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British Journal of Clinical Pharmacology Jul 2016Drug-induced Raynaud's phenomenon (RP) has long been associated with the use of different drugs, including cancer chemotherapy or β-adrenoceptor blockers. However,... (Review)
Review
AIM
Drug-induced Raynaud's phenomenon (RP) has long been associated with the use of different drugs, including cancer chemotherapy or β-adrenoceptor blockers. However, sources report extremely variable prevalence and the level of evidence for each class is heterogeneous. Moreover, new signals are emerging from case reports and small series. Our objective was therefore to review available evidence about this adverse drug effect and to propose a mechanistic approach of drug-induced RP.
METHODS
A systematic review of English and French language articles was performed through Medline (1946-2015) and Embase (1974-2015). Further relevant papers were identified from the reference lists of retrieved articles.
RESULTS
We identified 12 classes of drugs responsible for RP, with a variety of underlying mechanisms such as increased sympathetic activation, endothelial dysfunction, neurotoxicity or decreased red blood cell deformability. Cisplatin and bleomycin were associated with the highest risk, followed by β-adrenoceptor blockers. Recent data suggest a possible involvement of tyrosine kinase inhibitors (TKI), through an unknown mechanism.
CONCLUSION
Drug-induced RP is a probably underestimated adverse drug event, with limited available evidence regarding its prevalence. Although rare, serious complications like critical digital ischaemia have been reported. When these treatments are started in patients with a history of RP, careful monitoring must be made and, if possible, alternative therapies that do not alter peripheral blood flow should be considered.
Topics: Adrenergic beta-Antagonists; Animals; Drug-Related Side Effects and Adverse Reactions; Humans; Prevalence; Raynaud Disease
PubMed: 26949933
DOI: 10.1111/bcp.12912 -
The European Respiratory Journal Mar 2022Obstructive sleep apnoea and the related intermittent hypoxia (IH) are widely recognised as risk factors for incident cardiovascular diseases. Numerous studies support... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Obstructive sleep apnoea and the related intermittent hypoxia (IH) are widely recognised as risk factors for incident cardiovascular diseases. Numerous studies support the deleterious vascular impact of IH in rodents but an overall interpretation is challenging owing to heterogeneity in rodent species investigated and the severity and duration of IH exposure. To clarify this major issue, we conducted a systematic review and meta-analysis to quantify the impact of IH on systemic artery structure and function depending on the different IH exposure designs.
METHODS
We searched PubMed, Embase and Web of Science, and included 125 articles in a meta-analysis, among them 112 using wild-type rodents and 13 using apolipoprotein E knockout (ApoE) mice. We used the standardised mean difference (SMD) to compare results between studies.
RESULTS
IH significantly increased mean arterial pressure (+13.90 (95% CI 11.88-15.92) mmHg), and systolic and diastolic blood pressure. Meta-regressions showed that mean arterial pressure change was associated with strain and year of publication. IH altered vasodilation in males but not in females and increased endothelin-1-induced but not phenylephrine-induced vasoconstriction. Intima-media thickness significantly increased upon IH exposure (SMD 1.10 (95% CI 0.58-1.62); absolute values +5.23 (2.81-7.84) µm). This increase was observed in mice but not in rats and was negatively associated with age. Finally, IH increased atherosclerotic plaque size in ApoE mice (SMD 1.08 (95% CI 0.80-1.37)).
CONCLUSIONS
Our meta-analysis established that IH, independently of other confounders, has a strong effect on vascular structure and physiology. Our findings support the interest of identifying and treating sleep apnoea in routine cardiology practice.
Topics: Animals; Blood Pressure; Carotid Intima-Media Thickness; Disease Models, Animal; Female; Humans; Hypoxia; Male; Mice; Rats; Rodentia
PubMed: 34413154
DOI: 10.1183/13993003.00866-2021 -
Cerebrovascular Diseases Extra 2014Arachidonic acid (ARA) is a precursor of various lipid mediators. ARA metabolites such as thromboxane A2 cause platelet aggregation and vasoconstriction, thus may lead... (Review)
Review
BACKGROUND
Arachidonic acid (ARA) is a precursor of various lipid mediators. ARA metabolites such as thromboxane A2 cause platelet aggregation and vasoconstriction, thus may lead to atherosclerotic disease. It is unclear whether dietary ARA influences the ARA-derived lipid mediator balance and the risk for atherosclerotic diseases, such as cerebral ischemia. Considering the function of ARA in atherosclerosis, it is reasonable to focus on the atherothrombotic type of cerebral ischemia risk. However, no systematic reviews or meta-analyses have been conducted to evaluate the effect of habitual ARA exposure on cerebral ischemia risk. We aimed to systematically evaluate observational studies available on the relationship between ARA exposure and the atherothrombotic type of cerebral ischemia risk in free-living populations.
