Cardiology In Review[JOURNAL]
Sun
200 papers
Chronic Kidney Disease and Its Role in Cardiovascular Disease.
Swamynathan R, Dolan L, Frishman WH … +1 more , Aronow WS
Cardiol Rev · 2026 May · PMID 42115832 · Publisher ↗
Cardiovascular disease (CVD) is the leading cause of death and disability in the United States. Chronic kidney disease (CKD) is another public health concern, affecting roughly 1 in 7 individuals in the United States. Ch...
Cardiovascular disease (CVD) is the leading cause of death and disability in the United States. Chronic kidney disease (CKD) is another public health concern, affecting roughly 1 in 7 individuals in the United States. Characterized by kidney damage or decreased estimated glomerular filtration rate to below 60 mL/min/1.73 m 2 , there is a significant overlap in the mechanisms of disease progression for CVD and CKD. Among individuals between the ages of 18-64 with CKD, 38.4% of individuals have CVD, while in the population without CKD, only 7.1% of individuals have CVD. With this significant overlap, it is important to delve into the mechanisms for the progression of CKD and CVD to better understand how to treat and prevent overall disease burden. This paper reviews several mechanisms, including how impaired kidney function, the state of chronic inflammation, and dysregulation of the renin-angiotensin-aldosterone system affect the heart and vasculature. Based on these mechanisms, several treatment methods were delved into, including renin-angiotensin-aldosterone system inhibitors, sodium-glucose co-transporter 2 inhibitors, mineralocorticoid receptor antagonists, and glucagon-like peptide 1 receptor agonists, to better understand mechanisms of action and safety profile.
Trends and Disparities in Chronic Rheumatic Heart Disease Mortality in the United States (1999-2024) and Projections to 2050.
Jha M, Matawala K, Jairamani S … +8 more , Umar M, Kumar K, Dar A, Kumari P, Maheta D, Agrawal SP, Frishman WH, Aronow WS
Cardiol Rev · 2026 May · PMID 42115831 · Publisher ↗
Contemporary data on national mortality trends, projections, and evolving disparities remains limited. National rheumatic heart disease mortality data from 1999 to 2024 was assessed using Centers for Disease Control and...
Contemporary data on national mortality trends, projections, and evolving disparities remains limited. National rheumatic heart disease mortality data from 1999 to 2024 was assessed using Centers for Disease Control and Prevention's Wide-ranging Online Data for Epidemiologic Research database. Age adjusted mortality rates (AAMR) per 100,000 were calculated. Trends were assessed using joinpoint regression to compute the average annual percent change (AAPC), and predictive models were adopted to estimate rates through 2050. A total of 177,342 deaths were recorded from chronic rheumatic heart disease in the US between 1999 and 2024 with an AAPC of -0.46 [95% confidence interval, -1.20 to 0.26]. Mortality declined significantly between 1999 and 2010 [annual percent change (APC): 3.79: P < 0.001]; however, increased between 2017 and 2021 (APC: 6.04; P < 0.001). Females had a higher mortality burden than males (AAMR: 3.36 vs 2.65). AAMR declined across all racial groups, most prominently in Asian (AAPC: -0.82, P = 0.04) and Hispanics (AAPC: -0.87, P = 0.01). Mortality was higher in non-metropolitan areas (AAMR: 3.25) than metropolitan areas (AAMR: 2.91), though both showed significant decline (metropolitan: AAPC: -1.49, P < 0.001; non-metropolitan: AAPC: -0.54, P = 0.04). Geographically, the West had the highest AAMR (3.80), while Northeast experienced the steepest decline (AAPC: -1.06, P < 0.01). Mortality increased sharply with age, with those ≥65 years experiencing the highest mortality (AAMR: 12.57).
Cardiac Complications of Refeeding Syndrome: Pathophysiological Mechanisms, Clinical Manifestations, and Preventive Strategies.
Senthil A, Chalasani VB, Bonsu E … +4 more , Aman N, Trivedi YV, Alihsan B, Jain R
Cardiol Rev · 2026 May · PMID 42115821 · Publisher ↗
Refeeding syndrome (RFS) is a potentially life-threatening metabolic disorder that occurs when nutrition is rapidly reintroduced after prolonged starvation or malnutrition. It is characterized by insulin-driven shifts of...
