Spontaneous Dissection Research Articles

Assessment of Attenuation in Pericarotid Fat among Patients with Carotid Plaque and Spontaneous Carotid Dissection.

Changes in perivascular fat density (PFD) and its association with inflammation have been topics of interest in both atherosclerotic and nonatherosclerotic vasculopathies. The objective of this study was to assess the PFD in patients with spontaneous internal carotid artery dissection (SICAD) or carotid atherosclerotic plaque, with and without intraplaque hemorrhage (IPH). A cross-sectional retrospective bicentric analysis of 130 patients (30 with SICAD and 100 with carotid atherosclerotic plaque) who underwent CT angiography was performed. Among the subjects with atherosclerotic plaque, 36 showed the presence of IPH. PFD analysis was performed by 2 radiologists who placed 2 ROIs to identify the perivascular fat tissue attenuation. The Mann-Whitney U test was conducted to evaluate the difference between patient cohorts. Carotid arteries with SICAD and IPH demonstrated an average PFD of -68.97 HU (95% CI, -72.11 to -65.82 HU) and -69.97 HU (95% CI, -73.00 to -66.95 HU), respectively, in comparison with patients without IPH, who showed an average PFD -77.11 HU (95% CI,-78.78 to -75.44 HU) (P < .001 for both). Conversely, no significant differences were found between patients with SICAD and those with carotid plaque with IPH (P = .324). The average PFDs in patients with SICAD and carotid atherosclerosis plaque with IPH were similar and higher than those in patients with carotid plaque without IPH. This finding suggests a shared pathologic inflammatory mechanism in these 2 conditions. Studies comparing pathologic specimens directly with radiologic images may be needed to confirm this indirect hypothesis.

Spontaneous craniocervical dissection

Spontaneous dissections of the cerebral arteries are among the leading causes of stroke in young adults. They result from hemorrhage into the outer layers of the arterial wall, which can lead to stenosis or even complete vessel occlusion. Clinical presentations vary, ranging from localized pain to cerebral ischemic complications. Early recognition of dissection warning signs and diagnosis through imaging is crucial due to the high risk of recurrent transient ischemic attack (TIA) or stroke within the first two weeks following a dissection, necessitating immediate therapeutic or prophylactic intervention. Magnetic resonance imaging (MRI) is the imaging modality of choice, as it can reliably visualize all characteristic features of dissection. Typically, thin-slice, fat-saturated 3D black-blood sequences are sufficient to detect the pathognomonic intramural hematoma. Acute treatment and secondary prevention depend on the extent of neurological deficits, the location and size of the dissection, any sequelae, concomitant pathologies, and risk factors. In most cases, spontaneous vascular recanalization or regression of vessel stenosis occurs within several months due to resorption of the mural hematoma.

Spontaneous Coronary Dissection in Late Puerperium: Now What? A Case Report

Spontaneous coronary dissection is an infrequent cause of non-atherosclerotic or iatrogenic acute coronary syndrome, predominantly diagnosed in women under 50 years old during their reproductive phase, usually without associated cardiovascular risk factors. Various factors underlie its occurrence, ranging from connective tissue diseases to intense emotional stress, with fibromuscular dysplasia being a commonly associated nosological entity. Coronary angiography is the preferred diagnostic examination, and a conservative strategy is frequently recommended, especially in stable contexts. Invasive strategies, such as surgical revascularization or percutaneous coronary intervention, are reserved for more complex clinical situations involving severe arrhythmias or dissections involving the left coronary artery trunk, among others. We present the case of a postpartum woman with no known cardiovascular risk factors, diagnosed with spontaneous coronary dissection in the late puerperium of a twin pregnancy, resulting in a fatal outcome.

Thoracic and Cardiovascular Imaging Manifestations of Lupus.

