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Posts Tagged ‘secondary mr’

Hypertension is a prevalent condition in the general population, as is mitral regurgitation (MR). For most of us, HT traditionally conveys a “singular meaning” that is, high pressure within blood vessels. We often forget that the origin of blood pressure begins right inside the heart, i.e, the left ventricle, which is guarded by two valves – the aortic and mitral. (Though we are aware, LVH is the classical response to HT),

Obviously, there will be signiifcant consequences to the structural integrity of these valves when LV pressure is raised beyond the tolerable limit of endocardial layers that line these valves. Mind you, the bottom of the mitral valve is whipped from beneath 100 tousand times times a day & 2.5 billion times in life time at an average pressure of 140 mmHg, and during exertion, it can reach up to 200 mmHg .Apart from hemodynamic damage, It should be noted MR in HT can be consequence of altered geometery duE to LVH, (Concentric Initially & eccentric in late stages)

The MR-HT link : Not to be missed

It is basic bed-side teaching that any isometric activity will push the blood from LVOT towards the Mitral valve, if it is leaking. Hence, it may not be a great discovery to show that HT will aggravate MR. Now, what is the new message you are trying to tell? There is big data (Really massive one, available from 5 million HT patients Rahimi K, et al 2017) that confirms with authority that HT patients are at risk of developing both primary degenerative and secondary MR at a later age.

If HT accentuates MR , why vasodilators didn’t show much beneift in MR ?

It is true routine vasodilators didn’t do much in regression of MR, but the subgroup analysis of those patients who have intrinsic HT or tendency of hypertensive response during exertion did benefit from vasodilator. So, it is mandatory that anti-HT drug titration is an essential strategy to arrest progression MR or prevent new onset MR.( Mojadidi M, JACC  2014)

Since we can’t selectively identify who will benefit from vasodilator therapy, it is always worth a trial of ACEI or even Amlodipine in patients with significant MR.(Note guidelines prohibit vasodilator therapy in MR unless it is Ischemic or non Ischemic DCM with functional or secondary) One clinical clue is, if a HT patient shows undue fatigue, one must suspect he or she is prone to develop MR on exertion as forward cardiac output is interfered with and fatigue results. (Special efforts must be taken to ensure a competent MV in HT patients) .

*Special effort means just a simple echocardiogram. In India, it can be taken for as little as $20 in any cardiac clinics or labs scattered across major cities. (Curiously, in Western countries, it costs $1000 and has a worrying waiting time as well, so it really becomes special effort!)

Assessing MR in echocardiogram: A well known tip

All of us know how tricky is, to assess and grade MR accurately. As discussed above it can as labile as systemic BP. Try to document the Heart rate and BP at the time of assesment.

Does Aoritc valve gets damaged with hypertension ?

Logically, high blood pressure is expected to damage the aortic valve more than the mitral valve. Does that happen? When the high-pressure ventricle contracts, the aortic valve is not resisting the flow like the mitral valve. It opens respectfully, so guess which valve is likely to get injured more. (However, it must be noted that the diastolic pressure exerts pressure on the far side of the aortic valve and can trigger aortic regurgitation and degeneration on the far side of the aortic valve. While high systolic jets can dilate or dissect the aorta. ) So, let me clarify this post doesn’t convey a meaning that Aortic valve is sort of protected against HT related Injury.

Final message

It is unacademic to delink mitral regurgitation (MR) from systemic hypertension, both in etiological and therapeutic aspects. Hence, it is wiser to include MR within the “Complication basket” of hypertensive heart disease. Recognising it and tackling in a timely manner will reap definite symptomatic benefit.This simple concept should be emphasized to our students.

Reference

1.Rahimi K, Mohseni H, Otto CM, Conrad N, Tran J, Nazarzadeh M, Woodward M, Dwyer T, MacMahon S. Elevated blood pressure and risk of mitral regurgitation: A longitudinal cohort study of 5.5 million United Kingdom adults. PLoS Med. 2017 Oct 17;14(10):e1002404.

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Cardiologists have always struggled to classify, assess, and grade one important valve disease, which is Mitral regurgitation. While valve replacement is the ultimate treatment, the timing of MVR is still a big debate. Apart from valve replacement, valve repair is a strong contender in selected patients. In recent times, cardiologists have made great strides to grab MR patients from cardaic surgeons. MitraClip, a percutaneous edge stitching , is possible with a varying degree of success.

Mitral valve edge-to-edge repair (MEER) is an interventional clone of Alfieri surgery that has shown conflicting results in the MITRA-FR and COAPT studies. The reason for this discrepancy in the MITRA-FR population is that they had larger-sized ventricles, which continued to pose challenges for the clip, which is focused only on the leaflets.

A new subdivision of secondary MR

Now, some of the cardiologists want to classify SMR/FMR into Proportionate vs Disproportionate MR. It may not be a great innovation, but it sub-divides secondary MR for optimal therapy. It simply says if LV dilation is significant, clipping the leaflet alone will not be sufficient; it would rather need an annular restriction either at the time of the index clip procedure or in due course. While Disproportionate MR implies, it is more of a leaflet coaptation defect, dominating over annular contribution.

Who proposed this ? What is the implication?

It is an afterthought, I think, from the makers of annular restriction device makers. MEER is found to be less effective in proportional MR.The Carillon device is a new arrival to tackle secondary MR .It is actually a wire that forcibly tightens the AV annulus inserted through coronary sinus . This modality takes advaantage of the aantomical proximity of coronary sinus to mitral annulus. Coronary sinus encircles and from a virtual wall along significant circumference of mitral annulus.

Unlike mitraclip, the Carillon device is claimed to tackle secondary MR irrespective of whether it is proportional or disproportional. It also has the potential to reduce LV dimensions in the long run. We have another device called IRIS-Millipede (to compete with Carillon).

Front. Cardiovasc. Med., 20 November 2020
Sec. Structural Interventional Cardiology
Volume 7 – 2020 | https://doi.org/10.3389/fcvm.2020.576058

Final message

We are free to have as many classifications in MR (Primary, Secondary, Functional, Atrial MR, & now Proportionate Disproportionate.) It is not the aim to bring up a rivalry between leaflet vs annular intervention. Ultimately, the most powerful component of the mitral valve apparatus, i.e., the LV muscle that matters.

I would request the esteemed researchers in MR ,not to keep EROs, regurgitation fractions, or chamber dimensions as primary markers of success of a device. Having strong clinical outcomes as the endpoint should be made mandatory, i.e., prolonging good quality of life and survival (But, the reality can bite hard. Someone told me, walking 20 meters extra in a 6-minute walk test is enough to get device approval from the authorizing entities.)

Final message

1.Grayburn PA, Sannino A, Packer M. Distinguishing Proportionate and Disproportionate Subtypes in Functional Mitral Regurgitation and Left Ventricular Systolic Dysfunction. JACC Cardiovasc Imaging. 2021 Apr;14(4):726-729. doi: 10.1016/j.jcmg.2020.05.043. Epub 2020 Aug 26. PMID: 32861653.

Postamble : A surgeons perspetive

While we debate about devices, the true benefits may lie elsewhere. A good MVR done by a mitral heart surgeon is the need of the hour. Says this paper from a top heart surgeon in India. Yadava OP. Disseminating valve repairs – a clarion call. Indian J Thorac Cardiovasc Surg. 2020 Jan;36

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