Hypertension Journal

Show Contents

Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy
Assessment of End Organ Damage in Hypertension-Left
Ventricular Hypertrophy
1Mohan V Deshpande, 2Niteen V Deshpande
1Consultant, 2Director
1,2Department of Cardiology, Spandan Heart Institute andResearch Center, Nagpur, Maharashtra, India
Corresponding Author: Niteen V Deshpande, DirectorDepartment of Cardiology, Spandan Heart Institute and ResearchCenter, Nagpur, Maharashtra, India
Phone: +917122443333
e-mail: nvdesh@hotmail.com
Left ventricular Hypertrophy (LVH) is an important consequenceof systemic hypertension and is considered as target organdamage. LVH has significant impact on the prognosis and regressionof LVH correlates with better outcomes in hypertensiveindividuals. Electrocardiography (ECG) remains the basic toolto diagnose LVH in hypertension although it has significant limitationsin terms of sensitivity and specificity. Echocardiographynot only provides a better estimate of LVH but also allows betterquantification of left ventricular mass and volumes, while providingclues for other causes of LVH. Cardiac magnetic resonanceImaging (CMR) is considered the gold standard for estimationand characterization of LVH, but is limited due to its availabilityand cost. Computed Tomography of heart also offers reliableestimate of LVH at the cost of high radiation exposure and is notrecommended for this purpose. Assessment of LVH should bedone using ECG in every patient with hypertension while echocardiographyand CMR should be reserved for specific indications
Keywords: Electrocardiography, Hypertension, Left ventricularhypertrophy.
How to cite this article: Deshpande MV, Deshpande NV.Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy. Hypertens J 2017;3(3):139-146.
Source of support: Nil
Conflict of interest: None


Hypertension is an important health challenge, which isthe principal cause of death and disability. A systematicanalysis which included 135 population-based studies ofmore than 9 lakh adults from 90 countries observed thatprevalence of hypertension decreased by 2.6% in highincomegroup countries during 2000 to 2010, whereas itincreased by 7.7% in the low- and middle-income countries.1 This is because of improvements in public healthinterventions in high-income countries. India belongs tolow- to middle-income group countries and shows highprevalence of hypertension, which is steadily increasing. The age for standardized prevalence of hypertension is26.6%for men and 24.7% for women.2 Overall burden ofhypertension in India is estimated to be approximately118.2 million.3

Hypertension has a detrimental effect on almost allorgans of the body, and its effect on the heart is called ashypertensive heart disease or hypertensive cardiopathy.Hypertension leads to the remodeling of the myocardiumin response to chronically elevated blood pressure andwall stress.4

Hypertension leads to changes in both structure andfunction of the heart (Flow Chart 1).5 Hypertensive heartdisease has several recognizable stages, such as LVHand systolic and diastolic dysfunction, which progress toclinical heart failure and ischemic heart disease.6 The LVHtypically has the distinct importance due to being associatedwith a 3- to 15-fold increase in cardiovascular events.7

Hypertensive heart disease is asymptomatic in itsinitial stages. In its advanced stage, it can manifest asangina pectoris, dyspnea, and arrhythmias as a resultof reduced coronary reserve, impaired systolic anddiastolic function, and atrial and ventricular arrhythmias.7 It further leads to inappropriate activation of therenin-angiotensin-aldosterone system, which has beenidentified as a key pathologic pathway contributing tofibrosis, cardiomyocyte abnormalities, inflammation, andendothelial dysfunction.8

The LVH is defined as increased indexed LV massand classified as concentric or eccentric based on the ratioof LV wall thickness to chamber dimension. The LVHis concentric if the ratio is increased, else it is eccentric(Fig. 1).9 It takes months to years in order to develop LVH,and likewise regression is also a slow process.

Common tools to detect cardiac sequel of hypertension,most importantly LVH, include ECG and echocardiography,computed tomography (CT) scan, and CMRimaging. The CMR is considered to be the gold standardtoday, but is limited due to unavailability and cost.


