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Ventricular Hypertrophy (ventricular + hypertrophy)
Kinds of Ventricular Hypertrophy Selected AbstractsClinical Value of the Tissue Doppler S Wave to Characterize Left Ventricular Hypertrophy as Defined by EchocardiographyECHOCARDIOGRAPHY, Issue 4 2010Demian Chejtman M.D. Left ventricular hypertrophy (LVH) may be a physiological finding and may also be associated with different disease entities and hence, with different outcomes. Regional myocardial function can be assessed with color Doppler tissue imaging, specifically by the waveform of the isovolumic contraction (IC) period and the regional systolic wave ("s"). Methods and Results: We studied five groups (G): healthy, sedentary young volunteers (G1, n:10); healthy sedentary adult volunteers (G2, n:8); and subjects with LVH (left ventricular mass index >125 g/m2) including: high performance athletes (G3, n:21), subjects with hypertension (G4, n:21), subjects with hypertrophic cardiomyopathy (HCM) (G5, n:18). We measured peak "s" wave velocity (cm/sec) at the basal and mid septum, the IC/s ratio, and basal to mid-septal velocity difference (BMVD) of the "s" wave. Regional "s" wave values (cm/sec) were G1 = 5.6 ± 1; G2 = 5.4 ± 0.8; G3 = 5.7 ± 0.6; G4 = 5.3 ± 1.1; G5 = 4.2 ± 1.1 (P < 0.0001). The IC/s ratio was G1 = 0.28 ± 0.18; G2 = 0.39 ± 0.21; G3 = 0.23 ± 0.10; G4 = 0.42 ± 0.15; G5 = 0.64 ± 0.15 (P < 0.0001). The BMVD (cm/sec) was G1 = 2 ± 0.51; G2 = 1.71 ± 0.29; G3 = 1.78 ± 0.44; G4 = 1.26 ± 0.96; G5 = 0.45 ± 0.4 (P < 0.0001). IC/s < 0.38 discriminated physiological from pathological forms of hypertrophy (sensitivity 90%; specificity 88%). Peak "s" wave velocity discriminated HCM from other causes of hypertrophy, with a cutoff value of 4.46 cm/sec (sensitivity 72%; specificity 90%). BMVD <0.98 cm/sec detected HCM with 89% sensitivity and 86% specificity. Conclusions: Peak "s" wave velocity and two indices: IC/s and BMDV are novel parameters that may allow to discriminate physiological from pathological forms of hypertrophy as well as different subtypes of hypertrophy. (ECHOCARDIOGRAPHY 2010;27:370-377) [source] The Effects of Antihypertensive Treatment on the Doppler-Derived Myocardial Performance Index in Patients with Hypertensive Left Ventricular Hypertrophy: Results from the Swedish Irbesartan in Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA)ECHOCARDIOGRAPHY, Issue 7 2009Stefan Liljedahl M.D. Objectives: To investigate the effects of antihypertensive treatment on the Doppler-derived myocardial performance index (MPI) in patients with hypertensive left ventricular hypertrophy. Methods: The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol. Results: Antihypertensive treatment lowered MPI (mean difference ,0.03 ± 0.01, P = 0.04). Changes in MPI by treatment were associated with changes in left ventricular ejection fraction (,-coefficient ,0.35 P = 0.005), stroke volume/pulse pressure (reflecting arterial compliance, ,-coefficient ,0.39 P < 0.001) and peripheral vascular resistance (,-coefficient 0.28 P < 0.04). Furthermore, there was a borderline significant association between changes in MPI and changes in E-wave deceleration time (reflecting diastolic function, ,-coefficient 0.23, P = 0.06). No associations were found between changes in MPI and changes in blood pressure, E/A-ratio, left ventricular mass index, relative wall thickness or heart rate. A stepwise multivariable regression model confirmed the association between changes in MPI and changes in ejection fraction and stroke volume/pulse pressure (all P < 0.05), as well as the trend for E-wave deceleration time (P = 0.08), but not in the case of peripheral vascular resistance. Conclusion: The MPI exhibited a modest decrease after 48 weeks of antihypertensive treatment in patients with hypertensive left ventricular hypertrophy. Changes in MPI were associated with changes in left ventricular function and vascular compliance, rather than with changes in left ventricular remodeling or blood pressure. [source] Disproportionately High Risk of Left Ventricular Hypertrophy in Indo-Asian Women: A Call for More StudiesECHOCARDIOGRAPHY, Issue 8 2008F.A.C.C., Fahim H. Jafary M.D. Objective: Indo-Asians have one of the highest rates of cardiovascular disease worldwide. Estimates and determinants of left ventricular hypertrophy (LVH) in this population are not known. We sought to determine the prevalence of and risk factors for LVH in Karachi, Pakistan.Methods: We conducted a population-based cross-sectional study on 320 randomly selected adults from the general population aged 40 years or above. LVH was defined as increased left ventricular mass index (LVMI) on echocardiogram (>115 g/m2 in men and >95 g/m2 in women) employing the adjusted Devereux equation. Multivariable models were built and logistic regression analysis was done for the primary outcome of LVH.Results: Mean age of subjects was 52.7 (10.4) years, 50% were women. Mean LVMI (SD) was 72.0 (19.2) [median 71.1] g/m2 in men and 75.7 (25.9) [median 72.9] g/m2 in women. The overall prevalence of LVH was 21.9% in women and 2.5% in men (P < 0.001). The factors (odds ratio, 95% CI) independently associated with LVH were women versus men (11.35, 3.79,34.02), systolic blood pressure > versus < 140 mmHg (2.70, 1.23,5.93), waist circumference (1.05, 1.02,1.08 for each cm increase) and illiteracy (2.43, 1.07,5.52).Conclusions: Urban Pakistani women appear to have a disproportionately high risk of LVH compared to men using standard echocardiographic criteria. Further research is needed to verify these results by establishing population-specific reference values for LVH and correlating cut-points for increased LVMI with prognosis. Concerted efforts are needed to reduce the high burden of risk factors in Indo-Asian women. [source] What Is Left Ventricular Hypertrophy and Is There a Reason to Regress Left Ventricular