Posts Tagged ‘lvh’

We know LVH and SHT go together . Mind you , this is not an Intimate relationship.

Widespread utilisation  of echocardiography  has revealed  , definite  LVH occurs only in about 20% (A guess !) of  HT . (Do you know in the Famingham study the incidence of LVH  after 12 year follow up was a paltry 3 % .Will you agree with that ? Mind you , It was in 1969 when Echo was not there )

What determines LVH ?  The clear answer is elusive. It is easy to escape  from the issue by calling it  multi factorial !

Why don’t you try this question .

My guess would be ,  magnitude ( or  even duration of HT !)  is  less important than genetic predisposition  or  associated diabetes ,  renal involvement.Our analysis from  hypertension clinic reveals LVH is many fold common in secondary HT  when compared to primary HT !

I often used to provoke the students by saying if the LVH is gross in HT it can not be primary , 9/10 times  ! Invariably  we find some  other  association or reason for the HT !

Link to related topic in this site

Why-lvh-does-not-occur-in-all-patients-with-systemic-hypertension ?

How-diabetes-modifies-lvh-due-to-hypertension ?

incidence of lV left ventricular hypertrophy framingham study

Next  . . .

How does LVH regress with treatment ?

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  • LVH is classically diagnosed with high qrs voltage either in limb or chest leads or both.
  • High voltage is a specific ECG  sign,   presence  of  which  would strongly suggest LVH  ,   absence of which  is not  useful to rule out true LVH.
  • LVH with   flattish  or  down sloping   ST segment ,  with or without  T inversion  , can be a sole presentation of LVH . This should not be taken as sign of ischemia.  Here is  patient  with such an  ECG

Mechanism for LVH without high voltage

  • Intrinsic muscle  electrophysiological  property – Arrangement of muscle fibre orientation  will determine the voltage .(Parallel vs perpendicular, disarray etc)
  • Pathological LVH with fibrotic process and interstitial hypertrophy may not  record high voltage.
  • Presence of  high voltage LVH  would indicate a dominant physiological muscle mass that lacks interstitial reaction.
  • Finally , technical cause like thick chest wall in obese can dampen the LVH voltage.

Read a related  topic in this blog


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LVH can be diagnosed with fair degree of  accuracy  by surface ECG . We have a set criteria .The Estes  scoring is  the most popular. Very rarely we have all  the classical features of LVH in a given ECG .

With the advent of echocardiography ECG diagnosis of LVH has become redundant . Still , it is essential to  build the  foundations  in cardiology  for the current generation cardiologists.

The following are the  magnified views from the above   ECG

High Voltage

High voltage QRS is a hall mark of LVH .It increases in both chest  and  limb leads .In chest leads , both R and S wave gets amplified , while in limb leads only the R wave  is taller . We have to sum up R  from lead  V 5 and S from V2  (Practically any deep S and tall R can be added . LVH is diagnosed  if  sum qrs voltage  is  >35 mm . Voltage criterias in limb leads do not require these  addition business . An  R wave amplitude > 11mm  in limb leads by itself  would indicate an LVH (In the absence of bundle blocks )

Pit falls in voltage  criteria

It is our belief    qRS voltage  would faithfully   reflect the   quantum of cardiac muscle mass ,  but in general  to equate qRS voltage  to myocardial  mass  is   a  huge error we make ! (Of course  It  may be true in  some cases  following MI )  .

The qRS  voltage is determined by   numerous  factors (Important ones are :  chest wall thickness , age , LV cavity size ,  amount of blood inside LV cavity,  heart rate , conduction delays  etc ) This is the reason a 10-year-old boy’s   ECG will  satisfy the criteria of LVH  by 100 % .Do not ever report a ECG without knowing the age of the patient .

At high heart rates R wave amplitude increases(Broddy effect) due to high conductance of blood

Chest lead always balances RV and LV forces .One can mask the other .So be ready for surprises when you find a perfectly normal ECH in bi-ventricular  hypertrophies ) A balancing act !

Mini summary : Never diagnose LVH with high voltage alone

Left axis deviation

The axis deviation is again non specific  . The LV mass shifts the mean axis to left (Beyond -15 degrees) .The axis shift would also be contributed by mild forms of LAFB . This  fascicle  which criss crosses the LVOT  easily gets injured to hemodynamic stress ( or rather insulted ) and  lose its function . So its job is  transferred to  the posterior fascicle  which  shoots  towards  anterior and superior and left , hence the  left axis deviation) .The LAFB is generally a benign defect unless it occurs in an acute fashion as a response to ischemia.

