BACKGROUND Guidelines recommend nonstatin lipid-lowering agents in patients at very high risk for major adverse cardiovascular events (MACE) if low-density lipoprotein cholesterol (LDL-C) remains ≥70 mg/dL on maximum tolerated statin treatment. It is uncertain if this approach benefits patients with LDL-C near 70 mg/dL. Lipoprotein(a) levels may influence residual risk. OBJECTIVES In a post hoc analysis of the ODYSSEY Outcomes (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trial, the authors evaluated the benefit of adding the proprotein subtilisin/kexin type 9 inhibitor alirocumab to optimized statin treatment in patients with LDL-C levels near 70 mg/dL. Effects were evaluated according to concurrent lipoprotein(a) levels. METHODS ODYSSEY Outcomes compared alirocumab with placebo in 18,924 patients with recent acute coronary syndromes receiving optimized statin treatment. In 4,351 patients (23.0%), screening or randomization LDL-C was <70 mg/dL (median 69.4 mg/dL; interquartile range: 64.3–74.0 mg/dL); in 14,573 patients (77.0%), both determinations were ≥70 mg/dL (median 94.0 mg/dL; interquartile range: 83.2–111.0 mg/dL). RESULTS In the lower LDL-C subgroup, MACE rates were 4.2 and 3.1 per 100 patient-years among placebo-treated patients with baseline lipoprotein(a) greater than or less than or equal to the median (13.7 mg/dL). Corresponding adjusted treatment hazard ratios were 0.68 (95% confidence interval [Cl]: 0.52–0.90) and 1.11 (95% Cl: 0.83–1.49), with treatment-lipoprotein(a) interaction on MACE ( P interaction = 0.017). In the higher LDL-C subgroup, MACE rates were 4.7 and 3.8 per 100 patient-years among placebo-treated patients with lipoprotein(a) >13.7 mg/dL or ≤13.7 mg/dL; corresponding adjusted treatment hazard ratios were 0.82 (95% Cl: 0.72–0.92) and 0.89 (95% Cl: 0.75–1.06), with P interaction = 0.43. CONCLUSIONS In patients with recent acute coronary syndromes and LDL-C near 70 mg/dL on optimized statin therapy, proprotein subtilisin/kexin type 9 inhibition provides incremental clinical benefit only when lipoprotein(a) concentration is at least mildly elevated. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402 )

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Sažetak. Kardijalnu sinkopu karakteriše nagli gubitak svijesti, najčešće bez prethodećih znakova i simptoma, a najčešći uzrok su poremećaji srčanog provođenja i ritma. Cilj rada bio je da se utvrdi da li postojeća arterijska hipertenzija doprinosi većoj učestalosti kardijalne sinkope. Ispitana su 42 pacijenata sa kardijalnom sinkopom. Svim pacijentima je urađena anamneza, fizikalni pregled, standardni EKG, te Holter monitoring EKG na osnovu čega su, kao uzroci kardijalne sinkope utvrđeni poremećaji srčanog provođenja i ritma. Svi pacijenti su imali uredan neurološki nalaz. Ispitivanjem je obuhvaćeno 19 žena, prosječne starosti 52,4 godine, i 23 muškarca, prosječne starosti 59,3 godine. Prema tome da li su imali normalnu ili povišenu arterijsku tenziju, pacijenti su raspoređeni u dvije grupe. Arterijsku hipertenziju i kardijalne sinkope imalo je 29 (69,04%) pacijenata (grupa A), dok je 13 (30,95%) imalo kardijalnu sinkopu i normalnu arterijsku tenziju (grupa B). Sa tahibradikardnim sindromom u a u grupi B 2 (15,38%). Kod pacijenata sa arterijskom hipertenzijom kardijalna sinkopa češće se javljala, a i svi pojedinačno analizirani poremećaji provođenja i ritma. Ključne riječi: Kardijalna sinkopa, Arterijska hipertenzija, Poremećaji srčanog ritmaSummary. Cardiac syncope is characterized with a sudden loss of consciousness, most often without prior signs and symptoms, and the most frequent causes are disorders of cardiac conduction and rhythm. The aim of the work was to establish whether the existing arterial hypertension contributes to higher incidence of cardiac syncope. Forty two patients with cardiac syncope were examined. All of the patients had their anamnesis, physical examination, standard ECG and holter ECG monitoring done, on the basis of which the disorders of cardial conduction and rhythm were established as the causes of the cardiac syncope. All patients had regular neurological findings. The examination included 19 women of average age of 52.4 and 23 men of average age of 59.3. According to the findingsnormal or increased arterial tension respectively, the patients were divided in two groups. The arterial hypertension and cardiac syncope were found in 29 (69.04%) patients (group A), while 13 (30.95%) patients had cardiac syncope and normal arterial tension (group B). In the group A, there were 5 (17.24%) patients with tachy-brady syndrome and, in the group B, there were 2 (15.38%); in the group A, there were 4 (13.79%) patients with AV nodal reentrant tachycardia and, in the group B, there were2 (15.38%); in the group A, there were 3 (10.34%) patients with bradycardia (heart frequency under 40 per minute), and in the group B, there was 1 (7.69%) patient; in the group A, there were 5 (17.24%) patients with VTs and, in the group B, there were3 (23.07%); in the group A, there were 6 (20.69%) patients with sinus pauses and, in the group B, there were 2 (15.38%); in the group A, there were 6 (20.69%) patients with A-V block of II/III degree and, in the group B, there were2 (15.38%). In patients with arterial ...

Background Pleural effusion refractory to diuretic treatment is frequent in advanced heart failure. Therapeutic thoracentesis (TT) is a time-honored practice, recently made simpler and safer by guidance with lung ultrasound. Purpose In order to elucidate safety of lung ultrasound-driven TT in refractory heart failure, we compared incidence of pneumothorax requiring surgical drainage in patients undergoing TT with or without lung ultrasound. Methods and results In a single-centre retrospective analysis we recruited 373 patients with heart failure with reduced ejection fraction (26 ± 12%), New York Heart Association class ≥3, and pleural effusion ≥ moderate at lung ultrasound. They underwent overall 493 TT. Evacuated pleural fluid by passive drainage was 1030 ± 534 mL. The maximal interpleural space was 73.6 ± 15.6 mm before, and 12.4 ± 3.1 mm after TT (p &lt; .001). Two groups of TT were identified ex-post: 462 guided by lung ultrasound (Group 1); 31 without ultrasound guidance (Group 2), performed by cardiologist/pneumologist lacking access to ultrasound machine or expertise in lung ultrasound). The rate of complications (pneumothorax) was 0/462 in Group 1 and 3/31 in Group 2 (0 vs 10%, p &lt; 0.001) Conclusion Lung ultrasound-driven TT of pleural effusion in decompensated heart failure patients is feasible and safe when performed by cardiologists guided by lung ultrasound. A blind TT without ultrasound guidance is associated with higher rate of pneumothorax, and should be avoided.