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European Journal of Case Reports in... 2024Anomalous bronchial artery origins may have clinical implications beyond their anatomical curiosity. In this case, identification of such an anomaly led to the diagnosis...
UNLABELLED
Anomalous bronchial artery origins may have clinical implications beyond their anatomical curiosity. In this case, identification of such an anomaly led to the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH). A 49-year-old male with a history of recurrent deep vein thrombosis (DVT) and pulmonary embolism (PE) on anticoagulation presented with chest pain and shortness of breath. Laboratory analysis was remarkable for a troponin peak of 14.74 ng/ml, a brain natriuretic peptide level of 602 pg/ml and a D-dimer level of 0.62 μg/ml. Electrocardiogram showed non-specific ST elevation in the anterolateral and inferior leads. Computed tomography angiography (CTA) of the chest was positive for PE involving the right lower lobe pulmonary arterial tree. Echocardiogram showed reduced left ventricular function (ejection fraction 38%) and akinesis of the antero-apical and infero-apical segments. Cardiac catheterization revealed non-obstructive coronary arteries, and an anomalous origin of a right bronchial artery from the right coronary artery. The right bronchial hypertrophied as it supplied collateral flow to the occluded right pulmonary artery. This anomaly and the patient's history of multiple DVT/PEs while on therapeutic levels of warfarin with near normal D-dimer levels raised suspicion for a false positive PE. Pulmonary angiogram revealed chronic occlusion in branches of the right pulmonary artery, mean pulmonary artery pressure of 36 mmHg and no acute thrombus. Ventilation-perfusion scan confirmed the diagnosis of CTEPH. The patient underwent successful pulmonary thromboendarterectomy and subsequently had normalization of mean pulmonary artery pressure. This case underscores the importance of a comprehensive diagnostic approach, and consideration of alternative explanations for imaging findings, that unveiled the diagnosis of a complex and life-threatening condition such as CTEPH.
LEARNING POINTS
This case underscores the diagnostic significance of identifying anomalous bronchial artery origin which played a crucial role in the diagnosis of the underlying chronic thromboembolic pulmonary hypertension (CTEPH).It is important to understand the limitations of computed tomography angiography (CTA) chest for diagnosis of CTEPH.
PubMed: 38846648
DOI: 10.12890/2024_004616 -
Cureus May 2024Fibroblast growth factors (FGF) are a type of cell signaling proteins that are mostly produced by macrophages. They are essential for a variety of biological activities... (Review)
Review
Fibroblast growth factors (FGF) are a type of cell signaling proteins that are mostly produced by macrophages. They are essential for a variety of biological activities involved in normal development. Fibroblast growth factor 23 (FGF23) is the newest and youngest member of the FGF endocrine subfamily, along with fibroblast growth factor 19 (FGF19) and fibroblast growth factor 21 (FGF21). In this study, we conduct a systematic review of all known literature to identify the risk of elevated FGF23 in the cardiovascular system. The analysis includes the risk of cardiovascular disease for both primary and secondary causes of elevated FGF23, such as chronic renal insufficiency. This systematic literature review adhered to the Preferred Reporting Items and Meta-Analysis (PRISMA) standards. A total of 4,793 records were identified across different databases. After that, 273 records were retrieved and reviewed. After carefully examining the titles and summaries of each report, 249 additional entries were eliminated. About 24 studies from the remaining records were chosen by primary and secondary authors for screening, and they performed a quality assessment using common quality check tools. Finally, this review included 11 studies. Following a thorough analysis, we came to the conclusion that FGF23 can be regarded as a novel biomarker and should be included in the group of heart biomarkers that have already been identified, such as B-type natriuretic peptide (BNP), for the early identification of a variety of highly prevalent cardiovascular disorders.
PubMed: 38846254
DOI: 10.7759/cureus.59820 -
Respiratory Research Jun 2024Abnormal remodeling of distal pulmonary arteries in patients with pulmonary arterial hypertension (PAH) leads to progressively increased pulmonary vascular resistance,...
