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ΕΠΙΣΤΗΜΟΝΙΚΑ ΚΙ … ΑΛΛΑ”από τον Ομ. Καθηγητή, Ιωάννη Γουδέβενο, 2.7.2024 – Περί τροπονίνης

Το ΕΣΥ στην … Εντατική και η Εντατική στα πρωινάδικα

Η Ματίνα Παγώνη δίνει τα τελευταία νέα για την υγεία του τραγουδιστή

Στο τέλος θα δείτε που στην ΕΛΛΑΔΑ μόνο στο  ΔΕΛΦΙΝΑΡΙΟ θα συζητάνε σοβαρά!

Aπο την άλλη πλευρά δεν μπορούμε να μη εξάρουμε τη στάση του 45 χρονου χειρουργού της Ευροκλινικής που εξέτασε τη   Πολυζωγοπούλου-Λύτρα. Πέρα απο το καθήκον δεν παρουσιάσθηκε σε κανένα κανάλι ή  ΜΚΔ  παρά τις αφόρητες πιέσεις που σίγουρα  θα δέχτηκε.

  Ανακοινώθηκε η σύνθεση του  think tank υγείας του ΣΥΡΙΖΑ.  Βαριά γιορτή θα πείτε αλλά και δω κανένα ς καρδιολόγος Νέος Πρόεδρος στο ΠΙΕΔΙΚΑΡ ο Χάρης Γράσσος!

Είπαμε ο Εm Brilakis  ανήκει στη κατηγορία των ομογενών που βοηθάει! Ετσι στο συνέδριο του καλύπτει τα έξοδα 3 ειδικευομένων- θα διαγωνιστούν στα ημιτελικά με  clinical cases- από τη Καρδιολογική του Χατζηκώστα!

Περι τροπονίνης συνέχεια…

Γυναίκα ηλικίας 55 ετών προσήλθε στα ΤΕΠ για αναφερόμενη συγκοπή. Η ΦΕ χωρίς ευρήματα. ΗΚΓ ΦΒΚ ρυθμό και η τροπονίνη 2 500ng/l( οι επόμενες 2900 και 1200). Οι υπερηχοι και η ΣΦ χωρίς ευρήματα

CT εγκεφάλου; Oγκος

Περίεργοι που είμαστε και εμείς οι γιατροί. Εκεί που οι οδηγίες  συνιστούν να χορηγήσουμε ένα φάρμακο δε το χορηγούμε και το αντίθετο. Ετσι συμβαίνει με την ασπιρίνη. Ενας στους 3  > 60 ετών to 2021 ελάμβανε ασπιρίνη για πρωτογενή πρόληψη στις USA.

Patrono Carlo*. Low-Dose Aspirin for the Prevention of Atherosclerotic Cardiovascular Disease(CVD). Eur Heart J 2024;Jun 6:[Epub ahead of print].

*προσκεκλημένος ομιλητής στο ALPIC 2013,14,15 στο Μέτσοβο. Περασμένα μεγαλεία !

The following are key points to remember from a review on low-dose aspirin for the prevention of CVD.

  1. Thirty years ago, an overview of 145 RTs of prolonged antiplatelet therapy for the prevention of death, MI), and stroke (vascular events), supporting the use of medium-dose (75–325 mg/day) aspirin for the prevention of vascular events.
  2. At low doses, aspirin completely blocks platelet cyclooxygenase (COX)-1 activity while largely sparing clinically relevant sites of COX-2 activity (e.g., endothelial cells of the vasculature and renal cells), because of its short half-life and resynthesis of any acetylated COX-2 in nucleated cells within a few hours.
  3. Aspirin has relatively simple pharmacokinetics, with no requirement for metabolic activation, ∼50% oral bioavailability, and 15- to 20-minute half-life. However, lower bioavailability of some enteric-coated preparations of low-dose aspirin and poor absorption from the higher pH environment of the small intestine may result in inadequate platelet inhibition, particularly in heavier subjects.
  4. In the ISIS 2, once-daily dosing with low-dose aspirin (162.5 mg) started within 24 hours of the onset of symptoms of a suspected MI produced highly significant reductions in 5-week vascular mortality  by 23%, nonfatal reinfarction by 49%, and nonfatal stroke by 46% in over 17,000 patients.
  5. Based on a large number RCTs, long-term (2- to 3-year) aspirin therapy confers conclusive net benefit on the risk of subsequent MI, stroke, or vascular death among subjects at high risk of vascular complications.
  6. In a meta-analysis of nine RCTs with 42,108 patients randomly allocated to a P2Y12 inhibitor (ticlopidine, clopidogrel, or ticagrelor) or aspirin, patients who received a P2Y12 inhibitor had a borderline reduction in the risk of MI compared with those who received aspirin (odds ratio, 0.81; 95% confidence interval [CI], 0.66–0.99). Risks of stroke, all-cause death, and vascular death did not differ between patients who received a P2Y12 inhibitor and those who received aspirin.
  7. In the ASPREE trial involving 19,114 healthy elderly persons (median age, 74 years) who did not have known CVD, the use of low-dose aspirin did not result in a significantly lower risk of CVD than placebo. 
  8. Low-dose aspirin appears to spare COX-1 and COX-2 activity in the GI) mucosa, by virtue of its short half-life and rapid resynthesis of the acetylated COX isozymes in nucleated epithelial cells. Chronic use of low-dose aspirin will yield an absolute excess of GI complications ranging from as low as 6 per 10,000 in a young person with no prior GI history to as high as 600 per 10,000 in a very old person with a prior complicated ulcer. Although PPIs, reduce the risk of peptic ulcer disease and its complications in a wide range of clinical circumstances, their use in patients taking antiplatelet drugs is still quite limited.
  9. Traditional nonsteroidal anti-inflammatory drugs and COX inhibitors share COX-2–dependent renal effects, which may acutely reduce renal function and impair blood pressure control. Low-dose aspirin, by virtue of its relative COX-1 selectivity, does not impair renal function or blood pressure control and does not increase the risk of heart failure.

