Trends and Pattern of the Utilization of Cardiovascular Medicines in Lithuania in 2003–2012
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Supplementary Appendix 1. Search Strategy for the Systematic Review and Meta-Analysis
BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) Thorax Supplementary Appendix 1. Search strategy for the systematic review and meta-analysis # COVID-19 AND (ACEI or ARB) Pubmed #1. COVID-19 ((((novel[Title/Abstract]) AND (((corona[Title/Abstract]) AND virus[Title/Abstract]) OR (coronavirus[Title/Abstract]))) OR ((COVID[Title/Abstract]) OR (COVID-19[Title/Abstract]) OR (nCoV[Title/Abstract]) OR (2019-nCoV[Title/Abstract]) OR (Novel Coronavirus Pneumon.ia[Title/Abstract]) OR (NCP[Title/Abstract]) OR (severe acute respiratory infection[Title/Abstract]) OR (SARI[Title/Abstract]) OR (SARS-CoV-2[Title/Abstract]))) #2. ARB (("Angiotensin Receptor Antagonists"[Mesh]) OR (((angiotensin receptor blocker[Title/Abstract]) OR angiotensin receptor blockers[Title/Abstract]) OR ARB.*[Title/Abstract]) OR (((angiotensin[Title/Abstract]) AND receptor[Title/Abstract]) AND (antagonist.*[Title/Abstract] OR inhibitor.*[Title/Abstract] OR blocker.*[Title/Abstract]))) OR (ARB[Title/Abstract]) OR (olmesartan[Title/Abstract]) OR (valsartan[Title/Abstract]) OR (eprosartan[Title/Abstract]) OR (irbesartan[Title/Abstract]) OR (candesartan[Title/Abstract]) OR (losartan[Title/Abstract]) OR (telmisartan[Title/Abstract]) OR (azilsartan[Title/Abstract]) OR (tasosartan[Title/Abstract]) OR (embusartan[Title/Abstract]) OR (forasartan[Title/Abstract]) OR (milfasartan[Title/Abstract]) OR (saprisartan[Title/Abstract]) OR (zolasartan[Title/Abstract]) -
Inline-Supplementary-Material-1.Pdf
Appendix 1: STOPP/START criteria version 2 applied to the TRUST dataset Physiological system Criteria Criteria included Number (%) (The relevant () criteria for each participant were applied to the dataset and recorded in of Microsoft Office Excel ® (2013)) criteria included out of total criteria STOPP criteria Indication of medication A1. Any drug prescribed without an evidence-based clinical indication. X 1/3 (33.3) A2. Any drug prescribed beyond the recommended duration, where treatment duration is X well defined. A3. Any duplicate drug class prescription e.g. two concurrent NSAIDs, SSRIs, loop diuretics, ACE inhibitors, anticoagulants (optimisation of monotherapy within a single drug class should be observed prior to considering a new agent). Cardiovascular system B1. Digoxin for heart failure with preserved systolic ventricular function (no clear evidence X 7/13 (53.8) of benefit). B2. Verapamil or diltiazem with NYHA Class III or IV heart failure (may worsen heart failure). B3. Beta-blocker in combination with verapamil or diltiazem (risk of heart block). B4. Beta blocker with symptomatic bradycardia (< 50/min), type II heart block or complete heart block (risk of profound hypotension, asystole). B5. Amiodarone as first-line antiarrhythmic therapy in supraventricular tachyarrhythmias X (higher risk of side-effects than beta-blockers, digoxin, verapamil or diltiazem). B6. Loop diuretic as first-line treatment for hypertension (safer, more effective alternatives available). B7. Loop diuretic for dependent ankle oedema without clinical, biochemical evidence or radiological evidence of heart failure, liver failure, nephrotic syndrome or renal failure (leg elevation and /or compression hosiery usually more appropriate). B8. Thiazide diuretic with current significant hypokalaemia (i.e. -
Imidazoline Antihypertensive Drugs: Selective I1-Imidazoline Receptors Activation K
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by FarFar - Repository of the Faculty of Pharmacy, University of Belgrade REVIEW Imidazoline Antihypertensive Drugs: Selective I1-Imidazoline Receptors Activation K. Nikolic & D. Agbaba Faculty of Pharmacy, Institute of Pharmaceutical Chemistry, University of Belgrade, Vojvode Stepe, Belgrade, Serbia Keywords SUMMARY α2-Adrenergic receptors; Centrally acting antihypertensives; Clonidine; Hypertension; Involvement of imidazoline receptors (IR) in the regulation of vasomotor tone as well as in Imidazoline receptors; Rilmenidine. the mechanism of action of some centrally acting antihypertensives has received tremen- dous attention. To date, pharmacological studies have allowed the characterization of three Correspondence main imidazoline receptor classes, the I1-imidazoline receptor which is involved in central K. Nikolic, Faculty of Pharmacy, Institute of inhibition of sympathetic tone to lower blood pressure, the I2-imidazoline receptor which Pharmaceutical