Mini summary : Never diagnose LVH on the basis of left axis alone

Left Atrial  abnormality

This need not be present in every one with LVH . It happens only  if  LVH  is associated with relaxation defect , when   it calls for  LA’s  assistance .(In other words , presence  of LAE in hypertensive  patients is  a  sure and simple way to confirm diastolic dysfunction ) . Similarly absence of  LAE (  with a   significant LVH )  is a good sign as the LV is able to tackle the hypertensive stress in solo fashion in all likely hood free from significant diastolic dysfunction.

Apart from LAE , note also the p wave encroaches good part of PR interval .

Mini summary : LAE can be very useful parameter to diagnose LVH . (Is it not ironical  to note   LAE is more reliable to diagnose LVH ! . This is because qrs morphology is unreliable as it influenced by many factors  while p wave  changes are  not subjected to such influence )

Secondary repolarization changes

We know ventricular depolarization and repolarization are interlinked phenomenon .Both  occur in  opposite directions still  , able to  record   ECG deflection  in same direction  (positive QRS/positive T)  . This is due to the fact  the epicardium and endocardium has  action potential with different velocities . At times of   LVH this epicardial  , endocardial heterogeneity in repolarization becomes void. (Note : This is a simplified statement of a complex repolarization process)

Because of this the repolarization is recorded opposite to that of depolarization .Hence we get all sorts of secondary ST /T changes. (The  term secondary is used to denote secondary to alteration  in depolarisation ).

Many times  all of the following  could   mean the same  in the bed side clinical parlance !

  • Secondary ST/T changes
  • Non specific ST/T ,
  • LV strain
  • LV systolic over load etc .

Note : Primary ST depression occurs in true ischemia without any alteration in LV Mass or conduction defect.

*** For advanced readers  only : Some of the ST depression that occur in ischemia could again be secondary changes. This  needs further reading.


Echo is the gold standard for diagnosing LVH .There are two definitions .

  1. Based on septal thickness
  2. Based on LV mass*

LV mass > 200mg in men and 175mg in women is considered LVH . LVH based on LV mass is  ideal . But can be misleading in a dilated heart where the mass may be increased with a  relatively   thinned  out IVS .

Final message

There are numerous  ways to miss    LVH in ECG,  But the definite way  for not missing  is by echocardiogram !

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LVH is one of the commonest ECG abnormality . We know the hall mark  of LVH is increased QRS voltage .We also know , ECG is not a fool proof method to detect LVH .It has very good specificity , but little sensitivity , meaning that increase in  QRS voltage is  fairly accurate in predicting LVH  but absence of  which cannot exclude LVH.

Why Increased QRS voltage does not occur in many with LVH ?

Even though we think myocardial mass  is  the  sole determinant of QRS  voltage  , in reality  it   is determined by many other factors.

  • Distance between the ECG lead , and the myocardium is an important factor. In classical concentric LVH , the LV  cavity is not enlarged ,in fact it may shrink a little as the hypertrophy grow inwards and obliterate the LV cavity.(We do not know yet , how much of LVH grow out and how much  muscle grow in ! )
  • The blood volume within LV is a very good conductor of electricity.A good volumed LV may augment a QRS voltage.
  • This can be observed in some of the patients with DCM , where high voltage QRS  is recorded mimicking LVH.

But ,what really matters is the fine balance of blood volume and myocardial mass that determine the incidence and magnitude of LVH pattern in ECG.

QRS voltage as a tool to differentiate pathological from physiological  LVH

We know QRS current is generated from within the myocytes .If the myocytes  are  uniformly hypertrophy without altering the  basic mechanical and electrical architecture QRS complex will be amplified in a sm0oth manner and result in  classical high voltage  QRS  of LVH.

If the hypertrophy occurs in a disorganised fashion, where in myocardial fibres slips out of plane  with adjacent muscle bundles, the QRS  voltage may not increase and even be slurred or notched as we see in many cases of LVH with non specific intravascular conduction defects

The classical disarray of myocardial fibers that occur in HCM causes  pathological q waves.

* Other factors that determine LVH include bundle branch conduction delay or blocks which is not discussed here.(Ex: An incomplete LBBB can amplify the qrs without any LVH )

LVH with fibrosis

Fibrosis is not a standard feature of LVH. It occurs in few who are genetically predisposed , and  mediated by heightened sensitivity to circulating growth factors.

  • Fibrosis can have wide impact on the electrical as well as mechanical function of heart.
  • Fibrotic heart has a  potential to  blunt the  high voltage  QRS complex.
  • It  may even cause  pathological q waves .It predispose to ventricular arrhythmia
  • It prevents regression of LVH , even after the loading conditions corrected.

