Posted in CAD in HFpEF, Heart failure with preserved LV EF, HFpEF, HFrEF vs HFpEF, tagged diastolic dysfunction, dr venkatesan ppt prsentation, presentation on HFpEF and cad on January 7, 2021|
One of the topics rarely discussed in heart failure is CAD as a contributory factor in HFpEF.
This is a copy of the presentation done at the ECHO India Annual scientific meet 2019 at Kolkatta. India.
Will try to find out the recorded version with audio. Here is a GIF run through.
PDF version Download here
Posted in Atrial fibrillation, tagged atrial strain in atrial fibrillation, diastolic dysfunction, dual doppler probe in atrial fibrillation assessment, e velocity variation in atrial fibrillation, echocardiography, HFpEF, how to assess diastolic dysfunction in atrial fibrillation?, single beat doppler echo on October 23, 2019|
Assessment of LV diastolic function primarily depends on the Doppler flow profile across the mitral valve and also to be noted are the 2D features of LA and LV for associated abnormality like LVH, LAE etc.
Why diastolic dysfunction assessment difficult in AF ?
Since most diastolic doppler mitral inflow parameters involve analysis of atrial contraction A wave, atrial fibrillation makes it difficult to assess diastolic dysfunction. Since we have only early diastolic velocity to assess, the changes confined to this E velocity is of paramount importance. This E velocity again is subjected to cycle length dependent alteration in both its acceleration and deceleration time , making things still more complex.
However, the following features help diagnose diastolic dysfunction in AF
*LA dimension is a very good sign of chronic elevation of LAP and diastolic dysfunction in the absence of mitral valve disease. However, AF can dilate the LA making it a less useful parameter. But, it should be noted in AF both RA and LA dilate together.So, a disproportionate LA>RA (or if RA is normal size ) could still be a marker of baseline LV diastolic dysfunction.
Reference
Posted in Diastolic dysfunction, Echocardiography -Normal measurement, Echocardiography-hemodynamics, tagged diastolic dysfunction, diastolic dysfunction in dcm, e:a ratio >2, pseudo normal filling, what is the mechanism of tall e in diastolic dysfunction on May 31, 2017| Leave a Comment »
A 45 year old man came with recent onset breathlessness.His left ventricle was dilated along with left atrial enlargement.The LV EF was 42% (By current definition mid range preserved systolic function( Circ Heart Fail. 2016 Apr;9(4))
But, he was severely symptomatic because of combined systolic and diastolic dysfunction.Diagnosing and grading diastolic dysfunction has been extensively done in last decade.Now , we realise without significant diastolic dysfunction symptoms of pulmonary congestion can never occur in patients with DCM.
We don’t require complex tissue Doppler parameters to diagnose high-grade LV diastolic function.Just have a look at LA dimension, concentrate the E to A ratio. A tall E that humbles the A by more than 2 to 3 times is clear evidence for LA mean Pressure exceed 18 to 20 mmhg or so.
This , in combination with dilated LA is a marker of chronic severe diastolic dysfunction.The fact that A is diminutive in no way takes the Importance of Atrial contribution to LV filing at this critically compromised LV status.
Note E:A ratio is 3:1 .This simply means the early (and mid to a certain extent ) diastolic pressure in LA is high and most of the filling takes place before Atrial contraction .There is one more reason for diminutive A . Atrial contractility fails to prevail over E in late diastole as LV end diastolic pressure is significantly high in these patients with diastolic dysfunction.
A dilated left atrium is an Independent marker of significant LV diastolic dysfunction (In the absence of MR) .When does LA begin to enlarge in diastolic dysfunction ? There is uniform rule.Generally LA size more than 4.5cm indicate grade 3 or 4 LV diastolic dysfunction.
LA size and Pulmonary congestion
It’s a paradox , a roomy LA dampens the LA pressure curve and A reversal into lungs may not happen.
*AF irony on A reversal
Logic might suggest , loss of atrial contraction might attenuate A reversal and less blood flooding into pulmonary veins.No, It doesn’t happen that way.If AF is precipitated for any reason its going to be “switch on” for acute pulmonary edema.
What is the relation between systolic and diastolic dysfunction in DCM ?
