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Posts Tagged ‘dr svenkatesan’

Timing of valve replacement in AR vs MR : Why are they different ?

Posted in Uncategorized, tagged , , , , , , , , , , , , , on August 11, 2026|

Timing of AVR and MVR in AR and MR has always elicited huge discussion in cardiology literature. Mind you, if the patient is symptomatic and there is LV dysfunction, it is absolutely easy to make a decision.Here, the question of timing doesn’t arise at all. (Of course, the symptoms and LV dysfunction should be confirmed to arise because of valve disease, not because of any other systemic disease, or LV dysfunction might be due to associated CAD. *I know a women who got her leakinging mitral valve replaced because she developed symptoms of dyspnea due to anemia .

Timing becomes a big issue only in patients with no symptoms at all. Some cardiologists put them on a treadmill. It is controversial, as anyone will develop symptoms. But , somehow, we should make it sure, patients are truly asymptomatic.

For long, we relying on some gospel echo parameters. I don’t how good they are. But , no one really knows,how and when the onset of LV dysfunction would be , and how it will progress. But, we are bound by the guidelines , as on today. There is some critical difference between the echo parameters , based on we intervene.

For mitral valve the threshold is lower. It needs early MVR for same degree of regurgitation as AR. It is proposed by the author for the benefit of fellows to easily remember the cut offs. It may be called as the 40:60 rule for MVR and 50:50 rule for AVR. The former denoting LVESD and later referring to LV EF %. The difference in echocardiographic thresholds arises because the two lesions cause fundamentally different hemodynamic loads on the left atrium and ventricle .(Read the legend in Image)

Final message

With mortality and morbidity for valve replacement steadily falling, it is likely more and more patients will be taken for surgery early. Of course, intervention guys are raring to go with percutaneous TAVR and TMVR, so the thresholds are expected to fall.

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Why we mis-understood DIG-Trial for so long ? How can Digoxin reduce acute decompensation, but still doesn’t prevent death ?

Posted in Uncategorized, tagged , , , , , on May 12, 2026|

Here is a brand new study on Digoxin from AIIMS-India , in 2026 that triggered this post. (Ref 2)

The DIG trial published more than 3 decades ago,(1997) was a landmark study, that applied a disruptive break on the widespread usage of digoxin in heart failure for all the wrong reasons. It is one of the good examples of , how badly the mainstream academia could interpret a study. Though the study showed a consistent reduction in worsening heart failure and hospitalization, yet no overall mortality benefit was accrued in the full trial population. This apparent paradox deserves a more careful interpretation. We need to ask one simple question.

Did the DIG trial reported how many acute deaths (In hospital) occurred among patients who were on digoxin and who weren’t ?

The answer is No. While the paper details how many patients were hospitalized and how many died of  heart failure, it does not specify which of those heart failure deaths happened specifically while the patient was admitted in- hospital. Then, DIG trial also played the same old game of all major RCTs. Death and worsening heart failure was clubbed as a combined end point, for  analysis. So, we don’t know the exact acute deaths, that were prevented by Digoxin. Why no one asked this question for so long ?

Did we mis-understand the DIG-Trial ?

Further, it is plausible Digoxin’s   life-saving role probably  lies in  preventing the decompensated episode itself.

Of course,  patients ( Who were non on digoxin)may still survive because modern therapy , with powerful diuretics, ventilation, inotropes, and intensive care .Still, we  know there is a specific (could be high ) mortality rate in all acute decompensated heart failure cases despite the best treatment. The statistics ignored those lives that were lost due to decompensation , because of non-administration of digoxin.

Modified version of for DIG-Trial conclusion

“Digoxin may save lives by reducing the frequency and severity of decompensated heart-failure episodes, thereby preventing some acute deaths and the need for ICU care. However, DIG trial failed to show an overall mortality benefit in the study population in long term. This is understandable, as heart failure is a progressive disease.”

Final message

It doesn’t make sense to make a blanket statement that Digoxin doesn’t prevent deaths in heart failure. However huge/ popular a study may be, it need to undergo scrutiny  beyond evidence and  statistics. How ? They should be subjected to the vigorous test of bedside trial on individual patient* , common sense and experience.(* Recall N-1 study Ref 4)

Reference

We are gathering more evidence in favor of Digoxin in recent times.

1.DIGIT-HF study

2.Karthikeyan G, Devasenapathy N, Ghosh A, et al. Digoxin in Patients With Symptomatic Rheumatic Heart Disease: A Randomized Clinical Trial. JAMA. Published online May 10, 2026. doi:10.1001/jama.2026.7335

3.Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997 Feb 20;336(8):525-33. doi: 10.1056/NEJM199702203360801. PMID: 9036306.

4.Duan N, Kravitz RL, Schmid CH. Single-patient (n-of-1) trials: a pragmatic clinical decision methodology for patient-centered comparative effectiveness research. J Clin Epidemiol. 2013 Aug;66(8 Suppl):S21-8. doi: 10.1016/j.jclinepi.2013.04.006.

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