1. Complications of Acute Myocardial Infarction: Atrial Fibrillation
By Katie Hintz

2. About
Title: “New-Onset Atrial Fibrillation After Acute Myocardial Infarction and Its Relation to Admission Biomarkers (from the TRIUMPH registry)”
Authors: Susmita Parashar, MD, MPH, MSa,*, Danesh Kella, MDa, Kimberly J. Reid, MSb, John A. Spertus, MD, MPHb, Fengming Tang, MSb, Jonathan Langberg, Mda, Viola Vaccarino, MD, PhDa,c, Michael C. Kontos, MDd, Renato D. Lopes, MD, PhD, MHSe, and Michael S. Lloyd, MD
Journal: American Journal of Cardiology (112: )
Date published: 2013
How to retrieve: using MEDLINE through APU Library Resources
Search acute myocardial infarction AND complications AND women
I chose this article because I felt like it was a good refresher of pathophysiology of AMI and introduction to one of the major complications of AMI – Afib.

3. Article Summary
Purpose: analyze the relation between biomarkers linked to myocardial stretch (NT-pro-brain natriuretic peptide [NT-proBNP]), myocardial damage (Troponin-T [TnT]), and inflammation (high- sensitivity C-reactive protein [hs-CRP]) and new-onset atrial fibrillation (Afib) during acute myocardial infarction (AMI) to identify patients at high risk for Afib.
Problem: patients with new-onset Afib in the peri-AMI period have a higher rate of death and complications such as infarction, cardiogenic shock, and ventricular arrhythmias.
Operational definition of Afib: present if Afib or aflutter was identified on a 12-lead electrocardiogram or was seen for greater than 30 seconds on a rhythm strip at AMI presentation or during the AMI hospitalization.
Goal: observe relationship between biomarkers and occurrence of Afib post AMI  focusing on occurrence during hospitalization

4. What do Afib and Aflutter look like?
Afib: occurs because of multiple reentry circuits in the atria. Rapid impulses cause ineffectual atrial contraction  decrease in cardiac output and loss of atrial kick
*NO CLEAR P WAVE
- Baseline is erratic/wavy
Aflutter: ectopic atrial rhythm in which an irritable site depolarizes regularly at an extremely rapid rate
*Distinct characteristic = SAWTOOTH PATTERN
Source: EKGs made easy handbook

5. Article Summary Methods: Sample size: n=2,370
Inclusion criteria: AMI from April 2005-Dec 2008, 18 yo, elevated troponin levels w/in 24 hrs of hospital admin,
demonstrated AMI with at least one of following:
prolonged (>20 minutes) ischemic signs or symptoms
at least 1 electrocardiogram with ST elevation or ST depression in 2 consecutive leads
other clinical evidence of AMI, patients that donated blood for central analysis of lipid profile/genetics/biomarkers
Exclusion criteria: transferred from other facility more than a day after original presentation, didn’t speak English or Spanish, history of Afib prior to AMI
Participants from Translational Research Investigating Underlying disparities in recovery from acute Myocardial infarction: Patients’ Health status registry, a multicenter prospective cohort of patients with AMI from 24 United States hospitals.
Data collection: chart abstraction & interview by trained personnel within 72 hrs of admin, baseline venous blood samples drawn at enrollment w/in 72 hrs.
Data analysis: Demographic, clinical, treatment, and biomarker characteristics between patients with AF and those with non-AF myocardial infarction (MI) were compared using Student t test for normally distributed continuous variables, Wilcoxon rank sum test for skewed variables, and chi-square or Fisher’s exact tests for categorical variables.

6. Article Summary Results:
New-onset Afib was documented in 114 patients with AMI (4.8%; mean age 58 years; 32% women).
Patients with new-onset Afib had significantly higher levels of NT-proBNP and hs-CRP than those without Afib.
There were no statistically significant differences between the level of TnT between patients with and without new-onset Afib.
Observations:
Patients with AMI who developed new-onset AF were more likely to be older, Caucasian, and to have a higher prevalence of diabetes, hypertension, chronic lung disease, and chronic kidney disease. Also more likely to receive b blockers, calcium channel blockers, and antiplatelet agents on arrival and as likely to receive reperfusion and revascularization therapies as those without new-onset AF
less likely to smoke.
no significant association between AF and higher Killip class, LV ejection fraction (EF), ST elevation myocardial infarction, previous congestive heart failure, or previous coronary heart disease.

7. Shows that when NT-proBNP is high, so is the prevalence of Afib (p<0.001). Also CRP relation to Afib is significant (p<0.001).
For each twofold increase in the level of NT-proBNP, there was an 18% increase in the rate of AF (odds ratio 1.17, 95% confidence interval 1.02 to 1.34; p <0.02)
For every twofold increase in hs-CRP, there was a 15% increase in the rate of AF (odds ratio 1.15, 95% confidence interval 1.02 to 1.30; p = 0.02)
TnT was not independently associated with new AF (odds ratio 0.94, 95% confidence interval 0.84 to 1.06; p = 0.3; Figure 2)

8. Article Summary Conclusions:
The strength of association for NT-proBNP and hs-CRP was greater than other clinical covariates such as:
Left Ventricular Ejection Fraction
Killip class
Congestive heart failure
TnT was not independently associated with new-onset AF.
The association between biomarkers and the development of new-onset AF did not differ by race or gender.
Afib in MI appears to be multifactorial  use of NT-proBNP and hs-CRP as predictive indicators can only be speculative
Killip class: used to stratify the severity of left ventricular dysfunction and determine clinical status of patients after MI
Listening for 3rd heart sound
Presence of pulmonary edema or cardio genic shock
Source:

9. Article Summary Relevance:
Measurement of NT-proBNP and hs-CRP levels may provide an easier and faster way to identify AMI patients that are at high-risk for developing Afib.
Important to identify high-risk patients who may benefit from a more careful monitoring and early treatment during AMI hospitalization .
These biomarkers also provide insight into the pathophysiologic mechanisms of new-onset Afib after AMI by suggesting that inflammation and myocardial stretch, but not the amount of myocardial necrosis, are likely to be important drivers of new Afib in patients in the setting of AMI.
Why is this relevant? Although several studies have examined predictors of AF in the general population, there are limited data examining the association of biomarkers and new-onset AF after AMI. The findings in this study mostly agree with previous studies; however, it is unique in that it observes the association of post-AMI Afib with the three biomarkers independently.

10. How can we use this information?
Be aware of these biomarkers in lab values of our patients this semester
Seeing patients in ER / ICU / CICU who are either experiencing AMI or post AMI
Need for further study:
Clarify mechanisms of new-onset Afib
What is the pathophysiology?
Preventative impact of cardiac medications
What meds are most effective?
This relates to our studies this week and next week!
Observing atrial rhythms
Learning about complications of AMI

11. Question 1
Which biomarkers are independently associated with new in-hospital Afib after AMI?
A. Troponin-T
B. NT-proBNP
C. hs-CRP
D. B & C
Answer: B & C  NT-proBNP and hs-CRP

12. Question 2
For each twofold increase in NT-proBNP there was an 18% increase in the rate of Afib. What does the biomarker NT-proBNP represent?
A. Myocardial damage
B. Inflammation
C. Myocardial stretch
D. None of the above
Answer = C. Myocardial stretch
Or do question about Afib being a complication of AMI