We find about 30 % of DCM has documented resting diastolic dysfunction.This is actually a underestimation of true diastolic dysfunction as it can very well manifest only during exertion.
Though generally , there is good correlation of grade of diastolic and systolic dysfunction in terms of severity , some of the patients show severe diastolic dysfunction out of proportion with systolic dysfunction.
Note : In the above patient it’s actually a fairly preserved systolic function but still has advanced diastolic dysfunction.
Grading of diastolic dysfunction .Image courtesy MM Redfield et al: JAMA 289:194, 2003. Note E:A >1.5 is
Final message
Relying on E:A ratio to diagnose diastolic dysfunction may appear amateurish for some of us .The rampant reporting of E>A for grade 1 diastolic dysfunction has made this parameter a “Doppler cliché”. But , the fact of the matter is, it does help us confirm severe (Grade 4) diastolic dysfunction when E stands tall and towering over an almost dwarfed A.
Clinical Implication
Please realise ,In patients with DCM when you find an A that is too diminutive in combination with a menacingly tall E , it may be prudent to raise diuretic dosage. It’s a sure signal for impending pulmonary edema.
Queued queries
Can DT and IVRT normalise with progressive diastolic dysfunction ?
Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -unresolved questions, Cardiology hypertension, tagged circulation, diastolic dysfunction, diastolic dysfunction by ecg, doppler e a velocity, e propogation velocity, e vs e', hba1c and left atrium, hypertension, la size in hypertension lae and lvh, la volume, left atrium, limitations of doppler, mitral annular velocity, tissue doppler on May 29, 2011| Leave a Comment »
We presume ECG fails miserably against echocardiography for assessing hemodynamics , while echocardiogram has little value when it comes to studying electrophysiology . Ironically , we often ignore the fact , ECG can provide important long-term hemodynamic data . The pattern of chamber enlargement give us vital clues to the prevailing hemodynamic stress and loading conditions. While echo can be termed as an anatomical and physiologic modality , ECG apart from its unique capacity to record cardiac electrical finger prints , it provides useful , anatomical , hemodynamic information too !
While Doppler is a fascinating modality to measure hemodynamic data in a moment to moment fashion it can never ever tell us , what has been going around in the preceding months or years. This is were chamber size helps which give us chronic physiological information (Chronic Doppler ?)
A simple E:A reversal in mitral inflow doppler can be a innocuous finding in isolation . If it is associated with even minimal grades of LAE it gains huge importance. That is why left atrial size is funnily referred to as HB A1C of diastolic dysfunction ( A marker of chronicity of diastolic dysfunction)
If LAE is so important to diagnose diastolic dysfunction , why we are so obsessed with doppler filling profiles of mitral valve ,pulmonary veins, mitral annular tissue Doppler and what not ! .Many of these sophisticated doppler methods are extremely operator dependent and are subjected to technical and mathematical errors. Especially , with tissue doppler where we magnify the errors as we filter extremely slow tissue motion .
For many decades we have failed to impress ourselves , about the importance of subtle P wave abnormalities in the ECGs of hypertensive patients.
In fact those innocuous looking slurs and notches in P waves , suggest the left atrial stress and a definite marker of underlying LV diastolic dysfunction .
P wave is the only electrical wave that occur in diastole .Hence there is no surprise ,i gives us enormous information about this phase of cardiac cycle .
If only we look at them carefully, zoom it (Now it is made easy with so many softwares) analyse critically we can find a wealth of information about the atrial behavior in hypertension.
Experience from our hypertension clinic with periodic echocardiograms suggest , the following ECG findings can be good markers of significant diastolic dysfunction .
* Surprisingly , these abnormalities correlated with at least grade 1 diastolic dysfunction even in the absence of for LAE or LVH by echocardiogram.
** In an occasional patient P waves can widen due to inter atrial block or conduction delay. This a rare exception for wide P waves without LAE.
Final message
A well recorded and analysed ECG can predict diastolic dysfunction with fair degree of accuracy .This fact need to be emphasized by every one . Next to ECG , LA size and volume by 2d echo are excellent parameters to assess diastolic function in a long term fashion. Sophisticated but error prone , momentary doppler parameters are getting too much attention at the cost of simple , shrewd ECG and 2D echo !
