Comparison between the outcomes of transfemoral access and transfemoral access with adjunct upper extremity access in patients undergoing endovascular aortic repair: A pilot systematic review and meta-analysis.

Endovascular aortic repair is an emerging novel intervention for the management of abdominal aortic aneurysms. It is crucial to compare the effectiveness of different access sites, such as transfemoral access (TFA) and upper extremity access (UEA). An electronic literature search was conducted using PubMed, EMBASE, and Google Scholar databases. The primary endpoint was the incidence of stroke/transient ischemic attack (TIA), while the secondary endpoints included technical success, access-site complications, mortality, myocardial infarction (MI), spinal cord ischemia, among others. Forest plots were constructed for the pooled analysis of data using the random-effects model in Review Manager, version 5.4. Statistical significance was set at p < 0.05. Our findings in 9403 study participants (6228 in the TFA group and 3175 in the UEA group) indicate that TFA is associated with a lower risk of stroke/TIA [RR: 0.55; 95% CI: 0.40-0.75; p = 0.0002], MI [RR: 0.51; 95% CI: 0.38-0.69; p < 0.0001], spinal cord ischemia [RR: 0.41; 95% CI: 0.32-0.53, p < 0.00001], and shortens fluoroscopy time [SMD: -0.62; 95% CI: -1.00 to -0.24; p = 0.001]. Moreover, TFA required less contrast agent [SMD: -0.33; 95% CI: -0.61 to -0.06; p = 0.02], contributing to its appeal. However, no significant differences emerged in technical success [p = 0.23], 30-day mortality [p = 0.48], ICU stay duration [p = 0.09], or overall hospital stay length [p = 0.22]. Patients with TFA had a lower risk of stroke, MI, and spinal cord ischemia, shorter fluoroscopy time, and lower use of contrast agents. Future large-scale randomized controlled trials are warranted to confirm and strengthen these findings.

Palliative care in the cardiovascular intensive care unit: A systematic review of current literature.

BACKGROUND: There has been an evolution in the disease severity and complexity of patients presenting to the cardiac intensive care unit (CICU). There are limited data evaluating the role of palliative care in contemporary CICU practice. METHODS: PubMed Central, CINAHL, EMBASE, Medline, Cochrane Library, Scopus, and Web of Science databases were evaluated for studies on palliative care in adults (≥18 years) admitted with acute cardiovascular conditions - acute myocardial infarction, cardiogenic shock, cardiac arrest, advanced heart failure, post-cardiac surgery, spontaneous coronary artery dissection, Takotsubo cardiomyopathy, and pulmonary embolism - admitted to the CICU, coronary care unit or cardiovascular intensive care unit from 1/1/2000 to 8/8/2022. The primary outcome of interest was the utilization of palliative care services. Secondary outcomes of included studies were also addressed. Meta-analysis was not performed due to heterogeneity. RESULTS: Of 5711 citations, 30 studies were included. All studies were published in the last seven years and 90 % originated in the United States. Twenty-seven studies (90 %) were retrospective analyses, with a majority from the National Inpatient Sample database. Heart failure was the most frequent diagnosis (47 %), and in-hospital mortality was reported in 67 % of studies. There was heterogeneity in the timing, frequency, and background of the care team that determined palliative care consultation. In two randomized trials, there appeared to be improvement in quality of life without an impact on mortality. CONCLUSIONS: Despite the growing recognition of the role of palliative care, there are limited data on palliative care consultation in the CICU.

The role of renal denervation in cardiology and beyond: An updated comprehensive review and future directives.

Renal denervation (RDN) is a minimally invasive intervention performed by denervation of the nervous fibers in the renal plexus, which decreases sympathetic activity. These sympathetic nerves influence various physiological functions that regulate blood pressure (BP), including intravascular volume, electrolyte composition, and vascular tone. Although proven effective in some trials, controversial trials, such as the Controlled Trial of Renal Denervation for Resistant Hypertension (SYMPLICITY-HTN3), have demonstrated contradictory results for the effectiveness of RDN in resistant hypertension (HTN). In the treatment of HTN, individuals with primary HTN are expected to experience greater benefits compared to those with secondary HTN due to the diverse underlying causes of secondary HTN. Beyond its application for HTN, RDN has also found utility in addressing cardiac arrhythmias, such as atrial fibrillation, and managing cases of heart failure. Non-cardiogenic applications of RDN include reducing the intensity of obstructive sleep apnea (OSA), overcoming insulin resistance, and in chronic kidney disease (CKD) patients. This article aims to provide a comprehensive review of RDN and its uses in cardiology and beyond, along with providing future directions and perspectives.