10.Multiple lines of evidence support a chemo-preventive effect of aspirin against cancer, particularly tumors of the GI tract. These include observational studies suggesting a consistent association between regular aspirin use and reduced risk of esophageal, gastric, and colorectal cancer, and meta-analyses of post hoc, long-term follow-up of aspirin RCTs for primary and secondary prevention of CVD.

Προ φόρτωση στα ΟΣΣ:  εκεί που νομίσαμε ότι έχουμε τελειώσει.  STEMI pretreatment

Οι οδηγίες ESC ACS 2023 υποβάθμισαν(downgraded) τις συστάσεις για προ θεραπεία με αντιΑΜΠ στο STEMI από Ι στο ΙΙΒ(δηλ όχι προ φόρτιση). Eur Heart J. 2023;44:3720–3826.

Μικρή σε μέγεθος προοπτική καταγραφή από την Ισπανία  έδειξε ότι αν γνωρίζοντας τη γεωγραφία της περιοχής  και νομίζεται ότι ο ασθενής σας καθυστερήσει για prPCI μπορείτε να προ φορτίσετε.

 1,624 STEMI patients (mean age 63 years; 24 % female) undergoing prPCI between 2015 and 2019 In all, 1,033 received pretreatment with a P2Y12 inhibitor and the rest were treated in the cath lab. The median time difference between the two loading strategies was 88 minutes. The 30-day rate of MACE was 8.8%, with 55% events occurring within the first 72 hours of admission and approximately 40% happening within the first 24 hours. Those who received pretreatment had a lower rate of MACE at 30 days (7.5% vs 11.0%; adjusted HR 0.53; 95% CI 0.37-0.76). This was primarily driven by lower rates of all-cause mortality (adjusted HR 0.66; 95% CI 0.47-0.94), urgent TLR (adjusted HR 0.73; 95% CI 0.61-0.87), and definite stent thrombosis (adjusted HR 0.67; 95% CI 0.47-0.95). The risk of bleeding did not seem to differ between the treatment strategies (adjusted HR 0.47; 95% CI 0.26-0.86). If there’s going to be a time delay to get to the cath lab, you should be getting the antiplatelet drug on board as soon as possible

Παρ ότι πρόκειται για σύγχρονη αντιμετώπιση OΣΣ στη  πλειοψηφία των ασθενών χορηγήθηκε κλοπιδογρελη ( προ φόρτωση 75%,  όχι προφόρτωση 52% ). Στην  έξοδο τα ποσοστά χορήγησης κλοπιδογρέλης ήταν 37% και 44% αντίστοιχα.

Οι καταγραφές δεν αλλάζουν τις οδηγίες αλλά μη ανησυχείτε τρέχουν μελέτες.

Almendro-Delia M, Hernández-Meneses B, Padilla-Rodríguez G, et al. Timing of P2Y12 inhibitor administration in patients with STEMI undergoing primary PCI. J Am Coll Cardiol. 2024;83:2629-2639

ΣΙΔΗΡΟΘΕΡΑΠΕΙΑ και ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ:hot topic

Cheema B, Chokshi A, Orimoloye O, Ardehali H. Intravenous Iron Repletion for Patients With Heart Failure and Iron Deficiency: JACC State-of-the-Art Review. J Am Coll Cardiol 2024;83:2674-2689.

