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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 -
Annals of Indian Academy of Neurology 2021The current target of migraine treatment is focused on Triptans. Lasmiditan, a non-vasoconstrictive and highly selective 5HT receptor agonist is a novel therapeutic... (Review)
Review
BACKGROUND
The current target of migraine treatment is focused on Triptans. Lasmiditan, a non-vasoconstrictive and highly selective 5HT receptor agonist is a novel therapeutic discovery for migraine for patients with cardiovascular (CV) risk factors or stable cardiovascular diseases and who fail to respond to the existing treatment.
OBJECTIVE
To identify an optimal dosing of Lasmiditan 100 mg versus 200 mg for the treatment of acute migraine attacks in adult patients with cardiovascular risk factors.
METHODS
Systematic searches were run in databases such as Cochrane Central Register of Controlled Trials (CENTRAL), Scopus, Google scholar, and PUBMED. Out of 83 study records identified, two studies were included for quantitative analysis.
RESULTS
There was a significant headache pain freedom at 2 h [Odds Ratio (OR): 0.77; 95% Confidence interval (CI): 0.64-0.92] and sustained pain freedom at 24 h (OR): 0.75; 95% CI: 0.61-0.93] in patients taking Lasmiditan 200 mg compared to those taking Lasmiditan 100 mg. The results were statistically insignificant for parameters like most bothersome symptoms (MBS) free at 2 h, headache relief at 2 h, disability level at 2 h, and global impression of change at 2 h. A combined analysis of these parameters showed a remarkable difference between both the groups favoring Lasmiditan 200 mg [OR: 0.88; 95% CI: 0.81-0.95].
CONCLUSION
An oral dosing of Lasmiditan 200 mg is ideal for the treatment of acute migraine in adult patients with CV risk factors for attaining headache pain freedom at 2 h and sustained pain freedom at 24 compared to Lasmiditan 100 mg.
PubMed: 34220057
DOI: 10.4103/aian.AIAN_1223_20 -
European Review For Medical and... May 2021We aimed to analyze clinical characteristics, treatment patterns, and prognosis of patients with reversible cerebral vasoconstriction syndrome (RCVS).
OBJECTIVE
We aimed to analyze clinical characteristics, treatment patterns, and prognosis of patients with reversible cerebral vasoconstriction syndrome (RCVS).
MATERIALS AND METHODS
Two investigators independently searched PubMed and EMBASE, and 191 cases were included in this study. Information regarding demographics, triggering factors, brain imaging findings, treatment modalities, recurrence, and clinical outcome was collected.
RESULTS
The mean age of the patients was 39.9 years, and 155 (81.2%) were female. The most common triggering factor for RCVS was an exposure to vasoactive substances (41.4%), followed by pregnancy/postpartum (20.9%), and sexual intercourse (10.5%). Multifocal stenosis (84.0%) and beading shape (82.4%) were the leading abnormal findings on angiography, while cerebral ischemic lesions (47.6%) and cerebral hemorrhage (mainly subarachnoid hemorrhage) (35.1%) were the main findings on brain computed tomography (CT)/magnetic resonance imaging (MRI). Calcium channel blockers (nimodipine/verapamil) were the most commonly used medications (44.5%) in the treatment of RCVS. Multivariate analysis identified that RCVS was precipitated by trauma/surgery/procedure (hazard ratio (HR): 3.29, 95% confidence interval (CI) (1.21-8.88), p=0.019), and presence of aphasia/neglect/apraxia during the acute phase of the disease (HR: 3.83, 95% CI (1.33-11.05), p=0.013) were found to be the two independent risk factors for residual neurological deficit after RCVS.
CONCLUSIONS
In our systematic review, vasoactive substances were the most frequent triggers for RCVS, which was most commonly accompanied by angiographic findings of multifocal stenotic lesions. Patients with RCVS precipitated by trauma or surgical procedures and those with focal cortical deficits had a higher risk of residual neurological deficits, and these patients should closely be monitored.
