- Vasopressin Continuous Infusion Improves Intracranial Pressure and Patient Outcomes after Surgical Clipping or Endovascular Coiling of Cerebral Aneurysm. [Journal Article]Anesth Essays Res 2019 Jul-Sep; 13(3):528-534AE
- CONCLUSIONS: Vasopressin IVI improved ICP, MAP, CPP and patient outcomes safely by reducing the incidence of cerebral vasospasm, and 28-day mortality after clipping or coiling of the cerebral aneurysm.
- Increased Levels of Endothelin-1 in Cerebrospinal Fluid Are a Marker of Poor Visual Recovery after Optic Neuritis in Multiple Sclerosis Patients. [Journal Article]Dis Markers 2019; 2019:9320791DM
- CONCLUSIONS: Severity and failure in the recovery from ON in MS patients may depend from vascular hypoperfusion of the optic nerve induced by high intrathecally produced ET-1, a potential prognostic marker of ON recovery in MS. The detection of CSF ET-1 levels may allow identifying groups of ON patients potentially benefitting from treatment with ET-1 antagonists (e.g., bosentan).
- Novel Medications for the Treatment of Migraine. [Review]Headache 2019; 59(9):1597-1608H
- CONCLUSIONS: The development of new migraine-specific classes of medications provides more treatment options for both acute and preventive treatment of migraine.
- The role of arginine vasopressin in myocardial infarction and reperfusion. [Journal Article]Kardiol Pol 2019KP
- Little attention is paid to the coronary microvasculature when treating acute myocardial infarction (MI). Microvascular obstruction (MVO) contributes to ischaemia-reperfusion (I-R) injury which hampers distal blood flow to the myocardium despite recanalisation of the culprit epicardial vessel. One of the mechanisms behind reperfusion injury is MVO due to persistent vasoconstrictor tone during rep…
Little attention is paid to the coronary microvasculature when treating acute myocardial infarction (MI). Microvascular obstruction (MVO) contributes to ischaemia-reperfusion (I-R) injury which hampers distal blood flow to the myocardium despite recanalisation of the culprit epicardial vessel. One of the mechanisms behind reperfusion injury is MVO due to persistent vasoconstrictor tone during reperfusion. Arginine vasopressin (AVP) is a hormone with prominent vasoactive effect on the coronary microvessels. AVP levels are elevated as part of a stress response triggered by MI which can exert vasoconstrictive effects on coronary arteries in pre-clinical models, mainly in non-epicardial vessels of the microcirculation. Circulating AVP levels are up to 100-fold increased in MI and do not immediately decrease to baseline levels upon reperfusion. This would allow slow flow phenomenon and mediate I-R injury. Recently, the C-terminal fragment of pre-provasopressin, copeptin, has emerged to be a surrogate biomarker for AVP as it is more stable in the circulation. Multiple studies have shown the predictive value of both AVP and copeptin in regards to long-term prognoses of MI patients. We propose that both AVP and copeptin have more than just a predictive value but also play a role in the pathophysiology of adverse outcome post-MI. Therefore, the treatment of choice for MI should not only focus on epicardial vessel but also to target MVO that might pre-exist or might directly follow reperfusion. This mandates a clinical trial with an AVP-receptor antagonist in patients with acute MI undergoing reperfusion therapy.
- Magnesium-Based Resorbable Scaffold versus Permanent Metallic Sirolimus-Eluting Stent in Patients with ST-Segment Elevation Myocardial Infarction: The MAGSTEMI Randomized Clinical Trial. [Journal Article]Circulation 2019Circ
- CONCLUSIONS: When compared to SES, MgBRS demonstrated a higher capacity of vasomotor response to pharmacological agents (either endothelium-independent or-dependent) at 1 year. However, MgBRS was associated with a lower angiographic efficacy, a higher rate of target lesion revascularization, without thrombotic safety concerns. Clinical Trial Registration: URL: https://clinicaltrials.gov Unique Identifier: NCT03234348.
- Onset of Efficacy Following Oral Treatment With Lasmiditan for the Acute Treatment of Migraine: Integrated Results From 2 Randomized Double-Blind Placebo-Controlled Phase 3 Clinical Studies. [Journal Article]Headache 2019H
- CONCLUSIONS: Patients treated with lasmiditan for a migraine attack reported an earlier onset of efficacy compared with those treated with placebo. Some of the efficacy measures such as pain relief demonstrated improvement as early as the first assessment at 30 minutes after 100- or 200-mg lasmiditan treatment.
- [Cognitive impairments and microvascular endothelial dysfunction in unilateral occlusion of the carotid artery]. [Journal Article]Angiol Sosud Khir 2019; 25(3):17-22AS
- CONCLUSIONS: Unilateral occlusion of the common carotid artery in albino rats resulted in cognitive impairments, damage of neurons in the most vulnerable areas of the cortex of the cerebral hemispheres and hippocampus predominantly on the ipsilateral side. Cognitive impairments and ischaemic lesions of the brain structures are induced by endothelial dysfunction, enhanced desquamation of endotheliocytes and prevalence of vasoconstrictive reactions resulting from decreased production of the major vasorelaxing factor - nitric oxide.
- A comparative study between haemocoagulase and adrenaline in type 1 tympanoplasty. [Journal Article]J Otol 2019; 14(3):117-120JO
- CONCLUSIONS: Adrenaline is a better middle ear haemostatic than haemocoagulase. However, haemocoagulase can safely be used in patients with hypertension.
- NSAID associated bilateral renal infarctions: a case report. [Journal Article]Int J Nephrol Renovasc Dis 2019; 12:177-181IJ
- Renal infarctions (RIs) are caused by interruptions in the renal arterial blood flow. RIs are generally considered to be rare, however we present the case of a 37 year old woman whose renal infarction was likely due to the vasoconstrictive effects of non-steroidal anti-inflammatory drugs. Although high-dose non-steroidal anti-inflammatory drugs (NSAIDs) are known to cause a decrease in renal perf…
Renal infarctions (RIs) are caused by interruptions in the renal arterial blood flow. RIs are generally considered to be rare, however we present the case of a 37 year old woman whose renal infarction was likely due to the vasoconstrictive effects of non-steroidal anti-inflammatory drugs. Although high-dose non-steroidal anti-inflammatory drugs (NSAIDs) are known to cause a decrease in renal perfusion, they have not been accepted as causative agents in renal infarction. Theoretically, patients in prostaglandin dependent states should be more vulnerable to renovascular vasoconstriction and resulting hypoperfusion in the presence of NSAIDs. Given the high prevalence of NSAID use, we suspect that this mechanism of renal injury may be more prevalent than previously thought.
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- Sodium-activated potassium channels moderate excitability in vascular smooth muscle. [Journal Article]J Physiol 2019JP
- CONCLUSIONS: We report that a sodium-activated potassium current, IKNa , has been inadvertently overlooked in both conduit and resistance arterial smooth muscle cells. IKNa is a major K+ resting conductance and is absent in cells of IKNa knockout (KO) mice. The phenotype of the IKNa KO is mild hypertension, although KO mice react more strongly than wild-type with raised blood pressure when challenged with vasoconstrictive agents. IKNa is negatively regulated by angiotensin II acting through Gαq protein-coupled receptors. In current clamp, KO arterial smooth muscle cells have easily evoked Ca2+ -dependent action potentials.