BACKGROUND Severe coronary calcification remains one of the most challenging scenarios in interventional cardiology, predisposing to stent underexpansion, device entrapment, and procedural complications. CASE SUMMARY A 71-year-old man had a history of hypertension and dyslipidemia for 14 years, and presented with exertional chest pain for two days before admission. During initial percutaneous coronary intervention (PCI) for a calcified left anterior descending artery (LAD) lesion, the coronary stent balloon shaft fractured and became entrapped. Percutaneous retrieval failed; emergent open-heart surgery with coronary endarterectomy successfully extracted the fractured coronary stent balloon shaft and two embedded stents, followed by saphenous vein grafting. Two months later, recurrent angina with dynamic electrocardiographic changes prompted coronary computed tomography angiography, revealing native LAD occlusion at the anastomosis with significant diagonal branch disease. During re-PCI, intravascular ultrasound (IVUS) identified a 270° calcific arc; intravascular lithotripsy (IVL) balloon rupture occurred on the second pulse cycle. The balloon was retrieved; high-pressure non-compliant balloon dilatation achieved calcium fracture, and three drug-eluting stents were implanted with TIMI 3 flow. CONCLUSION This case sequentially documents three rare complications with complete photographic documentation, providing practical lessons on calcium preparation, coronary endarterectomy as salvage, IVUS guidance, and IVL rupture management.
BACKGROUND Mitochondria are considered a promising target for the treatment of cardiovascular disease. However, there has not been a direct association confirmed between mitochondrial ultrastructure in cardiac myocytes and cardiovascular death (CVD) in patients with heart failure (HF). AIM To evaluate the association between mitochondrial ultrastructure in cardiac myocytes and CVD in patients with HF who underwent coronary artery bypass grafting (CABG). METHODS It was a prospective study of HF patients that used electron microscopy of human cardiac myocytes. A total of 40 patients with HF (left ventricular ejection fraction < 50%) with coronary artery disease who underwent CABG were included (ClinicalTrials.gov: NCT05770349). Right atrial appendage biopsies were obtained during CABG. Ultrastructural analysis of mitochondria was performed using a JEM-1400 transmission electron microscope. The “Total area of interfibrillar mitochondria” and the “Ratio of mitochondrial membrane lengths” were calculated. Patients were followed for 12 months: 6 CVDs were recorded (15%). Statistical analysis was performed using IBM SPSS Statistics version 21; statistical significance was defined as P < 0.05. RESULTS From 3 to 5 Longitudinal sections were examined at 5000 × magnification and at 15000 × magnification for each patient (a total of over 250 micrographs were analyzed). The median of the total area of interfibrillar mitochondria was 41% (34; 63); the median of the ratio of the outer membrane length to the inner mitochondrial membrane length was 30% (22; 36). Univariate analysis demonstrated statistically significant differences between the ratio of mitochondrial membrane lengths in patients with and without CVD [29% (20, 33.5) vs 41% (35, 45), P = 0.001]. Patients with CVDs were also more often hospitalized due to HF before CABG and had a long duration of hospitalization after CABG. CONCLUSION A disruption in the mitochondrial ultrastructure in cardiomyocytes in the right atrial auricle might be associated with the development of CVD in patients with HF who underwent CABG.