Management of coronary artery disease in patients with aortic stenosis in the era of transcatheter aortic valve replacement.

Aortic stenosis (AS) is a common valve disorder among the elderly, and these patients frequently have concomitant coronary artery disease (CAD). Risk factors for calcific AS are similar to those for CAD. Historically, the treatment of these conditions involved simultaneous surgical replacement of the aortic valve (AV) with coronary artery bypass grafting. Since the advancement of transcatheter AV therapies, there have been tremendous advancements in the safety, efficacy, and feasibility of this procedure with expanding indications. This has led to a paradigm shift in our approach to the patient with AS and concomitant CAD. Data regarding the management of CAD in patients with AS are largely limited to single-center studies or retrospective analyses. This article aims to review available literature around the management of CAD in patients with AS and assist in the current understanding in approaches toward management.

Targeted Temperature Management in Cardiac Arrest: An Updated Narrative Review.

The established benefits of cooling along with development of sophisticated methods to safely and precisely induce, maintain, monitor, and reverse hypothermia have led to the development of targeted temperature management (TTM). Early trials in human subjects showed that hypothermia conferred better neurological outcomes when compared to normothermia among survivors of cardiac arrest, leading to guidelines recommending targeted hypothermia in this patient population. Multiple studies have sought to explore and compare the benefit of hypothermia in various subgroups of patients, such as survivors of out-of-hospital cardiac arrest versus in-hospital cardiac arrest, and survivors of an initial shockable versus non-shockable rhythm. Larger and more recent trials have shown no statistically significant difference in neurological outcomes between patients with targeted hypothermia and targeted normothermia; further, aggressive cooling is associated with a higher incidence of multiple systemic complications. Based on this data, temporal trends have leaned towards using a lenient temperature target in more recent times. Current guidelines recommend selecting and maintaining a constant target temperature between 32 and 36 °C for those patients in whom TTM is used (strong recommendation, moderate-quality evidence), as soon as possible after return of spontaneous circulation is achieved and airway, breathing (including mechanical ventilation), and circulation are stabilized. The comparative benefit of lower (32-34 °C) versus higher (36 °C) temperatures remains unknown, and further research may help elucidate this. Any survivor of cardiac arrest who is comatose (defined as unarousable unresponsiveness to external stimuli) should be considered as a candidate for TTM regardless of the initial presenting rhythm, and the decision to opt for targeted hypothermia versus targeted normothermia should be made on a case-by-case basis.

Takotsubo cardiomyopathy following liver transplantation and COVID-19 infection.

Takotsubo cardiomyopathy involves transient systolic dysfunction of the left ventricle thought to be caused by a physiologic stress response and associated catecholamine release. We present a previously undocumented cause of this stress response involving a 53-year-old man with hepatocellular carcinoma and alcohol-associated cirrhosis who initially presented for liver transplantation. Shortly after successful transplantation, the patient developed a COVID-19 infection and takotsubo cardiomyopathy.

Role of Lipid-Lowering Therapy in Peripheral Artery Disease.

Atherosclerosis is a multifactorial, lipoprotein-driven condition that leads to plaque formation within the arterial tree, leading to subsequent arterial stenosis and thrombosis that accounts for a large burden of cardiovascular morbidity and mortality globally. Atherosclerosis of the lower extremities is called peripheral artery disease and is a major cause of loss in mobility, amputation, and critical limb ischemia. Peripheral artery disease is a common condition with a gamut of clinical manifestations that affects an estimated 10 million people in the United States of America and 200 million people worldwide. The role of apolipoprotein B-containing lipoproteins, such as LDL and remnant lipoproteins in the development and progression of atherosclerosis, is well-established. The focus of this paper is to review existing data on lipid-lowering therapies in lower extremity atherosclerotic peripheral artery disease.

The BRASH syndrome, a synergistic arrhythmia phenomenon.

