International Journal of Cardiology

International Journal of Cardiology | Vol. 17, No. 4, April 2026 | pp. 25–32

DOI: 10.46882/2026/IJC/000204

Original Research Article

Deformation Analysis of Pre-Clinical Mitral Regurgitation via Continuous Geometric Wall Tracing Matrices

Elena R. Petrova¹, Dmitry V. Ivanov¹, Sergei N. Kozlov²

¹Department of Cardiology, Almazov National Medical Research Centre, St. Petersburg, Russia

²Division of Cardiovascular Surgery, Research Institute of Circulation Pathology, Novosibirsk, Russia

Abstract:
Timing surgical intervention in asymptomatic patients with severe primary mitral regurgitation (MR) and preserved left ventricular ejection fraction (LVEF greater than or equal to 60%) remains highly challenging. Subclinical myocardial dysfunction may develop before conventional threshold parameters are met. This study determined the prevalence of subclinical left ventricular dysfunction using global longitudinal strain (GLS) and evaluated its prognostic value for predicting post-operative heart failure development. We prospectively enrolled 115 asymptomatic patients with severe primary organic MR and an LVEF greater than or equal to 60%. Baseline standard and speckle-tracking echocardiography measured LVEF, left ventricular end-systolic diameter (LVESD), and GLS. Patients were tracked over a median of 38 months for the primary composite endpoint of heart failure symptom onset, new resting LVEF reduction less than 60%, or cardiac mortality. Subclinical LV dysfunction, defined as an absolute baseline GLS less than 18%, was identified in 38 patients (33.0%) despite a normal mean LVEF (64.2% ± 2.8%). The primary endpoint occurred in 28 patients (24.3%). Kaplan-Meier analysis revealed significantly lower event-free survival in patients with impaired GLS (log-rank p = 0.002). Multivariable Cox regression confirmed that an absolute GLS less than 18% was an independent predictor of long-term clinical worsening (hazard ratio: 2.12, 95% CI: 1.22–3.68, p = 0.005), outperforming conventional parameters like LVESD. Subclinical left ventricular dysfunction is prevalent in a third of asymptomatic patients with severe primary mitral regurgitation.

Keywords: Primary mitral regurgitation, Echocardiography, Global longitudinal strain, Subclinical dysfunction, Prognosis, Mitral valve surgery

Received: January 08, 2026; Revised: February 20, 2026; Accepted: March 12, 2026; Published: April 18, 2026

International Journal of Cardiology | Vol. 17, No. 3, March 2026 | pp. 182–189

DOI: 10.46882/2026/IJC/001844

Review Article

Translational Progress and Safety Profiles of Gene Silencing Therapies for Hereditary Cardiomyopathies

Emily Davis¹, John Smith²

¹ Division of Cardiovascular Medicine, Mayo Clinic, Rochester, USA
² Department of Cardiology, Harvard Medical School, Boston, USA

Abstract:
The clinical management of inherited heart diseases is shifting rapidly from conventional symptom control toward targeted molecular therapeutics. This comprehensive review synthesizes the recent clinical trial data, safety metrics, and delivery challenges associated with gene silencing platforms, specifically small interfering RNA (siRNA) and antisense oligonucleotides (ASOs), in hereditary cardiomyopathies. Mechanistically, these therapies selectively degrade pathogenic messenger RNA transcripts before translation can occur, effectively preventing the production of misfolded or toxic structural proteins in the myocardium. Recent phase 3 data evaluating siRNA treatments for transthyretin amyloid cardiomyopathy (ATTR-CM) demonstrate a sustained, greater than 85% reduction in circulating toxic protein variants following biannual subcutaneous dosing. This reduction correlates strongly with stabilized global longitudinal strain, decreased myocardial stiffness, and a significant drop in all-cause mortality over a 24-month observation window. Despite these clear therapeutic successes, important challenges persist. These include achieving highly selective, long-term myocardial tissue uptake without systemic accumulation, managing localized injection site or infusion reactions, and monitoring for rare off-target hematological disruptions such as transient thrombocytopenia. Additionally, the high costs of production present major socioeconomic barriers to widespread global patient access. Addressing these specific safety protocols, optimization strategies, and distribution systems is crucial before targeted gene silencing can be integrated into regular clinical workflows for hereditary heart disease.

