Prevalence Of Left Ventricular Hypertrophy In Patients Research Articles

Prevalence of abnormal left ventricular geometry and predictors of left ventricular hypertrophy in patients with rheumatoid arthritis

Abstract Background Rheumatoid arthritis (RA) patients have an excess risk of cardiovascular morbidity and mortality. Left ventricular hypertrophy (LVH) is generally considered a target organ damage of hypertensive patients, but it is an overlooked condition in the RA. In addition, LVH is one-sixth prevalence in RA patients and reflects a greater risk of cardiovascular events. Purpose We aimed to study the prevalence of LVH in patients with RA without symptomatic cardiovascular disease and explore the associated factors of LVH. Methods A cross-sectional study was conducted among adult RA patients and a retrospectively review of echocardiography from the database in non-RA participants. LVH was defined as LV mass index greater than 115 g/m2 in males or 95 g/m2 in females. The prediction model for LVH was constructed by stepwise logistic regression. The prediction model's performance on the test data is evaluated using receiver operator characteristic (ROC) curves to predict the presence of LVH and optimal cut-off point determined by the Youden index. Results This study included 109 RA patients and 119 age- and sex-matched non-RA participants. RA participants showed a significantly greater CV risk factor profile; hypertension, diabetes, and dyslipidemia than non-RA participants. Fifty two of 109 (47.7%) RA patients had abnormal LV geometry; eccentric hypertrophy, concentric remodeling, and concentric hypertrophy were 8/109 (7.3%), 28/109 (25.7%), and 16/109 (14.7%), respectively. The prevalence of LVH in RA patients was comparable to non-RA participants 24/109 (22%) and 28/119 (23.5%), p=0.91, respectively. However, there was significantly higher relative wall thickness in RA than non-RA participants 0.4±0.1 and 0.3±0.1, p<0.001, respectively. The diagnostic performance of the score prediction [(0.025×systolic blood pressure) + (non-steroidal anti-inflammatory drug × (0 or 1)) + (0.141×Troponin T level) ≥3.948] was to predict LVH in RA patients showed 91% sensitivity and 39% specificity (AUC = 0.689, 95% CI 0.564–0.814). Conclusion RA was associated with higher abnormal LV geometry compared to the non-RA participant. LVH is not uncommon in RA patients, and we could consider it as a target organ damage despite no obvious cardiovascular risk factors. The risk predictor score may be applied for fundamental screening tool for LVH in RA patients before sending the patients for echocardiography. Funding Acknowledgement Type of funding sources: None.

The high normal ankle brachial index is associated with left ventricular hypertrophy in hypertension patients among the Han Chinese

Left ventricular hypertrophy (LVH) is the most common target organs damage in the hypertension patients. Abnormal low (≤0.9) or high (≥1.40) ankle brachial index (ABI) are associated with an increased risk of cardiovascular events. However, the relationships between a high ABI in the normal range (0.9–1.4) and LVH in Han Chinese hypertension are not entirely elucidated. This study included 3953 hypertension patients aged 40–75 years among Han Chinese. Hypertension was defined as systolic blood pressure≥140 mm Hg, diastolic blood pressure≥90 mm Hg, or history of antihypertensive drug use. Left ventricular mass (LVM) was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of LVM ≥49.2 g/m2.7 for men and 46.7 g/m2.7 for women. Our study suggested that the ABI was higher in patients with LVH than in those without (1.13±0.11, 1.11±0.11, p < 0.001). The prevalence of LVH in patients with the lowest (0.9 < ABI≤1.03), second (1.04≤ABI≤1.11), the third (1.12≤ABI≤1.20), and the highest quartile (1.21≤ABI < 1.40) of ABI was 37.2%, 38.2%, 45.5%, 45.7%, respectively. Logistic regression analysis suggested that the highest and third quartile of ABI were significantly associated with increased LVH risk (multivariate‐adjusted OR of highest group:1.83; third group:1.61). The association of ABI at second quartile with LVH was nonsignificant. Similar results were observed in less than 60 years and without coronary heart disease or diabetes group. Our observations in Chinese patients with hypertension indicated high ABI may be an important risk factor for LVH in hypertension patients among Han Chinese, even in the normal range.