Systemic lupus erythematosus (SLE), commonly referred to as lupus, is a widely prevalent chronic autoimmune disease that can affect any organ system in the body. Although the pathogenesis of this disease is rather complex and poorly understood, ultimately there is an overproduction of multiple self-reactive antinuclear antibodies. These autoantibodies are one of the laboratory hallmarks of the diagnosis and disease activity of SLE. Lupus has a myriad of symptoms and imaging manifestations. Serositis, one of the most common manifestations of the disease, usually occurs with pleural or pericardial effusion with or without associated serosal inflammatory changes. The pulmonary manifestations are heterogeneous, with mostly acute (eg, diffuse alveolar hemorrhage, acute lupus pneumonitis) and some chronic (eg, fibrosing interstitial lung disease, shrinking lung syndrome) lung findings. Cardiac and vascular manifestations include myocarditis; coronary artery disease, including accelerated atherosclerosis; myocardial infarction; and spontaneous dissections, along with vasculitis, aneurysms, Libman-Sacks endocarditis, and arterial and venous thromboembolism. Although patient history and risk factor assessment have a vital role in diagnosing lupus, familiarity with the imaging manifestations aids radiologists in optimizing patient care, assessing for complications, and uncovering undiagnosed cases of lupus. This fact emphasizes the importance of recognizing the complex multisystem involvement of lupus seen at imaging. In this article, the authors review the thoracic and cardiovascular imaging manifestations of lupus. © RSNA, 2024.

Spontaneous dissection of the right coronary artery complicated by an intra-ventricular thrombus: A case report

Spontaneous dissection of the right coronary artery complicated by an intra-ventricular thrombus: A case report

Deficiency of ATF3 facilitates both angiotensin II-induced and spontaneously formed aortic aneurysm and dissection development by activating cGAS-STING pathway.

Sporadic aortic aneurysm and dissection (AAD) is a critical condition characterised by the progressive loss of vascular smooth muscle cells (VSMCs) and the breakdown of the extracellular matrix. However, the molecular mechanisms responsible for the phenotypic switch and loss of VSMCs in AAD are not fully understood. In this study, we employed a discovery-driven, unbiased approach. This approach encourages us to explore the unknown functions of activating transcription factor 3 (ATF3) rather than merely confirming existing hypotheses, while no assumptions were made about ATF3 prior to the experiments. We ensured the unbiased nature of our assessment by conducting morphological evaluations with two independent observers in a blinded manner. We identified elevated expression of ATF3 in both human sporadic AAD tissues and mouse AAD models. VSMC-specific ATF3 conditional knockout (Atf3 cKO) mice showed notable enlargement, dissection and rupture in both thoracic and abdominal aortic regions after exposure to Ang II. Interestingly, older Atf3 cKO mice exhibited spontaneous aortic dissections and senescence of the aortic wall. Mechanistically, ATF3 deficiency led to the degradation of P21 through ubiquitination. Impaired DNA repair in VSMCs resulted in micronuclei formation in the cytoplasm, activating the cyclicGMP-AMP synthase- stimulator of interferon genes (cGAS-STING) pathway and inducing VSMC phenotypic switching and apoptosis. Finally, both pharmacological complementation of P21 function and knockdown of STING expression alleviated ATF3 deficiency-induced AAD. Our study indicates that ATF3 is essential for genomic DNA stability in VSMCs through the P21-cGAS-STING pathway, suggesting that enhancing ATF3 expression in VSMCs could help prevent sporadic AAD. ATF3 deficiency led to degradation of P21 through ubiquitination, which abolished the G1 phase arrest. VSMCs had no time window to repair the damaged DNA, leading to generation of micronuclei in cytoplasm. Cytoplasmic micronuclei facilitating the activation of cGAS-STING pathway, thus inducing the phenotypic switch and apoptosis of VSMCs.

Giant left ventricular pseudoaneurysm: a rare complication of coronary spontaneous dissection in a young female patient

Giant left ventricular pseudoaneurysm: a rare complication of coronary spontaneous dissection in a young female patient

Cervical Artery Tortuosity Is Associated With Dissection Occurrence and Late Recurrence: A Nested Case-Control Study.