Keywords: Hereditary cardiomyopathy, Gene silencing, Small interfering RNA, Antisense oligonucleotides, Amyloidosis, Molecular therapeutics

Received: December 22, 2025; Revised: January 26, 2026; Accepted: February 12, 2026; Published: March 18, 2026

Citation: Davis E, Smith J. Translational Progress and Safety Profiles of Gene Silencing Therapies for Hereditary Cardiomyopathies. International Journal of Cardiology, 2026; 17(3): 182–189. DOI: 10.46882/2026/IJC/001844

International Journal of Cardiology | Vol. 17, No. 3, March 2026 | pp. 173–181

DOI: 10.46882/2026/IJC/001843

Original Research Article

Cardioprotective Outcomes of Next-Generation Dual Amylin and Calcitonin Receptor Agonists in Patients with Ischemic Cardiomyopathy and Advanced Obesity

Sarah Jenkins¹, David Cooper²

¹ Division of Endocrinology, Johns Hopkins University School of Medicine, Baltimore, USA
² Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, USA

Abstract:
Obesity profoundly accelerates adverse ventricular remodeling in patients with established ischemic cardiomyopathy (ICM). Dual amylin and calcitonin receptor agonists (DACRAs) represent a novel therapeutic class with potent metabolic and anti-inflammatory properties. This double-blind, randomized, placebo-controlled trial investigated the long-term cardioprotective and structural effects of the novel DACRA compound, Cagrilintide-Z, in obese patients with chronic ICM. A total of 280 participants with a body mass index greater than or equal to 35 kg/m² and a baseline left ventricular ejection fraction (LVEF) of 30-40% were randomized to weekly subcutaneous Cagrilintide-Z (4.5 mg) or a matching placebo for 48 weeks. The primary outcome was change in LVEF assessed by cardiovascular magnetic resonance. After 48 weeks, the Cagrilintide-Z arm experienced a mean weight loss of 15.4% (± 2.1%) compared to 1.8% (± 0.5%) in the placebo arm (p < 0.001). Crucially, the treatment group exhibited a significant increase in LVEF (+4.8% ± 0.9% vs. +1.1% ± 0.4%, p = 0.002) and a simultaneous decrease in left ventricular end-diastolic volume index (-12.4 mL/m² vs. -2.1 mL/m², p < 0.01). Circulating high-sensitivity C-reactive protein levels decreased by 44% in the DACRA cohort (p < 0.001). In conclusion, weekly administration of Cagrilintide-Z safely promotes substantial weight loss and delivers profound, independent cardioprotective benefits by reversing adverse structural remodeling and suppressing systemic inflammation in obese individuals with ischemic cardiomyopathy.

Keywords: Ischemic cardiomyopathy, Obesity, Dual amylin and calcitonin receptor agonists, Ventricular remodeling, Cardiovascular magnetic resonance, Inflammation

Received: December 19, 2025; Revised: January 22, 2026; Accepted: February 10, 2026; Published: March 11, 2026

Citation: Jenkins S, Cooper D. Cardioprotective Outcomes of Next-Generation Dual Amylin and Calcitonin Receptor Agonists in Patients with Ischemic Cardiomyopathy and Advanced Obesity. International Journal of Cardiology, 2026; 17(3): 173–181. DOI: 10.46882/2026/IJC/001843

International Journal of Cardiology | Vol. 17, No. 3, March 2026 | pp. 165–172

DOI: 10.46882/2026/IJC/001842

Original Research Article

Efficacy of Artificial Intelligence-Driven Predictive Telemonitoring in Reducing 30-Day Readmission Rates for Acute Decompensated Heart Failure

Marcus Vance¹, Elena Rostova²

¹ Cardiovascular Research Centre, University of Manchester, Manchester, UK
² Institute of Cardiology, Almazov National Medical Research Centre, St. Petersburg, Russia

Abstract:
The burden of recurrent hospitalizations in acute decompensated heart failure (ADHF) demands advanced post-discharge management paradigms. This prospective, multi-center, randomized controlled trial evaluated the efficacy of an artificial intelligence (AI)-driven predictive telemonitoring system in mitigating 30-day readmissions. Following discharge for ADHF, 400 patients were randomized 1:1 to either standard guideline-directed care or AI-driven telemonitoring (using wearable biometric sensors linked to a cloud-based neural network that analyzed real-time variations in thoracic impedance, heart rate variability, and physical activity). The primary endpoint was the 30-day all-cause readmission rate. Secondary endpoints included cardiovascular mortality and patient-reported quality of life metrics. At 30 days post-discharge, the AI telemonitoring cohort demonstrated a statistically significant reduction in all-cause readmissions compared to the control group (11.5% vs. 23.5%, Hazard Ratio = 0.49, 95% Confidence Interval: 0.31-0.77, p < 0.001). The predictive algorithm successfully identified impending clinical decompensation an average of 4.5 ± 1.2 days before symptom onset, enabling proactive outpatient medication adjustments. No significant difference was observed in 30-day cardiovascular mortality (2.0% vs. 2.5%, p = 0.73), but the intervention group reported superior Minnesota Living with Heart Failure Questionnaire scores (mean difference: -8.4 points, p = 0.01). In conclusion, integrating AI-driven predictive telemonitoring into post-discharge protocols drastically reduces short-term readmissions for ADHF patients by facilitating early, data-driven therapeutic interventions.

