Comparative Assessment of 2-Dimensional Echocardiography vs Cardiac Magnetic Resonance Imaging in Measuring Left Ventricular Mass in Patients With and Without End-Stage Renal Disease

Background

While echocardiography (ECHO)-measured left ventricular mass (LVM) predicts adverse cardiovascular events that are common in hemodialysis (HD) recipients, cardiac magnetic resonance imaging (CMR) is now considered the reference standard for determination of LVM. This study aimed to evaluate concordance between LVM measurements across ECHO and CMR among chronic HD recipients and matched controls.

Methods

A single-centre, cross-sectional study of 41 chronic HD patients and 41 matched controls with normal kidney function was performed to compare LVM measurements and left ventricular hypertrophy (LVH) designation by ECHO and CMR.

Results

In both groups, ECHO, compared with CMR, overestimated LVM. Bland-Altman analysis demonstrated wider agreement limits in LVM measurements by ECHO and CMR in the chronic HD group (mean difference, 60.8 g; limits −23 g to 144.6 g) than in the group with normal renal function (mean difference, 51.4 g; limits −10.5 g to 113.3 g). LVH prevalence by ECHO and CMR in the chronic HD group was 37.5% and 22.5%, respectively, while 17.5% and 12.5% had LVH by ECHO and CMR, respectively, in the normal kidney function group. Intermodality agreement in the designation of LVH was modest in the chronic HD patients (κ = 0.42, P = 0.005) but strong (κ = 0.81, P < 0.001) in the patients with preserved kidney function. Agreement was strong in assessing LVH by ECHO and CMR only in those with normal kidney function.

Conclusions

Our results suggest that the limitations of LVM measurement by ECHO may be more pronounced in patients receiving HD, and provide additional support for the use of CMR in research and clinical practice when rigourous assessment of LVM is essential.     

Reclassification of adolescent hypertension by ambulatory blood pressure monitoring using adult norms and association with left ventricular hypertrophy

2017 pediatric blood pressure (BP) guidelines applied adult BP norms to define clinic hypertension (HTN) in patients ≥ 13 years. 2014 pediatric ambulatory BP monitor (ABPM) guidelines recommend age‐ and sex‐specific percentile norms for patients < 18 years. The authors evaluated reclassification of HTN when applying adult ABPM norms in patients ≥ 13 years and assessed the association of left ventricular hypertrophy (LVH) with HTN. Charts of patients 13–17 years with ABPM 9/2018–5/2019 were reviewed for sex, age, height, weight, BP medication, ABPM results, and left ventricular mass index (LVMI). American Heart Association 2005 (AHA 2005), AHA 2017 (AHA 2017), and European Society of Hypertension 2018 (ESH 2018) guidelines for adult ABPM were compared with 2014 AHA pediatric norms (pABPM). HTN was defined by each guideline using only ABPM. ABPM and clinic BP were used to classify white coat hypertension (WCH) and masked hypertension (MH). LVH was defined as LVMI > 51 g/m^2.7. 272 patients had adequate ABPM. 124 patients also had echocardiogram. All adult norms resulted in significant reclassification of HTN. LVMI correlated significantly with systolic BP only. The odds of a patient with HTN having LVH was significant using AHA 2005 (OR: 8.75 [2.1, 36.4], p = .03) and ESH 2018 (OR: 4.94 [1, 24.3], p = .002). Significant reclassification of HTN occurs with all adult norms. HTN is significantly associated with LVH using AHA 2005 and ESH 2018. Applying pediatric norms for ABPM while using adult norms for clinic BP causes confusion. Guideline selection should balance misdiagnosis with over‐diagnosis.     