SUMMARY
The PubMed database was searched for articles registered up to June 24, 2014. We designed a PubMed search formula as follows: key words for humans AND brain ischemia AND study designs AND ARA exposure. Thirty-three articles were reviewed against predefined criteria. There were 695 bibliographies assessed from the articles that included both ARA and cerebral ischemia descriptions. Finally, we identified 11 eligible articles and categorized them according to their reporting and methodological quality. We used the Strengthening the Reporting of Observational Studies in Epidemiology Statement (STROBE) checklist to score the reporting quality. The methodological quality was qualitatively assessed based on the following aspects: subject selection, ARA exposure assessment, outcome diagnosis, methods for controlling confounders, and statistical analysis. We did not conduct a meta-analysis due to the heterogeneity among the studies. All eligible studies measured blood ARA levels as an indicator of exposure. Our literature search did not identify any articles that evaluated dietary ARA intake and tissue ARA as assessments of exposure. Seven of the 11 eligible articles were considered to be of low quality. No articles reported a dose-dependent positive association between an increased cerebral ischemia risk and ARA exposure. However, most studies did not assess the risk in each subtype of cerebral ischemia, thus various etiological types of cerebral ischemia risk were involved in their results.
KEY MESSAGES
We did not find a positive association between ARA exposure and cerebral ischemia risk. Eligible studies reported inconsistent findings: cerebral ischemia risk did not change or significantly decreased. We could not draw any conclusions due to the limited number of eligible high-quality studies. Further evidence from well-designed observational studies is required. Simultaneously, in order to develop effective preventive measures against cerebral ischemia, it is imperative to establish standardized definitions, nomenclatures, classifications, and diagnostic procedures.
PubMed: 26225134
DOI: 10.1159/000367588 -
Frontiers in Medicine 2024Methylene blue is an interesting approach in reducing fluid overload and vasoactive drug administration in vasodilatory shock. The inhibition of guanylate cyclase...
BACKGROUND
Methylene blue is an interesting approach in reducing fluid overload and vasoactive drug administration in vasodilatory shock. The inhibition of guanylate cyclase induced by methylene blue infusion reduces nitric oxide production and improves vasoconstriction. This systematic review and meta-analysis aimed to assess the effects of methylene blue administration compared to placebo on the hemodynamic status and clinical outcomes in patients with sepsis and septic shock.
METHODS
The authors specifically included randomized controlled trials that compared the use of methylene blue with placebo in adult patients with sepsis and septic shock. The outcomes were length of intensive care unit stay, hemodynamic parameters [vasopressor use], and days on mechanical ventilation. We also evaluated the abnormal levels of methemoglobinemia. This systematic review and meta-analysis were recorded in PROSPERO with the ID CRD42023423470.
RESULTS
During the initial search, a total of 1,014 records were identified, out of which 393 were duplicates. Fourteen citations were selected for detailed reading, and three were selected for inclusion. The studies enrolled 141 patients, with 70 of them in the methylene blue group and 71 of them in the control group. Methylene blue treatment was associated with a lower length of intensive care unit stay (MD -1.58; 95%CI -2.97, -0.20; = 25%; = 0.03), decreased days on mechanical ventilation (MD -0.72; 95%CI -1.26, -0.17; = 0%; = 0.010), and a shorter time to vasopressor discontinuation (MD -31.49; 95%CI -46.02, -16.96; = 0%; < 0.0001). No association was found with methemoglobinemia.
CONCLUSION
Administering methylene blue to patients with sepsis and septic shock leads to reduced time to vasopressor discontinuation, length of intensive care unit stay, and days on mechanical ventilation.