Vitamin D and fibroplastic processes in myocardium in spontaneously hypertensive rats with initial kidney dysfunction

Background. Even a moderate decrease in glomerular filtration rate leads to an increased risk of cardiovascular diseases (CVD), which is the leading cause of mortality in patients with chronic kidney disease (CKD). Left ventricular hypertrophy (LVH) underlies CVD development in renal dysfunction. The prevalence of LVH in patients with CKD stages 2–4 is 50–70 % and reaches 95 % at the beginning of dialysis, which significantly exceeds the number of cases in general population (15–21 %). Common hemodynamic factors associated with chronic kidney damage —hypertension (HTN), activation of the renin-angiotensin system, anemia, fluid and sodium retention, and others largely explain the high prevalence of LVH among patients with CKD. Nevertheless, the existence of additional non-hemodynamic mechanisms of myocardial remodeling (MR) is evident.Objective. To investigate the associations between the MR physiological/histological characteristics and laboratory parameters of calcium-phosphate metabolism in the initial stages of experimental CKD. Design and methods. Four groups of spontaneously hypertensive rats (SHR) were studied (n = 35): 3/4 nephrectomized rats (Nx) one month exposed after surgery (Nx(1), n = 9), 5/6 Nx two months after surgery (Nx(2), n = 8), sham operated rats one month after surgery (SO(1), n = 9) and two months after surgery (SO(2), n = 9). Myocardial mass index (MMI), systolic blood pressure (BP), proteinuria, creatinine (Cr) concentration, total calcium (Ca) and inorganic phosphate (Pi), 25-OH vitamin D (25OHD) and parathyroid hormone (PTH) in serum, myocardial morphology were studied in all experimental animals.Results. The models corresponded to the 1–3 stages CKD. There were no significant changes in serum total Ca (p = 0,066), Pi (p = 0,051) and PTH (p = 0,015) concentrations, the level of 25OHD was significantly lower in Nx(2) rats vs control (p = 0,015). MMI increased in all nephrectomized rats (p = 0,008). The cardiomyocytes (CM) thickness increased in Nx(1) and Nx(2) animals compared to the corresponding controls (p = 0,010, p = 0,002). A significant increase in interstitial (IF) and perivascular (PF) fibrosis occurred in Nx(2) rats with more damaging influence (p = 0,017, p = 0,004). CM thickness, IF and PF increased with the elevation of BP (r = 0,39, p = 0,038, r = 0,47, p = 0,026, r = 0,49, p = 0,031) and serum Cr (r = 0,68, p = 0,001, r = 0,61, p = 0,003, r = 0,69, p = 0,001), and the decrease in serum 25OHD concentration (r = –0,045, p = 0,047, r = –0,50, p = 0,020, r = –0,52, p = 0,012). Multiple linear regression analysis showed, that 25OHD is an independent predictor of myocardial fibrosis (IF: β = –0,38 ± 0,18, p = 0,047, PF: β = –0,34 ± 0,15, p = 0,032).Conclusions. The initial stages of CKD accompanied with HTN are associated with serum 25OHD concentration decrease CM hypertrophy and myocardial fibrosis. The CM growth is an earlier event in relation to the interstitial fibrosis. The obtained data suggest a possible role of vitamin D deficiency in the development of myocardial fibrotic lesions.

Increased Serum Uric Acid Level Is a Risk Factor for Left Ventricular Hypertrophy but Not Independent of eGFR in Patients with Type 2 Diabetic Kidney Disease.

Background Although the relation between serum uric acid (SUA) and left ventricular hypertrophy (LVH) has been studied for decades, however, their association remains debatable. Methods This is a retrospective study in which a total of 435 hospitalized Chinese patients with type 2 DKD were enrolled. The subjects were stratified into quartiles according to SUA level. LVH was assessed by two-dimensional guided M-mode echocardiography. Results There was a significant increase in the prevalence of LVH in patients with type 2 DKD across SUA quartiles (28.9, 26.5, 36.1, and 49.5%; p < 0.001). The Spearman analysis indicated that SUA was positively correlated to LVMI and negatively correlated to eGFR. The logistic regression analysis revealed that the odd ratio for LVH in the highest SUA quartile was 2.439 (95% CI 1.265–4.699; p = 0.008; model 1) or 2.576 (95% CI 1.150–5.768; p = 0.021; model 2) compared with that in the lowest SUA quartile. However, there was no significant increased risk of LVH in the subjects with the highest SUA quartile after adjusting the eGFR (OR = 1.750; 95% CI 0.685–4.470; p = 0.242; model 3). Conclusions In selected population, such as type 2 DKD, the elevated SUA level is positively linked with the increased risk of LVH, but this relationship is not independent of eGFR.

