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

Cesare Cuspidi; Rita Facchetti; Carla Sala; Michele Bombelli; Marijana Tadic; Guido Grassi; Giuseppe Mancia

doi:10.1111/jch.12834

. 2016 May 10;18(9):846–854. doi: 10.1111/jch.12834

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

Cesare Cuspidi ^1,^2,^✉, Rita Facchetti ¹, Carla Sala ³, Michele Bombelli ¹, Marijana Tadic ⁴, Guido Grassi ^1,⁵, Giuseppe Mancia ^1,²

PMCID: PMC8032070 PMID: 27160298

Abstract

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.

Left ventricular (LV) hypertrophy (LVH) as detected by electrocardiography (ECG) or echocardiography (ECHO) is a powerful predictor of nonfatal and fatal cardiovascular (CV) events and all‐cause death in a variety of clinical settings.1, 2, 3, 4, 5 Standard ECG is regarded as the first‐line method for detecting LVH, owing to its large availability, good reproducibility, and limited cost.6 In addition to these strengths, ECG provides clinically relevant information on cardiac rhythm, myocardial ischemia, ventricular “strain,” and conduction alterations.7

Numerous observational studies and randomized trials have shown that regression‐reduction of ECG LVH is associated with a lower likelihood of incident CV disease and all‐cause mortality.8, 9 Hence, hypertension guidelines support LVH detection by ECG at the initial workup and during treatment of hypertensive patients as a useful tool for improving CV risk estimation and treatment.6 A strong line of evidence, however, indicates that ECG criteria for detecting LVH have an unsatisfactory sensitivity, as proven by studies where cardiac mass was also estimated by ECHO10, 11 or by more sophisticated imaging techniques such as computerized tomography and magnetic resonance imaging.12

The array of clinical and prognostic information provided by ECHO (LV geometry, global systolic/diastolic function, regional kinesis, left atrial size, aortic diameter, and chamber mechanics), in addition to its superior accuracy for detecting LVH compared with standard ECG, are strong arguments for considering ECG findings of limited relevance in the evaluation of CV risk in clinical practice.13

Whether the increased risk is related to isolated ECHO LVH or ECG LVH is well documented, but the additional prognostic value provided by LVH positivity on both tests has been addressed by few studies in the general population.14, 15

Therefore, we aimed to investigate whether patients from a general population with LVH according to both tests have a higher risk of CV mortality than patients with LVH according to either ECG or ECHO. Furthermore, we extended, for the first time, such investigation to subtypes of ECHO LVH, as defined by the updated classification suggested by the Dallas Heart Study investigators based on four patterns: eccentric nondilated, eccentric dilated, concentric nondilated, and concentric dilated LVH.16 To this purpose we have analyzed the data obtained in the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study,16 a population study performed in a north region of Italy.

Methods

Population

The PAMELA study was carried out in a sample of 3200 patients representative of the population of Monza (a town near Milan, Italy) for sex and age decades (25–74 years). The participation rate was 64%; thus, data were collected from 2051 patients. Demographic characteristics of nonparticipants and participants were similar; this was also the case for CV risk factors as assessed by data collected via phone interviews. Overall, 1716 of 2051 patients without significant cardiac valve disease (>1+ valve regurgitation, any degree of valve stenosis, or presence of prosthesis) and preserved LV systolic function (ie, LV ejection fraction >50%) had an ECHO evaluation of LV mass (LVM) at baseline. A total of 1691 of 1716 participants also had a suitable ECG for detection of LVH (see ECG methods).

Entry Data

Methods employed in the PAMELA study have been previously described in detail.17 Briefly, after informed consent, patients were invited to undergo a comprehensive clinical evaluation at the outpatient clinic of the S. Gerardo University Hospital of Monza in the morning of a working day. Collected data included a full medical history, blood and urine samples, physical examination, and three sphygmomanometric blood pressure (BP) measurements in the sitting position, standard 12‐lead ECG, and ECHO. Body weight was recorded to the nearest 0.1 kg using a calibrated electronic scale with patients wearing indoor clothing without shoes. Height was recorded to the nearest 0.5 cm using a standardized wall‐mounted height board. Data collection included ambulatory BP, which was obtained by a monitoring device (Spacelabs 90207; Spacelabs Healthcare, Snoqualmie, WA) set to obtain automated BP and heart rate oscillometric readings every 20 minutes over 24 hours. During the monitoring period, participants were asked to pursue their normal activities and to self‐measure BP at home twice, namely at 8 am and 8 pm using a semiautomatic oscillometric device (Philips model HP 5331; Philips Healthcare, Andover, MA) on the arm contralateral to the one used for ambulatory BP monitoring.

Electrocardiography

Standard 12‐lead ECGs were recorded by our technical staff at 25 mm/s and 1 mV/cm calibration with equipment having frequency response characteristics in accordance with American Heart Association recommendations7 ECG findings were coded and assessed by two physicians blinded to clinical data. All R‐wave and S‐wave measurements were performed to the nearest 0.1 mV (ie, 100 μm) with calipers and metal rulers on three consecutive cycles. Patients with complete bundle branch block, previous myocardial infarction, or Wolff‐Parkinson‐White syndrome were excluded from the analysis because of the interference of these abnormalities with LVH detection. For the purpose of the present analysis, the following ECG criteria for LVH were tested at baseline examination: (1) Sokolow‐Lyon voltage (sum of the amplitude of S wave in V₁ and R wave in V₅ or V₆, whichever the larger ≥3500 μm)18; (2) Cornell voltage (sum of the amplitude of S wave in V₃ and R wave in aVL >2000 μm in women and >2800 μm in men19; and (3) R‐wave voltage in aVL >700 μm.20