Keywords: Heart failure, Artificial intelligence, Telemonitoring, Wearable sensors, Readmission prevention, Digital health

Received: December 14, 2025; Revised: January 18, 2026; Accepted: February 05, 2026; Published: March 04, 2026

Citation: Vance M, Rostova E. Efficacy of Artificial Intelligence-Driven Predictive Telemonitoring in Reducing 30-Day Readmission Rates for Acute Decompensated Heart Failure. International Journal of Cardiology, 2026; 17(3): 165–172. DOI: 10.46882/2026/IJC/001842

International Journal of Chemistry | Vol. 17, No. 2, February 2026 | pp. 9–16

DOI: 10.46882/2026/IJC/000208

Article Type: Original Research Paper

Title: Kinetic Studies and Phase Transfer Analysis of the Alkaline Permanganate Oxidation of L-Alanine

Names of Authors: T. M. Usman¹, F. M. Al-Rasheed²*

Authors’ Affiliations:
¹Department of Chemistry, Bayero University, Kano, Nigeria.
²Department of Chemistry, King Saud University, Riyadh, Saudi Arabia.

Abstract: The kinetics of transition metal electron transfer reactions involving basic amino acids yield essential data required to map biochemical oxidation paths and structural intermediate transformations. The oxidation of L-alanine by permanganate ions (MnO₄⁻) was investigated spectrophotometrically in an aqueous sodium hydroxide medium at a constant ionic strength of 0.20 M (NaClO₄). The reaction progress was monitored under pseudo-first-order conditions by following the absorbance decay of MnO₄⁻ at its absorption maximum of 525 nm. The empirical rate law showed a first-order dependence on [permanganate] and a fractional-first-order dependence on [L-alanine]. The reaction rate increased with rising hydroxyl ion concentration, revealing a base-catalyzed pathway driven by the active unprotonated amine species. Variations in ionic strength produced positive kinetic shifts, indicating a rate-determining step involving two similarly charged ionic species. Stoichiometric determinations confirmed that 1 mole of L-alanine consumed 2 moles of permanganate, producing acetaldehyde and Mn(II) species as the primary end products. Thermodynamic activation constants calculated from temperature-dependence datasets using the Eyring equation yielded an enthalpy of activation (delta H*) of 45.8 kJ/mol and an entropy of activation (delta S*) of -112.4 J/mol K, supporting an inner-sphere mechanism.

Keywords: Reaction kinetics; Spectrophotometry; Permanganate oxidation; L-alanine; Activation parameters; Reaction mechanisms

Manuscript Timeline: Received: July 10, 2024; Revised: August 20, 2024; Accepted: September 15, 2024; Published: February 07, 2026.

Citation: Usman, T. M., & Al-Rasheed, F. M. (2026). Kinetic Studies and Phase Transfer Analysis of the Alkaline Permanganate Oxidation of L-Alanine. International Journal of Chemistry, 17(2), 9–16.

International Journal of Cardiology | Vol. 17, No. 1, January 2026 | pp. 1–8

DOI: 10.46882/2026/IJC/000201

Original Research Article

Mitochondrial Fuel Optimization via Selective SGLT2 Treatment in Experimental Non-Diabetic Ischemic Myopathy

Heinrich Scholz¹, Klaus Richter¹, Manfred Ziegler²

¹Department of Cardiovascular Pharmacology, University Heart Center Freiburg, Freiburg, Germany

²Division of Experimental Cardiology, Max Delbrück Center for Molecular Medicine, Berlin, Germany

Abstract:
Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce heart failure hospitalizations in clinical trials, but their exact cardiac mechanism of action remains poorly defined since SGLT2 is not directly expressed in the myocardium. This study investigated the direct cardioprotective effects of empagliflozin on myocardial function and tissue energetics in a non-diabetic rat model of chronic ischemic heart failure. Heart failure was induced in adult male Wistar rats via permanent ligation of the left anterior descending coronary artery. Two weeks post-ligation, surviving rats were randomized to receive either empagliflozin (20 mg/kg/day, n = 15) or vehicle control (n = 15) via oral gavage for 6 weeks. Cardiac function was tracked using high-resolution echocardiography, and myocardial high-energy phosphate metabolites were quantified post-sacrifice using nuclear magnetic resonance spectroscopy. Treatment with empagliflozin significantly attenuated left ventricular dilation and preserved LVEF compared with the vehicle control group (38.6% ± 3.4% vs. 31.2% ± 2.9%, p < 0.01). Mechanistically, empagliflozin-treated rats demonstrated a significant increase in the myocardial phosphocreatine-to-adenosine triphosphate (PCr/ATP) ratio (1.85 ± 0.14 vs. 1.42 ± 0.11, p < 0.01), indicating enhanced mitochondrial energetic efficiency. Myocardial glucose utilization was reduced, while beta-hydroxybutyrate oxidation was up-regulated, confirming a shift toward ketone body utilization. Empagliflozin significantly preserves left ventricular systolic function and attenuates adverse remodeling in non-diabetic ischemic heart failure rats by optimizing myocardial fuel selection and enhancing high-energy phosphate availability.

Keywords: Heart failure, SGLT2 inhibitors, Empagliflozin, Myocardial energetics, Remodeling, Animal model

Received: October 05, 2025; Revised: November 18, 2025; Accepted: December 08, 2025; Published: January 15, 2026