Angiogram results after Myocardial Infraction

[rashmideepthi]

my father is 64 yrs old, has a stent in mid LAD (9 yrs back angioplasty was done), non diabetic, hypertensive, quit smoking 9 years back . till now he was doing well since last week he started having heart burn and pressure in chest which lasted for an hour or so, he went in for a thorough check up TMT, echo were all normal, his BP during TMT was lil high hence medicines were changed, howevr after 2 days he experienced heart burn and nausea, there was no change in ecg but cardiac markers were slightly elevated
CKMB-15.2ng/ml   Tropinin-1.44ng/ml Myoglobin- 428ng/ml
they told us it is non-ST segment elevation myocardial infraction
he was on anticoagulants for 6 hours angiography was done report follows
LMCA-normal
LAD-type III vessel
Patent stent in mid LAD with mild neointimal hyperplasia
Distal LAD 50% stenosis, D1, D2, D3 small vessels
LCX- non dominant vessel normal
OMI ostioproximal 60%stenosis, OM2 normal
RCA- Large dominant vessel. Ectatic vessel
Distal RCA filled with 100% thrombiotic occlusion
PDA. PLV fills via left to right collaterals
IMP-SVD
ADV-48 hrs infusion with tirofiban and check angio followed BT delayed PCI stent to RCA

After 48 hours the angiogram was repeated report is below

Distal RCA has fully opened up with TIMI grade 3 flow in RCA.
PDA PLV has diffuse disease with residual clots underlying residual clot with 80%stenosis in distal RCA
Adv- Plan elective PCI stent to RCA after 2-3 weeks

can somebody give me a clear picture of his condition, did he really have an heart attack as enzyme levels are only slightly high and ecg also don confim MI,  how serious he is and what kind of treatment would best suit him, angioplasty or medications alone, are there any other concerns i shud be worried about

[ed34]

Hi, yes he certainly did have a heart attack, but it was in the distal part of the Right Coronary Artery so would have had less effect than if in the middle or top of the vessel. It isn't easy from the notes to determine the exact events, but at a guess I would say...
A diseased area in the lower part of the RCA ruptured, releasing clotting material from within the artery wall. This travelled a little further down and became lodged. He then developed a blood clot where the rupture occurred. This is a natural repair function, but would have blocked the artery. So I think he had 2 blockages, one slightly above the other. Anticoagulant meds dissolved the natural blood clot, completely opening that part of the vessel, but there is a 80% blockage still there, from the stuff which ruptured out of the diseased area. I think they will want to stent across the ruptured area PLUS the 80% blockage so the bottom of the RCA is totally clear.
This is how it reads to me, but as I say, it's not easy from the noted they have written.
Would I have the stents or rely on meds? I would definitely have it stented. With such a rough surface inside the artery where the rupture occurred, there is a high chance of another natural clot forming. Also, the 80% blockage will probably grow to 100% in a matter of months. It's very sticky and nasty stuff. The reason his troponin was only slightly elevated is probably because only a small portion of heart muscle was affected, because the problem was right at the lower end of the right artery.
The stent he had 9 years ago is still fully open, suggesting he is a good candidate for successful stenting long term. I would ask them to look at the images from 9 years ago and see if there was any signs of the blockage in his obtuse marginal 1 vessel. There is now a 60% blockage. If there was no sign, perhaps they will consider dealing with that one now.

[rashmideepthi]

thanks a ton for this reply, ur suggestions r of great help, i checked the angiogram report done 9 yrs ago. typed the report below

LMCA: normal
LAD: proximal normal, mid 100%occlusion after d2, distal vessel not visualised
diagonals: d1- normal, d2 proximal 50-60% leison
CX: proximal normal, distal plaquing
marginals: OM1 normal, major OM2 shows proximal eccentric 30% leison
RCA: proximal normal, mid and distal RCA show plaquing
PDA/PLV: PLV- mid 80% lesion, PDA- normal
LV: anterolateral and apical hypokinesia, LVEF= 40%
final diagnosis: CAD- Acute anterior wall myocardial infraction, mild LV dysfunction, systemic hypertension.
recomendation: primary angioplasty to LAD

i can see in the recent angiogram OMI ostioproximal 60%stenosis, OM2 normal whereas 9 years back angiogram report typed above says OM1 normal, major OM2 shows proximal eccentric 30% leison, is this a typo error of the hospital report am not sure. one more ques what does it mean when they say PDA PLV has diffuse disease?
we are surprised that his TMT and echo done 2 days before these events showed no abnormalities, he showed only gastric symptoms and no changes in ecg also, in such situations how can we be sure its a heart attack? cardiac markers also need time to show up right?