BACKGROUND
Abnormal remodeling of distal pulmonary arteries in patients with pulmonary arterial hypertension (PAH) leads to progressively increased pulmonary vascular resistance, followed by right ventricular hypertrophy and failure. Despite considerable advancements in PAH treatment prognosis remains poor. We aim to evaluate the potential for using the cytokine resistin as a genetic and biological marker for disease severity and survival in a large cohort of patients with PAH.
METHODS
Biospecimens, clinical, and genetic data for 1121 adults with PAH, including 808 with idiopathic PAH (IPAH) and 313 with scleroderma-associated PAH (SSc-PAH), were obtained from a national repository. Serum resistin levels were measured by ELISA, and associations between resistin levels, clinical variables, and single nucleotide polymorphism genotypes were examined with multivariable regression models. Machine-learning (ML) algorithms were applied to develop and compare risk models for mortality prediction.
RESULTS
Resistin levels were significantly higher in all PAH samples and PAH subtype (IPAH and SSc-PAH) samples than in controls (P < .0001) and had significant discriminative abilities (AUCs of 0.84, 0.82, and 0.91, respectively; P < .001). High resistin levels (above 4.54 ng/mL) in PAH patients were associated with older age (P = .001), shorter 6-min walk distance (P = .001), and reduced cardiac performance (cardiac index, P = .016). Interestingly, mutant carriers of either rs3219175 or rs3745367 had higher resistin levels (adjusted P = .0001). High resistin levels in PAH patients were also associated with increased risk of death (hazard ratio: 2.6; 95% CI: 1.27-5.33; P < .0087). Comparisons of ML-derived survival models confirmed satisfactory prognostic value of the random forest model (AUC = 0.70, 95% CI: 0.62-0.79) for PAH.
CONCLUSIONS
This work establishes the importance of resistin in the pathobiology of human PAH. In line with its function in rodent models, serum resistin represents a novel biomarker for PAH prognostication and may indicate a new therapeutic avenue. ML-derived survival models highlighted the importance of including resistin levels to improve performance. Future studies are needed to develop multi-marker assays that improve noninvasive risk stratification.
Topics: Humans; Male; Female; Resistin; Middle Aged; Adult; Severity of Illness Index; Biomarkers; Predictive Value of Tests; Pulmonary Arterial Hypertension; Aged; Cohort Studies; Polymorphism, Single Nucleotide; Survival Rate; Hypertension, Pulmonary
PubMed: 38844967
DOI: 10.1186/s12931-024-02861-8 -
Journal of the American Heart... Jun 2024The aim of this study was to evaluate the association between obesity and risk of incident left ventricular hypertrophy (LVH) in community-dwelling populations with... (Observational Study)
Observational Study
BACKGROUND
The aim of this study was to evaluate the association between obesity and risk of incident left ventricular hypertrophy (LVH) in community-dwelling populations with hypertension and investigate whether this association would be attenuated by a lower achieved systolic blood pressure (SBP).
METHODS AND RESULTS
We used the EMINCA (Echocardiographic Measurements in Normal Chinese Adults) criteria, which were derived from healthy Chinese populations to define LVH. A total of 2069 participants with hypertension and without LVH (obesity 20.4%) were included. The association between obesity and risk of incident LVH was evaluated using Cox proportional hazard models and stratified by achieved follow-up SBP levels (≥140, 130-139, and <130 mm Hg). These analyses were also assessed using the American Society of Echocardiography/European Association of Cardiovascular Imaging criteria, which were derived from European populations to define LVH. After a median follow-up of 2.90 years, the rates of incident LVH in the normal-weight, overweight, and obese groups were 13.5%, 20.3%, and 27.8%, respectively (<0.001). In reference to normal weight, obesity was associated with increased risk of incident LVH (adjusted hazard ratio [aHR], 2.51 [95% CI, 1.91-3.29]), which was attenuated when achieved SBP was <130 mm Hg (aHR, 1.78 [95% CI, 0.99-3.19]). This association remained significant when achieved SBP was ≥140 mm Hg (aHR, 3.45 [95% CI, 2.13-5.58]) or at 130 to 139 mm Hg (aHR, 2.32 [95% CI, 1.23-4.36]). Differences in these findings were noted when LVH was defined by the American Society of Echocardiography/European Association of Cardiovascular Imaging criteria.
