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).
3- First, despite recovery of ejection fraction, #Takotsubo might lead to long-term cardiac damage, at least in some patients (nice #WhyCMR studies by @dana_dawson16
and colleagues, ref #31 #32 #33).
4- Dyspnea at presentation might identify those in which uncomplete recovery could influence prognosis in the chronic phase: in the future, it would be interesting to investigate the prognostic relevance of #NativeT1#WhyCMR in these patients @dana_dawson16@v_puntmann@GoetheCVI
6- Hence, additionally, dyspnea could be the presenting symptom of those higher vulnerable patients (reads: highly comorbid) in which acute functional abnormalities of #Takotsubo lead to an “expressed heart failure phenotype”, otherwise not detectable.
7- In the chronic phase, cardiac function largely recovers, but higher comorbidity burden still exerts its action on prognosis: KM curves progressively diverge across years.
8- These hypotheses would need to be confirmed by specific studies. As for now, our data from >1000 patients would encourage assessment of symptoms at presentation in #Takotsubo to aid risk-stratification.
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(1/9) Interesting study recently published in @ehj_ed providing a comprehensive description of microvascular function in an animal model of 💔#takotsubo💔 - however, can we call it a microvascular disease? Some thoughts to challenge this view (thread 🧵)academic.oup.com/eurheartj/arti…
(2/9) The authors used transaortic contriction to elicit #takotsubo in mice. They performed it on mice null for Kv1.5 channels and double transgenic mice with inducible Kv1.5 (plus controls): this elegantly reiterates the role of microvascular dysfunction (MD)...
(3/9)...as a relevant predisposing or contributing factor for #takotsubo, yet it does not demonstrate its pivotal action. In an animal model of isoprenaline induced #takotsubo MD was absent minutes after ballooning onset, implying that...academic.oup.com/ehjcimaging/ar…
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
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)