The pathogenesis of spontaneous cervical artery dissection remains unclear, and no established predictors of recurrence exist. Our goal was to investigate the potential association between cervical artery tortuosity, a characteristic of patients with connective tissue disorder, and spontaneous cervical artery dissection. The ReSect study (Risk Factors for Recurrent Cervical Artery Dissection) is an observational study that invited all spontaneous cervical artery dissection patients treated at the Innsbruck University Hospital between 1996 and 2018 for clinical and radiological follow-up. Internal carotid and vertebral artery tortuosity was assessed on magnetic resonance angiography using a validated 3-dimensional algorithm. Differences between patients and healthy controls as well as dependent on recurrence status were assessed by applying χ2, Mann-Whitney U test, and Kruskal-Wallis test where applicable, and confounders were established by bivariable Pearson correlation. Logistic regression was used to address the impact of tortuosity on dissection occurrence and recurrence as well as its association to extracellular matrix proteome data derived from skin biopsies in a subset of patients. Magnetic resonance angiography was performed a median of 6.5 years after dissection in the included dissection patients. Patients with dissection (n=125) had significantly increased values of internal carotid artery tortuosity compared with healthy controls (n=24; odds ratio, 2.65 [95% CI, 1.68-3.86], 1 SD increase; P<0.01). This was also true for patients with long-term dissection recurrence (n=7) when compared with those with single time-point dissection (n=118; odds ratio, 2.00 [95% CI, 1.47-3.99], 1 SD increase; P<0.01). In patients with dissection and available extracellular matrix protein data (n=37), 6 of 13 (46.2%) proteins previously found linked with dissection recurrence were also associated with increased tortuosity. All 3 proteins associated with both anterior and posterior circulation tortuosity belonged to the desmosome-related cluster. Internal carotid artery tortuosity is elevated in spontaneous cervical artery dissection patients compared with healthy controls, and this difference is most pronounced if individuals suffer from long-term dissection recurrence. Additionally, an association between tortuosity, being a readily measurable biomarker in routine magnetic resonance angiography, and proteomic markers of dissection recurrence exists, further enhancing the prospect of underlying subclinical connective tissue disease in dissection patients.

Double strike without stroke: a postpartum headache with too many causes.

Pregnancy and postpartum are phases in the women's life where the thrombotic risk is increased both on the venous and on the arterial side. We are presenting the case of a young woman at the third pregnancy, carried out without complications until delivery, whose postpartum was characterized by the occurrence of headache. Neuroimaging studies were performed, firstly brain computed tomography (CT) with CT Angiography and after brain Magnetic Resonance Imaging (MRI) with MR Angiography. The main finding was the simultaneous presence of two cerebrovascular vascular diseases, i.e. cerebral venous thrombosis (CVT) and left carotid dissection, without stroke. The neuroimaging features of both the diseases were analyzed and both CVT and dissection had neuroimaging markers of acute timing. After starting heparin therapy at anticoagulant dose the clinical symptoms disappeared within a few days. CVT is a rare event with a peak in the late pregnancy and puerperium, but other arterial cerebrovascular events, as spontaneous dissection, have not an increased incidence in the postpartum. Headache is one of the main symptoms for all these cerebrovascular diseases, but usually stroke is the accompanying event. This is not always true and the presented case illustrates this unexpected occurrence. Headache is a nonspecific and highly prevalent symptom and in the postpartum period it could raise the suspicion of CVT. Sometimes several different causes are found for the same symptom and concurrent acute cerebrovascular diseases might be considered. Neuroimaging investigations may help for diagnosis and timing concurrent thrombotic diseases, particularly DWI-MRI.

Epidemiology of traumatic cervical artery dissections.

Unlike spontaneous cervical artery dissection (CeAD), the incidence of CeAD after a major trauma is not well characterized. This population-based observational study investigates the epidemiology and natural history of traumatic cervical artery dissection (CeADs) using data from the Rochester Epidemiology Project (REP) in Olmsted County, USA. The REP system database has a high likelihood of complete case ascertainment and comparable demographics (age, sex) to the US population. After the initial screening of the database with ICD-based codes for carotid and vertebral dissections, meticulous review was performed to select patients with CeAD due to major trauma. We used Poisson regression to assess the association of age, sex, and time-period using crude incidence rates. Analyzing cases from 2002 to 2020, we identified 21 patients with traumatic CeAD, noting a significant 3.5-fold increase in incidence from 2002 to 2011-2012-2020 (0.37-1.29 per 100,000 person-years, p = 0.005). Only 23.8 % of cases experienced traumatic CeAD-related cerebral infarction. No patients received acute reperfusion therapies. Antithrombotic treatment predominantly involved single antiplatelet therapy (47.6 %) with aspirin. However, increasing use of dual antiplatelet therapy (11.8 %) along with declining use of anticoagulation (17.6 %) was also noted over time. We observed no recurrent strokes, dissections, or de-novo pseudoaneurysms. at the final follow-up. The population-based incidence of traumatic CeAD is on the rise, potentially due to an increased screening in real-life practice leading to improved identification of cases that may have otherwise gone unrecognized. Our study also shows that traumatic CeADs tend to have a favorable prognosis.

