Cardiology In Review[JOURNAL]
Sun
200 papers
Meta-Analysis of Oral PCSK9 Inhibitors for Hypercholesterolemia in Adults: A Systematic Review and GRADE Assessment.
Abomohsen M, Rifai M, Mohamed AE … +10 more , Bakr HM, Elgendy MS, Alkuwaiti MA, Dewedar MS, Almakadma AH, Ghannam M, Mojahedi A, Idries I, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42269009 · Publisher ↗
Oral PCSK9 inhibitors are emerging once-daily therapies intended to simplify PCSK9 pathway inhibition, but trial-level evidence varies across agents, populations, and follow-up. We searched PubMed, Scopus, Web of Science...
Oral PCSK9 inhibitors are emerging once-daily therapies intended to simplify PCSK9 pathway inhibition, but trial-level evidence varies across agents, populations, and follow-up. We searched PubMed, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials from inception to February 5, 2026 for double-blind randomized trials comparing oral PCSK9 inhibitors with placebo on background lipid-lowering therapy. Five trials (n = 4232) evaluating AZD0780, NNC0385-0434, MK-0616, and enlicitide were included. Compared with placebo, oral PCSK9 inhibitors significantly reduced low-density lipoprotein cholesterol (mean difference, -52.42 percentage points; 95% confidence interval, -62.84 to -42.00) and ApoB (mean difference, -43.03 percentage points; 95% confidence interval, -52.12 to -33.94), with consistent reductions in nonhigh-density lipoprotein cholesterol and total cholesterol. High-density lipoprotein cholesterol was not significantly changed. No significant differences were observed in discontinuation due to adverse events, any adverse events, serious adverse events, or treatment-related adverse events. Oral PCSK9 inhibitors provide substantial short-term reductions in atherogenic lipoproteins without an apparent excess of short-term adverse events; longer-term cardiovascular outcome trials are needed.
Childhood Obesity: Epidemiology, Risk Factors, Prevention, and Emerging Treatment Strategies.
Hadid S, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42269007 · Publisher ↗
Childhood obesity is a growing global public health concern influenced by genetic, environmental, behavioral, psychological, and socioeconomic factors. Increasing consumption of ultra-processed foods and increasingly sed...
Childhood obesity is a growing global public health concern influenced by genetic, environmental, behavioral, psychological, and socioeconomic factors. Increasing consumption of ultra-processed foods and increasingly sedentary lifestyles have contributed significantly to rising obesity rates among children and adolescents. Childhood obesity is associated with serious long-term health complications, including type 2 diabetes, cardiovascular disease, and psychological disorders. Current childhood obesity management emphasizes early identification and intensive lifestyle intervention through nutrition counseling, physical activity promotion, behavioral therapy, and family-based treatment. Recent advances in pharmacologic therapy, particularly glucagon-like peptide-1 receptor agonists, as well as bariatric surgery, have demonstrated meaningful improvements in body mass index and metabolic outcomes in adolescents with severe obesity. This review summarizes the epidemiology, risk factors, clinical consequences, prevention strategies, and emerging treatment approaches for childhood obesity.
Antithrombotic Therapy After Lower Limb EndoVascular Interventions: Are We Overtreating or Undertreating? - A Narrative Review.
Bozzani A, Destefanis Gallo E, Salzillo I … +4 more , Arici V, Rossini R, Rota M, Visciglia E
Cardiol Rev · 2026 Jun · PMID 42269003 · Publisher ↗
Peripheral arterial disease patients undergoing lower limb revascularization remain at high risk of thrombotic complications, yet optimal postprocedural antithrombotic therapy remains uncertain. Current strategies vary w...
Peripheral arterial disease patients undergoing lower limb revascularization remain at high risk of thrombotic complications, yet optimal postprocedural antithrombotic therapy remains uncertain. Current strategies vary widely, reflecting the difficulty of balancing ischemic protection against bleeding risk. This review critically examines the evidence supporting antithrombotic approaches after lower limb revascularization and explores whether contemporary practice is characterized by overtreatment, undertreatment, or both. Randomized controlled trials, subgroup analyses, and recent meta-analyses evaluating dual pathway inhibition (DPI), dual antiplatelet therapy (DAPT), and single antiplatelet therapy were reviewed, with particular attention to efficacy, safety, treatment duration, and patient selection. DPI is supported by robust randomized evidence demonstrating reductions in major adverse cardiovascular and limb events, particularly after revascularization. In contrast, DAPT remains widely used despite limited and methodologically heterogeneous evidence. Available meta-analyses suggest potential reductions in myocardial infarction, cardiac mortality, and reintervention with DAPT compared with single antiplatelet therapy, although certainty remains low and no randomized trial has directly compared DAPT with DPI. This evidentiary gap contributes to a clinical paradox in which some patients receive prolonged combination therapy with excess bleeding risk, whereas others at particularly high ischemic risk may remain undertreated. Current guideline-based approaches insufficiently account for procedural complexity, patient phenotype, and temporal changes in thrombotic risk. A more personalized and dynamic antithrombotic strategy is needed to optimize outcomes in peripheral arterial disease after revascularization.