BACKGROUND Diabetic cardiomyopathy (DCM) is characterized by ventricular remodeling and cardiac dysfunction, with limited therapies targeting the underlying myocardial remodeling process. AIM To investigate the effects of 5-methoxytryptophan (5-MTP) on cardiac structure and function in a rat model of DCM. METHODS Forty-eight Sprague-Dawley rats with DCM induced by a high-fat, high-fructose diet and streptozotocin (25 mg/kg) were randomized to a control group or 5-MTP treatment groups (25 mg/kg, 50 mg/kg, or 100 mg/kg). Animals were evaluated after 8 days, 16 days, or 32 days of treatment. Cardiac structure and systolic and diastolic functions were assessed by echocardiography, and serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured and compared among groups. RESULTS 5-MTP significantly reduced NT-proBNP levels after 16 days and 32 days of treatment (vs controls; P = 0.029 and P < 0.05, respectively) but not after 8 days. At day 8, 5-MTP significantly reduced left ventricular end-diastolic diameter (LVEDD; P = 0.026) and left ventricular end-systolic diameter (LVESD; P = 0.044). Significant reductions in LVEDD and LVESD from baseline were observed in the 25 mg/kg and 50 mg/kg treatment groups. Preservation of interventricular septal thickness in diastole and left ventricular posterior wall thickness in diastole was observed during the early treatment phase. However, these structural effects were not maintained after 16 days or 32 days of treatment. No significant improvements in systolic or diastolic function were observed in any treatment group. CONCLUSION 5-MTP reduced NT-proBNP levels and attenuated early structural remodeling in this rat model of DCM, although these structural effects were not sustained nor accompanied by improvements in cardiac function. Additional studies are needed to determine whether alternative dosing strategies or longer treatment durations can produce durable structural and functional benefit.
BACKGROUND Right heart thrombi (RHT) are associated with high mortality in patients with pulmonary embolism (PE). Thrombolytic therapy (TLT) and anticoagulation therapy (ACT) are the main treatment options. However, the optimal treatment strategy remains controversial due to a lack of randomized controlled trials. AIM To compare the efficacy and safety of TLT vs isolated ACT in patients with RHT and PE. METHODS We searched PubMed, Scopus, and Wiley Online Library from database inception to January 20, 2026, using a comprehensive strategy combining terms for RHT (including “right heart thrombus”, “right ventricular thrombus”, “atrial thrombus”, “thrombus in transit”), PE (“pulmonary embolism” OR “PE”), and thrombolysis (“thrombolysis”, “fibrinolysis”, “alteplase”, “tenecteplase”, and “streptokinase”). Inclusion criteria involved the following: Adults with confirmed RHT in acute PE; direct comparison of TLT + ACT vs ACT alone; intention-to-treat design; and case series with n > 5 per group. RESULTS Five observational studies (n = 205 patients) were included. TLT did not significantly reduce early all-cause mortality during hospitalization (OR = 0.36, 95%CI: 0.10-1.29, and P = 0.12). The heterogeneity of the results across the included studies was low and not statistically significant (I 2 = 18% and P = 0.30). TLT also did not significantly reduce all-cause mortality at 30 days (OR = 0.26, 95%CI: 0.04-1.64, and P = 0.15). The heterogeneity of the results across the included studies was moderate and not statistically significant (I 2 = 51% and P = 0.13). No subgroup analyses by hemodynamic status or thrombus type were possible. CONCLUSION Routine thrombolysis does not significantly reduce mortality compared with ACT alone in the overall cohort of RHT and PE patients.
Heart failure with preserved ejection fraction (HFpEF) remains a complex and heterogeneous syndrome without robust disease-modifying therapies. In this context, the retrospective analysis comparing beta-blockers and calcium channel blockers offers intriguing signals that beta-blockers may reduce all-cause mortality and heart failure hospitalizations, albeit at the expense of increased symptomatic bradycardia and treatment discontinuation. While these findings are not definitive, they highlight the potential relevance of heart-rate control and autonomic modulation in selected HFpEF phenotypes. This article discusses the clinical implications and limitations of the study by Mansoor et al published in World Journal of Cardiology , emphasizing the need for precision-based treatment strategies and calling for prospective trials to clarify the true prognostic impact of beta-blockers in HFpEF. Ultimately, the study reinforces the notion that therapeutic decisions in HFpEF must be individualized, integrating hemodynamic, rhythm-related, and comorbidity-driven considerations.
