cardiovascular-agents and Intracranial-Aneurysm

To compare the effectiveness of various drug interventions in improving the clinical outcome of postoperative patients after aneurysmal subarachnoid hemorrhage (aSAH) and assist in determining the drugs of definite curative effect in improving clinical prognosis.. Eligible Randomized Controlled Trials (RCTs) were searched in databases of PubMed, EMBASE, and Cochrane Library (inception to Sep 2020). Glasgow Outcome Scale (GOS) score, Extended Glasgow Outcome Scale (GOSE) score or modified Rankin Scale (mRS) score was used as the main outcome measurements to evaluate the efficacy of various drugs in improving the clinical outcomes of postoperative patients with aSAH. The network meta-analysis (NMA) was conducted based on a random-effects model, dichotomous variables were determined by using odds ratio (OR) with 95% confidence interval (CI), and a surface under the cumulative ranking curve (SUCRA) was generated to estimate the ranking probability of comparative effectiveness among different drug therapies.. From the 493 of initial citation screening, forty-four RCTs (n = 10,626 participants) were eventually included in our analysis. Our NMA results showed that cilostazol (OR = 3.35,95%CI = 1.50,7.51) was the best intervention to improve the clinical outcome of patients (SUCRA = 87.29%, 95%CrI 0.07-0.46). Compared with the placebo group, only two drug interventions [nimodipine (OR = 1.61, 95%CI 1.01,2.57) and cilostazol (OR = 3.35, 95%CI 1.50, 7.51)] achieved significant statistical significance in improving the clinical outcome of patients.. Both nimodipine and cilostazol have exact curative effect to improve the outcome of postoperative patients with aSAH, and cilostazol may be the best drug to improve the outcome of patients after aSAH operation. Our study provides implications for future studies that, the combination of two or more drugs with relative safety and potential benefits (e.g., nimodipine and cilostazol) may improve the clinical outcome of patients more effectively.

Topics: Cardiovascular Agents; Cilostazol; Humans; Intracranial Aneurysm; Network Meta-Analysis; Neuroprotective Agents; Nimodipine; Postoperative Period; Prognosis; Randomized Controlled Trials as Topic; Subarachnoid Hemorrhage; Treatment Outcome

Delayed cerebral ischemia seriously affects the prognosis of patients surviving the initial aneurysmal subarachnoid hemorrhage. Application of cilostazol was reported to ameliorate vasospasm and improve outcomes in series and clinical trials. But the effectiveness and feasibility of cilostazol on aneurysmal subarachnoid hemorrhage remained controversial. We performed a systematic review to clarify this issue.. PubMed, Ovid and Cochrane library database were systematically searched up to May 2018 for eligible publications in English. Quality assessment was conducted for included studies. Meta-analysis was conducted to evaluate the overall effect on events of interest. Subgroup analyses and sensitivity analyses were used to check whether the results were robust. Publication bias was evaluated with the funnel plot.. Pooled analyses found cilostazol significantly reduced incidences of severe angiographic vasospasm (p = 0.0001), symptomatic vasospasm (p < 0.00001), new cerebral infarction (p < 0.00001) and the poor outcome (p < 0.0001). Subgroup and sensitivity analyses achieved consistent results. There was no statistical difference between cilostazol and the control group in reducing mortality (p = 0.07). But sensitivity analysis changed the result after excluding one study. Under the prescribed dosage, complication was few and non-lethal.. Cilostazol was effective and safe to reduce incidences of severe angiographic vasospasm, symptomatic vasospasm, new cerebral infarction and poor outcome in patients after aneurysmal subarachnoid hemorrhage. However, its effect on mortality and the interactive effect with nimodipine warranted further research.