Obesity and Atrial Fibrillation: Epidemiology, Mechanisms, and Therapeutic Implications in the Era of Metabolic Therapies.
Zine-Eddine H, Alam W, Lellouche N … +1 more , Moini C
Cardiol Rev · 2026 Jun · PMID 42269002 · Publisher ↗
Obesity has become a major modifiable risk factor for atrial fibrillation (AF) and contributes significantly to its rising global prevalence. Beyond epidemiological associations, obesity induces a specific form of atrial...
Obesity has become a major modifiable risk factor for atrial fibrillation (AF) and contributes significantly to its rising global prevalence. Beyond epidemiological associations, obesity induces a specific form of atrial cardiomyopathy characterized by structural remodeling, fibrosis, expansion of epicardial adipose tissue, inflammation, autonomic imbalance, and metabolic dysfunction, all of which promote AF initiation and progression. This review synthesizes current evidence linking obesity to AF, focusing on epidemiology, pathophysiological mechanisms, and therapeutic implications, including catheter ablation, bariatric surgery, and metabolic pharmacotherapies. The analysis is based on a structured, nonsystematic review of the literature, with studies identified primarily through PubMed using keywords related to obesity and AF. Priority was given to large population-based cohorts, mechanistic investigations, randomized controlled trials, and recent high-impact publications, with additional references identified through manual screening. Evidence consistently demonstrates a graded relationship between increasing body mass index and the incidence, progression, and recurrence of AF. Mechanistically, obesity contributes to atrial remodeling through fibrosis, inflammation, dysregulated adipose signaling, autonomic dysfunction, and metabolic disturbances. Interventional studies indicate that sustained weight loss reduces AF burden and improves rhythm control outcomes, while bariatric surgery and glucagon-like peptide-1 receptor agonists show promise as disease-modifying strategies. Overall, obesity plays a central role in AF pathogenesis and represents a key therapeutic target, with integrated management of weight and metabolic factors offering potential to improve outcomes, although further research is needed to clarify the direct atrial effects of metabolic therapies.
Nonocclusive Mesenteric Ischemia in Cardiogenic Shock: Mechanisms of Splanchnic Hypoperfusion and Strategies for Early Detection.
Heydari H, Weisberg IS, Kothari M … +3 more , Weingarten JA, Frishman WH, Peterson SJ
Cardiol Rev · 2026 Jun · PMID 42258757 · Publisher ↗
Nonocclusive mesenteric ischemia (NOMI) is an underappreciated and lethal sequelae of cardiogenic shock (CS), forming the bulk of acute mesenteric ischemia in critically ill patients. In the setting of CS, reduced cardia...
Nonocclusive mesenteric ischemia (NOMI) is an underappreciated and lethal sequelae of cardiogenic shock (CS), forming the bulk of acute mesenteric ischemia in critically ill patients. In the setting of CS, reduced cardiac output, exposure to high doses of vasopressors, and nonpulsatile mechanical circulatory support (MCS) result in a "perfect storm" of hemodynamic insults to the splanchnic circulation. Mortality from NOMI in this population exceeds 70-90%, largely attributable to late diagnosis after irreversible transmural necrosis has already occurred. In this review, we describe the pathophysiology of NOMI in the setting of CS, considering the effects of sympathoadrenergic and renin-angiotensin mediated vasoconstriction, the loss of mesenteric pulsatility due to contemporary MCS, and the gut-heart axis as an enhancer of systemic injury. We address topics such as the under detection of limb ischemia with current imaging modalities, the potential of new markers of gut dysfunction, such as intestinal fatty acid-binding protein and citrulline, and bedside imaging, including contrast-enhanced ultrasound and assessment of portal vein pulsatility. We review strategies for prevention and management, including early MCS escalation, minimizing vasopressor requirements, and careful enteral feeding. Finally, we recognize the need for prospective multicenter registries and AI-based risk stratification to facilitate the diagnosis of this under-recognized condition. Understanding that the gut is not a "mere" bystander in the pathophysiology of CS, but rather a central participant, it may be the gateway to reducing the ongoing high mortality of this syndrome.
Role of Personalized Medicine in Myocardial Infarction With Nonobstructive Coronary Artery Disease (MINOCA): An Updated Review.