A clinical case of spontaneous coronary artery dissection in a young patient

Аim. To describe a clinical case of acute myocardial infarction in a young patient caused by spontaneous dissection of the coronary artery.Material and methods. The patient, a 32-year-old man, was hospitalized in the cardiology department with a clinical picture of acute coronary syndrome. When collecting anamnestic data, it was established that the patient has an aggravated cardiovascular, hereditary, pharmacological anamnesis and concomitant pathology. A special attitude of the patient to hisdisease in the form of an anosognosic reaction was revealed. The data of the coronary angiography study determined further tactics of patient management at the inpatient stage.Results. Taking into account the clinical picture, the dynamics of electrocardiograms, the results of laboratory diagnostics, acute myocardial infarction with ST segment elevation on the electrocardiogram was preliminarily diagnosed. During coronary angiography, spontaneous coronary artery dissection was detected in the patient, which was the main cause of acute left ventricular myocardial infarction. A decision was made to implant 3 stents in order to completely cover the dissection zone of the anterior interventricular branch of the left coronary artery. The choice of conservative and/or surgical tactics for managing patients with spontaneous coronary artery dissection is debatable. After percutaneous coronary intervention, drug therapy was prescribed, including dual antiplatelet therapy. The patient noted an improvement in his well-being, without relapses of pain syndrome. In the dynamics of inpatient treatment, according to echocardiographic examination, an aneurysm of the apex of the left ventricle with a mural thrombus was detected, which required correction of drug therapy, taking into account the increased risks of thromboembolic and hemorrhagic complications.Conclusion. This clinical case demonstrates that spontaneous dissection of the coronary artery is one of the pathogenetic mechanisms of the formation of the clinical picture of acute coronary syndrome and affects the development of complications and further prognosis.

Revascularization with superficial temporal artery-middle cerebral artery anastomosis in spontaneous intracranial internal carotid artery dissection: illustrative case.

Because of ischemic symptoms, intracranial internal carotid artery (IICA) dissection has no established treatment guidelines. The authors report a case of IICA dissection in which an emergency superficial temporal artery-middle cerebral artery (STA-MCA) bypass was performed. A 46-year-old woman presented with a headache and left hemiplegia. Her cortical symptoms appeared on day 10, and an STA-MCA bypass was performed because of cerebral hypoperfusion. Her postoperative patency was good, and cortical symptoms improved. Contrast-enhanced magnetic resonance imaging (MRI) was performed in the acute phase with wall contrast. From day 18, the internal carotid artery delineation improved, and the patient was transferred for rehabilitation without worsening symptoms. A literature review of spontaneous IICA dissection with revascularization procedures was conducted to discuss the indications, timing, treatment modalities, and surgical outcomes. The STA-MCA bypass provides supplemental cerebral blood flow and can prevent critical complications. Contrast-enhanced MRI in the acute phase of dissection can show a wall contrast effect and assist in predicting disease progression. https://thejns.org/doi/10.3171/CASE24332.