The ECG is an inexpensive, initial screening tool to assesstarget organ damage in a hypertensive patient. It can be used to assess the presence of left atrial enlargement,LVH, myocardial ischemia or infarction, ventricularpremature beats, and atrial fibrillation. The sensitivityand specificity of ECG vary widely depending uponthe gold standard used [echo or magnetic resonanceimaging (MRI) or necropsy] and severity of LVH. Overall,sensitivity of ECG in detecting moderate-to-severe LVHranges from 30 to 60%, while specificity ranges from80 to 90%. Despite its relative insensitivity, ECG doeshave prognostic significance. Hypertensive patients withECG-documented LVH, who meet ECG criteria, have agreater LV mass than those who do not meet ECG criteria.10 Associated abnormalities of ST-T changes signifyhigh LV mass in patients with LVH.

Hypertension Journal, July-September, Vol 3, 2017 139

Mohan V Deshpande, Niteen V Deshpande

Flow Chart 1: Structural and functional changes in heart due to hypertension(Adapted from: Schmieder5)
Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy

Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy
Fig. 1: Types of LV hypertrophy (Adapted from: Khouri et al9)


The LVH produces five major changes in the ECG, whichinclude increased QRS voltage, increased QRS duration,left axis deviation, repolarization (ST-T) changes, and leftatrial enlargement.

Increased QRS Voltage and Duration

Increased LV mass augments amplitude of voltage generated,which is reflected on the surface ECG as positiveforces on the left precordial leads (increased R waves) andnegative forces on the right precordial leads (S waves).The R wave amplitude is also increased in leads I andaVL. Widening of QRS duration is also known to occur with development of LVH, which may be subtle or pronounced.Widening of QRS eventually may result intocomplete left bundle branch block (LBBB) pattern on theECG. However, LBBB may result from other pathologicalchanges like calcification or fibrosis of the proximalconduction system. A number of criteria have been suggestedfor diagnosis of LVH.

Assessment of End Organ Damage in Hypertension

Cornell Criteria

Add the R wave in aVL and the S wave in V3. If the sumis greater than 28 mm in males or greater than 20 mm infemales, LVH is present.

Modified Cornell Criteria

Examine the R wave in aVL. If the R wave is greater than12 mm in amplitude, LVH is present.

Sokolow-Lyon Criteria

Add the S wave in V1 plus the R wave in V5 or V6. If thesum is greater than 35 mm, LVH is present.

Romhilt-Estes LVH Point Score System

If the score equals 4, LVH is present with 30 to 54%sensitivity.If the score is greater than 5, LVH is present with83 to 97% specificity.
  • Amplitude of largest R or S in limb leads ≥ 20 mm = 3 points
  • Amplitude of S in V1 or V2 ≥ 30 mm = 3 points
  • Amplitude of R in V5 or V6 ≥ 30 mm = 3 points
  • ST and T wave changes opposite QRS without digoxin = 3 points
  • ST and T wave changes opposite QRS with digoxin = 1 point
  • Left atrial enlargement = 3 points
  • Left axis deviation = 2 points
  • QRS duration ≥ 90 ms = 1 point
  • Intrinsicoid deflection in V5 or V6 > 50 ms = 1 point

These scores are not full proof and there are fallaciesassociated with these scores. The QRS voltage increaseswith both thickening of the wall (pressure overload)and dilatation of the chamber (volume overload) of theleft ventricle. There is significant day-to-day variabilityin QRS voltage due to lead placement, respiration, andbody position. In addition, young black males may haveincreased voltage in the absence of hypertension.11

The LVH is also seen in aortic stenosis and aorticinsufficiency, mitral valve insufficiency, some congenitalcardiac defects, and hypertrophic obstructive cardiomyopathyin addition to hypertension. Classical ECG criteriafor detection of LVH have a satisfactory specificity, butlow sensitivity. The sensitivity declines dramatically in the presence of obesity. The most sensitive, but leastspecific criteria are high voltages in the precordial leads.11
Repolarization Abnormalities