Refeeding syndrome (RFS) is a potentially life-threatening metabolic disorder that occurs when nutrition is rapidly reintroduced after prolonged starvation or malnutrition. It is characterized by insulin-driven shifts of phosphate, potassium, and magnesium into cells, leading to severe hypophosphatemia, hypokalemia, and hypomagnesemia. These electrolyte derangements impair myocardial energy metabolism, contractility, and conduction, resulting in arrhythmias, heart failure, and sudden cardiac arrest. Thiamin deficiency and fluid overload further exacerbate cardiac instability, making cardiovascular complications the most fatal manifestations of RFS. Despite recognition for over 7 decades, RFS remains underdiagnosed due to inconsistent definitions, variable diagnostic criteria, and limited clinical awareness. Reported incidence ranges widely from 0% to 62%, with the highest rates in malnourished, critically ill, and elderly patients, as well as those with anorexia nervosa or chronic alcoholism. Prevention remains the cornerstone of management and includes risk stratification, gradual caloric initiation (10-20 kcal/kg/d), thiamin supplementation before feeding, and vigilant monitoring of phosphate, potassium, and magnesium levels during the initial refeeding period. Adherence to established guidelines has been shown to reduce morbidity and mortality. By summarizing the pathophysiological mechanisms, cardiac sequelae, and preventive strategies, this review underscores the importance of early recognition and standardized protocols to mitigate the cardiovascular consequences of RFS and improve outcomes in high-risk populations.
Atrial Cardiomyopathy: A Cardiologist's Guide to Stroke, Heart Failure, and Arrhythmias.
Niazi M, Akram MB, Chaudhary AS … +7 more , Bashir S, Rao A, Fatima A, Masood MA, Arshad MMUD, Maktoob M, Khan A
Cardiol Rev · 2026 May · PMID 42115815 · Publisher ↗
Atrial cardiomyopathy has emerged as a comprehensive pathophysiological construct encompassing structural, architectural, contractile, and electrophysiological abnormalities of the atrial myocardium. Traditionally, atria...
Atrial cardiomyopathy has emerged as a comprehensive pathophysiological construct encompassing structural, architectural, contractile, and electrophysiological abnormalities of the atrial myocardium. Traditionally, atrial fibrillation (AF) has been regarded as the primary manifestation of atrial disease; however, accumulating evidence suggests that atrial cardiomyopathy often precedes AF and independently contributes to adverse cardiovascular outcomes, including ischemic stroke, heart failure with preserved ejection fraction, and a spectrum of atrial arrhythmias. This paradigm shift has significant clinical and research implications. Atrial fibrosis, inflammation, oxidative stress, and endothelial dysfunction collectively drive atrial remodeling, which impairs atrial reservoir and booster pump function while promoting thrombogenesis even in the absence of overt AF. Advanced imaging modalities, including speckle-tracking echocardiography and cardiac magnetic resonance imaging (CMR), coupled with emerging biomarkers, have enabled earlier detection, phenotyping, and risk stratification of atrial disease. Furthermore, the recognition of atrial cardiomyopathy challenges the current AF-centric approach to anticoagulation, rhythm management, and preventive cardiology. This narrative review synthesizes current evidence on the pathophysiology, diagnostic strategies, clinical consequences, and therapeutic implications of atrial cardiomyopathy. Emphasis is placed on its role as a unifying substrate for stroke, heart failure, and arrhythmias, as well as on potential strategies for early identification and precision-based interventions. Understanding atrial cardiomyopathy as a distinct disease entity has the potential to transform clinical practice, optimize patient outcomes, and guide future research directions in cardiovascular medicine.
Vagus Nerve Stimulation in Cardiac Disease: A Systematic Review of Randomized Clinical Trials.
Alrabadi B, Bandak N, Badwan A … +4 more , Abu-Irsheid L, Refai Y, Marouf M, Alomari O
Cardiol Rev · 2026 May · PMID 42113803 · Publisher ↗
Cardiac arrhythmias remain a major cause of morbidity and mortality, and current therapies have notable limitations. Vagus nerve stimulation (VNS), which modulates autonomic tone, has emerged as a potential adjunctive tr...
Cardiac arrhythmias remain a major cause of morbidity and mortality, and current therapies have notable limitations. Vagus nerve stimulation (VNS), which modulates autonomic tone, has emerged as a potential adjunctive treatment. This systematic review evaluated the efficacy of invasive and noninvasive VNS in patients with atrial fibrillation, heart failure, myocardial infarction, and other rhythm disorders. A search of PubMed, Scopus, and Web of Science identified 21 randomized controlled trials, including 11,368 patients. Overall, VNS was associated with reduced atrial fibrillation incidence and burden, improved autonomic function and left ventricular ejection fraction in heart failure, and reduced arrhythmic events and infarct biomarkers after myocardial infarction. Additional benefits were observed in conditions such as vagally mediated atrioventricular block and postural orthostatic tachycardia syndrome. Across studies, VNS demonstrated a favorable safety profile. These findings suggest that VNS may be a promising multimodal strategy for reducing arrhythmia burden and improving cardiac autonomic regulation, although larger confirmatory trials are needed.
Understanding Dysfunctional Autophagy and Mitophagy in Inflammatory Cardiovascular Disease.