Kumar D, Nirander F, Raza H … +4 more , Rani S, Raj P, Adnan F, Malik J
Cardiol Rev · 2026 Jul-Aug 01 · PMID 42246870 · Publisher ↗
Cardiovascular diseases, notably myocardial infarction (MI), contribute significantly to global mortality. While traditional MIs are often associated with notable coronary artery blockages, a subgroup experiences MI with...
Cardiovascular diseases, notably myocardial infarction (MI), contribute significantly to global mortality. While traditional MIs are often associated with notable coronary artery blockages, a subgroup experiences MI without such blockages, termed myocardial infarction with nonobstructive coronary arteries (MINOCA). Current diagnostic methods, like invasive coronary angiograms, are inadequate in diagnosing MINOCA due to the absence of visible vessel blockages. Personalized medicine endeavors to introduce novel diagnostic tools for early identification and tailored management of MINOCA. Unlike percutaneous coronary intervention, which lacks efficacy in MINOCA, personalized medical management aligned with the specific underlying pathophysiological cause is essential. Treatments may include statins, agents modulating the renin-angiotensin system, and antiplatelet therapies if linked to plaque disruption. At the same time, calcium channel blockers may be pivotal if coronary artery spasm is the primary cause. Research is ongoing to refine tailored therapies and discover new biomarkers, highlighting the crucial need for individualized approaches in managing MINOCA.
Spot Urinary Electrolytes and Creatinine for Guiding Loop Diuretic Therapy in Acute Heart Failure: Pathophysiologic Rationale, Evidence, and Practical Implementation.
Khan AA, Rohatgi D, Dogra K … +2 more , Agarwal SP, Elgabry I
Cardiol Rev · 2026 Jun · PMID 42237083 · Publisher ↗
Congestion is the dominant driver of hospitalization in acute heart failure and relief of congestion remains a central therapeutic target. Loop diuretics are first-line therapy for decongestion, yet their dosing and esca...
Congestion is the dominant driver of hospitalization in acute heart failure and relief of congestion remains a central therapeutic target. Loop diuretics are first-line therapy for decongestion, yet their dosing and escalation in routine practice often rely on subjective bedside assessment, variable urine output thresholds, weight change, and delayed laboratory trends approaches that incompletely capture the primary pharmacodynamic goal of diuretic therapy: natriuresis. Neurohormonal activation and renal sodium avidity in heart failure can lead to poor diuretic response despite apparently adequate diuretic dosing, and persistent congestion is consistently associated with adverse outcomes. In this context, early measurement of spot urinary electrolytes especially urinary sodium, and potentially urinary chloride and urinary creatinine offers an objective, rapid method to quantify natriuretic response and identify inadequate decongestion early enough to adjust therapy. This review summarizes the pathophysiologic basis linking renal sodium handling to congestion, critiques traditional metrics used to titrate diuretics, synthesizes the clinical evidence supporting spot urinary sodium-based assessment (observational cohorts and emerging randomized/protocolized strategies), and outlines pragmatic implementation considerations, including confounders such as chronic kidney disease, concomitant SGLT2 inhibitors, and timing of sampling. While natriuresis-guided strategies reliably improve natriuresis and process-of-care metrics, definitive evidence for improved hard outcomes remains evolving, underscoring the need for standardized protocols and larger outcomes trials.
Does Anatomy Dictate Outcome?: Self-Expanding vs Balloon-Expandable Transcatheter Aortic Valve Replacement in Small and Extra-Small Annuli.
Abdelrahman AK, Elkholy M, Arce JE … +6 more , Al-Muhaisen R, Ahmed K, Omara G, Altujjar M, Leon MB, Beohar N
Cardiol Rev · 2026 Jun · PMID 42237081 · Publisher ↗
The optimal transcatheter aortic valve replacement strategy in patients with a small aortic annulus (SAA) remains unclear. We performed a systematic review and meta-analysis comparing self-expanding valves (SEVs) to ball...
The optimal transcatheter aortic valve replacement strategy in patients with a small aortic annulus (SAA) remains unclear. We performed a systematic review and meta-analysis comparing self-expanding valves (SEVs) to balloon-expandable valves (BEVs) in SAA patients. We searched PubMed, Embase, Web of Science, and Scopus for studies comparing SEVs and BEVs in patients with SAA defined by computed tomography. A random-effects model using the Der Simonian and Laird estimator was used to pool odds ratios (ORs) and mean differences (MDs). We identified 25 studies encompassing 13,846 patients (5633 BEV; 8213 SEV). SEVs demonstrated superior hemodynamics, including a larger indexed effective orifice area (MD: 0.20 cm2/m2; P < 0.00001), a lower mean transvalvular gradient (MD: -4.11 mm Hg; P < 0.00001), and a lower risk of severe patient-prosthesis mismatch (OR: 0.37; P < 0.00001). However, SEVs were associated with a higher risk of permanent pacemaker implantation (PPI) (OR: 1.63; P = 0.0008) and moderate or severe paravalvular leak (PVL) (OR: 2.26; P < 0.00001). There was no significant difference in all-cause mortality at 1 year (OR: 0.96; P = 0.55) or stroke at 30 days (OR: 1.34; P = 0.18). Notably, in a subgroup analysis restricted to patients with extra-small annuli (area <400 mm2 or diameter <23 mm), the hemodynamic advantages of SEVs persisted while the elevated risks of PPI and PVL were no longer statistically significant. In patients with SAA, SEVs provide better hemodynamics but carry safety concerns including higher risks of PVL and PPI in the overall population. These risks were not observed in the extra-small annulus subgroup. Valve selection should be individualized based on patient anatomy and procedural risk profile.