BACKGROUND A simple method for evaluating renal function is the estimated glomerular filtration rate (eGFR), which reveals prognostic implications. However, it is not yet known which equation should be applied to elderly Chinese individuals. AIM To compare the ability of Modification of Diet in Renal Disease (MDRD), Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), and the Asian/Chinese-modified equations and their predictive performance for clinical outcomes. METHODS A total of 3257 community-dwelling elderly Chinese participants (>= 65 years) in northern Shanghai were prospectively recruited in the present study. The GFR was estimated by creatinine-based MDRD and CKD-EPI and modified Asian/Chinese (c-aMDRD, aCKD-EPI, and cCKD-EPI) equations. The outcomes included major adverse cardiovascular events (MACE), cardiovascular mortality, and all-cause mortality. RESULTS The prevalence of eGFR < 60 mL/minute, based on different eGFR equations, ranged from 5.7% (c-aMDRD) to 16.5% (cCKD-EPI). The rate and risk of adverse outcomes were higher in patients with eGFR < 60 mL/minute (P < 0.05). Low eGFR (< 60 mL/minute) estimated by the c-aMDRD equation was associated with MACE and cardiovascular mortality, whereas low eGFR (< 60 mL/minute) estimated by the MDRD, c-aMDRD, CKD-EPI, aCKD-EPI, and cCKD-EPI equations was associated with all-cause mortality. The CKD-EPI, aCKD-EPI, and cCKD-EPI equations demonstrated significantly better predictive abilities for outcomes than the MDRD and c-aMDRD equations. CONCLUSION eGFR is an independent predictor of long-term outcomes. When estimated by the c-aMDRD equation, eGFR predicts MACE and cardiovascular mortality, while all equations predict all-cause mortality. The CKD-EPI, aCKD-EPI, and cCKD-EPI equations might be better than MDRD and c-aMDRD for risk stratification in the elderly Chinese population.
BACKGROUND Sodium-glucose co-transporter-2 inhibitors (SGLT-2Is), originally developed as anti-hyperglycemic medications, have emerged as cornerstone therapies for heart failure (HF) due to their cardioprotective effects. While their mortality benefits in HF are established, their role in patients with both HF and chronic obstructive pulmonary disease (COPD) remains unclear. AIM To evaluate the effects of SGLT-2Is in patients with HF with coexisting COPD, focusing on hospitalization, cardiovascular (CV) mortality, and drug-related complications. METHODS A systematic search of PubMed and Cochrane Library databases was conducted through February 17, 2025, for randomized controlled trials assessing the safety and efficacy of SGLT-2I in HF patients with coexistent COPD. Outcomes analyzed included composite first hospitalization for HF (HHF), CV death, all-cause mortality, and time-to-first HHF. Safety endpoints included drug discontinuation, serious adverse events (AE), volume depletion, major hypoglycemia, and renal AE, reported as relative risk (RR) with 95% confidence intervals. RESULTS Four trials (n = 3224) met inclusion criteria. Of these, 1727 patients (53.6%) received SGLT-2Is, while 46.4% received placebo. Compared with placebo, SGLT-2I significantly reduced the risk of composite HHF + CV death (RR = 0.80, 95%CI: 0.70-0.91, P = 0.0006, I 2 = 0%), HHF (RR = 0.77, 95%CI: 0.67-0.88, P < 0.0001, I 2 = 0%), and time-to-first HHF (RR = 0.75, 95%CI: 0.57-0.99, P = 0.04, I 2 = 47%). No significant differences were observed for CV death (RR = 1.01, P = 0.88) or all-cause mortality (RR = 0.94, P = 0.46). SGLT-2I did not increase risk of drug discontinuation, serious AE, renal AE, volume depletion, nor hypoglycemia. CONCLUSION In patients with HF and COPD, SGLT-2Is significantly reduce HF hospitalizations but do not lower all-cause mortality or CV mortality. Importantly, these drugs are well tolerated without excess AE, supporting their role as a safe therapeutic option in this population.
