LV dysfunction , perhaps is the most common medical term used by physicians world over.But surprisingly , It is not easy to infer what they mean by it ! The term literally means left ventricle is not functioning all right .
LV dysfunction can be classified by many ways.
- Symptomatic vs Asymptomatic
- Global vs Regional
- Reversible vs Permanent
- Systolic vs Diastolic
- Ischemic vs Nonischemic
- Primary vs Secondary ( Muscle vs valve etc)
If you analyse the above classification LV dysfunction can mean different things to different people , at different times.Though systolic dysfunction , as reflected by low EF % ( Less than 50% ) is the major cause of LV dysfunction the issue is not simple.
Is coronary artery disease ( CAD ) a must for LV to become dysfunctional ?
No , not at all .CAD is the leading cause of LV dysfunction .Primary muscle disorders -cardiomyopathy is an equally common entity. Valve disorders especially aortic valve stenosis is another common cause for LV dysfunction. Further , systemic hypertension, diabetes mellites, renal failure, can result in serious impairment of LV function .Some drugs ( Adriamycin ) can either precipitate or aggravate LV dysfunction.
If physicians themselves are confronted with such complexity , how are , our other medical colleagues (Forget about the patients ! ) will understand the concept of LV dysfunction.
But , the crux of the matter is every doctor believes LV dysfunction is synonymous with low ejection fraction. A surgeon or an anesthetist is quiet happy to operate if the ejection fraction is above 60% .
Can a patient have significant LV dysfunction with normal Ejection fraction ? (EF )
Yes , this can occur in advanced degrees of diastolic dysfunction, where cardiac contractility is normal but
fails to relax adequately .
Is diastolic dysfunction less dangerous than systolic dysfunction?
May be , that is the dominant opinion , but there are sufficient evidence emerging that opinion is wrong.The main reason for diastolic dysfunction to send a ” not so sinister signal ” is over diagnosis of grade 1 diastolic dysfunction in the general population . The echocardiologists considered it fashionable for a quiet a longtime (Many have changed since then !) to report all patients with reversed E :A ratio in the mitral inflow doppler profile as diastolic dysfunction. This has resulted in thousands of asymptomatic , healthy people getting labelled as grade 1 diastolic dysfunction undermining the importance of this entity.
The fact of the matter is true diastolic dysfunction is indeed dangerous , if not more dangerous than systolic dysfunction for the simple reason , there is no specific treatment for this condition
To improve the specificity to diagnose genuine LV diastolic dysfunction it is suggested to remove grade 1 diastolic dysfunction from the literature .
Other causes of LV dysfunction with normal EF
- Some times , there can be wall motion defects and mitral regurgitation but still the EF can be normal .
- Mitral valve dysfunction can be a part of LV dysfunction .The EF is either not affected as ischemic damage might be confined to papillary muscle.
- Vigorous compensation from non ischemic areas can normalise an EF
What is the difference between LV dysfunction and LV failure ?
Many times both these terms are perceived to convey the same meaning .But it can never be used synonymously .Cardiac failure is a clinical entity while LV dysfunction is a derived technical parameter by and large an echocardiographic enity. Cardiac failure is defined classically as a clinical syndrome .(elevated jvp, edema * S 3 rales etc) Neuroueohormonal activation can occur with both.
A patient with LV dysfunction when destabilsed develops LV failure and after stabilisation of LV failure he is brought back to the baseline LV dysfunction
*What is the link between LV dysfunction and RV dysfunction ?
RV can not be silent companion when the LV fails . There always have been link between the two.
LV dysfucntion begets RV dysfunction and LV failure can trigger a total heart failure
Apart from the classical concept of ventricular interdependence , where inter ventricular septum plays a pivotal role , now there is strong evidence to prove both LV and RV myocardial muscle bundles are interwoven . In fact failing LV drags the muscle bundles over RV also (Friendly pull , let us die together !) and this is classically seen in idiopathic dilated cardiomyopathy where all four chambers of the heart dilate. There is also biochemical evidence the RV myocytes deplete thier norepinephrine stores in LV failure.
Is there an entity called transient or temporary LV dysfunction ?
The classical chronic reversible LV dysfunction also called hibernating myocardium is a different topic shall be discussed later.
Can acute ischemia cause LV dysfunction ?
Yes .This can occur during ischemic stunning of myocardium during NSTEMI .This can result in acute pulmonary edema* at times.This can be termed as ischemic LV dysfunction as there is no myocardial necrosis .
* The pulmoanry edema mentioned here is the flash pulmonary edema carries very dis prognosis.
What is the cause of LV dysfunction in critical aortic stenosis ?
Is it fibrotic ?
Is it necrotic ?
Is it ischemic ? (Associated CAD )
Or is it simply a mechanical inability* to contract as the outflow is closed ?
There is no specific answer . All the above factors may contribute .*But the fact that most patients recover full normal LV function following aortic valve replacement would make the last explanation more likely.
What does the term LV dysfunction mean to a cardiac surgeon when he plans for a CABG ?
LV dysfunction becomes an important determinant of overall outcome in patients who are going to receive a CABG .The surgeon will have contingent strategies during peroperative and post operative phase while operating in hearts with severe LV dysfunction.
How much of LV function is going to recover after CABG ?
This can not be predicted accurately but CABG may not resucitate all dying myocytes and bring life in them .The buttressing effect of blood within the dysfunctional segement can improve contractility and reduce the wall motion defect(This is an indirect mechanism of improving EF )
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Dr.S.Venkatesan MD 