Explore chapters and articles related to this topic
Plantago ovata (Isabgol) and Rauvolfia serpentina (Indian Snakeroot)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Ankur Anavkar, Nimisha Patel, Ahmad Ali, Hina Alim
P. ovata seed husk contains a high proportion of polysaccharides. The extracted polysaccharides have been studied as a super disintegrant for fast-dissolving tablets. Valsartan, used for treating hypertension, was the model drug for the study. Tablets with concentration of 7.5% w/w polysaccharide showed rapid wetting and disintegration time when compared with the same concentration of the control Crospovidone, a synthetic super disintegrant (Pawar and Varkhade, 2014). Another study used P. ovata husk powder in the manufacture of orodispersible tablets of the model drug meloxicam. The formulations having lowest wetting and disintegration time with highest water absorption ratio had 16 mg of psyllium husk powder. It outperformed the control and other formulations. Thus, P. ovata can be used in orodispersible tablets and its formulations (Draksiene et al., 2019). The P. ovata husk polysaccharide is inexpensive and nontoxic and has fewer side effects, good stability, patient compliance; it is also highly bioavailable, and manufacture-friendly. Thus, P. ovata could be used as a natural super-disintegrant (Pawar and Varkhade, 2014).
Congestive Heart Failure
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Brooks Willar, E. Wilson Grandin
Providers need to consider a few important clinical factors when initiating inpatient ARNI therapy. A 36-hour washout period from ACEi is needed prior to starting ARNI due to the significant risk of angioedema with concomitant ACE and neprilysin inhibition, both of which can potentiate bradykinin levels. For patients admitted with decompensated heart failure, particularly those who require the ICU for low cardiac output, this 36-hour washout without any ACEi/ARB/ARNI therapy should be avoided as withdrawal of that afterload reduction can be highly detrimental in these vulnerable patients. A sensible approach for patients with marginal blood pressure is starting a low-dose ARB, which, if tolerated, can be transitioned to low-dose sacubitril-valsartan (24–26 mg). The ionic form of valsartan found in sacubitril-valsartan is 40% more bioavailable than the salt used in stand-alone valsartan, so 26 mg of valsartan in sacubitril-valsartan is roughly equivalent to 40 mg of traditional valsartan [9]. For patients with marginal blood pressure, we suggest initiating valsartan at 20 mg twice daily and uptitrating to 40 mg twice daily before transitioning to low-dose sacubitril-valsartan. When titrating ARNI therapy in patients with marginal blood pressure, allow 48–72 hours at a stable dose before considering an increase to the next dosing level.
Essential Oils as Carrier Oils
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Romana Aichinger, Gerhard Buchbauer
Anethol, menthone, and eugenol are oxygen-containing terpenes that act as penetration enhancers for valsartan, a lipophilic specific angiotensin 2 receptor blocker used for treating hypertension. Valsartan should be delivered through human skin due to its low oral bioavailability, its low melting point, and its molecular weight. For the terpenes, 1% (w/v) concentration is the optimum to increase the flux by interacting with the SC lipids, whereas anethol, the most lipophilic enhancer, causes the maximum lipid extraction and thereby improves the drug enhancement rate 4.4 times, followed by menthone. It is always important that penetration enhancers and drugs conform with each other in polarity; thus eugenol, the least lipophilic enhancer, leads to the lowest permeation rate of the highly lipophilic valsartan. Anethol and eugenol promote the drug penetration by keratin denaturation and lipid extraction while menthone only works with lipid extraction. Overall, it is supposed that the following terpenes are preferred over the other ones, because of the better enhancement effects they provoke; namely, liquid terpenes and terpenes with higher Log P values due to the better mixture properties from lipophilic terpenes with SC intercellular lipids (Ahad et al., 2016).