Many acute coronary syndromes or strokes occur in patients without arterial hypertension, diabetes mellitus, dyslipidaemia, or smoking habits. Therefore, it is essential to identify new cardiovascular (CV) risk factors, among which psychosocial elements are gaining increasing importance. Recent guidelines recognize psychosocial factors, such as mental stress, as risk modifiers that can improve risk prediction and clinical decision-making. Stressful stimuli are processed by cortical and subcortical brain regions, which, through the autonomic nervous system and the hypothalamic-pituitary-adrenal axis, generate neuroendocrine, hemodynamic, and immune changes. Mental stress can be acute or chronic. Acute stress results from sudden emotions and may trigger acute cardiac or cerebral events. Chronic stress, instead, develops from prolonged exposure to family, work, or financial problems. It can induce endothelial dysfunction and low-grade systemic inflammation, contributing to atherogenesis. Like physical stress tests, mental stress tests can provoke transient myocardial ischemia even without significant coronary obstruction. Therapeutic strategies reducing adrenergic activity or mitigating negative emotions associated with psychological stress may lower CV risk. This narrative review synthesizes current epidemiological data on interactions between stress and CV disease, explores potential mechanisms, and outlines future research directions for holistic treatment approaches.
BACKGROUND Metformin, a first-line therapy for type 2 diabetes mellitus (T2DM), has demonstrated potential preventive effects in high-risk individuals, especially in those with prediabetes. However, its role in preventing diabetes specifically among non-diabetic patients with established cardiovascular disease (CVD) remains unclear. Given the clinical and public health importance of diabetes prevention in this high-risk group, a systematic evaluation of existing evidence from randomized controlled trials is necessary to inform treatment strategies. AIM To investigate the effectiveness of metformin in preventing T2DM among patients with CVD who do not have diabetes. METHODS We searched PubMed, the Cochrane Central Register of Controlled Trials, and Scopus (from January 1, 2000 to July 31, 2024) for eligible randomized controlled trials (RCTs). A meta-analysis was conducted to evaluate the effect of metformin on the prevention of T2DM in patients with CVD and or coronary artery disease (CAD) without diabetes. RESULTS A total of 933 patients with CVD, all of whom had CAD, were included (470 in the metformin group and 463 in the control group). Fifty-six participants (11.9%) in the intervention groups and fifty-seven (12.3%) in the control groups developed T2DM. Patients with CAD receiving metformin showed no statistically significant difference in the development of T2DM compared with those not receiving metformin (odds ratio: 0.97; 95% confidence interval: 0.65-1.45; P = 0.89). Heterogeneity was rather low (Q = 2.38, P = 0.50; I 2 = 0%, 95% confidence interval: 0%-84%), showing satisfactory results across studies; however, the overall quality of evidence was very low. The results remained non-significant in subgroup analyses restricted to: (1) Studies conducted in similar countries; (2) Studies with or without post-intervention follow-up; (3) Studies with a predominance of male or female participants; (4) Studies with a mean participant age above or below 60 years; (5) Studies including central adiposity as an additional diabetes risk factor or not; (6) Studies including prediabetes and/or hypertension as additional risk factors or not; (7) Studies using different daily metformin dosages; and (8) Studies with different intervention durations. CONCLUSION The administration of metformin does not appear to be effective in preventing the development of T2DM in non-diabetic patients with CAD. However, this finding is based on a limited number of small RCTs. Therefore, results should be interpreted cautiously, and further high-quality studies are needed before definitive clinical recommendations can be made.