Kaiser M, Lewis TA, Malekan M … +4 more , Parikh MA, Turitto G, Frishman WH, Peterson SJ
Cardiol Rev · 2026 May · PMID 42113734 · Publisher ↗
Mitochondria are critical cellular powerhouses that produce adenosine triphosphate to maintain the structure and integrity of the cell. Mitochondria generate 90% of the energy of a cell. Chronic inflammation causes damag...
Mitochondria are critical cellular powerhouses that produce adenosine triphosphate to maintain the structure and integrity of the cell. Mitochondria generate 90% of the energy of a cell. Chronic inflammation causes damage to mitochondria. When enough mitochondria are dysfunctional, the involved organ will suffer. Mitochondria become dysfunctional in the setting of chronic inflammation. Under noninflammatory conditions, the body generates new mitochondria (mitochondrial biogenesis) and removes old and damaged mitochondria via mitophagy. When mitochondria are damaged, they "spontaneously" leak out reactive oxygen species, mitochondrial DNA, and damage-associated molecular patterns, generating erroneous innate immune responses. Autophagy is a recycling and housekeeping process that removes dysfunctional components, organelles, and proteins, promoting the recovery and maintenance of cell health. Mitophagy is a specific variant of this process that removes dysfunctional mitochondria from the cell. Mitophagy declines with age, allowing dysfunctional mitochondria to accumulate, and chronic inflammation leads to cardiovascular disease (CVD). In CVD, impairment of both autophagy and mitophagy leads to more chronic inflammation, characterized by hyperactivation of the nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)- and pyrin domain-containing protein 3 (NLRP3) inflammasome, a key component of the immune system. Once activated, it triggers inflammation, leading to excessive cytokine activity, proinflammatory macrophage polarization, pyroptosis, and increased immune cell infiltration into cardiac and vascular tissues. Pyroptosis is a form of inflammatory cell death triggered by programmed cues; however, in autoimmunity and cancer, when overactivated, this process can become detrimental. Adequate regulation of these events reduces oxidative stress, inflammatory cascades, fibrosis, and maladaptive remodeling, thereby improving overall cardiovascular health. Targeted therapeutic enhancement of autophagy and mitophagy represents a promising strategy to modulate immune-driven pathology and improve outcomes in cardiovascular conditions. We will review the mechanisms of how this inflammation causes CVD.
Triple Hormone Receptor Agonism: The Role of Retatrutide in Addressing Cardiovascular-Kidney-Metabolic (CKM) Syndrome: A Comprehensive Review.
Pillai AA, Godin SL, Frishman WH … +1 more , Aronow WS
Cardiol Rev · 2026 May · PMID 42108533 · Publisher ↗
Retatrutide is a first-in-class, unimolecular triple hormone receptor agonist targeting glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, and glucagon receptors. By synergizing incretin-mediated cent...
Retatrutide is a first-in-class, unimolecular triple hormone receptor agonist targeting glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, and glucagon receptors. By synergizing incretin-mediated central satiety with glucagon-driven thermogenesis, retatrutide circumvents the compensatory metabolic resistance that often limits traditional weight-loss therapies. Phase 2 clinical data demonstrate that a 12-mg maximal weekly dose yields a 24.2% reduction in total body weight at 48 weeks, with 63% of participants achieving a total body weight loss of ≥20%. In patients with type 2 diabetes, retatrutide achieved an absolute HbA1c reduction of 2.02%, with 27% of participants reaching normoglycemia (HbA1c < 5.7%). Beyond global weight reduction, dual-energy X-ray absorptiometry substudies confirm a 23.2% reduction in fat mass, comparable to bariatric surgery. Retatrutide demonstrates potent efficacy in resolving metabolic dysfunction-associated steatotic liver disease, achieving an 82.4% relative reduction in hepatic fat and normalization of liver fat in 86% of patients. These metabolic improvements are accompanied by systemic hemodynamic unloading, including an 8.79 mm Hg reduction in systolic blood pressure and significant attenuation of the urine albumin-to-creatinine ratio. The safety profile is consistent with established incretins: clinicians must monitor for a dose-dependent chronotropic effect. De-escalation of concurrent antihypertensive therapies may also be required.
Dapagliflozin: Potential Role in Pediatric Cardiac Patient Care.
Bitar K, Abdul Khalek J, Zareef R … +2 more , Bitar F, Arabi M
Cardiol Rev · 2026 May · PMID 42108523 · Publisher ↗
Sodium-glucose cotransporter 2 inhibitors have demonstrated substantial cardiovascular and renal benefits in adults, including reduced heart failure events across diabetic and nondiabetic populations. However, pediatric...