Topics: Cerebrovascular Disorders; Headache Disorders, Primary; Humans; Magnetic Resonance Imaging; Tomography, X-Ray Computed; Vasoconstriction
PubMed: 34002826
DOI: 10.26355/eurrev_202105_25834 -
Pharmacology Research & Perspectives Oct 2020Intravenous norepinephrine (NE) is utilized commonly in critical care for cardiovascular support. NE's impact on cerebrovasculature is unclear and may carry important...
Intravenous norepinephrine (NE) is utilized commonly in critical care for cardiovascular support. NE's impact on cerebrovasculature is unclear and may carry important implications during states of critical neurological illness. The aim of the study was to perform a scoping review of the literature on the cerebrovascular/cerebral blood flow (CBF) effects of NE. A search of MEDLINE, BIOSIS, EMBASE, Global Health, SCOPUS, and Cochrane Library from inception to December 2019 was performed. All manuscripts pertaining to the administration of NE, in which the impact on CBF/cerebral vasculature was recorded, were included. We identified 62 animal studies and 26 human studies. Overall, there was a trend to a direct vasoconstriction effect of NE on the cerebral vasculature, with conflicting studies having demonstrated both increases and decreases in regional CBF (rCBF) or global CBF. Healthy animals and those undergoing cardiopulmonary resuscitation demonstrated a dose-dependent increase in CBF with NE administration. However, animal models and human patients with acquired brain injury had varied responses in CBF to NE administration. The animal models indicate an increase in cerebral vasoconstriction with NE administration through the alpha receptors in vessels. Global and rCBF during the injection of NE displays a wide variation depending on treatment and model/patient.
Topics: Administration, Intravenous; Animals; Brain Injuries; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Dose-Response Relationship, Drug; Humans; Norepinephrine; Vasoconstriction
PubMed: 32965778
DOI: 10.1002/prp2.655 -
International Journal of Chronic... 2020Exacerbations of chronic obstructive pulmonary disease (COPD) are currently diagnosed based on changes in respiratory symptoms. Characterizing the imaging manifestation... (Review)
Review
Exacerbations of chronic obstructive pulmonary disease (COPD) are currently diagnosed based on changes in respiratory symptoms. Characterizing the imaging manifestation of exacerbations could be useful for objective diagnosis of exacerbations in the clinic and clinical trials, as well as provide a mechanism for monitoring exacerbation treatment and recovery. In this systematic review, we employed a comprehensive search across three databases (Medline, EMBASE, Web of Science) to identify studies that performed imaging of the thorax at COPD exacerbation. We included 51 from a total of 5,047 articles which met all our inclusion criteria. We used an adapted version of the Modified Newcastle-Ottawa Quality Assessment Scale for cohort studies to assess the quality of the included studies. Conclusions were weighted towards higher-quality articles. We identified a total of 36 thoracic imaging features studied at exacerbation of COPD. Studies were generally heterogeneous in their measurements and focus. Nevertheless, considering studies which performed consecutive imaging at stable state and exacerbation, which scored highest for quality, we identified salient imaging biomarkers of exacerbations. An exacerbation is characterized by airway wall and airway calibre changes, hyperinflation, pulmonary vasoconstriction and imaging features suggestive of pulmonary arterial hypertension. Most information was gained from CT studies. We present the first ever composite imaging signature of COPD exacerbations. While imaging during an exacerbation is comparatively new and not comprehensively studied, it may uncover important insights into the acute pathophysiologic changes in the cardiorespiratory system during exacerbations of COPD, providing objective confirmation of events and a biomarker of recovery and treatment response.
Topics: Disease Progression; Humans; Pulmonary Disease, Chronic Obstructive
PubMed: 32801677
DOI: 10.2147/COPD.S250746 -
International Journal of Environmental... Jun 2020The fatigue of the respiratory muscles causes the so-called metabolic reflex or metaboreflex, resulting in vasoconstriction of the blood vessels in the peripheral... (Meta-Analysis)
Meta-Analysis
The fatigue of the respiratory muscles causes the so-called metabolic reflex or metaboreflex, resulting in vasoconstriction of the blood vessels in the peripheral muscles, which leads to a decrease in respiratory performance. Training the respiratory muscles is a possible solution to avoid this type of impairment in intermittent sports. The objective of this systematic review was to evaluate the results obtained with inspiratory muscle training (IMT) in intermittent sports modalities, intending to determine whether its implementation would be adequate and useful in intermittent sports. A search in the Web of Science (WOS) and Scopus databases was conducted, following the Preferred Reporting Elements for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The methodological quality of the articles was assessed using the PEDro (Physiotherapy Evidence Database) scale. In conclusion, the introduction of specific devices of IMT seems to be a suitable method to improve performance in intermittent sports, mainly due to a reduction of the metaboreflex, fatigue sensation, and dyspnea. The ideal protocol would consist of a combination of acute and chronic treatment, and, even if IMT is done daily, the duration will not exceed one hour per week.