Topics: Brain Ischemia; Cardiovascular Agents; Cerebral Infarction; Cilostazol; Humans; Intracranial Aneurysm; Outcome Assessment, Health Care; Subarachnoid Hemorrhage; Vasospasm, Intracranial

To perform a systematic review of the techniques for transient circulatory arrest during intracerebral aneurysm surgery according to the PRISMA guidelines. Search of PubMed and Google Scholar using the following: ("heart arrest" OR "cardiac standstill"[All Fields]) AND ("intracranial aneurysm" OR "intracranial"[All Fields] AND "aneurysm"[All Fields]). A total of 41 original articles were retrieved, of which 17 were excluded (review articles, editorials and single-case reports). A total of 24 separate articles published between 1984 and 2018 were included in the final analysis, where the majority of patients harbored anterior circulation giant or large aneurysms. Adenosine-induced cardiac arrest gave a short, temporary asystole. The method had benefits in aneurysm with a broad neck, a thin wall, in specific localizations with narrow surgical corridors or in case of intraoperative rupture. Rapid ventricular pacing (RVP) allows a longer and more easily controlled hypotension. Its use is largely limited to elective cases. Deep hypothermic circulatory arrest required a complex infrastructure, and fatal procedure complications lead to a 11.5-30% 30-day mortality rate, limiting its application to giant or complex aneurysm of the basilar artery or to residual posterior circulation aneurysm after endovascular treatment. Adenosine and RVP are both effective options to facilitate clipping of complex aneurysms. However, their use in patient with ischemic heart disease and cardiac arrhythmias should be avoided, and their safety in the context of subarachnoid hemorrhage is yet to be determined. Today, deep hypothermic circulatory arrest is almost obsolete due to endovascular alternatives.

Topics: Adenosine; Cardiac Pacing, Artificial; Cardiovascular Agents; Circulatory Arrest, Deep Hypothermia Induced; Heart Arrest, Induced; Humans; Hypotension; Intracranial Aneurysm; Neurosurgical Procedures

Sensorineural deafness and vertigo have different causes among them immunological, vascular and infectious. Vascular causes of sensorineural hearing loss are unusual and among them are the vertebral artery aneurysms. Knowledge by neurosurgeons, neurointerventional and otolaryngologists aneurysms involving the development of sensorineural hearing loss is critical to establishing and determining a targeted therapeutics. We report the case of an adult handled with endovascular techniques and review the current literature of similar cases.

Topics: Angioplasty, Balloon, Coronary; Cardiovascular Agents; Cerebral Angiography; Combined Modality Therapy; Endovascular Procedures; Hearing Loss, Sensorineural; Hearing Loss, Unilateral; Humans; Imaging, Three-Dimensional; Intracranial Aneurysm; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Male; Middle Aged; Multimodal Imaging; Myocardial Infarction; Risk Factors; Smoking; Stents; Tinnitus; Vertebral Artery; Vertigo

The purpose of this article is to describe the modern management of delayed cerebral ischemia (DCI) in patients with aneurysmal subarachnoid hemorrhage (SAH). SAH causes an inflammatory reaction to blood products in the basal cisterns of the brain, which may produce cerebral ischemia and strokes through progressive narrowing of the cerebral artery lumen. This process, known as cerebral vasospasm, is the most common cause of DCI after SAH. Untreated DCI may result in strokes, which account for a significant portion of the death and long-term disability after SAH.. A number of publications, including two recent consensus statements, have clarified many best practices for defining, diagnosing, monitoring, preventing, and treating DCI. DCI is best defined as new onset of focal or global neurologic deficits or strokes not attributable to another cause. In addition to the clinical examination, radiographic studies such as transcranial Doppler ultrasonography, CT angiography, and CT perfusion may have a role in determining which patients are at high risk for developing DCI. The mainstay of prevention and treatment of DCI is maintenance of euvolemia, which can be a difficult therapeutic target to measure. Hemodynamic augmentation with induced hypertension with or without inotropic support has become the first-line treatment of DCI. The ideal method of measuring hemodynamic values and volume status in patients with DCI remains elusive. In patients who do not adequately respond to or cannot tolerate hemodynamic augmentation, endovascular therapy (intraarterial vasodilators and balloon angioplasty) is a complementary strategy. Optimal triggers for escalation and de-escalation of therapies for DCI have not been well defined.. Recent guidelines and consensus statements have clarified many aspects of prevention, monitoring, and treatment of DCI after SAH. Controversies continue regarding the optimal methods for measurement of volume status, the role of invasive neuromonitoring, and the targets for hemodynamic augmentation therapy.