Diagnostic Accuracy of Left Ventricular Hypertrophy in Patients with Myocardial Infarction by Computer‐Assisted Electrocardiography (ELECTROPRES)

Information is limited about the classification accuracy of electrocardiographic (ECG) criteria for left ventricular hypertrophy (LVH) in the presence of myocardial infarction (MI). We evaluated LVH classification accuracy for a set of 16 ECG criteria and some combinations derived from them in 1642 patients (105 with MI) suspected of coronary heart disease with two-dimensional echocardiography evaluation and a standard 12-lead ECG recorded at the same time. Patients with left bundle branch block had previously been excluded. Measures of classification accuracy included sensitivity, specificity, likelihood ratios, and positive and negative predictive values. Diagnostic accuracy varied widely for different LVH criteria. The criteria with the best overall performance had highest sensitivity in the presence of MI and sensitivities of approximately 30% with relatively low specificities ranging from 72% to 78%. However, the classification accuracy for them was similar to that for patients without MI. The prevalence of LVH in patients with MI was higher (56%) than in those with no MI (31%). Classification accuracy of the best single previously published LVH criteria was comparable to that of the best combinations of any three of them. The classification accuracy of LVH criteria in the presence of MI is comparable to that in patients without MI, in part possibly due to the higher LVH prevalence in the MI group. The presence of a well-validated computer database facilitates comparative evaluation of ECG-LVH criteria and derivation of optimal combinations of criteria for any given clinical application.

The α2C-Del322–325 adrenoceptor polymorphism and the occurrence of left ventricular hypertrophy in hypertensives

Objectives. Sympathetic activation has a role in the development of left ventricular hypertrophy (LVH). The presynaptic α2C-adrenoceptor inhibits the release of norepinephrine from sympathetic nerve terminals in the heart. A deletion polymorphism in the α2C-adrenoceptor (α2CDel322–325) generates a hypofunctional α2C-adrenoceptor, which may result in chronic adrenergic signalling. This study aimed to investigate whether the α2CDel322–325 polymorphism was associated with an increased prevalence of LVH in patients with systemic hypertension. Methods. Left ventricular mass was measured in 205 patients with systemic hypertension and 60 normal volunteers using a 1.5-T Philips MRI system. Genotyping was performed using a restriction fragment length polymorphism assay. Results. No significant difference was observed between the distribution of the α2CDel322–325 genotypes in hypertensive patients with LVH compared with those without LVH. Adjusting for confounding variables the odds ratio (OR) of being ins/del for the α2CDel322–325 and having LVH was 0.49 (95% CI 0.14–1.69, p = 0.256). Conclusions. These observations suggest that there is little evidence for an association between α2CDel322–325 polymorphism and an increased prevalence of LVH in patients with systemic hypertension.

Left ventricular mass in hypertensive patients with mild‐to‐moderate reduction of renal function

Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular (CV) morbidity and mortality. The aim of the present study was to evaluate the relationship between LV mass and mild-to-moderate renal dysfunction in a group of non-diabetic hypertensives, free of CV diseases, participating in the Renal Dysfunction in Hypertension (REDHY) study. Patients with diabetes, a body mass index (BMI) of more than 35 kg/m(2), secondary hypertension, CV diseases and a glomerular filtration rate (GFR) of less than 30 mL/min per 1.73 m(2) were excluded. The final sample included 455 patients, who underwent echocardiographic examination and ambulatory blood pressure monitoring. There was a significant trend for a stepwise increase in LV mass, indexed by both body surface area (LVMI) and height elevated to 2.7 (LVMH(2.7)), with the declining renal function, that remained statistically significant after correction for potential confounders. The prevalence of LVH, defined either as LVMI of 125 g/m(2) or more or as LVMH(2.7) of 51 g/m(2.7) or more, was higher in subjects with lower values of GFR than in those with normal renal function (P < 0.001 in both cases). The multiple regression analysis confirmed that the inverse association between GFR and LVM was independent of confounding factors. The present study confirms the high prevalence of LVH in patients with mild or moderate renal dysfunction. In the patients studied (all with a GFR of 30 mL/min per 1.73 m(2)), the association between LVM and GFR was independent of potential confounders, including 24 h blood pressure load. Taking into account the negative prognostic impact of LVH, further studies focusing on a deeper comprehension of the mechanisms underlying the development of LVH in chronic kidney disease patients are needed.

