European Heart Journal: Acute Cardiovascular Care最新文献

Background and aims: Low-density lipoprotein cholesterol (LDL-C) is causally associated with myocardial infarction (MI). However, MI covers two clinically different entities: ST-segment elevation MI (STEMI) and non-STEMI (NSTEMI). We aimed to assess whether high LDL-C confers greater risk of STEMI than NSTEMI in statin-treated patients with ischemic heart disease (IHD).

Methods: We included statin-treated patients with IHD determined by coronary angiography from the Western Denmark Heart Registry between 2011-2020. LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C) levels were measured within 1 year after coronary angiography. The risk of STEMI and NSTEMI was estimated as adjusted hazard ratios (aHR). The comparison of STEMI versus NSTEMI and 30-day mortality after STEMI versus NSTEMI was estimated as adjusted odds ratios (aOR).

Results: The study included 36,739 statin-treated patients with IHD: 26,178 (71%) men, median age 66 years. During median follow-up of 4.9 years, 531 STEMI and 1,614 NSTEMI events occurred. Per 1 mmol/L higher LDL-C, the aHRs of STEMI and NSTEMI were 1.43 (95% CI: 1.30-1.57) and 1.23 (95% CI: 1.16-1.31), corresponding to an aOR of 1.18 (95% CI: 1.04-1.32) for STEMI versus NSTEMI. Patients at LDL-C goal ≤1.4 mmol/L versus >2.2 mmol/L had a lower risk of STEMI and NSTEMI, with 22% lower odds of STEMI than NSTEMI. Results were similar for non-HDL-C.STEMI was associated with higher 30-day mortality than NSTEMI: aOR 1.62 (95% CI: 1.02-2.57).

Conclusions: High LDL-C confers greater risk of STEMI than NSTEMI in statin-treated patients with IHD. This is important given the higher early mortality associated with STEMI.

Background: Electrical storm (ES) is a highly heterogeneous condition with wide-ranging clinical presentations. The absence of standardized classification hampers risk stratification and limits effective multidisciplinary coordination.

Objective: To develop a classification system based on simple clinical characteristics and stratify 30-day mortality in ES patients.

Methods: Patients admitted to intensive care units for ES between 2010-2023 across four tertiary centers were retrospectively included. The five-stage STORM severity-response classification, based on treatment intensity during hospitalization, incorporated four clinically relevant parameters: signs of acute heart failure or hemodynamic instability, need for inotropes or vasopressors, use of advanced supportive therapies (including deep sedation) and renal replacement therapy, and implementation of mechanical circulatory support. The primary outcome was all-cause mortality at 30 days.

Results: 788 patients were included. The cohort was predominantly male (84.3%), with median age 66.0 years (57.0-74.0). The majority had ischemic cardiomyopathy (65.6%), with median LVEF 30.0% (20.0-45.0). According to the STORM classification, 421 patients (53.4%) were categorized as STORM-1, 45 (5.7%) as STORM-2, 86 (10.9%) as STORM-3, 220 (27.9%) as STORM-4, and 16 (2.0%) as STORM-5. Overall, 117 patients (14.8%) died within 30 days. A stepwise increase in 30-day mortality was observed across STORM stages-5.0%, 6.7%, 20.9%, 30.5%, and 50.0% for stages 1 through 5, respectively (p<0.01).

Conclusion: The STORM classification may facilitate standardized multidisciplinary management strategies and effectively stratifies 30-day mortality risk in ES patients, ranging from 5% in stage 1 to 50% in stage 5. Further prospective studies are warranted to validate our findings.

Background: Contemporary guidelines support the use of a pharmaco-invasive (PI) strategy with immediate transfer to a percutaneous coronary intervention (PCI)-capable hospital for ST-elevation myocardial infarction (STEMI) when timely primary PCI (pPCI) is unattainable. However, when reperfusion with fibrinolysis fails to occur, rescue PCI is recommended.

Methods: In a pre-specified analysis from STREAM-2, we explored patients randomized to PI treatment and compared those receiving half-dose tenecteplase who required rescue intervention to those with successful fibrinolysis undergoing scheduled angiography. To provide context for those randomized pPCI, we also explored the relationship between site of randomization, i.e., community hospital (CH) versus ambulance on clinical outcomes. Resolution of ST-elevation following angiography and the composite of 30-day all-cause death, shock, heart failure and reinfarction, as well as safety, reflected by stroke and non-intracranial bleeding, were measured.