Sodium-glucose cotransporter 2 inhibitors have demonstrated substantial cardiovascular and renal benefits in adults, including reduced heart failure events across diabetic and nondiabetic populations. However, pediatric cardiac data remain limited, and real-world use is increasing in specialized centers despite the absence of standardized pediatric protocols. We synthesized a literature review, which was conducted using multiple databases, covering records available through January 2026, to include studies reporting cardiovascular outcomes in children with heart failure receiving dapagliflozin. Given the heterogeneity in study designs and endpoints, findings were synthesized qualitatively without conducting a meta-analysis. Six key studies were identified: 1 open-label pilot randomized trial, 1 prospective cohort, 3 retrospective cohorts, and 1 case series, encompassing heterogeneous etiologies, including dilated cardiomyopathy, myocarditis-related cardiomyopathy, congenital heart disease/Fontan physiology, and post-transplant graft dysfunction. Across observational cohorts, dapagliflozin was associated with modest improvements in ventricular function and frequent improvement in New York Heart Association/Ross functional class. Natriuretic peptide responses were variable, with reductions that were inconsistent. The pilot randomized trial did not demonstrate significant between-group differences in composite clinical outcomes or key cardiac measures over a 6-month period. Reported adverse events were predominantly genitourinary infections and transient renal events, with few discontinuations and no consistent signal of ketoacidosis, severe hypoglycemia, or clinically significant hypotension. Available data suggest a potential signal for modest improvement in cardiac function and clinical status, alongside an overall reassuring short-term safety profile. Multicenter prospective studies with standardized endpoints are needed to define efficacy, optimal patient selection, and long-term safety in pediatric cardiac care.
Finerenone and Empagliflozin in Type 2 Diabetes.
Abdullah M, Khalid N, Frishman WH … +1 more , Aronow WS
Cardiol Rev · 2026 May · PMID 42108478 · Publisher ↗
Cardiovascular disease and chronic kidney disease remain the leading causes of morbidity and mortality in patients with type 2 diabetes, even when conventional risk factors are well managed. Two drug classes have emerged...
Cardiovascular disease and chronic kidney disease remain the leading causes of morbidity and mortality in patients with type 2 diabetes, even when conventional risk factors are well managed. Two drug classes have emerged over the past decade that reduce these risks through mechanisms that are largely independent of glucose lowering effect: sodium-glucose cotransporter 2 inhibitors and nonsteroidal mineralocorticoid receptor antagonists. Empagliflozin demonstrated reductions in cardiovascular mortality, heart failure hospitalization, and kidney disease progression in the EMPA-REG OUTCOME trial and was subsequently shown to benefit patients with heart failure across the ejection fraction spectrum in the EMPEROR trials. Finerenone, the first nonsteroidal mineralocorticoid receptor antagonist with phase III cardiorenal outcome data, reduced both cardiovascular and kidney composite endpoints in the FIDELIO-DKD and FIGARO-DKD trials, effects that were confirmed and strengthened in the pooled FIDELITY analysis of over 13,000 patients. These 2 agents target distinct pathophysiological pathways. Sodium-glucose cotransporter 2 inhibition acts primarily through hemodynamic and tubuloglomerular mechanisms, whereas finerenone addresses mineralocorticoid receptor driven inflammation and fibrosis in cardiac and renal tissue. The CONFIDENCE trial, published in 2025, was the first prospective study to test their combination; finerenone plus empagliflozin reduced urinary albumin.
From Lumen to Myocardium With Artificial Intelligence: A Clinician's Guide to Comprehensive Cardiac CT.
Mohammadi A, Khatami S, Ebrahimi S … +4 more , Chattha SS, Mohammadi A, Frishman WH, Aronow WS
Cardiol Rev · 2026 May · PMID 42101950 · Publisher ↗
Coronary artery disease assessment has long focused on stenosis severity, yet luminal narrowing alone fails to capture ischemic burden, plaque vulnerability, or myocardial health. This mismatch drives unnecessary invasiv...
Coronary artery disease assessment has long focused on stenosis severity, yet luminal narrowing alone fails to capture ischemic burden, plaque vulnerability, or myocardial health. This mismatch drives unnecessary invasive coronary angiography and delays preventive therapy. Cardiac computed tomography (CT) has evolved from a simple anatomical gatekeeper into a comprehensive, noninvasive platform that addresses this gap. This review synthesizes current evidence and provides practical guidance for clinicians, with an emphasis on artificial intelligence integration. High-quality coronary CT angiography now serves as a foundational anatomical roadmap, with trials demonstrating its feasibility for planning complex revascularization (SYNTAX III REVOLUTION) and safely reducing invasive procedures (DISCHARGE). CT-derived fractional flow reserve improves diagnostic specificity, reduces nonobstructive catheterization, and guides revascularization decisions, though prognostic evidence remains mixed and image-quality constraints apply. Quantitative plaque characterization, particularly low-attenuation and total plaque volumes, strongly predicts myocardial infarction and mortality, outperforming stenosis severity and supporting proactive preventive therapy even in nonobstructive disease. Emerging applications include CT-derived extracellular volume for detecting diffuse fibrosis and cardiac amyloidosis, with prognostic value across aortic stenosis and heart failure.