Posted in Cardiology - Clinical, echocardiography, tagged diastolic dysfunction, heart rate and diastolic function on May 12, 2011| Leave a Comment »
Heart is mainly perceived as a pumping organ but it need to be realised it also has a reservoir function (Temporarily though , for about .5 seconds every beat ) . Contrary to the popular belief heart is not continuously and tirelessly working .For every contractile beat it takes a brief period of rest .This is called diastole. But , even here it is not a complete rest , as it has to receive the blood from the atria and get filled and be ready for the next beat.
Many think diastole is an active energy-consuming process . . . but it can be debated still , as passive elastic properties may contribute substantially to cardiac relaxation blunting the energy requirement
God is so scientific (Greatest scientist !) he made it sure the resting phase(Diastole) is slightly more than the contractile phase (Systole ).
This makes the organ relax a bit more than it stresses in its entire life time . At any given heart rate diastole will be slightly more than systole , peculiarly for the same reason during tachycardia diastole suffers more than systole.
What happens in diastolic dysfunction ?
Pathologically the ventricles become stiff and rigid and the filling of the ventricle is impaired . The commonest cause for diastolic dysfunction are hypertension, diabetes, and ischemic CAD some forms of myopathies .In systole ,the calcium is pumped into actin myosin complex while in diastole the same calcium molecules (Or different !) are ejected back into the cytosol and sarcoplasmic reticulum. The later process is impaired in many situations of diastolic dysfunction.
It should also be realised not every one with diastolic dysfunction has a calcium release /unloading defect .Many have structural diastolic dysfunction like interstitial fibrosis .Here the mechanism goes beyond calcium kinetics.These are the patients who get maximum benefit out of heart rate reduction.
It is all Time . . . Time as a lusiotropic drug !
If the ventricle finds difficult to relax (or slow /sluggish to relax ) we have two options to tackle this .
Prolonging diastole makes it certain , the LV relaxation process is completed as the excess time compensates for the slowness of calcium reuptake into the sarcoplasmic reticulum . In fact , we have observed at slow heart rates (<60) it is very difficult to document diastolic dysfunction by doppler .
In many of dilated cardiomyopathies the beneficial effect of beta blockers , could be linked to simple reduction in heart rate and prolongation of diastole .(Note In DCM about 30-40 % have restrictive filling )
Final message
As we have no specific drugs to augment the process of cardiac diastole, currently heart rate reduction could be the simple and best method* to improve diastolic function .In many cases diastolic dysfunction simply vanishes at low heart rate.Bradycardia and diastolic dysfunction will remain as foes forever ! Please give the benefit of this simple concept to all your patients with diastolic dysfunction .Your patients can breath lot more easier !
*Apart from controlling the underlying cause like DM, SHT and CAD , anti fibrotic drugs, interstitial relaxants ,selective cardiac collagen uncouplers are the future areas of research .
Posted in Uncategorized, tagged diastolic dysfunction on January 8, 2010| Leave a Comment »
Diastolic dysfunction as concept has come a long way after initial hiccups . Now, it is a well established left ventricular pathology , and has a sound physiological and molecular basis. Even though there are variety of methods available to quantify LV diastolic function, echocardiogram is the simple method to identify and grade diastolic dysfunction.
There are 4 grades of diastolic dysfunction
1.Impaired relaxation (without elevated filling pressure)
Some describe another grade 1 a with elevated filling pressure
2.Pseudonormal mitral inflow
3.Restrictive -Reversible
4.Restrictive -irreversible
What is pseudo normal pattern ?
The grade 1 is the most common type diagnosed . It is diagnosed when the A velocity is more than E velocity . This simply implies , ventricular filling needs greater assistance from atrial contraction than in resting conditions. It is so common , especially in elderly , many thought it should not be considered a pathology . In youngsters it is definitely pathological especially if it is persistent.
The issue that really concerns us is this : When the diastolic dysfunction progress from grade 1 to grade 2 , the mitral the inflow doppler pattern , instead of showing any new changes simply nullifies the changes that occurred in grade 1 and records a normal E : A velocity .
So , a person with grade 2 diastolic dysfunction will have a near normal pattern .Of course deceleration time, and IVRT is shorter than in grade 1 but it is not very useful in differentiating it from normal .