CONCLUSIONS
Obesity was associated with incident LVH and an SBP target <130 mm Hg might be needed to attenuate this risk in patients with hypertension and obesity.
Topics: Humans; Hypertrophy, Left Ventricular; Male; Hypertension; Obesity; Female; Middle Aged; Incidence; Blood Pressure; China; Risk Factors; Independent Living; Aged; Echocardiography; Risk Assessment; Adult
PubMed: 38842284
DOI: 10.1161/JAHA.123.033521 -
Journal of the American Heart... Jul 2024The aim of this study was to assess how early-adulthood body mass index (BMI) and waist circumference (WC) relate to long-term cardiovascular structure, function, and...
BACKGROUND
The aim of this study was to assess how early-adulthood body mass index (BMI) and waist circumference (WC) relate to long-term cardiovascular structure, function, and prognosis in individuals without obesity and with low cardiovascular risk factor (CVRF) burden.
METHODS AND RESULTS
A total of 2024 participants aged 18 to 30 from the CARDIA (Coronary Artery Risk Development in Young Adults) study, without obesity and with low CVRFs defined as the absence of cardiovascular disease (CVD), diabetes, hypertension, current smoking, and dyslipidemia were included. A CVRF-optimal subgroup was also defined, with blood pressure<120/80 mm Hg, fasting glucose <100 mg/dL, total cholesterol <200, low-density lipoprotein cholesterol <130, and women with high-density lipoprotein cholesterol ≥50 mg/dL. Coronary artery calcification, carotid intima-media thickness, left ventricular mass, left ventricular ejection fraction, longitudinal peak systolic strain, and diastolic function were assessed in midlife. Cox regression was used to calculate hazard ratios of BMI and WC for all-cause death and CVD events. Logistic regression was used to estimate odds ratios for subclinical CVD. Over 33.9 years (median follow-up), 5.2% (n=105) died, and 2.6% (n=52) had CVD events. Each 1-SD BMI increase was associated with 27% (95% CI, 1.10-1.47), 24% (1.08-1.43), 42% (1.20-1.68), 28% (1.05-1.57), 51% (1.20-1.90), and 49% (1.10-2.02) higher odds of coronary artery calcification presence, increased carotid intima-media thickness, left ventricular hypertrophy, reduced left ventricular ejection fraction, low longitudinal peak systolic strain, and diastolic dysfunction, respectively, in the CVRF-low group. Generally, similar associations were found for WC and in the CVRF-optimal subgroup. No significant associations between BMI and WC with CVD and death were found.
CONCLUSIONS
Elevations in BMI and WC among young low-risk individuals, even within the nonobesity range, are associated with midlife cardiovascular health.
Topics: Humans; Female; Male; Adult; Body Mass Index; Young Adult; Waist Circumference; Adolescent; Cardiovascular Diseases; Heart Disease Risk Factors; Risk Assessment; Carotid Intima-Media Thickness; United States; Risk Factors; Prognosis; Age Factors
PubMed: 38842274
DOI: 10.1161/JAHA.123.033355 -
Journal of the American Heart... Jun 2024The mineralocorticoid receptor plays a significant role in the development of chronic kidney disease (CKD) and associated cardiovascular complications. Classic steroidal...
BACKGROUND
The mineralocorticoid receptor plays a significant role in the development of chronic kidney disease (CKD) and associated cardiovascular complications. Classic steroidal mineralocorticoid receptor antagonists are a therapeutic option, but their use in the clinic is limited due to the associated risk of hyperkalemia in patients with CKD. Finerenone is a nonsteroidal mineralocorticoid receptor antagonist that has been recently investigated in 2 large phase III clinical trials (FIDELIO-DKD [Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease] and FIGARO-DKD [Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease]), showing reductions in kidney and cardiovascular outcomes.
