Magnesium is one of the inconspicuous cations involved in multiple systems of the human body. Yet, laboratory evaluation of this ion is not routinely conducted. It plays a crucial role in the cardiac system, and abnormal levels can lead to arrhythmias by disrupting the flow of other ions involved in the cardiac membranes. This review aimed to highlight the common etiologies of hypomagnesemia and the fundamental roles of magnesium in the body with particular attention to the mechanism of action of magnesium related to suppression and termination of cardiac arrhythmias, as well as its crucial roles in the treatment of ventricular arrhythmias and reperfusion injuries after myocardial infarction.

Patients with chronic liver disease are systematically excluded from acute myocardial infarction (AMI) trials, and prior real-world data rely on administrative coding alone. Whether ICD-coded liver disease and laboratory-defined liver fibrosis identify the same patients, and whether they predict the same outcomes, is unknown. We conducted a single-center retrospective cohort study of 1037 consecutive adults admitted with AMI (ICD-10 I21.x) to a tertiary New York center between November 2022 and December 2024. The primary exposure was ICD-defined advanced liver disease (cirrhosis, hepatic failure, or portal hypertension/decompensation; n = 102). The secondary, lab-based exposure was the Fibrosis-4 (FIB-4) index calculated from earliest admission AST, ALT, and platelet count (computable in 1031 patients, 99.4%), stratified as low (3.25). Co-primary outcomes were invasive management (diagnostic angiography, percutaneous coronary intervention, or coronary artery bypass grafting) and in-hospital mortality. Multivariable logistic regression adjusted for age, sex, diabetes, chronic kidney disease, heart failure, and ST-elevation; the trend across FIB-4 tiers was assessed with the Cochran–Armitage test. Denominators throughout (including the 168/909 occult-fibrosis estimate) use the full exposure group as denominator under a missing-as-not-exposed convention; the four no-LD and two advanced-LD patients with missing FIB-4 are counted as non-advanced fibrosis for this calculation. Patients with ICD-defined advanced liver disease received invasive management less often (12.7% vs. 50.4%; adjusted odds ratio [aOR] 0.17, 95% CI 0.09–0.32) and died in hospital more often (43.1% vs. 7.9%; aOR 8.22, 95% CI 5.02–13.46) than patients without coded liver disease. Outcomes worsened monotonically across FIB-4 tiers (mortality 4.4% → 9.2% → 27.5%; invasive management 55.2% → 45.6% → 33.5%; both p < 0.001 by Cochran–Armitage trend test). Critically, 168 of 909 patients with no coded liver disease (18.5%) had FIB-4 > 3.25, representing a substantial population of unrecognized advanced fibrosis missed by clinical coding. Coded liver disease identifies a small, severely affected subgroup with markedly lower rates of invasive management and 6- to 8-fold higher mortality after AMI. Routine FIB-4 calculation, a free, three-variable lab score, identifies a much larger population with occult advanced fibrosis and graded excess risk that ICD codes miss entirely. Pending prospective validation, FIB-4 may serve as a low-cost adjunct to bedside risk stratification in AMI care.

Background: Dual-chamber leadless pacing with the Aveir DR system restores atrioventricular synchrony without transvenous leads. The labeled implant workflow calls for a separate delivery catheter for each device. The second catheter adds cost and adds steps to the procedure, and whether it is actually needed has not been examined in a large series. Objective: To describe the acute procedural feasibility, the rate of delivery-catheter malfunction, and the effect on direct disposable supply cost of implanting both devices of a dual-chamber leadless pacemaker system through one delivery catheter. Methods: We reviewed 102 consecutive patients who received a dual-chamber leadless pacemaker at a single center between February 2024 and February 2025, implanted by five operators at that center. Twenty earlier dual-chamber implants performed with two catheters, before the single-catheter workflow was adopted, precede the study period and are not part of this cohort. The right ventricular device was placed first in every case. The same catheter was then reloaded with the atrial device and used for the second implant, and a new catheter was opened only if the first one failed. We recorded acute implant success, catheter malfunction, procedure time, fluoroscopy time, complications through 30 days after implantation, and direct disposable supply cost. Results: Both devices were implanted through the original catheter in 100 of 102 patients (98.0%, 95% CI 93.1 to 99.8%). Two patients (2.0%, 95% CI 0.2 to 6.9%) needed a catheter exchange because of a mechanical failure that arose during ventricular deployment; in both, the ventricular device had been recaptured and redeployed with repeated torque beforehand. No catheter failed during atrial implantation. Mean time from sheath insertion to removal was 69 min, and mean fluoroscopy time was 16.0 ± 6.6 min. Two device dislodgements occurred (2.0%, 95% CI 0.2 to 6.9%), one intraprocedural and one a right atrial device that embolized the day after implant; neither was related to the delivery catheter. There was no perforation, pericardial effusion, or access-site complication, and no other complication occurred in any patient through 30 days after implant. Omitting the second catheter lowered direct disposable supply cost by USD 1505 per case, 6.1% of the USD 24,510 two-catheter supply total. Conclusions: With experienced operators, one delivery catheter completed both implants in 98% of cases and lowered disposable supply cost. The study is single arm aand the number of events is small, so these findings support feasibility, with 30-day freedom from complications of 98.0%, and a supply cost difference.

Background: Sepsis-associated cardiac dysfunction has historically been characterized as predominantly systolic, yet the burden of heart failure with the preserved ejection fraction (HFpEF) phenotype among patients with heart failure (HF) first documented during sepsis remains poorly defined. Methods: In a single-center retrospective cohort of adults (≥18 years) admitted to a tertiary-care hospital between 1 January 2022 and 31 December 2024, we identified patients whose first sepsis diagnosis (ICD-10) coincided with their first HF diagnosis (ICD-10 I50.x) during the same encounter, with no prior HF in the EHR. Patients were classified by ICD-10 subtype as HFpEF, HFrEF, combined, or unspecified; the unspecified group underwent echocardiographic reclassification when LVEF was documented. Demographics, selected comorbidities, peak inflammatory markers, and unadjusted in-hospital and subsequent-encounter outcomes were compared between HFpEF and HFrEF. Results: Of 924 patients with HF first documented during sepsis, 438 (47.4%) were ICD-10–coded HFpEF and 405 (43.8%) HFrEF. HFpEF patients were older (74.0 vs. 69.2 years; p < 0.001) and more often female (53.0% vs. 37.0%; p < 0.001), with higher prevalence of COPD exacerbation (21.5% vs. 13.1%; p = 0.004) and hypothyroidism (26.3% vs. 17.5%; p = 0.034). HFrEF patients exhibited higher peak lactate (2.88 vs. 2.48 mmol/L; p = 0.009) and procalcitonin (8.52 vs. 7.24 ng/mL; p = 0.011). Unadjusted in-hospital mortality (28.1% vs. 27.7%; p = 0.95), ICU admission (75.8% vs. 74.8%; p = 0.80), and length of stay did not differ. Subsequent encounters were descriptively more frequent after HFpEF (11.0% vs. 6.2%). Conclusions: ICD-10–coded HFpEF and HFrEF occurred at nearly equal frequency among adults with HF first documented during sepsis, challenging the systolic-centric paradigm. Despite distinct demographic and biochemical profiles, unadjusted in-hospital outcomes did not differ. These descriptive findings, limited by administrative-coding-based phenotype classification, the absence of multivariable adjustment, and unmeasured sepsis-severity and comorbidity variables, are hypothesis-generating and support phenotype-aware prospective study of HF arising during sepsis.