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.

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.

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.

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 The impact of obesity on left ventricular mass and left ventricular systolic function in children

2016 ◽  
Vol 45 (4) ◽  
pp. 171
Author(s):  
Ria Nova ◽  
Bambang Madiyono ◽  
Sudigdo Sastroasmoro ◽  
Damayanti R Sjarif
Keyword(s):  
Wall Thickness ◽  
Systolic Function ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Obese Children ◽  
Normal Children ◽  
Posterior Wall Thickness ◽  
Lv Mass ◽  
Lv Systolic Function

Background Obesity causes cardiovascular disturbances. Theincidence of cardiovascular disease is higher even in mildly obesepatients than in lean subjects.Objectives The purpose of this study was to compare left ven-tricular (LV) mass, LV internal dimensions, and LV systolic func-tion between obese and normal children; and to determine the as-sociation of the degree of obesity with LV mass and LV systolicfunction.Methods This cross-sectional study was conducted on elemen-tary school students in Jakarta from February to April 2003. Wemeasured the subjects’ body weight and height, and performedlipid profile and echocardiography examinations. Measurementsof LV mass, LV internal dimensions with regard to septum thick-ness, LV internal diameter, and LV posterior wall thickness; andLV systolic function as indicated by shortening fraction and ejec-tion fraction, were performed echocardiographically. The differ-ences in measurements between obese and normal children aswell as between obese children with and without lipid abnormalitywere analyzed. The correlation between the degree of obesity withLV size and systolic function was determined.Results Twenty-eight normal children and 62 obese children wereenrolled in the study. Mean LV mass was 35.7 (SD 5.16) g/cm 3 inobese children versus 24.0 (SD 3.80) g/cm 3 in normal children(P<0.0001). Mean septum thickness was 0.8 (SD 0.14) mm inobese children versus 0.6 (SD 7.90) mm in normal children (P<0.0001). Mean posterior wall thickness was 0.9 (SD 0.14) mm inobese children versus 0.6 (SD 9.97) mm in normal children(P<0.0001). Mean LV internal diameter was 4.0 (SD 0.34) mm inobese children versus 3.9 (SD 0.29) mm in normal children(P=0.300). There was strong correlation between the degree ofobesity and LV mass (r=0.838, P<0.0001). LV systolic function(shortening fraction) was 37.1 (SD 4.20) percent in obese childrenversus 35.8 (SD 4.99) percent in normal children (P=0.19). Ejec-tion fraction was 67.4 (SD 5.32) percent in obese children versus65.5 (SD 6.29) percent in normal children (P=0.13). There wasweak correlation between LV systolic function and the degree ofobesity (shortening fraction r=0.219, P=0.038; ejection fractionr=0.239, P=0.023).Conclusions Obese children had significantly greater LV mass,septum thickness, and posterior wall thickness than normal chil-Backgrounddren. Such significant difference was absent for LV internal diam-eter and measures of LV systolic function. There was no signifi-cant difference in LV mass and LV systolic function between obesechildren with or without abnormality of lipid profile. A strong corre-lation exists between the degree of obesity and LV mass, but thecorrelation between degree of obesity and LV systolic function wasweak

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.

Abstract 2292: Torsional Deformation Delay: a Novel Echocardiographic Index of Left Ventricular Peak Rotation Sequence Between Basal and Apical Level.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Lukasz Chrzanowski ◽  
Barbara Uznanska ◽  
Michal Plewka ◽  
Piotr Lipiec ◽  
Jaroslaw Drozdz ◽  
...  
Keyword(s):  
Systolic Function ◽  
Temporal Distribution ◽  
Left Ventricular ◽  
Torsional Deformation ◽  
Lv Mass ◽  
Echocardiographic Parameters ◽  
The Difference ◽  
Lv Systolic Function ◽  
Rotation Sequence