Prevalence of left ventricular hypertrophy detected by Cornell voltage‐duration product in a hypertensive population

Introduction. Detection and treatment of left ventricular hypertrophy (LVH) in hypertension is important in order to reduce cardiovascular risk. The product of QRS voltage and duration (e.g. Cornell voltage‐duration product; CorP), is a good marker of LVH and the current study was designed to determine the prevalence of LVH in patients with essential hypertension treated in general practice. Methods. This study was a multicenter, cross‐sectional survey in outpatient hypertensive patients attending clinics across Spain. The primary endpoint for detection of LVH was a CorP >2.440 mm·ms on ECG recordings, which were independently assessed. Results. Seven hundred and eighty‐two patients were evaluated (66.1±10.4 years; 50.6% males; body mass index 28.2±6.1 kg/m2) with a mean baseline blood pressure (BP) of 155.7±17.7/90.8±10.6 mmHg. Only 13.2% of the study population had BP that was adequately controlled. LVH was detected in 23.4% of patients using the CorP method. Predictors of LVH were prior history of LVH, hypertensive retinopathy, age, grade II hypertension and male gender. Conclusions. Almost one‐quarter of hypertensive patients who attended outpatient clinics in Spain had LVH detected by CorP. The CorP criterion appears to be a useful method for detecting LVH in general practice.

The Cardiovascular Risk Factor, Left Ventricular Hypertrophy, Is Highly Prevalent in Stable, Treated Angina Pectoris

In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy (LVH). However, LVH will only have a large impact overall in CAD if it is highly prevalent. Therefore we aimed to assess the prevalence of LVH in patients with stable, treated angina and its relationship with blood pressure (BP). Three hundred twenty-two consecutive patients with angiographically confirmed coronary artery disease were recruited. Echocardiographic LV mass was performed and correlated with both office and 24-h ambulatory BP. Of the 267 patients with LV mass measurements, 195 (73%) had LVH. The mean 24-h ambulatory BP reading was systolic 125 +/- 12 mm Hg and diastolic 68 +/- 8 mm Hg in the LVH group. Of the LVH patients 62% had a nonhypertensive 24-h BP reading. On multivariate logistic regression analysis, factors independently related to LVH were history of hypertension (odds ratio [OR] 1.848, 95% confidence interval [CI] 1.051-3.248), body mass index (OR 1.085, 95% CI 1.011-1.165), and age (OR 1.039, 95% CI 1.004-1.076). We conclude that echo LVH is very common in patients with stable, treated angina and the majority of these patients had a nonhypertensive BP at the time of study. Studies are now required to determine whether identifying and vigorously treating LVH in CAD would reduce the risk of premature death in these patients.

Left ventricular hypertrophy is present in one-half of newly-diagnosed peripheral arterial disease patients

Peripheral arterial disease (PAD) patients are at high risk of cardiac death. Coincidental but silent coronary disease is obviously a major contributor but left ventricular hypertrophy (LVH) could be a second major contributor. To investigate whether LVH could really be making a large contribution to cardiac death in PAD, we assessed the prevalence of LVH when PAD was first diagnosed. The prevalence of echo LVH when left ventricular mass was indexed to body surface area was 50%. Although office blood pressure and 24-h blood pressure were both significantly higher in those with LVH, in clinical practice, a contemporaneous blood pressure measurement (office or 24 h) at the time of PAD diagnosis would only partially identify those with LVH. For example, an office blood pressure cut-off of < 140/90 mmHg was found in 27% of all LVH cases and a 24-h blood pressure cut-off of < 125/80 mmHg was found in 24% of all LVH cases. In conclusion, there is already a high prevalence of LVH in patients at first diagnosis of PAD. LVH is therefore common enough in PAD patients to potentially make a major contribution to cardiac death, which means that future research should now investigate whether screening for and regressing LVH when present would actually reduce cardiac deaths over and above merely achieving target blood pressure.