Pseduonormal is actually equivalent to moderate diastolic dysfunction , but the abnormality is masked as near normal filling is restored with atrial assistance . So, technically it a assisted LV filling . A superficial look at the doppler pattern may exactly mimic normal . But there will be a 2 D echo abnormality that makes the patient pathological . Our eyes need to look beyond doppler ( in coherence with 2 D ) to differentiating normal or pseudo normal.
It is learnt , 2D abnormality of LV or LA occurs in nearly 90 % of grade 2 diastolic dysfunction .(There can be a pure functional grade 2 diastolic dysfunction without structural changes in LA/LVH in minority -This is poorly understood form of silent sub clinical CAD manifesting only as diastolic dysfunction )
Traditionally there are few methods taught in echocardiaographic schools all over the world to differentiate normal from pseudonormal
1.Pulmonary vein doppler
2.Response to valsalva maneuver
3.Tissue doppler etc
One simple echo feature that is often forgotten , that can be really useful in differentiation of normal from pseudo normal is left atrial dimension
While patient with pseudonormal who have progressed into stage 2 will show a definite left atrial abnormality .
When does a left atrium begins to enlarge in diastolic dysfunction?
It is yet unclear , the onset of LA enlargement in diastolic dysfunction .This is potentially a research topic for the fellows !
It is not uncommon to find LA enlarge like a balloon even in stage 2 of diastolic dysfunction. So , in patients who are suspected to have pseduonormal doppler profile , look for the presence of LAE , (however mild it may be !) , there is no business for LA to enlarge in normal persons.
Ofcourse , if you are a echo expert one can measure A reversal in PV doppler, tissue doppler echo etc .But remember a simple 2D echo feature like a LA dimension / LVH may score over the sophisticated (Also read complex . . .) parameters in the grading of diastolic dysfunction
Final message
While we immerse ourself in sophisticated doppler methods to differentiate normal from psedunormal pattern, the fact that , normal persons will have normal hearts is often forgotten , and presence of left atrial enlargement (Which is all too common in pseudonormal !) straightaway settles the issue . Detailed diastolic function studies are warrented only if the LA size is normal .
*Correction: in table A reversal in normal is less than 35cm/sec
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged angina relief, cabg, canadian cardiovascualr, cardiomyopathy, courage study, diastolic dysfunction, dilated cardiomyopathy, dyspnea, functional class, ischemic dcm, lv dysfunction, lv fucntion, nyha class 3, nyha class 4, oat study, pci, ptca, stable angina, toat study, unstable angina on December 30, 2009| Leave a Comment »
It is a well known fact , CABG and PCI provides immediate relief for patients with angina , which is refractory to medical therapy. Of course , this happens only if a critical occlusion of at least one epicardial coronary artery is opened . It need to be realised , angina due to microvascular disease can not be cured by maintaining epicardial patency .
While angina relief is prompt , dyspnea is not ! . If we believe, opening up a coronary artery in a patient with LV dysfunction will restore the LV function , it is grossly mistaken !
Why is it so ?
Angina relief requires simple restoration of oxygen supply and correction of local ischemia . This happens without any issue as the blood seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals . While , for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this, there need to be an intact cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is zig zag orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of extracellular matrix namely the collagen frame work is also vital . Note , angina relief is not concerned with any of the above .
And now , we also realise dyspnea in failing ventricles is vitally dependent on diastolic function , which is also very much impaired in ischemic DCM .There is little proof for PCI/CABG to correct the molecular mysteries in diastolic dysfunction !
Dysfunctional LV means what ? (read the link )
It is a collection of variety of myocardial tissues . Viz : Fully necrosed , partially necrosed , ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments may also be perfused normally by spontaneous reopening of an IRA.
One can imagine the complexity of events in these segments once we do the PCI /CABG . The response is highly variable and unpredictable. The major concept we , the physicians believe or ( to be precise made to believe !) is the sanctity devoted to the viable myocardium .For many us , it is considered a holy exercise to identify viable myocardium in patients following MI and then revascularise them if found to have significant viable myocardium (Atleast 20% of infarcted area )
A full 2 decades were lost or (shall we say wasted on this futile exercise !) as we have since realised most of the cardiologists do not follow this rule .
Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where there is no contradiction for not doing a PCI /CABG with reference to LV dysfunction.