Atrioventricular Junction Ablation for Cardiac Resynchronization Therapy in Atrial Fibrillation: An Updated Systematic Review, Meta-Analysis, and Meta-Regression Including Contemporary Randomized Trials.
Abomohsen M, Mohamed AE, Almakadma AH … +8 more , Ghannam M, Hasson M, Idries I, Kholeif Z, Rifai M, Duodu E, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42237079 · Publisher ↗
Atrial fibrillation is a common cause of suboptimal cardiac resynchronization therapy (CRT) delivery because intrinsic atrioventricular conduction reduces effective biventricular capture. We performed an updated systemat...
Atrial fibrillation is a common cause of suboptimal cardiac resynchronization therapy (CRT) delivery because intrinsic atrioventricular conduction reduces effective biventricular capture. We performed an updated systematic review and meta-analysis evaluating atrioventricular junction ablation (AVJA) versus no AVJA or pharmacological rate control in CRT recipients with atrial fibrillation. PubMed, Scopus, and Cochrane Library were searched through February 16, 2026. Sixteen studies were included, comprising 14 observational cohorts and 2 randomized trials. AVJA significantly increased biventricular pacing (mean difference 8.80 percentage points, 95% confidence interval [CI] 5.99-11.61). All-cause mortality (risk ratio [RR] 0.74, 95% CI 0.51-1.10), cardiovascular mortality (RR 0.79, 95% CI 0.49-1.27), and heart failure hospitalization (RR 0.73, 95% CI 0.18-2.97) were directionally favorable but not statistically significant. Remodeling, functional, quality-of-life, and clinical responder outcomes were modest or neutral. Contemporary device-therapy data suggested fewer inappropriate shocks and ventricular arrhythmia-related therapies with AVJA, although reporting heterogeneity precluded formal pooling. AVJA remains a dependable CRT-optimization strategy for selected patients with atrial fibrillation, especially when biventricular pacing is inadequate, but contemporary evidence supports a more measured interpretation of downstream clinical benefit.
Medical Management of Nonobstructive Coronary Artery Disease.
Agrawal SP, Maniyar P, Raval M … +3 more , Maheta D, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42237077 · Publisher ↗
Nonobstructive coronary artery disease (CAD) is increasingly recognized as a common cause of ischemic symptoms, especially in women, despite the absence of significant epicardial artery stenosis. This review summarizes t...
Nonobstructive coronary artery disease (CAD) is increasingly recognized as a common cause of ischemic symptoms, especially in women, despite the absence of significant epicardial artery stenosis. This review summarizes the epidemiology and pathophysiology of nonobstructive CAD, encompassing entities such as angina or ischemia with nonobstructive coronary arteries and myocardial infarction with nonobstructive arteries. We discuss diagnostic approaches-including coronary angiography, coronary computed tomography angiography, and functional testing-that can uncover microvascular dysfunction or vasospasm as underlying mechanisms. Evidence-based medical management focuses on aggressive risk factor modification and symptomatic relief, mirroring guideline-directed therapies for obstructive CAD. Key interventions include antiplatelet agents, statins, angiotensin-converting enzyme inhibitors, beta blockers, and lifestyle changes, tailored to patient risk profiles. We highlight findings from recent clinical trials and studies (2020 onward) that inform management, such as the importance of stratified therapy guided by invasive physiology or advanced imaging, and discuss sex-based differences, with women disproportionately affected by nonobstructive CAD. Future directions point toward emerging therapies (eg, PCSK9 inhibitors, anti-inflammatory agents) and advanced imaging or invasive techniques to better characterize disease and personalize treatment.
Coronary Artery Involvement in Kawasaki Disease and Multisystem Inflammatory Syndrome in Children: Imaging, Risk Stratification, and Long-Term Cardiovascular Considerations.
Fatima A, Akram MB, Asghar AH … +5 more , Sabah NU, Rana MA, Khan A, Masood MA, Arshad MMUD
Cardiol Rev · 2026 Jun · PMID 42237075 · Publisher ↗
Kawasaki disease (KD) and multisystem inflammatory syndrome in children (MIS-C) are pediatric inflammatory conditions with significant cardiovascular involvement, particularly affecting the coronary arteries. KD remains...