PCSK9 as a Biomarker and Therapeutic Target for Anthracycline Cardiotoxicity Prevention: Recent Advancements and Future Perspectives.
Gadelmawla AF, Alkuwaiti MA, Alsubaiei AA … +6 more , AlSejari NY, Alharran AM, Abdul-Hafez HA, Mohamed AE, Frishman WH, Aronow WS
Cardiol Rev · 2026 May · PMID 42101949 · Publisher ↗
Anthracycline-induced cardiotoxicity continues to be a significant clinical challenge in oncology, affecting up to 30% of patients who are subjected to sequential chemotherapy regimens and substantially restricting the t...
Anthracycline-induced cardiotoxicity continues to be a significant clinical challenge in oncology, affecting up to 30% of patients who are subjected to sequential chemotherapy regimens and substantially restricting the therapeutic potential of these highly effective anticancer agents. Despite the fact that anthracycline-based chemotherapy has an overall 5-year survival rate of 80%, dose-dependent cardiotoxicity is a rising safety concern which manifests as cardiomyopathy or congestive heart failure. This highlights the need for novel cardioprotective strategies are required as the currently available regimens are insufficiently effective. Anthracycline exposure induces proprotein convertase subtilisin/kexin type 9 (PCSK9) upregulation in cardiomyocytes in a concentration- and time-dependent manner. The nuclear accumulation induces apoptosis through the degradation of karyopherin subunit beta-1 (KPNB1). Elevated PCSK9 levels are linked to pathological remodeling, increased myocardial fibrosis, and a reduced left ventricular ejection fraction. Cardioprotection against Anthracycline-induced cardiotoxicity is primarily achieved through lipid-independent mechanisms, including the suppression of inflammasome-mediated injury, modulation of innate immune signaling, attenuation of myocardial fibrosis, and restoration of mitochondrial homeostasis, which are regulated by PCSK9 inhibition. The inhibition of PCSK9 has been demonstrated in preclinical models to enhance anticancer efficacy by reducing chemoresistance and increasing cardiomyocyte viability by 35-88% during anthracycline/trastuzumab exposure.
The Role of Uric Acid in the Pathogenesis of Heart Failure With Preserved Ejection Fraction.
Tan J, Ke J, Qiu X … +1 more , Gu J
Cardiol Rev · 2026 May · PMID 42101948 · Publisher ↗
With advancing age and the development of risk factors such as hypertension, type 2 diabetes, obesity, and atrial fibrillation, the incidence of heart failure with preserved ejection fraction (HFpEF) has shown a year-on-...
With advancing age and the development of risk factors such as hypertension, type 2 diabetes, obesity, and atrial fibrillation, the incidence of heart failure with preserved ejection fraction (HFpEF) has shown a year-on-year increase and is projected to become the most common form of heart failure in the near future. Uric acid (UA) is the end product of purine metabolism in the body and is closely associated with metabolic syndrome. Studies indicate that elevated serum uric acid levels constitute an independent risk factor for the onset, progression, and prognosis of HFpEF. UA can directly participate in the pathophysiological process of HFpEF by inducing oxidative stress, activating the inflammasome and pro-inflammatory signaling pathways, and impairing both cardiomyocyte function and microvascular endothelial integrity. This systematic review examines the epidemiological association between UA and HFpEF, the underlying mechanisms of UA involvement in HFpEF, and the potential benefits of urate-lowering therapy, including xanthine oxidase inhibitors and sodium-glucose cotransporter 2 inhibitors, for patients with HFpEF. It aims to enhance awareness of serum uric acid management in HFpEF patients and promote further exploration of pharmacological interventions in this field.
Cyanotic Congenital Heart Disease in Pregnancy: A Comprehensive Review of Pathophysiology, Maternal-Fetal Outcomes, and Contemporary Management.
Frangaj K, Strubchevska K, Strubchevska O … +4 more , Kozyk M, Ahmad R, Frishman WH, Aronow WS
Cardiol Rev · 2026 May · PMID 42101946 · Publisher ↗
Advances in pediatric cardiac surgery and medical management have enabled an increasing number of women with cyanotic congenital heart disease to reach reproductive age and contemplate pregnancy. Maternal complications o...