Case report: Cervical arterial dissections in the setting of recent COVID-19 infection

BackgroundCOVID-19 infections have been implicated in cerebral ischemia, but their relationship to cervical arterial dissections remains poorly characterized. Descriptions of cervical arterial dissections in patients with COVID-19 infections with details regarding their presenting symptomatology, imaging findings, and responses to treatment with antithrombotic therapy may be helpful to clinicians.Methods and observationsWe present six adult cases of cervical arterial dissections in the setting of recent COVID-19 infections from 2021 to 2022 at our institution. Four cases presented with dissections involving the internal carotid artery, while two cases had dissections of bilateral vertebral arteries. In one patient, we found imaging evidence for a possible inflammatory process. All patients were treated with either antiplatelet agents or direct oral anticoagulants.Conclusions and relevanceCOVID-19 infections may predispose patients to spontaneous cervical arterial dissections. Such patients can have variable neurologic presentations, though headaches and neck pain were common complaints. Most patients responded well to antithrombotic therapy, with improvement in symptoms and radiologic findings at follow-up. Clinicians should maintain a high degree of suspicion for cervical arterial dissections in patients who present acutely with severe headache/neck pain and/or new neurologic deficits in the setting of COVID-19 infections.

Giant left ventricular pseudoaneurysm: a rare complication of coronary spontaneous dissection in a young female patient.

Giant left ventricular pseudoaneurysm: a rare complication of coronary spontaneous dissection in a young female patient.

Duodenal Obstruction Caused by an Isolated Spontaneous Celiac Artery Dissection.

Duodenal Obstruction Caused by an Isolated Spontaneous Celiac Artery Dissection.

Abstract 384: Rapid accumulation of spontaneous intracranial dissection cases within two years

Introduction Spontaneous intracranial dissection is very uncommon and there are few cases reported so far. Interestingly most cases reported are from Asia. Genetic perspective would be one of the speculative causes. Making a definite diagnosis is also one of the pitfalls and distinguishing from other more common diseases, intracranial atherosclerosis which is also much more prevalent in Asia is sometimes difficult. With such a limited case, clinical progression and appropriate treatment would possibly be hard to define. Method We present a series of 11 cases directed or transferred to our hospital referral center from 2022‐2024. All patient information retrospectively collected in demographic, clinical presentation, and radiologic workups including relevant investigation, treatment, and clinical outcomes were described. Outcome All patients are between 29 and 82 years old with the six decades being the most prevalent composed of 8 cases of middle cerebral artery dissection, M1 segment and one case of M2 segment of middle cerebral artery dissection, one case of anterior cerebral artery dissection, and one case of posterior cerebral artery dissection, P2 segment. These cases have intracranial dissection spontaneously, there are no connective tissue disorders related to physical examination and there is no history of head injury before the event. Most of them present with acute ischemic stroke or transient ischemic attack and a few of them with headaches from subarachnoid hemorrhage. Interestingly there is another case that has transient ischemic attack and hyperkinetic movement disorders. Magnetic resonance imaging or cerebral angiogram reveals an intimal flap, double lumen, or string sign in all cases. These findings could distinguish from intracranial atherosclerosis if looked at carefully. The case of M2 segment middle cerebral artery dissection shows rapid progressive change in the dissecting aneurysm. Most of them had no anterograde flow impairment therefore these cases received antiplatelet treatment but four cases (36%) present with acute large vessel occlusion or severe stenosis received endovascular treatment and two of them ended up with rescue permanent stenting. One of two cases who has subarachnoid hemorrhage receives surgical clipping and bypass. All cases presenting with ischemic stroke have good clinical outcomes at three months follow up including cases with subarachnoid hemorrhage. Conclusion Spontaneous intracranial dissection is uncommon and underdiagnosed. Differentiating from intracranial atherosclerosis is important, and recognizing intracranial dissection features is useful. Clinical features or progression may not be benign since some of them may present with acute large vessel occlusion or stenosis. Providing treatment in this type is very challenging otherwise complications from endovascular treatment may be devastating.

