Myocardial edema largely represented, correlations with interstitial expansion, ECG changes and systolic function. Some considerations below 🧵
1/ In #takotsubo syndrome myocardial edema features the acute phase: #WhyCMR T1 and T2 mapping have the advantage of a parametric quantification of edema. T2 specific for water, but native T1 can read it too (ahajournals.org/doi/full/10.11…) and ECV not water-independent in this setting
2/ Several measurements approach were used (i.e. global, per slice, septal) with similar results obtained ➡️ septal ROI likely the best one, given higher reproducibility (ConSept study jcmr-online.biomedcentral.com/articles/10.11…)
3/ The higher the myocardial water content (⬆️native T1, T2 and ECV) the worse the systolic function. Interesting finding: basal segments had preserved circumferential strain BUT slightly increase mapping values 🟰 subtle edema.
5/ … the classic #takotsubo sub-acute ECG with diffuse T-wave inversion and long QT seems not related to septal T2 (absolute myocardial water content) BUT rather to edema dispersion (apex-base) – replication of data obtained by using T2-STIR sequences (heartrhythmjournal.com/article/S1547-…)
1/8 Males represent approx. 10% of #Takotsubo patients within the registry. As comapred with females, they have ⬆️comorbid burden (malignancies, COPD etc.), ⬆️physical trigger ⬇️LVEF, worse in-hospital and long-term outcome.
2/8 These results were expected, when looking at smaller previously published studies, but why is that? Is the #takotsubo attack itself worse in men or do they just suffer because of the vulnerable comorbid background?
1/ Premessa - “Nell’università italiana il reclutamento segue nei fatti logiche slegate dai regolamenti concorsuali ”
Senza polemiche e moralismi, se si nega questo stato dell’arte, si può interrompere qua la lettura
2/ Il reclutamento nell’accademia è fatto di cooptazione, in Italia come nel resto del mondo. Necessariamente, per selezionare, il giudizio deve essere espresso da chi è esperto della materia, il cortocircuito è inevitabile e i grandi grant internazionali non ne sono esenti
We found independent associations between increasing natriuretic peptide/hsTropT on one side and myocardial involvement as assessed by native T1 and T2 mapping on the other ➡️ cardiac biomarkers=cardiac involvement (not only reduced elimination). (1/3)
Is cardiac involvement characterized by diffuse fibrosis only? Likely not: increased T2=contribution of myocardial edema. ❗️❗️T2 decreases after hemodialysis, proportionally to revomed volume❗️❗️ (2/3)
1. Increase of troponin/BNP was common in our sample, higher in patients with worse in-hospital prognosis (consistently shown in literature). Take into account epidemiological characteristics of the population: older age, high rate of comorbidity and fatal outcome.
2. Troponin and BNP generally had parallel increase, both in relation to A) markers of disease severity (D-dimer, CRP, P/F) and B) pre-existing condition of vulnerability (age, previous CVD, renal insufficiency etc.). However,
1- Dyspnea was associated with both worse in-hospital and long-term outcome. Similarly described in AMI (ref #12 and #13) in which heart failure symptoms at presentation might reflect wider myocardial damage. Why is it so even for a “transient” condition such as #Takotsubo?
2- Dyspnea was independently associated with both higher cardiac impairment and comorbidity burden, intuitively linked to the worse prognosis in the acute phase. And long-term, after recovery of cardiac function? We tried to give two possible explanations (just hypothesis).