BRASH syndrome is a relatively novel clinical entity with profound bradycardia secondary to simultaneous metabolic derangement and drug toxicity. The syndrome is a clinical pentad of bradycardia, acute kidney injury, use of atrioventricular nodal blocking agents, shock, and hyperkalemia. It is widely underrecognized with selectively few reports, mainly in the elderly population. We present a 43-year-old woman on two oral atrioventricular blocking agents who presented with 1 week of increasing lethargy with rapid deterioration into cardiac arrest with subsequent shock postresuscitation. She was found to have hyperkalemia, metabolic acidosis, and acute kidney injury on arrival. Her initial electrocardiogram was remarkable for sinus arrest and junctional bradycardia. She was treated with a temporary pacemaker, renal replacement therapy, and potassium-lowering agents, with subsequent improvement resulting in conversion to normal sinus rhythm.

Chronic Stress-Related Neural Activity Associates With Subclinical Cardiovascular Disease in Psoriasis: A Prospective Cohort Study.

OBJECTIVES: This study hypothesized that there is an association between chronic stress (as indexed by resting amygdalar activity [AmygA]), hematopoietic system activity (HMPA), and subclinical cardiovascular indexes (aortic vascular inflammation [VI] and noncalcified coronary plaque burden [NCB]) in psoriasis (PSO). The study also hypothesized that treatment of PSO would improve these parameters. BACKGROUND: PSO is a stress-related chronic inflammatory condition that is associated with increased prevalence of subclinical cardiovascular disease (CVD). In individuals without PSO, stress has been linked to CVD through a serial biological pathway that involves the amygdala, hematopoietic tissues, and atherosclerotic plaques. METHODS: A total of 164 consecutive patients with PSO and 47 healthy volunteers underwent 18-fluorodeoxyglucose positron emission tomography/computed tomography scans for assessment of AmygA, HMPA, and VI, as well as coronary computed tomography angiography scans for quantifying NCB. Furthermore, a consecutive subset of 30 patients with severe PSO (Psoriasis Area Severity Index Score >10) were followed at 1 year to assess the relationship between skin disease improvement and AmygA, HMPA, VI, and NCB. RESULTS: The PSO cohort was middle-aged (mean age: 50 years), had low cardiovascular risk (Framingham risk score: median: 3) and had mild to moderate PSO activity (median Psoriasis Area Severity Index Score: 5.6). AmygA was higher in patients with PSO compared to volunteer participants. AmygA was associated with HMPA (bone marrow activity: ß = 0.20, p = 0.01) and subclinical CVD (VI: ß = 0.31, p < 0.001; NCB: ß = 0.27, p < 0.001) The AmygA-CVD association was in part mediated by HMPA (VI: 20.9%, NCB: 36.7%). Following 1 year of PSO treatment in those with severe disease, improvement in skin disease was accompanied by a reduction in AmygA, bone marrow activity, and VI, with no progression of NCB. CONCLUSIONS: In PSO, a chronic inflammatory disease state, AmygA, which is a manifestation of chronic stress, substantially contributes to the risk of subclinical CVD. Additional studies that use psychometric measures of stress are required to explore therapeutic impact.

Association Between Soluble Lectinlike Oxidized Low-Density Lipoprotein Receptor-1 and Coronary Artery Disease in Psoriasis.