Hypertrophy?JOURNAL OF CLINICAL HYPERTENSION, Issue 8 2009Matthew R. Weir MD First page of article [source] Electrocardiographic Indices of Left Ventricular Hypertrophy and Repolarization Phase Share the Same Genetic Influences: A Twin StudyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2009Sara Mutikainen M.Sc. Background: Both left ventricular hypertrophy (LVH) and repolarization phase (RP) are known to be attributable to genetic influences, but less is known whether they share same genetic influences. The aim of this study was to investigate to what extent individual differences in electrocardiographic (ECG) LVH and RP are explained by genetic and environmental influences and whether these influences are shared between these two traits. Methods: Resting ECG recordings were obtained from 186 monozygotic and 203 dizygotic female twin individuals, aged 63 to 76 years. Latent factors, called LVH and RP, were formed to condense the information obtained from LVH indices (Cornell voltage and Cornell product) and T-wave amplitudes (leads V5 and II), respectively. Multivariate quantitative genetic modeling was used both to decompose the phenotypic variances into additive genetic, common environmental, and unique environmental influences, and for the calculation of genetic and environmental correlations between LVH and RP. Results: Additive genetic influences explained 16% of individual differences in LVH and 74% in RP. The remaining individual differences were explained by both common and unique environmental influences. The genetic correlation and unique environmental correlation between LVH and RP were ,0.93 and ,0.05, respectively. Conclusions: In older women without overt cardiac diseases, RP is under stronger genetic control than LVH. The majority of genetic influences are shared between LVH and RP whereas environmental influences are mainly specific to each. [source] Electrical and Structural Remodeling in Left Ventricular Hypertrophy,A Substrate for a Decrease in QRS Voltage?ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007Ljuba Bacharova M.D., M.B.A., Ph.D. Electrical remodeling in advanced stages of cardiovascular diseases creates a substrate for triggering and maintenance of arrhythmias. The electrical remodeling is a continuous process initiated already in the early stages of cardiological pathology. The aim of this opinion article was to discuss the changes in electrical properties of myocardium in left ventricular hypertrophy (LVH), with special focus on its early stage, as well as their possible reflection in the QRS amplitude of the electrocardiogram. It critically appraises the classical hypothesis related to the QRS voltage changes in LVH. The hypothesis of the relative voltage deficit is discussed in the context of supporting evidence from clinical studies, animal experiments, and simulation studies. The underlying determinants of electrical impulse propagation which may explain discrepancies between "normal" ECG findings and increased left ventricular size/mass in LVH are reviewed. [source] Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular HypertrophyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2004Laura Maria Lonati M.D. Objective:,The objective of this article is to assess whether left ventricular hypertrophy (LVH) due to physical training or of hypertensive patients shows similarities in QT length and QT dispersion. Methods:,A total of 51 subjects were studied: 17 essential hypertensive patients (27.7 ± 5.6 years), 17 athletes involved in agonistic activity (canoeing) (24.8 ± 6.1 years), and 17 normotensive healthy subjects as control group (24.8 ± 3.6 years). The testing protocol consisted of (1) clinic BP measurement, (2) echocardiography, (3) 12-lead electrocardiographic examination (QT max, QTc max, QT min, QTc min, ,QT, ,QTc). Results:,There were no significant differences between the body surface area, height, and age of the three groups. Clinic blood pressure was higher in hypertensives (146.5 ± 45.2/93.5 ± 4.9 mmHg) versus athletes (120.9 ± 10.8/77.1 ± 6.0 mmHg) and controls (123.5 ± 4.8/78.8 ± 2.9 mmHg) by definition. Indexed left ventricular mass (LVM/BSA) was significantly greater in both athletes (148.9 ± 21.1 g/m2) and hypertensives (117.1 ± 15.2 g/m2) versus controls (81.1 ± 14.5 g/m2; P < 0.01), there being no statistical difference among them. LVH (LVMI > 125 g/m2) was observed in all athletes, while the prevalence in hypertensives was 50%. In spite of this large difference in cardiac structure there were no significant differences in QT parameters between athletes and the control group, while hypertensive patients showed a significant increase in QT dispersion versus the two other groups (,QT 82 ± 2.1, 48 ± 1.3, 49 ± 2.3 ms; P < 0.01; ,QTc 88 ± 2.0, 47 ± 1.4, 54 ± 2.7; P < 0.01). Conclusions:,LVH induced by physical training activity is not associated with an increase in QT dispersion, whereas pathological increase in LVM secondary to hypertension is accompanied by an increased QT dispersion. [source] Metoprolol Treatment Lowers Thrombospondin-4 Expression in Rats with Myocardial Infarction and Left Ventricular HypertrophyBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2010Erja Mustonen In this study, we characterised left ventricular thrombospondin-1 and -4 expression in rats treated with a beta-blocker metoprolol during the remodelling process in response to pressure overload and acute myocardial infarction. Left ventricular thrombospondin-1 and thrombospondin-4 mRNA levels increased 8.4-fold (p < 0.001) and 7.3-fold (p < 0.001) post-infarction, respectively. Metoprolol infusion by osmotic minipumps (1.5 mg/kg/hr) for 2 weeks after myocardial infarction decreased thrombospondin-1 and thrombospondin-4 mRNA levels (55% and 50%, respectively), improved left ventricular function, and attenuated left ventricular remodelling with reduction of left ventricular atrial natriuretic