Topics: Breathing Exercises; Humans; Muscle Strength; Physical Therapy Modalities; Respiratory Muscles; Sports
PubMed: 32575827
DOI: 10.3390/ijerph17124448 -
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 -
Frontiers in Neurology 2019Posterior reversible encephalopathy syndrome (PRES) is a rare clinical and radiological entity characterized by a typical brain edema. Although several case reports...
Posterior reversible encephalopathy syndrome (PRES) is a rare clinical and radiological entity characterized by a typical brain edema. Although several case reports have described PRES in a context of poisoning, to our knowledge, a comprehensive assessment has not been performed. The aim of this systematic review was to raise awareness on poisoning-specific PRES features and to encourage consistent and detailed reporting of substance abuse-and drug overdose-associated PRES. Medline/PubMed, Web of Science, and PsycINFO were screened through May 31, 2019, to systematically identify case reports and case series describing PRES associated with poisoning (i.e., alcohol, drugs, illicit drugs, natural toxins, chemical substances) in accidental context, intentional overdose, and substance abuse. The methodological quality of eligible case reports/series was assessed. Patients and exposure characteristics were recorded; relevant toxicological, radiological, and clinical data were extracted. Forty-one case reports and one case series reporting 42 unique cases were included. The median time to PRES onset from the start of exposure was 3 days (IQR 2-10). Acute high blood pressure, visual disturbance, and seizure were reported in 70, 55, and 50% of patients, respectively. The initial clinical presentation was alertness disorders in 64% of patients. Nine patients (21%) required mechanical ventilation. One-third of patients had at least one risk factor for PRES such as chronic hypertension (17%) or acute/chronic kidney failure (24%). The main imaging pattern (67%) was the combination of classical parieto-occipital edema with another anatomical region (e.g., frontal, basal ganglia, posterior fossa involvement). Vasogenic edema was found in 86% of patients. Intracranial hemorrhage occurred in 14% of patients. Both brain infarction and reversible cerebral vasoconstriction syndrome were diagnosed in 5% of patients. Three patients (12%, 3/25) had non-reversible lesions on follow-up magnetic resonance imaging. The median time required to hospital discharge was 14 days (IQR 7-18). Mortality and neurological recurrence rate were null. Comorbidities such as chronic hypertension and kidney failure were less frequent than in patients with other PRES etiologies. Imaging analysis did not highlight a specific pattern for poisoning-induced PRES. Although less described, PRES in the context of poisoning, which shares most of the clinical and radiological characteristics of other etiologies, is not to be ignored.
PubMed: 32116991
DOI: 10.3389/fneur.2019.01420 -
Clinical Orthopaedics and Related... Mar 2020Blood flow restriction (BFR) is a process of using inflatable cuffs to create vascular occlusion within a limb during exercise. The technique can stimulate muscle...
BACKGROUND
Blood flow restriction (BFR) is a process of using inflatable cuffs to create vascular occlusion within a limb during exercise. The technique can stimulate muscle hypertrophy and improve physical function; however, most of these studies have enrolled healthy, young men with a focus on athletic performance. Furthermore, much of the information on BFR comes from studies with small samples sizes, limited follow-up time, and varied research designs resulting in greater design, selection, and sampling bias. Despite these limitations, BFR's popularity is increasing as a clinical rehabilitation tool for aging patients. It is important for practitioners to have a clear understanding of the reported effects of BFR specifically in older adults while simultaneously critically evaluating the available literature before deciding to employ the technique.
