Search Results (178)

Tuberculosis (TB) is an ancient and re-emerging granulomatous infectious disease that continues to challenge public health. Early diagnosis and prompt effective treatment are crucial for preventing disease progression and reducing both morbidity and mortality. These steps play a vital role in infection control and in lowering death rates at both individual and population levels. Although diagnostic methods have improved sufficiently in recent decades, TB can still present with ambiguous laboratory and imaging features. This ambiguity can lead to diagnostic pitfalls and potentially disastrous outcomes due to delayed diagnosis. In this article, we present a case of TB that was difficult to diagnose. The disease had invaded the mediastinum, right atrium, right coronary artery, and inferior vena cava (IVC), resulting in Budd–Chiari syndrome. This rare presentation created clinical, laboratory, and radiological confusion, resulting in a diagnostic dilemma that ultimately led to open cardiac surgery. The patient initially presented with progressive shortness of breath on exertion and fatigue, which suggested possible heart disease. This suspicion was reinforced by computed tomography (CT) imaging, which showed infiltrative mass lesions predominantly in the right side of the heart, invading the right coronary artery and IVC, with imaging features mimicking angiosarcoma. Although laboratory findings revealed an exudative effusion with lymphocyte predominance and elevated adenosine deaminase (ADA), the Gram stain was negative for bacteria, and an acid-fast bacilli (AFB) smear was also negative. These findings contributed to diagnostic uncertainty and delayed the confirmation of TB. Open surgery with excisional biopsy and histopathological analysis ultimately confirmed TB. We conclude that TB should not be ruled out solely based on negative Mycobacterium bacteria in pericardial effusion or AFB smear. TB can mimic aggressive tumors such as angiosarcoma or lymphoma with invasion of the surrounding tissues and blood vessels. Awareness of the clinical presentation, imaging findings, and potential diagnostic pitfalls of TB is essential, especially in endemic regions. Full article

Ischemic stroke following percutaneous coronary intervention (PCI) is a rare complication, with an overall incidence of 0.56%. Most embolic strokes result from the dislodgement of atherosclerotic plaques, thrombi formed on catheter surfaces, procedural maneuvers, or, less commonly, air or metallic emboli originating from fractured guidewires. We present a unique case of stroke following PCI due to a previously unreported mechanism—arterial tunica media embolization associated with arterial access. A 57-year-old female presented with chest pain at rest and with exertion, accompanied by episodes of anxiety and fluctuating blood pressure, for which coronary angiography was performed, revealing 90–99% stenosis of the left anterior descending artery and necessitating PCI. During the procedure, the patient developed an eye deviation, aphasia, and left-sided hemiparesis. Cerebral angiography identified a M2 segment occlusion of the right middle cerebral artery (MCA) and a subocclusion of the right anterior cerebral artery (ACA). Thrombectomy was performed, retrieving two white, tubular emboli resembling fragments of a vessel wall, histologically confirmed to be arterial tunica media. While PCI is associated with a low complication rate, its increasing frequency necessitates awareness of emerging complications. This case underscores a previously undocumented potential embolic complication arising from the performance of PCI. Full article

Background/Objectives: The severity of coronary artery disease (CAD) depends on several factors. Oxidative stress contributes to the oxidation of lipoproteins, thereby promoting ischemic events (IEs) and damaged blood vessels (DBVs). This study aimed to compare biochemical variables and levels of oxidized lipoproteins in CAD patients stratified by the number of IEs and DBVs. Methods: A cross-sectional study was performed, including 51 patients diagnosed with CAD. Serum oxidized lipoproteins were measured by ELISA. Results: CAD patients with ≥2 IEs and ≥2 DBVs showed higher oxLDL levels than those with one IE and one DBV (8293.35 ng/mL [7131.32–9287.39] vs. 6474.26 ng/mL [5374.52–7574.01], p = 0.029). OxLDL levels were positively associated with the number of IEs (r² = 15.2, B = 0.142 [0.046–0.239], p = 0.005) and DBVs (r² = 19.2, B = 0.196 [0.018–0.374], p = 0.020). Conclusions: This study identified a positive association between elevated serum oxLDL levels and the presence of ≥2 IEs and ≥2 DBVs in CAD patients. Full article