peptide and brain natriuretic peptide gene expression. Thrombospondin-1 and -4 mRNA levels correlated positively with echocardiographic parameters of left ventricular remodelling as well as with atrial natriuretic peptide and brain natriuretic peptide gene expression. Moreover, there was a negative correlation between left ventricular ejection fraction and thrombospondin-1 mRNA levels. In 12-month-old spontaneously hypertensive rats with left ventricular hypertrophy, metoprolol decreased left ventricular thrombospondin-4 levels and attenuated remodelling while thrombospondin-1, atrial natriuretic peptide and brain natriuretic peptide mRNA levels as well as left ventricular function remained unchanged. In metoprolol-treated spontaneously hypertensive rats, thrombospondin-4 gene expression correlated with parameters of left ventricular remodelling, while no correlations between thrombospondins and natriuretic peptides were observed. These results indicate that thrombospondin-1 expression is linked exclusively to left ventricular remodelling process post-infarction while thrombospondin-4 associates with myocardial remodelling both after myocardial infarction and in hypertensive heart disease suggesting that thrombospondins may have unique roles in extracellular matrix remodelling process. [source] Late Presentation of Pulmonary Valve Stenosis Confirmed by Cardiovascular Magnetic ResonanceCONGENITAL HEART DISEASE, Issue 3 2008Didier Locca MD ABSTRACT We describe the case of a 70-year-old man who presented with increasing exertional dyspnea. He was found to have an ejection systolic murmur and evidence of right ventricular outflow tract obstruction, with a peak velocity of 4.5 m/s recorded by transthoracic Doppler echocardiography. Cardiovascular magnetic resonance showed right ventricular hypertrophy, pulmonary valve stenosis, peak recorded velocity 4.2 m/s, with thickened pulmonary valve leaflets of reduced mobility, and poststenotic dilatation of the main pulmonary artery. The case illustrates that severe pulmonary valve stenosis can present late in life and that cardiovascular magnetic resonance can be useful in clarifying nature and level of right ventricular outflow tract obstruction in an adult. [source] Protein kinase C mRNA and protein expressions in hypobaric hypoxia-induced cardiac hypertrophy in ratsACTA PHYSIOLOGICA, Issue 4 2010M. Uenoyama Abstract Aim:, Protein kinase C (PKC), cloned as a serine/threonine kinase, plays key roles in diverse intracellular signalling processes and in cardiovascular remodelling during pressure overload or volume overload. We looked for correlations between changes in PKC isoforms (levels and/or subcellular distributions) and cardiac remodelling during experimental hypobaric hypoxic environment (HHE)-induced pulmonary hypertension. Methods:, To study the PKC system in the heart during HHE, 148 male Wistar rats were housed for up to 21 days in a chamber at the equivalent of 5500 m altitude level (10% O2). Results:, At 14 or more days of exposure to HHE, pulmonary arterial pressure (PAP) was significantly increased. In the right ventricle (RV): (1) the expression of PKC-, protein in the cytosolic and membrane fractions was increased at 3,14 days and at 5,7 days of exposure respectively; (ii) the cytosolic expression of PKC-, protein was increased at 1,5, 14 and 21 days of exposure; (3) the membrane expressions of the proteins were decreased at 14,21 (PKC-,II), 14,21 (PKC-,), and 0.5,5 and 21 (PKC-,) days of exposure; (4) the expression of the active form of PKC-, protein on the plasma membrane was increased at 3 days of exposure (based on semiquantitative analysis of the immunohistochemistry). In the left ventricle, the expressions of the PKC mRNAs, and of their cytosolic and membrane proteins, were almost unchanged. The above changes in PKC-,, which were strongly evident in the RV, occurred alongside the increase in PAP. Conclusion:, PKC-, may help to modulate the right ventricular hypertrophy caused by pulmonary hypertension in HHE. [source] Elevated plasma ACE activity: no guarantee for enhanced left ventricular hypertrophy during trainingACTA PHYSIOLOGICA, Issue 2 2008Hans DegensArticle first published online: 5 SEP 200 No abstract is available for this article. [source] The muscle,collagen ratio in left ventricular hypertrophy and aorta remodelling in hypertensionACTA PHYSIOLOGICA, Issue 1 2008Marcos A. RossiArticle first published online: 1 AUG 200 No abstract is available for this article. [source] Cardiovascular effects of the thiazolidinedionesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2006Rehan Qayyum Abstract Thiazolidinediones, used for the treatment of diabetes mellitus type 2, modulate gene expression by binding to nuclear transcription factor, peroxisome proliferator-activated receptor-gamma. Peroxisome proliferator,activated receptor-gamma is expressed in several tissues, therefore, thiazolidinediones have biological effects on multiple organ systems. Here, we describe evidence that thiazolidinediones have beneficial effects on the cardiovascular system independent of their antidiabetic effect. Studies in animals have clearly shown that thiazolidinediones decrease blood pressure, left ventricular hypertrophy, development of atherosclerotic lesions, and protect myocardium from ischemia/reperfusion injury. Although relatively few studies in humans have been reported, the preponderance of available evidence suggests a beneficial effect of thiazolidinediones. Thus, by modulating gene expression, thiazolidinediones may provide a novel method for the prevention and treatment of cardiovascular diseases. Copyright © 2005 John Wiley & Sons, Ltd. [source] Prediction of cardiovascular risk in people with diabetesDIABETIC MEDICINE, Issue 7 2003P. H. Winocour Abstract People with diabetes are at high risk of cardiovascular morbidity and mortality, especially if they have already developed