Echocardiography

ECHO studies were performed according to standardized procedures, as previously reported.21 In brief, M‐mode and two‐dimensional ECHO examinations were carried out with a commercially available instrument (computed sonography 128 CF; Acuson, Mountain View, CA). End‐diastolic (d) and end‐systolic (s) LV internal diameters (LVIDs), interventricular septum (IVS) thickness, and posterior wall thickness (PWT) were measured offline from two‐dimensionally guided M‐mode tracings recorded at 50 cm/s to 100 cm/s during at least three consecutive cycles. Relative wall thickness (RWT) was defined by the ratio of PWT plus IVS thickness to LVIDd; LVM was estimated by using the corrected ASE method: 0.8 × (1.04 × [(IVSd + LVIDd + PWTd)³−LVIDd³]) + 0.618 and normalized to body surface area.22 ECHO tracings were obtained by two skilled operators and read by a third independent observer: intraobserver coefficient of variation was 0.6% for LVIDd, 3.1% for IVSd thickness, and 3.2% for PWd thickness.

Partition values for defining LVH and LV geometric patterns were derived from the distribution of LVM normalized to body surface area, RWT, and LVIDd diameter (Table 1), using 1.96 standard deviation (SD) above the mean from 675 healthy persons from the PAMELA population after excluding a total of 376 patients with isolated home or ambulatory hypertension, obesity, diabetes mellitus, and CV diseases.21

Table 1.

Demographic and Clinical Baseline Characteristics of 1691 Participants in the PAMELA Population According to Type of LV Geometric Abnormality

	LV Geometric Patterns (LVH With h^2.7)					P Value^a
	Normal LV Geometry	Concentric LV Remodeling	Eccentric Nondilated LVH	Concentric Nondilated LVH	Eccentric Dilated LVH	P Value^a
No.	1252	131	145	107	56
Men, No. (%)	639 (51)	71 (54.2)	73 (50.3)	48 (44.9)	27 (48.2)	.3466
Age, y	47.1±13.3	58.2±11.4	59.4±10.4	60.6±10.4	60.8±10.7	<.0001
Office SBP, mm Hg	126.8±17.6	141.6±21	146±20.3	153.9±23.2	149±20.7	<.0001
Office DBP, mm Hg	81.5±9.7	87.7±9.8	88.9±9.7	93.2±11.7	86.9±9.7	<.0001
Office HR, beats per min	70.5±9.4	75.4±13.5	70.1±11.2	73.6±11.4	69.4±9.3	<.0772
24‐h SBP, mm Hg	117.4±10	124±12	125.7±12.8	128.6±13.3	125.5±14.3	<.0001
24‐h DBP, mm Hg	73.1±6.7	76.6±7.5	76.6±8.5	78.7±9.1	74.3±8.1	<.0001
BMI, kg/m²	24.5±3.5	26.5±4.2	28.7±4.2	29.6±4.7	28.7±4.8	<.0001
Total cholesterol, mg/dL	219.4±42.8	232.7±40.6	225.6±40.8	235.3±40.9	230.1±48.4	<.0001
HDL cholesterol, mg/dL	56.4±15.7	53.5±14.2	53.3±14.3	52.4±15.2	50.2±14.5	.0005
Serum glucose, mg/dL	87.7±15.5	100.5±37.2	95.3±23.1	99.7±26.5	96±35.9	<.0001
eGFR, mL/min	89.5±14.8	80.4±16.2	82.1±17.1	79.5±17.1	81.9±19.0	<.0001
Antihypertensive drugs, No. (%)	121 (9.7)	45 (34.4)	53 (36.6)	62 (57.9)	31 (55.4	<.0001
History of CVD, No. (%)	28 (2.2)	3 (2.3)	12 (8.3)	5 (4.7)	13 (23.2)	<.0001
Smoking, No. (%)	375 (30.0)	30 (22.9)	31 (21.4)	26 (24.3)	9 (16.1)	.0017

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Abbreviations: CVD, cardiovascular disease; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; HDL, high‐density lipoprotein; HR, heart rate; SBP, systolic blood pressure. Cutoffs used for defining left ventricular (LV) geometric patterns: LV mass index (51 g/h^2.7 men, 47 g/h^2.7 women), relative wall thickness (0.45 men, 0.44 women), and LV internal diastolic dimension (5.8 cm men, 5.3 cm women). ^a P value for trend.

According to the new classification system,16 patients were divided into six groups: those with (1) normal LV geometry (ie, normal LVM index, LVIDd, and RWT), (2) concentric remodeling (ie, normal LVM index and LVIDd and increased RWT), (3) eccentric nondilated LVH (ie, increased LVM index, normal LVIDd, and RWT); (4) eccentric dilated LVH (ie, increased LVM index and LVIDd and normal RWT), (5) concentric nondilated LVH (ie, increased LVM index and RWT and normal LVIDd), and (6) concentric dilated LVH (ie, increased LVM index, LVIDd, and RWT).

Follow‐Up

Participants were followed from the time of the initial medical visit (from 1990 to 1993) to September 30, 2008. Death certificates were retrieved from the National Institute of Statistics database and coded using the International Classification of Diseases and Causes of Death, 10th Revision (ICD‐10).23 ICD‐10 codes from I‐0 to I‐99 were considered as CV deaths. Each event was validated by MONICA criteria (http://www.thl/publications/monica/maual/index.htm). At the end of follow‐up, reliable data on survival were collected in 99.6% of participants.

Data Analysis

In each patient, three office BP measurements and two home BP measurements were obtained at the initial visit and separately averaged. Ambulatory BP readings were also averaged after editing for artifacts, based on preselected criteria.24 The average of three measurements was used to define ECHO parameters.