Severe pressure overload is often associated with STdepression and T wave inversion in the leads with relativelytall R waves. This pattern may be a result of primaryalteration in the repolarization of the hypertrophiedmuscle or due to relative subendocardial ischemia.12

The "strain pattern" is characterized by ST depression≥1 mm in lateral leads I, aVL, and V4 to V6 (mostcommonly just V5 or V6 is used). The direction of theT wave is in the opposite of the direction of the uprightQRS complex (Fig. 2). Furthermore, the T wave is asymmetricwith a gradual down slope (upward convex)followed by a rapid up slope and a terminal positiveovershoot. The presence of a "strain pattern" impliesa poor prognosis. Increased LVM and coronary arterydisease are associated with the strain pattern.

The ECG LVH with "strain pattern" is the most lethalclassic Framingham cardiovascular risk factor (Graph 1).

Fragmented QRS on ECG

Fragmented QRS complexes (fQRS) on surface ECGare defined as an rSR' pattern in the absence of typicalbundle branch block. Morphologically, it represents analtered QRS complex that has a duration < 120 ms andhas either an additional R wave, notching in the nadirof the S wave, or an additional R' wave.13 In one study,24-hour ambulatory blood pressure monitoring and ECGscreening were done in 548 "healthy" persons withoutcardiac hypertrophy. It was observed that fQRS patternwas significantly higher in patients with hypertensionand prehypertension as against those with normal bloodpressure. The fQRS on a 12-lead ECG has been demonstratedas a marker of myocardial fibrosis. The fQRS has been shown to be an independent predictor of newonset atrial fibrillation in postoperative period in patientsundergoing coronary artery bypass graft.14

Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy
Fig. 2: The LVH with strain pattern (Adapted from: Cifkova11)

Hypertension Journal, July-September, Vol 3, 2017 141

Mohan V Deshpande, Niteen V Deshpande

Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy
Graph 1: The LVH and Framingham cardiovascular risk (Adapted from: Cifkova11)

Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy
Fig. 3: The LA enlargement on ECG (Adapted from: Cifkova11)

Left Atrial Enlargement

Left atrial enlargement is one of the early change seenin hypertensive heart disease. Surface ECG finding ofincreased duration of terminal portion of P wave andamplitude of P wave is one of the earliest finding of hypertensiveheart disease. P wave duration more than 0.04seconds and depth of more than 1 mm or their product> -0.04mm sec is indicative of left atrial enlargement11are indicative of left atrial enlargement (Fig. 3).


The LVH on echocardiography may be detected in 20 to40% patients with arterial hypertension. Two-dimensional(2D) echocardiography allows more accurate and reproduciblemeasurements of LV volumes and mass and ismost commonly calculated using the Devereux equation.15

Echocardiography offers more reliable detection of LVHas compared with ECG in women,16 in obese individuals17with body mass index > 30 kg/m2, and in smokers.18 TheDevereux formula for calculating LV mass is
LV mass = 0.8 × (1.04 [(LVIDd + PWTd + SWTd)
3 - (LVIDd) 3]) + 0.6 gm

where LVIDd is the LV internal diameter in diastole,PWTd is the posterior wall thickness in diastole, andSWTd is the septal wall thickness in diastole. Thisformula is applicable only to patients without majordistortion of their LV geometry (e.g., LV aneurysm). Forpatients with an increased LV mass (LV mass > 125 gm/m2in men and > 110 gm/m2 in women), calculation of relativewall thickness (RWT) using the equation (2 × PWTd/LVIDd) will aid in classification of concentric or eccentricLVH. Patients with an increased RWT (RWT ≥ 0.42) haveconcentric hypertrophy, whereas patients with a normalvalue (RWT ≤ 0.42) have eccentric hypertrophy. Patientswith concentric remodeling are those with normal LVmass, but increased RWT. Echocardiography-derived LVmass and RWT measurements have been shown to carryprognostic significance in hypertensive patients, eventhose without LVH.19