SYSTEMATIC REVIEW REGISTRATION
https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023423470, CRD42023423470.
PubMed: 38698779
DOI: 10.3389/fmed.2024.1366062 -
Frontiers in Physiology 2018While cannabis is perceived as a relatively safe drug by the public, accumulating clinical data suggest detrimental cardiovascular effects of cannabinoids. Cannabis has... (Review)
Review
While cannabis is perceived as a relatively safe drug by the public, accumulating clinical data suggest detrimental cardiovascular effects of cannabinoids. Cannabis has been legalized in several countries and jurisdictions recently. Experimental studies specifically targeting cannabinoids' effects on the cerebral vasculature are rare. There is evidence for transient vasoconstrictive effects of cannabinoids in the peripheral and cerebral vasculature in a complex interplay of vasodilation and vasoconstriction. Vasoreactivity to cannabinoids is dependent on the specific molecules, their metabolites and dose, baseline vascular tone, and vessel characteristics as well as experimental conditions and animal species. We systematically review the currently available literature of experimental results in and animal studies, examining cannabinoids' effects on circulation and reactive vasodilation or vasoconstriction, with a particular focus on the cerebral vascular bed.
PubMed: 29896112
DOI: 10.3389/fphys.2018.00622 -
International Journal of Trichology 2022Smoking and its role in Androgenetic Alopecia has long been debated. Smoking may lead to hair loss by vasoconstriction, by forming DNA adducts, free radical damage to... (Review)
Review
Smoking and its role in Androgenetic Alopecia has long been debated. Smoking may lead to hair loss by vasoconstriction, by forming DNA adducts, free radical damage to hair follicle, by enhancing senescence and hormonal effects. We have reviewed the available literature on AGA and smoking. Data available show that there is a significant association between smoking and AGA. However, studies demonstrating the benefit of avoidance of smoking in improving hair loss are lacking. Furthermore, large controlled studies with histological documentation are still unavailable to affirm the findings.
PubMed: 35531482
DOI: 10.4103/ijt.ijt_59_21 -
BMJ Open Nov 2017Current guidelines suggest limiting the use of vasopressors following traumatic injury; however, wide variations in practice exist. Although excessive vasoconstriction... (Review)
Review
OBJECTIVES
Current guidelines suggest limiting the use of vasopressors following traumatic injury; however, wide variations in practice exist. Although excessive vasoconstriction may be harmful, these agents may help reduce administration of potentially harmful resuscitation fluids. This systematic review aims to compare early vasopressor use to standard resuscitation in adults with trauma-induced shock.
DESIGN
Systematic review.
DATA SOURCES
We searched MEDLINE, EMBASE, ClinicalTrials.gov and the Central Register of Controlled Trials from inception until October 2016, as well as the proceedings of 10 relevant international conferences from 2005 to 2016.
ELIGIBILITY CRITERIA FOR SELECTING STUDIES
Randomised controlled trials and controlled observational studies that compared the early vasopressor use with standard resuscitation in adults with acute traumatic injury.
RESULTS
Of 8001 citations, we retrieved 18 full-text articles and included 6 studies (1 randomised controlled trial and 5 observational studies), including 2 published exclusively in abstract form. Across observational studies, vasopressor use was associated with increased short-term mortality, with unadjusted risk ratios ranging from 2.31 to 7.39. However, the risk of bias was considered high in these observational studies because patients who received vasopressors were systematically sicker than patients treated without vasopressors. One clinical trial (n=78) was too imprecise to yield meaningful results. Two clinical trials are currently ongoing. No study measured long-term quality of life or cognitive function.
CONCLUSIONS
Existing data on the effects of vasopressors following traumatic injury are of very low quality according to the Grading of Recommendations, Assessment, Development and Evaluation methodology. With emerging evidence of harm associated with aggressive fluid resuscitation and, in selected subgroups of patients, with permissive hypotension, the alternatives to vasopressor therapy are limited. Observational data showing that vasopressors are part of usual care would provide a strong justification for high-quality clinical trials of early vasopressor use during trauma resuscitation.
TRIAL REGISTRATION NUMBER
CRD42016033437.