Clinical characteristics and predictors of recurrence from the Australia-New Zealand Spontaneous Coronary Artery Dissection (ANZ-SCAD) registry

Abstract Background Spontaneous coronary artery dissection (SCAD) is an increasingly recognised cause of acute coronary syndrome (ACS), particularly in young women. Our understanding of SCAD remains incomplete with limited prospective data on determinants of SCAD recurrence. Purpose We aimed to describe the clinical characteristics, incidence and predictors of SCAD recurrence and major adverse cardiovascular events (MACE) in patients with SCAD from a large, multicentre registry. Methods Observational, multi-centre prospective and retrospective cohort study recruiting patients with SCAD from 23 hospitals in Australia and New Zealand. Patients aged=&amp;gt;18 years with SCAD and an ACS were eligible for inclusion. Prospectively recruited patients gave their informed consent while a waiver of consent was granted for retrospectively recruited patients. An independent core laboratory adjudicated invasive coronary angiography images to confirm the diagnosis of SCAD. The primary outcome was SCAD recurrence, defined as de novo spontaneous dissection with new ACS symptoms and cardiac enzyme elevation, not due to extension of the index lesion. Cox proportional hazard models were used to evaluate the association between SCAD recurrence and predefined clinical variables. Results From a total 487 patients recruited, 423 (132 prospective and 291 retrospective) patients with SCAD confirmed on core laboratory review were included for analysis. Mean age was 52.4±10.7 years, 89.7% were female and 73.1% were Caucasian. At discharge, 75.2% were on beta-blockers, 27.9% single antiplatelet and 61.9% dual antiplatelet (DAPT). At 15 (interquartile range 5-36) months median follow-up, SCAD recurrence occurred in 3.3%, with an overall MACE of 6.6%. On multivariate analysis, the presence of fibromuscular dysplasia (FMD) or other extra-cardiac vascular abnormalities [adjusted hazard ratio (HR) 5.63, 95% confidence interval (CI), 2.09-15.3, p&amp;lt;0.001], and past history of stroke (adjusted HR 7.99, 95% CI, 1.51-42.4, p=0.015) were associated with higher SCAD recurrence. Discharge beta-blockers was not independently associated with SCAD recurrence, while dual antiplatelet therapy that combined ticagrelor with aspirin was associated with a higher risk of recurrence (adjusted HR 2.47, 95% CI, 1.9-15.6, p=0.048). Conclusion SCAD recurrence comprised half of overall MACE in people with SCAD. The risk of SCAD recurrence was more than 5-fold higher in patients with FMD or other extra-cardiac vascular abnormalities. Dual-antiplatelet therapy that comprised ticagrelor and aspirin was associated with a higher risk of SCAD recurrence.

Lipoprotein(a) induces spontaneous aortic dissection via increasing monocyte mediated vascular smooth muscle cell phenotype transformation in human Lp(a) transgenic mice

Abstract Background Elevated lipoprotein(a) [Lp(a)] is a prevalent, independent risk factor of atherosclerotic cardiovascular disease and aortic valve stenosis. Recent studies have reported that high levels of Lp(a) are strongly associated with aortic dissection (AD), independent of other cardiovascular risk factors. However, orthologues of Lp(a) are only found in humans, Old World monkeys, apes, and hedgehogs. The lack of a proper animal model has hindered elucidation of the true pathophysiological mechanisms of Lp(a). Here, we conducted the first humanized Lp(a) transgenic mice experiment to verify the pathological mechanism of Lp(a) in aortic dissection. Methods We conducted ApoE knock out and human ApoA transgenic mice via CRISPR-Cas9 and then crossed with human ApoB transgenic mice to achieve high levels of human-like Lp(a) particles in plasma. Plasma was assayed by ELISA for the concentrations of each lipoprotein. Echocardiography was performed to detect aortic morphology in vivo. Single cell transcriptome analysis was performed on the dissection lesion. Cell interaction was examined in macrophage from Lp(a) transgenic mice and vascular smooth muscle cell (VSMC) coculture system. Result Our results indicate that the concentration of ApoA and ApoB in plasma were increased in transgenic mice fed a chow diet. Low density lipoprotein (LDL) levels were increased and shows that LDL is the major cholesterol carrier in these mice. We were surprised to find that the dissection of the ascending aortic arch could be seen by echocardiography in transgenic mice as early as 2 months, and transgenic mice showed significant increase in aortic enlargement, dissection, and rupture in both the thoracic and abdominal aortic regions, resulting in a survival rate of only 58% after 12 months. Single cell transcriptome analysis revealed that Lp(a) transgene induced the inflammatory response, dedifferentiation and pathological VSMC phenotypical switch, and matrix metalloproteinase expression in macrophages. Monocytes isolated from transgenic mice with elevated Lp(a) remain in a long-lasting primed state, as evidenced by an increased capacity to transmigrate and produce proinflammatory cytokines on stimulation. Monocytes isolated from wild type mice cultured in media with high level Lp(a) for 24h also showed the ability to facilitated cocultured VSMC phenotype transformation, which was reversed by E06, a monoclonal antibody blocking the oxidized phospholipids in Lp(a). Conclusion These findings demonstrate that Lp(a) induces spontaneous aortic dissection via increasing monocyte trafficking to the arterial wall, mediating proinflammatory responses and VSMC phenotype transformation through its OxPL content. The study presents a rodent model of spontaneous aortic dissection and provide a novel mechanism by which Lp(a) mediates aortic dissection.Graphical abstract