Coronary artery disease and vitamin D deficiency are both widespread conditions with a high incidence worldwide. Coronary artery disease is a complex illness with variable manifestation and pathogenesis. It often involves the development of atherosclerosis, and it frequently has serious or even fatal consequences for the patient. Vitamin D receptor expression is found in many tissues throughout the body, which results in a broad effect of the vitamin. Studies have found correlations between vitamin D deficiency and the development of coronary artery disease as well as other cardiovascular diseases, such as hypertension. This review will discuss randomized controlled trials conducted from 2020 forward, aiming to elucidate whether vitamin D supplements have the potential to be used as an add-on treatment for coronary artery disease. The randomized controlled trials all used vitamin D as intervention and tested a population suffering from coronary artery disease or the risk of developing it. Even though animal studies found evidence that vitamin D can regulate inflammation, lipid profile, foam cell formation, vessel reactivity, and blood pressure, which are all mediators in the development of atherosclerosis, the results from the randomized controlled trials were ambiguous. The general older population did not seem to benefit from the treatment, but different subgroups such as patients with type 2 diabetes and patients with more developed coronary artery disease exhibited some positive effects from the treatment. Furthermore, vitamin D showed cardioprotective effects following coronary artery bypass surgery, which make it a possible add-on treatment before invasive coronary intervention. The question in focus still needs further research and a more focused approach on subgroups that may benefit from treatment. Full article

Cardiovascular diseases represent one of the leading causes of mortality worldwide, underscoring the need for accurate simulations of blood flow to improve diagnosis and treatment. This study examines blood flow dynamics in two different vascular structures—the aorta and the right coronary artery (RCA)—using Computational Fluid Dynamics (CFD). Utilizing COMSOL Multiphysics^®, various mathematical models were applied to simulate blood flow under physiological conditions, assuming a steady-flow regime. These models include both Newtonian and non-Newtonian approaches, such as the Carreau and Casson models, as well as viscoelastic frameworks like Oldroyd-B, Giesekus, and FENE-P. Key metrics—such as velocity fields, pressure distributions, and error analysis—were evaluated to determine which model most accurately describes hemodynamic behavior in large vessels like the aorta and in smaller and more complex vessels like the RCA. The results highlight the importance of shear-thinning and viscoelastic properties in small vessels like the RCA, which contrasts with the predominantly Newtonian behavior observed in the aorta. While computational challenges remain, this study contributes to a deeper understanding of blood rheology, enhancing the accuracy of cardiovascular simulations and offering valuable insights for diagnosing and managing vascular diseases. Full article

Background and Objectives: Nonischemic cardiomyopathies comprise a wide spectrum of heart muscle disorders characterized by different morphological, functional, and tissue abnormalities. Cardiovascular magnetic resonance (CMR) represents the gold standard imaging modality for assessing cardiac morphology, systolic function, and tissue characterization, thereby aiding in early diagnosis, precise phenotyping, and tailored treatment. The aim of this review is to provide an up-to-date overview of CMR techniques for studying myocardial perfusion and their applications to nonischemic cardiomyopathy, not only to rule out an underlying ischemic aetiology but also to investigate the pathophysiological characteristics of microcirculatory dysfunction in these patients. Materials and Methods: We performed a structured review of the literature focusing on first-pass gadolinium perfusion sequences, stress protocols, and emerging pixel-wise perfusion mapping approaches. Studies were selected to illustrate the methods for image acquisition, post-processing, and quantification of myocardial blood flow (MBF) and myocardial perfusion reserve (MPR), as well as to highlight associations with clinical endpoints. Results: First-pass CMR perfusion imaging reliably detects diffuse and regional microvascular dysfunction across cardiomyopathies. Semi-quantitative parameters (e.g., upslope, MPRI) and quantitative MBF mapping (mL/g/min) have demonstrated that impaired perfusion correlates with disease severity, extent of fibrosis, and adverse outcomes, including heart failure hospitalization, arrhythmias, and mortality. Novel automated pixel-wise mapping enhances reproducibility and diagnostic accuracy, distinguishing coronary microvascular dysfunction from balanced three-vessel disease. Microvascular dysfunction—present in approximately 50–60% of dilated cardiomyopathy (DCM), 40–80% of hypertrophic cardiomyopathy (HCM), and >95% of cardiac amyloidosis (CA) patients—has emerged as a key driver of adverse outcomes. Perfusion defects appear early, often preceding overt hypertrophy or fibrosis, and provide incremental prognostic value beyond conventional CMR metrics. Conclusions: CMR represents a powerful tool for detecting myocardial perfusion abnormalities in nonischemic cardiomyopathies, improving phenotyping, risk stratification, and personalized management. Further standardization of quantitative perfusion techniques will facilitate broader clinical adoption. Full article

