Funding Acknowledgements Type of funding sources: None. Introduction Historically, the prognosis of those women suffering a STelevation myocardial infarction (STEMI), has been worse compared to men. Some causal factors are presentation at later ages, atypical symptoms, lower perception of risk and less sensitivity of the health care providers. Purpose Our hypothesis is that there are still differences in the presentation of STEMI based on gender, which could be identified to guide new public campaigns in this perspective. Therefore our primary outcome is to find gender differences in symptoms and time delays in a cohort of STEMI patients, and secondary outcomes are differences in mortality and bleeding. Methods We conducted a retrospective analysis carried out in the Acute Cardiac Care Unit (ACCU) of a tertiary care hospital, where 50% of the medical staff are women. Patients hospitalized for STEMI for one year were included and a detailed caracterization of symptoms, time delays, and adverse events was recorded. Finally, the patients were classified according to gender, and differences in primary and secondary outcomes between both groups were analyzed. Results Between May/2020 and May/2021, 1056 patients were admitted to the ACCU, 33% were women. A total of 115 STEMI patients were included for the analysis, 21% were women. Basal characteristics of both groups were equivalent, except for a non significand trens towards less prevalence of peripheral arterial disease in women (0% vs. 11%; OR 0.890, IC 95% 0.828-0.957; p=0.089). Opressive chest pain was the most frequent symptom, but it was less frequent in women (75% vs. 91.4%, OR 0.284, IC 95% 0.085-0.948; p=0.033), whereas they presented more frequently with stabbing pain (13% vs. 2.4%, OR 6, IC 95% 1.073-38.35; p=0.035), and their pain was more frequently radiated towards the neck (28.6% vs. 4.9%, OR 7.7, IC 95% 1.1936-30.631; p=0.001), and associated to nausea/vomiting (45% vs. 1.3%, OR 5.809, IC 95% 1.930-17.486; p=0.001). There was a non-significant trend towards a longer time delay between pain onset and seek for help in women (185min IQR 747 vs. 60min IQR 454, p=0.098), being the other system time delays equivalent between both gender groups. Women had an increased bleeding risk, with a higher CRUSADE score (47.48 ± 22.92 vs. 28.60 ± 16.72, p=0.001) and higher incidence of bleeding events (12.55% vs. 0%, OR 11.68, IC 95% 9.82-13.29, p=0.001). There were no differences in the treatments administered or in mortality (12.5% vs. 14.3%, p=0.822). Conclusions Women suffering a STEMI more often reported stabbing chest pain, radiating to the neck, and associated to nausea/vomiting compared with men, and took longer to seek for help. These findings could help in the design of future campaigns to minimize time delays, targeting these different symptoms in female population.
Funding Acknowledgements Type of funding sources: None. Background Thrombocytopenia post transcatheter aortic valve implantation (TPPT) in its most severe manifestation is an independent predictor of mortality. However, mechanisms that favors TPPT remain unknown. Purpose To establish the prognostic value and risk factors of TPPT in a real-life population of patients treated with transcatheter aortic valve implantation (TAVI) in a tertiary hospital. Methods We analyzed retrospectively clinical, laboratory, echocardiographic and procedure-related variables from 203 consecutive patients, treated with TAVI between January 2019 and October 2021. Results This cohort had mean age of 82,3 ±5,9 years, 56% male, 83% hypertensive, 62% dyslipidemia, 35% diabetic, 20% chronic kidney disease, 22% chronic obstructive pulmonary disease, 32% coronary artery disease, 20% had previous ICP, 38% Atrial Fibrillation (AF), 18% peripheral arterial disease, 12% neurovascular disease, 23% history of cancer, 10% pacemaker carriers. 