Other conditions that  attenuate LVH features in ECG

  • Diabetic hypertensive show less ECG voltage than isolated HT .
  • CKD patients often do not show ECG features of LVH inspite of LVH

Final message

Diagnosis  of  LVH by ECG is a  simple clinical exercise , but we realise now , the underlying mechanisms are too complex .

A simple question , ie  Why  every one  with LVH  do not increase  their  QRS voltage  ?  . . . exposes  our ignorance on the subject!

But one thing is clear, physiological LVH (Meaning LVH ,  purely due to loading conditions including SHT/Aortic stenosis)  more often result in high voltage , while  in true pathological LVH(infested with fibrosis ) the  increase in voltage is not consistent .

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The most common ECG dilemmas one encounters is to differentiate between the ST segment depression and T wave inversion due to LVH from that of primary ischemia.

Very often  , the entity is misdiagnosed . The implication can be serious , and adding further complexity is exercise stress testing is alos prone for errors in these group of patients as false negative or positive results are very common due to basline  ST/T changes.So it needs a CAG to confirm or rule out CAD in many .

Still the clinical acumen with the help of ECG can help us to a great extent !

A rough and approximate way to identify primary ischemia is given below.

Though these  humble ECG features may not be specific to diagnose CAD . One  need to remember even a normal coronary angiogram is  not synonymous with normal coronary arteries !

Read this blog on limitations of CAG .

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Left ventricular  hypertrophy (LVH) is one of the most common  structural heart disease.Systemic hypertension, aortic valve disease are responsible for the bulk of the cases .Some  of the LVH occur due to cardiomyopathy (HCM/Non HCM variants).Athlete’s heart is a physiological response to exercise and  it  is largely a normal entity.

How many patients with SHT develop LVH ?

It is surprising to note , not every patient with SHT develop LVH .In fact estimates suggest only  about 30-40% of chronic  hypertensive individuals develop SHT .

What are the determinants of LVH in SHT ?

  • Magnitude of systolic pressure
  • Magnitude of diastolic pressure
  • Pulse pressure
  • Duration of SHT
  • Age
  • Gender
  • Body  weight/Obesity
  • Effect of treatment

While any of the above factors may operate in determining LVH

none of the above are important than this

“Genetic susceptibility ”

The myosin isoforms are determined by the genes .The re expression of   fetal isoforms in adults is responsible for LVH in many .This is determined by the genetic homogeneity

LVH  in  renal disease

Secondary hypertension due to renal dysfunction is a major determinant of LVH. This is espcially true if the pateints are dialysis dependent.The mechanism are not clear .

Diabetes and SHT :  LVH  friendly forces

When diabetes alone and SHT alone is less likely to result in LVH the combination of these two entities greatly increase the likely hood of LVH.DM induced microangitis amplifies the after load effect of HT and result in early LVH.Further this LVH is different from pure forms of hypertensive LVH  in that the interstitium goes for hypertrophy and in some cases neovascualrisation. In hypertensive LVH it is predominately myocyte hypertrophy  with little interstitial  proliferation. this has important therapeutic implication as any drug which reduce the blood pressure can regress pure myocytic hypertrophy, while in diabetic LVH  regression is difficult to achieve .

Lipid levels inversely related to LVH ?

There is no consistent relation between lipids and LVH .Occasional reports suggest a negative correlation.

Which LVH is associated with diastolic dysfunction ?

It is a well known fact , LVH has major effect on LV diastolic function.But it is also a fact only some forms of LVH develop this. Now it is clear only if the interstitial hypertrophy occur  diastolic dysfunction is manifested.  Even as the as the hypertrophied  myocyte  continue to  relax  the interstitium do not have molecular mechanisms to relax .Hence, as discussed earlier , diabetic hypertensive patient often  develop diastolic dysfunction .

Final message

LVH is not a simple expression of raised after load.It has major  non hemodynamic determinants which if identified , could have important therapeutic implication.

Coming soon . . .

Can  coronary artery  disease induce LVH in the absence of SHT or DM ?


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The quantum of electrical energy reaching the surface of the chest wall varies widely .It depends upon myocardial mass, proximity to the chest wall  and the thickness of chest wall.

Apart from this ,  the amount of blood within the left ventricle also determine the QRS voltage of ECG.

In dilated LV due to a regurgitant lesion , the LVEDV is increased . Since  blood is a very good conductor of  electricity , it amplifies the transmural  activation front and results  in high voltage QRS complex.This is referred to as Brody’s effect.

Where else , we  can  visualise the Brody effect  ?