METHODS AND RESULTS
We tested whether finerenone improves renal and cardiac function in a preclinical nondiabetic CKD model. Twelve weeks after 5/6 nephrectomy, the rats showed classic signs of CKD characterized by a reduced glomerular filtration rate and increased kidney weight, associated with left ventricular (LV) diastolic dysfunction and decreased LV perfusion. These changes were associated with increased cardiac fibrosis and reduced endothelial nitric oxide synthase activating phosphorylation (ser 1177). Treatment with finerenone prevented LV diastolic dysfunction and increased LV tissue perfusion associated with a reduction in cardiac fibrosis and increased endothelial nitric oxide synthase phosphorylation. Curative treatment with finerenone improves nondiabetic CKD-related LV diastolic function associated with a reduction in cardiac fibrosis and increased cardiac phosphorylated endothelial nitric oxide synthase independently from changes in kidney function. Short-term finerenone treatment decreased LV end-diastolic pressure volume relationship and increased phosphorylated endothelial nitric oxide synthase and nitric oxide synthase activity.
CONCLUSIONS
We showed that the nonsteroidal mineralocorticoid receptor antagonist finerenone reduces renal hypertrophy and albuminuria, attenuates cardiac diastolic dysfunction and cardiac fibrosis, and improves cardiac perfusion in a preclinical nondiabetic CKD model.
Topics: Animals; Mineralocorticoid Receptor Antagonists; Renal Insufficiency, Chronic; Naphthyridines; Ventricular Dysfunction, Left; Male; Disease Models, Animal; Fibrosis; Nitric Oxide Synthase Type III; Glomerular Filtration Rate; Ventricular Function, Left; Diastole; Kidney; Phosphorylation; Myocardium; Rats, Sprague-Dawley; Rats; Nephrectomy
PubMed: 38842271
DOI: 10.1161/JAHA.123.032971 -
Frontiers in Veterinary Science 2024Studies on aberrant bronchoesophageal arteries are limited. Herein, we report a case of a multi-origin systemic-to-pulmonary shunt with suspected bronchoesophageal...
INTRODUCTION
Studies on aberrant bronchoesophageal arteries are limited. Herein, we report a case of a multi-origin systemic-to-pulmonary shunt with suspected bronchoesophageal artery hypertrophy and fistula in a dog.
CASE REPORT
A 4-year-old castrated male beagle weighing 11 kg underwent routine medical screening. Physical examination revealed a right-sided continuous murmur of grades 1-2. Thoracic radiography revealed a mild cardiomegaly. Echocardiography revealed a continuous turbulent shunt flow distal to the right pulmonary artery (RPA) branch from the right parasternal short axis pulmonary artery view. Computed tomography demonstrated systemic-to-pulmonary shunts originating from the descending aorta at the level of T7-8, the right 5th and 6th dorsal intercostal arteries, and the right brachiocephalic trunk, which formed anomalous networks around the trachea and esophagus that anastomosed into a large tortuous vessel at the level of T6-7 and entered the RPA. Surgical ligation of multiple shunting vessels was performed. Postoperative echocardiography and computed tomography showed decreased left ventricular volume overload and markedly decreased size of the varices. Additionally, most of the shunting vessels were without residual shunt flow.
CONCLUSION
The present study provides information regarding imaging features and the successful surgical management of multiple systemic-to-pulmonary shunts originating from the descending aorta, right brachiocephalic trunk, and intercostal arteries and terminating at the RPA. Multimodal imaging features after surgical ligation have also been described.
PubMed: 38840636
DOI: 10.3389/fvets.2024.1400076 -
Drug Metabolism and Disposition: the... Jun 2024This research aimed to clarify the impacts of cannflavin-C on angiotensin II (Ang II)-induced cardiac hypertrophy and their potential role in modulating cytochrome P450...