vascular problems. For patients who are apparently free of vascular complications, risk tables are often used to assess the risk of cardiovascular events in the following years, and to decide on treatment with statins or anti-platelet therapy. These risk prediction tables include estimates of traditional cardiovascular risk factors and are based on populations, some of which only contained a very small number of people with diabetes. Multiple problems can be identified with these tables, and many seriously underestimate cardiovascular risk in people with diabetes. Possible ways of addressing this include using risk estimation tools based solely on diabetic populations, adding in additional traditional variables such as triglycerides or left ventricular hypertrophy, including novel cardiovascular risk factors, or intervening at a lower level of estimated risk in people with diabetes compared with non-diabetic subjects. Alternatively, estimates of individual risk could be abandoned and all people with diabetes could be treated with statins and other effective agents. Diabet. Med. 20, 515,527 (2003) [source] Clinical Value of the Tissue Doppler S Wave to Characterize Left Ventricular Hypertrophy as Defined by EchocardiographyECHOCARDIOGRAPHY, Issue 4 2010Demian Chejtman M.D. Left ventricular hypertrophy (LVH) may be a physiological finding and may also be associated with different disease entities and hence, with different outcomes. Regional myocardial function can be assessed with color Doppler tissue imaging, specifically by the waveform of the isovolumic contraction (IC) period and the regional systolic wave ("s"). Methods and Results: We studied five groups (G): healthy, sedentary young volunteers (G1, n:10); healthy sedentary adult volunteers (G2, n:8); and subjects with LVH (left ventricular mass index >125 g/m2) including: high performance athletes (G3, n:21), subjects with hypertension (G4, n:21), subjects with hypertrophic cardiomyopathy (HCM) (G5, n:18). We measured peak "s" wave velocity (cm/sec) at the basal and mid septum, the IC/s ratio, and basal to mid-septal velocity difference (BMVD) of the "s" wave. Regional "s" wave values (cm/sec) were G1 = 5.6 ± 1; G2 = 5.4 ± 0.8; G3 = 5.7 ± 0.6; G4 = 5.3 ± 1.1; G5 = 4.2 ± 1.1 (P < 0.0001). The IC/s ratio was G1 = 0.28 ± 0.18; G2 = 0.39 ± 0.21; G3 = 0.23 ± 0.10; G4 = 0.42 ± 0.15; G5 = 0.64 ± 0.15 (P < 0.0001). The BMVD (cm/sec) was G1 = 2 ± 0.51; G2 = 1.71 ± 0.29; G3 = 1.78 ± 0.44; G4 = 1.26 ± 0.96; G5 = 0.45 ± 0.4 (P < 0.0001). IC/s < 0.38 discriminated physiological from pathological forms of hypertrophy (sensitivity 90%; specificity 88%). Peak "s" wave velocity discriminated HCM from other causes of hypertrophy, with a cutoff value of 4.46 cm/sec (sensitivity 72%; specificity 90%). BMVD <0.98 cm/sec detected HCM with 89% sensitivity and 86% specificity. Conclusions: Peak "s" wave velocity and two indices: IC/s and BMDV are novel parameters that may allow to discriminate physiological from pathological forms of hypertrophy as well as different subtypes of hypertrophy. (ECHOCARDIOGRAPHY 2010;27:370-377) [source] Overestimation of Left Ventricular Mass and Misclassification of Ventricular Geometry in Heart Failure Patients by Two-Dimensional Echocardiography in Comparison with Three-Dimensional EchocardiographyECHOCARDIOGRAPHY, Issue 3 2010Dmitry Abramov M.D. Background: Accurate assessment of left ventricular hypertrophy (LVH) and ventricular geometry is important, especially in patients with heart failure (HF). The aim of this study was to compare the assessment of ventricular size and geometry by 2D and 3D echocardiography in normotensive controls and among HF patients with a normal and a reduced ejection fraction. Methods: One hundred eleven patients, including 42 normotensive patients without cardiac disease, 41 hypertensive patients with HF and a normal ejection fraction (HFNEF), and 28 patients with HF and a low ejection fraction (HFLEF), underwent 2DE and freehand 3DE. The differences between 2DE and 3DE derived LVM were evaluated by use of a Bland,Altman plot. Differences in classification of geometric types among the cohort between 2DE and 3DE were determined. Results: Two-dimensional echocardiography overestimated ventricular mass compared to 3D echocardiography (3DE) among normal (166 ± 36 vs. 145 ± 20 gm, P = 0.002), HFNEF (258 ± 108 vs. 175 ± 47gm, P < 0.001), and HFLEF (444 ± 136 vs. 259 ± 77 gm, P < 0.001) patients. The overestimation of mass by 2DE increased in patients with larger ventricular size. The use of 3DE to assess ventricular geometry resulted in reclassification of ventricular geometric patterns in 76% of patients with HFNEF and in 21% of patients with HFLEF. Conclusion: 2DE overestimates ventricular mass when compared to 3DE among patients with heart failure with both normal and low ejection fractions and leads to significant misclassification of ventricular geometry in many heart failure patients. (Echocardiography 2010;27:223-229) [source] The Effects of Antihypertensive Treatment on the Doppler-Derived Myocardial Performance Index in Patients with Hypertensive Left Ventricular Hypertrophy: Results from the Swedish Irbesartan in Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA)ECHOCARDIOGRAPHY, Issue 7 2009Stefan Liljedahl M.D. Objectives: To investigate the effects of antihypertensive treatment on the Doppler-derived myocardial performance index (MPI) in patients with hypertensive left ventricular hypertrophy. Methods: The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol. Results: Antihypertensive treatment lowered MPI (mean difference ,0.03 ± 0.01, P = 0.04). Changes in MPI by treatment were associated with changes in left ventricular ejection fraction (,-coefficient ,0.35 P = 0.005), stroke volume/pulse pressure (reflecting arterial compliance, ,-coefficient ,0.39 P < 0.001) and peripheral vascular resistance (,-coefficient 0.28 P < 