Strain Rate Imaging Differentiates Hypertensive Cardiac Hypertrophy from Physiologic Cardiac...

Strain Rate Imaging DifferentiatesHypertensive Cardiac Hypertrophy

from Physiologic Cardiac Hypertrophy(Athlete’s Heart)

Mohammed Saghir, MD, Marianela Areces, MD, and Majesh Makan, MD, FACC,

Background: This study sought to determine whetherstrain rate imaging could distinguish between individ-uals with hypertensive left ventricular hypertrophy(LVH) and those with strength-training athletic LVH.Methods: In all, 108 participants (30 hypertensiveLVH, 30 strength-training LVH, 48 control) wereenrolled. In addition to a baseline echocardiogram,strain, peak systolic strain rate (SRS), peak earlydiastolic strain rate (SRE), and peak late diastolicstrain rate values were compared in the apical4-chamber view.Results: Athletes had no significant differences in

doi:10.1016/j.echo.2006.08.006

pared with control subjects (P � .11, .99, .85, and .09,respectively). Individuals with hypertensive LVH hadsignificantly decreased strain, SRS, and SRE (�16.8 �3.2%, �0.99 � 0.15 s�1, and 1.54 � 0.40 s�1, respec-tively) compared with control subjects (�21.7 � 3.5%,�1.31 � 0.27 s�1, and 2.35 � 0.57 s�1, respectively; allP < .0001).Conclusion: Hypertensive LVH has significant longitu-dinal strain, SRS, and SRE reductions versus control.The lack of these reductions in athletes suggests thatstrain rate imaging may have clinical use in discerningthe physiologic LVH state. (J Am Soc Echocardiogr 2007;

Hypertensive cardiac hypertrophy is a conditionassociated with significant morbidity and mortality.1

This includes, but is not limited to, coronary arterydisease, arrhythmias, diastolic dysfunction, heartfailure, and sudden death. Athletes who engage inrigorous strength training also exhibit a concentriccardiac hypertrophy pattern similar to that of hyper-tensive hypertrophy.2 However, athletic hypertro-phy is thought to be a benign, physiologic responsewithout the prognostic significance of hypertensivehypertrophy.3

Noninvasive studies have uncovered characteris-tics associated with these two types of left ventric-ular (LV) hypertrophy (LVH). Vinereanu et al4

achieved high sensitivity and specificity using amean systolic mitral annulus velocity of less than0.09 m/s in distinguishing hypertensive LVH fromphysiologic LVH. Schannwell et al5 reported de-creased early diastolic mitral blood filling velocity

From the Division of Cardiovascular Diseases, Washington Uni-versity School of Medicine.Supported by the Doris Duke Charitable Foundation, New York,New York.Reprint requests: Majesh Makan, MD, FACC, Washington Uni-versity School of Medicine, 660 S Euclid Ave, Campus Box 8086,St Louis, MO 63110 (E-mail: mmakan@im.wustl.edu).0894-7317/$32.00Copyright 2007 by the American Society of Echocardiography.

and increased late diastolic mitral filling velocity inhypertensive LVH with no such occurrence intrained athletes. Strain rate imaging (SRI) may ex-pound on these findings.

SRI is a modality of Doppler tissue imaging and arelatively new tool to quantify regional myocardialfunction. Studies have shown that it may provide agood assessment of myocardial contractility.6 Cur-rently, there is little work that documents the strainand strain rate profile associated with physiologicLVH. To that end, this study aimed to determinewhether SRI could distinguish between pathologicand physiologic LVH. As hypertensive LVH is asso-ciated with decreased mitral annulus velocity,4 thisstudy hypothesized that hypertensive LVH wouldexhibit lower strain parameters in the longitudinalaxis relative to control. Physiologic LVH, by con-trast, should demonstrate normal strain parametersrelative to control. Therefore, SRI may be able todifferentiate between physiologic and pathologiccardiac hypertrophy.

METHODS

Participants

Our institutional review board approved the study, and

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Journal of the American Society of Echocardiography152 Saghir, Areces, Makan February 2007

total of 108 participants were enrolled into the study: 30patients with LVH secondary to hypertension; 30 strength-training athletes with concentric LVH (13 rowers, 14weight lifters, and 3 contact-sport players), and 48healthy, sedentary control subjects.