Endothelial cells respond to forces generated by laminar blood flow with changes in vasodilation, anticoagulant, fibrinolytic, or anti-inflammatory functions which preserve vessel patency. These responses to flow shear stress are primarily mediated by the modulation of the following transcription factors: Krüppel-like factors 2 and 4 (KLF2 and KLF4). Notably, disturbed flow patterns, which are found in vascular areas predisposed to atherosclerosis, significantly reduce the endothelial expression of KLF2 and KLF4, resulting in changes in the transcriptome that exacerbate inflammation and thrombosis. The endothelial CCM (Cerebral Cavernous Malformation) complex, comprising KRIT1 (Krev1 interaction trapped gene 1), CCM2 (Malcavernin), and CCM3 (Programmed cell death protein 10), suppresses the expression of KLF2 and KLF4. Loss of function of the CCM complex has recently been suggested to protect from coronary atherosclerosis in humans. We thus hypothesized that the silencing of KRIT1, the central scaffold of the CCM complex, can normalize the atherogenic effects of disturbed flow on the human endothelial transcriptome. Bulk RNA sequencing (RNA-seq) was conducted on human umbilical vein endothelial cells (HUVECs) after the expression of KRIT1 was silenced using specific small interfering RNA (siRNA). The endothelial cells were exposed to three different conditions for 24 h, as follows: pulsatile shear stress (laminar flow), oscillatory shear stress (disturbed flow), and static conditions (no flow). We found that silencing the KRIT1 expression in HUVECs restored the expression of the transcription factors KLF2 and KLF4 under oscillatory shear stress. This treatment resulted in a transcriptomic profile similar to that of endothelial cells under pulsatile shear stress. These findings suggest that inhibition of the CCM complex in endothelium plays a vasoprotective role by reactivating a protective gene program to help endothelial cells resist disturbed blood flow. Targeting CCM genes can activate well-known vasoprotective gene programs that enhance endothelial resilience to inflammation, hypoxia, and angiogenesis under disturbed flow conditions, providing a novel pathway for preventing atherothrombosis. Full article

Pre-eclampsia is a severe pregnancy complication affecting 5–8% of pregnancies worldwide, marked by high blood pressure and organ damage typically occurring after 20 weeks of gestation. It is a leading cause of maternal and fetal morbidity and mortality. Though its exact cause is unknown, it involves placental abnormalities and improper blood vessel development. Risk factors include a history of pre-eclampsia, chronic hypertension, diabetes, obesity, and autoimmune disorders. Symptoms include high blood pressure, proteinuria, headaches, vision changes, and abdominal pain. Untreated, it can lead to seizures, stroke, preterm birth, or death. Delivery is the definitive treatment, with management strategies such as monitoring and blood pressure control. Pre-eclampsia significantly increases long-term cardiovascular disease (CVD) risks, including hypertension, ischemic heart disease, and stroke, linked to shared mechanisms like endothelial dysfunction and inflammation. Women with severe or recurrent pre-eclampsia have heightened risks, often developing chronic hypertension within a decade postpartum. It also impacts offspring, with daughters at elevated risk for pre-eclampsia and CVD. Hypertensive disorders of pregnancy, including pre-eclampsia, induce changes like left ventricular hypertrophy and diastolic dysfunction, raising risks for heart failure with preserved ejection fraction and coronary atherosclerosis. Overlapping with peripartum cardiomyopathy, pre-eclampsia underscores a spectrum of pregnancy-related cardiovascular disorders. Long-term monitoring and lifestyle interventions are crucial for managing risks, with research into genetic and biological mechanisms offering the potential for targeted prevention. Full article