Purpose: left ventricular (LV) torsion (TOR) results from oppositely directed rotation (ROT) at the basal (BAS) and apical (AP) level. Speckle Tracking Echocardiography (STE) allows TOR assessment, but little is known of LV ROT temporal distribution. The aim was to evaluate the sequence of BAS and AP level ROT and to identify associated echocardiographic parameters. Methods: 48 patients (PTS) were studied (mean age 54±13 years, 23 men). LV systolic function was normal in 23 PTS (LVEF 60% or more), and various degrees of dysfunction were present in 25 PTS (mean LVEF 40±10%). Digital short axis loops at BAS and AP level were analyzed using STE algorithm to measure ROT in degrees (°). After adjustment for heart rate, Torsional Deformation Delay (TDD) was calculated as the difference between the time from the onset of QRS complex to the peak average systolic ROT at BAS and AP level (figure ). Results: mean TOR, BAS ROT and AP ROT was 14.3±7.3°, −6.8±4.7° and 7.5±6.1° respectively. Mean TDD was 19±107 ms (range from −285 to 248 ms); negative TDD indicated shorter time to BAS peak ROT. No difference of mean TDD was found between PTS with normal and decreased LVEF. TDD outside the range of −28 ms to 28 ms, derived by ROC analysis, was shown to have 96% specificity in detecting PTS with LVEF <60%. It was also associated with higher LV mass index as compared to TDD ranging from −28 to 28 ms (130 g/m2 vs 100 g/m2, p=0.025). Conclusions: a novel TDD index allows evaluation of LV ROT temporal distribution between BAS and AP level. TDD values outside the range of −28 ms to 28 ms are associated with decreased LVEF and presence of LV hypertrophy. Further studies are required to assess the role of TDD in cardiac imaging.

scholarly journals Genetic inhibition of calcineurin induces diastolic dysfunction in mice with chronic pressure overload

2009 ◽  
Vol 297 (5) ◽  
pp. H1814-H1819 ◽  
Author(s):  
Ricardo J. Gelpi ◽  
Shumin Gao ◽  
Peiyong Zhai ◽  
Lin Yan ◽  
Chull Hong ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Systolic Function ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Aortic Banding ◽  
Lv Systolic Function ◽  
Calcineurin Inhibition ◽  
Lv Diastolic Function ◽  
Isovolumic Relaxation

Calcineurin is a Ca2+/calmodulin-dependent protein phosphatase that induces myocardial growth in response to several physiological and pathological stimuli. Calcineurin inhibition, induced either via cyclosporine or genetically, can decrease myocardial hypertrophy secondary to pressure overload without affecting left ventricular (LV) systolic function. Since hypertrophy can also affect LV diastolic function, the goal of this study was to examine the effects of chronic pressure overload (2 wk aortic banding) in transgenic (Tg) mice overexpressing Zaki-4β (TgZ), a specific endogenous inhibitor of calcineurin, on LV diastolic function. As expected, in the TgZ mice with calcineurin inhibitor overexpression, aortic banding reduced the degree of LV hypertrophy, as assessed by LV weight-to-body weight ratio (3.5 ± 0.1) compared with that in non-Tg mice (4.6 ± 0.2). LV systolic function remained compensated in both groups with pressure overload. However, the LV end-diastolic stress-to-LV end-diastolic dimension ratio, an index of diastolic stiffness and LV pressure half-time and isovolumic relaxation time, two indexes of isovolumic relaxation, increased significantly more in TgZ mice with aortic banding. Protein levels of phosphorylated phospholamban (PS16), sarco(endo)plasmic reticulum Ca2+-ATPase 2a, phosphorylated ryanodine receptor, and the Na+/Ca2+ exchanger were also reduced significantly ( P < 0.05) in the banded TgZ mice. As expected, genetic calcineurin inhibition inhibited the development of LV hypertrophy with chronic pressure overload but also induced LV diastolic dysfunction, as reflected by both impaired isovolumic relaxation and increased myocardial stiffness. Thus genetic calcineurin inhibition reveals a new mechanism regulating LV diastolic function.

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