Blood pressures values during evaluation of 24-h ambulatory blood pressure monitoring and left ventricular hypertrophy in patients with chronic renal failure treated with hemodialysis (HD)

Left ventricular hypertrophy (LVH) is common and important predictor of risk of death in end-stage renal failure. In the present study we have analysed the relationship between 24-h ambulatory blood pressure (BP) profile and LVH. The effect of parathyroid hormone (PTH) on was also assessed. From a cohort of 85 patients with crf we selected for analysis 59 stable patients. Ambulatory BP 24-h monitoring, echocardiography (ECHO), body mass index (BMI), serum creatinine, hemoglobin, total protein, albumin, electrolytes and PTH concentrations were assessed in all patients. Concentric LVH was detected by ECHO in 46 patients, in 13 patients excentric LVH was observed. Mean 24-h ambulatory sBP, dBP, mean 24-h ambulatory day sBP, dBP as well as night sBP and dBP were significantly higher than in a control group 60 healthy subjects. It was a correlation between mean 24-h ambulatory sBP and left ventricular mas (LVM) r = 0.606 (p < 0.0001), between mean dBP and (LVM) r = 0.498 (p < 0.001), between mean day sBP and (LVM) r = 0.591 (p < 0.0001), between mean day dBP and (LVM) r = 0.479 (p < 0.001), between mean night dBP and (LVM) r = 0.548 (p < 0.0001), between left ventricular mass index (LVMI) and mean sBP r = 0.428 (p < 0.05), between LVMI and mean day sBP r = 0.442 (p < 0.05). The loss in physiological night-time BP was observed in all patients. It was also correlations between PTH and (LVM) r = 0.704 (p < 0.001), and between BMI and LVMI r = -0.451 (p < 0.05). LVH is common in crf patients. These results confirmed that strong correlations between BP values and LVH and between serum PTH concentrations and LVH indicate that both hypertension and hyperparathyroidism play an important role in the LVH development.     

The Initial Stage of Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats is Manifested by a Decrease in the QRS Amplitude/Left Ventricular Mass Ratio

In this study we tested the hypothesis of the relative voltage deficit, i.e. the discrepancy between increased left ventricular mass (LVM) and QRS amplitudes, in an experimental model of spontaneously hypertensive rats (SHR) during the period of a moderate increase in blood pressure. To address this issue we recorded orthogonal electrocardiograms of male SHR at the age of 12 and 20 weeks. During this period the systolic blood pressure (sBP) increased from 165 ± 3 mmHg to 195 ± 1 mmHg (p < 0.001). Age and sex matched WKY rats were used as control groups. The sBP values in WKY normotensive control groups were within normal limits (122 ± 8 mmHg and 130 ± 4mmHg, respectively). The maximum QRS spatial vector magnitude (QRSmax) was calculated from X, Y, Z amplitudes of the orthogonal electrocardiograms. The animals were sacrificed and the left ventricular mass was weight. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The LVM in SHR (0.86 ± 0.05 g and 1.05 ± 0.07 g, respectively) was significantly higher as compared to WKY (0.65 ± 0.07 g and 0.70 ± 0.02 g), and the increase of LVM closely correlated with the sBP increase. On the other hand, QRSmax in SHR did not follow either the increase of sBP, or LVM. The QRSmax values in SHR did not differ from those of WKY at the age of 12 weeks (0.59 ± 0.14 mV compared to 0.46 ± 0.05 mV), and they were even lower in SHR at the age of 20 weeks (0.74 ± 0.08 mV compared to 0.44 ± 0.05 mV, p < 0.001). The values of SP, quantifying the relative voltage deficit, were significantly lower in SHR as compared to the WKY control. The values decreased significantly in SHR with increasing age, sBP and LVM, i.e., with the progression of hypertrophic remodeling of the left ventricle. The results of this study support the hypothesis of the relative voltage deficit in LVH. These results are consistent with the finding of a high number of false negative ECG results in clinical ECG diagnostics of LVH, and could contribute to an understanding of the diagnostic importance of the false negative ECG results, their re‐evaluation and utilization for clinical diagnosis and prognosis.     