Background and Objectives: Screening, primary prevention, and the early identification of high-risk individuals are crucial for minimising the burden of cardiovascular diseases (CVDs). In this study, we aimed to evaluate the association of retinal microvascular features with myocardial dysfunction and CVD risk factors in a group of patients with significant coronary artery disease (CAD) compared to patients with newly diagnosed isolated arterial hypertension and healthy controls. Materials and Methods: We performed a single-centre cross-sectional study on 214 individuals divided into three groups: a group of 99 cases diagnosed with significant CAD, a group of 61 cases with newly diagnosed isolated arterial hypertension, and a control group of 54 cases with no confirmed cardiovascular pathology. Colour optic disc-centred retinal photographs were taken in all cases, and the following parameters were quantified using MONA REVA 3.0.0 software (VITO Health, Mol, Belgium): central retinal arteriolar equivalent, central retinal venular equivalent, arteriovenous ratio, fractal dimension, tortuosity index, and lacunarity. Univariable and multivariable statistical analyses were performed to assess changes in retinal microvascular features in CVD. Results: Dyslipidaemia (p = 0.009), systolic blood pressure (p = 0.008), and LDL cholesterol (p = 0.003) were negatively associated while left ventricular (LV) strain (0.043) was positively associated with the CRAE. In the case of the CRVE, the coronary Agatston score (p = 0.016) proved a positive and HDL cholesterol (p = 0.018) a negative association. A lower fractal dimension was associated with the presence of diabetes mellitus (p = 0.006), dyslipidaemia (p = 0.011), and a history of acute myocardial infarction (p = 0.018), while a higher fractal dimension was associated with increased left ventricular ejection fraction (LVEF) (p = 0.006) and medical treatment (p = 0.005). Lacunarity was higher in patients of female gender (p = 0.005), with decreased HDL (p = 0.014) and LVEF (0.005), and with increased age (p < 0.001) and Agatston score (p = 0.001). The vessel tortuosity index increased with LV strain (p = 0.05), medical treatment (p = 0.043), and male gender (p = 0.006). Conclusions: Retinal microvascular features may serve as additional risk stratification tools in patients with CVD, particularly CAD, pending prospective validation. Full article

Background and Objectives: The neutrophil-percentage-to-albumin ratio (NPAR) has been recognized as an independent risk factor for cardiovascular diseases. In our study, we investigated whether the NPAR is associated with the formation of coronary collateral circulation (CCC) in patients with chronic coronary syndrome (CCS). Materials and Methods: A total of 681 patients with CCS were included in this study. Of these patients, 571 had chronic total occlusion in at least one major vessel and developed collateral vessels. In total, 110 patients were in the control group, who had CCS but did not have complete occlusion in a major vessel and did not develop collateral vessels. Patients with collateral vessels on coronary angiography were divided into two groups according to the Rentrop score: poor CCC (Rentrop 0–1) and good CCC (Rentrop 2–3). Blood samples were taken for the NPAR and other biochemical parameters in all patients during hospitalization. The NPAR was calculated as the neutrophil-percentage-to-albumin ratio. Results: The group of patients with poor CCC had a higher white blood count (WBC), neutrophil, C-reactive protein (CRP), neutrophil–lymphocyte ratio (NLR), CRP/albumin ratio (CAR), and NPAR values than patients with good CCC (p < 0.001, for all). Multivariate logistic regression analysis showed that high NPAR levels were an independent predictor of poor CCC (OR: 2.79, 95% CI:1.7–4.6, p < 0.001), accompanied by neutrophil, CRP, CAR, and NLR levels. In the receiver operator characteristic curve (ROC analysis), the cut-off value for the NPAR to indicate poor CCC was 1.78 with a sensitivity of 76.6% and specificity of 81.4% (area under ROC curve = 0.804 95% CI (0.753–0.854), p < 0.001). Conclusions: We demonstrated that the NPAR may be an independent predictor of poor CCC development in clinical practice. Full article