Topics: Angioplasty, Balloon; Brain Ischemia; Calcium Channel Blockers; Cardiovascular Agents; Cerebral Angiography; Combined Modality Therapy; Consensus Development Conferences as Topic; Disease Management; Fluid Therapy; Hemodynamics; Humans; Hypertension; Intracranial Aneurysm; Neuroimaging; Nimodipine; Practice Guidelines as Topic; Rupture, Spontaneous; Subarachnoid Hemorrhage; Ultrasonography, Doppler, Transcranial; Vasospasm, Intracranial

Late cerebral vasospasm after subarachnoid hemorrhage (SAH) is a disastrous phenomenon for the patients and a definite treatment has not been established. We studied 48 consecutive patients receiving high-dose diltiazem (5 micrograms/kg/min) injection combined with dextran and hydrocortisone to late cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). All but 2 patients underwent surgery within 72 hours after SAH. Diltiazem was continuously given via a central venous line for up to 2 weeks in conjunction with simple cisternal drainage. 5% of dextran solution (500 ml/day) was infused for 7-10 days. Hydrocortisone was given 1,600 mg on the first day, then the dose was gradually decreased over 14 days. Symptomatic vasospasm (SVS) occurred in 5 patients (10.4%), 4 patients recovered, but 1 had severe neurological deficit. A low density area on CT-scan was observed in 2 patients. Thirty patients (62.5%) had good recovery, 10 patients (20.8%) had moderate disability, 3 (6.3%) had severe disability and 3 (6.3%) had vegetative survival. Two patients died of the initial brain damage. There were no severely hypotensive side effects. However, 3 patients showed atrioventricular blockage on electrocardiogram. These side effects subsided after the dose of the drug was decreased or administration was stopped altogether. These findings show that high-dose calcium antagonist diltiazem therapy combined with dextran and hydrocortisone injection is safe and effective for prevention of late cerebral symptomatic vasospasm after SAH.

Topics: Adult; Aged; Aged, 80 and over; Aneurysm, Ruptured; Anti-Inflammatory Agents; Anticoagulants; Blood Pressure; Cardiovascular Agents; Dextrans; Diltiazem; Drug Therapy, Combination; Female; Heart Rate; Humans; Hydrocortisone; Intracranial Aneurysm; Ischemic Attack, Transient; Male; Middle Aged; Subarachnoid Hemorrhage; Tomography, X-Ray Computed

Aspirin is a promising medical therapy for the prevention of intracranial aneurysm (IA) rupture. Recently, we found that men have a better response to aspirin than women. The purpose of this study was to determine whether a sex differential exists in the level of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in the lumen of human IAs.. Consecutive patients undergoing coiling or stent-assisted coiling for a saccular IA at our institution were enrolled. Two samples (A and B) were collected from IA lumens, and the plasma level of 15-PGDH was measured using an ELISA-based method. The study included 38 patients, with 20 women and 18 men. Women and men were comparable on baseline characteristics. The mean plasma concentration of 15-PGDH did not differ statistically between sample A (62.8±16.2 ng/mL) and sample B (61.8±17.9 ng/mL; 95% confidence interval -6.6 to 9.4). The mean plasma concentration of 15-PGDH in IA lumens of samples A and B was significantly higher in men (73.8±13.5 ng/mL) than women (49.6±7.8 ng/mL;. Higher enzyme levels of 15-PGDH exist in the lumen of IAs of men compared with women. This observation could explain why aspirin confers better protection against IA rupture in men than in women. The susceptibility of an individual to aspirin may differ according to the level of 15-PGDH.