Left Ventricular Hypertrophy Phenotype in Childhood‐Onset Essential Hypertension

The aim of this study was to determine the risk factors associated with left ventricular (LV) hypertrophy (LVH) among 89 untreated children with primary hypertension. Clinic hypertension was confirmed by 24‐hour ambulatory blood pressure (BP) monitoring. LV mass (LVM) index was calculated as LVM (g)/height (m)^2.7 and LVH was defined as LVM index >95th percentile. Children with (n=32) and without (n=57) LVH were compared. Both obesity and systolic BP were independently associated with LVH, with a higher contribution by body mass index. Obesity contributed significantly, with a nearly nine‐fold increased risk of LVH. There was evidence of effect modification by the presence or absence of obesity on the relationship between systolic BP and LVH, whereby the relationship existed mainly in nonobese rather than obese children. Hence, to achieve reversal of LVH, clinicians should take into account both BP control and weight management.     

Excessive increase in left ventricular mass identifies hypertensive subjects with clustered geometric and functional abnormalities

BACKGROUND: Left ventricular mass (LVM) exceeding needs to sustain haemodynamic load has been termed 'inappropriate left ventricular mass'. We hypothesized that inappropriate LVM identifies hypertensive patients with clustered cardiac geometric and functional abnormalities. METHODS: For this purpose, 359 hypertensive individuals without prevalent cardiovascular disease underwent Doppler echocardiography. Observed LVM exceeding more than 28% of the value predicted for individual cardiac work, body size and sex was defined as inappropriate LVM. Concentric left ventricular geometry was defined as age-adjusted relative wall thickness (RWT) greater than 0.40. Systolic dysfunction was defined as ejection fraction less than 50% or midwall shortening less than 14.7%. Diastolic dysfunction was defined as isovolumic relaxation time (IVRT) greater than 100 ms, E-velocity deceleration time greater than 220 ms or age and heart rate-normalized early/late (E/A) ratio less than 0.66. Left ventricular hypertrophy (LVH) was defined as an LVM index greater than 49.2 g/m2.7 in men and 46.7 g/m2.7 in women. RESULTS: As expected, inappropriate LVM was associated with higher RWT, lower left ventricular systolic function, longer IVRT and prolonged E-deceleration time (all P < 0.05). Patients with inappropriate LVM had a higher prevalence of concentric geometry (65.5 versus 40.4%), systolic dysfunction (67.9 versus 47.4%) and diastolic dysfunction (46.4 versus 39%; all P < 0.001) than those with LVH. Inappropriate LVM had greater sensitivity (0.89 versus 0.54) and specificity (0.82 versus 0.62; both P < 0.01) than LVH in identifying patients with clustered left ventricular concentric geometry, systolic and diastolic dysfunction. CONCLUSIONS: Inappropriate LVM is associated with a cluster of concentric left ventricular geometry, delayed left ventricular relaxation and reduced systolic performance. Compared with LVH, inappropriate LVM is more accurate at identifying patients with clustered left ventricular geometric and functional abnormalities.     

Relation Between QRS Amplitude and Left Ventricular Mass in the Initial Stage of Exercise-Induced Left Ventricular Hypertrophy in Rats

The aim of the study was to analyze the relationship between QRS amplitude and left ventricular mass (LVM) in early stages of two different experimental models of left ventricular hypertrophy (LVH) in rats: in exercise-induced hypertrophy and pathological hypertrophy due to genetically conditioned pressure overload. Three groups of experimental animals were studied: healthy control Wistar-Kyoto rats (WKYs), spontaneously hypertensive rats (SHRs), and WKY rats exposed to training by intermittent swimming (SWIM). Orthogonal electrocardiograms were recorded in each group at the age of 12 and 20 weeks, and the maximum spatial QRS vector (QRSmax) was calculated. Then the animals were sacrificed and LVM was measured. The specific potential of myocardium (SP) was calculated as a ratio of QRS_max to LVM. The QRSmax values did not follow the changes in LVM. At the end of the follow-up period, the highest values of QRSmax were recorded in the control WKY rats (0.80 ± 0.05 mV). The QRSmax values in both groups with experimental LVH were significantly lower as compared with control animals (SHR 0.44 ± 0.02 mV, p < 0.001; SWIM 0.53 ± 0.04 mV, p < 0.001). Similarly, the SP values were significantly lower in both groups with experimental LVH as compared with control animals (SHR 0.42 ± 0.02 mV/g, p < 0.001; SWIM 0.55 ± 0.05 mV/g, p < 0.001). A decrease in QRSmax and SP was observed in both models of experimental LVH. We attributed these findings to the changes in electrogenetic properties of myocardium in the early stage of developing LVH. In other words, it is changes of nonspatial determinants that influence the resultant QRS voltage in terms of the solid angle theory.     