Septal bulge (basal septal wall thickness ≥ 2 mmthicker than midseptal wall thickness) is an early echocardiographicsign in patients with hypertension. In astudy, it was observed that when resting blood pressure(BP) was used to diagnose hypertension, septal bulgewas a reasonable predictive sign with a sensitivityof 73% and specificity of 76%. However, when cycleergometer test or ambulatory BP monitoring was usedto diagnose hypertension, septal bulge strongly predictedarterial hypertension with sensitivity of 93% andspecificity of 86%.20

The LVH is seen many other conditions apart fromhypertension like hypertrophic cardiomyopathy (HCM).

Assessment of End Organ Damage in Hypertension

Assessment of End Organ Damage in Hypertension-LeftVentricular Hypertrophy
Fig. 4: Tricuspid annular velocity (Adapted from: Hayashi et al21)

Echocardiography can differentiate the two conditions.Apart from other echocardiographic signs, RV wall thicknessis greater in HCM than in hypertensive patients.Tricuspid annular motion velocity determined by pulsedtissue Doppler echocardiography can be used to detectright ventricular dysfunction in HCM. Early diastolictricuspid annular motion velocity (TAM-e') was foundto be significantly lower in HCM than those with hypertension(Fig. 4).21

Strain rate (SR) imaging derived from tissue Dopplerimaging is able to discriminate HCM from hypertensiveLVH. The septum/posterior wall thickness ratio andsystolic strain (? sys) are able to discriminate HCM fromhypertensive LVH. An ? sys cutoff value of -10.6% discriminatedbetween HCM and H-LVH with a sensitivityof 85.0%, specificity of 100.0%, and predictive accuracyof 91.2%. The combination of the septum/posterior wallthickness ratio and ? sys discriminates HCM from H-LVHwith a predictive accuracy of 96.1%.22 Strain rate imagingcan also be used to distinguish between individualswith hypertensive LVH and those with strength-trainingathletic LVH. Hypertensive LVH has significant longitudinalstrain, peak systolic strain rate [SR (S)], peakearly diastolic strain rate [SR (E)], reductions vs control.The lack of these reductions in athletes suggests that SRimaging may have clinical use in discerning the physiologicLVH state.23

Implication of LVH on Echocardiography

Levy et al24 studied the relation of LV mass to the incidenceof cardiovascular disease, mortality from cardiovasculardisease, and mortality from all causes in 3,220subjects enrolled in the Framingham Heart Study, whowere 40 years of age or older and free of clinically apparentcardiovascular disease, in whom LV mass was determinedechocardiographically. During a 4-year follow-upperiod, there were 208 incident cardiovascular events, 37deaths from cardiovascular disease, and 124 deaths from all causes. Left ventricular mass (corrected for height) wasassociated with death from all causes with a relative riskof 1.49 in men and 2.01 in women. Increase in LV masswas associated with all outcome events, and the relationwas seen in LV mass not considered as "hypertrophic."Cardiovascular disease and death rates had a 1.5-foldincrease for each 50 gm/m of LV mass indexed by height.Thus, it is hypothesized that LVH is an independent riskmarker of long-term exposure to the combined effectsof various risk factors for atherosclerosis, especially incontext of cerebrovascular disease.25 Further, regressionof LVH has been shown to confer protection fromcardiovascular disease.26 In the Losartan Interventionfor End-Point reduction (LIFE) study carried out inhypertensive patients with LVH, patients randomizedto losartan showed greater regression of LVH and lesserrisk of stroke.27,28 A prespecified analysis of the LIFE trialparticipants for prognostic effects of serial changes inECG and echocardiographic indices of LVH confirmedits independent value.29,30

Three-dimensional Echocardiography

Three-dimensional (3D) echocardiography has severaladvantages over M-mode and 2D methods, as it does notrely on geometric assumptions. It is highly reproduciblefor assessment of LV mass and volumes, but as with anyechocardiography technique, it relies on adequate acousticwindows and an experienced practitioner.31 The availabilityof 3D echocardiography is still limited to selectedfew centers and its use in hypertensive patients is limited.

