[TachyBrady]

My BIL is 57 years old and an athelete. He has no risk factors or prior heart problems. The other night he developed chest pain, was taken to our small community hospital (which only does diagnostic caths/ no interventions) and was airlifted to a large city hospital where his cath showed a clot and otherwise normal arteries. He was given a 'clot buster'.

This info was given to me by my sister so I don't have info first hand. Anyway, my questions are: can a clot just appear in the arteries or are all clots related to a plaque disruption? If there is no arterial narrowing or rupture, could the clot formation have been caused by dehydration? (It was hot and he ran a 4 mile race earlier in the day.)

What will his treatment and recovery involve? Will he be put on blood thinners? Will he eventually be able to run again?

I've worked on telemetry for almost 14 years so I feel pretty confident in basic heart stuff. We occasionally transfer pts out with acute problems but then never hear what happens with them or what the outcomes are. Could those of you that work in the cath labs and CCUs share what you know about the differences in stent placement vs angioplasty vs clot busters.

Thanks for responding. Any info or links to treatment of ACS/MI's is appreciated for this specific instance and also in general for expanding my knowledge as a telemetry nurse.

Bern

[ZASHAGALKA]

http://www.cardiologyrounds.org/crus/402-011.pdf

Blockages can be caused in 3 ways:

1. increasing occlusion by plaque formation over time.

2. Sudden occlusion by a clot floating into an arterial lumen of smaller diameter.

3. Plaque rupture and platelet mediated clot formation on site.

Only the first route involves slowly building plaque over time. In the 2nd scenario, you could have no plaque one day, 100% occlussion the next. It isn't plaque causing the clot; the clot migrated to that spot from another sources. (This is why afib pts are on blood thinners - to prevent this very thing.) In the case of #3 above, you could have a 20% blockage one day, and a total occlusion the next.

Platelets tend to be a prime culprit. In a normal system, platelets are heroes to the blood, preserving supply in case of damage to the system and acting as primary spotters for inflammatory situations.

In a diseased system, I've heard platelets referred to as a 'self-perpetuating pathogenic loop'. Platelets form clots by aggregation. The very things that makes them heroes under normal circumstances makes them accomplices under these circumstances. These situations can normally dealt with by thrombolytics: clot busters.

In the 3rd route, above, platelets have inflammatory mediators that can release in and around plaque formations and cause them to become unsteady, or, weak. Once ruptured, platelets attack the ruptured products, creating, in effect, a thrombosed cascade across the lumen of the artery.

This is why primary therapy for AMI is ASA and a platelet aggregate inhibitor, such as plavix or integrillin (rarely, reopro). Both are aimed to reduce platelet clotting by changing the characteristics of the platelet-platelet binding sites.

So, think plavix and asa long term. In addition, B-Blockers and ACE inhibitors are standard post-MI drugs, because they prevent negative cardiac remodeling post MI, and, as a result, reduces the risks of future MIs and decreased Left Ventricular Ejection Fraction over time.

But, there is no reason, assuming a decent EF, that someone can't resume a relatively normal lifestyle after MI. That is patient specific however, and THAT is something your BIL has to get cleared from his doc.

~faith,
Timothy.

[TachyBrady]

Thanks Timothy. The article you posted looks good and I will read it more thoroughly tomorrow. I was not aware that clots formed due to afib could migrate to the coronaries. It's still a mystery how/where BIL's clot formed. Do you think dehydration contributed?

Fascinating stuff.