High prevalence of cardiac hypertophy without detectable signs of fibrosis in patients with untreated active acromegaly: an in vivo study using magnetic resonance imaging

Objective Left ventricular (LV) hypertrophy and myocardial fibrosis are considered the main pathological features of acromegalic cardiomyopathy. The aim of the study was to evaluate the proportion of LV hypertrophy and the presence of fibrosis in acromegalic cardiomyopathy in vivo using cardiac magnetic resonance (CMR). Design and patients Fourteen consecutive patients (eight women, mean age 46 ± 10 years) with untreated active acromegaly were submitted to two‐dimensional (2D) colour Doppler and integrated backscatter (IBS) echocardiography and CMR. Measurements LV volume, mass and wall thickness and myocardial tissue characterization (IBS and CMR). Results On echocardiography: mean LV mass (LVM) and LVM index (LVMi) were 209 ± 48 g and 110 ± 24 g/m², respectively; hypertrophy was revealed in five patients (36%); abnormal diastolic function [evaluated by isovolumic relaxation time (IVRT) or early (E) to late or atrial (A) peak velocities (E/A ratio)] was found in four patients (29%). Systolic function evaluated by measuring LV ejection fraction (LVEF) was normal (mean 72 ± 12%) in all patients. Six patients (43%) had increased IBS (mean 57·4 ± 6·2%). On CMR: mean LVM and LVMi were 151 ± 17 g and 76 ± 9 g/m², respectively; 10 patients (72%) had LV hypertrophy. Contrastographic delayed hyperenhancement was absent in all patients; on the contrary, mild enhancement was revealed in one patient. Systolic function was normal in all patients (LVEF 67 ± 11%). LVMi was not related to serum IGF‐1 concentrations or the estimated duration of disease. Conclusions CMR is considered to be the gold standard for evaluating cardiac hypertrophy, fibrosis and systolic function. Using CMR, 72% patients with untreated active acromegaly had LV hypertrophy, which was only detected in 36% patients by echocardiography. However, cardiac fibrosis was absent in all patients irrespective of the estimated duration of disease. Although a very small increase in collagen content (as suggested by increased cardiac reflectivity at IBS), not detectable by CMR, could not be ruled out, it is unlikely that it would significantly affect cardiac function.     

Indexation criteria of ventricular mass and predictive role of blood pressure and body composition

BACKGROUND: There is no definite consensus on which indexation of left ventricular mass (LVM) should be used to better identify left ventricular hypertrophy (LVH). Left ventricular mass has been adjusted to height, to height2.7(h2.7) and to body surface area (BSA). The aims of the present study were to evaluate the prevalence of LVH according to different indexations and different cut-offs and to identify the most useful indexation of LVM to detect hypertension-related LVH. METHODS: Echocardiographic LVH was defined as LVM to h2.7, LVM to BSA, LVM to height, LVM values in the upper 5th percentile of our gender-related LVM distribution, using different partition values suggested in previous population-based studies. RESULTS: Prevalence of LVH in the general population was 32% using the less restrictive criterion (LVH 49.2/46.7 g/m2.7), 15% with the criterion of LVH 116/104 g/m2, and 3.8% with the most restrictive one (LVH 134/110 g/m2). Prevalence of LVH in hypertensive subjects was almost twice than in normotensive subjects with all criteria. Only 20 subjects out of the 707 evaluated were found to have LVH with all six criteria. In multiple regression analysis SBP was independently associated with nonindexed LVM and was indexed to both BSA and h2.7. On the other hand, fat-free mass was a powerful predictor of nonindexed LVM or of LVM to BSA, whereas body mass index was the strongest predictor of LVM to h2.7. CONCLUSIONS: The indexation of LVM to BSA, possibly with the cut-off of LVH 116/104, is probably the best criterion for identifying blood pressure-related LVH.     

