Archive for November, 2018

We learn from basic physiology  lessons that human body is made up of 60 % water. What about heart ? There is no reason for the heart should behave differently from rest of the body . If my  assumptions are correct when the normal heart weighs 300g  , 180g of which should be  be water. The same thing could be applicable for LV mass( * Reference requested)

Is there myocardial congestion in cardiac failure ?

Genesis of edema in any tissue depends on local hydrostatic pressures, tissue resistive forces, osmotic balance, and cell membrane permeability. In the myocardium individual contribution of above factors are not known. Apart from total myocardial water content  , myocardial water logging depends upon the trans myocardial venous gradient and the coronary sinus exit pressure in right atrium.Technically ,any severe right heart failure should lead to myocardial congestion at least to some degree.Unlike the lungs , the myocardial edema fluid doesn’t produce crackle , (May cause S -3 gallop instead) . However ,we have modern technology to image water inside the myocardium. Yes, it is called proton / hydrogen imaging or simply called MRI .

This is especially evident In chronic kidney disease , where in the fractional water content within the myocardium is expected to increase further as the whole body is water logged.


myocardial edema by mri in ckd 2

We have seen time and again patients with CKD  improve in LV function immediately  after dialysis . It happens like a magic . The mechanism  is simple .The over-hydrated cardiac Interstitium  threatening to drown the myocytes  is promptly dehydrated by dialysis. This was my wild guess  until I came across this paper which proved the exact points.

myocardial edema in ckd chronic renal failure recovery of lv function after dialysis


Other situations  where myocardial edema may play a significant clinical Impact  (*Includes increased permeability of myocardial capillaries)

  1. Myocarditis
  2. Transplant rejection
  3. Stress cardiomyopathy (Takotsubo)
  4. Congestive heart failure
  5. Acute ischemic injury
  6. No Reflow situation after PCI

Final message

Myocardial interstitial edema in cardiac failure is a grossly under diagnosed  entity.  A water-logged myocardium is classical at least in CKD. We know it can severely compromise the LV function especially, the diastolic function that explains the all too common flash pulmonary edema in CKD.

The number of studies in this  topic (Myocardial Hydrology !)  is minuscule compared to other areas of research in cardiology literature.There is a need to involve both  Nephrologist and cardiologists to explore this curious concept of  dialysable  left ventricular mass in CKD/Cardio renal syndromes !

medical quotes new idea

One more area of research 

It is reasonable to believe,  cardiomegaly in cardiac failure  is primarily related to the increased end diastolic volumes .Still , we are not clear whether there is net increase in cardiac mass as the surface area of the heart increases with dilatation. (Even in DCM ? ) Whenever myocardial mass increases relative increase water is likely. Does the beneficial effect of diuretics in cardiac failure , and the restoration of  LV dimension is due to myocardial interstitial diuresis as well ?


myocardail edema water content congestion mri n myocardial diuresis interstitial

2.Andrés-Villarreal, M., Barba, I., Poncelas, M., Inserte, J., Rodriguez-Palomares, J., Pineda, V., & Garcia-Dorado, D. (2016). Measuring Water Distribution in the Heart: Preventing Edema Reduces Ischemia-Reperfusion Injury. Journal of the American Heart Association5(12), e003843. doi:10.1161/JAHA.116.003843

3.Cardiovascular magnetic resonance of myocardial edema using a short inversion time inversion recovery (STIR) black-blood technique: Diagnostic accuracy of visual and semi-quantitative assessment Darach O h-Ici, John P Ridgway, Titus Kuehne , Journal of Cardiovascular Magnetic Resonance 2012, 14:22  


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Evening cardiac clinic is generally a relaxing place until an occasional patient  with vague chest discomfort present with this sort of an ECG .

He was a 68 y old hypertensive and was on Tablet Amlodipine .After a cursory look at his ECG , eyes wandered to look for some specifics. Suddenly ,my  ECG reading skill was stretched . Is it really LVH ? or Ischemia ? I asked for any old ECG which he couldn’t provide. I had to blink  more than a moment , before asking him to describe his chest pain in detail one more time . I got almost convinced it was not ACS  since he was having only localized pain over left side of chest. Still , I didn’t have the courage to send him home. An Echo was done.

Curious to know what the Echo showed ?


Yes , you also probably guessed right . It is LVH and there is no wall motion defect either.

How to differentiate between Ischemia and LVH ?

This is a common question asked in the board exams.There are number of ECG clues to differentiate the two .Mostly it will help  fellows  to pass exams. Academics rarely comes to your rescue when patients land with  chest pain  especially at odd hours.

Find the answer in this link



Now comes the real twister , Does presence of LVH  exclude Ischemia in any way ?

Why can’t be ACS in a patient with LVH ?

When I posed these questions , some one suggested global longitudinal strain  with speckle  tracking to rule out ischemic wall motion defect, my resident suggested  high sensitivity Troponin and Ischemia modified albumin.

Whatever is the technological assistance , one thing  is certain,  we need to finally fall back  on patient’s symptoms . Unstable angina is neither an ECG diagnosis nor biochemical  or Echo diagnosis . (Its all about patient description about his angina , that clinches the  diagnosis !)

It remains a fact normal spot Troponin can never rule out  ACS on time ,( Even patients with unstable angina who  harbor  tight  LAD lesion can be both ECG /Enzyme negative )

When we are not sure ,the traditional coronary care dictum  shall operate .It demands admit, observe, with serial ECGs and enzymes. This protocol cant’t be followed strictly for a variety of reasons . We may have to rely entirely on our clinical Intuition accrued over the years.

A modern-day cardiologist might have a different dictum .The simplest solution in such situations is a diagnostic radial snap shot coronary angiogram .It is an easy way out  . . . , and avoids the trouble of spending wasteful minutes of personal conversation with the patient .The ethics of outsourcing history taking , patient record review or even clinical examination has pushed the definition of professional competence in coronary care into murky grey zone.

One more reason we should hesitate to rush these patient to cath lab is the detection of  incidental insignificant CAD (Which will loom larger than life when they are wheeled in from  ER)  that will  lead on to  further inappropriate chain of events.

How relevant is clinical acumen in modern era ?

Clinical acumen in medicine can never be taught in class rooms or read in text books. It is the innate ability to  combine  knowledge, experience ,skill  and  lastly (and most importantly) courage to ignore conflicting and pervasive data from new generation Investigations. Instead of helping us ,they often directly affect our increasingly vulnerable native medical cognition.

Even if some one is blessed with a good clinical acumen it seems to have little value many times as power of Investigations and fear of missing a event will prevail over it ! I have been victim of this phenomenon many times and not able to follow what my mind preach me !

What happened to this patient ?

I had to admit him against my  wish (Of course I was safe!)  He too got admitted reluctantly and was observed till morning , spent Rs 5000 for pack of investigations and stay , was discharged without any issues with a diagnosis of simple Hypertension and LVH.

The non academic bug  didn’t stop there  . . . again  contrary to my conscience  I had to suggest  optional coronary angiogram to rule out true CAD as a precautionary statutory advisory !



How do you know this is really not CAD  ? I won’t believe unless and until I see the CAG and its normal.

Ok, Let me post his angiogram if he decides to  undergo it.

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