[rashmideepthi]

i forgot to mention, his blood pressure is now 110/70 and not on any medications for hypertension, but prior to this he used to have cardace 10 mg still his BP would fluctuate, what could be the reason for low BP, is it because of the anticoagulant medication they gave tirofiban , heparin etc, he was on tirofiban for 48 hours. from past 24 hours his BP is 110/70

[ed34]

Hi. Well, different cardiologists will report different levels of disease in different ways. Some will only report 50% and above, as with the latest report. Some will report everything, even 10%. So the 30% in OM2 wasn't seen as an issue by the cardiologist this time and in some sense he is correct. The older report does seem more detailed, as it mentions the 30% in the OM2 and so I would suspect there was no disease in the OM1 9 years ago. Now it has reached 50% so it's growing. One to watch. It's also odd how the Diagonal 2 (D2) in the first report says 50-60% lesion, but now it just says small vessel? Questions to ask the cardiologist I think?
Diffuse just means scattered, not in one tight location. If I had a report which said diffuse disease in distal LAD, it would mean basically the distal LAD has a coating of plaque over the entire area. This isn't a concern, you are looking for tight blockages.
If his BP is 110/70 after stenting, I would celebrate. This is not low, it's absolutely perfect. The fact that he isn't on any BP meds now, would suggest that his heart is working in tandem with his arteries perfectly.
Non-stemi means it will not show up on ECG. I had a non stemi in 2007 and a standard echo won't reveal anything unless the muscle is being seriously compramised. It was his distal RCA, so very little muscle would be affected and the echo is done with the heart at rest, not working very hard at all. If they did a stress echo, where the heart is raced, it would have likely shown something up. Yes you are correct about the troponin. It takes around 12 hours to get into the blood and give accurate readings. It can remain elevated for up to 2 weeks. A good Doctor should know when its heart attack, by the symptoms. Unfortunately not all general Doctors seem to recognise the signs and pass it off as a stomach problem.
If you have any other questions, please don't hesitate to ask, we are here to give any advice we can.

[rashmideepthi]

recent echo report (10/9/12)is as follows

echo final diagnosis: EF= 52
                             S/P PTCA
                             concentric LV hypertrophy
                             Fair LV systolic function
                             RWMA involving inferior segment
                             Grade 1 MR
                             reduced LV diastolic compliance
                             trival TR/mild PAH
                             no clot/effussion
wall motion abnormalities: basal septum, basal, mid inferior segment hypokinetic
following is the echo report on 5/9/12 (just 5 days bck) which was part of his routine health check up.
   Final diagnosis: S/P PTCA
                           normal LV systolic function
                           LVEF - 57%
                           MR - trivial
wall motion abnormalities: Distal septum, apex mild hypokinetic

what i understand from this report is the recent MI has considerably damaged his heart further and the sad part inspite of several visits to the hospital and all the precautionry health check ups we could not avoid it.

please give your opinion on the treatment which he is going through now
Discharge summary

Diagnosis: essential hypertension.
CAD, old ASMI, S/P primary PCI stent to LAD- DES-TAXUS 2004
fair LV systolic function
acute evolved IWMI, PWMI - delayed presentaation >48 hours
CAG- Patent stent, distal RCA occlusion with heavy thrombus burden, PDA, PLV well collateralised - 9/9/12
tirofban infusion for 48 hours- check angio- RCA patency restored with residual thrombus burden - 12/9/12
Adv- elective PTCA stent to RCA after 2 weeks

tab ecosprin 150 mg(0-1-0)
tab effient 10mg (1-0-1)
tab tonact 40 mg(1-0-0)
tab neksium 40 mg(1-0-0)
tab nikoran 5mg (1-0-1)
tab ranozex 500mg (1-0-1)
review with doctor after 2 weeks