0.04). Furthermore, there was a borderline significant association between changes in MPI and changes in E-wave deceleration time (reflecting diastolic function, ,-coefficient 0.23, P = 0.06). No associations were found between changes in MPI and changes in blood pressure, E/A-ratio, left ventricular mass index, relative wall thickness or heart rate. A stepwise multivariable regression model confirmed the association between changes in MPI and changes in ejection fraction and stroke volume/pulse pressure (all P < 0.05), as well as the trend for E-wave deceleration time (P = 0.08), but not in the case of peripheral vascular resistance. Conclusion: The MPI exhibited a modest decrease after 48 weeks of antihypertensive treatment in patients with hypertensive left ventricular hypertrophy. Changes in MPI were associated with changes in left ventricular function and vascular compliance, rather than with changes in left ventricular remodeling or blood pressure. [source] Disproportionately High Risk of Left Ventricular Hypertrophy in Indo-Asian Women: A Call for More StudiesECHOCARDIOGRAPHY, Issue 8 2008F.A.C.C., Fahim H. Jafary M.D. Objective: Indo-Asians have one of the highest rates of cardiovascular disease worldwide. Estimates and determinants of left ventricular hypertrophy (LVH) in this population are not known. We sought to determine the prevalence of and risk factors for LVH in Karachi, Pakistan.Methods: We conducted a population-based cross-sectional study on 320 randomly selected adults from the general population aged 40 years or above. LVH was defined as increased left ventricular mass index (LVMI) on echocardiogram (>115 g/m2 in men and >95 g/m2 in women) employing the adjusted Devereux equation. Multivariable models were built and logistic regression analysis was done for the primary outcome of LVH.Results: Mean age of subjects was 52.7 (10.4) years, 50% were women. Mean LVMI (SD) was 72.0 (19.2) [median 71.1] g/m2 in men and 75.7 (25.9) [median 72.9] g/m2 in women. The overall prevalence of LVH was 21.9% in women and 2.5% in men (P < 0.001). The factors (odds ratio, 95% CI) independently associated with LVH were women versus men (11.35, 3.79,34.02), systolic blood pressure > versus < 140 mmHg (2.70, 1.23,5.93), waist circumference (1.05, 1.02,1.08 for each cm increase) and illiteracy (2.43, 1.07,5.52).Conclusions: Urban Pakistani women appear to have a disproportionately high risk of LVH compared to men using standard echocardiographic criteria. Further research is needed to verify these results by establishing population-specific reference values for LVH and correlating cut-points for increased LVMI with prognosis. Concerted efforts are needed to reduce the high burden of risk factors in Indo-Asian women. [source] Real Time Three-Dimensional Echocardiography Evaluation of Mitral Annular Characteristics in Patients with Myocardial HypertrophyECHOCARDIOGRAPHY, Issue 4 2008Fatih Yalçin M.D. It has been shown that systolic excursion of the mitral annulus (MA) correlates well with left ventricular (LV) systolic function. Evaluation of the complicated shape and dynamics of the mitral annulus, however, may require rigorous methodology. The aim of this study was to investigate differences in MA motion between hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) patients due to hypertension or aortic stenosis using real time three-dimensional echocardiography (RT3DE). We studied 10 HCM, 10 LVH, and 10 controls. Mean MA area changes between early and late systole were 9.5 ± 4.3% in HCM, 26 ± 15% in LVH and 19 ± 10% in normal controls. MA apicobasal motion was 5.8 ± 4 mm in HCM, 11 ± 4 mm in LVH, and 13.6 ± 6 mm in normal controls. RT3DE with digital reconstruction of MA accurately display complicated MA geometry and dynamics during a cardiac cycle. Annular function in LVH was similar to that of the normal group while annular apicobasal motion and area changes were reduced in HCM. [source] Aortic Valve Sclerosis: Is It a Cardiovascular Risk Factor or a Cardiac Disease Marker?ECHOCARDIOGRAPHY, Issue 3 2007F.I.S.C.U., Pasquale Palmiero M.D. Background: Aortic valve sclerosis, without stenosis, has been associated with an increased cardiovascular mortality and morbidity due to myocardial infarction. However, it is unclear whether it is a cardiovascular risk factor or a cardiac disease marker. The goal of our study is to evaluate the difference in the prevalence of cardiovascular disease and risk factors among patients with or without aortic sclerosis. Methods: This observational study compared a group of 142 consecutive subjects with aortic valve sclerosis, assigned as group S, with a group of 101 subjects without aortic sclerosis, assigned as group C. Patients with bicuspid aortic valves and those with antegrade Doppler velocity across aortic valve leaflets exceeding 2.0 m/sec were excluded. Results: Mean ages of groups S and C were 71 ± 8, and 68.8 ± 6 years, respectively (P value = not significant). The prevalence of smoking, diabetes, hypercholesterolemia, hypertension, pulse pressure, left ventricular diastolic dysfunction, atrial fibrillation, and stroke was not significantly different between the two groups. However, there was a significantly higher prevalence of left ventricular hypertrophy (P = 0.05), ventricular arrhythmias (P = 0.02), myocardial infarction (P = 0.04), and systolic heart failure (P = 0.04) in aortic sclerosis group. Conclusions: Aortic sclerosis is associated with a higher prevalence of left ventricular hypertrophy, ventricular arrhythmias, myocardial infarction, and systolic heart failure, while the prevalence of cardiovascular risk factors is not different between aortic sclerosis patients and controls. Hence, aortic sclerosis represents a cardiac disease marker useful for early identification of high-risk patients beyond cardiovascular risk factors rate. [source] Methodological Analysis of Diagnostic Dobutamine Stress