemical parameters, we also determined cardiac troponins and echocardiographic parameters of LV morphology and function (LV mass index, LV fractional shortening, LV ejection fraction). The results were analyzed using the Student's t test and Mann-Whitney U test. Results. The patients with adverse outcome had significantly lower serum albumin (p < 0.01) and higher serum homocystein, troponin I and T, and LV mass index (p < 0.01). Hyperhomocysteinemia, anemia, hypertriglyceridemia and uncontrolled hypertension had the highest prevalence (86.09%, 76.52%, 43.48% and 36.52%, respectively) among all investigated cardiovascular risk factors. Hypertrophy of the LV was presented in 71.31% of the patients and congestive heart failure in 8.70%. Heart valve calcification was found in 48.70% of the patients, pericardial effusion in 25.22% and disrrhythmia in 20.87% of the investigated patients. The average annual overall mortality rate was 13.74%, while average cardiovascular mortality rate was 8.51%. Conclusion. Patients on HD have high risk for cardiovascular morbidity and mortality.

scholarly journals Estrogen therapy for arterial hypertension in menopansal females

2003 ◽  
Vol 49 (4) ◽  
pp. 51-54
Author(s):  
A. N. Karachentsev ◽  
I. V. Kuznetsova
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
High Blood Pressure ◽  
Estrogen Therapy ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Rational Pharmacotherapy ◽  
Cardiovascular Morbidity And Mortality ◽  
History Of ◽  
Practical Recommendations

The epidemiology of arterial hypertension in women with menopause Arterial hypertension, according to many experts, "is the greatest non-infectious pandemic in the history of mankind that determines the structure of cardiovascular morbidity and mortality"; Thus, only in Russia AG about 40% of the population suffers. Due to the wide prevalence of hypertension, it has become an interdisciplinary problem, and today doctors of different specialties need practical recommendations for rational pharmacotherapy of high blood pressure in specialized patients.

Cardiovascular Benefits of Extended-Time Nocturnal Hemodialysis

2020 ◽  
Vol 19 (1) ◽  
pp. 21-33
Author(s):  
Athanasios Roumeliotis ◽  
Stefanos Roumeliotis ◽  
Christopher Chan ◽  
Andreas Pierratos
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sleep Apnea ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Lv Function ◽  
Plasma Norepinephrine ◽  
Nocturnal Hemodialysis ◽  
Cardiovascular Morbidity And Mortality

Hemodialysis (HD) remains the most utilized treatment for End-Stage Kidney Disease (ESKD) globally, mainly as conventional HD administered in 4 h sessions thrice weekly. Despite advances in HD delivery, patients with ESKD carry a heavy cardiovascular morbidity and mortality burden. This is associated with cardiac remodeling, left ventricular hypertrophy (LVH), myocardial stunning, hypertension, decreased heart rate variability, sleep apnea, coronary calcification and endothelial dysfunction. Therefore, intensive HD regimens closer to renal physiology were developed. They include longer, more frequent dialysis or both. Among them, Nocturnal Hemodialysis (NHD), carried out at night while asleep, provides efficient dialysis without excessive interference with daily activities. This regimen is closer to the physiology of the native kidneys. By providing increased clearance of small and middle molecular weight molecules, NHD can ameliorate uremic symptoms, control hyperphosphatemia and improve quality of life by allowing a liberal diet and free time during the day. Lastly, it improves reproductive biology leading to successful pregnancies. Conversion from conventional to NHD is followed by improved blood pressure control with fewer medications, regression of LVH, improved LV function, improved sleep apnea, and stabilization of coronary calcifications. These beneficial effects have been associated, among others, with better extracellular fluid volume control, improved endothelial- dependent vasodilation, decreased total peripheral resistance, decreased plasma norepinephrine levels and restoration of heart rate variability. Some of these effects represent improvements in outcomes used as surrogates of hard outcomes related to cardiovascular morbidity and mortality. In this review, we consider the cardiovascular effects of NHD.

Abstract 3435: Left Ventricular Hypertrophy is Resistant to Inhibition of Expression of the R403Q Alpha-Myosin Heavy Chain Cardiac Hypertrophy-Inducing Mutant Protein

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Leah Cannon ◽  
Tadeusz Marciniec ◽  
Bryony Mearns ◽  
Robert M Graham ◽  
Diane Fatkin
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Interstitial Fibrosis ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Familial Hypertrophic Cardiomyopathy ◽  
Lv Function ◽  
Dependent Manner ◽  
Cardiovascular Morbidity And Mortality ◽  
Lv Mass