[ed34]

I can't see anywhere that it says considerable damage? There are areas of the heart which are mildly hypokinetic, but you would expect that with a blockage. His systolic function is fine, he has an EF of 57%, something you wouldn't get with a lot of damage. Normal EF is 50-70%.
Nikoran is Nicorandil, a medication which helps keep blood vessels open more. This is basically a BP lowering medication. 5mg is a low dosage though. The meds look fine, but I'm wondering why he isn't on a beta blocker to keep the heart from over working.
With regards to the prevention of the heart attack. Sadly, this happens more than hospitals would like to admit. People go in for a complete medical and pass with flying colours, only to die a few days later of heart attack. When I get chest pains now I go to the ER and refuse to let the general Doctors touch me, I ask for a Cardiologist on duty.

[rashmideepthi]

when he was on betablocker his HR was 53 so doc had changed those medicines to cardace before hospitalization, right now he is not on beta blocker i can c HR 60 above rarely crosses 70
am from india, here very few hosp and doc value for patients life, todays visit i asked the doc regarding the question u asked me how d2 in first report says 50-60% leison is now referrd as small vessels, he was fuming at me

[rashmideepthi]

hi ed34
my dad had angioplasty 2 dys back, the blockages remain the same even after 2 week medicines hence doc did an angioplasty on the distal RCA, this time we went to another hospital because the stent which suited him last time (Taxus DES) was nt availble in the old hospital. however after the procedure i was told they have used XIENCE DES as it is a better option and lesser chances of restenosis, i was little worried because the doctor did not ask our opinion on which stent to use after the angiogram which he initially said he will. and one more thing i noticed was my dad asked to pop 3 effient tablets before the procedure, nurse told me it is to ease up the blood flow, but i found it somewhat strange giving an overdose of the medicine which he is already using, now i feel my dad could have had excess bleeding due to which the doctor was left with no time to discuss about stent with us and finished the procedure soon wat do u think?. now he is in the ward complaining of headache and they are still giving LMW heparin injections to him. this is his 3rd angiogram in last 3 weeks am really worried we are always at the wrong places for treatment, had they done the stenting in the first angiogram it cud have saved him from the effects of 2 angios, as it did no good by waiting for so long, the block in OM1 60%  doc told we need not worry, and his D1, D2, D3 vessels still remain small vessels, what could be the treatment plan for these small vessels ?

[rashmideepthi]

there is another less invasive procedure to diagnose blockages, 64 slice CT scan, why is it not preferred to angio? any idea

[ed34]

Vessels that are considered too small for stenting are a problem. They used to use a balloon, but nearly all vessels soon shrunk back down or developed scar tissue which closed them entirely. They now have a drug eluting balloon for small vessels. A drug stent, because it's mesh, only touches about 2% of the artery lining, meaning not much drug is delivered. The drug coated balloon touches 90-98% of the lining, delivering far much more and stopping restenosis. I don't know much about effient, just that it's a replacement for plavix, but for every angio procedure i've had, they've given me 8 pills = 600mg.
It has a very short half life, but you certainly don't want clots forming while the cardiologist is doing his procedure. It simply helps to stop clotting, preventing heart attacks or stroke during the procedure.
His OM1 (obtuse marginal 1 vessel) has taken 9 years to reach 60% so with a healthier diet this could stop the progression.
Don't worry about the stent manufacturer, let the cardiologist deal with it, they have the experience for which one is best in a given situation.
64 slice CT scans are limiting and are not liked by many cardiologists. There is nothing better than getting inside the artery and looking around. When in the artery you can also measure flow rate and pressure at any point in any artery to see the effect a blockage is having on the patient.
The term 'small vessels' used for D1 D2 D3 may simply mean they are anatomically small, but healthy. They are simply keeping his blood thin with injections to greatly lower the risk of a clot forming in the coronary arteries where the procedure was done. It will give the vessel a very good head start in beginning repairs.
Now that the distal RCA is open again, he should have the ability to open natural bypass vessels if necessary, called collaterals. It sounds very successful.