Left ventricular mass and hypertrophy assessment by means of the QRS complex voltage-independent measurements

ECG QRS-complex voltage-based criteria are relatively insensitive for detection of increased left ventricular mass (LVM). We developed and evaluate a new ECG index for LV hypertrophy (LVH) detection regardless of the QRS voltage. METHODS: Study population consisted of 106 patients (73 m, 33 f, aged 60 +/- 10 years) with established coronary artery disease (CAD). All patients had LVM assessed echocardiographically and indexed to BSA (LVMI(ECHO)). LVH was diagnosed if LVMI(ECHO) >117 g/m2 in men and >104 g/m2 in women. LV geometry was also determined. Analysed ECG variables, obtained from 12 leads recorded simultaneously, were: the QRS complex duration (QRSd, ms), the average 12-lead time to maximal deflection (TMD, ms), the average 12-lead QRS complex voltage (12QRSV, mV), the average product of 12 lead QRS voltage and duration (12QRSVd, mV ms), Sokolow-Lyon voltage and V-d product (SLV, SLVd), Cornell voltage and V-d product (CV, CVd). A newly developed index, LVM(ECG), was calculated, as LVM(ECG) = [(2 x TMD+QRSd/pi)3-(QRSd/pi)3]*0.0001 (ms3), and indexed to BSA (LVMI(ECG), ms3/m2). RESULTS: Means of the QRS voltage-related parameters were similar in patients with LVH and normal LVM. Greater differences existed between both groups when the QRS voltage-duration products were compared. LVMI(ECG) was most powerful in distinguishing between groups (130 +/- 33 LVH vs 91 +/- 21 normal LVM, p < 0.001). LVMI(ECG) correlated with LVMI(ECHO) better (r = 0.77, p < 0.001) than other indices (r coefficients between 0.24 for SLV and 0.49 for CVd). None of the examined indices allowed for distinction between eccentric and concentric LVH. The new index showed better statistical performance (area under ROC = 0.861) compared to the other indices (AUC range 0.545-0.697, p<0.001 vs LVMI(ECG)). At the specificity level of 92%, the value of LVMI(ECG) > 120 ms3/m2 had the sensitivity of 64% for detection of increased LVM. The sensitivities of the other parameters were significantly lower (sensitivity range 18-42%). Relative intra- and interobserver errors and correlation coefficients for LVMI(ECG) calculation were 0.4% and 1.6% and r = 0.94 and 0.98, respectively. CONCLUSIONS: In patients with CAD an assessment of LV mass and detection of hypertrophy using the QRS complex time-dependent index is feasible. The new index correlated well with echocardiographically-determined LVM and showed better statistical performance than indices which include QRS-voltage measurements. The results are promising and warrant further studies to evaluate the utility of the new index as a risk predictor.     

Appropriate or inappropriate left ventricular mass in the presence or absence of prognostically adverse left ventricular hypertrophy

OBJECTIVES: To evaluate whether assessment of appropriateness of left ventricular mass (LVM) adds to the traditional definition of left ventricular hypertrophy (LVH). DESIGN: Cross-sectional, relational. METHODS: Echocardiographic LVH and appropriateness of LVM were studied in 562 subjects (231 normotensive controls, aged 35+/-11 years, 142 women; 331 hypertensive patients, aged 47+/-11 years, 135 women) classified on the basis of either the presence or the absence of both LVH (LVM index > or = 51 g/m2.7) and inappropriate LVM (LVM > 128% of the value predicted by an equation including age, sex and stroke work). RESULTS: Body mass index was comparable in hypertensive patients and controls. Hypertensive patients without LVH but with inappropriate LVM (n = 21) had higher relative wall thickness and total peripheral resistance than all other groups, whereas cardiac output was lower (all P < 0.001). Midwall mechanics was normal with appropriate LVM, independently of presence of LVH, whereas it was depressed in inappropriate LVM, either with or without LVH (both P < 0.0001). There was no substantial difference in ejection fraction among controls and hypertensive groups. Stress-corrected midwall shortening was more closely related to deviation of LVM from the value appropriate for stroke work, body size and gender (r = -0.56, P < 0.0001) than to LVM index (r = -0.26). CONCLUSIONS: Inappropriate LVM is associated with concentric geometry, high peripheral resistance and depressed wall mechanics. The deviation of LVM from the value appropriate for stroke work, body size and sex correlates with measures of myocardial function better than LVM.     