Values were expressed as means±SDs or as percentages. Between‐group trends for demographic and clinical variables were tested using integer values (1, 2, 3, 4, and 5) in a linear regression model. Prevalence trend was evaluated by Cochran‐Armitage trend test. A P value <.05 was considered statistically significant. The strength of linear correlation between ECG variables and LVM, RWT, and LVIDd was tested by the Pearson correlation coefficients.

Follow‐Up Analysis

Crude and adjusted hazard ratios (HRs) of fatal CV events were calculated by Cox's proportional hazard model.25 The HR of CV death was calculated by the Cox proportional hazard models in patients with isolated ECHO LVH, isolated ECG LVH, and combined ECHO LVH and ECG LVH and taking as reference group patients with normal LV geometry and ECG.

HRs were also calculated for each LVH subtype (ie, eccentric nondilated, concentric nondilated LVH, and eccentric dilated hypertrophy) with or without ECG LVH, having as reference normal LV geometry and ECG. For this aim, ECG LVH was defined according to Cornell voltage criterion, as only this criterion, at variance from the Sokolow‐Lyon index and R‐wave amplitude in aVL, predicted CV prognosis independently of traditional risk factors in the PAMELA population.20 Data were adjusted for age, sex, previous CV disease, average 24‐hour systolic BP, fasting blood glucose, low‐ and high‐density lipoprotein cholesterol, estimated glomerular filtration rate (eGFR), tobacco consumption, and antihypertensive drugs.

All tests were two‐sided and P<.05 was considered statistically significant. Statistical analysis was performed by SAS version 9.4 (SAS Institute Inc, Cary, NC).

Results

The present analysis included 1691 participants with valuable ECG and ECHO‐measurable LV dimensions at baseline and preserved LV systolic function. Mean office BP was 132±21/83±10 mm Hg and mean 24‐hour BP was 120±11/74±7 mm Hg. Average body mass index (BMI) and waist circumference was 25.4±4.2 kg/m² and 85±12 cm, respectively. Obesity was present in 13% and type 2 diabetes mellitus in 4% of cases.

Prevalence of ECG LVH and Abnormal LV Geometric Patterns

Prevalence rates of ECG LVH according to Sokolow‐Lyon index, Cornell voltage index, and R‐wave voltage in aVL criteria were 0.8%, 7.8%, and 12.9%, respectively.

ECHO LVH was defined according to sex‐specific criteria as LVM index ≥51 g/h^2.7 in men and 47 g/m^2.7 in women. These cutoffs, as described in the Methods section, are derived from sex‐specific upper limits of normality (mean plus 1.96 SD) for LVM index in 675 healthy individuals with sustained normotension.

Overall, prevalence of abnormal LV geometric patterns was 26.0%, with eccentric nondilated LVH the most common abnormality (8.6%) followed by concentric remodeling (7.7%), concentric nondilated LVH (6.3%), and eccentric dilated LVH (3.3%). No patients fulfilled criteria for concentric dilated LVH.

Association of LV Geometric Patterns With Baseline Clinical Characteristics and ECG Markers of LVH

Table 1 shows the demographic and clinical characteristics of participants. Patients with LV geometric abnormalities compared with those with normal LV geometry were older; had higher BMI, office and ambulatory BPs, total cholesterol levels, and glucose; and lower high‐density lipoprotein cholesterol and eGFR. Furthermore, they were more frequently taking antihypertensive drugs and had a higher prevalence of previous CV events.

Significant differences were also detected among groups with abnormal LV geometry: patients with eccentric nondilated LVH, concentric nondilated LVH, and eccentric dilated LVH exhibited higher BMI and office systolic BP levels than those with concentric LV remodeling.

As reported in Table 2, a progressive increase in average LVM and LVM indexed to height^2.7 (and body surface area) was observed from normal LV geometry to eccentric dilated LVH. In parallel, ECG voltages were significantly higher in patients with ECHO LVH subtypes than in those with normal LV geometry and concentric LV remodeling. In particular, Cornell voltage and R‐wave amplitude in aVL were highest in participants with concentric LVH, whereas Sokolow‐Lyon index was highest in those with eccentric nondilated LVH. Again, the highest prevalence of ECG LVH, treated as a binary variable, according to Cornell voltage and R‐wave amplitude in aVL, was observed in patients with concentric nondilated LVH, while those with eccentric dilated LVH had the highest rate of ECG LVH according to Sokolow‐Lyon index.

Table 2.

ECG Indexes of LVH^a and Average Values of LVM and LVM Indexed to Body Surface Area and Height to 2.7 of 1694 Participants in the PAMELA Population According to Type of LV Geometric Abnormality

	LV Geometric Patterns (LVH With h^2.7)					P Value^b
	Normal LV Geometry	Concentric LV Remodeling	Eccentric Nondilated LVH	Concentric Nondilated LVH	Eccentric Dilated LVH	P Value^b
No.	1252	131	145	107	56
R in aVL, μV	340±260	430±270	570±290	610±310	550±270	<.0001
SL index, μV	1910±530	1970±530	2110±520	2007±670	2090±620	<.0001
CV index, μV	1440±550	1580±490	1780±590	1940±570	1930±780	<.0001
ECG LVH (R in aVL), %	9.7	12.8	28.1	33.3	23.3	<.0001
ECG LVH SL criterion, %	0.9	–	0.8	–	2.3	0.9049
ECG LVH CV criterion, %	5.4	6.0	11.3	29.8	19.5	<.0001
LVM, g	138.2±33.0	155.0±35.4	196.1±38.5	206.4±47.0	237.8±50.4	<.0001
LVMI, g/m²	79.2±14.3	86.6±13.8	111.4±16.4	115.4±19.3	132.2±22.3	<.0001
LVMI, g/m^2.7	35.5±6.8	40.2±6.3	55.2±6.4	58±8.6	64.7±11.9	<.0001