Post-cardiac arrest care is key in determining neurological recovery and survival after return of spontaneous circulation (ROSC). Despite recent advances, post-arrest mortality remains high due to myocardial dysfunction, cerebral injury, and systemic inflammation. Guidelines recommend avoiding hypotension and using individualized hemodynamic targets with a mean arterial pressure ≥ 65 mmHg commonly used as an initial threshold, although higher targets may be considered in select patients with impaired cerebral autoregulation. Early coronary angiography and revascularization are indicated for ST-elevation myocardial infarction but have not demonstrated a mortality benefit in non-ST-elevation cohorts. Current evidence increasingly emphasizes strict fever prevention and individualized temperature management strategies, while uncertainty remains regarding which patient subgroups may benefit from deeper hypothermia. Post-ROSC ventilation strategies suggest avoiding both hypoxemia and severe hyperoxemia, targeting peripheral oxygen saturation of 92%-98% and normocapnia. Sedation with propofol or dexmedetomidine and analgesia with fentanyl/remifentanil, with appropriate shivering control, enhances targeted temperature management tolerance. Multimodal neuroprognostication incorporating neurological examination, electrophysiology, neuroimaging, and biomarkers (such as neuron-specific enolase and neurofilament light chain) should be performed. Early prognostic findings should be interpreted cautiously to minimize premature withdrawal of life-sustaining therapy. Future research should refine hemodynamic, temperature, and prognostic targets to optimize individualized post-resuscitation care for patients with cardiac arrest.
BACKGROUND Transthyretin amyloid cardiomyopathy (ATTR-CM) is a rare and fatal cardiomyopathy resulting from myocardial deposition of misfolded transthyretin protein. The literature on review of prognostic tools in this patient population is limited. AIM To determine which parameters are commonly used in prognostication of ATTR-CM. METHODS We conducted a systematic review of studies assessing prognostic role in ATTR-CM amyloidosis. Studies published from inception till December 2022 were included in this review. The databases searched were PubMed, EMBASE, Scopus and ACP Journal Club, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, Cochrane Methodology Register Database, Database of Abstracts of Reviews of Effects, Health Technology Assessment Database, National Health Service Economic Evaluation Database. RESULTS Of 7272 studies initially identified, 42 studies comprising 13145 transthyretin amyloid (ATTR) patients were included. The median mortality of patients with ATTR was 33.6%. Majority of studies assessed biomarkers [Troponin, B type Natriuretic peptide (BNP), NTpro-BNP, glomerular filtration rate (eGFR)], echocardiographic findings [interventricular septal diameter (IVSd), posterior wall thickness, left ventricle ejection fraction (LVEF)], New York heart association (NYHA) class, Gillmore staging in predicting mortality, they were included in meta-analysis. In meta-analysis, higher Gillmore staging, BNP, N Terminal pro-B Type Natriuretic peptide (NT-proBNP), troponin-T, IVSd, and NYHA were associated with higher risk of mortality. On other hand, higher eGFR, was associated with lower risk of mortality. CONCLUSION Most commonly used parameters for prognostication of ATTR-CM studies included Gillmore staging, eGFR, Trop-T, NT pro-BNP and LVEF. Prognostication of ATTR-CM patients can help predict disease severity, survival outcomes and subsequently timely initiation of appropriate treatment strategies.
BACKGROUND MicroRNAs (miRNAs) have emerged as key regulators and promising biomarkers in cardiovascular diseases (CVDs). To date, numerous miRNAs associated with CVDs have been identified. Machine learning (ML) models play a critical role in integrating multiple miRNAs into a unified predictive framework, thereby enhancing diagnostic accuracy in CVDs. AIM To synthesize the current evidence on the development and/or validation of ML-based diagnostic models using miRNA expression profiles for the classification and differentiation of CVDs, and to evaluate their diagnostic performance. METHODS A literature search was conducted from inception to December 2025 across PubMed, the Cochrane Library, and ScienceDirect databases with specific keywords. Two reviewers independently screened the studies, and disagreements were resolved through discussion with the third reviewer. The reviewers then used a predefined eligibility criterion to determine the eligibility of the studies for inclusion. All the selected studies were qualitatively synthesized. RESULTS The initial search identified 390 records, of which nine met the eligibility criteria and were included in this review. The included studies evaluated the diagnostic performance and clinical applicability of ML algorithms incorporating miRNA expression profiles across multiple CVD phenotypes, including acute coronary syndrome, acute myocardial infarction, coronary artery disease, essential hypertension (HTN), atrial fibrillation, pulmonary arterial HTN, and angina. Overall, the included studies consistently demonstrated that ML-based approaches enabled identification of miRNAs with potential diagnostic relevance in CVDs. In addition, models derived from these miRNA profiles showed good to high discriminative performance for classification and differentiation of CVD subtypes. CONCLUSION This review found that the integration of ML models and miRNA profiles for CVD diagnosis represents a promising strategy, with the potential to improve diagnostic accuracy through multivariable panels. However, the current evidence base remains limited, and further well-designed studies are needed to validate these models, standardize methodological approaches, and define their role in routine clinical diagnosis of CVDs.