Patterns of QT Dispersion in Athletic and Hypertensive Left Ventricular Hypertrophy

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, ΔQT, ΔQTc). 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 (ΔQT 82 ± 2.1, 48 ± 1.3, 49 ± 2.3 ms; P < 0.01; ΔQTc 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.     

Comparison of electrocardiographic versus echocardiographic detection of left ventricular mass changes over time and evaluation of new onset left ventricular hypertrophy

We assessed the value of 3 electrocardiographic (EKG) voltage criteria in detecting variations of left ventricular mass (LVM) over time, taking echocardiographic (ECHO) LVM as reference, in the Pressioni Arteriose Monitorate E Loro Associazioni study. In 927 subjects (age 47 ± 13 years on entry, 49.9% men) an ECHO evaluation of LVM and EKG suitable for measurement of EKG-LVH criteria (Sokolow-Lyon voltage, Cornell voltage and R-wave voltage in aVL) were available at baseline and at a 2^nd evaluation performed 10 years later. Δ (delta) LVM, Δ LVMI, and Δ EKG parameters values were calculated from 2^nd evaluation to baseline. The sensitivity of the EKG criteria in the diagnosis of LVH, poor at baseline, becomes even worse after 10 years, reaching very low values. Only the sensitivity of R-wave amplitude exhibited slight increase over time but with unsatisfactory absolute values. Despite the prevalence of ECHO-LVH at the 2^nd evaluation was threefold increased compared to baseline (29.3% and 33.7% for LVM indexed to BSA and height^2.7, respectively), the prevalence of EKG-LVH was unchanged when evaluated by Sokolow-Lyon criteria, significantly reduced when assessed by Cornell voltage index, while significantly increased using R-wave voltage in aVL criteria. Despite an ECHO-LVM increase over the time, mean EKG changes were of opposite sign, except for R-wave amplitude in aVL. Our study highlights the discrepancy between ECHO and EKG in monitoring LVM changes over the time, especially for Sokolow-Lyon and Cornell voltage. Thus, EKG is an unsuitable method for the longitudinal evaluation of LVM variations.     

Left ventricular mass and atrial volume determined by cine magnetic resonance imaging in essential hypertension

To evaluate the relationship between left atrial volume determined by cine magnetic resonance imaging and progression of left ventricular hypertrophy (LVH), left atrial volume and echocardiographic left ventricular mass (LVM) were measured in 30 hypertensive patients (15 without LVH and 15 with LVH) and 10 normotensive control subjects. We also evaluated the effects of antihypertensive therapy on the cardiac chamber volumes and LVM in hypertensive patients. The cardiac chamber volumes and LVM were indexed by body surface area. Although there were no significant differences in left ventricular chamber volumes among the three groups, both maximum and minimum left atrial volume indexes, and the LVM index were greater in hypertensive patients with LVH than in the other two groups. The LVM index was correlated with maximum left atrial volume index (r = 0.74, P < .0001), and minimum left atrial volume index (r = 0.76, P < .0001), respectively. Furthermore, in multivariate models, the LVM index was significantly correlated with maximum left atrial volume index. In hypertensive patients with LVH, both maximum and minimum left atrial volume indexes, and the LVM index significantly reduced after treatment. The percent of changes in maximum left atrial volume index after treatment was significantly correlated with the percent of changes in LVM index after treatment. In conclusion, our data indicate that LVH is an independent determinant of left atrial enlargement, and both LVH and left atrial enlargement may be reversed by some effective therapeutic interventions.     