Kawasaki disease (KD) and multisystem inflammatory syndrome in children (MIS-C) are pediatric inflammatory conditions with significant cardiovascular involvement, particularly affecting the coronary arteries. KD remains the leading cause of acquired heart disease in children worldwide, while MIS-C has emerged as a postinfectious complication of severe acute respiratory syndrome coronavirus 2 with overlapping but distinct cardiovascular manifestations. Coronary artery abnormalities, including dilation and aneurysm formation, represent the most important cardiovascular sequelae in KD, whereas coronary involvement in MIS-C appears less frequent and often transient, although its long-term implications remain incompletely understood. Early detection and longitudinal assessment of coronary involvement are essential for optimizing outcomes. Echocardiography is the first-line imaging modality for both KD and MIS-C due to its accessibility and high sensitivity in detecting proximal coronary abnormalities. However, advanced imaging techniques such as coronary computed tomography angiography and cardiac magnetic resonance imaging provide superior visualization of distal coronary segments, vessel wall characteristics, myocardial perfusion, and fibrosis. These modalities are increasingly integrated into follow-up strategies, especially in patients with complex or persistent lesions. Risk stratification is guided by coronary artery Z scores, inflammatory biomarkers, and clinical severity, enabling tailored therapeutic approaches, including antiplatelet and anticoagulation therapy. Despite advances in treatment, a subset of patients with KD develops persistent coronary artery abnormalities with potential progression to ischemic heart disease later in life. In contrast, current evidence suggests that most cardiovascular abnormalities in MIS-C improve over time, although long-term longitudinal data remain limited. This review synthesizes current evidence on the pathophysiology, imaging strategies, risk assessment, and long-term cardiovascular outcomes in KD and MIS-C. A multimodal imaging approach combined with individualized risk stratification is essential for improving prognosis and guiding lifelong surveillance in affected patients.
The Neuroimmune-Cardiac Axis: Inflammation and Autonomic Remodeling as Drivers of Cardiac Arrhythmogenesis.
Fahad Bin Imtiaz M, Maqsood R, Fatima A … +2 more , Akhtar S, Khalid N
Cardiol Rev · 2026 Jun · PMID 42237074 · Publisher ↗
Cardiac arrhythmias are traditionally attributed to structural and electrophysiological abnormalities; however, increasing evidence highlights the critical role of systemic inflammation and autonomic dysregulation in arr...
Cardiac arrhythmias are traditionally attributed to structural and electrophysiological abnormalities; however, increasing evidence highlights the critical role of systemic inflammation and autonomic dysregulation in arrhythmogenesis. The neuroimmune-cardiac axis represents a bidirectional communication network between the autonomic nervous system and immune signaling pathways that collectively modulate cardiac electrical stability. Pro-inflammatory cytokines and immune mediators influence central autonomic regulatory centers, leading to sympathetic overactivation and parasympathetic withdrawal, reflected by reduced heart rate variability and increased arrhythmic susceptibility. Conversely, autonomic dysfunction further amplifies inflammatory signaling, establishing a self-perpetuating feed-forward loop that promotes electrical instability and adverse cardiac remodeling. Key neuroanatomical structures, including circumventricular organs and the stellate ganglion, serve as critical interfaces linking systemic inflammation to autonomic cardiac control. Inflammatory mediators such as interleukin (IL)-17A and metabolic adipokines like leptin contribute to stellate ganglion remodeling, enhanced sympathetic discharge, and increased vulnerability to ventricular arrhythmias. At the molecular level, activation of the NLRP3 inflammasome plays a central role in integrating inflammatory and electrical signaling pathways by promoting IL-1β and IL-18 release, oxidative stress, calcium handling abnormalities, and gap junction disruption, thereby establishing a proarrhythmic substrate. Importantly, sustained arrhythmias may further potentiate inflammasome activation, reinforcing the vicious cycle between inflammation and electrical instability. Anti-inflammatory and immunomodulatory mediators, including adiponectin and IL-1 receptor antagonists, demonstrate protective effects by restoring autonomic balance and reducing arrhythmic risk. Collectively, the neuroimmune-cardiac axis provides a unified mechanistic framework for understanding arrhythmogenesis and highlights novel therapeutic opportunities targeting both inflammatory and autonomic pathways beyond conventional antiarrhythmic strategies.
Treatment of Premature Ventricular Contractions: A Review of Medical Therapy, Catheter Ablation, and Emerging Treatments.