Results: Of the 583 patients in the current study, 168 patients required rescue intervention [43.5%], 218 patients had successful fibrinolysis scheduled for angiography and 197 were randomized to pPCI. Rescue PCI patients, compared to those undergoing scheduled angiography, had less ST resolution ≥50% (76.3% versus 92.5%, P<0.001) and worse clinical composite outcomes at 30 days (16.7% versus 6.0%, P<0.001) with a higher risk of intracranial hemorrhage (2.4% versus 0.5%). Intermediate outcomes were observed for patients undergoing pPCI (ST resolution ≥50%: 78.7%; 30-day composite outcome: 12.2%). Rescue intervention deployed in CH patients required 10 minutes longer compared to ambulance patients: however, there was similar ST resolution ≥50% (72.2% versus 80.5%, P=0.219) and comparable 30-day composite outcome (17.6% versus 15.7%, relative risk [RR] 0.97, 95% confidence interval [CI] 0.50 - 1.87), irrespective of location. pPCI required 48 minutes longer in CH patients, but resulted in similar outcomes to ambulance patients (ST resolution ≥50%: 77.0% versus 80.2%, P=0.595; 30-day composite outcome: 9.3% versus 15.6%, RR 1.57, 95% CI 0.72-3.41, respectively).

Conclusion: Contemporary PI with half-dose tenecteplase in older patients requiring rescue intervention led to less ST resolution and worse 30-day outcomes compared to those with successful fibrinolysis receiving scheduled angiography. Notably, delays to deploying rescue PCI in CH patients were shortened over those previously achieved thereby resulting in similar outcomes to those randomized in the ambulance. Our results reinforce the benefits of functional hub and spoke models with rapid transfer to a PCI-capable facility.

Aims: Acute heart failure (AHF) is a leading cause of frequent hospitalizations and poor outcomes. While chronic HF is treated with guideline-directed medical therapy, acute hospital care often requires loop diuretics, vasodilators, inotropes, and vasopressors. This study aimed to evaluate the inpatient use, dosing, and determinants of guideline-recommended therapies in patients hospitalized with AHF.

Methods and results: This nationwide, register-based cohort study included 6,009 patients aged ≥45 years hospitalized with AHF with (left ventricular ejection fraction [LVEF] ≤40%) in Denmark from 2018-2023. Data from the Danish Heart Failure Registry were linked to national healthcare registers. The main outcomes were inpatient use and doses of loop diuretics, vasodilators, inotropes, and vasopressors. Loop diuretics were used in 88.7% of patients (median dose [MD] of furosemide: 50 mg parenteral, 40 mg oral). Vasodilators were administered to 36.1% (MD of nitroglycerin: 30 mg parenteral, 7.5 mg oral). Inotropes were administered to 3.0%, including dopamine (0.5%), dobutamine (1.0%), milrinone (0.9%), and levosimendan (1.1%). Vasopressors were used in 8.4%, with norepinephrine (7.3%) and epinephrine (2.0%). Older patients (≥75) had lower prevalence of vasodilator, inotrope, and vasopressor use. Severe HF (LVEF <25%) was associated with lower prevalence of vasodilator and vasopressor use. In contrast, chronic kidney disease and recurrent HF hospitalization were linked to higher prevalence of use of all AHF therapies.

Conclusions: Loop diuretics were widely used, while vasodilators, inotropes, and vasopressors had lower utilization. The observed variation in treatment reflects complexity of inpatient AHF management, warranting further studies to assess treatment outcomes.

Aims: There are limited clinical data for beta blockers in Takotsubo syndrome (TTS). This real-world analysis aims to evaluate the impact of beta-blockers on all-cause mortality in TTS.

Methods and results: This retrospective analysis was conducted using the Global Collaborative Network of the TriNetX database. Patients with TTS were identified between 01/01/2005 and 06/06/2025 and stratified based on post-diagnosis beta-blocker use. Propensity-score matching using the greedy nearest-neighbor matching was utilized to balance the cohorts. Outcomes of interest was in-hospital mortality at 1-, 3-, and 5-years. During the study period, 54,855 patients with TTS were identified (beta-blocker group 39,108, control: 15,747). The beta blocker group was on average older (71 vs 69.7 years), of white race (74.2% vs 68.9%), and had higher rates of comorbidities. Following matching, both cohorts had 14,268 patients each with a mean age of 70 years and well balanced in demographics, comorbidities, medications, and laboratory data. Matched cohort analysis demonstrated beta blocker use was associated with lower all-cause mortality at 1-year (risk ratio [RR]: 0.67; 95% confidence interval [CI]: 0.63-0.71], 3 years (RR: 0.78; 95% CI: 0.74-0.82), and 5 years (RR: 0.81; 95% CI: 0.76-0.84).

Conclusions: Beta blocker use in patients with TTS was associated with a lower risk of short- and long-term mortality up to 5 years.