Electrocardiographic criteria for the diagnosis of abnormal hypertensive cardiac phenotypes

This article compared the performance of 18 electrocardiographic (ECG) left ventricular hypertrophic (LVH) criteria and four P‐wave indices for the diagnosis of echocardiographic (ECHO) LVH and left atrial enlargement (LAE), including the deepest S‐wave amplitude added to the S‐wave amplitude of lead V₄ (S_D+SV₄) and P‐wave terminal force in lead V₁ (PTFV₁). A total of 152 middle‐aged hypertensive patients without evident cardiovascular diseases (CVDs) were enrolled. The gold standard for the diagnosis of LVH and LAE was ECHO left ventricular mass index (LVMI) and largest left atrial volume index (LAVI). For the detection of LVH, Sokolow‐Lyon voltage, Cornell voltage, Cornell product, S_D+SV₄, Manning, and R+S in any precordial lead had relatively higher sensitivity, especially S_D+SV₄ criteria. Their combination could further increase sensitivity (43% vs 29% [S_D+SV₄], P = 0.016). PTFV₁ was the only criterion that had significant diagnostic value for ECHO LAE (AUC, 0.68; 95% CI: 0.54‐0.73, P = 0.008). For middle‐aged hypertensive patients without evident cardiovascular diseases, S_D+SV₄ had the highest sensitivity for the diagnosis of LVH and the combination of several ECG LVH criteria might further increase sensitivity. PTFV₁ had significant diagnostic value for ECHO LAE.     

Do Combined Electrocardiographic and Echocardiographic Markers of Left Ventricular Hypertrophy Improve Cardiovascular Risk Estimation?

The authors estimated the risk of cardiovascular mortality associated with echocardiographic (ECHO) left ventricular hypertrophy (LVH) and subtypes of this phenotype in patients with and without electrocardiographic (ECG) LVH. A total of 1691 representatives of the general population were included in the analysis. During a follow‐up of 211 months, 89 cardiovascular deaths were recorded. Compared with individuals with neither ECHO LVH nor ECG LVH, fully adjusted risk of cardiovascular mortality increased (hazard ratio [HR], 3.36; 95% confidence interval [CI], 1.51–7.47; P=.003) in patients with both ECHO‐LVH and ECG‐LVH, whereas the risk entailed by ECHO‐LVH alone was of borderline statistical significance (P=.04). Combined concentric nondilated LVH and ECG‐LVH, but not concentric nondilated LVH alone, predicted cardiovascular death (HR, 3.79; 95% CI, 1.25–11.38; P=.01). Similar findings were observed for eccentric nondilated LVH (HR, 3.37; 95% CI, 1.05–10.78; P=.04.). The present analysis underlines the value of combining ECG and ECHO in the assessment of cardiovascular prognosis related to abnormal left ventricular geometric patterns.     

Blood Pressure Variability in Children With Primary vs Secondary Hypertension

Increased blood pressure variability (BPV) is correlated with adverse cardiovascular (CV) events in adults. However, there has been limited research on its effect in the pediatric population. Additionally, BPV differences between primary and secondary hypertension (HTN) are not known. Children with primary and secondary HTN underwent 24‐hour ambulatory blood pressure monitoring and echocardiography studies. BPV measures of standard deviation (SD), average real variability (ARV), and range were calculated for the 24‐hour, daytime, and nighttime periods. Seventy‐four patients (median age, 13.5 years; 74% boys) were examined, 40 of whom had primary HTN. Body mass index z score and age were independent predictors of systolic ARV (R²=0.14) and SD (R²=0.39). There were no statistically significant differences in overall or wake period BPV measures between secondary or primary HTN groups, but sleep period diastolic SD was significantly greater in the secondary HTN group (9.26±3.8 vs 7.1±2.8, P=.039). On multiple regression analysis, secondary HTN was associated with increased sleep period diastolic SD (P=.025). No metrics of BPV in the overall, wake, and sleep periods were found to be significantly associated with left ventricular hypertrophy (LVH). The results of this study do not show a strong relationship between overall or wake BPV with primary vs secondary HTN, but the association of secondary HTN with sleep period diastolic BPV deserves further exploration. Contrary to expectation, the findings of this study failed to indicate a relationship between BPV and LVH for all patients as well for primary hypertensive and secondary hypertensive patients.     