Importance: Psoriasis, a chronic inflammatory skin disease associated with accelerated noncalcified coronary burden (NCB) by coronary computed tomography angiography (CCTA), accelerates lipoprotein oxidation in the form of oxidized modified lipoproteins. A transmembrane scavenger receptor for these oxidized modified lipoproteins is lectinlike oxidized low-density lipoprotein receptor-1 (LOX-1), which has been reported to be associated with coronary artery disease. It is unknown whether this receptor is associated with coronary artery disease in psoriasis. Objective: To assess the association between soluble LOX-1 (sLOX-1) and NCB in psoriasis over time. Design, Setting, and Participants: In a cohort study at the National Institutes of Health, 175 consecutive patients with psoriasis were referred from outpatient dermatology practices between January 1, 2013, and October 1, 2017. A total of 138 consecutively recruited patients with psoriasis were followed up at 1 year. Exposures: Circulating soluble lectinlike oxidized low-density lipoprotein receptor-1 levels were measured blindly by field scientists running undiluted serum using an enzyme-linked immunosorbent assay. Main Outcomes and Measures: Coronary computed tomography angiography scans were performed to quantify NCB in all 3 major epicardial coronary arteries by a reader blinded to patient demographics, visit, and treatment status. Results: Among the 175 patients with psoriasis, the mean (SD) age was 49.7 (12.6) years and 91 were men (55%). The cohort had relatively low median cardiovascular risk by Framingham risk score (median, 2.0 [interquartile range (IQR), 1.0-6.0]) and had a mean (SD) body mass index (calculated as weight in kilograms divided by height in meters squared) suggestive of overweight profiles (29.6 [6.0]). Elevated sLOX-1 levels were found in patients with psoriasis compared with age- and sex-matched controls (median, 210.3 [IQR, 110.9-336.2] vs 83.7 [IQR, 40.1-151.0]; P < .001), and were associated with Psoriasis Area Severity Index (PASI) score (ß = 0.23; 95% CI, 0.082-0.374; P = .003). Moreover, sLOX-1 was associated with NCB independent of hyperlipidemia status (ß = 0.11; 95% CI, 0.016-0.200; P = .023), an association which persisted after adjusting for traditional cardiovascular risk factors, statin use, and biologic psoriasis treatment (ß = 0.10; 95% CI, 0.014-0.193; P = .03). At 1 year, in those who had clinical improvement in PASI (eg, >50% improvement), a reduction in sLOX-1 (median, 311.1 [IQR, 160.0-648.8] vs median, 224.2 [IQR, 149.1 - 427.4]; P = .01) was associated with a reduction in NCB (ß = 0.14; 95% CI, 0.028-0.246; P = .02). Conclusions and Relevance: Soluble lectinlike oxidized low-density lipoprotein receptor-1 levels were elevated in patients with psoriasis and were associated with severity of skin disease. Moreover, sLOX-1 associated with NCB independent of hyperlipidemia status, suggesting that inflammatory sLOX-1 induction may modulate lipid-rich NCB in psoriasis. Improvement of skin disease was associated with a reduction of sLOX-1 at 1 year, demonstrating the potential role of sLOX-1 in inflammatory atherogenesis in psoriasis.

Coronary artery plaque characteristics and treatment with biologic therapy in severe psoriasis: results from a prospective observational study.

AIMS: The use of biologic therapy has increased over the past decade well beyond primary autoimmune diseases. Indeed, a recent trial using an anti-IL-1beta antibody reduced second myocardial infarction (MI) in those who have had MI. Psoriasis is a chronic inflammatory disease often treated with biologics when severe, is associated with increased risk of MI, in part driven by high-risk coronary plaque phenotypes by coronary computed tomography angiography (CCTA). We hypothesized that we would observe a reduction in inflammatory-driven phenotypes of coronary plaque, including non-calcified coronary plaque burden and lipid-rich necrotic core in those treated with biologic therapy after one-year compared with non-biologic therapy. METHODS AND RESULTS: In a prospective, observational study, 290 participants were recruited from 1 January 2013 through 31 October 2018 with 215 completing one-year follow-up. Of the 238, 121 consecutive participants who were biologic treatment naïve at baseline were included. A blinded reader (blinded to patient demographics, visit and treatment) quantified total coronary plaque burden and plaque subcomponents (calcified and non-calcified) in the three main coronary vessels >2 mm using dedicated software (QAngio, Medis, Netherlands). Psoriasis patients were middle-aged [mean (standard deviation) age, 50.5 (12.1) years], mostly male (n = 70, 58%) with low cardiovascular risk by Framingham score [median (interquartile range, IQR), 3 (1-6)] and had moderate to severe skin disease at baseline [median (IQR) Psoriasis Area Severity Index, PASI, 8.6 (5.3-14.0)]. Biologic therapy was associated with a 6% reduction in non-calcified plaque burden (P = 0.005) reduction in necrotic core (P = 0.03), with no effect on fibrous burden (P = 0.71). Decrease in non-calcified plaque burden in the biologic treated group was significant compared with slow plaque progression in non-biologic treated (Δ, -0.07 mm2 vs. 0.06 mm2; P = 0.02) and associated with biologic treatment beyond adjustment for traditional cardiovascular risk factors (ß = 0.20, P = 0.02). CONCLUSION: In this observational study, we demonstrate that biologic therapy in severe psoriasis was associated with favourable modulation of coronary plaque indices by CCTA. These findings highlight the importance of systemic inflammation in coronary artery disease and support the conduct of larger, randomized trials.