The inclusion criteria for patients with hypertensiveLVH were: (1) age 18-65 years; (2) past clinical diagno-sis of hypertension; (3) exercise stress echocardiogramnegative for ischemia and hypertensive response; and(4) LV mass (LVM) index greater than 110 g/m2 inwomen (�135 g/m2 in men) or symmetric interventric-ular septum and posterior wall hypertrophy greaterthan 1.1 cm. Exclusion criteria included: (1) moderateor severe valvular disease; (2) history of coronary arterydisease, myocardial infarction, or diabetes mellitus; (3)ejection fraction less than 50% by echocardiogram; and(4) history of cardiomyopathy, congenital heart defect,open heart surgery, or ongoing arrhythmia. All patients withhypertension discontinued �-blockers and calcium-channelblockers 24 hours before study echocardiogram. Theseparticipants were enrolled from consecutive eligible pa-tients at a stress echocardiogram facility. Inclusion criteriafor athletes were: (1) age 18-65 years; (2) engaged instrength-training activities greater than 10 h/wk for thepast year; and (3) LVM index greater than 110 g/m2 inwomen (�135 g/m2 in men) or symmetric interventricu-lar septum and posterior wall hypertrophy greater than1.1 cm. Exclusion criteria for athletes were identical to thehypertensive group with the addition of past clinicaldiagnosis of hypertension. Athletes were recruited fromlocal sports teams, clubs, and training facilities. Inclusioncriterion for control subjects was age 18-65 years. Exclu-sion criteria were identical to the hypertensive group butalso included: (1) echocardiographic evidence of LVH; (2)history of hypertension; and (3) heavily engaged in exer-cise or athletics (�10 h/wk for past year). Control subjectswere recruited from local healthy volunteers.

Echocardiography

Studies were performed with a commercially availabletissue Doppler ultrasound system (Vivid 7, GE Systems,Milwaukee, Wis). The echocardiographic examinationconsisted of 2-dimensional views from the parasternal andapical positions, M-mode, and conventional and tissueDoppler modes. Interventricular and posterior wall thick-ness were recorded from the parasternal long-axis view.LV internal dimensions were recorded from the midpap-illary parasternal short-axis view. In each echocardio-graphic view, 3 consecutive cardiac cycles were recorded.Obtained measurements were a mean of these 3 cycles.Blood pressure was recorded before the echocardio-graphic examination. Heart rate was measured from theelectrocardiographic tracing taken during the echocardio-graphic examination. Longitudinal strain parameters, mi-tral inflow velocities, presence of mitral valve regurgita-tion or stenosis, and septal mitral annular velocities wereobtained from the apical 4-chamber view. Aortic valvemeasurements were recorded from the apical 5-chamber

Simpson’s method. LVM was calculated by Penn conven-tion.7 Conventional echocardiographic measurementswere recorded from studies by M. S.

Strain Imaging

Doppler tissue imaging recordings were taken at 134 � 22frames/s with a 5.0-MHz phased-array transducer in theapical 4-chamber view. Analysis was independently andseparately performed on a commercially available analysiscomputer (Echopac, GE Systems) by two cardiologists(M. M. and M. A.) trained in SRI analysis and blinded to thecategorization of participants. For all strain parametermeasurements, the sample size was a 12- � 6-mm oval.Semiautomated tissue tracking was used to keep the samplein the myocardium throughout the cardiac cycles. Strain,peak systolic strain rate (SRS), peak early diastolic strain rate(SRE), and peak late diastolic strain rate measurements for 3consecutive cardiac cycles were averaged for each partici-pant. Forty-millisecond gaussian curve smoothening wasapplied to all strain rate curves. For longitudinal measure-ments, samples were placed at the basal, mid, and apicalseptum in the apical 4-chamber view. Participants wereexcluded from the study if the axis of the septum deviatedfrom the line of the Doppler beam by more than 15degrees.

Exercise Stress Testing

All patients with hypertension enrolled in the studyunderwent an exercise stress test after the resting echo-cardiogram and tissue Doppler recordings. The stress testwas read by cardiologists blinded to the study. Participantswere excluded from the study if they demonstratedpositive results for myocardial ischemia or a hypertensiveresponse.

Variability

Presented results are the mean values of the two blindedcardiologists’ (M. M. and M. A.) data sets. Interobservervariability was assessed from the variability between thedata sets. Intraobserver variability was determined with are-examination of 20 randomly selected participants 1month after the original analysis. Variability was calculatedwith a Bland-Altman analysis.