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Electrocardiographic (ECG) criteria used for defining left ventricular hypertrophy (LVH): R‐wave voltage in aVL >700 μV; Sokolow‐Lyon (SL): (sum of the amplitude of S wave in V₁ and R wave in V₅ or V₆, whichever the larger ≥3500 μV); Cornell voltage (CV): (sum of the amplitude of S wave in V₃ and R wave in aVL >2000 μV in women and >2800 μV in men. Cutoffs used for defining left ventricular (LV) geometric patterns: LV mass (LVM) index (LVMI) (51 g/h^2.7 men, 47 g/h^2.7 women), relative wall thickness (0.45 men, 0.44 women), and LV internal diastolic dimension (5.8 cm men, 5.3 cm women). ^aContinuous variables and prevalence rates of LVH according to R‐wave amplitude in aVL and SL and CV criteria. ^b P value for trend.

The strength of correlations, adjusted for age and sex, between Sokolow‐Lyon index and ECHO parameters defining LV geometry (LVM/height^2.7, RWT, and LVIDd) was markedly lower as compared with other indexes in the whole population. Cornell index showed the closest correlation with RWT (r=0.10, P<.0001) and the same level of association as R aVL amplitude with LVM/height^2.7 (r=0.31 vs r=0.30, P=.0001 for both) and with LVIDd (r=0.14 vs r=0.16, P<.0001 for both).

ECHO LVH, ECG LVH, and CV Death

During a follow‐up of 211 months, a total of 89 fatal CV events occurred in the whole population with reliable baseline ECHO and ECG data.

Incidence of fatal CV events was lowest in patients with normal LVM with or without ECG LVH (1.4% and 2.9%, respectively), intermediate in those with isolated ECHO LVH (12.9%), and highest in those with both ECHO LVH and ECG LVH (22.0%). Compared with the reference group of individuals with neither ECHO LVH nor ECG LVH, the fully adjusted (see Methods) risk of fatal CV events exhibited a clear‐cut increase (HR, 3.36; 95% CI, 1.51–7.47; P=.003) in patients with both ECHO LVH and ECG LVH. A modest increase of risk (P=.04) occurred when isolated ECHO LVH and no ECG LVH was present (Figure 1).

Fatal cardiovascular events (hazard ratios [HRs] and 95% confidence intervals [CIs]) associated with isolated electrocardiographic (ECG) left ventricular hypertrophy (LVH) by Cornell voltage index (n=57), isolated echocardiographic (ECHO) LVH (n=201), and combined ECG and ECHO LVH (n=50). The reference group is represented by patients with normal left ventricular geometry and ECG findings (n=1252). Data were adjusted for age, sex, average 24‐hour systolic blood pressure, previous cardiovascular disease, fasting blood glucose, low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, tobacco consumption, antihypertensive drugs, and estimated glomerular filtration rate. ECHO‐LVH indicates all subtypes of LVH.

Abnormal LV Geometric Patterns, ECG LVH, and CV Death

Figure 2 shows the risk of CV mortality, adjusted for age, sex, average 24‐hour SBP, low‐ and high‐density lipoprotein cholesterol, serum glucose, eGFR, smoking status, antihypertensive treatment, and previous CV disease, in patients with concentric nondilated ECHO LVH with and without ECG LVH, in patients with isolated ECG LVH (by Cornell voltage index), and in the reference group. The association of concentric nondilated LVH and ECG LVH, but not concentric nondilated LVH alone, predicted the long‐term incidence and risk of fatal CV events (HR, 3.79; 95% CI, 1.25–11.38; P=.01). Similar findings were observed for eccentric nondilated LVH (Figure 3). This was not the case for eccentric dilated LVH, probably because of the small number of patients with ECHO LVH and ECG LVH on both tests at baseline evaluation (data not shown).

Additional Analyses

In order to avoid the risk of overfitting the models, we performed additional analyses after excluding the following covariables: use of antihypertensive drugs, high‐density lipoprotein cholesterol, and the Modification of Diet in Renal Disease formula (all these variables did not show any significant correlation with CV events, according to the analysis of maximum likelihood estimates). Compared with the reference group, the adjusted (seven covariables) HR in patients with both ECHO LVH and ECG LVH (HR, 3.49; 95% CI, 1.59–7.65, P=.002) and in those with isolated ECHO LVH (HR, 1.83; 95% CI, 1.06–3.13; P=.03) were not different from previous values. Similar results were obtained for LVH subtypes (data not shown).

Discussion

The present study provides several interesting findings. First, the association between ECG LVH and ECHO LVH markedly increased the risk of CV fatal events independently of other risk factors known to predict mortality. Indeed, LVH as assessed by both tests at baseline examination conveyed a stronger mortality risk than isolated ECHO LVH. Second, ECG LVH without a concomitant increase in ECHO LVM index failed to predict CV death. Third, the combination of ECG LVH with LVH subtypes (ie, concentric nondilated LVH and eccentric nondilated LVH) predicted CV mortality (HRs, 3.8; P<.01, 5.6; P=.02, respectively); this was not the case when such subtypes of LVH were associated with a normal ECG. Several aspects of our results deserve to be further discussed in relation to previous reports in this area. The predictive value of ECHO LVH and ECG LVH, separately, for CV mortality (and all‐cause death) have been consistently documented in different populations, with robust evidence for a continuous relationship between increased LVM, ECG voltages, and risk.26

In a prior analysis of the PAMELA population, ECHO LVH, defined according to four sex‐specific criteria, entailed an increased risk of CV mortality and all‐cause death, independently of type of indexation to body size; similar results were obtained when the continuous variable LVM index was considered instead of the dichotomous LVH.27 The value of three ECG voltage criteria in predicting CV events and all‐cause mortality has been previously assessed by our group in the same population.20 After adjustment for age, sex, and average 24‐hour ambulatory BP, only Cornell voltage index turned out to predict an increased risk of CV events and all‐cause mortality (HR for a 100 μm increase, 1.032; 95% CI, 1.0–1.066; P<.05), a difference from the Sokolow‐Lyon index and R aVL amplitude. Again, when the relationship between ECG LVH as a categorical variable and CV outcomes was investigated in multiple models, only LVH identified by the Cornell voltage criterion retained an independent relationship with CV events.