Amiodarone remains a mainstay in the treatment of potentially life-threatening cardiac arrhythmias, yet its long-term use is well known to induce cornea verticillata, an epithelial alteration related to intracellular phospholipid accumulation. In most cases these deposits are clinically silent, but some patients may report glare, halos, blurred vision, or ocular discomfort, symptoms that can negatively affect visual quality and, in selected cases, influence treatment adherence, particularly in individuals with severe cardiovascular disease. This mini-review examines the current evidence on the pathophysiological basis, clinical manifestations, and diagnostic features of amiodarone-related corneal changes, with a focus on slit-lamp biomicroscopy and newer multimodal imaging approaches, including in vivo confocal microscopy. Management is considered within a multidisciplinary framework, where ophthalmic findings must be interpreted alongside the often-essential role of amiodarone in cardiac care. Special attention is given to ophthalmic follow-up, symptom-guided management, and patient counseling. By bringing together the perspectives of ophthalmology and cardiology, this review outlines practical strategies to maintain visual comfort without compromising the systemic benefits of antiarrhythmic therapy.
Diabetes mellitus (DM) has a significant negative impact on the global health. Its burden on the medical sector is tremendous as its complications affect all body organs across all age groups. The most dramatic complications of DM include cardiovascular and neurological disorders. Microvascular damage can start years before the diagnosis of type 2 diabetes (T2DM) is made; therefore, early screening is of utmost value. Moreover, subclinical electrocardiographic (ECG) changes are common in patients with T2DM without evident cardiac disease. I have read with great interest the recent study published in World Journal of Cardiology by Karbovskaya et al , on the utility of a single-lead ECG for diagnosing DM, using machine learning and multinomial regression. The utility of single-lead ECG for predicting glycemic levels appears questionable. It should be interpreted with caution, particularly in light of the model’s limited explanatory power and elevated maximum error. A single-center, non-randomized study with a small sample size in the DM groups and misclassification bias are limitations of the study. A simple, easily accessible tool for early detection or prediction of cardiac dysfunction in DM or in people at risk is more valuable than merely distinguishing healthy from DM or type 1 diabetes from T2DM. A single-lead ECG, especially with artificial intelligence, can flag risk and help bridge some gaps in predicting event risk. However, this study needs validation with a precise aim to predict high-risk diabetics and not only to diagnose DM.
The recent 2025 European Society of Cardiology (ESC)/European Association for Cardio-Thoracic Surgery (EACTS) guidelines for the management of valvular heart disease (VHD) state that treatment should be tailored to patient’s preferences. Durability is the main limitation of bioprosthetic heart valves (BHVs), due to structural valve degeneration and increased pannus formation. There is no definitive evidence that bovine pericardium protheses (BPP) are inferior to porcine xenografts (PX) in terms of durability. Muslim patients, due to their religious belief, may prefer to be treated with BPP rather than PX, except for Darurah (emergency) and Istihalah (physicochemical transmutation) conditions. Our paper highlights two key point. First, Italian Muslim professionals have little information concerning the presence of porcine derivatives in BHVs and regarding the existence of an alternative to PX with BPP. Second, the quality and quantity of biological material in BHVs is only known by bio-manufacturers that do not disclose this data spontaneously. To comply with the 2025 ESC/EACTS guidelines for the management of VHD, we believe that the heart team could benefit from the advice of qualified Islamic religious leaders in delivering to Muslim patients the scenario of BHV utilization with complete, relevant, and accessible information.