Computed Tomography

The CT is used when a patient has contraindicationsfor CMR, offering an excellent spatial resolution andunrestricted field of view. However, the relatively lowtemporal resolution and the radiation exposure (rangingfrom 5 to 20 mSv) make cardiac CT the least preferredtechnique among the three for LVH assessment.32
Hypertension Journal, July-September, Vol 3, 2017 143

Mohan V Deshpande, Niteen V Deshpande

In a study, multidetector row computed tomography(MDCT) was compared with MRI in the assessmentLV wall thickness. It was observed that in assessablesegments by both modalities, a significant correlationbetween MDCT and MRI was found for end-diastolicwall thickness (EDWT) and end-systolic wall thickness(ESWT) and percent systolic wall thickening %SWT.However, mean EDWT and ESWT values by MDCT wereslightly lower than those by cine MRI.33

Cardiac Magnetic Resonance Imaging

The MRI has emerged as a powerful imaging modalityfor assessment of hypertensive heart disease, as it is notrestrained by acoustic windows, provides accurate andreproducible measures of LV function and mass, andenables myocardial fibrosis assessment.34 It is also areliable and reproducible measurement of cardiac parameterslike volume, ejection fraction, and cardiac mass. Itcan also differentiate the etiology of LVH by providinginformation about tissue characterization.

Presently, the methodology of choice for measuringLVM by CMR is steady-state free precession (SSFP) cineimaging. The absolute values of LVM measured by CMRtend to be lower than those for echocardiography becauseSSFP cine imaging allows the visualization of myocardialtrabeculae and thus, includes trabeculae in the LV volumemeasurement excluding it from the mass. Echocardiography,however, generally includes trabeculations in themeasurement of LV mass. Although CMR has excellentreproducibility for measuring LVM and is widely perceivedas the gold standard, its accuracy has not beenvalidated against necropsy LV weight in humans.35

The MRI is useful in differentiating hypertrophybecause of hypertension from other causes like HCM.When the EDWT is ≥ 15 mm, indexed LV mass wassignificantly greater in hypertensive patients as HCM.However, midwall late gadolinium enhancement andsystolic anterior motion of mitral valve were present inHCM as compared with hypertensive patients.36

Hypertension leads to myocardium remodeling due tocardiomyocyte hypertrophy, fibroblast stimulation, andincreased collagen stimulation, which leads to fibrosis.The MRI is useful to detect this fibrosis. In a study, it wasobserved that hypertensive patients with LVH exhibitedgreater diffuse fibrosis and reduced circumferentialstrain and circumferential SRs compared with hypertensionwithout LVH and control subjects. Hypertensivepatients with LVH had higher ECV (extracellular volume),and higher ADC (apparent diffusion coefficient). Basedon these observations, it was suggested that ADC measurementmay be a novel target to monitor hypertensivepatients.37

Evaluation of LVH-How and When?

Although LVH is important end organ damage due tohypertension, and its regression is shown to improveoutcomes, no current guidelines recommend monitoringof its progression/regression. Since most of the currentlyrecommended first-line therapeutic agents for hypertensionalso reduce LVH significantly (except diuretics), thefocus of the current guidelines is adequate control of BPrather than LVH regression. Serial ECG monitoring mayhelp to demonstrate changes in the ECG voltage over time,which correlates with regression of LVH. However, lossof ECG voltage could be due to many other factors likealteration in the leads position, development of anasarca,pericardial or pleural effusion, weight gain, and increasedseverity of chronic obstructive pulmonary disease. Thus,the investigation to monitor LVH regression today isechocardiography rather than ECG.