Advances in pediatric cardiac surgery and medical management have enabled an increasing number of women with cyanotic congenital heart disease to reach reproductive age and contemplate pregnancy. Maternal complications occur in approximately 32% of pregnancies in women with uncorrected cyanotic heart disease, with heart failure, arrhythmias, and thromboembolism representing the primary adverse events. Fetal outcomes are critically dependent on maternal oxygen saturation, with live birth rates of 92% when saturation exceeds 90% but plummeting to 12% when saturation falls below 85%. This review synthesizes current evidence regarding the pathophysiology of major cyanotic lesions, maternal cardiovascular adaptations and risks, fetal and neonatal outcomes, risk stratification approaches, and contemporary management strategies from preconception through the postpartum period. Particular attention is given to lesion-specific considerations, guideline-based recommendations from the American Heart Association, American College of Cardiology, and the European Society of Cardiology, and the essential role of multidisciplinary cardio-obstetrics teams in optimizing outcomes for this high-risk population. The 2025 American College of Cardiology/American Heart Association/Heart Rhythm Society/International Society for Adult Congenital Heart Disease/Society for Cardiac angiography and Interventions Guideline for the Management of Adults with Congenital Heart Disease reinforces the importance of structured preconception counseling, individualized risk stratification, and coordinated multidisciplinary care in specialized ACHD centers.
Treatment and Outcomes for Acute Ischemic Stroke in Cardiomyopathy Patients With Heart Failure: A Retrospective Cross-Sectional Study.
Kishore Jain A, Gozum N, Wong S … +12 more , Nolan BE, Clare KM, Feldstein E, Vazquez S, Russo B, Thomas A, Lui A, Pandit M, Kaur G, Medicherla C, Gandhi CD, Al-Mufti F
Cardiol Rev · 2026 May · PMID 42092332 · Publisher ↗
Cardiomyopathy (CM) is a common cause of heart failure (HF), and those with HF have up to a 3-fold increased risk of stroke. This study aims to examine the incidence of intravascular thrombolysis and endovascular thrombe...
Cardiomyopathy (CM) is a common cause of heart failure (HF), and those with HF have up to a 3-fold increased risk of stroke. This study aims to examine the incidence of intravascular thrombolysis and endovascular thrombectomy and the functional outcomes in acute ischemic stroke (AIS) patients with CM and HF. International Classification of Diseases-10 codes were used to query the National Inpatient Sample database for patients with AIS and concurrent CM and HF from 2016 to 2019. Incidence of reperfusion therapy, medical complications, discharge disposition, length of hospital stay, and mortality between patients with and without CM and HF were compared using propensity score matching and multivariable logistic regression analysis. Of 2,939,160 patients identified with AIS, 80,915 (2.8%) had concomitant diagnoses of CM and HF. Patients in this population had more severe strokes (25.9% vs 19.6%, P < 0.001) and received endovascular thrombectomy at higher rates (8.8% vs 5.6%, P < 0.001) but equivalent rates of intravascular thrombolysis (3.0% vs 2.9%, P = 0.107). Additionally, CM/HF patients were more likely to experience inpatient death (6.6% vs 5.4%, P < 0.001). Despite this, those who survived were statistically more likely to have a favorable discharge disposition (45.7% vs 43.9%, P < 0.001). Although CM and HF patients are more likely to experience complications, prolonged length of stay, and inpatient death, those who survive have higher rates of favorable discharge disposition. These results suggest that stroke intervention is safe and efficacious in patients with CM and HF.
Contemporary Management of Ascending Aortic and Arch Dissection: Integrating Open, Hybrid, and Endovascular Strategies.
Filho AAM, Maia ADS, Rascov L … +10 more , Alves HFA, Aragão YM, Júnior FASL, Rzazade A, da Fonseca GDP, Rossi Ribeiro R, Ribeiro BS, Cividanes FR, Kilic A, da Fonseca JHAP
Cardiol Rev · 2026 May · PMID 42092326 · Publisher ↗
Acute aortic dissection is the most frequent presentation of acute aortic syndromes and remains a rapidly progressive and life-threatening condition requiring immediate diagnosis and treatment. Advances in surgical techn...
Acute aortic dissection is the most frequent presentation of acute aortic syndromes and remains a rapidly progressive and life-threatening condition requiring immediate diagnosis and treatment. Advances in surgical techniques, hybrid strategies, and endovascular technologies have expanded treatment options, particularly for high-risk and anatomically complex patients. This narrative review summarizes current evidence and guideline-based strategies for the management of aortic dissection, with emphasis on acute type A disease. The review integrates data from registries, contemporary clinical trials, meta-analyses, and recent international guidelines. Open surgical repair remains the standard of care for acute type A aortic dissection, providing reliable entry tear exclusion, restoration of true lumen perfusion, and prevention of rupture. Expanded surgical strategies such as frozen elephant trunk improve distal aortic remodeling and reduce late reinterventions in selected patients. Hybrid and adjunctive technologies, including modular dissection stents and branched stented anastomosis techniques, aim to improve distal perfusion and simplify arch reconstruction. Endovascular repair of the ascending aorta is emerging as a potential alternative for high-risk or inoperable patients, supported by early feasibility data and dedicated device development. Management of aortic dissection is rapidly evolving toward individualized, anatomy-driven strategies that integrate open, hybrid, and endovascular therapies. While open surgery remains the cornerstone for acute type A dissection, emerging endovascular technologies may expand treatment eligibility in selected patients. Future progress will depend on continued device innovation, multidisciplinary aortic team models, and prospective clinical trials to define optimal treatment algorithms.