Echocardiography StudiesECHOCARDIOGRAPHY, Issue 8 2004Boudewijn J. Krenning M.D. Background: Dobutamine stress echocardiography (DSE) is an accepted test for the diagnosis of coronary artery disease (CAD), despite its wide diagnostic accuracy. Aim: Which factors cause test variability of DSE for the diagnosis of CAD. Methods: In a retrospective analysis of 46 studies in 5,353 patients, the potential causes of diagnostic variability were systematically analyzed, including patient selection, definition of CAD, chest pain characteristics, confounding factors for DSE (left ventricular hypertrophy, left bundle branch block, female gender), work-up bias (present when patient's chance to undergo coronary angiography is influenced by the result of DSE), review bias (present when DSE is interpreted in relation to CAG), DSE protocol and definition of a positive DSE. Results: Diagnostic variability was related to definition of a positive test, but not related to the definition of CAD or DSE protocol. However, only three of eight methodological standards for research design found general compliance. Differences in the selection of the study population (quality of echocardiographic window, angina pectoris), handling of confounding factors and analysis of disease in individual coronary arteries were observed. Lack of data on analysis of relevant chest pain syndromes and handling of nondiagnostic test results hampered further evaluation of these standards. Conclusion: Methodological problems may explain the wide range in diagnostic variability of DSE. An improvement of clinical relevance of DSE testing is possible by stronger adherence to common and new methodological standards. [source] Echocardiographic Left Ventricular Mass in African-AmericansECHOCARDIOGRAPHY, Issue 2 2003The Jackson Cohort of the Atherosclerosis Risk in Communities Study Characterization of target organ damage from hypertension is of particular interest in African-Americans, and evidence from electrocardiographic studies suggests that left ventricular hypertrophy is a frequent clinical finding of considerable prognostic importance. Echocardiographic studies may permit more precise characterization of the pathologic impact of hypertension on cardiac structure and function. The objective of this study is to characterize left ventricular (LV) structure including measures of wall thickness, septal thickness, internal dimension, and mass in a middle-aged sample of African-Americans using echocardiography. This study is a cohort (cross-sectional) study in which 2445 middle-aged African-American study participants from a population-based sample initially enrolled by the Atherosclerosis Risk in Communities, Jackson, Mississippi Examination Center in 1987,1989 underwent an M-mode echocardiograpic examination at their third or fourth clinic visit in 1993,1996. Measures of LV mass, even where indexed by size were conspicuously greater in men compared to women, and men exhibited a demonstrably steeper gradient of LV mass across the rather restricted age range of the study. However, when gender specific thresholds for LV hypertrophy were utilized, African-American men appear to have lower prevalence of LV hypertrophy than women. The lowest prevalence of LV hypertrophy was observed in African-American men who did not have hypertension (28.4%). The findings confirm previous suggestions from electrocardiographic investigations that cardiac hypertrophy is common, if not epidemic in middle-aged African-American men and women, whether or not they have hypertension. (ECHOCARDIOGRAPHY, Volume 20, February 2003) [source] Arterial structural and functional alterations in uraemiaEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2005A. P. Guérin Abstract Epidemiological and clinical studies have shown that cardiovascular disease in patients with end-stage renal disease (ESRD) is frequently related to damage of large conduit arteries. Arterial disease is responsible for the high incidence of ischaemic heart disease, peripheral artery diseases, left ventricular hypertrophy and congestive heart failure. The vascular complications in ESRD are ascribed to two different but associated mechanisms, namely atherosclerosis and arteriosclerosis. Whereas the former principally affects the conduit function with ischaemic lesions being the most characteristic consequence, the latter primarily disturbs the dampening function of large arteries. Arteriosclerosis in ESRD patients is characterized by diffuse dilation and wall hypertrophy of large conduit arteries and stiffening of arterial walls. These changes represent a clinical form of an accelerated ageing process. The main clinical characteristics due to arterial stiffening are isolated increase in systolic blood pressure with normal or lower diastolic pressure resulting in an increased pulse pressure. The consequences of these alterations are: (i) an increased left ventricular afterload with development of left ventricular hypertrophy and increased myocardial oxygen demand; and (ii) altered coronary perfusion and subendocardial blood flow distribution. Epidemiological studies have identified arterial remodelling and stiffening as independent predictors of overall and cardiac mortality in ESRD patients. [source] ACE and angiotensinogen gene genotypes and left ventricular mass in athletesEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2001F. Diet Background Genetic factors may be important in modifying heart size due to long-term athletic training. The significance of polymorphisms of genes of the renin,angiotensin system in myocardial mass in a population of athletes participating in different disciplines is not known. Methods The angiotensin I-converting enzyme gene insertion/deletion (I/D) polymorphism, angiotensinogen gene M235T polymorphism and angiotensin II type 1 receptor gene A1166C polymorphism were determined in 83 male Caucasian endurance athletes