Statistical Analysis

All values are expressed as a mean � SD. The study isdesigned to detect a 7.5% effect size with a power of 80%.With a substantial age difference between the athlete andhypertensive groups, each group was compared with thecontrol group. Analysis was performed with commerciallyavailable software (SPSS 13, SPSS Inc, Chicago, Ill). A2-tailed Student t test was used to compare strain param-eter differences among athletes, patients with hyperten-sion, and control subjects. A P value less than .006 wasconsidered statistically significant by Bonferroni’s correc-tion. A discriminant analysis was used to examine inde-pendent predictors of a hypertensive LVH state. Studied

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annular velocity, peak early diastolic mitral annular veloc-ity (Em), ratio of peak early mitral valve flow to Em(E/Em), and isovolumetric relaxation time. A receiveroperating characteristic curve analysis was used to deter-mine sensitivity and specificity of strong independentpredictors.

RESULTS

Table 1 summarizes the baseline clinical character-istics of the 3 groups. There were significant agedifferences among athletes, patients with hyperten-sion, and control subjects. The hypertensive grouphad significantly elevated systolic and diastolic

Table 1 General clinical characteristics (mean � SD)

AT (n � 30) CT (n � 48) HT (n � 30)

Age, y 27 � 7* 38 � 14 48 � 11*Male 73% 47% 30%BSA, m2 1.87 � 0.17 1.90 � 0.22 2.06 � 0.37*SBP, mm Hg 124 � 13 126 � 18 149 � 20*DBP, mm Hg 75 � 7 79 � 12 86 � 15*RHR, beats/min 61 � 9* 72 � 15 68 � 11

AT, Athletes; BSA, body surface area; CT, control subjects; DBP, diastolicblood pressure; HT, patients with hypertension; RHR, resting heart rate;SBP, systolic blood pressure.*P � .05 compared with control.

Table 2 General echocardiographic characteristics

AT (n � 30) CT (n � 48) HT (n � 30)

LVIDd, cm 5.32 � 0.46* 5.03 � 0.52 5.22 � 0.54LVIDs, cm 3.66 � 0.48* 3.37 � 0.53 3.31 � 0.73IVST, cm 1.14 � 0.11* 0.87 � 0.09 1.32 � 0.13*PWT, cm 1.14 � 0.12* 0.87 � 0.09 1.30 � 0.13*RWT 0.43 � 0.06* 0.35 � 0.05 0.51 � 0.07*EDV, mL 138 � 30* 112 � 26 128 � 43*ESV, mL 50 � 14* 41 � 12 42 � 21SV/BSA 47.1 � 10.1* 37.3 � 7.2 41.7 � 10.4LVEF, % 64 � 6 64 � 6 67 � 8E/A 1.73 � 0.42 1.52 � 0.53 1.19 � 0.40*Sm, m/s 0.09 � 0.01 0.09 � 0.02 0.08 � 0.01*Em, m/s 0.13 � 0.02* 0.12 � 0.03 0.07 � 0.02*Am, m/s 0.08 � 0.02 0.09 � 0.03 0.09 � 0.02E/Em 5.85 � 0.82* 7.23 � 2.01 12.71 � 4.40*LVM, g 288 � 52* 179 � 44 340 � 73*LVMI, g/m2 154 � 21* 94 � 18 165 � 38*IVRT, ms 98 � 12 100 � 20 131 � 29*

A, Late diastolic filling; Am, peak late diastolic mitral annular velocity; AT,athletes; CT, control subjects; E, early diastolic filling; EDV, end-diastolicvolume; Em, peak early diastolic mitral annular velocity; ESV, end systolicvolume; HT, patients with hypertension; IVRT, isovolumetric relaxationtime; IVST, interventricular septal thickness; LVEF, LV ejection fraction;LVIDd, left ventricular (LV) internal dimension end diastole; LVIDs, LVinternal dimension end systole; LVM, LV mass; LVMI, LVM index; PWT,posterior wall thickness; RWT, relative wall thickness; Sm, peak systolicmitral annular velocity; SV/BSA, stroke volume/body surface area.*P � .05 compared with control.

blood pressure relative to the control group. Table 2

shows the baseline echocardiographic characteris-tics of each group. The hypertensive group exhib-ited significantly decreased mitral annulus velocityin systole and diastole relative to control subjects.E/Em, a noninvasive index proportional to LV end-diastolic pressure,8 and isovolumetric relaxationtime were also significantly elevated in patients withhypertension. Athletes exhibited a significantly dif-ferent stroke volume indexed to body surface area,E/Em, and diastolic mitral annulus velocity withrespect to control subjects.

