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1.
J Am Heart Assoc ; 13(6): e032951, 2024 Mar 19.
Artigo em Inglês | MEDLINE | ID: mdl-38471832

RESUMO

BACKGROUND: Cardiogenic shock (CS) is a significant complication of Takotsubo syndrome (TTS), contributing to heightened mortality and morbidity. Despite this, the Society for Cardiovascular Angiography and Interventions (SCAI) staging system for CS severity lacks validation in patients with TTS and CS. This study aimed to characterize a patient cohort with TTS using the SCAI staging system and assess its utility in cases of TTS complicated by CS. METHODS AND RESULTS: From a TTS national registry, 1591 consecutive patients were initially enrolled and stratified into 5 SCAI stages (A through E). Primary outcome was all-cause in-hospital mortality; secondary end points were TTS-related in-hospital complications and 1-year all-cause mortality. After exclusions, the final cohort comprised 1163 patients, mean age 71.0±11.8 years, and 87% were female. Patients were categorized across SCAI shock stages as follows: A 72.1%, B 12.2%, C 11.2%, D 2.7%, and E 1.8%. Significant variations in baseline demographics, comorbidities, clinical presentations, and in-hospital courses were observed across SCAI shock stages. After multivariable adjustment, each higher SCAI shock stage showed a significant association with increased in-hospital mortality (adjusted odds ratio: 1.77-29.31) compared with SCAI shock stage A. Higher SCAI shock stages were also associated with increased 1-year mortality. CONCLUSIONS: In a large multicenter patient cohort with TTS, the functional SCAI shock stage classification effectively stratified mortality risk, revealing a continuum of escalating shock severity with higher stages correlating with increased in-hospital mortality. This study highlights the applicability and prognostic value of the SCAI staging system in TTS-related CS.


Assuntos
Choque Cardiogênico , Cardiomiopatia de Takotsubo , Humanos , Feminino , Pessoa de Meia-Idade , Idoso , Idoso de 80 Anos ou mais , Masculino , Choque Cardiogênico/diagnóstico , Choque Cardiogênico/etiologia , Choque Cardiogênico/terapia , Prognóstico , Cardiomiopatia de Takotsubo/diagnóstico , Cardiomiopatia de Takotsubo/diagnóstico por imagem , Morbidade , Angiografia , Mortalidade Hospitalar
2.
Eur Heart J Case Rep ; 7(10): ytad508, 2023 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-37900663

RESUMO

Background: D-Transposition of the great arteries (d-TGA) is characterized by the aorta positioned above the right ventricle and the pulmonary artery above the left ventricle. Acute pulmonary artery dissection (PAD) is a rare and often lethal condition. We present a case report of acute PAD in an adult with d-TGA and pulmonary hypertension. Case summary: A 49-year-old male with history of d-TGA palliated with an atrial switch (Mustard) operation, pulmonary venous baffle stenosis treated percutaneously, chronic pulmonary hypertension (mixed group 1 and 2), and severe dilatation of pulmonary arteries (pulmonary trunk of 75 mm) presented to the emergency department with chest pain and acute respiratory failure. Blood pressure was 106/78 mmHg, heart rate 93 b.p.m., and oxygen saturation 88% on room air. A computed tomography (CT) scan showed acute right PAD. He was not considered suitable for surgery nor percutaneous procedure. Epoprostenol was initiated to reduce parietal stress, but after initial stabilization, pulmonary venous stent baffle gradient increased and acute pulmonary oedema occurred. Epoprostenol was withdrawn, and furosemide was initiated, with good clinical response. A follow-up CT scan showed dissection morphological stabilization and false lumen thrombosis, and the patient was discharged. Discussion: Pulmonary hypertension and previous pulmonary artery dilatation are reported as the main underlying conditions leading to PAD. No previous cases of PAD are described in patients with history of d-TGA and atrial switch procedure. Evidence regarding the best treatment of PAD is lacking, but it seems reasonable to reduce parietal stress using pulmonary vasodilators. Nevertheless, in patients with post-capillary pulmonary hypertension, pulmonary vasodilatation may cause important pulmonary congestion.

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