QUESTIONS/PURPOSES
(1) Does BFR induce skeletal muscle hypertrophy in adults older than 50 years of age? (2) Does BFR improve muscle strength and/or physical function in adults older than 50 years?
METHODS
Using PubMed, Google Scholar, Web of Science, and Science Direct, we conducted a systematic review of articles using Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to assess the reported effects of BFR on skeletal muscle in older adults. Included articles enrolled participants 50 years of age or older and used BFR in conjunction with exercise to study the effects of BFR on musculoskeletal outcomes and functionality. The following search terms were used: "blood flow restriction" OR "KAATSU" OR "ischemic training" AND "clinical" AND "elderly." After duplicates were removed, 1574 articles were reviewed for eligibility, and 30 articles were retained with interventions duration ranging from cross-sectional to 16 weeks. Sample sizes ranged from 6 to 56 participants, and exercise tasks included passive mobilization or electrical stimulation; walking; resistance training using machines, free weights, body weight, or elastic bands; and water-based activities. Furthermore, healthy participants and those with cardiovascular disease, osteoarthritis, osteoporosis, sporadic inclusion body myositis, spinal cord injuries, and current coma patients were studied. Lastly, retained articles were assigned a risk of bias score using aspects of the Risk of Bias in Nonrandomized Studies of Interventions and the Cochrane Collaboration's tool for assessing the risk of bias in randomized trials.
RESULTS
BFR, in combination with a variety of exercises, was found to result in muscle hypertrophy as measured by muscle cross-sectional area, thickness, volume, mass, or circumference. Effect sizes for BFR's ability to induce muscle hypertrophy were calculated for 16 of the 30 papers and averaged 0.75. BFR was also shown to improve muscle strength and functional performance. Effect sizes were calculated for 21 of the 30 papers averaging 1.15.
CONCLUSIONS
Available evidence suggests BFR may demonstrate utility in aiding rehabilitation efforts in adults older than 50 years of age, especially for inducing muscle hypertrophy, combating muscle atrophy, increasing muscle strength, and improving muscle function. However, most studies in this systematic review were at moderate or high risk of bias; that being so, the findings in this systematic review should be confirmed, ideally using greater sample sizes, randomization of participants, and extended follow-up durations.
LEVEL OF EVIDENCE
Level II, systematic review.
Topics: Aged; Exercise Therapy; Female; Humans; Hypertrophy; Male; Middle Aged; Muscle Strength; Muscle, Skeletal; Orthopedic Procedures; Regional Blood Flow; Vasoconstriction
PubMed: 31860546
DOI: 10.1097/CORR.0000000000001090 -
PloS One 2019Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II which causes vasoconstriction. ACE inhibitors reduce blood pressure by inhibiting ACE. A...
Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II which causes vasoconstriction. ACE inhibitors reduce blood pressure by inhibiting ACE. A well-known adverse drug reaction to ACE inhibitors is ACE inhibitor-induced angioedema (ACEi-AE). Angioedema is a swelling of skin and mucosa, which can be fatal if the airway is compromised. We have performed a systematic review of the evidence suggesting that genetic polymorphisms are associated with ACEi-AE and evaluated the methodological approaches of the included studies. The Cochrane Database of Systematic Reviews, Google Scholar, and PubMed were searched. Studies investigating the association between genetic markers and ACEi-AE were included. The Q-genie tool was used to evaluate the quality of the study methodologies. Seven studies were included. With the exception of one whole genome study, all of the included studies were candidate gene association studies. Study quality assessment scores ranged from 36 to 55. One study was found to be of good quality, suggesting that the detected associations may be unreliable. The inferior quality of some studies was due to poor organization, lack of analyses and missing information. Polymorphisms within XPEPNP2, BDKRB2-9/+ 9 and neprilysin genes, were reported to be associated with increased risk of ACEi-AE. However, due to low quality, these associations need to be confirmed in larger studies.
Topics: Angioedema; Angiotensin-Converting Enzyme Inhibitors; Genetic Predisposition to Disease; Humans; Outcome Assessment, Health Care; Polymorphism, Genetic
PubMed: 31710633
DOI: 10.1371/journal.pone.0224858