A total of 1296 strain parameter measurementswere taken. Of these, 10 were dropped secondary todifficulties in obtaining a SRI curve. Table 3 summa-rizes the strain characteristics of the study popula-tion. Negative values denote myocardial contractionand positive values imply relaxation. In the averagedlongitudinal axis, the hypertensive group had signif-icantly lower strain, SRS, and SRE in comparison withcontrol subjects (P � .0001). The most notablereductions in strain parameters between patientswith hypertension and control subjects occurred inthe basal and midseptal sections. Athletes, by con-trast, exhibited a significantly increased basal strain.Otherwise they demonstrated no significant strainor strain rate differences from control subjects with

Table 3 Strain and strain rate characteristics(mean � SD)

AT (n � 30) CT (n � 48) HT (n � 30)

Basal septumStrain �26.3 � 4.7% �22.5 � 5.7% �14.2 � 4.1%SRS, s�1 �1.45 � 0.39 �1.31 � 0.43 �0.88 � 0.23SRE, s�1 2.63 � 0.91 2.48 � 0.95 1.39 � 0.51SRA, s�1 1.66 � 0.65 1.53 � 0.64 1.37 � 0.45

MidseptumStrain �21.6 � 3.6% �21.7 � 4.6% �16.9 � 4.4%SRS, s�1 �1.34 � 0.31 �1.36 � 0.36 �1.04 � 0.30SRE, s�1 2.05 � 0.50 2.13 � 0.75 1.39 � 0.56SRA, s�1 0.97 � 0.36* 1.30 � 0.64 1.34 � 0.47

Apicalseptum

Strain �20.8 � 4.8% �21.0 � 6.3% �18.6 � 4.5%SRS, s�1 �1.13 � 0.36 �1.21 � 0.37 �1.03 � 0.21*SRE, s�1 2.43 � 0.54 2.45 � 0.72 1.79 � 0.60SRA, s�1 0.73 � 0.27* 0.99 � 0.59 1.39 � 0.47

Averageseptum

Strain �22.9 � 2.4% �21.7 � 3.5% �16.8 � 3.2%SRS, s�1 �1.31 � 0.19 �1.31 � 0.27 �0.99 � 0.15SRE, s�1 2.37 � 0.40 2.35 � 0.57 1.54 � 0.40SRA, s�1 1.12 � 0.25 1.28 � 0.46 1.38 � 0.37

AT, Athletes; CT, control subjects; HT, patients with hypertension; SRA,peak late diastolic strain rate; SRE, peak early diastolic strain rate; SRS, peaksystolic strain rate.Shading denotes P � .006 compared with control.*P � .05 compared with control.

average strain, SRS, SRE, and peak late diastolic strain

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rate having P values of .11, .99, .85, and .09,respectively. Figure breaks down longitudinal strainby septal section. The largest decrease in the hyper-tensive group’s strain relative to control subjectsoccurred in the basal portion of the septum. Thiswas less apparent as the sample size was movedapically. The hypertensive group had significantlylower basal and midstrain performance (P � .00005)with no significant difference in apical strain relativeto control subjects (P � .069).

Discriminant analysis revealed average longitudi-nal strain and SRS were the strongest predictors of ahypertensive LVH state. Receiver operating charac-teristic curve analysis shows an averaged longitudi-nal strain cutoff of less than �20.3% separateshypertensive LVH from control with a sensitivity of93% and a specificity of 73%. An averaged longitu-dinal SRS cutoff of less than �1.17 s�1 separateshypertensive LVH from control with a sensitivity of97% and a specificity of 61%. In the study popula-tion, average longitudinal strain and SRS were supe-rior to SRE, peak systolic mitral annular velocity, Em,E/Em, and isovolumetric relaxation time in distin-guishing hypertensive LVH. Table 4 summarizes areceiver operating characteristic analysis of strainparameters compared with conventional echocar-diographic parameters associated with a hyperten-sive state. An averaged longitudinal measurementwas also superior to using basal, mid, or apical strainparameters alone. Between athletes and the hyper-tensive group, a septal wall thickness less than 1.20cm separated athletes from patients with hyperten-sion with a sensitivity of 80% and a specificity of77%. However, this is obviously confounded by thestudy eligibility criteria for LVH of a septal thicknessgreater than 1.1 cm.

