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?
3/8 To answer this question, we compared male patients with a propensity score matched group of female #takotsubo with similar distribution of age, kind of trigger, underlying comorbidities.
4/8 Despite matching, we found that male patients still suffered higher in-hospital mortality, albeit having similar long-term prognosis as compared with females
5/8 Trying to make some hypothesis: male patients are less prone to develop #takotsubo➡️when this happen, ⬆️adrenergic drive is likely at play, leading to ⬇️LVEF and ⬆️cardiogenic shock/in-hospital mortality
6/8 After the acute phase, LVEF substantially recovers. For the survivors, mortality is then mainly driven by underlying comorbid conditions, and so, males and matched comorbid females with #takotsubo have the same long-term outcome
7/8 In summary, male #takotsubo is a high-risk phenotype requiring close in-hospital monitoring and long-term follow-up. ❗️Different pathophysiologic mechanisms are likely involved❗️
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).