Glucose effectiveness is strongly related to left ventricular mass in subjects with stage I hypertension or high-normal blood pressure

BACKGROUND: Evidence suggests that "glucose effectiveness," (SG) or the effect of glucose per se to enhance net glucose disposal, may be at least as important as the insulin sensitivity index (SI) in the assessment of glucose tolerance. Our objective was to study the relationship of SG and SI parameters to left ventricular mass in a group of untreated, nondiabetic, and nonobese subjects recently diagnosed with stage I or high-normal blood pressure (BP). METHODS: In this sample of subjects, among whom the expected prevalence of insulin resistance is low, we assessed SG and SI parameters using the intravenous glucose tolerance test and minimal model analysis. We also measured left ventricular mass (LVM) index and diastolic function by echocardiography. RESULTS: We observed a strong relationship between SG and LVM index (r = -0.61, P <.0001). Patients with left ventricular hypertrophy (LVH) had lower SG than those without LVH (0.1114 +/- 0.04 v 0.2088 +/- 0.08 x 10(-1). min(-1), P <.001). In contrast, patients below the lowest quartile of the SG parameter distribution had higher LVM index (126.4 +/- 23.1 v 94.8 +/- 22.3 g/m(2), P <.001) and also had higher prevalence of LVH than the other patients (P <.0001). The SI related only to diastolic dysfunction, suggesting that SG may be an earlier marker of LVH than SI in hypertension. CONCLUSION: In this sample of nonobese and glucose-tolerant subjects with an early stage of hypertension, SG but not SI was related to LVM.     

Echocardiographic definition of left ventricular hypertrophy in the hypertensive: which method of indexation of left ventricular mass?

OBJECTIVES: It has been suggested that hypertensives at high risk of cardiovascular complications can be identified on the basis of their left ventricular mass as determined echographically. However, there is as yet a lack of consensus on the mode of indexation (body surface area, height, height 2.7) of left ventricular mass (LVM), and on the cut-off values for definition of left ventricular hypertrophy (LVH). The main objective of this study is to test the influence of the different modes of indexation for LVM on the prevalence of LVH in a population of never treated hypertensive patients on the basis of cut-offs for LVM based upon its relationship with ambulatory blood pressure (BP) measurement. METHODS: A population of 363 untreated hypertensives was investigated using a standardised procedure. The men and women were analysed separately. We studied the relationship between mean daytime ambulatory systolic BP and LVM and calculated the LVM cut-off for a BP of 135 mm Hg using three different methods of indexation. On the basis of these criteria, the population was divided into those with and those without LVH. RESULTS: The prevalence of LVH was found to be higher when LVM was indexed to height2.7 (50.4%) or height (50.1%). Prevalence was lowest when LVM was indexed to body surface area (48.2%), which tended to minimise the hypertrophy in obese individuals. Only indexation by height 2.7 fully compensates for relationships between height and ventricular mass in this population. CONCLUSIONS: Indexing LVM to height 2.7 thus appeared to give a more sensitive estimate of LVH by eliminating the influence of growth. Cut-offs of 47 g/m2.7 in women and 53 g/m2.7 in men corresponded to a cardiovascular risk indicated by a daytime systolic BP >/=135 mm Hg.     

The Role of ECG in the Diagnosis of Left Ventricular Hypertrophy

The traditional approach to the ECG diagnosis of left ventricular hypertrophy (LVH) is focused on the best estimation of left ventricular mass (LVM) i.e. finding ECG criteria that agree with LVM as detected by imaging. However, it has been consistently reported that the magnitude of agreement is rather low as reflected in the low sensitivity of ECG criteria. As a result, the majority of cases with true anatomical LVH could be misclassified by using ECG criteria of LVH. Despite this limitation, it has been reported that the ECG criteria for LVH provide independent information on the cardiovascular risk even after adjusting for LVM. Understanding possible reasons for the frequent discrepancy between common ECG LVH criteria and LVH by echo or MRI would help understanding the genesis of ECG changes that occur as a consequence of increased LV mass.