Left ventricular hypertrophy (LVH) develops as a compensatory response to myocardial dysfunction due to diverse causes, but is nonetheless a major risk factor for premature cardiovascular morbidity and mortality. It is thus unclear if regressing LVH is beneficial or may worsen patient outcome. To evaluate the effects of LVH regression, we developed a transgenic mouse model in which the expression of a familial hypertrophic cardiomyopathy (FHC)-inducing mutation (R403Q alpha-MHC) can be regulated in a temporal and dose-dependent manner. In this model, transgene expression can be shut off by feeding with a tetracycline analogue (doxycycline). Serial echocardiography and histology studies were performed in a cohort of mice expressing the FHC mutant (“gene-on”) and in wildtype (WT) littermates. A second cohort of WT and 403/+ mice was randomised to placebo or doxycycline (“gene off”) from 6 (Dox6) or 20 weeks (Dox20) and evaluated at 40 weeks of age. Compared to WT littermates, “gene on” 403/+ mice showed increased LV mass, LV end-diastolic diameter (LVDD) and left atrial diameter (LAD), and reduced fractional shortening (LVFS), with changes evident from 12 weeks of age. LV sections from 403/+ mice showed typical features of FHC: myofibre disarray and interstitial fibrosis. LV mass, LV function and myocardial histology were unchanged in both male and female placebo- vs Dox6 or Dox20 mice at 40 weeks (Table 1 ). Thus, consistent with the major LV thickening in FHC humans occurring in adolescence, overexpression of R403Q for only 6 weeks is sufficient to trigger the complete LVH phenotypic response. Moreover, switching off the genetic trigger for LVH in 403/+ mice at 6 weeks (prior to overt disease manifestation) or 20 weeks (established disease) does not induce regression of LVH or exacerbate contractile dysfunction. Interventions to induce LVH regression may, therefore, need to be directed at downstream factors in hypertrophic pathways. Table 1. Echo data for male WT and 403/+ mice aged 40 weeks

Abstract 3269: Association of Aortic Regurgitation with Cardiovascular Morbidity and Mortality in Hypertensive Patients with Left Ventricle Hypertrophy: The LIFE study

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Zhibin Li ◽  
Kristian Wachtell ◽  
Sverre E. Kjeldsen ◽  
Stevo Julius ◽  
Michael H. Olsen ◽  
...  
Keyword(s):  
Aortic Regurgitation ◽  
Cox Regression ◽  
Left Ventricular ◽  
Morbidity And Mortality ◽  
Hypertensive Patients ◽  
Life Study ◽  
Cardiovascular Morbidity And Mortality ◽  
Increased Risk ◽  
Lv Mass ◽  
Ventricle Hypertrophy

Background : Whether aortic regurgitation (AI) is associated with higher cardiovascular (CV) morbidity and mortality in hypertension with electrocardiographic (ECG) left ventricular hypertrophy (LVH) is unknown. Methods : Hypertensive patients with ECG-LVH were randomized to losartan- or atenolol-based treatment and followed for 4.8 years in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. In the LIFE echo substudy, echocardiograms were used to detect AI. Baseline clinical, echocardiographic variables and cardiovascular endpoints data were used in current analyses. Results: The presence of AI was detected in 132 participants (68 women; 68.4 ± 7.3 years). AI was associated with older age (p < 0.001) but not gender. After adjustment for age, AI was associated with significantly increased LV mass indexed by body surface area (BSA) and height 2.7 (both p < 0.005), echocardiographic eccentric LVH (p < 0.05) but not concentric left ventricular (LV) geometry (p < 0.05). After adjusting for significant confounders including history of CV disease, Framingham risk score, randomized antihypertensive therapy, LV eccentric geometry, LV mass indexed by BSA and height 2.7 , multivariate Cox regression analyses showed that AI was independently associated with 2.83-fold more CV death (95% confidence interval [CI] 1.12 to 7.13), 2.24-fold more all-cause mortality (95% CI 1.17 to 4.28) (both p < 0.05). Conclusion : In hypertensive patients with ECG-LVH, AI independently identifies patients at increased risk of CV and all-course mortality.

scholarly journals Left ventricular hypertrophy in patients treated with regular hemodialyses

2008 ◽  
Vol 61 (7-8) ◽  
pp. 369-374 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic
Keyword(s):  
Risk Factors ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Concentric Hypertrophy ◽  
Cardiovascular Morbidity And Mortality

Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.

Evaluation of diastolic LV function

2015 ◽  
pp. 323-335
Author(s):  
Johan De Sutter ◽  
Jean-Louis J. Vanoverschelde
Keyword(s):  
Diastolic Function ◽  
Daily Practice ◽  
Tissue Doppler ◽  
Left Ventricular ◽  
Doppler Imaging ◽  
Lv Function ◽  
Prognostic Information ◽  
Heart Failure Patients ◽  
Lv Mass ◽  
Deformation Measurements

The evaluation of diastolic function in patients with reduced (HFREF) or preserved (HFPEF) left ventricular (LV) ejection fraction is important as it carries both diagnostic and prognostic information. In daily practice, this is most frequently done by standard echocardiographic techniques, including the evaluation of LV mass and LA volumes, as well as transmitral and pulmonary venous PW Doppler, CW Doppler for evaluation of the IVRT, and tissue Doppler imaging of the septal and lateral annular velocities. This permits grading the severity of diastolic dysfunction, which is related to outcome and may be used to estimate LV filling pressures. The latter needs further validation, especially in patients with HFPEF. Newer echocardiographic and cardiac magnetic resonance techniques, including myocardial deformation measurements during diastole, LV twist and untwisting, and parameters of left atrial function, are promising and will hopefully in the future help clinicians to make a more precise evaluation of diastolic function and filling pressures in heart failure patients.

Ventricular performance and myocardial water content during hemodilution in dogs

1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  
Keyword(s):  
Water Content ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Ventricular Performance ◽  
End Diastolic Volume ◽  
Lv Mass ◽  
Right Heart Bypass ◽  
Water Gain

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

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