In the averaged longitudinal axis, interobservervariability in strain, SRS, SRE, and peak late diastolicstrain rate was �4.6%, �7.1%, �4.7%, and �9.2%,respectively. Intraobserver variability for the sameparameters was �9.1%, �12.0%, �9.5%, and�12.5%, respectively. There were no significantdifferences between observers with regard to mea-

Table 4 Performance of echocardiographic criteria indifferentiating between pathologic left ventricularhypertrophy and control

Sensitivity Specificity

Longitudinal strain cutoff � �20.3% 93% 73%Longitudinal SRS cutoff � �1.17s�1 97% 61%Early diastolic annular velocity � 9 cm/s 85% 78%Systolic annular velocity � 9 cm/s 66% 69%

SRS, Peak systolic strain rate.

surement of strain parameters.

DISCUSSION

Differentiation between pathologic and physiologicLVH is a diagnostic challenge. To that end, this studysought to uncover the strain and strain rate profilesassociated with these conditions. These profileshave clinical use and may help in understanding theproperties behind the respective forms of LVH.

The ventricular septum receives longitudinallyarranged subendocardial fibers from both the LV andright ventricle.9 These fibers are thought to play animportant role in ventricular long-axis movement,and longitudinal motion of the mitral annulus isoften measured to help assess LV function.10 Thisstudy reveals a significant defect in longitudinalseptal strain and strain rate in patients with hyper-tensive LVH. Whereas strain measures the deformityof muscle, strain rate measures the myocardial gra-dient of velocities and is translatable to myocardialcontractility in systole.6 The deficit of these param-eters in hypertensive LVH suggests this state may beassociated with subendocardial dysfunction.

Hypertensive LVH is associated with decreasedmyocardial efficiency and perfusion reserve.11 Suchcases have increased basal coronary blood flow butdecreased coronary resistance and dilation capabili-ties12 and are less able to respond to increases inmyocardial demand. In canine models of pathologicLVH, the subendocardium has impaired coronaryautoregulation and is more sensitive to relativedecreases in coronary blood flow.13 A similar phe-nomenon is seen in human patients with pathologicLVH secondary to aortic stenosis or hypertrophiccardiomyopathy.14,15 As compromises in myocardialblood flow can produce a dysfunction in strain andstrain rate,16 a suboptimal perfusion of the subendo-cardium in hypertensive LVH may be responsible forthe decreased strain parameters uncovered by thisstudy.

Hypertensive LVH has a different gene expressionprofile from physiologic LVH, which may also affectcontractility. Pressure overloaded hypertrophied rathearts demonstrate increased cardiac messengerRNA expression of beta myosin heavy chain anddecreased expression of sarcoplasmic reticulum cal-cium2� adenosine triphosphatase.17 The beta myo-sin chain is associated with decreased contractionvelocities,18 and sarcoplasmic reticulum calcium2�

adenosine triphosphatase is believed to be involvedin relaxation.19 Normal and physiologic LVH rats, bycontrast, have greater expression of the more con-tractile alpha myosin heavy chain and sarcoplasmicreticulum calcium2� adenosine triphosphatase.17,20

The systolic dysfunction seen in this study isconfounded by the decreased compliance and in-creased fibrosis of the hypertensive LVH heart.Diastolic function was depressed in the hyperten-

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with control group. It is possible that this increasedstiffness also restricts systolic movement. Whetherpoor perfusion, myocyte dysfunction, or fibrosis,this study reveals a maladaptive process in thesubendocardium of the hypertrophied hypertensiveheart. Further research is necessary to uncover theproperties of this process.

