Fusiform aneurysms of anterior cerebral artery: center experience and systematic literature review.

Fusiform aneurysms of the anterior cerebral artery (ACA) are uncommon, and the natural history of this entity is poorly characterized. Along with our center experience, we conducted a systematic literature review to help shed light on the clinical course of ACA fusiform aneurysms. We queried our institutional database to identify cases with fusiform aneurysms of ACA. In addition, following the PRISMA algorithm, we identified all reported cases published in the English literature from the inception of PubMed until December 2022. We categorized clinical presentations into three categories: (i) traumatic/iatrogenic, (ii) spontaneous symptomatic ruptured/unruptured, and (iii) spontaneous asymptomatic aneurysms. We utilized descriptive statistics. We identified seven cases from our center along with 235 patients from published literature. Blunt trauma was responsible for the development of 19 aneurysms. Sixty-three percent of these aneurysms tend to rupture within 2 weeks from the initial trauma, and despite treatment, only 74% of these patients had good clinical outcomes. Spontaneous symptomatic presentation occurred in 207 patients and was often associated with previous/concomitant ACA dissection. Subarachnoid hemorrhage from ruptured aneurysms was the most common presentation. Spontaneous symptomatic fusiform aneurysm is rapidly evolving lesions, and treatment is necessary. Three of our own cases were treated with an endovascular flow diverter (pipeline) stenting with good outcomes. Spontaneous asymptomatic aneurysms were reported in nine patients. These lesions are often associated with other vascular abnormalities. Treatment included surgical clipping with good clinical outcomes. Instead, four patients from our center database were managed conservatively with equally good outcomes. Our study demonstrates good clinical outcomes when fusiform aneurysms of ACA, especially when symptomatic, are treated promptly with either reconstructive or deconstructive therapies.

Lipoprotein(a): a genetic marker for cardiovascular disease and target for emerging therapies.

Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor, and growing evidence indicates its causal association with atherosclerotic disease because of the proatherogenic low-density lipoprotein (LDL)-like properties and the prothrombotic plasminogen-like activity of apolipoprotein(a) [apo(a)]. As genetics significantly influences its plasma concentration, Lp(a) is considered an inherited risk factor of atherosclerotic cardiovascular disease (ASCVD), especially in young individuals. Moreover, it has been suggested that elevated Lp(a) may significantly contribute to residual cardiovascular risk in patients with coronary artery disease and optimal LDL-C levels. Nonetheless, the fascinating hypothesis that lowering Lp(a) could reduce the risk of cardiovascular events - in primary or secondary prevention - still needs to be demonstrated by randomized clinical trials. To date, no specific Lp(a)-lowering agent has been approved for reducing the lipoprotein levels, and current lipid-lowering drugs have limited effects. In the future, emerging therapies targeting Lp(a) may offer the possibility to further investigate the relation between Lp(a) levels and cardiovascular outcomes in randomized controlled trials, ultimately leading to a new era in cardiovascular prevention. In this review, we aim to provide an updated overview of current evidence on Lp(a) as well as currently investigated therapeutic strategies that specifically address the reduction of the lipoprotein.

Coronary Physiology Assessment for the Diagnosis and Treatment of Coronary Artery Disease.

Functionally significant coronary lesions identification is necessary for appropriate revascularization. This review aims to provide an overview of the available options for coronary stenosis physiologic evaluation with a focus on the latest developments in the field.

Antihypertensive treatment with beta-blockers in the metabolic syndrome: a review.

Metabolic syndrome, a "cluster" of metabolic disorders including hypertension, increases the cardiovascular risk, and insulin resistance plays a key role in its pathogenesis. In this syndrome antihypertensive treatment with beta-blockers is underused because of their adverse metabolic effects. The aim was to review the evidences supporting the reasons for underusing beta-blockers in hypertensive patients with metabolic syndrome. A review of Literature has been carried out via PubMed from 1998 to 2008: most of beta-blockers have adverse effects on insulin sensitivity, carbohydrate and lipid metabolism, and are not recommended in metabolic syndrome. However, some recent large studies have shown a better metabolic profile with newer third generation vasodilating beta-blockers, such as Carvedilol and Nebivolol. Vasodilating action of Carvedilol and Nebivolol, due respectively to alpha1-blocking effect and release of nitric oxide, explains the lack of adverse metabolic effects of these beta-blockers that could also be used in hypertensive patients with metabolic syndrome.

A case of ischemic stroke in acute promyelocytic leukemia at initial presentation. Relevance of all-trans retinoic acid treatment.

Acute promyelocytic leukemia (APL) is frequently associated, often from the earliest phases, with a life-threatening coagulation/bleeding syndrome; disseminated intravascular coagulation (DIC) is described in majority of patients. We report a case of 49-year-old male, without cardiovascular risk factors, who suddenly developed ischemic stroke and splenic infarction as presenting symptoms of APL and related DIC. The patient was immediately treated with all-trans retinoic acid (ATRA) and the alterations of hemocoagulation parameters promptly returned in normal range. The coagulation/bleeding syndrome of the onset of APL is associated with high mortality; both diagnostic and therapeutic approaches require special and timely consideration of this condition. Treatment with ATRA is essential.

Percutaneous ethanol injection plus radioiodine versus radioiodine alone in the treatment of large toxic thyroid nodules.

UNLABELLED: Therapeutic options for toxic thyroid nodules (TTNs) are surgery, radioiodine (RAI), and percutaneous ethanol injection (PEI). Surgery is generally considered for TTNs larger than 4 cm. However, some patients may be at high surgical risk. The purpose of the study was to evaluate the efficacy of 2 nonsurgical modalities for these TTNs. METHODS: Twenty-two patients with TTNs larger than 4 cm were randomly assigned to 2 different treatments: to 11 (subgroup A), RAI was administered at a dose of 12,580 kBq/mL of nodular volume (NV) and was corrected for 100% 24-h (131)I uptake (RAIU); to 11 (subgroup B), 2-4 PEI sessions (ethanol injected = 30% NV) preceded 2 mo of 24-h RAIU and RAI dosing. Inclusion criteria were clinical and biochemical hyperthyroidism; a single palpable, hot nodule at (99m)Tc scintigraphy; and high surgical risk or refusal to have surgery. Patients gave informed consent. Local symptoms were evaluated by a previously validated score (symptom score, or SYS). RESULTS: Both treatments were well tolerated. Subgroup B showed a significant reduction of NV 2 mo after PEI: 33.6 +/- 18.5 versus 60.8 +/- 29.5 mL. Their 24-h RAIU was similar to that of subgroup A: 53.9 +/- 13.9 versus 61.8% +/- 11.0%. Consequently, the administered RAI dose was significantly lower for subgroup B (730 +/- 245 MBq) than for subgroup A (1,048 +/- 392 MBq). Twelve months after RAI, subgroup B had a higher NV reduction and a lower SYS than did subgroup A. In subgroup A, 1 patient was subclinically hyperthyroid, 2 showed a slight increase of thyroid-stimulating hormone, and 1 was clinically hypothyroid. In subgroup B, 1 patient had a slight increase of thyroid-stimulating hormone. CONCLUSION: We demonstrated that RAI, alone or with PEI, can be considered a valid alternative for TTNs larger than 4 cm when surgery is either refused or contraindicated. PEI plus RAI can be considered when marked shrinkage of a nodule is required or when reduction of the RAI dose can prevent hospitalization.