LVH is an adaptive response to the higher impedance to ventricular emptying induced by a progressive increase of large artery stiffness and/or peripheral resistances. Increased intravascular volume has been shown to play a relevant role in the pathogenesis of LVH in both normotensive and hypertensive individuals. The mechanism(s) linking this cardiac phenotype to overt CV disease and mortality is complex. In addition to myocyte hypertrophy, myocardial fibrosis, a key pathological process in LVH, contributes to the impairment of systolic/diastolic function and to the reduction of coronary reserve and increase in electrical activity.28, 29, 30 Overall, these abnormalities adversely affect clinical outcomes even in patients with less advanced forms of LVH. If standard ECHO does not provide information on myocardial fibrosis, cardiac perfusion, and electrical remodeling, ECG, on the other hand, provides only indirect evidence of LVM increments by recording electric changes related to the hypertrophic process.31 Furthermore, several factors other than LVH have been reported to influence the amplitude of ECG voltages. Body size, age, sex, and chest impedance may interfere with ECG markers of LVH, thus reducing the accuracy of voltage‐based criteria. Therefore, ECG and ECHO offer complementary information on cardiac hypertrophy by reflecting different pathological alterations at the cardiac level.32 Few studies have previously analyzed the additive value of ECG and ECHO in refining prediction of CV events. This question has been addressed in different clinical settings, including in elderly men from a general population,14 in American Indians with a high prevalence of type 2 diabetes,15 in patients with previous ischemic stroke,33 and in hypertensive patients with ECG LVH.34

In a seminal paper by Sundström and coworkers14 conducted in a population‐based sample of 475 men aged 70 years, the authors reported that ECHO LVH and ECG LVH (defined by Cornell voltage duration product) independently predicted CV and all‐cause death during a 5‐year follow‐up. Furthermore, when the population was separated into groups with or without LVH on one or both examinations, participants with LVH on both tests exhibited the highest rates of CV and all‐cause mortality. The prognostic value of combining ECHO LVH and ECG strain was examined by Okin and coworkers15 in 2193 American Indian participants in the Strong Heart Study. The authors documented that combined ECHO LVH and ECG strain improved risk stratification for both CV and all‐cause death compared with either test alone. After adjustment for major confounders, ECHO LVH combined with ECG strain was associated with a 6.3‐fold increased risk of CV death. More recently, this topic was examined in 922 hypertensive patients in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension ECHO substudy.34 Patients were grouped according to presence of LVH on both ECG and ECHO, on a single test or no test. Incidence of hospitalization for heart failure during a mean follow‐up period of 4.8 years was 5.3 and 2.6 times higher in patients with LVH on both tests compared with patients with LVH only on ECHO or ECG, respectively.

Study Strengths and Limitations

Some aspects of the above‐mentioned studies, however, need to be addressed. The conclusions of the study by Sundstrom and coworkers14 about the superiority of combining ECG LVH and ECHO LVH for predicting outcomes were valid only in the hypertensive fraction of the population. Moreover, the authors used a restrictive (and obsolete) criterion for detecting ECHO LVH (ie, 150 g/m²), thus excluding a consistent portion of patients with mild cardiac hypertrophy.14 Finally, the LIFE study reported that patients with LVH according to both diagnostic tests did not exhibit a higher incidence of combined myocardial infarction, stroke, or CV death as compared with their counterparts with LVH on a single test.34

Our study reporting the prognostic value of combined ECG LVH and subtypes of ECHO LVH in a sample from a Caucasian general population provides a novel contribution in this area.

A large body of evidence supports the view that increased LVM related only to LV wall thickening has a more unfavorable clinical and prognostic significance than LVM increments secondary to increases in both wall thickness and LV diameter/volume.35 Concentric hypertrophy, indeed, has been shown to be associated with more severe alterations in LV diastolic function, myocardial perfusion, and texture than other nonconcentric LV geometric abnormalities.36 In our analysis, we used the Dallas classification of LVH16 based on cardiac magnetic resonance imaging parameters to ECHO linear measurements.37, 38 By combining LVM index, LVIDd, and RWT, we found that alterations in LV geometry were present in approximately one quarter of the entire population. This updated classification allowed us to identify three types of hypertrophy: eccentric nondilated LVH, eccentric dilated LVH, and concentric nondilated LVH; this last geometric phenotype was associated with the highest prevalence of ECG LVH (30% according to Cornell voltage criterion), followed by eccentric dilated and eccentric nondilated LVH. The new finding of the present study is that concentric nondilated or eccentric nondilated LVH combined with ECG LVH predicted CV mortality independently of major confounders. This was not the case when concentric nondilated or eccentric nondilated LVH was dissociated from ECG LVH. This observation suggests that concentric nondilated LVH, the most unfavorable LV geometric alteration, in the absence of concomitant ECG alterations, does not convey a significant increase of CV risk over traditional factors in a Caucasian population. However, the failure of eccentric nondilated or concentric nondilated ECHO LVH alone (as well as of ECG LVH alone) to stratify CV risk may be related to the small size of subgroups as well as the limited number of events and cannot be regarded as a strong argument against the usefulness of performing an ECHO in patients with normal ECG findings. Some other limitations of our study deserve to be mentioned. The absence of serial ECHOs and ECGs did not allow us to analyze the time course of ECG and/or LVM changes and their impact on CV risk. ECG evaluation in the PAMELA study was restricted to QRS voltages and, in particular, did not include QRS duration, which precluded the use of Cornell product for detection of LVH, as recommended by current guidelines. Our results represent a sample of a general Caucasian population including normotensive, treated, and untreated hypertensive patients with a relatively low incidence of CV mortality; therefore, they should not be extended to different ethnic groups or settings with higher CV risk such as the hypertensive fraction of the general population.