Prospective trials on anemia of chronic disease: The Trial to Reduce Cardiovascular Events with Aranesp® Therapy (TREAT): Management of comorbidities in kidney disease in the 21st century: Anemia and bone disease

Chronic kidney disease (CKD) is emerging as a major public health problem in the United States. Between 1973 and 1999 there was a more than 30-fold increase in the number of patients enrolled in the Medicare funded end-stage renal disease (ESRD) program, from approximately 10,000 to 340,000 [1]. The annual incidence of ESRD has nearly doubled from 48,350 patients (190 per million) in 1991 to 89,252 (317 per million) in 1999. Estimates from the Third National Health and Nutrition Examination Survey (NHANES III), using the glomerular filtration rate (GFR) equation from the Modification of Diet in Renal Disease (MDRD) study [2, 3], showed that the prevalence of CKD, defined as a GFR 60 mL/min /1.73 m2, was approximately 8.3 million individuals, or 4.7% [4]. The MDRD Study indicated that 85% of patients with impaired kidney function (GFR 55 mL/min/1.73m2) have progressive losses of kidney function at a rate of 4 mL/min per year [5]. The progressive nature of CKD, and epidemiologic factors that include population aging, increasing prevalence of type II diabetes and hypertension, improved survival of patients on dialysis, and the acceptance of higher risk patients into ESRD programs, explain the ongoing and projected increases in the numbers of patients with ESRD. The increasing incidence and prevalence of ESRD and CKD is a global trend not just confined to the United States [6]. Although incidence rates for the United States and Japan are nearly two-fold higher than those of other industrialized nations, the rates of growth appear to be quite similar, best described by an exponential growth curve at the rate of 7.36% per year [7]. The impact of these numbers must be interpreted from

Relationship of the electrocardiographic strain pattern to left ventricular structure and function in hypertensive patients: the LIFE study

OBJECTIVES This study was designed to assess the relation of electrocardiographic (ECG) strain to increased left ventricular (LV) mass, independent of its relation to coronary heart disease (CHD). BACKGROUND The classic ECG strain pattern, ST depression and T-wave inversion, is a marker for left ventricular hypertrophy (LVH) and adverse prognosis. However, the independence of the relation of strain to increased LV mass from its relation to CHD has not been extensively examined. METHODS Electrocardiograms and echocardiograms were examined at study baseline in 886 hypertensive patients with ECG LVH by Cornell voltage-duration product and/or Sokolow-Lyon voltage enrolled in the Losartan Intervention For End point (LIFE) echocardiographic substudy. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite to the QRS axis in leads V 5 and/or V 6. RESULTS Strain occurred in 15% of patients, more commonly in patients with than without evident CHD (29%, 51/175 vs. 11%, 81/711, p < 0.001). When differences in gender, race, diabetes, systolic pressure, serum creatinine and high density lipoprotein cholesterol were controlled, strain on baseline ECG was associated with greater indexed LV mass in patients with (152 ± 33 vs. 131 ± 32 g/m 2, p < 0.001) or without CHD (131 ± 24 vs. 119 ± 22 g/m 2, p < 0.001). In logistic regression analyses, strain was associated with an increased risk of anatomic LVH in patients with CHD (relative risk 5.14, 95% confidence interval [CI] 1.16 to 22.85, p = 0.0315), without evident CHD (relative risk 2.91, 95% CI 1.50 to 5.65, p = 0.0016), and in the overall population when CHD was taken into account (relative risk 2.98, 95% CI 1.65 to 5.38, p = 0.0003). CONCLUSIONS When clinical evidence of CHD is accounted for, ECG strain is likely to indicate the presence of anatomic LVH. Greater LV mass and higher prevalence of LVH in patients with strain offer insights into the known association of the strain pattern with adverse outcomes.

Severe left ventricular hypertrophy in pediatric dialysis: prevalence and predictors.

Left ventricular hypertrophy (LVH) has been recognized as an independent risk factor for cardiovascular morbidity and mortality in adults with end-stage renal disease. However, the prevalence and severity of LVH in children on chronic dialysis therapy is not well established. Retrospectively, 64 chronic dialysis patients, aged 20 months to 22 years, on chronic dialysis had echocardiographic evaluation of LV mass (LVM) and geometry. Forty-eight (75%) children had LVH, including 22 of 26 (85%) on hemodialysis (HD) and 26 of 38 (68%) on peritoneal dialysis (PD). The prevalence of LVH in patients on HD was significantly higher than those on PD (P=0.02). Abnormal LV geometry was found in 51 of 64 (80%) patients: 25 patients (39%) had eccentric hypertrophy, 3 (5%) had concentric remodelling, and 23 (36%) had concentric LVH. Twenty-six children (41%) had severe LVH, defined as LVM index greater than 51 g/m2.7, which is associated with a fourfold greater risk for development of cardiovascular disease in adults. Patients with severe LVH had a significantly lower hemoglobin level (P=0.027) and longer duration of renal disease prior to the start of dialysis therapy (P=0.003) than patients without LVH. Multiple logistic regression analysis revealed HD as opposed to PD as a significant independent predictor for severe LVH (P=0.036). Higher systolic blood pressure remained in the final model as an independent predictor with a borderline level of significance (P=0.065). The results indicate that severe LVH and abnormal left ventricular geometry are common in young dialysis patients. Better control of blood pressure, anemia, and hypervolemia may be important in prevention or improving LVH.