Coronary atherosclerosis in patients with diabetes mellitus is the most significant pathophysiological mechanism responsible for ischemic heart disease. Atherosclerosis in diabetes is premature, more diffuse, and more progressive, and it affects more coronary blood vessels compared to non-diabetics. Atherosclerosis begins with endothelial dysfunction, continues with the formation of fatty streaks in the intima of coronary arteries, and ends with the appearance of an atherosclerotic plaque that expands centrifugally and remodels the coronary artery. If the atherosclerotic plaque is injured, a thrombus forms at the site of the damage, which can lead to vessel occlusion and potentially fatal consequences. Diabetes mellitus and atherosclerosis are connected through several pathological pathways. Among the most significant factors that lead to atherosclerosis in diabetics are hyperglycemia, insulin resistance, oxidative stress, dyslipidemia, and chronic inflammation. Chronic inflammation is currently considered one of the most important factors in the development of atherosclerosis. However, to date, no adequate anti-inflammatory therapeutic measures have been found to prevent the progression of the atherosclerotic process, and they remain a subject of ongoing research. In this review, we summarize the most significant pathophysiological mechanisms that link atherosclerosis and diabetes mellitus. Full article

Coronary arteries may vary in quantity, point of origin, or course. These variations fall under the category of anatomical variants/anomalies of the coronary arteries, representing congenital abnormalities of the coronary vascular system. Generally, they are benign, asymptomatic, and identified inadvertently during coronary angiography conducted for alternative indications. However, in some cases, the anomaly’s characteristics or its interaction with surrounding structures may cause hemodynamic disturbances. These disturbances can lead to turbulent blood flow, which in turn poses an increased likelihood for the development of atherosclerosis and myocardial ischemia. If symptomatic, potential manifestations include chest pain, arrhythmias, syncope, myocardial infarction, and sudden cardiac death. Given the potential for life-threatening complications in certain cases, the early and accurate diagnosis of coronary artery anomalies is of paramount importance. The most common diagnostic procedures used for the evaluation of coronary vessels are coronary angiography and multi-detector row computed tomography (MDCT) coronary angiography. MDCT angiography is a non-invasive, dependable, safe, and sensitive method for the detailed visualization of coronary anatomy. It offers high-resolution imaging that enables precise assessment of congenital coronary variations, aiding in both clinical decision-making and long-term patient management. We conducted a narrative review to analyze and integrate the body of literature on coronary artery varieties and anomalies. Our objective was to provide a comprehensive, albeit non-exhaustive, overview of essential concepts and findings related to their definition, classification, and detection with MDCT angiography. By integrating current knowledge in MDCT imaging, we seek to contribute to a better understanding of the clinical implications of coronary artery variations and their role in cardiovascular health. Full article

Blood vessel segmentation in X-ray coronary angiography (XCA) plays a crucial role in diagnosing cardiovascular diseases, enabling a precise assessment of arterial structures. However, segmentation is challenging due to a low signal-to-noise ratio, interfering background structures, and vessel bifurcations, which hinder the accuracy of deep learning models. Additionally, deep learning models for this task often require high computational resources, limiting their practical application in real-time clinical settings. This study proposes a lightweight variant of the U-Net architecture using a structured kernel pruning strategy inspired by the Lottery Ticket Hypothesis. The pruning method systematically removes entire convolutional filters from each layer based on a global reduction factor, generating compact subnetworks that retain key representational capacity. This results in a significantly smaller model without compromising the segmentation performance. This approach is evaluated on two benchmark datasets, demonstrating consistent improvements in segmentation accuracy compared to the vanilla U-Net. Additionally, model complexity is significantly reduced from 31 M to 1.9 M parameters, improving efficiency while maintaining high segmentation quality. Full article