and associated with left ventricular mass. Results No association with left ventricular mass was found for the polymorphisms of angiotensin I-converting enzyme gene I/D, angiotensinogen gene M235T and angiotensin II type 1 gene A1166C when studied separately. However, combined analysis of the angiotensin I-converting enzyme gene I/D polymorphism and angiotensinogen gene M235T polymorphism genotypes suggested an association with left ventricular mass (g m,2) (P = 0·023). Athletes with the angiotensin I-converting enzyme gene DD/angiotensinogen gene TT genotype combination had greater left ventricular mass compared with all other genotype combinations (179·8 ± 26·1 g m,2 vs. 145·2 ± 27·3 g m,2, P = 0·003). Conclusions These results suggest an association of combined angiotensin I-converting enzyme gene I/D polymorphism genotypes, and angiotensinogen gene M235T polymorphism genotypes with left ventricular hypertrophy due to long-term athletic training. A synergistic effect of angiotensin I-converting enzyme gene DD genotype and angiotensinogen gene TT genotype on left ventricular mass in endurance athletes appears to occur. [source] Higher arteriovenous fistulae blood flows are associated with a lower level of dialysis-induced cardiac injuryHEMODIALYSIS INTERNATIONAL, Issue 4 2009Shvan KORSHEED Abstract Native arteriovenous fistulae (AVF) remain the vascular access of choice for hemodialysis (HD). Despite being associated with superior long-term outcomes (cf. catheter use), little is known about the systemic hemodynamic consequences of AVFs. Repetitive myocardial injury (myocardial stunning) is an under-recognized common consequence of HD. The aim of this study was to examine the impact of AVF flow (Qa) on dialysis-induced cardiac injury. We studied 50 chronic HD patients. All patients underwent echocardiography (and subsequent quantitative offline analysis) at baseline, during and post dialysis, to assess left ventricular function and the development of regional wall motion abnormalities. Qa was measured using ionic dialysance. Patients were divided into Qa tertiles (<500, mean 291±101 mL/min, 500,1000, mean 739±130 mL/min and >1000, mean 1265±221 mL/min). There were no significant differences between the groups in terms of age, sex, diabetes, or resting ejection fraction. Patients with Qa>1000 mL/min had a lower prevalence of left ventricular hypertrophy (55% vs. 76%, P=0.01). Dialysis-induced myocardial stunning (seen in 65% of the patients studied) was significantly and sequentially reduced in those patients with higher Qas. This was seen in a lower number of segments and ventricular regions developing regional wall motion abnormalities, as well as a significantly reduced mean and cumulative percentage reduction in fractional shortening of those ventricular segments affected (,187±37%, ,161±26%, and ,101±25%, respectively, P=0.04). Relatively higher AVF flows appear to be associated with a lower level of observed HD-induced cardiac injury. [source] Interdialytic blood pressure obtained by ambulatory blood pressure measurement and left ventricular structure in hypertensive hemodialysis patientsHEMODIALYSIS INTERNATIONAL, Issue 3 2008Siddig MOMINADAM Abstract Unlike in subjects with normal renal function, the relationship between hypertension and cardiovascular morbidity and mortality in dialysis patients is still being debated. In order to clarify this issue, we performed 44-hour ambulatory blood pressure measurements (ABPM) during the interdialytic period in a group of 164 hypertensive patients, the blood pressure (BP) control based on conventional antihypertensive strategy previously, on chronic hemodialysis treatment in the Mediterranean region of Turkey. These results were then compared with their echocardiographic data. This is a cross-sectional analysis. The mean ABPM during 44 hours was close to the manually measured predialysis value, but there was a gradual increase in the ABPM values in the interdialytic period. When divided into a group with mild or no left ventricular hypertrophy (LVH) (45 patients) and severe LVH (119 patients), the latter had significantly higher BP levels in all separate periods, while the difference in predialysis BP was not significant. Patients with severe LVH had larger left atrium and left ventricular diameters, and consumed more antihypertensive drugs. Systolic BP during the night before dialysis showed the strongest relation to LVH, but interdialytic weight gain was also independently related to LVH. Yet, 56% of the patients with systolic BP <135 had severe LVH. There is not only an association between BP and presence of LVH, but it is shown that volume expansion is also an important independent determinant of LVH. This may explain the difficulty in identifying hypertension as a cardiac risk factor in these patients. [source] Effect of acetate-free biofiltration with a potassium-profiled dialysate on the control of cardiac arrhythmias in patients at risk: A pilot studyHEMODIALYSIS INTERNATIONAL, Issue 1 2008Rosa I. MUÑOZ Abstract Cardiac arrhythmias are a frequent event in chronic hemodialysis patients. The aim of this study was to evaluate the efficacy and safety of acetate-free hemofiltration with potassium-profiled dialysate (AFB-K) dialysis compared with constant potassium acetate-free biofiltration (AFB). Twelve patients (mean age 79 years) affected by cardiac arrhythmias or at a high risk for arrhythmia (advanced age, hypertension, left ventricular hypertrophy, heart valve disease, coronary artery disease, diabetes, paroxysmal atrial fibrillation) participated in a single-center, sequential cohort study. All were treated with hemodialysis 3 times per week, using constant potassium AFB for the first 3 weeks, followed by an AFB-K dialysate for the subsequent 3 weeks. The hemofilter, duration of dialysis, and electrolyte concentration were the same in both treatments. Both AFB-K and constant