BACKGROUND Anthracyclines cause dose-dependent, irreversible cardiac dysfunction, whereas trastuzumab leads to dose-independent, reversible cardiotoxicity. Both beta-blockers and angiotensin-converting enzyme inhibitor (ACEI) have shown protective effect against anti-cancer agents-induced cardiotoxicity, however to date there is no head-to head comparison. Our metanalysis focuses on bridging this gap. AIM To compare the efficacy of ACEI and beta-blockers in preventing cardiotoxicity and to evaluate whether either class offers superior cardio-protection. METHODS PubMed, EMBASE, and Cochrane Library were searched for randomized controlled trials comparing beta-blockers with ACEI in patients of chemotherapy. 4 studies including 680 patients were analyzed using Revman random-effects model, and results were generated in form of relative risk and mean difference (MD). RESULTS There was no difference in the two groups in regards to: Change in E/E’ [MD = -0.25; 95% confidence interval (CI): -0.50 to 0.01; P = 0.06], change of left ventricular (LV) ejection fraction (MD = 0.38%; 95%CI: -0.35 to 1.11; P = 0.31), cardiotoxicity (MD = 1.07; 95%CI: 0.66-1.75, P = 0.77), change in LV end diastolic diameter (MD = -0.41%; 95%CI: -0.98 to 0.16; P = 0.16), change in LV end systolic diameter (MD = -0.20%; 95%CI: -0.70 to 0.30; P = 0.43) and change in E/A (MD = -0.01; 95%CI: -0.25 to 0.23; P = 0.92). While risk of total adverse events and palpitation were same in two groups, hypotension (11% vs 3%, P = 0.004) and dizziness (13% vs 6%, P = 0.01) were more frequent with ACEI. CONCLUSION Our study demonstrates that both groups offer similar protection against cardiotoxicity, with ACEI associated with more side-effects. Therefore, choice of agent should be guided by individual tolerability and clinical context.
Kos et al recently published a study in World Journal of Cardiology report that an acute myocardial infarction patient’s outcome is more strongly determined by whether the culprit artery is totally occluded than by the initial electrocardiographic presentation. In this Letter, we highlight the clinical significance of their finding that ST-segment elevation on electrocardiogram was not an independent predictor of 30-day mortality, underscoring the importance of angiographic occlusion status. We discuss the utility and caveats of using troponin levels as a surrogate for infarct size, the observed protective association of chronic statin therapy with lower likelihood of occlusion, and the need for earlier detection of occlusions. We share the authors’ view that integrating culprit vessel patency into acute myocardial infarction risk assessment is essential and that an “occlusion myocardial infarction” approach may improve triage decisions and outcomes.
We read with great interest the meta-analysis by Parsi et al showing the strong therapeutic effects of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in heart failure. Because the expression of sodium-glucose cotransporter-2 in cardiomyocytes is minimal, the exact pathways for their direct cardioprotective actions are not fully defined. In this correspondence, we summarize emerging evidence and advance an integrated view that places Ca2+/calmodulin-dependent protein kinase II (CaMKII) as a central molecular target. CaMKII is a key factor in heart failure progression. By phosphorylating a host of key substrates such as ryanodine receptor 2, L-type calcium channels and voltage-gated sodium channel voltage-gated sodium channel type V 1.5, it facilitates ionic imbalance, predisposition to arrhythmia, and structural remodeling. We highlight the way SGLT2i may exercise their benefits through coordinated suppression of CaMKII activity via enhanced ionic homeostasis, decreased oxidative injury and suppressed inflammatory signaling. This mechanistic framework offers a unified explanation for the reported clinical and experimental improvements associated with SGLT2i, such as improved electrical stability, improved systolic and diastolic function, and reduction of pathological cardiac remodeling.