Conclusions

The major clinical implication of the present study is the value of combining ECG and ECHO reports in the assessment of CV risk related to the presence of LVH. The predictive value of both combined noninvasive techniques in refining CV risk prediction is still valid when LVH is subclassified according to concentric or eccentric LV patterns.

Disclosure

The authors report no conflicts of interest.

References

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4. Ghali JK, Liao Y, Simmons B, et al. The prognostic role of left ventricular hypertrophy in patients with or without coronary artery disease. Ann Intern Med. 1992;117:831–836. [DOI] [PubMed] [Google Scholar]
5. Chen SC, Chang JM, Liu WC, et al. The ratio of observed to predicted left ventricular mass is independently associated with increased cardiovascular events in patients with chronic kidney disease. Hypertens Res. 2012;35:832–838. [DOI] [PubMed] [Google Scholar]
6. Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens. 2013;31:1281–1357. [DOI] [PubMed] [Google Scholar]
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8. Mathew J, Sleight P, Lonn E, et al; Heart Outcomes Prevention Evaluation (HOPE) Investigators . Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin‐converting enzyme inhibitor ramipril. Circulation. 2001;104:1615–1621. [DOI] [PubMed] [Google Scholar]
9. Okin PM, Devereux RB, Jern S, et al; LIFE Study Investigators . Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events. JAMA. 2004;292:2343–2349. [DOI] [PubMed] [Google Scholar]
10. Pewsner D, Juni P, Egger M, et al. Accuracy of electrocardiography in diagnosis of left ventricular hypertrophy in arterial hypertension: systematic review. BMJ. 2007;335:771–775. [DOI] [PMC free article] [PubMed] [Google Scholar]
11. da Costa W, Riera ARP, de Assis Costa F, et al. Correlation of electrocardiographic left ventricular hypertrophy criteria with left ventricular mass by echocardiogram in obese hypertensive patients. J Electrocardiol. 2008;41:724–729. [DOI] [PubMed] [Google Scholar]
12. Bacharova L, Chen H, Estes EH, et al. Determinants of discrepancies in detection and comparison of the prognostic significance of left ventricular hypertrophy by electrocardiogram and cardiac magnetic resonance imaging. Am J Cardiol. 2015;115:515–522. [DOI] [PMC free article] [PubMed] [Google Scholar]
13. Schillaci G, de Simone G, Reboldi G, et al. Change in cardiovascular risk profile by echocardiography in low‐ or medium‐risk hypertension. J Hypertens. 2002;20:1519–1525. [DOI] [PubMed] [Google Scholar]
14. Sundstrom J, Lind L, Arnlov J, et al. Echocardiographic and electrocardiographic diagnoses of left ventricular hypertrophy predict mortality independently of each other in a population of elderly men. Circulation. 2001;103:2346–2351. [DOI] [PubMed] [Google Scholar]
15. Okin PM, Roman MJ, Lee ET, et al. Combined echocardiographic left ventricular hypertrophy and ST depression improve prediction of mortality in American Indians. The Strong Heart Study. Hypertension. 2004;43:769–774. [DOI] [PubMed] [Google Scholar]
16. Khouri MG, Peshock RM, Ayers CR, et al. A 4‐tiered classification of left ventricular hypertrophy based on left ventricular geometry: the Dallas Heart Study. Circ Cardiovasc Imaging. 2010;3:164–171. [DOI] [PubMed] [Google Scholar]
17. Sega R, Trocino G, Lanzarotti A, et al. Alterations of cardiac structure in patients with isolated office, ambulatory, or home hypertension: data from the general population (Pressioni Arteriose Monitorate E Loro Associazioni [PAMELA] Study). Circulation. 2001;104:1385–1392. [DOI] [PubMed] [Google Scholar]
18. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37:161–186. [DOI] [PubMed] [Google Scholar]
19. Hsieh BP, Pham MX, Froelicher VF. Prognostic value of electrocardiographic criteria for left ventricular hypertrophy. Am Heart J. 2005;150:161–167. [DOI] [PubMed] [Google Scholar]
20. Cuspidi C, Facchetti R, Bombelli M, et al. Accuracy and prognostic significance of electrocardiographic markers of left ventricular hypertrophy in a general population: findings from the PAMELA population. J Hypertens. 2014;32:921–928. [DOI] [PubMed] [Google Scholar]
21. Cuspidi C, Facchetti R, Sala C, et al. Normal values of left ventricular mass: findings from the PAMELA study. J Hypertens. 2012;30:997–1003. [DOI] [PubMed] [Google Scholar]
22. Devereux RB, Reickek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation. 1977;55:613–618. [DOI] [PubMed] [Google Scholar]
23. Anderson RN, Rosemberg HM. Disease classification: measuring the effect of the Tenth Revision of the International Classification of Diseases on cause‐of‐death in the United States. Stat Med. 2003;15:1551–1570. [DOI] [PubMed] [Google Scholar]
24. Groppelli A, Omboni S, Parati G, Mancia G. Evaluation of non invasive blood pressure monitoring devices Spacelabs 90202 and 90207 versus resting and ambulatory 24 h intra‐arterial blood pressure. Hypertension. 1992;20:227–232. [DOI] [PubMed] [Google Scholar]
25. Wiley Cox DR. Regression models and life tables (with discussion). J R Stat Soc Series B. 1972;34:187–220. [Google Scholar]
26. Schillaci G, Verdecchia P, Porcellati C, et al. Continuous relationship between left ventricular mass and cardiovascular risk in essential hypertension. Hypertension. 2000;35:580–586. [DOI] [PubMed] [Google Scholar]
27. Cuspidi C, Facchetti R, Bombelli M, et al. Prognostic value of left ventricular mass normalized to different body size indexes: findings from the PAMELA population. J Hypertens. 2015;33: 1082–1089. [DOI] [PubMed] [Google Scholar]
28. Frohlich E, Gonzales A, Diez J. Hypertensive left ventricular hypertrophy risk: beyond adaptive cardiomyocytic hypertrophy. J Hypertens. 2011;29:17–26. [DOI] [PubMed] [Google Scholar]
29. Rimoldi O, Rosen SD, Camici PG. The blunting of coronary flow reserve in hypertension with left ventricular hypertrophy is transmural and correlates with systolic blood pressure. J Hypertens. 2014;32:2465–2471. [DOI] [PubMed] [Google Scholar]
30. Contaldi C, Imbriaco M, Alcidi G, et al. Assessment of the relationships between left ventricular filling pressures and longitudinal dysfunction with myocardial fibrosis in uncomplicated hypertensive patients. Int J Cardiol. 2016;202:84–86. [DOI] [PubMed] [Google Scholar]
31. Schillaci G, Battista F, Pucci G. A review of the role of electrocardiography in the diagnosis of left ventricular hypertrophy in hypertension. J Electrocardiol. 2012;45:617–623. [DOI] [PubMed] [Google Scholar]
32. Bacharova L. Changing role of ECG in the evaluation of left ventricular hypertrophy. J Electrocardiol. 2012;45:609–611. [DOI] [PubMed] [Google Scholar]
33. Kohsaka S, Sciacca RR, Sugioka K, et al. Additional impact of electrocardiographic over echocardiographic diagnosis of left ventricular hypertrophy for predicting the risk of ischemic stroke. Am Heart J. 2005;149:181–186. [DOI] [PubMed] [Google Scholar]
34. Gerdts E, Okin PM, Boman K, et al. Association of heart failure hospitalizations with combined echocardiography and electrocardiography criteria for left ventricular hypertrophy. Am J Hypertens. 2012;25:678–683. [DOI] [PubMed] [Google Scholar]
35. Muiesan ML, Salvetti M, Monteduro C, et al. Left ventricular concentric geometry during treatment adversely affects cardiovascular prognosis in hypertensive patients. Hypertension. 2004;43:731–738. [DOI] [PubMed] [Google Scholar]
36. Müller‐Brunotte R, Kahan T, Malmqvist K, Edner M. Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy. J Hum Hypertens. 2003;17:841–849. [DOI] [PubMed] [Google Scholar]
37. de Simone G, Izzo R, Aurigemma GP, et al. Cardiovascular risk in relation to a new classification of hypertensive left ventricular geometric abnormalities. J Hypertens. 2015;33:745–754. [DOI] [PubMed] [Google Scholar]
38. Cuspidi C, Facchetti R, Bombelli M, et al. Risk of mortality in relation to an updated classification of left ventricular geometric abnormalities in a general population: the Pamela study. J Hypertens. 2015;33:2133–2140. [DOI] [PubMed] [Google Scholar]

