Blood transfusion as a risk factor of recurrent thrombosis in ACS patients

Blood transfusion is a common procedure in hospital care, especially in trauma patients and operated patients which loss lots of blood. But the risk of getting a transfused blood might be bigger than we expected, especially in acute coronary syndrome patients. A study by Silvain J et al, proved that transfused blood might increase the platelet reactivity in ACS patients which responsible for the recurrent ischemic event and mortality in ACS patients.

Here's the writing:

Impact of Red Blood Cell Transfusion on Platelet Aggregation and Inflammatory Response in Anemic Coronary and Non-Coronary Patients The TRANSFUSION-2 study 

Johanne Silvain, MD-PhD1; Jérémie Abtan, MD1; Mathieu Kerneis, MD1; Réjane Martin, BCh1; Jonathan Finzi, PharmMD1; Jean-Baptiste Vignalou, MD1; Olivier Barthélémy, MD1; Stephen A. O’Connor, MD1; Charles-Edouard Luyt, MD-PhD2; Nicolas Brechot, MD-PhD2; Anne Mercadier, MD-PhD3; Delphine Brugier, PhD1; Sophie Galier, BCh1; Jean-Philippe Collet, MD-PhD1; Jean Chastre, MD-PhD2; Gilles Montalescot, MD-PhD1

Objectives  To determine whether RBC transfusion increases in-vivo platelet aggregation and inflammation in coronary and non-coronary patients.

Background Red blood cell (RBC) transfusion increases in-vitro platelet activation and aggregation in healthy volunteers, providing a possible explanation for the increase in recurrent ischemic events and mortality reported after RBC transfusion in ACS patients.

Methods Platelet reactivity was measured before and after RBC transfusion in 61 patients (33 ACS patients and 28 non-ACS patients). Relative changes between baseline and post-transfusion measurements of maximum (MPA) and residual platelet aggregation (RPA) were considered with different agonists as well as changes in Vasodilatator-Stimulated Phosphoprotein Platelet Reactivity Index (VASP-PRI) and P-selectin expression. Inflammatory and thrombotic biomarkers were also measured before and after transfusion.

Results After RBC transfusion, platelet reactivity was increased when measured with adenosine diphosphate (ADP)-induced light transmission aggregometry (+11.6% relative increase of MPA; p = 0.004 and +10.8% increase of RPA; p = 0.005) and VASP PRI (relative increase of +20.7%; p=0.002) while there was a non-significant trend towards an increase of P-selectin expression. Similar results were found with the non-specific agonist thrombin receptor activated peptide (TRAP) (relative increase of +11.7% for MPA p=0.04 and+12.7% for RPA; p=0.02) but not with collagen or arachidonic acid agonists. There were no significant differences in inflammatory and thrombotic biomarkers before and after transfusion. 

Conclusions After red blood cell transfusion, there is an increase in platelet reactivity, especially with tests measuring the ADP-P2Y12receptor pathway without significant variation in inflammatory or thrombotic biomarkers. This in-vivo effect may account for the excess in ischemic events observed in the context of ACS treated by PCI and P2Y12inhibitors.

Basic Life Support with no kissing scene? Where's the fun?!?

When we watch some action movies, we tend to see CPR a.k.a cardiac pulmonary resuscitation with the component of chest compressions and the heroic kissing scenes. Well....not exactly kissing, blowing air to be frank, giving the artificial breathing.

Mouth-to-mouth artificial breathing has been a component of Basic Life Support (BLS) sequence for ages. Though some people might grossed out to do so for a very reasonable reason: exchanging bodily fluids with unknown person which might lead to transmission of infectious disease. Well, since it is a guideline, the BLS providers are encouraged to do so. But, how about the evidence, does giving mouth-to-mouth artificial breathing give more benefit?

Removing mouth-to-mouth artificial breathing is rather a new concept which come from several reasons regarding the downside of giving artificial breathing, which are:

1. Transmissible disease between the patient and the provider
2. An unnecessary distraction (especially for the untrained BLS provider) for the most vital component of CPR: chest compression 

Moreover, the part of giving the patient artificial breathing may be replaced by the automatous breathing effect from the chest compression. Giving a chest compression might give secondary effect of pushing the air out and pulling it in, which supposedly give quite sufficient oxygen to the patient (compared to the breathe-out air from the patient which also contains more CO2).

Those are mainly the talk about the theory and stuffs, but how's the survival rate reported in the study? This is an interesting paper where the evidence come to play: Compression-Only CPR or Standard CPR in Out-of-Hospital Cardiac Arrest, comparing the survival rate in 1-day and 30-days between the use of compression-only CPR and the standard CPR. 

"The result showed a 30-day survival rate of 8.7% in the group receiving compression-only CPR and 7.0% in the group receiving standard CPR, while 24.0% of the patients receiving compression-only CPR survived for 1 day, as did 20.9% of those receiving standard CPR. There were no significant differences between the two groups with respect to the other secondary end points."

Well, we might see a little difference in survival rate, quite visible in compression-only CPR result for both 1-day and 30-days survival rate, though it was considered as no significant differences. Meaning? mouth-to-mouth artificial breathing supposedly will not give better result, considering the "extra miles" we have to go through doing it, than compression-only CPR.

As for now, compression-only CPR hasn't been approved as a guideline, though I have a standpoint of  doing so when doing BLS for outpatient setting.

Kudos to dr. Rahul Goswami for introducing me to this topic. His blog, emergence phenomena, can be accessed here: singem.blogspot.com

"Myocardial infarct? Naah...just send her home!!"

That sentence may be heard a lot in our workplace. A chest pain may be interpreted as an angina or just a muscle pain. Indeed the muscle is in pain, but to determine "which muscle?" may be the most difficult choice we've ever made. Either we send a patient home because of the nontypical chest pain leading to costochondritis, or we have to keep the patient in because we suspect of an angina.

Well, we learned from med school that we HAVE TO suspect a person for having an angina by several typical criteria:
1. Dull chest pain (heaviness or pressure on the chest), cannot be exactly pointed by the patient
2. Pain radiating to left arm or shoulder
3. Pain radiating to the jaw or to the back

However, we tend to exclude the possibility of someone having angina pectoris if they don't have any of the symptoms mentioned above. How wrong could this be??
Well, based on a review by Swap and Nagurney (2005), some symptoms were accounted and calculated to show the likelihood ratio of having acute myocardial Infarction:

1. Pain radiating to the right arm or shoulder (LR, 4.7)
2. Pain radiating to both arms or shoulders (LR, 4.1)
3. Association between pain and exertion (LR, 2.4)
4. Pain radiating to the left arm (LR, 2.3)
5. Diaphoresis (LR, 2.0)
6. Pain described as worse than previous angina or similar to previous MI (LR, 1.8)
7. Pain described as pressure was not very predictive of ACS (LR, 1.3)

I believe these facts might just slap your face. Well, believe it or not, you just have to prove it for yourself in the ER. Just remember what A/Prof. Amal Mattu said, there is no patient with chest pain can be considered as "no risk" for MI.