Now every patient with post MI LV dysfunction is considered to have some amount of viable myocardium that is fit enough for revascularization
Are we justified in doing this ?
Many clinical trials have revealed , the recovery of LV function in these segments has not been consistent at all .
The most surprising discovery is a viable myocardium need not be ischemic .It might get adequate blood supply either from invisible collaterals or trickle of antegrade flow . Hence an adequately perfused myocardial segment can still be non contractile . This shatters the myth that revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.
The other major finding is , even ischemic viable myocardium ( documented by metabolic activities PET etc) need not regain it’s original contractility after the ischemia is fully corrected .
*reference for both the above statements are available from variety of sources including real life experiences .(Type C evidence )
Final message
Counter point
If the above statements are really true , How does PCI/CABG help relieving dyspnea and functional class what is your answer for thousands of patients with CAD and ischemic DCM who have greatly benefited from CABG ?
The answer could be simple , The revascularization piggybacks over the medical management (which , these patients pursue vigorously) like ACEI, statins, salt restriction, betablockers , optimal diuretics and tend to hijack the credits from the poor drugs !
Read a related blog
Posted in cardiac surgery, Cardiology - Clinical, Uncategorized, tagged diastolic dysfunction on December 14, 2009| Leave a Comment »
Diastolic dysfunction is a common clinical cardiac problem which has no specific therapy.It can occur either in isolation or in combination with systolic dysfunction.The later may be more common.
Isolated diastolic dysfunction
In association with systolic dysfunction
General principles of management
Even though there is no specific drugs to tackle diastolic dysfunction the following measures may have significant impact.
What are the treatments in the horizon ?
Antifibrotic drugs ,Antiproliferative drugs
Collagen breakers ,
Posted in Cardiology - Clinical, tagged diastolic dysfunction on December 13, 2009| Leave a Comment »
Cardiac failure is the number one killer of mankind. So far we have believed the major function of the heart is to contract . Relaxation was thought to be a passive process .Now we know, for myocardium to relax properly the calcium which was pumped in to acto myosin complex, has to be taken back into the sarcoplasmic reticulum during diastole .This is mediated by SERCA 2 , Phospholamban the active calcium uptaking kinase.Clinical diastolic dysfunction as a concept has been disputed for too long that has delayed our knowledge gap .
Myocardial relaxation is much more complex than we think !
We have given too much importance to calcium kinetics and diastolic dysfunction .While impaired relaxation and diastolic dysfunction are used interchangably by both researchers and clinicians resting myocardial stiffness is an important parameter that has been overlooked .
The myocardium is made up of not only myocytes , in fact it has more non myocytic components than myocytes themself. Myocytes constitute only 33 % of cardiac mass . The interstitial cells, fibroblasts the extracellular matrix (This is in fact a vague terminology in use !) It is nothing but sheets of tissues made up of collagen criss crossing the myocardial planes. The type 1 collagen is as powerful as stainless steel . Type 3 collagen is little more flexible. The issue here is , how to flex these rigid collagens without compromising it’s contractile role. One can realise , how ignorant it would be be , if we thought altering calcium kinetics within the myocardium is the ultimate answer to tackle diastolic dysfunction .
So our aim is to reduce the resting stiffness of cardiac muscle in pathological states like SHT/LVH/CAD etc . . .
How to do augment myocardial relaxation ?
Altering calcium kinetics within the cell is one option. But as we have discussed much of the stiffness comes from cells which do not have calcium at all (Fibroblasts) or from life less molecules like collagen etc
The proliferation of interstitial cells and fibroblasts make the myocardium stiff.So drugs which inhibit these reactive events may help.ACE inhibitors, ACE receptor blockers, anti aldosterone (Spirinolactone) are vigorously tried by respective patent holders to bring in another indication for these drugs namely positive lusiotropic agents .But the crux of the issue and the fact of the matter is we have not made any break through in finding a positive lusiotropic drug. (Milrinone was shownto have some promise !)
We need to try new concepts instead of trying the existing band of drugs .
The following are some of the options
Collagen – The interstitial collagen may be modified.The so called MMP matrix metalloprotinase which lyse collagen cross linkages can make the myocardium agile and fit.Tissue inhibitors of MMP has a role.