The following are key points to remember from a state-of-the-art review about intravenous (IV) iron repletion for patients with heart failure (HF) and iron deficiency:

  1. Guidelines from the AHA/ACC and ESC recommend IV iron replacement in patients with HFrEF and iron deficiency with or without anemia to improve functional status and quality of life(Class IIa και Class I αντίστοιχα). An additional update has been added to the ESC guidelines also recommending IV iron in patients with symptomatic HFrEF or HF with mid-range EF( Class 2A ).
  2. Iron deficiency can occur due to inadequate total body stores called absolute iron deficiency and is caused by nutritional deficiencies or blood loss. It can also be caused by inadequate access to stores despite normal store called functional iron deficiency. The gold standard for diagnosing iron deficiency is iron staining of bone marrow biopsy but due to the invasive nature of this study, in clinical practice, iron indices are used including ferritin, transferrin saturation (Tsat), and serum iron levels.
  3. Serum ferritin is an acute phase reactant that varies in inflammatory states such as HF, making it challenging to rely upon. Definition of iron deficiency in HF and for clinical trials in HF have been modeled off chronic kidney disease literature and suggest using ferritin <100 or ferritin 100-299 with Tsat <20%.
  4. Studies suggest that 1/3 of patients diagnosed with iron deficiency using ferritin and Tsat criteria as stated above have normal bone marrow iron stores. A Tsat level of <20% and serum iron level <13 μg/dL instead correlate more strongly with decreased bone marrow iron stores.
  5. Serum iron indices in HF fluctuate over time and can normalize even without iron replacement. However, those with persistent iron deficiency at 1 year had a higher mortality and those with normalized iron indices had a lower mortality in the absence of iron replacement. These observations raise the question of whether serum iron indices accurately reflect iron deficiency in all circumstances.
  6. Studies  suggest a detrimental effect of erythropoiesis-stimulating agents in HF. Darbepoetin use in HFrEF correlated with thromboembolic events and ischemic stroke.
  7. Three moderate-sized RCTs (FAIR-HF, CONFIRM-HF, and EFFECT-HF with 174-459 patients enrolled) suggest ferric carboxymaltose in HFrEF patients with iron deficiency (as defined by transferrin <100 or transferrin 100-299 with Tsat <20%) without anemia was associated with functional and subjective improvements. These trials largely included a majority White population with ischemic cardiomyopathy and a substantial burden of angina. In addition, EFFECT-HF used a controversial imputation strategy for patients who died during the trial and when this was abandoned, benefit with IV iron was no longer seen.
  8. Τhree larger sized trials  (AFFIRM-HF, IRONMAN, and HEART-FID with 1,132-3,065 patients enrolled) have not shown a benefit with IV iron in their primary composite endpoint. AFFIRM-HF was impacted by the COVID-19 pandemic. While IRONMAN showed a reduction in the secondary endpoint of CV death or hospitalization for stroke, HF, or MI, this was not replicated in AFFIRM-HF. HEART-FID had a hierarchical composite primary endpoint of death, HF hospitalizations at 12 months, and change in 6-minute walk test that was negative.
  9. IV iron bypasses typical regulation of iron mediated by hepcidin resulting in potential damage to endothelial cells as elemental iron produces free radicals. Oral iron is tightly regulated by hepcidin, making iron toxicity unlikely but is associated with GI side effects. In humans, IV iron has been associated with reduction in endothelial cell health. It is also associated with higher risk of infection than oral iron and hypophosphatemia. Current HF trials do not have adequate long-term data on iron safety nor do they compare oral iron to IV iron.

10.Newer data suggest there may be alternative serum markers of iron deficiency such as soluble transferrin receptor (sTFR) but these have not been investigated in HF. Alternate measures of iron deficiency are needed in HF due to variability in serum iron indices seen with HF treatment without iron replacement.

10.Newer oral formulations such as oral sucrosomial iron suggest a better GI side-effect profile and are being studied in HF with preserved EF and HFrEF patients compared with IV iron.

  1. Authors of this review use IV iron in hospitalized HF patients with Tsat <20% and serum iron <13 μg/dL. For other HF patients not meeting these criteria but with ferritin <100 or 100-299 with Tsat <20%, they use oral iron. However, oral iron has yet to be evaluated in a clinical trial in HF. They do not use IV iron in patients with ACS and use serum ferritin only when levels are very low.

Tαυτόχρονη δημοσίευση στο Circulation May 24.  Milton Packer, Stefan D. Anker, Javed Butler, et al. Redefining Iron Deficiency in Patients With Chronic Heart Failure. 1161/CIRCULATIONAHA.124.068883

Πρώτη γραμμή: “biological function”;

2η γραμμή “triggers and biological significance”;

3η γραμμή “diagnostic utility”; 

4η περιγράφει “assay limitations”.

H Ψέριμος είναι νησάκι απέναντι στη Κάλυμνο και έχει περίπου 30 μόνιμους κατοίκους!  Τα αιώνια προβλήματα με τους αγροτικούς γιατρούς.  Αν δεν δώσεις διαπιστευτήρια στο καφενείο ή στους νταλαβερτζήδες(κράχτες) του χωριού δεν έχεις  μοίρα

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