Topics: Fluid Therapy; Humans; Observational Studies as Topic; Randomized Controlled Trials as Topic; Resuscitation; Shock, Traumatic; Vasoconstrictor Agents
PubMed: 29151048
DOI: 10.1136/bmjopen-2017-017559 -
Pulmonary Circulation 2020Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricular afterload, which causes right ventricular... (Review)
Review
Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricular afterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of the mechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased right ventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonary vasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexes and hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin, thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenous administration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemic vasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulators of the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandin pathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim of this review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimental and human investigations of pulmonary vasodilation in acute pulmonary embolism.
PubMed: 32180938
DOI: 10.1177/2045894019899775 -
BJS Open Sep 2023Conflicting evidence exists regarding the optimal waiting time for stable analgesic and vasoconstrictive effects after local infiltration of lidocaine with epinephrine....
BACKGROUND
Conflicting evidence exists regarding the optimal waiting time for stable analgesic and vasoconstrictive effects after local infiltration of lidocaine with epinephrine. An objective review is needed to dispel surgical dogma.
METHODS
This systematic review (PROSPERO ID: CRD42022362414) included RCTs and prospective cohort studies. Primary outcomes were (1) onset of analgesia and (2) onset of stable hypoperfusion, assessed directly, or measured indirectly using perfusion imaging. Other data extracted include waiting strategies, means of outcome assessment, anaesthetic concentrations, volume/endpoint of infiltration, and injection sites. Methodological quality was evaluated using the Cochrane risk-of-bias tool for randomized trials. Articles describing waiting strategies were critically appraised by the Joanna Briggs Institute tools.
RESULTS
Twenty-four articles were analysed, comprising 1013 participants. Ten investigated analgesia onset. Their pooled mean was 2.1 min (range 0.4-9.0 min). This varied with anatomic site and targeted nerve diameter. Fourteen articles investigated onset of stable hypoperfusion. Four observed bleeding intraoperatively, finding the minimum time to hypoperfusion at 7.0 min in the eyelid skin and 25.0 min in the upper limb. The ten remaining studies used perfusion imaging, reporting a wide range of results (0.0-30.0 min) due to differences in anatomic sites and depth, resolution and artefacts. Studies using near-infrared reflectance spectroscopy and hyperspectral imaging correlated with clinical observations. Thirteen articles discussed waiting strategies, seven relating to large-volume tumescent local infiltration anaesthesia. Different waiting strategies exist for emergency, arthroscopic and cosmetic surgeries, according to the degree of hypoperfusion required. In tumescent liposuction, waiting 10.0-60.0 min is the norm.
CONCLUSION
Current literature suggests that around 2 min are required for most patients to achieve complete analgesia in all sites and with all anaesthesia concentrations. Waiting around 7 min in eyelids and at least 25 min in other regions results in optimal hypoperfusion. The strategies discussed inform decisions of when and how long to wait.
Topics: Humans; Anesthesia, Local; Prospective Studies; Pain Management; Epinephrine; Lidocaine
PubMed: 37768699
DOI: 10.1093/bjsopen/zrad089 -
Expert Review of Cardiovascular Therapy Oct 2010Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder associated with multifocal arterial constriction and dilation. RCVS is associated with... (Review)
Review
Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder associated with multifocal arterial constriction and dilation. RCVS is associated with nonaneurysmal subarachnoid hemorrhage, pregnancy and exposure to certain drugs. The primary clinical manifestation is recurrent sudden-onset and severe (‘thunderclap’) headaches over 1–3 weeks, often accompanied by nausea, vomiting, photophobia, confusion and blurred vision. The primary diagnostic dilemma is distinguishing RCVS from primary CNS arteritis. Diagnosis requires demonstration of the characteristic ‘string of beads’ on cerebral angiography with resolution within 1–3 months, although many patients will initially have normal vascular imaging. Many treatments have been reported to ameliorate the headaches of RCVS, but it is unclear whether they prevent hemorrhagic or ischemic complications.
Topics: Arteritis; Cerebral Angiography; Cerebral Arterial Diseases; Diagnosis, Differential; Female; Headache Disorders, Primary; Humans; Pregnancy; Syndrome; Time Factors; Vasoconstriction; Vasospasm, Intracranial
PubMed: 20936928
DOI: 10.1586/erc.10.124