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[jch12834-bib-0003] 3. Koren MJ, Devereux RB, Casale PN, et al. Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med. 1991;114:345–352. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0004] 4. Ghali JK, Liao Y, Simmons B, et al. The prognostic role of left ventricular hypertrophy in patients with or without coronary artery disease. Ann Intern Med. 1992;117:831–836. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0005] 5. Chen SC, Chang JM, Liu WC, et al. The ratio of observed to predicted left ventricular mass is independently associated with increased cardiovascular events in patients with chronic kidney disease. Hypertens Res. 2012;35:832–838. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0006] 6. Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens. 2013;31:1281–1357. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0007] 7. Hancock FW, Deal BJ, Mirvis DM, et al. AHA/ACCF/HRS Recommendations for the standardization and interpretation of the electrocardiogram. Part V: electrocardiogram changes associated with chamber hypertrophy a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology: the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol. 2009;53:992–1002. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0008] 8. Mathew J, Sleight P, Lonn E, et al; Heart Outcomes Prevention Evaluation (HOPE) Investigators . Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin‐converting enzyme inhibitor ramipril. Circulation. 2001;104:1615–1621. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0009] 9. Okin PM, Devereux RB, Jern S, et al; LIFE Study Investigators . Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events. JAMA. 2004;292:2343–2349. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0010] 10. Pewsner D, Juni P, Egger M, et al. Accuracy of electrocardiography in diagnosis of left ventricular hypertrophy in arterial hypertension: systematic review. BMJ. 2007;335:771–775. [DOI] [PMC free article] [PubMed] [Google Scholar]

[jch12834-bib-0011] 11. da Costa W, Riera ARP, de Assis Costa F, et al. Correlation of electrocardiographic left ventricular hypertrophy criteria with left ventricular mass by echocardiogram in obese hypertensive patients. J Electrocardiol. 2008;41:724–729. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0012] 12. Bacharova L, Chen H, Estes EH, et al. Determinants of discrepancies in detection and comparison of the prognostic significance of left ventricular hypertrophy by electrocardiogram and cardiac magnetic resonance imaging. Am J Cardiol. 2015;115:515–522. [DOI] [PMC free article] [PubMed] [Google Scholar]

