Every day thousands of hearts end their life due to terminal heart failure . Much more lives are confined to their bed rooms.In refractory cardiac failure and severe LV dysfunction the only long-term option is cardiac transplantation.
Medical therapy has reached its saturation point. Neuro- humoral modulation shows some promise. The other modalities like cardiac resynchronisation ,LV assist devices , ventricular reduction surgeries , restriction devices , mitral valve splinting are still experimental .
Simply watch this Image : Your heart will get Energy
Modern day cardiology is trying to add life to these dying hearts .
There are two aims
- To prolong survival
- Improve functional capacity (Make them at least take care of daily activities and live a fairly independent live)
This is the purpose of the mushrooming heart failure clinics all over the world . These clinics , though started with good intention , ultimately become feeding centres for so many experimental bridge modalities , sometimes with an infinite wait for a potential donor or at the mercy of their insurance companies . (Many time it turns out to be a bridge to heaven as the patient fails to cross it !) .
Even though there is strict criteria for terminal heart failure , in practical terms it has many issues .Temporary functional deterioration is misinterpreted often .
Premature dependence on LV assist devices and indulgence in inappropriate mitral valve reconstructive procedures are the currently most important pseudo cardiac interventions .( Myosplint/AV groove tying etc) Some where along the academic corridors , we failed to realise many patients can bridge themselves to a transplant (or even self de-list from transplant programme ) provided we are willing to wait and take few risks .
It is observed exercise training programme is awfully inadequate in most centres who deal with late stages of cardiac failure.
The hidden link between skeletal muscle and cardiac muscle
Skeletal muscle function is impaired in cardiac failure . This impairment is attributable to both dis-use and low cardiac output. Proper training of these muscles can not only improve the functional capacity but also sets in a positive hemodynamic cycle that ultimately improves cardiac function as well.
In our country we have data of thousands of patients with severe LV dysfunction living with the much ridiculed digoxin , diuretics , ACEI and minimal exercise living a comfortable life for over 10 years . It is often said in cardiology class rooms , do not whip a tired horse as the failed heart needs rest .This statement has truth in it even in this space age cardiology !
Whipping a failing heart with electrodes in the name of CRT could be as bad as whipping with inotropic agents . This is not a personal joke ! This fact has been repeatedly proved by various inotropic studies in terminal heart failure(Dobutamine to be specific ) Even CRT is a suspect .These patients walk for 30 meters further with no convincing survival benefits .(Of course it requires a ICD -Combo to prevent sudden deaths ) Zero impact in non sudden deaths ?
Can we propose a new therapeutic concept to our patients ?
Do you want to live with a low functional capacity (Restricted life still happy ) for 5 years or live apparently unrestricted life and die prematurely ?
In simple terms, for all those patients with severe grades of heart failure the best advice could be . . .to avoid the levels of exertion that cause dyspnea / Modern gadgets may help relieve exertion for a short while , but it can cut short your longevity * (* This is not a threatening message. This applies to near terminal stages of cardiac failure .All other minor grades of CHF are encouraged to exert up to 70 % of their limits.)
Peripheral mechanism in cardiac failure.
We know cardiac failure is not a simple mechanical failure of heart , it activates a complex neuro endocrine system which makes it a systemic disorder .Many of the current research is aimed at favorably modify this. It is now certain Skeletal muscle function is a major determinant of cardiac failure outcome and hence a therapeutic target .
If you have good muscle mass , good diaphragm and intercostal muscles one can compensate the compromise inflicted by the heart to a large extent. We know, the entire vascular tree has a mechanical function to do . The stiffness and compliance of aorta , other major vessels, the muscles through which these vessels traverse determine the ultimate efficiency of circulation.We know the pulse wave , as it travels to the periphery , gets amplified. This amplification is not without any significance. It aids in muscle blood flow . This agumnetation is missing in poorly trained cardiac failure patients. Further muscle respiration is synonymous with functional capacity . Numerous defects (Both structural and functional ) in skeletal muscle mitochondria are reported.
This is why meticulous exercise training becomes an important intervention in cardiac failure . There are very good studies that document muscle respiration defects getting reverted with proper exercise training and muscle care . Among all muscles the calf and thigh muscles show great promise. We have observed cardiac failure patients with good calf muscles , outperform others with identical ejection fraction.(Will be published shortly )
Strangely there is no comparative studies between calf muscle efficiency and other available modalities in cardiac failure .
The concept of Venous pump vs Arterial pump
Skeletal muscle mass acts not only as venous pump it also has a modulating effect on the arterial pulse transmission .A good venous pump will activate vascular tone . In congestive heart failure a the RV filling pressure is raised, blood tends to move sluggishly in right heart chambers . A proper venous tone can alleviate this . Well trained calf muscle can exactly do this by a controlled elevation of IVC pressure at times of exertion .
Dyspnea of muscular origin (Peripheral dyspnea)
The symptomatology of cardiac failure has an intimate realtionship with skeletal muscle integrity !
Lactate in blood and hypoxia in exercising muscles can trigger non hemodynamic dyspnea . Further , there is strong reason to believe the sensation of dyspnea is perceived at the chest muscle level (By muscle spindle length/tension mismatch ) .It is not known whether lower limb muscles can generate a feeling of dyspnea !
But , one thing is certain by altering the tone of the muscle spindle and the optimising the stretch signals the peripheral component of cardiac dyspnea can be significantly neutralised . This is what happens in well-trained cardiac failure patients .
How to train the skeletal muscles ? ( In to heart friendly muscle )
- Passive stretch
- Simple 6 minute walking three times a day will help .
- Muscle massage and toning
- Drugs like Trimetazidine may improve muscle metabolism by better ATP utilisation
- Diligent use of diuretics (Excess diuretic can make your muscle exhausted )
- Chest exercise for improving intercostal muscle function
Final message
Skeletal muscle training in cardiac failure could be as important as the digoxins , diurteics and ACEI .When a 300 grams of heart muscle is struggling , God is willing to help it with huge muscle mass that lies elsewhere , we should read the silent signals of nature . Many cardiac failure patients realise this and live a happy live without artificial assistance .This applies in all grades of cardiac failure .
For all those physicians out there in modern hospitals who treat cardiac failure , spend at least few minutes for prescribing a good exercise program with a specific mention about calf muscle function . After all , it may turn out be the most efficient RV/LV assist device !
References
http://content.onlinejacc.org/cgi/content/abstract/30/7/1758
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