Baseline evaluation of hypertensive patient includesbiochemistry along with ECG for detection of any preexistingabnormality at the onset of the treatment. Follow-upECG is indicated only when the clinical situation demandsevaluation for additional supportive information regardingdevelopment of ischemic heart disease. Routine followupECG monitoring is not indicated in uncomplicatedhypertension. Echocardiography, on the contrary, is notindicated for measurement of LVH/mass routinely forhypertensive patients owing to its cost and availability.Indications for echo in hypertensive patient include:
  • Patients with mild diastolic hypertension without anyother risk factors or end organ damage (no LVH onECG). Demonstration of LVH by echo is generally anindication for instituting medical therapy, while lackof LVH generally supports nonpharmacologic therapy.
  • Patients with severely elevated blood pressure in theclinic (suspected white coat hypertension) withoutevidence of end organ damage. Absence of LVHon echo in these patients suggests either white coathypertension or hypertension of recent onset. Ambulatoryblood pressure monitoring would be the mostimportant in this situation.
  • Patients with suspected or documented heart disease,which needs further evaluation.
  • Patients with bundle branch blocks.

Since the indications of echocardiography for detectionof LVH are very few and limited even at baseline,routine follow-up echo for monitoring LVH regressionis not recommended. A significant change in the clinicalscenario should, however, prompt repeat echo evaluation.


The LVH is an important target organ damage in hypertensionand correlates with increased risk of morbidity and mortality. The ECG and echocardiography are thetwo common tools to detect LVH in clinical practice,which are widely available to most of the clinicians today.Although MRI is the gold standard to evaluate LVH, itsuse is restricted to research settings. Documentation ofLVH regression although satisfying has no bearing on thetreatment of hypertension and, thus, routine follow-upECG/ECHO for LVH monitoring are not currently recommended.Documenting good BP control using either clinicor home BP monitoring or ambulatory BP monitoring isthe more important part of follow-up of hypertensivepatients than monitoring LVH, as adequate control ofhypertension is the key to improve long-term outcomes.


Assessment of End Organ Damage in Hypertension

  1. Mills KT, Bundy JD, Kelly TN, Reed JE, Kearney PM, Reynolds K,Chen J, He J. Global disparities of hypertension prevalenceand control. A systematic Analysis of Population basedStudies from 90 Countries. Circulation 2016 Aug;134:441-450.
  2. Global Health Observatory Data Repository. Raised bloodpressure (SBP> 140 OR DBP> 90) age standardized (%) Globalestimates. Geneva: WHO; 2015; [cited 2017 Jul 13]. Availablefrom: http://apps.who.int/gho/data/view.main.2464GLOBALSTANDARD?lang=en.
  3. Chaturvedi V, Parakh N, Seth S, Bhargava B, Ramakrishnan S,Roy A, Saxena A, Gupta N, Misra P, Rai SK, et al. Heart failurein India: The INDUS (INDia Ukieri Study) study. J PractCardiovasc Sci 2016 Jan-Apr;2(1):28-35.
  4. Alvarez Aliaga A, Gonzalez Aguilera JC, Maceo Gomez Ldel R.Factors associated to hypertensive heart disease development:a prospective cohort study in Bayamo, Cuba. Medwave2016 Jul;16(6):e6492.
  5. Schmieder RE. End organ damage in hypertension. DtschArztebl Int 2010 Dec;107(49):866-873.
  6. Ramakrishnan S, Kothari SS, Bahl VK. Hypertensive heartfailure. Indian Heart J 2003 Jun;55:21-26.
  7. Kannel WB. Left ventricular hypertrophy as a risk factor: theFramingham experience. J Hypertens (Suppl) 1991 Dec;9(2):S3-S8, discussion S8-S9.
  8. Volpe M, McKelvie R, Drexler H. Hypertension as an underlyingfactor in heart failure with preserved ejection fraction.J Clin Hypertens (Greenwich) 2010 Apr;12(4):277-283.
  9. Khouri MG, Peshock RM, Ayers CR, de Lemos JA, Drazner MH.A 4-tiered classification of left ventricular hypertrophy basedon left ventricular geometry: the Dallas heart study. CircCardiovasc Imaging 2010 Mar;3(2):164-171.
  10. Fragola PV, Colivicchi F, Fabrizi E, Borzi M, Cannata D.Assessment of left ventricular hypertrophy in patients withessential hypertension. A rational basis for the electrocardiogram.Am J Hypertens 1993 Feb;6(2):164-169.
  11. Cifkova R. Advantages and disadvantages of ECG diagnosis inleft ventricular hypertrophy. Vnitr Lek 2002 Dec;48(Suppl 1):103-108.
  12. Prisant LM. Hypertensive heart disease. J Clin Hypertens(Greenwich) 2005 Apr;7(4):231-238.
  13. Mani A. Fragmented QRS: a marker of hypertensive heartdisease? J Clin Hypertens (Greenwich) 2017 Sep;19(9):866-867.
  14. Bekar L, Katar M, Yetim M, Celik O, Kilci H, Onalan O. FragmentedQRS complexes are a marker of myocardial fibrosis in hypertensive heart disease. Turk Kardiyol Dern Ars 2016Oct;44(7):554-560.
  15. Devereux RB, Alonso DR, Lutas EM, Gottlieb GJ, Campo E,Sachs I, Reichek N. Echocardiographic assessment of leftventricular hypertrophy: comparison to necropsy findings.Am J Cardiol 1986 Feb;57(6):450-458.

