Summary PRIVATE-ATLANTIC (P2Y12 Receptor Inhibition with VASP Testing using Elisa kit during the ATLANTIC study) is a pre-specified substudy of the randomised, double-blind ATLANTIC trial in patients with ST-segment elevation myocardial infarction, designed to help interpret the main trial results. The primary objective of ATLANTIC was to assess coronary reperfusion prior to percutaneous coronary intervention (PCI) with pre- vs in-hospital ticagrelor 180 mg loading dose (LD). PRIVATE-ATLANTIC assessed platelet inhibition in 37 patients by measurement of vasodilator-associated stimulated phosphoprotein (VASP) platelet reactivity index (PRI) and VerifyNow platelet reactivity units (PRU) before angiogram (T1), immediately after PCI (T2), 1 (T3), and 6 (T4) hours (h) after PCI, and before next study drug administration (T5). The median time difference between the two ticagrelor LD was 41 minutes. Platelet reactivity was unaffected at T1 when measured by VASP-PRI (89.8 vs 93.9% for pre- and in-hospital ticagrelor, respectively; p = 0.18) or PRU (239 vs 241; p = 0.82). Numerical differences were apparent at T2 and maximal at T3. Morphine administration significantly delayed onset of platelet inhibition at T3 (VASP-PRI 78.2 vs 23.4% without morphine; p = 0.0116) and T4 (33.1 vs 11.0%; p = 0.0057). In conclusion, platelet inhibition in ATLANTIC was unaffected by pre-hospital ticagrelor administration at the time of initial angiogram due to the short transfer delay. The maximum difference in platelet inhibition was detected 1 h after PCI (T3). Morphine administration was associated with delayed onset of action of ticagrelor and appeared more important than timing of ticagrelor administration.
To assess the safety, feasibility, and prognostic value of stress cardiovascular magnetic resonance (CMR) in patients with pacemaker (PM).Between 2008 and 2021, we conducted a bi-centre longitudinal study with all consecutive patients with MR-conditional PM referred for vasodilator stress CMR at 1.5 T in the Institut Cardiovasculaire Paris Sud and Lariboisiere University Hospital. They were followed for the occurrence of major adverse cardiovascular events (MACE) defined as cardiac death or non-fatal myocardial infarction. Cox regression analyses were performed to determine the prognostic value of CMR parameters. The quality of CMR was rated by two observers blinded to clinical details. Of 304 patients who completed the CMR protocol, 273 patients (70% male, mean age 71 ± 9 years) completed the follow-up (median [interquartile range], 7.1 [5.4-7.5] years). Among those, 32 experienced a MACE (11.7%). Stress CMR was well tolerated with no significant change in lead thresholds or pacing parameters. Overall, the image quality was rated good or excellent in 84.9% of segments. Ischaemia and late gadolinium enhancement (LGE) were significantly associated with the occurrence of MACE (hazard ratio, HR: 11.71 [95% CI: 4.60-28.2]; and HR: 5.62 [95% CI: 2.02-16.21], both P < 0.001). After adjustment for traditional risk factors, ischaemia and LGE were independent predictors of MACE (HR: 5.08 [95% CI: 2.58-14.0]; and HR: 2.28 [95% CI: 2.05-3.76]; both P < 0.001).Stress CMR is safe, feasible and has a good discriminative prognostic value in consecutive patients with PM.
Abstract— Treatment of hypertensive patients with β-blockers reduces heart rate and decreases central blood pressure less than other antihypertensive drugs, implying that reducing heart rate without altering brachial blood pressure could increase central blood pressure, explaining the increased cardiovascular risk reported with β-blocker. We describe a randomized, double-blind study to explore whether heart rate reduction with the I f inhibitor ivabradine had an impact on central blood pressure. We included 12 normotensive patients with stable coronary artery disease, heart rate ≥70 bpm (sinus rhythm), and stable background β-blocker therapy. Patients received ivabradine 7.5 mg BID or matched placebo for two 3-week periods with a crossover design and evaluation by aplanation tonometry. Treatment with ivabradine was associated with a significant reduction in resting heart rate after 3 weeks versus no change with placebo (−15.8±7.7 versus +0.3±5.8 bpm; P =0.0010). There was no relevant between-group difference in change in central aortic systolic blood pressure (−4.0±9.6 versus +2.4±12.0 mm Hg; P =0.13) or augmentation index (−0.8±10.0% versus +0.3±7.6%; P =0.87). Treatment with ivabradine was associated with a modest increase in left ventricular ejection time (+18.5±17.8 versus +2.8±19.3 ms; P =0.074) and a prolongation of diastolic perfusion time (+215.6±105.3 versus −3.0±55.8 ms with placebo; P =0.0005). Consequently, ivabradine induced a pronounced increase in Buckberg index, an index of myocardial viability (+39.3±27.6% versus −2.5±13.5% with placebo; P =0.0015). In conclusion, heart rate reduction with ivabradine does not increase central aortic blood pressure and is associated with a marked prolongation of diastolic perfusion time and an improvement in myocardial perfusion index. Clinical Trial Registration— URL: https://www.clinicaltrialsregister.eu . Unique identifier: 2011-004779-35.
The appropriate duration of treatment with beta-blocker drugs after a myocardial infarction is unknown. Data are needed on the safety and efficacy of the interruption of long-term beta-blocker treatment to reduce side effects and improve quality of life in patients with a history of uncomplicated myocardial infarction.
On-admission coronary angiogram (CA) with angioplasty (percutaneous coronary intervention, PCI) may improve survival in patients resuscitated from out-of-hospital cardiac arrest (OHCA), but long-term survival data are scarce. We assessed long-term survival in OHCA patients managed with on-admission CA and PCI if indicated and compared survival rates in patients with/without acute coronary syndrome (ACS).Retrospective single-centre study including patients aged ≥18 years resuscitated from an OHCA without noncardiac cause, with sustained return of spontaneous circulation, undergoing on-admission CA with PCI if indicated. ACS was diagnosed angiographically. Survival was recorded at hospital discharge and at 5-year follow up. Survival probability was estimated by Kaplan-Meier survival curves.A total of 300 comatose patients aged 56 years (IQR 48-67 years) were included, 36% with ST-segment elevation. All had on-admission CA; 31% had ACS. PCI was attempted in 91% of ACS patients and was successful in 93%. Hypothermia was performed in 84%. Survival to discharge was 32.3%. After discharge, 5-year survival was 81.7 ± 5.4%. Survival from admission to 5 years was 26.2 ± 2.8%. ACS patients had better survival to discharge (40.8%) compared with non-ACS patients (28.5%, p=0.047). After discharge, 5-year survival was 92.2 ± 5.4% for patients with ACS and 73.4 ± 8.6% without ACS (hazard ratio, HR, 2.7, 95% CI 0.8-8.9, p=0.1). Survival from admission to 5 years was 37.4 ± 5.2% for ACS patients, 20.7 ± 3.0%, for non-ACS patients (HR 1.5, 95% CI 1.12-2.0, p=0.0067).OHCA patients undergoing on-admission CA had a very favourable postdischarge survival. Patients with OHCA due to ACS had better survival to discharge at 5-year follow up than patients with OHCA due to other causes.