Elattar S, Hodhod A, Basha NR … +9 more , Ahmed S, Elattar S, Elsayed O, Elganainy M, Salem A, Rojas L, Frishman WH, Aronow WS, Rojas RA
Cardiol Rev · 2026 Jul · PMID 42237073 · Publisher ↗
Premature ventricular contractions (PVCs) are common arrhythmia encountered in patients with and without structural heart disease. Although often benign and asymptomatic, they may also cause palpitations, exercise intole...
Premature ventricular contractions (PVCs) are common arrhythmia encountered in patients with and without structural heart disease. Although often benign and asymptomatic, they may also cause palpitations, exercise intolerance, presyncope, and reduced quality of life, and in some patients can contribute to PVC-induced cardiomyopathy or trigger malignant ventricular arrhythmias. Their clinical significance depends on symptom burden, PVC frequency, ventricular function, and the presence of underlying myocardial disease. Diagnostic evaluation includes electrocardiography, ambulatory rhythm monitoring, echocardiography, exercise testing, and cardiac magnetic resonance imaging for tissue characterization and risk stratification. Management ranges from reassurance and lifestyle modification to pharmacologic therapy and catheter ablation. Beta-blockers and nondihydropyridine calcium channel blockers remain common first-line options, whereas antiarrhythmic drugs may be considered in carefully selected patients. Catheter ablation is an effective treatment for symptomatic PVCs, high PVC burden, and PVC-induced cardiomyopathy, with high procedural success rates and favorable effects on arrhythmic burden and ventricular function. Novel approaches, including electrocardiographic imaging-guided planning, pulsed field ablation, stereotactic radioablation, neuromodulation, and renal denervation, may further expand future therapeutic options. This review summarizes the pathophysiology, clinical implications, diagnostic evaluation, and contemporary management of PVCs, with emphasis on medical therapy, catheter ablation, and emerging treatments.
DOAC Pharmacokinetics in Malabsorptive States.
Chaudhry MQ, Patel H, Ramesh J … +7 more , Alkasabrah O, Jajja FA, Thukral J, Kaur A, Fnu V, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42231091 · Publisher ↗
Direct oral anticoagulants, such as dabigatran, rivaroxaban, apixaban, and edoxaban, are becoming more popular for the prevention of stroke and treatment of venous thromboembolism, although their effectiveness relies on...
Direct oral anticoagulants, such as dabigatran, rivaroxaban, apixaban, and edoxaban, are becoming more popular for the prevention of stroke and treatment of venous thromboembolism, although their effectiveness relies on adequate gastrointestinal absorption. However, in the setting of malabsorption, such as after bariatric surgery, short bowel syndrome, or during the course of active inflammatory bowel disease, the pharmacokinetic profile of the drugs can be altered. Recent literature indicates that, although rivaroxaban and apixaban are effective in stable patients after bariatric surgery, such as sleeve gastrectomy or Roux-en-Y gastric bypass, dabigatran is not effective because it requires the acidic environment of the stomach for adequate absorption. However, in the setting of severe malabsorption, such as very short bowel syndrome, the gold standard, which is warfarin, is recommended because the effect of the drug can be monitored. Guidelines recommend avoiding the use of direct oral anticoagulants during the acute postoperative period, which is defined as 0-4 weeks, and using drug-specific assays, such as antiXa or dilute thrombin time, to ensure adequate absorption.
Efficacy and Safety of Sacubitril/Valsartan in Protecting Cardiac Function in Patients Undergoing Chemotherapy: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Abuelazm M, Alsejari N, Alsubaiei AA … +3 more , Alsaffar H, Mohammed ZA, Rashed M
Cardiol Rev · 2026 Jun · PMID 42228808 · Publisher ↗
Contemporary chemotherapy has significantly improved cancer survival, yet cancer therapy-related cardiac dysfunction (CTRCD) remains a major cause of morbidity and mortality. Current cardioprotective strategies often fai...
Contemporary chemotherapy has significantly improved cancer survival, yet cancer therapy-related cardiac dysfunction (CTRCD) remains a major cause of morbidity and mortality. Current cardioprotective strategies often fail to preserve left ventricular (LV) function robustly. Sacubitril/valsartan (Sac/Val) has shown promise in mitigating CTRCD. A comprehensive search was conducted across PubMed, Web of Science, CENTRAL, Scopus, and Google Scholar for randomized controlled trials up to December 2025. The primary outcomes were the incidence of CTRCD and the mean change in LV ejection fraction. Data were pooled using risk ratios (RRs) and mean differences (MDs) with 95% confidence intervals (CIs). PROSPERO: CRD420261280152. Four randomized controlled trials involving 412 patients were included. Sac/Val was associated with a significant preservation of LV ejection fraction [MD: 1.71%, 95% CI (0.73-2.68); P < 0.001] and a greater improvement in global longitudinal strain [MD: -0.99, 95% CI (-1.94 to -0.04); P = 0.04] compared to controls. However, there was no significant difference in the incidence of CTRCD [RR: 0.44, 95% CI (0.15-1.32); P = 0.14]. Also, Sac/Val significantly increased the risk of hypotension [RR: 4.35, 95% CI (1.71-11.08); P = 0.001] but showed no significant differences in death (P = 0.86), heart failure (P = 0.52), or treatment discontinuation due to adverse events (P = 0.75). Sac/Val significantly preserves LV function and improves subclinical myocardial global longitudinal strain in patients undergoing chemotherapy. Although it increases the risk of hypotension, its overall safety profile regarding hard outcomes is favorable. Further large-scale trials are needed to assess its impact on long-term clinical cardiotoxicity.