Current and emerging pharmacotherapy for the management of hypertrophic cardiomyopathy
Published in Expert Opinion on Pharmacotherapy, 2023
Akiva Rosenzveig, Neil Garg, Shiavax J. Rao, Amreen K. Kanwal, Arjun Kanwal, Wilbert S. Aronow, Matthew W. Martinez
Angiotensin II receptor blockers (ARBs) have been suggested to be beneficial in the cases of left ventricular hypertrophy and fibrosis related to HCM, leading to a protective effect in these patient populations [72]. Mechanistically, these drugs function by selective inhibition of angiotensin II, allowing for blood pressure lowering effects by antagonism of angiotensin II vasoconstriction, mineralocorticoid, catecholamine, ADH release, and hypertrophic remodeling response [72]. Several trials have demonstrated a decrease in morbidity and mortality with the use of ARBs in patients with heart failure [72]. The inhibition of the renin angiotensin system in hypertrophic cardiomyopathy and its effect on hypertrophy (INHERIT) trial evaluated the effect of 100-mg Losartan on the regression of LV hypertrophy [73]. This randomized placebo controlled double-blind trial enrolled 133 patients and found that Losartan treatment is considerably safe in HCM patients, however the drug does not significantly affect remodeling—compared to placebo [73]. Another clinical trial, the valsartan for attenuating disease evolution in early sarcomeric hypertrophic cardiomyopathy (VANISH), enrolled 178 participants in a double-blinded, randomized placebo-controlled manner [74]. The VANISH trial utilized a younger, more diverse cohort, and ultimately concluded that treatment with Valsartan in HCM improved the outcome when compared to the placebo group in metrics, such as cardiac function, structure, and remodeling. Valsartan was also proven to be safe in patients with early-stage HCM with no recorded increase in adverse outcomes [74].
Investigating the root cause of N-nitrosodimethylamine formation in metformin pharmaceutical products
Published in Expert Opinion on Drug Safety, 2021
Nasr Eldin Hussein Nasr, Metwaly Gamel Metwaly, Eman Osama Ahmed, Ahmed Roshdy Fares, Aliaa Nabil ElMeshad
In 2019, Food and Drug Administration (FDA) raised the flag that NDMA is formed as a contaminant in the active pharmaceutical ingredient (API) of valsartan (angiotensin II receptor blockers) and extended to include other members irbesartan and losartan [11]. The NDMA daily dose was assessed by the FDA in different valsartan products and ranged from 330 to 20,190 ng/tablet [12]. The EU authorities were notified on June 2018 that an API manufacturer (Zhejiang Huahai Pharmaceutical, China) has detected the presence of a previously undetected process impurity, NDMA, in the valsartan API manufactured at its site in Chuannan. NDMA is formed at the tetrazole ring-forming step in Zhejiang Huahai valsartan manufacturing process [13]. As a result, 22 countries issued recalls for approximately 2300 valsartan batches [14].
Cardiovascular outcomes at recommended blood pressure targets in middle-aged and elderly patients with type 2 diabetes mellitus and hypertension
Published in Blood Pressure, 2021
Eirik Olsen, Björn Holzhauer, Stevo Julius, Sverre E. Kjeldsen, Anne Cecilie K. Larstorp, Giuseppe Mancia, Maria H. Mehlum, Rune Mo, Morten Rostrup, Camilla L. Søraas, Dion Zappe, Michael A. Weber
Both treated and untreated hypertensive patients were considered for inclusion into the trial. Untreated patients were recruited if their systolic BP was between 160 and 210 mmHg and diastolic BP was <115 mmHg. Treated patients were recruited if their systolic BP was <210 mmHg or diastolic BP <115 mmHg. The recruited patients were rolled-over into one or the other arm of the trial without a run-in phase. For valsartan treatment started with 80 mg daily and for amlodipine with 5 mg daily. The dose of either drug was doubled and hydrochlorothiazide (12.5 mg and 25 mg daily) and other antihypertensive drugs were added in sequential steps if BP was not reduced <140/90 mmHg. Angiotensin receptor blockers were excluded from the treatment algorithms and ACE inhibitors and calcium channel blockers only allowed if required for conditions other than hypertension. Patients were followed-up for 4–6 years with visits performed monthly during the initial 6 months of treatment and at 6 months intervals thereafter. Blood pressure was measured three times during each visit, with the patient in the sitting position, after 5 min rest and 24 h post-dose. Blood pressure was measured using a calibrated standard sphygmomanometer or a validated digital device, and mean BP was calculated as the mean of all three readings.