[jch12834-bib-0013] 13. Schillaci G, de Simone G, Reboldi G, et al. Change in cardiovascular risk profile by echocardiography in low‐ or medium‐risk hypertension. J Hypertens. 2002;20:1519–1525. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0014] 14. Sundstrom J, Lind L, Arnlov J, et al. Echocardiographic and electrocardiographic diagnoses of left ventricular hypertrophy predict mortality independently of each other in a population of elderly men. Circulation. 2001;103:2346–2351. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0015] 15. Okin PM, Roman MJ, Lee ET, et al. Combined echocardiographic left ventricular hypertrophy and ST depression improve prediction of mortality in American Indians. The Strong Heart Study. Hypertension. 2004;43:769–774. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0016] 16. Khouri MG, Peshock RM, Ayers CR, et al. A 4‐tiered classification of left ventricular hypertrophy based on left ventricular geometry: the Dallas Heart Study. Circ Cardiovasc Imaging. 2010;3:164–171. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0017] 17. Sega R, Trocino G, Lanzarotti A, et al. Alterations of cardiac structure in patients with isolated office, ambulatory, or home hypertension: data from the general population (Pressioni Arteriose Monitorate E Loro Associazioni [PAMELA] Study). Circulation. 2001;104:1385–1392. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0018] 18. Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37:161–186. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0019] 19. Hsieh BP, Pham MX, Froelicher VF. Prognostic value of electrocardiographic criteria for left ventricular hypertrophy. Am Heart J. 2005;150:161–167. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0020] 20. Cuspidi C, Facchetti R, Bombelli M, et al. Accuracy and prognostic significance of electrocardiographic markers of left ventricular hypertrophy in a general population: findings from the PAMELA population. J Hypertens. 2014;32:921–928. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0021] 21. Cuspidi C, Facchetti R, Sala C, et al. Normal values of left ventricular mass: findings from the PAMELA study. J Hypertens. 2012;30:997–1003. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0022] 22. Devereux RB, Reickek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation. 1977;55:613–618. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0023] 23. Anderson RN, Rosemberg HM. Disease classification: measuring the effect of the Tenth Revision of the International Classification of Diseases on cause‐of‐death in the United States. Stat Med. 2003;15:1551–1570. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0024] 24. Groppelli A, Omboni S, Parati G, Mancia G. Evaluation of non invasive blood pressure monitoring devices Spacelabs 90202 and 90207 versus resting and ambulatory 24 h intra‐arterial blood pressure. Hypertension. 1992;20:227–232. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0025] 25. Wiley Cox DR. Regression models and life tables (with discussion). J R Stat Soc Series B. 1972;34:187–220. [Google Scholar]

[jch12834-bib-0026] 26. Schillaci G, Verdecchia P, Porcellati C, et al. Continuous relationship between left ventricular mass and cardiovascular risk in essential hypertension. Hypertension. 2000;35:580–586. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0027] 27. Cuspidi C, Facchetti R, Bombelli M, et al. Prognostic value of left ventricular mass normalized to different body size indexes: findings from the PAMELA population. J Hypertens. 2015;33: 1082–1089. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0028] 28. Frohlich E, Gonzales A, Diez J. Hypertensive left ventricular hypertrophy risk: beyond adaptive cardiomyocytic hypertrophy. J Hypertens. 2011;29:17–26. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0029] 29. Rimoldi O, Rosen SD, Camici PG. The blunting of coronary flow reserve in hypertension with left ventricular hypertrophy is transmural and correlates with systolic blood pressure. J Hypertens. 2014;32:2465–2471. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0030] 30. Contaldi C, Imbriaco M, Alcidi G, et al. Assessment of the relationships between left ventricular filling pressures and longitudinal dysfunction with myocardial fibrosis in uncomplicated hypertensive patients. Int J Cardiol. 2016;202:84–86. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0031] 31. Schillaci G, Battista F, Pucci G. A review of the role of electrocardiography in the diagnosis of left ventricular hypertrophy in hypertension. J Electrocardiol. 2012;45:617–623. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0032] 32. Bacharova L. Changing role of ECG in the evaluation of left ventricular hypertrophy. J Electrocardiol. 2012;45:609–611. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0033] 33. Kohsaka S, Sciacca RR, Sugioka K, et al. Additional impact of electrocardiographic over echocardiographic diagnosis of left ventricular hypertrophy for predicting the risk of ischemic stroke. Am Heart J. 2005;149:181–186. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0034] 34. Gerdts E, Okin PM, Boman K, et al. Association of heart failure hospitalizations with combined echocardiography and electrocardiography criteria for left ventricular hypertrophy. Am J Hypertens. 2012;25:678–683. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0035] 35. Muiesan ML, Salvetti M, Monteduro C, et al. Left ventricular concentric geometry during treatment adversely affects cardiovascular prognosis in hypertensive patients. Hypertension. 2004;43:731–738. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0036] 36. Müller‐Brunotte R, Kahan T, Malmqvist K, Edner M. Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy. J Hum Hypertens. 2003;17:841–849. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0037] 37. de Simone G, Izzo R, Aurigemma GP, et al. Cardiovascular risk in relation to a new classification of hypertensive left ventricular geometric abnormalities. J Hypertens. 2015;33:745–754. [DOI] [PubMed] [Google Scholar]

[jch12834-bib-0038] 38. Cuspidi C, Facchetti R, Bombelli M, et al. Risk of mortality in relation to an updated classification of left ventricular geometric abnormalities in a general population: the Pamela study. J Hypertens. 2015;33:2133–2140. [DOI] [PubMed] [Google Scholar]

PERMALINK

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

Cesare Cuspidi, MD

Rita Facchetti, PhD

Carla Sala, MD

Michele Bombelli, MD

Marijana Tadic, MD

Guido Grassi, MD

Giuseppe Mancia, MD

Abstract