GLP-1 RAs in Substance Use Disorders: Emerging Evidence and Future Directions.
Macanian J, Frishman WH
Cardiol Rev · 2026 Jun · PMID 42219586 · Publisher ↗
Substance use disorders (SUDs) are the leading causes of both global mortality and morbidity, and alcohol, nicotine, and opioids account for most of this burden. Existing pharmacotherapies are only moderately effective,...
Substance use disorders (SUDs) are the leading causes of both global mortality and morbidity, and alcohol, nicotine, and opioids account for most of this burden. Existing pharmacotherapies are only moderately effective, have inconsistent compliance and regular relapse, and therefore, new treatment modalities are required. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), which have been licensed to treat type 2 diabetes and obesity, have emerged as potential therapeutic candidates for SUDs due to their central action on neural reward circuits. GLP-1 receptors are expressed in mesolimbic regions, and preclinical studies show decreases in drug use, suppression of nucleus accumbens efflux of dopamine, and inhibition of relapse-like behaviors in models of alcohol, nicotine, and opioids. Early clinical findings, particularly those from semaglutide, indicate reductions in both alcohol and cigarette consumption, although the results remain inconsistent and are limited by small sample size. Subgroup analysis and observational findings suggest that GLP-1RAs may have potentially larger effects in individuals with obesity and metabolic disease, which could also be due to metabolic modes of action. In opioid use disorder, evidence is currently limited to animal models but demonstrates comparable efficacy to established therapies. Collectively, GLP-1RAs represent an emerging and mechanistically novel therapeutic option for SUDs. Future research should prioritize large-scale randomized controlled trials, patient stratification, and long-term safety assessments to define their potential role as adjunct or standalone treatments in addiction medicine.
The Temporal Dissociation of Vascular Leak and Myocardial Dysfunction in Dengue: Pathophysiology, Diagnostic Challenges, and Implications for Phase-Specific Management.
Egli C, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42219576 · Publisher ↗
Dengue virus infection is a leading cause of arboviral disease worldwide, with severe cases characterized by plasma leakage and hypovolemic shock. Increasing evidence suggests that cardiovascular involvement is clinicall...
Dengue virus infection is a leading cause of arboviral disease worldwide, with severe cases characterized by plasma leakage and hypovolemic shock. Increasing evidence suggests that cardiovascular involvement is clinically significant, challenging the conventional paradigm of dengue-associated hemodynamic compromise. This review synthesizes mechanistic, clinical, and population-based evidence to propose a temporal, phase-dependent framework of dengue cardiovascular pathology. Cardiovascular involvement evolves across distinct phases, beginning with direct viral myocardial effects and endothelial glycocalyx disruption during the febrile phase, followed by immune-mediated injury, vascular leak, and myocardial dysfunction. While vascular permeability typically resolves within 48-72 hours of defervescence, myocardial dysfunction may persist for up to 2 weeks, creating a temporal dissociation with important clinical consequences. Hemodynamic studies demonstrate that dengue shock frequently reflects a mixed phenotype, with approximately equal contributions of hypovolemic and cardiogenic shock. This mismatch creates a narrow therapeutic window in which aggressive fluid resuscitation may exacerbate cardiac dysfunction and increase the risk of pulmonary edema. Dengue-associated shock is therefore better understood as a dynamic, phase-dependent syndrome characterized by shifting contributions of vascular and myocardial dysfunction. Recognition of this mixed shock paradigm is essential for phase-specific management and highlights the need for accessible tools to identify shock phenotypes in real time.
Prognostic Value of Left Atrial Strain for Atrial Fibrillation After Cryptogenic Stroke and Embolic Stroke of Undetermined Source.
Gancarczyk U, Prochownik P, Jakiel M … +3 more , Tworek M, Płazak W, Komar M
Cardiol Rev · 2026 Jun · PMID 42219573 · Publisher ↗
Subclinical atrial fibrillation (AF) is increasingly recognized as an important underlying mechanism of cryptogenic stroke (CS) and embolic stroke of undetermined source (ESUS). Early identification of patients at increa...