  1. Okin PM, Roman MJ, Devereux RB, Kligfield P. Gender differencesand electrocardiogram in left ventricular hypertrophy.Hypertension 1995 Feb;25(2):242-249.
  2. Lauer MS, Anderson KM, Kannel WB, Levy D. The impact ofobesity on left ventricular mass and geometry. The FraminghamHeart Study. JAMA 1991 Jul;266(2):231-236.
  3. Schillaci G, Verdecchia P, Sacchi N, Vignai E, Benemio G,Porcellati C. Influence of cigarette smoking on the electrocardiographicdiagnosis of left ventricular hypertrophy inarterial hypertension. G Ital Cardiolo 1999 Jan;29(1):34-38.
  4. Li L, Shigematsu Y, Hamada M, Hiwada K. Relative wallthickness is an independent predictor of left ventricularsystolic and diastolic dysfunctions in essential hypertension.Hypertens Res 2001 Sep;24(5):493-499.
  5. Gaudron PD, Liu D, Scholza F, Hu K, Florescu C, Herrmann S,Bijnens B, Ertl G, Stork S, Weidemann F. The septal bulge-anearly echocardiographic sign in hypertensive heart disease.J Am Soc Hypertens 2016 Jan;10(1):70-80.
  6. Hayashi S, Yamada H, Nishio S, Hotchi J, Bando M, Takagawa Y,Saijo Y, Hirata Y, Sata M. Tricuspid annular motion velocity asa differentiation index of hypertrophic cardiomyopathy fromhypertensive heart disease. J Cardiol 2015 Jun;65(6):519-525.
  7. Kato TS, Noda A, Izawa H, Yamada A, Obata K, Nagata K,Iwase M, Murohara T, Yokota M. Discrimination of nonobstructivehypertrophic cardiomyopathy from hypertensiveleft ventricular hypertrophy on the basis of strain rateimaging by tissue doppler ultrasonography. Circulation 2004Dec;110(25):3808-3814.
  8. Saghir M, Areces M, Makan M. Strain rate imaging differentiateshypertensive cardiac hypertrophy from physiologiccardiac hypertrophy (athlete's heart). J Am Soc Echocardiogr2007 Feb;20(2):151-157.
  9. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP.Prognostic implications of echocardiographically determinedleft ventricular mass in the Framingham Heart Study. N EnglJ Med 1990 May;322(22):1561-1566.
  10. Benjamin EJ, Levy D. Why is left ventricular hypertrophy sopredictive of morbidity and mortality? Am J Med Sci 1999Mar;317(3):168-175.
  11. Verdecchia P, Angeli F, Borgioni C, Gattobigio R, de Simone G,Devereux RB, Porcellati C. Changes in cardiovascular riskby reduction of left ventricular mass in hypertension: ameta-analysis. Am J Hypertns 2003 Nov;16(11 Pt 1):895-899.
  12. Okin PM, Devereux RB, Jern S, Kjeldsen SE, Julius S, NieminenMS, Snapinn S, Harris KE, Aurup P, Edelman JM, et al.;Losartan Intervention for End-Point Reduction Study Investigators.Regression of electrocardiographic left ventricularhypertrophy by losartan versus atenolol: the Losartan Interventionfor End-Point Reduction (LIFE) Study. Circulation2003 Aug;108(6):684-690.
  13. Dahlof B, Devereux RB, Kjeldsen SE, Julius S, Beevers G, deFaire U, Fyhrquist F, Ibsen H, Kristiansson K, Lederballe-Pedersen O, et al.; LIFE Study Group. Cardiovascular morbidityand mortality in the Losartan Intervention for End PointReduction in hypertension (LIFE) study: a randomized trialagainst atenolol. Lancet 2002 Mar;359(9311):995-1003.