Long-Term Oxygen Therapy and Cardiovascular Physiology: Divergent Effects in Heart Failure and Pulmonary Hypertension.
Kusayev J, Nayak S, Frishman WH … +1 more , Aronow WS
Cardiol Rev · 2026 May · PMID 42087317 · Publisher ↗
Long-term oxygen therapy (LTOT) is a cornerstone of management for chronic hypoxemic respiratory diseases, such as chronic obstructive pulmonary disease, yet its physiological impact as a potent modulator of cardiovascul...
Long-term oxygen therapy (LTOT) is a cornerstone of management for chronic hypoxemic respiratory diseases, such as chronic obstructive pulmonary disease, yet its physiological impact as a potent modulator of cardiovascular function remains a subject of ongoing investigation. While oxygen is primarily prescribed to correct arterial desaturation, its role as a regulator of vascular tone and cellular metabolism suggests it can exert significant, and sometimes contrasting, effects on the heart and systemic circulation. This review evaluates the evidence for LTOT in heart failure and pulmonary hypertension, 2 conditions where oxygen is frequently utilized despite varying levels of baseline hypoxemia. In heart failure, LTOT has not been shown to improve key hemodynamic variables and relevant endpoints, such as exercise capacity, in normoxemic patients. Some studies suggest that supplemental oxygen may even impose hemodynamic strain in this population by increasing systemic vascular resistance and reducing cardiac output. On the other hand, LTOT shows promise in improving relevant hemodynamic variables in pulmonary hypertension, such as mean pulmonary arterial pressure, as well as exercise capacity and other clinical measures across various baseline oxygen saturation levels. These findings suggest that the cardiovascular response to LTOT is highly dependent on the specific underlying pathology.
Anticoagulation in Patients With Gastrointestinal Disease.
Alkasabrah O, Ramesh J, Shah RK … +4 more , Chaudhry MQ, Jajja FA, Frishman WH, Aronow WS
Cardiol Rev · 2026 May · PMID 42087312 · Publisher ↗
Gastrointestinal (GI) disease complicates anticoagulation by simultaneously increasing bleeding risk and maintaining high thromboembolic vulnerability. Mucosal injury, portal hypertension, malignancy, inflammatory bowel...
Gastrointestinal (GI) disease complicates anticoagulation by simultaneously increasing bleeding risk and maintaining high thromboembolic vulnerability. Mucosal injury, portal hypertension, malignancy, inflammatory bowel disease, and vascular lesions predispose to hemorrhage, whereas interruption of therapy increases the risk of stroke, venous thromboembolism, and stent thrombosis. Contemporary management follows an indication-first, risk-balanced approach that integrates thrombotic urgency, GI disease phenotype, and patient-specific bleeding-risk factors. Direct oral anticoagulants demonstrate heterogeneous GI bleeding profiles, with higher risk observed with dabigatran and rivaroxaban, while apixaban is comparatively safer in high-risk populations. Periprocedural management is guided by procedural bleeding risk, renal function, and drug pharmacokinetics, with strategies emphasizing appropriate interruption and minimal use of bridging. In acute GI bleeding, management prioritizes hemodynamic stabilization, restrictive transfusion strategies, and early endoscopic or interventional radiology-guided source control, with selective use of reversal agents in severe cases. Adjunctive measures, including proton pump inhibitor therapy and Helicobacter pylori eradication, reduce recurrent bleeding risk. Resumption of anticoagulation is generally associated with improved survival and reduced thromboembolic events when timed appropriately. Key knowledge gaps remain regarding optimal reversal strategies, lesion-specific restart timing, and management in cirrhotic populations.
Catheter Ablation Versus Antiarrhythmic Drugs in the Management of Ventricular Tachycardia in Ischemic Cardiomyopathy: An Updated Systematic Review and Meta-analysis.
Elnashar M, Abdelsayed K, Mohamed AE … +12 more , Abomohsen M, Gadelmawla AF, Kholeif Z, Almakadma AH, Tahhan IS, Rashwan R, Elnady M, Jain H, Agrawal SP, Alahwany SH, Frishman WH, Aronow WS
Cardiol Rev · 2026 May · PMID 42087310 · Publisher ↗
Ventricular tachycardia (VT) is a major cause of morbidity and mortality in patients with ischemic cardiomyopathy. Prior randomized controlled trials comparing catheter ablation (CA) with antiarrhythmic drug (AAD) therap...