Metabolic stress on the heart can cause dilation of coronary arterioles for blood flow recruitment. Although potassium ions (K⁺) released from the myocardium are a major mediator for this response, the underlying signaling pathways for vasodilation are incompletely understood. Herein, the roles of smooth muscle inward-rectifier K⁺ channel subtype 2.1 (K_ir2.1) and Na⁺/K⁺-ATPase were examined. Porcine coronary arterioles were isolated, cannulated, and pressurized for vasomotor study. Vessels developed basal tone and dilated concentration-dependently to extraluminal K⁺ from 7 to 20 mM. Higher K⁺ concentrations (25–40 mM) caused graded vasoconstriction. Vasodilation to K⁺ (10 mM) was not altered by endothelial removal, and blockade of ATP-sensitive K⁺ channels, voltage-sensitive K⁺ channels, or calcium-activated K⁺ channels did not affect K⁺-induced vasodilation. However, sustained but not abrupt transient vasodilation to K⁺ was reduced by the nonspecific K_ir channel inhibitor Ba²⁺ or K_ir2.1 channel blocker chloroethylclonidine. The Na⁺/K⁺-ATPase inhibitor ouabain attenuated K⁺-elicited vasodilation, and ouabain with Ba²⁺ abolished the response. Transfection of arterioles with K_ir2.1 antisense oligonucleotides abolished sustained but not transient dilation. It is concluded that extraluminal K⁺ elevation within the physiological range induces initial transient dilation of porcine coronary arterioles by activating smooth muscle Na⁺/K⁺-ATPase and sustained dilation via smooth muscle K_ir2.1 channels. Full article

Inhibition of HIF-prolyl hydroxylases (PHD1, PHD2, and PHD3) causes the stabilization of hypoxia-inducible factor-1α and -2α (HIF-1α and HIF-2α) to regulate various cell signaling pathways. Hypoxia-inducible factor (HIF) is crucial in regulating signal responses mediated by hypoxia. HIF regulates the transcription of many genes involved in the response to hypoxia and ischemic insult. Our current work investigates the protective effects of PHD1 knockout in mice against myocardial infarction. Study Design: Myocardial infarction (MI) was induced by left anterior descending coronary artery (LAD) ligation (8–12-week-old mice) in both wild-type (WT) and PHD1 knockout (PHD1^−/−) mice. WT sham (S) and PHD1^−/−S group mice underwent surgery without LAD ligation. Thirty days post-surgery, cardiac functions were measured by echocardiogram. Mice in all the groups were euthanized at various time points for tissue collection post-MI 8 h (gel shift and microarray analysis), 4 days (Western blot analysis), 7 days (blood vessel density), or 30 days (histological analysis). For microarray analysis, WTMI and PHD1^−/−MI group mices’ heart tissue was used for RNA isolation, then hybridization to a GeneChip™ Mouse Gene 1.0 ST Array as per the manufacturer’s instructions. Bioinformatic analysis was performed using the transcriptome analysis console (TAC) to generate a list of differentially regulated genes, followed by ingenuity pathway analysis. Results: The study findings revealed a significant increase in vessel density (capillary and arteriolar density) in the PHD1^−/−MI mice compared to those with WTMI. The echocardiographic examination demonstrated that the PHD1^−/−MI mice group had an increased ejection fraction and fractional shortening than the WT mice 30 days post-MI. HIF-1α DNA binding activity was higher in PHD1^−/−MI mice than in WTMI. The Western blot analysis showed a significant increase in the expression of HSPA12B in the PHD1^−/−MI compared to WTMI mice. Bioinformatic analysis using TAC software, Version 4.0.2.15 (1.5 fold, p < 0.05) showed 174 differentially regulated genes. Conclusions: In conclusion, our study showed PHD1 knockout activates several important molecules and signaling pathways, resulting in increased angiogenesis and cardioprotection against myocardial infarction. Full article