50% of TAVIs were balloon-expandable and 50% self-expandable. Mean procedure duration was 138 ±109min, size 26,6±3mm, contrast dose 233 ±88mL. During in-hospital stay 192/203 patients had TPPT. Platelets before TAVI, 187.000 (IQR 148.000-222.000) Vs a minimum post-TAVI (PlqMin) of 135.000 (IQR 105.000-164.000); P<0,05. Platelet fall (DeltaPlq) 48.000 ±38.000. We observed a Minimum Kidney clearance (ClMin) 46 ±20,75mL/min/m2, a maximum ultrasensitive Troponin-T (Tr-TusMax) 250 ±450 pg/L, a Maximum C Reactive Protein (PCRMax) 6,68 ±6,4, and a Minimum Hemoglobin (HbMin) 9,8 ±1,7 g/dL. 31/203 (15,3%) patients were exitus at the end of follow-up. We observed a non-lineal statistically significant association between TPPT quartiles and all-cause mortality (P<0,05): 21 exitus occurred in the extreme quartiles (1 and 4) while only 11 at the central ones (2 and 3). DeltaPlq was associated with PCRMax (Pearson 0,25; P<0,001), CliMin (Pearson -0,23; P0,005), HbMin (Pearson -0,27; P 0,001), AF. The only protective factor for DeltaPlq was history of previous ICP. Among exitus patients PlqMin was observed later than in survivors (3,5 vs 2,2 days; P<0,05). TPPT’s quartiles, previous ICP, time to PlqMin, HbMin, PCRMax and Tr-TusMax were the variables found to be independent associated with all-cause mortality (P<0,05). Conclusions The non-linear association between TPPT and mortality, the temporal relation between TPPT and mortality and the linear correlation between TPPT and HbMin and PCRMax suggest that late TPPT may have a mortality prognostic value through an increased risk of low Hb in the context of an increased inflammatory status. The fact that history of ICP was associated with les platelet fall suggests that revascularization, or ICP associated drug therapy, may confer protection against after TAVI mortality.
Funding Acknowledgements Type of funding sources: None. Background Aadverse left ventricle remodeling’s natural evolution without proper therapy leads to low left ventricle ejection fraction (LVEF) and high morbidity and mortality. LVEF evolution after discharge in patients with de novo LV dysfunction (≤40%) detected during an intensive cardiac care unit (ICCU) hospitalization is not well known. Purpose To characterize LVEF evolution after discharge in patient with de novo LV dysfunction (≤40%) detected during an Intensive Cardiac Care Unit (ICCU) admission according to etiology: ischemic etiology (IE)Vs non-ischemic etiology (NIE). Methods We retrospectively analyzed clinical, echocardiographyc, pharmacological and coronary angiography -related variables from 154 consecutive patients admitted from May 2020 to July 2022 in the ICCU of a tertiary hospital and whose LVEF at discharge was ≤40%. Patients were grouped according to LV dysfunction etiology in ischemic and non-ischemic. LVEF at follow-up was registered when available. Results This cohort had a mean age of 64.8 ±14 years and 127 (82%) were male. Mean left ventricle ejection fraction was 30 ±6.8%. Among them, 119 (77%) had ischemic etiology (IE) and 35 (23%) non-Ischemic (NIE). Inotropes during admission were required in 29 (19%) and 151 (98%) were studied with coronary angiography. 70 (46%) were also studied with MRI during hospitalization; 35 (23%) had right ventricular dysfunction (RVD) and 39 (25%) had any kind of bundle branch block at discharge’s EKG. At discharge, 121 (78%) received betablockers (BB), 69 (45%) received Angiotensin Converser Enzyme Inhibitor (ACEI), 17 (11%) received Angiotensin Receptor Blocker (ARB), 24 (16%) received sacubitril-valsartan (ARNI), 88 (57%) received Mineralcorticoid Receptor Antagonist (ARM) and 39 (25%) received Sodium-Glucos type-2 inhibitors. At discharge, LVEF in patients with IE was 31 ±6% and 27 ±8% in NIE (p=0,01). Follow-up echocardiography was available in 119 (77%) of them. Mean last available follow-up LVEF was 46% ±11 in NIE while among IE was 40% ±11 (p=0,02). LVEF increase was of 17±11% in NIE and 9±9% in IE (p=0,0004). Among all, 36 patients normalized LVEF, 14 (50%) in NIE group and 22 (25%) in IE (P=0.01). In a multiple linear regression model adjusting by age, sex, QRS duration, left bundle branch block, TRC implantation and modifying-disease drugs, NIE etiology was independently associated with a 7,6% increase in LVEF compared to IE (p=0,003). Conclusions Our findings support that LVEF improvement after admission to ICCU with de novo LV dysfunction is strongly dependent on etiology. Patients with NIE tend to have an initial worse LVEF but greater improvement at follow-up.
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