Impact of Blood Pressure Control on Prevalence of Left Ventricular Hypertrophy in Treated Hypertensive Patients

Aim: The aim of the present study was to evaluate (1) the prevalence and patterns of left ventricular hypertrophy (LVH) and (2) the impact of blood pressure (BP) control, assessed by clinical and 24-hour ambulatory BP monitoring (ABPM) criteria on the persistence of LVH in a representative sample of treated patients attending our Hypertension Clinic. Methods: One hundred consecutive essential hypertensives (61 m/39 f, age 56± 9 years) regularly followed up by the same medical team (average period 52 months, 12–156 months) were included in the study and underwent 24-hour ABPM and complete echocardiographic examination. Results: Twenty-eight of the 100 patients were found to have LVH [left ventricular mass index (LVMI) >125 g/m² in men and >110 g/m² in women]; LVH was eccentric in 20 patients and concentric in the remaining 8. LVMI did not correlate with clinical BP values but only with ABPM values (mean 24 h systolic r = 0.34, p <0.01; diastolic r = 0.37, p <0.01). The prevalence of LVH in patients controlled according to clinical BP criteria (n = 43, BP <140/90 mm Hg) was 19%, in patients controlled according to ABPM criteria (n = 30, BP during daytime <132/85 mm Hg) 17%, and in those controlled with both criteria (n = 16) 6% (p <0.01). Conclusions: The results of this study suggest that the eccentric type of LVH is the prevalent pattern in chronically treated patients. The persistence of LVH is significantly dependent on BP levels achieved during treatment; indeed the prevalence of LVH is very low in patients with an optimal BP control, whereas it is elevated (37%) in uncontrolled patients.

Prevalent left ventricular hypertrophy in the predialysis population: Identifying opportunities for intervention

Left ventricular hypertrophy (LVH) is present in over 70% of patients commencing dialysis. It is an independent risk factor for cardiac death, which is the cause of death in approximately 45% of patients on dialysis. The prevalence of LVH in patients earlier in the course of renal insufficiency is unknown. As part of a prospective longitudinal study evaluating the progression of comorbid diseases in patients with progressive renal disease, we evaluated LVH. In 175 consecutive patients attending a renal insufficiency clinic we obtained technically adequate echocardiograms and estimated left ventricular mass index (LVMI) using two-dimensional targeted M-mode echocardiography. We calculated LVMI using the American Society of Echocardiography cube formula method regressed to anatomic validation. The population consisted of 115 men and 60 women ranging in age from 20 to 82 years (mean age, 51.5 years). The mean creatinine was 403 ± 207 μmol/L (±SD), representing a creatinine clearance (Ccr) of 25.5 ± 17 mL/min. Left ventricular hypertrophy was defined as LVMI greater than 131 g/m 2 in men and greater than 100 g/m 2 in women, and was present in 38.9% of the population studied. We demonstrate that the prevalence of LVH increases with progressive renal decline: 26.7% of patients with Ccr greater than 50 mL/min had LVH, 30.8% of those with Ccr between 25 and 49 mL/min had LVH, and 45.2% of patients with severe renal impairment (Ccr <25 mL/min) had LVH ( P = 0.05). The mean LVMI was significantly different among the three groups (97.5 g/m 2 v 100.8 g/m 2 v 114.4 g/m 2, respectively; P < 0.001). Univariate analyses revealed that age, hemoglobin, systolic blood pressure, and Ccr were significantly different between the groups with and without LVH. The logistic regression model confirmed the findings of the univariate analysis: an increase in age of 5 years was associated with an increase of 3% in risk of LVH ( P = 0.0094), as was an increase in systolic blood pressure and for each 5 mL/min decline in Ccr the risk increased by 3% ( P = 0.0168). We demonstrate the high prevalence of LVH in patients with renal insufficiency prior to the need for dialysis, which is associated with severity of renal impairment, and identity two modifiable factors (systolic blood pressure anemia) as important predictors of LVH. We suggest that future studies should focus on interventions aimed attenuating the impact of these factors.