Subclinical atrial fibrillation (AF) is increasingly recognized as an important underlying mechanism of cryptogenic stroke (CS) and embolic stroke of undetermined source (ESUS). Early identification of patients at increased risk of AF remains a major clinical challenge. Assessment of left atrial strain (LAS) by transthoracic echocardiography has emerged as a promising method for evaluating atrial function and may provide incremental information for AF risk stratification. We performed a systematic review in accordance with Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines to evaluate the association between LAS and AF detection in patients with CS and ESUS. PubMed, Embase, the Cochrane Library, and Google Scholar were searched up to December 7, 2025. Thirteen studies, including 2132 patients, were eligible for qualitative synthesis. Random-effects meta-analyses using the inverse-variance method were conducted where appropriate. Eleven studies reporting LAS as mean values with standard deviation were included in a comparative meta-analysis, comprising 525 patients with AF and 1185 without AF. LAS was significantly lower in patients with AF (standardized mean difference -0.80; 95% confidence interval, -1.09 to -0.50; P < 0.001), although heterogeneity was substantial (I2 = 83%). In an exploratory prognostic meta-analysis, 3 studies reporting multivariable-adjusted odds ratios from logistic regression models were pooled. Lower LAS was associated with AF detection (pooled odds ratio 0.87 per 1% increase; 95% confidence interval, 0.79-0.97; P = 0.009), with considerable heterogeneity across studies (I2 = 86.6%). Overall, LAS is generally lower in patients with AF and may support risk stratification for AF detection in patients with CS and ESUS; however, substantial heterogeneity and methodological differences across studies should be acknowledged.
From Adipose Tissue to the Heart: Leptin, Exercise, and Cardiovascular Risk in Women.
Gera P, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42219570 · Publisher ↗
Cardiovascular disease (CVD) is a leading cause of mortality in women, with sex-specific risk factors still underrepresented in research. Leptin is an adipokine released primarily from adipose tissue, with multifaceted r...
Cardiovascular disease (CVD) is a leading cause of mortality in women, with sex-specific risk factors still underrepresented in research. Leptin is an adipokine released primarily from adipose tissue, with multifaceted roles contributing to cardiometabolic health. Hyperleptinemia and associated resistance influence appetite regulation, cardiac remodeling, vascular health, and sympathetic nervous system activation. The interplay of leptin and CVD health is mediated by estrogen, and the lack thereof in menopause, modifying cardiac health across the lifespan. Exercise is an important lifestyle modifier that reduces leptin levels and increases central sensitivity. Weight loss and energy intake both influence the relationship between leptin and exercise, but the exact mechanism is still unclear. Nonetheless, moderately intense aerobic exercise has promising benefits, especially for postmenopausal women. Leptin should be considered as a biomarker for CVD risk assessment and be targeted with exercise as a nonpharmacological intervention in women.
Cardiac Biomarkers and Multimodality Imaging in Surveillance During Oncologic Therapy: An Integrated Approach to Cardio-Oncology.
Agrawal SP, Lussier A, Patel DS … +6 more , Thukral J, Gopu SS, Shah RK, Patel H, Frishman WH, Aronow WS
Cardiol Rev · 2026 Jun · PMID 42219561 · Publisher ↗
Modern oncologic therapy has dramatically improved cancer survival, yet many of the agents responsible for these gains-anthracyclines, human epidermal growth factor receptor 2-targeted therapies, vascular endothelial gro...
Modern oncologic therapy has dramatically improved cancer survival, yet many of the agents responsible for these gains-anthracyclines, human epidermal growth factor receptor 2-targeted therapies, vascular endothelial growth factor inhibitors, immune checkpoint inhibitors, and chest radiotherapy-carry meaningful cardiovascular risk. The emerging discipline of cardio-oncology has transformed the clinical approach to this challenge, and the 2022 European Society of Cardiology guidelines on cardio-oncology have provided the first comprehensive framework for cancer therapy-related cardiovascular toxicity, including its early detection through cardiac biomarkers and advanced imaging. Cardiac troponin (preferably high sensitivity) and natriuretic peptides (B-type natriuretic peptide or N-terminal pro B-type natriuretic peptide) serve as reliable, accessible markers of cardiomyocyte injury and hemodynamic stress, respectively, and are now formally embedded in surveillance algorithms across all major society documents. Growth differentiation factor 15, a stress-responsive cytokine, has emerged as a particularly promising next-generation biomarker, with recent data demonstrating predictive value for cardiotoxicity in human epidermal growth factor receptor 2-targeted breast cancer therapy. On the imaging side, global longitudinal strain by speckle-tracking echocardiography enables sensitive detection of subclinical left ventricular dysfunction long before left ventricular ejection fraction declines, and the SUCCOUR and SUCCOUR-MRI trials have provided important randomized data on strain-guided cardioprotection.
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