Hypertension Journal, July-September, Vol 3, 2017 145

Mohan V Deshpande, Niteen V Deshpande

  1. Okin PM, Devereux RB, Jern S, Kjeldsen SE, Julius S, NieminenMS, Snapinn S, Harris KE, Aurup P, Edelman JM, et al.;LIFE Study Investigators. Regression of electrocardiographicleft ventricular hypertrophy during antihypertensive treatmentand the prediction of major cardiovascular events.JAMA 2004 Nov;292(19):2343-2349.
  2. Devereux RB, Wachtell K, Gerdts E, Boman K, NieminenMS, Papademetriou V, Rokkedal J, Harris K, Aurup P,Dahlof B. Prognostic significance of left ventricular masschange during treatment of hypertension. JAMA 2004Nov;292(19):2350-2356.
  3. Kuhl HP, Schreckenberg M, Rulands D, Katoh M, Schafer W,Schummers G, Bucker A, Hanrath P, Franke A. Highresolutiontrans-thoracic real-time three-dimensional echocardiography:quantitation of cardiac volumes and functionusing semi-automatic border detection and comparison withcardiac magnetic resonance imaging. J Am Coll Cardiol 2004Jun;43(11):2083-2090.
  4. Alkema M, Spitzer E, Soliman OI, Loewe C. Multimodalityimaging for left ventricular hypertrophy severity grading:a methodological review. J Cardiovasc Ultrasound 2016Dec;24(4):257-267.

  1. Kanza RE, Higashino H, Kido T, Kurata A, Saito M, Sugawara Y,Mochizuki T. Quantitative assessment of regional left ventricularwall thickness and thickening using 16 multidetectorrowcomputed tomography: comparison with cine magneticresonance imaging. Radiat Med 2007 Apr;25(3):119-126.
  2. Hoey ET, Pakala V, Teoh JK, Simpson H. The role of imagingin hypertensive heart disease. Int J Angiol 2014 Jun;23(2):85-92.
  3. Janardhanan R, Kramer CM. Imaging in hypertensiveheart disease. Expert Rev Cardiovasc Ther 2011 Feb;9(2):199-209.
  4. Rodrigues JC, Rohan S, Ghosh Dastidar A, Harries I, Lawton CB,Ratcliffe LE, Burchell AE, Hart EC, Hamilton MC, Paton JF,et al. Hypertensive heart disease versus hypertrophic cardiomyopathy:multi-parametric cardiovascular magneticresonance discriminators when end-diastolic wall thickness≥ 15 mm. Eur Radiol 2017 Mar;27(3):1125-1135.
  5. Wu LM, Wu R, Ou YR, Chen BH, Yao QY, Lu Q, Hu J, Jiang M,An DA, Xu JR. Fibrosis quantification in Hypertensive HeartDisease with LVH and Non-LVH: Findings from T1 mappingand Contrast-free Cardiac Diffusion-weighted imaging. SciRep 2017 Apr;7(1):559.