potassium AFB dialytic techniques were safe and well tolerated. The results of biochemical tests were similar, except for serum potassium levels after 2 hr of dialysis, which were significantly higher in the AFB-K group (4.0 mmol/L) than in the constant potassium AFB group (3.6 mmol/L) (p<0.001). All cardiac variables improved during AFB-K dialysis. There was a significant reduction of postdialysis QT intervals corrected for heart rate in the AFB-K group (448.8 ms) compared with the constant potassium AFB group (456.8 ms) (p=0.039). The severity and mean number of ventricular extasystoles also decreased (163.5 vs. 444.5/24 hr). Potassium profiling during hemodialysis treatment may be beneficial for patients with arrhythmias or at those risk of arrhythmias, particularly those with predialysis hyperkalemia. [source] Fallacies of High-Speed HemodialysisHEMODIALYSIS INTERNATIONAL, Issue 2 2003Zbylut J. Twardowski Chronic hemodialysis sessions, as developed in Seattle in the 1960s, were long procedures with minimal intra- and interdialytic symptoms. Financial and logistical pressures related to the overwhelming number of patients requiring hemodialysis created an incentive to shorten dialysis time to four, three, and even two hours per session in a thrice weekly schedule. This method spread rapidly, particularly in the United States, after the National Cooperative Dialysis Study suggested that time of dialysis is of minor importance as long as urea clearance multiplied by dialysis time and scaled to total body water (Kt/Vurea) equals 0.95,1.0. This number was later increased to 1.3, but the assumption remained unchanged that hemodialysis time is of minimal importance as long as it is compensated by increased urea clearance. Patients accepted short dialysis as a godsend, believing that it would not be detrimental to their well-being and longevity. However, Kt/Vurea measures only removal of low molecular weight substances and does not consider removal of larger molecules. Besides, it does not correlate with the other important function of hemodialysis, namely ultrafiltration. Whereas patients with substantial residual renal function may tolerate short dialysis sessions, the patients with little or no urine output tolerate short dialyses poorly because the ultrafiltration rate at the same interdialytic weight gain is inversely proportional to dialysis time. Rapid ultrafiltration is associated with cramps, nausea, vomiting, headache, fatigue, hypotensive episodes during dialysis, and hangover after dialysis; patients remain fluid overloaded with subsequent poor blood pressure control, left ventricular hypertrophy, diastolic dysfunction, and high cardiovascular mortality. Short, high-efficiency dialysis requires high blood flow, which increases demands on blood access. The classic wrist arteriovenous fistula, the access with the best longevity and lowest complication rates, provides "insufficient" blood flow and is replaced with an arteriovenous graft fistula or an intravenous catheter. Moreover, to achieve high blood flows, large diameter intravenous catheters are used; these fit veins "too tightly," so predispose the patient to central-vein thrombosis. Longer hemodialysis sessions (5,8 hrs, thrice weekly), as practiced in some centers, are associated with lower complication rates and better outcomes. Frequent dialyses (four or more sessions per week) provide better clinical results, but are associated with increased cost. It is my strong belief that a wide acceptance of longer, gentler dialysis sessions, even in a thrice weekly schedule, would improve overall hemodialysis results and decrease access complications, hospitalizations, and mortality, particularly in anuric patients. [source] Left ventricular hypertrophy in rats with biliary cirrhosisHEPATOLOGY, Issue 3 2003Javier Inserte Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague-Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P < .01), 87% increase in cardiac index and 30% increase in heart weight (P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (P < .01) increase in cross-sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK-B genes (P < .01). Isolated perfused CBDL hearts showed pressure/end-diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N -nitro-L-arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis. [source] Fabry Disease: Treatment and diagnosisIUBMB LIFE, Issue 11 2009Paula A. Rozenfeld Abstract Fabry disease is an X-linked lysosomal disorder that results from a deficiency of the lysosomal enzyme ,-galactosidase A leading to accumulation of glycolipids, mainly globotriaosylceramide in the cells from different tissues. Classical Fabry disease affects various organs. Clinical manifestations start at early age and include angiokeratoma, acroparesthesia, hypohydrosis, heat/exercise intolerance, gastrointestinal pain, diarrhea, and fever. The main complications of Fabry disease are more prominent after the age of 30 when kidney, heart, and/or cerebrovascular disorders appear. Most of the heterozygous females are symptomatic. Enzyme replacement therapy (ERT) is the only specific treatment for Fabry disease. The beneficial effect of ERT on different organs/systems has been extensively evaluated. Quality of life of patients receiving ERT is improved. Enzyme replacement stabilizes or slows the decline in renal function and reduces left ventricular hypertrophy. Fabry disease may be underdiagnosed because of nonspecific and multiorgan symptoms. Different screening strategies have been carried out in different at-risk populations in order to detect undiagnosed Fabry patients. An increasing knowledge about Fabry disease within the medical community increases the chances of patients to receive a timely diagnosis and, consequently, to access the appropriate therapy. © 2009 IUBMB IUBMB Life, 61(11): 1043,1050, 2009 [source] | |||||||||||||||||||||||||||||||||||||||||||