Unusual Causes of Myocardial Infarction -ESC Webinar

There are some quite remarkable cases presented . It also highlights how careful an EKG needs to be looked at in  evaluating a patient suspected of myocardial ischemia . A multi- imaging approach is often necessary. When in doubt remember " the dye don't lie" (but may not tell the truth ).

Refer to to an older post at the bottom of the page referring to the recent published Fourth Universal Definitions of Myocardial Infarction

CardioMems already part of history?

https://vectoriousmedtech.com/

A Case from a long time ago.....

Patient was sent to Duke University down further on Tobacco Road , for a myocardial biopsy. The following report was returned.....

Do you think this patient has cardiac /AL amyloid or Fabry disease, or another diagnosis....

The patient lived in Greensboro, but could not him to get myocardial biopsy done in Greensboro..

Interpretation of High Sensitivity Troponin

I have collected several articles on the interpretation of hs cTnT/I. The interpretation of this new and ultra sensitive test can be very challenging in critically ill patients that have additional co-morbidity's, particularly in septic shock , ARDS etc...

If you do not want to read all the literature just refer to the ACCA (Acute Cardiovascular Care Association , part of ESC ) poster, which is extremely helpful .

How to interpret high-sensitivity assays, from Circulation:

Commenting on the ever increasing sensitivity and decreasing specificity of troponin assays, Robert Jesse crypt, "when troponin was a lousy assay he was a great test, but now that it is becoming a great assay is getting to be a lousy test.  Recommendation however is is that frequent monitoring of troponin kinetics, along with careful attention to the noncoronary causes of troponin elevations we will keep the high-sensitivity troponin assays extremely useful markers for myocardial injury.

Data from the SWEDEHEART registry, points out that a large proportion of patients will have minor cardiac troponin increases the majority would do not have a myocardial infarction.  However despite remaining a heterogeneous group be adjusted mortality rate start to increase at the level of the 99th percentile in healthy controls.

From BMJ February 2019: In the hospital population of 20,000 consecutive patients, 1 in 20 of all patients had a  high-sensitivity troponin I concentration greater than the manufactures recommended 99th percentile.  In most of these patients there was no clinical suspicion of acute myocardial infarction.  In this particular study the  99th percentile of the high-sensitivity troponin I for the whole population was 296 ng/L compared with the manufactures quoted level of 40 ng/L currently used clinically as upper limit of normal for high-sensitivity troponin I.

Among patients with infection [ including the post-infection period ] there is also an increased risk of myocardial infarction.  Pathophysiology is discussed in this article from New England Journal of Medicine referred to in an earlier posting.

QTc prolongation

A young woman, who had been binge drinking, admitted with severe agitation and hallucinations......

Initial Mg 1.3, K=2.8 , iCa++ low normal

2gm MgSO4 was given and potassium IV. Mg level 3.2,  one hour after the magnesium infusion .Telemetry showed the following (pic/video)

......and < 24 hours after treatment still with QTc prolongation.

What's the primary abnormality, besides QTc prolongation ?

How much Magnesium was given in less then 24 h with a Mg level of 3.2. Any ?

Should we use NIV or HFNC for acute hypoxaemic respiratory failure?

Acute Decompensated HF with congestion - ESC Guideline Approach

Learning objectives:

Current guidelines regarding diuretic use in HF patients

Different mechanism of action of different diuretic agents

Using diuretics in real clinical practice

When to switch to mechanical fluid removal

Define future needs for new diuretic agents

Key points are actually interesting

1) measuring UNa+ @ 2 hours if no UOP >100 cc/hr. UNa+ has to be > 50 mEq/ L to make sure you actually achieve "natriuresis" ( poor fellow running around all night checking Una + levels !)
2) A rise in creatinine is to be expected in many cases and should not lead to backing off from diuresis. I think we see as soon as creatinine goes up MDs back off on diuresis , which is the exact wrong thing to if congestive symptoms are still present
3) Inotropes are discouraged , unless the patient has "true" low output symptoms...and dopamine is not on this list, milrinone is preferred. Any inotrope in the acute setting is associated with increased mortality and purely provides symptomatic relief.