[rashmideepthi]

thanx for the reply, i was told the d2, d2 d3 are diseased and not anatomically small by the doc, does the collaterals form naturally or with excercise, will there be any symptoms if they block, what are the chances of restenosis for a stent

[ed34]

" does the collaterals form naturally or with excercise"

naturally, it's believed to be done by pressure.
I've not heard of them blocking. There are many of them over the surface of the heart. The only way they will stop is if the blood feeding them becomes blocked.
I wouldn't start to look at statistics for failure. Every single person is different. I've known stents to fail in people after a couple of days, but I have one that has been doing great since feb 2007.

[rashmideepthi]

in the first angio after his MI it is stated "Distal RCA filled with 100% thrombotic occulsion, PDA PLV fills via left to right collaterals"
does it mean he had already developed or developing collaterals, there was one doc  who wanted to treat it medically as he belived in natural bypass, but consulting him regularly was extremely difficult and i cud meet him just once, and all the other doc's we met wanted us to go for angioplasty and we din want to wait as its risky

[ed34]

Yes, he was developing them already, but with the right artery now open at the bottom, he stands a better chance of developing more of them.

[ed34]

Has your Father noticed any improvements since the stent?

[rashmideepthi]

he says nothing very significant but he feels better psychologically.
his recent report says the following
1. Coronary angiogrm reveled intraluminal narrowing of 99% in the distal RCA with diffuse plaquing in the mid PLV segment
2. Sucessful PTCA and stenting was done to distal RCA with Xience-V(DES) stent 2.75mm* 18mm
in a span of 2 weeks the 80% stenosis had turned 99% meaning it ws about to close again?
what abt the collaterals which was initially formed, now it has turned to diffuse disease after tirofiban and stenting
my father's BP is now 130/80, heart rate is 82, before angioplasty his pulse rate was 60 range and he was not on betablockers, is it gud or bad, will opening up of arteries increase the heart rate

[ed34]

2,   Yes it was. It says nothing about the collaterals in the recent report, the collaterals will still exist because they are from the LEFT side, which hasn't been touched. Stenting does not cause Diffuse disease.
Heart rate increase? it CAN. After my triple bypass, my HR was about 82-84 from normally being 68. After a few weeks, it dropped again. I was told by the cardiologist that over years, my heart had been adapting/adjusting to less oxygen. Suddenly, in a matter of minutes, the muscle in certain areas goes from getting 1% to 100%, so it will suddenly become more reactive. Over time it adapts and adjusts back to a lower rate again. It takes regular exercise and healthy diet to get the heart back to normal again.

[rashmideepthi]

i have a question, does PTCA and stenting procedure include angiogram, because am not able to find angiogram report in my fathers hospital reports

[ed34]

When they do an angiogram they look inside the coronary arteries with a catheter. This is exactly the same procedure when they fit stents, they use a catheter and the same equipment.

[rashmideepthi]

my dad has been prescribed cilodoc 50 mg, along with effient(10mg), ecosprin(150), tonact(40) and cardace (2.5), i was wondering what is the  drug cilodoc for? googled about this drug and found it is for muscle cramps, he doesn complain of leg cramps...one more ques he had URI and is on antibiotics, will it have any impact on his heart

[ed34]

Has the Doctor mentioned anything about bad circulation in the leg arteries? that's the only thing I can think of for Cilodoc.

With regards to antibiotics, no, unless you are allergic to the medication, they will not affect the heart.

[rashmideepthi]

i was told d1 d2 d3 are diseased, are they arteries which supply blood to the legs

[ed34]

No, they are on the heart. D1 D2 and D3 have a fuller name, they are the Diagonal vessels and branch off of the Left Anterior Descending.
Cilodoc also increases cAMP-dependent protein kinase which is an enzyme
which controls metabolism of sugar, glucose and lipids.