Association of Mineralocorticoid Receptor Antagonist Use With All-Cause Mortality and Hospital Readmission in Older Adults With Acute Decompensated Heart Failure

Use of MRA at discharge from ADHF  ( acute decompensated heart failure in HFrEF/HFpEF) hospitalization appeared to be associated with a lower risk of heart failure hospitalization but not with lower all-cause mortality or overall rate of hospitalization. No in this end- point was seen  benefit in 94% of patients with average age of 80 years old .

These findings suggest that MRA use might be associated with minimal, if any, clinical advantage. Further studies appear to be needed to identify the patient groups that may find value in MRA treatment and for findings to be confirmed by RCTs in patients hospitalized for ADHF.

This reminds me of the digoxin story in HF patients - high risk medication with essentially no benefit . Another med to de-escalate elderly patients often complicated HF medication list .

Tako-tsubo Cardiomyopathy and its multiple variants

Tako - Tsubo Cardiomyopathy

The correct answer is a Tako-Tsubo Cardiomyopathy. [Stress cardiomyopathy or broken heart syndrome]. Typical presentation is a patient with chest pain after emotional distress and EKG presentation suggestive of an ST elevation myocardial infarction.[ST elevation]



ST elevation myocardial infarction is not entirely an incorrect answer. The patient still is treated initially as a STEMI, but then in the catheterization laboratory the usual findings are no significant obstructive coronary artery disease with typical ballooning of the apex of the heart on left ventriculogram. Therefore the syndrome was also called apical ballooning syndrome or Octopus trap syndrome, first described in the mid 1980s by a Japanese scientist

.

However more recently several variants have been noted, one variant is where there is akinesis of the mid ventricle and hypercontractility of the apex and the base [see article] and yet another form is reversed Tako-Tsubo syndrome, or also called “squid syndrome”. This gives an image on ventriculogram and echocardiogram with apical hypercontractility and basilar akinesis




There are specific ECG criteria that differentiates Tako-Tsubo Cardiomyopathy from a true STEMI secondary to plaque rupture or type I myocardial infarction.



Although this EKG looks like an ST elevation myocardial infarction , the distribution of the ST segment elevation is unusual as well as the shape of the ST segments. There is also no reciprocal ST segment depression. The frontal axis is typically shifted more leftward.

The EKG at first glance can also look like pericarditis, but the history is not compatible with this and although there are a few leads with what appears to be PR depression there is no PR elevation in aVR and is also no ST elevation in all leads and/or T wave inversion. Squid syndrome ( reverse tako -tsubo syndrome) presents with ST depression and QTC prolongation. No J wave's are seen which would be associated with hypothermia, hypercalcemia, idiopathic VT or even Brugada syndrome.



The point of this question is to alert you that when elderly people complain of a "bad dream" or go through emotional/physical distress and then develop chest pain, and particularly when they complain of associated shortness of breath either at rest or on exertion, always keep this syndrome and its multiple variants in mind. Call EMS and get an EKG in the interim if you can, and if not one available call EMS and refer the patient to the hospital. Often the patient will minimize her/his symptoms and and will say "it's nothing and just felt bad".There is no reason to remember all the criteria and EKG features, as the answer lies in the patient's history. Often this is a benign syndrome but not always.Also this patient has 3+ ( on a scale of 4) mitral regurgitation and likely presented with crackles and left sided heart failure symptoms. The other video I attached is a NC female school bus driver , who ended up in a ditch and some of the kids were hurt . She was emotionally so shaken she developed also a stress cardiomyopathy

Attached articles

Here is the distribution of the answers of the initial 25 answers.

Lung ultrasound for the diagnosis of weaning-induced pulmonary oedema

Weaning-Induced Pulmonary Oedema (WIPO) is a common cause of failure of weaning from mechanical ventilation. The change in heart-lung interactions during Spontaneous Breathing Trials (SBT) can lead to WIPO, which can be detected by pulmonary artery occlusion pressure, left ventricular filling pressure, or extravascular lung water. Detection of multiple B lines by lung ultrasound may used to detect WIPO.

To test this hypothesis, a mixed population of ICU patients was enrolled. B-lines were counted in a rib short-axis scan at four points on the anterior chest. WIPO was diagnosed a posteriori by two experts using several criteria.

43 patients were included in the cohort, who had 27% WIPO overall and 52% WIPO in patients with failed SBT. The best accuracy to diagnose WIPO was reached when delta B lines were ≥6, with 88% sensitivity and 91% specificity, and with 79% of PPV. Accuracy was similar when considering only failed SBT trials.

The authors conclude that WIPO has a high incidence in mixed population of ICU patients, and that lung ultrasound may be used to diagnose WIPO with high accuracy using a cut-off of ≥6 B-lines counted on the anterior chest.

TAKE HOME MESSAGE

WIPO is a frequent complication of weaning from mechanical ventilation.Lung Ultrasound may be used to detect WIPO with high accuracy, when the number of B-lines on the anterior chest increases by ≥6.

REFERENCES

1) Ferré A, Guillot M, Lichtenstein D, Mezière G, Richard C, Teboul JL, Monnet X, Lung ultrasound allows the diagnosis of weaning-induced pulmonary oedema. Intensive Care Med. 2019 May;45(5):601-608. doi: 10.1007/s00134-019-05573-6. Epub 2019 Mar 12. PubMed PMID: 30863935.

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.