Association Between Aortic Vascular Inflammation and Coronary Artery Plaque Characteristics in Psoriasis.

Importance: Inflammation is critical to atherosclerosis. Psoriasis, a chronic inflammatory disease associated with early cardiovascular events and increased aortic vascular inflammation (VI), provides a model to study the process of early atherogenesis. Fludeoxyglucose F 18 positron emission tomography/computed tomography (18F-FDG PET/CT) helps quantify aortic VI, and coronary computed tomography angiography provides coronary artery disease (CAD) assessment through evaluation of total plaque burden (TB) and noncalcified coronary plaque burden (NCB), luminal stenosis, and high-risk plaques (HRP). To our knowledge, association between aortic VI and broad CAD indices has not yet been assessed in a chronic inflammatory disease state. Such a study may provide information regarding the utility of aortic VI in capturing early CAD. Objective: To assess the association between aortic VI and CAD indices, including TB, NCB, luminal stenosis, and HRP prevalence, in psoriasis. Design, Setting, and Participants: In a cross-sectional cohort study at the National Institutes of Health, 215 consecutive patients with psoriasis were recruited from surrounding outpatient dermatology practices. All patients underwent 18F-FDG PET/CT for aortic VI assessment, and 190 of 215 patients underwent coronary computed tomography angiography to characterize CAD. The study was conducted between January 1, 2013, and May 31, 2017. Data were analyzed in March 2018. Exposures: Aortic VI assessed by 18F-FDG PET/CT. Main Outcomes and Measures: Primary outcome: TB and NCB. Secondary outcomes: luminal stenosis and HRP. Results: Among 215 patients with psoriasis (mean [SD] age, 50.4 [12.6] years; 126 men [59%]), patients with increased aortic VI had increased TB (standardized ß = 0.48; P < .001), and higher prevalence of luminal stenosis (OR, 3.63; 95% CI, 1.71-7.70; P = .001) and HRP (OR, 3.05; 95% CI, 1.42-6.47; P = .004). The aortic VI and TB association was primarily driven by NCB (ß = 0.49; P < .001), whereas the aortic VI and HRP association was driven by low-attenuation plaque (OR, 5.63; 95% CI, 1.96-16.19; P = .001). All associations of aortic VI remained significant after adjustment for cardiovascular risk factors: aortic VI and TB (ß = 0.23; P < .001), NCB (ß = 0.24; P < .001), luminal stenosis (OR, 3.40; 95% CI, 1.40-8.24; P = .007), and HRP (OR, 2.72; 95% CI, 1.08-6.83; P = .03). No association was found between aortic VI and dense-calcified coronary plaque burden. Conclusions and Relevance: Aortic VI is associated with broad CAD indices, suggesting that aortic VI may be a surrogate for early CAD. Larger prospective studies need to assess these associations longitudinally and examine treatment effects on these outcomes.

Chronic skin inflammation accelerates macrophage cholesterol crystal formation and atherosclerosis.

Inflammation is critical to atherogenesis. Psoriasis is a chronic inflammatory skin disease that accelerates atherosclerosis in humans and provides a compelling model to understand potential pathways linking these diseases. A murine model capturing the vascular and metabolic diseases in psoriasis would accelerate our understanding and provide a platform to test emerging therapies. We aimed to characterize a new murine model of skin inflammation (Rac1V12) from a cardiovascular standpoint to identify novel atherosclerotic signaling pathways modulated in chronic skin inflammation. The RacV12 psoriasis mouse resembled the human disease state, including presence of systemic inflammation, dyslipidemia, and cardiometabolic dysfunction. Psoriasis macrophages had a proatherosclerotic phenotype with increased lipid uptake and foam cell formation, and also showed a 6-fold increase in cholesterol crystal formation. We generated a triple-genetic K14-RacV12-/+/Srb1-/-/ApoER61H/H mouse and confirmed psoriasis accelerates atherogenesis (~7-fold increase). Finally, we noted a 60% reduction in superoxide dismutase 2 (SOD2) expression in human psoriasis macrophages. When SOD2 activity was restored in macrophages, their proatherogenic phenotype reversed. We demonstrate that the K14-RacV12 murine model captures the cardiometabolic dysfunction and accelerates vascular disease observed in chronic inflammation and that skin inflammation induces a proatherosclerotic macrophage phenotype with impaired SOD2 function, which associated with accelerated atherogenesis.