By contrast, strength-training athletes face only atransient increase in afterload. By not experiencing achronically increased afterload or the vascular ef-fects of hypertension, the athletic heart may bespared the deleterious longitudinal effects that oc-cur with hypertensive LVH. The similarity of athletichearts to control hearts suggests that from a perspec-tive of contractility and compliance, athletic hyper-trophy is a benign process. The similarity betweenathletes and control subjects is supported by pastresearch that used tissue Doppler velocities andmyocardial velocity gradients derived from M-modetissue Doppler.4,21 A recent study found pronouncedlongitudinal strain and strain rate abnormalities inhearts with hypertrophic cardiomyopathy or hyper-tensive LVH in comparison with control hearts.22

The results of our patients with hypertension are inconcordance with that study. Moreover, this studyprovides a strain and strain rate profile for physio-logic strength-training LVH. This profile may even-tually make it possible to use SRI to determine thecause of LVH in the athletic patient.

In both the athletes and control subjects, the basalportion of the septum had larger strain and strainrates compared with the mid and apical septum.However, in the hypertensive state the basal septumhad comparatively lower strain values (Figure). Dis-

Figure Septal strain versus participant group. Ahypertension.

section studies of hypertrophied hypertensive hu-

man hearts show an increased proportion of suben-docardial connective tissue in the basal septumrelative to mid and apical portions,23 which may bea histologic correlate to the functional phenomenonwitnessed by this study.

This study obtained superior sensitivity and spec-ificity in separating hypertensive LVH from controlby using an averaged septal strain rather than anysingle septal section. This measurement was partlyused to improve signal-to-noise ratio. It was alsorecorded with the knowledge that LVH is not ahomogeneous process, and the hemodynamicswithin the LV can vary based on clinical character-istics of the participant and the disease condition.24

Varying LV chamber hemodynamics may cause dif-ferent contractility and compliance profiles alongthe septum. As such, an averaged septal measure-ment helps to compensate for this variance toproduce a net effect of the examined condition.Although this study shows a predominately basaland midseptal defect in hypertensive LVH, differinghemodynamics within hypertensive LVH may ex-plain why averaged strain parameter measurementsare more sensitive and specific than using any singleseptal section.

Limitations

This study is limited by the disparate ages of theathletic, control, and hypertensive groups. It hasinsufficient enrollment to discern the strain profileof the young patient with hypertension or the olderathlete. Instead, it functions on the supposition thatthe normal strain characteristics of the young ath-

hletes; CT, control subjects; HT, patients with

lete’s heart hold at older ages. In nonhypertrophied

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hearts, a study revealed a linear decay in strain ratewith a positive movement of 0.004 s�1 per year ofage.25 The amount of strain rate decay seen in ourstudy’s hypertensive group is too large to be ex-plained by aging alone. Further research is neededto determine whether strain rate decays in a linearfashion in the hypertrophied heart. Studies and apast meta-analysis suggest that the LVH induced byathletics trends toward normal in terms of LVM andseptal and posterior wall thickness after an extendedperiod of inactivity.26 However, this does not com-ment on strain profiles, and more work will need tobe done regarding the effect of age on both hyper-tensive and athletic LVH.

There are proportionally more men in the athleticgroup than either the hypertensive or control group.This may be secondary to the tendency of physio-logic LVH to surface more often in trained men thanwomen. A study on healthy individuals found nosignificant strain or strain rate variations based onsex.25 However, this does not comment on sexdifferences in the LVH state.

The hypertensive group underwent exercisestress testing. As this group was hypothesized tohave poorer strain parameters, it was desirable forthe patients with hypertension to have a normalexercise stress test to lower suspicion of moderateto severe coronary artery disease confounding thestudy results. If the criteria of a normal exercisestress test was applied to the athletic and controlgroups, it might have increased the difference instrain parameters between the control and hyper-tensive groups–enhancing the significance of thestudy’s results.

With the exception of basal septum strain, thisstudy found no significant strain or strain rate differ-ences between control subjects and athletes withLVH. Consequentially, the possibility exists for atype II error. As previously mentioned, the studydesign could have found an effect size as small as7.5% with a power of 80%. It is possible thatsignificant differences exist between control andathletic LVH groups, but the study is underpoweredto detect it.

Conclusions

This study used SRI to discern the differences be-tween physiologic and hypertensive hypertrophy. Ituncovered a pronounced abnormality in longitudi-nal strain, SRS, and SRE in the hypertensive heart thatmay allude to a subendocardial defect. A SRI longi-tudinal strain cutoff of �20.3% separated hyperten-sive LVH from control group with a sensitivity andspecificity of 93% and 73%, respectively. AthleticLVH, by comparison, had a strain profile similar tocontrol. As such, SRI may hold clinical use in helpingto determine whether LVH in a patient is physio-

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