One should remember we can not afford to play the dangerous game of manipulating myocardial structural protein frames . If the myocardium becomes too flabby it will forget it’s primary job that is contraction
Final message
There are thousands of articles in cardiology literature that cry fowl over diastole and few hundred of them devoted to quantify diastolic dysfunction by various imaging technique .
It is unfortunate there is no single drug or intervention that has a meaningful impact on this entity. We look forward for cardiac scientists to divert the resources to find an answer to this problem instead of simply documenting the presence of it .
Common sense has taught us the most effective method that can reverse established diastolic dysfunction is by simple , regular exercise .Exercise not only make the skeletal muscles agile & fit it does the same to cardiac muscle too !
Posted in Cardiology - Clinical, Cardiology -unresolved questions, Cardiology-Land mark studies, tagged chf, diastolic dysfunction, diastolic heart failure, diastology, ejection fraction, heart failure, heart failure with preserved EF, myocardium, nejm, restrictive lv function on August 11, 2008| 1 Comment »
The perception that diastolic heart failure ( Now renamed as heart failure with preserved EF ) is less dangerous than systolic HF has been exposed by this land mark study by Owan TE, in 2006 (nejm) But unfortunately this information is not yet fully disseminated among the physician community. Hence this post, with due acknowledgment to NEJM & Owan et all.
Experts from the article
“The nosology of heart failure has been the
subject of much current debate, and some extreme
positions have been taken. The observation
that 22 to 29 percent of patients with diastolic
heart failure die within one year of hospital
discharge, and 65 percent die within five years,
is a reminder that we are facing a lethal condition,
regardless of its name. Owan et al. also
show that, in recent years, there has been little
improvement in survival rate among patients with
diastolic heart failure, in contrast to the improvement
in survival rate over time among patients
with systolic heart failure”Have a look at the survival curve below, almost similar , surprise surprise ! DHF survival is not only worse ( in many ), than systolic CHF and further they respond poorly to treatment, compared to conventional systolic CHF .
Click below for the link to full text article
Short abstract :
Trends in prevalence and outcome of heart failure with preserved ejection fraction.
Cardiorenal Research Laboratory, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.
BACKGROUND: The prevalence of heart failure with preserved ejection fraction may be changing as a result of changes in population demographics and in the prevalence and treatment of risk factors for heart failure. Changes in the prevalence of heart failure with preserved ejection fraction may contribute to changes in the natural history of heart failure. We performed a study to define secular trends in the prevalence of heart failure with preserved ejection fraction among patients at a single institution over a 15-year period. METHODS: We studied all consecutive patients hospitalized with decompensated heart failure at Mayo Clinic Hospitals in Olmsted County, Minnesota, from 1987 through 2001. We classified patients as having either preserved or reduced ejection fraction. The patients were also classified as community patients (Olmsted County residents) or referral patients. Secular trends in the type of heart failure, associated cardiovascular disease, and survival were defined. RESULTS: A total of 6076 patients with heart failure were discharged over the 15-year period; data on ejection fraction were available for 4596 of these patients (76 percent). Of these, 53 percent had a reduced ejection fraction and 47 percent had a preserved ejection fraction. The proportion of patients with the diagnosis of heart failure with preserved ejection fraction increased over time and was significantly higher among community patients than among referral patients (55 percent vs. 45 percent). The prevalence rates of hypertension, atrial fibrillation, and diabetes among patients with heart failure increased significantly over time. Survival was slightly better among patients with preserved ejection fraction (adjusted hazard ratio for death, 0.96; P=0.01). Survival improved over time for those with reduced ejection fraction but not for those with preserved ejection fraction. CONCLUSIONS: The prevalence of heart failure with preserved ejection fraction increased over a 15-year period, while the rate of death from this disorder remained unchanged. These trends underscore the importance of this growing public health problem. Copyright 2006 Massachusetts Medical Society.
Other interesting article
Heart failure with preserved ejection fraction: dangerous, elusive, and difficult.
Eur Heart J. 2008 Feb;29(3):339-47. Nielsen OW, Køber L, Torp-Pedersen C.
BMJ editorail 2009
http://www.bmj.com/cgi/content/full/338/jan27_1/b52?ijkey=c7a29d35dc9d9dddf7d0e75c5b8d05014315c564