Characteristics, treatment, and outcomes of spontaneous renal artery dissection: a 10-year retrospective single-center experience.

Spontaneous renal artery dissection (SRAD) is a rare cause of renal failure and renovascular hypertension, with the diagnosis often being delayed and treatment varying across different centers. The objective of this retrospective cohort study was to scrutinize the characteristics, treatment modalities, and outcomes of patients with SRAD at our center over the past ten years. Furthermore, the study sought to identify the most suitable treatment options for different categories of patients with SRAD. Data from 21 consecutive patients who presented with symptoms of SRAD from December 2013 to December 2023 were collected. Lesion characteristics, treatment options, blood pressure (BP) control, serum creatinine and estimated glomerular filtration rate (eGFR) were analyzed. A paired t-test was used for comparisons of BP, serum creatinine, and eGFR. An independent samples t-test was used to analyze baseline BP and BP change in different treatment groups. The mean age, weight, and height of patients with SRAD was 49.2±13.0 (range, 18-69) years, 69.0±9.7 (range, 50-80) kg, and 1.7±0.1 (range 1.6-1.8) m, respectively. New-onset hypertension was found in 8 (38.1%) patients. Renal artery dissecting aneurysm and renal artery stenosis were found in 1 (4.8%) and 4 (19.0%) patients, respectively. Supportive medical treatment alone, endovascular intervention, and nephrectomy were required in 15, 4 and 2 cases, respectively. Stable renal function and satisfactory hypertension control were obtained in all treatment groups, with a median follow-up of 18.1 (range, 12-32) months. Medical management is a reasonable choice in most patients with SRAD. Interventional management is an efficacious strategy for the management of renovascular hypertension and the preservation of renal function.

Optical Coherence Tomography in Myocardial Infarction Management: Enhancing Precision in Percutaneous Coronary Intervention

In acute myocardial infarction (AMI), the urgency of coronary revascularization through percutaneous coronary intervention (PCI) is paramount, offering notable advantages over pharmacologic treatment. However, the persistent risk of adverse events, including recurrent AMI and heart failure post-revascularization, underscores the necessity for enhanced strategies in managing coronary artery disease. Traditional angiography, while widely employed, presents significant limitations by providing only two-dimensional representations of complex three-dimensional vascular structures, hampering the accurate assessment of plaque characteristics and stenosis severity. Intravascular imaging, specifically optical coherence tomography (OCT), significantly addresses these limitations with superior spatial resolution compared to intravascular ultrasound (IVUS). Within the context of AMI, OCT serves dual purposes: as a diagnostic tool to accurately identify culprit lesions in ambiguous cases and as a guide for optimizing PCI procedures. Its capacity to differentiate between various mechanisms of acute coronary syndrome, such as plaque rupture and spontaneous coronary dissection, enhances its diagnostic potential. Furthermore, OCT facilitates precise lesion preparation, optimal stent sizing, and confirms stent deployment efficacy. Recent meta-analyses indicate that OCT-guided PCI markedly improves safety and efficacy in revascularization, subsequently decreasing the risks of mortality and complications. This review emphasizes the critical role of OCT in refining patient-specific therapeutic approaches, aligning with the principles of precision medicine to enhance clinical outcomes for individuals experiencing AMI.