This research aimed to clarify the impacts of cannflavin-C on angiotensin II (Ang II)-induced cardiac hypertrophy and their potential role in modulating cytochrome P450 1B1 (CYP1B1) and arachidonic acid (AA) metabolites. Currently there is no evidence to suggest that cannflavin-C; a prenylated flavonoid, has any significant effects on the heart or cardiac hypertrophy. The metabolism of arachidonic acid (AA) into midchain hydroxyeicosatetraenoic acids (HETEs), facilitated by CYP1B1 enzyme, plays a role in the development of cardiac hypertrophy which is marked by enlarged cardiac cells. Adult human ventricular cardiomyocytes cell line (AC16) were cultured and exposed to cannflavin-C in the presence and absence of Ang II. The assessment of mRNA expression pertaining to cardiac hypertrophic markers and CYPs was conducted via real-time polymerase chain reaction (PCR) while the quantification of CYPs protein levels was carried out through western blot analysis. Ang II induced hypertrophic markers myosin heavy chain (β/α-MHC), atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) and increased cell surface area, while cannflavin-C mitigated these effects. Gene and protein expression analysis revealed that cannflavin-C downregulated CYP1B1 gene expression, protein level as well as the enzyme activity assessed by 7-methoxyresorufin O-deethylase (MROD). Arachidonic acid metabolites analysis, using LC-MS/MS, demonstrated that Ang II increased midchain (R/S)-HETEs concentrations, which were attenuated by cannflavin-C. This study provides novel insights into the potential of cannflavin-C in modulating arachidonic acid metabolites and attenuating Ang II-induced cardiac hypertrophy, highlighting the importance of this compound as potential therapeutic agents for cardiac hypertrophy. This study demonstrates that cannflavin-C offers protection against cellular hypertrophy induced by Ang II. The significance of this research lies in its novel discovery, which elucidates a mechanistic pathway involving the inhibition of CYP 1B1 by cannflavin-C. This discovery opens up new avenues for leveraging this compound in the treatment of heart failure.
PubMed: 38839111
DOI: 10.1124/dmd.124.001705 -
Annals of Vascular Surgery Jun 2024This study's objective is to describe outcomes of adult patients who underwent thoracic stent graft placement treatment for primary or recurrent aortic coarctation.
OBJECTIVE
This study's objective is to describe outcomes of adult patients who underwent thoracic stent graft placement treatment for primary or recurrent aortic coarctation.
METHODS
This is a retrospective study of 30 adult patients who underwent thoracic stent graft placement for aortic coarctation at our institution. Average age was 46.5 years, with 53.3% of patients presented with no prior treatment or repair for coarctation. Indications for repair included gradient ≥20 mm Hg with anatomic evidence of coarctation on imaging with left ventricular hypertrophy, pseudoaneurysm, aneurysm, refractory hypertension, or claudication. Stent grafts used for repair included MDT (Medtronic, Santa Rosa, CA) and GORE TAG (W. L. Gore & Associates, Flagstaff, AZ).
RESULTS
Patients were observed for a median of 979 days, with one death during the study. All patients had complete resolution of symptoms with no recurrences. TEVAR significantly reduced the gradient across the coarctation (p <0.0001). Aortic coarctation diameter significantly increased at 30-days postoperatively and continued to increase up to 5 years post-treatment. At 3+ years, aortic remodeling was observed at the coarctation site and surrounding regions. At 30 days, systolic, diastolic, and mean arterial pressure were all reduced. Systolic and diastolic blood pressure as well as MAP continued to significantly improve 1-year post-treatment.
CONCLUSIONS
Stent grafts are a safe and effective treatment for aortic coarctation. We observed a clinically significant improvement in blood pressure, and longitudinal aortic remodeling of the coarctation segment and the entire aorta that persisted over more than 3 years.
PubMed: 38838987
DOI: 10.1016/j.avsg.2024.03.009