During excercise stress testing , when  the heart rate and   the  LV diastolic volume increases .There is  a significant increase in QRS  voltage in leads facing LV, especially V5 and V6.

This is  usually a benign response in healthy individuals. However in patients  with preexisting CAD and LV dysfunction an  increase in R wave amplitude may  be a marker of  exercise induced LV dilatation  which  could  predict an adverse outcome .

Is there  a reversed Brody effect , where Q waves get deepened on exercise ?

This has not been described in literature , but it is seen often in patients with post MI stress testing .Q gets deepened .If the q gets minimised* it could indicate presence of significant viable tissue  , as it gets recruited during the excercise induced positive inotrpism mediated by   catecholamine .Lengthening or deepening of Q indicate less viable tissue.

*Study in progress : Will  be referenced shortly .

Brody effect is a complex phenomenon.

Advanced readers follow the link for illustration on Brody effect


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                                Hypertension is the most common clinical  cardiovascular entity.Left ventricular hypertrophy (LVH) is  an important consequence of  HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.


                              Though LVH is considered  as a close companion of  HT  it is  surprising  only a minority (15-30%)  show evidence of LVH .Some  experienced clinicians (Level C evidence)  quote even lower < 10 %  .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.

What determines the LVH ?

It will be suprising to note , answer to this question  is  still not  clear .

  • Is it the duration of elevated blood pressure ?
  •  Is it the absolute level of blood pressure ?
  • If so , is it  the systolic BP  , diastolic BP or the mean BP ?
  • Or is it related to the etiology of HT ?
  • There has been no significant correlation between the above parameters

When we don’t know  the answer to a question in medicine , the answer will  generally will be inside the genes !

So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain  response .

and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.

An excellent study  on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1

It implicates , gender, age, race etc in the genesis of LVH

Final message

So , the  myocardium does not respond with LVH   in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but  the major factor is  the alteration of genetic switches  within the myocytes How this switches are going to  behave ,  is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression  of LVH , later disputed )

*LVH is more consistently seen  in hypertension due to reno vascular  or parenchymal disorders .It is also an observed fact , a  combination of diabetes and HT is more likely to result in  LVH.

The other major issue  that needs explanation in HT/LVH  is   , how much of LVH is due to  myocyte hypertrophy perse  and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)

This issue will be discussed soon

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This is a 15-year-old post about LVH, written in 2008. Few of my colleagues, now agree with this, still hesitate to oblige in the open, suggesting it is too good to be true! Re-posting it for your own assessment. Surprised, why cardiology community didn’t consider this observation worthy to pursue.

Advantages of Left ventricular hypertrophy (LVH)

Left ventricular hypertrophy is one of the most common clinical cardiac entity.It is recognised either by ECG or echocardiography.LVH has a unique place in cardiology as it can imply a  grossly pathological state or  a marker of healthy heart as in physiological hypertrophy in athletes.

Logic would suggest, in this era of  stem cells and  nano medicine ,  every muscle fibre in ventricle is worth in gold !. So when the nature provides an  extra reserve of myocardium in the form of LVH one should welcome it , if otherwise not harmful.

Is LVH due to systemic hypertension benign ?

Not really, LVH has been shown to be an independent cardiac risk factor. (The famous Framingham study)Further LVH can result in diastolic dysfunction and the risk of cardiac failure increases.

But in spite of these observations, an  astute clinician with considerable experience will appreciate , patients with LVH fare better during an acute coronary syndrome !

This has been a consistent clinical observation . (Shall we call it as class C . ACC /AHA evidence ? )

Is LVH  an asset during ACS ?

  • A hypertrophied heart takes ischemic injury very easy , it doesn’t really hurt much . Another possibility is that in  LVH myocytes are relatively resistant to hypoxia .
  • Patients with LVH rarely show  significant wall motion defect following an STEMI.This is probably because the full thickness transmural necrosis is almost never possible even if extensive MI occurs.
  • This is also reflected in ECG  as these patients   rarely develop q waves in  following STEMI .
  • Persistent ST elevation and failed thrombolysis is very uncommon in pateints with LVH.
  • LVH provides  a relative immunity against development of cardiogenic shock . It requires 40% of LV mass destruction to produce cardiogenic shock.This can rarely happen in LVH. In a  long term analysis we have found none of the patient with LVH developed cardiogenic shock following STEMI.
  • LVH patients  are also protected against development of free wall rupture.

 Concluding message

                   “Lack of published evidence is the weakest evidence to dismiss a true myth”

LVH , either pathological or physiological, has a hitherto unreported beneficial effect.It acts as a myocardial reserve and helps limit the impact of STEMI.



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