Ventricular tachycardia (VT) is a major cause of morbidity and mortality in patients with ischemic cardiomyopathy. Prior randomized controlled trials comparing catheter ablation (CA) with antiarrhythmic drug (AAD) therapy have reported inconsistent findings. We conducted an updated meta-analysis to compare the efficacy and safety of CA versus AAD therapy in this population. Four randomized controlled trials involving 846 patients were included. The weighted mean age was 58.7 years, the weighted mean left ventricular ejection fraction was 33.5%, and 88% of participants were male. In the AAD group, amiodarone and sotalol were used in 60% and 40% of patients, respectively. CA significantly reduced the primary composite outcome compared with AAD therapy (risk ratio [RR] = 0.85, 95% confidence interval [CI]: 0.75-0.97, P = 0.01), mainly driven by a lower incidence of treated sustained VT below the implantable cardioverter-defibrillator detection limit (RR = 0.25, 95% CI: 0.15-0.43, P < 0.01). CA also significantly reduced treatment-related adverse events (RR = 0.49, 95% CI: 0.36-0.65, P < 0.01). No significant differences were observed in all-cause mortality, appropriate implantable cardioverter-defibrillator shocks, or VT storm. In patients with ischemic cardiomyopathy and VT, CA reduces arrhythmic events and treatment-related adverse events compared with AAD therapy, although a survival benefit remains unproven.
Long-Term Exposure to PM2.5 and Risk of Incident Dementia: A Systematic Review and Meta-Analysis of Cohort Studies.
Rocheeld J, Gluck B, Frishman WH … +1 more , Aronow WS
Cardiol Rev · 2026 May · PMID 42087308 · Publisher ↗
Exposure to ambient fine particulate matter (PM2.5) is associated with cardiovascular and inflammatory pathways implicated in neurodegeneration. However, epidemiologic findings linking PM2.5 exposure to dementia incidenc...
Exposure to ambient fine particulate matter (PM2.5) is associated with cardiovascular and inflammatory pathways implicated in neurodegeneration. However, epidemiologic findings linking PM2.5 exposure to dementia incidence remain heterogeneous. We conducted a systematic review and meta-analysis of existing cohort studies evaluating the association between PM2.5 exposure and incident dementia. A literature search yielded 909 records, of which 15 cohort studies, including approximately 65 million participants in Europe, Asia, and North America, were included in the meta-analysis. Hazard ratios were standardized to a 1 μg/m3 increase in PM2.5 exposure using logarithmic transformation. Effect estimates were then pooled using a random-effects model. Long-term PM2.5 exposure was associated with an increased risk of incident dementia (pooled HR 1.04, 95% confidence interval 1.01-1.06). Substantial heterogeneity was observed across studies (I2 = 88.3%). These findings support growing evidence that chronic exposure to fine particulate air pollution may contribute to the development of dementia and highlight air pollution as a potentially modifiable environmental risk factor for neurodegenerative disease.
Why Do Blue Zone Populations Live Longer? Mechanistic Insights Into Cardiovascular Longevity.
Mehta K, Senthil A, Banker H … +4 more , Trivedi YV, Manucharyan A, Sahu N, Jain R
Cardiol Rev · 2026 May · PMID 42087302 · Publisher ↗
Growing interest in Blue Zone populations and a focus on cardiovascular protection are leading to significant discoveries about human longevity. These regions-Okinawa, Sardinia, the Nicoya Peninsula, Ikaria, and Loma Lin...
Growing interest in Blue Zone populations and a focus on cardiovascular protection are leading to significant discoveries about human longevity. These regions-Okinawa, Sardinia, the Nicoya Peninsula, Ikaria, and Loma Linda-are characterized by a high prevalence of centenarians and relatively low rates of cardiovascular mortality. Despite cardiovascular disease remaining the leading global cause of morbidity and mortality, its relationship with exceptional longevity remains incompletely understood. Much of the existing literature on Blue Zones is descriptive, with limited integration of cardiovascular epidemiology and the biological mechanisms underlying healthy cardiac aging. This narrative review aims to bridge this gap by examining key cardiovascular features associated with longevity, including vascular aging, myocardial remodeling, and autonomic regulation. In addition, we explore mechanistic pathways derived from centenarian studies, such as reduced inflammation, enhanced metabolic efficiency, and favorable neurohormonal balance, to better understand how these factors collectively shape a distinct cardiovascular aging trajectory. By integrating epidemiological patterns with mechanistic insights, this work seeks to provide a more comprehensive framework for understanding cardiovascular longevity and its potential translation into preventive cardiology.
About
- Frequency
- Sun
- Papers found
- 200
- RSS feed
- Subscribe