blood pressure

Background: Studies explored the therapeutic role of agents inhibiting RAS in epilepsy. Fewer studies addressed the electrophysiological changes associated with angiotensin converting enzyme inhibitors (ACEIs) in terms of sustained seizures (status epilepticus). Sodium valproate (SVPA), a broad-spectrum anticonvulsant, has been associated with adverse cardiac events upon long-term use, in contrast to the beneficial role of ACEIs in cardiovascular disorders.  This work explored the potential effects of ramipril, an ACEI, compared to SVPA, on the behavior, and electrophysiology of the brain and heart in a rat model of status epilepticus. The dose dependent pattern of the presumed ramipril activities was investigated. Methods: Adult male rats were assigned into seven groups, controls, IP pyridostigmine (36 mg/kg)-induced status epilepticus (PISE), oral SVPA (5 mg/kg), and three groups receiving oral ramipril at respective doses of 5 (R5), 10 (R10), and 20 mg/kg (R20). Rat behavior was assessed using Racine’s motor convulsion scoring for 10 minutes.  Blood pressure was recorded, and electroencephalography (EEG) and electrocardiography (ECG) were performed on the sedated rats 24 hours after recovery. Results: Despite the partial behavioral improvement of motor convulsions with R5 and R10 exhibited epileptogenic activity, as indicated by the increased relative power of fast and slow gamma waves and total EEG power. R10 triggered arrhythmia and cardiac ischemia as indicated by absence of P wave, along with ST elevation and tall T wave, slowed heart rate and prolonged QRS, QTc, and RR intervals. Conclusion: PISE was resistant to sodium valproate and ramipril. Ramipril at low and moderate doses induced epileptogenic activity and, especially at moderate dose, precipitated cardiac ischemia and arrhythmia. SummaryThe debatable role of ramipril in epilepsy was studied in a rat model of pyridostigmine-induced status epilepticus, compared to sodium valproate. Increasing ramipril doses did not resolve status epilepticus in rats. Instead, low and moderate doses exhibited epileptogenic activity, opposite to high dose ramipril and sodium valproate. Blood pressure was dose-dependently reduced with ramipril. Electrocardiography showed evidence of cardiac arrythmia and ischemia, especially with the moderate ramipril dose. The behavioral and EEG indices correlated with systolic blood pressure and ECG changes.

Stress in acute stroke may increase mortality and complications, but there is a paucity of information on the efficacy of beta blockers  over other anti-hypertensive. To report efficacy of metoprolol over amlodipine in reducing mortality, disability and infections in acute stroke. CT/MRI confirmed stroke patients within 3 days of onset were included whose age was 18 to 75 years. Patients with secondary intracerebral hemorrhage, organ failure, pregnancy, malignancy, and immunosuppressant or on beta-blocker/amlodipine were excluded. Stroke risk factors, Glasgow Coma Scale (GCS) score, National Institute of Health Stroke Scale (NIHSS) score and CT/MRI findings were noted. Patients with a blood pressure of > 160/90 mm of Hg were randomized using 1:1 randomization to metoprolol (25 mg on day 1, 50 mg if BP is not controlled) or amlodipine (2.5 mg on day 1, then 5 mg then 10 mg on, subsequent days if BP is not controlled). Other standard treatment was continued. The primary outcome was mortality at 1 month; secondary outcomes included  were in-hospital gastrointestinal hemorrhage, pneumonia, sepsis and 3 months functional outcome based on modified Rankin Scale (mRS). Side effects were noted. 18 (14.4%) patients died; 6 (9.7%) in metoprolol and 12 (19%) in amlodipine (p = 0.20) group. At 3-months, 66 patients had good outcome; 45 (80.4%) in metoprolol and 21 (43.3%) in amlodipine group (p < 0.001). The other secondary outcomes were comparable between the two groups. Metoprolol was withdrawn in 6 patients due to bradycardia, and amlodipine in 5 due to hypotension and in 1 due to allergic reaction. Metoprolol is associated with improved functional outcomes in acute stroke  compared to amlodipine.

Background: Absence of nocturnal decrease in Blood Pressure (BP) (“non-dipping”) has been shown to be a strong and independent predictor of cardiovascular events, target organ damage, cardiovascular sequela and cardiovascular mortality. Obstructive Sleep Apnea (OSA) has been associated with non-dipping with an estimated prevalence of approximately 50%, but factors associated with non-dipping in OSA patients remain poorly understood. In this study, we examined clinically relevant variables associated with non-dipping in OSA.Methods: Patients (n = 35) undergoing overnight valuation for OSA, laboratory-based polysomnography, structured clinical interviews, and comprehensive metabolic and anthropometric evaluations, and ambulatory BP monitoring for 24 hours. Patients were classified into a) dipping BP group or b) non-dipping BP group, based on (a) a nocturnal systolic BP decrease of 10% - 20% or (b) a systolic BP decrease of < 10%. Results: Patients had moderate and severe OSA (AHI = 34.8 ± 29.1), and 42.9% demonstrated a non-dipping BP pattern. The severity of OSA measures did not differ between dipping group and non-dipping group. However, Wake after Sleep Onset (WASO) and chronicity of insomnia predicts non-dipping BP independent of demographics, sleep stages, anthropometrics, metabolic measures, or arterial stiffness. Conclusion: These findings contribute to a better understanding of the cardiovascular impacts of OSA and indicate that sleep quality should be incorporated into clinical assessments and management of OSA patients.