Topics: Adult; Aged; Aspirin; Biomarkers; Cardiovascular Agents; Embolization, Therapeutic; Female; Humans; Hydroxyprostaglandin Dehydrogenases; Intracranial Aneurysm; Male; Middle Aged; Sex Factors; Stents; Up-Regulation

Cardiac abnormalities attributed to adrenergic surge are common after aneurysmal subarachnoid hemorrhage. Prescribed medications that block adrenergic stimulation may suppress the onset of cardiopulmonary compromise in patients after aneurysmal subarachnoid hemorrhage.. To compare the incidence of early cardiac complications between patients who reported prescribed use of β-blockers and/or angiotensin-converting enzyme inhibitors before aneurysmal subarachnoid hemorrhage and patients who did not.. A retrospective review of 254 adult patients after acute aneurysmal subarachnoid hemorrhage who were enrolled in an existing R01 study. Demographic data and history were obtained from patients'/proxies' reports and charts. Cardiac enzyme levels, 12-lead electrocardiograms, and chest radiographs were obtained on admission. Holter monitoring and echocardiograms were completed as a part of the R01 study.. Patients reporting prescribed use of angiotensin-converting enzyme inhibitors or β-blockers before aneurysmal subarachnoid hemorrhage had more ventricular and supraventricular ectopy on a Holter report than did patients who did not (P < .05). When age, race, sex, and injury (Fisher grade) were controlled for, patients reporting use of β-blockers were 8 times more likely than others to have occasional to frequent ventricular ectopy (P = .02).. No concrete evidence was found that exposure to adrenergic blockade before aneurysmal subarachnoid hemorrhage provides protection from neurocardiac injury.

Topics: Adrenergic beta-Antagonists; Adult; Age Distribution; Aged; Aneurysm, Ruptured; Angiotensin-Converting Enzyme Inhibitors; Cardiovascular Agents; Female; Heart; Heart Diseases; Humans; Intracranial Aneurysm; Male; Middle Aged; Retrospective Studies; Sex Distribution; Subarachnoid Hemorrhage; Survival Analysis; Young Adult

BRIEF SUMMARY: We describe the use of adenosine-induced cardiac arrest to facilitate intracranial aneurysm clip ligation.. Cerebral aneurysms are highly variable which may result in difficult surgical exposure for clip ligation in select cases. Secure clip placement is often not feasible without temporarily decompressing the aneurysm. This can be accomplished with temporary clip ligation of proximal vessels, or with deep hypothermic circulatory arrest on cardiopulmonary bypass, although these methods have their own inherent risks. Here we describe an alternate method of decompressing the aneurysm via adenosine-induced transient asystole.. We examined the records of 27 patients who underwent craniotomy for cerebral aneurysm clipping in which adenosine was used to induce transient asystole to facilitate clip ligation. Duration of adenosine-induced bradycardia (heart rate <40) and hypotension (SBP < 60) recorded on the electronic anesthesia record and outcome data including incidence of successful clipping, intraoperative and postoperative complications, and mortality were recorded.. Satisfactory aneurysm decompression was achieved in all cases, and all aneurysms were clipped successfully. The median dose of intravenous adenosine resulting in bradycardia greater than 30 seconds was 30 mg. The median dose of adenosine resulting in hypotension greater than 30 seconds was 15 mg, and greater than 60 seconds was 30 mg. One case of prolonged hypotension after rapid redosing of adenosine required brief closed chest compressions before circulation was spontaneously restored. No other adverse events were observed.. Adenosine cardiac arrest is a relatively novel method for decompression of intracranial aneurysms to facilitate clip application. With appropriate safety precautions, it is a reasonable alternative method when temporary clipping of proximal vessels is not desirable or not possible.

Topics: Adenosine; Aged; Anesthesia, General; Antihypertensive Agents; Cardiovascular Agents; Dose-Response Relationship, Drug; Female; Heart Arrest, Induced; Humans; Intracranial Aneurysm; Intraoperative Care; Length of Stay; Male; Middle Aged; Neurosurgical Procedures; Nicardipine; Patient Selection; Postoperative Complications; Retrospective Studies; Treatment Outcome; Vasospasm, Intracranial