Chemistry, University of is an allosteric binding site of monoamine oxidase B (MAO-B), and the I3-imidazoline re- Belgrade, Vojvode Stepe 450, 11000 Belgrade, ceptor which regulates insulin secretion from pancreatic β-cells. All three imidazoline re- Serbia. ceptors represent important targets for cardiovascular research. The hypotensive effect of + Tel: 381-63-84-30-677; clonidine-like centrally acting antihypertensives was attributed both to α2-adrenergic re- + Fax: 381-11-3974-349; ceptors and nonadrenergic I1-imidazoline receptors, whereas their sedative action involves E-mail: [email protected] activation of only α2-adrenergic receptors located in the locus coeruleus. Since more selec- tive I1-imidazoline receptors ligands reduced incidence of typical side effects of other cen- trally acting antihypertensives, there is significant interest in developing new agents with higher selectivity and affinity for I1-imidazoline receptors. -
Low Dose of Moxonidine Within the Rostral Ventrolateral Medulla Improves the Baroreflex Sensitivity Control of Sympathetic Activity in Hypertensive Rat
npg Acta Pharmacologica Sinica (2009) 30: 1594–1600 © 2009 CPS and SIMM All rights reserved 1671-4083/09 $32.00 www.nature.com/aps Original Article Low dose of moxonidine within the rostral ventrolateral medulla improves the baroreflex sensitivity control of sympathetic activity in hypertensive rat Jia-ling WANG1, 2, #, Long WANG3, #, Zhao-tang WU4, #, Wen-jun YUAN1, Ding-feng SU4, Xin NI1, Jian-jun YAN5,*, Wei-zhong WANG1,* Department of 1Physiology and 4Pharmacology, Second Military Medical University, Shanghai 200433, China; 2Department of Emergency, Changhai Hospital, Shanghai 200433, China; 3Shanghai Research Center for Biomodel Organism, Shanghai 200433, China; 5The First Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Shanghai 200433, China Aim: To determine the effects of the centrally antihypertensive drug moxonidine injected into the rostral ventrolateral medulla (RVLM) on baroreflex function in spontaneously hypertensive rats (SHR). Methods: Baroreflex sensitivity control of renal sympathetic nerve activity (RSNA) and barosensitivity of the RVLM presympathetic neu- rons were determined following application of different doses of moxonidine within the RVLM. Results: Three doses (0.05, 0.5, and 5 nmol in 50 nL) of moxonidine injected bilaterally into the RVLM dose-dependently reduced the baseline blood pressure (BP) and RSNA in SHR. At the highest dose (5 nmol) of moxonidine injection, the maximum gain (1.24%±0.04%/mmHg) of baroreflex control of RSNA was significantly decreased. However, the lower doses (0.05 and 0.5 nmol) of moxonidine injection into the RVLM significantly enhanced the baroreflex gain (2.34%±0.08% and 2.01%±0.07%/mmHg). The moxoni- dine-induced enhancement in baroreflex function was completely prevented by the imidazoline receptor antagonist efaroxan but not by the α2-adrenoceptor antagonist yohimbine. -
What to Do When You Find Your Patient Is Non-Adherent to Antihypertensive Therapy ?
What to do when you find your patient is non-adherent to antihypertensive therapy ? Indranil Dasgupta Consultant in nephrology and hypertension Heartlands Hospital Birmingham Honorary Reader, University of Birmingham Conflict of interest • Received – Research grants: Medtronic and Daiichi Sankyo – Speaker fees: Sanofi, MSD, Pfeizer, GSK, Mitshubishi pharma, Otsuka, Agenda • Case studies • Size of the problem • Cost to the NHS • Detection • Factors responsible • Measures to improve adherence • Further research Case study 1 Case study 1 • 57 year old lady, FH of hypertension, BMI 38 • Mean BP in clinic: 171/92 mmHg • Mean daytime ABP: 147/84 mmHg • Current medications: – Amlodipine 10 mg once daily – Bisoprolol 2.5 mg once daily – Doxazosin MR 8 mg once daily – Furosemide 40 mg once daily – Indapamide 2.5 mg once daily – Losartan 100 mg once daily • Urine sent for antihypertenive drug assay Urine antihypertensive drug assay • She was advised to take amlodipine 5mg only and given life style advice especially to lose weight Case study 2 • 55 year old lady, teacher – Deputy Head of English • Recent clinic BP 175/104, 177/75, 222/114 • Known white coat effect, BMI 41 • Medication: – Losartan 100 mg once daily – Felodipine 20 mg once daily – Doxazosin 8 mg twice daily – Furosemide 60 mg once daily – Bisoprolol 7.5 mg once daily • Urine AHT assay requested She wouldn’t accept the result but since then her BP control has improved! Case study 3 • 41 year old man, engineer Rolls Royce • Referred a year ago for drop in GFR 64 to 23 • Losartan 150mg, -
"Coaprovel, INN-Irbesartan+Hydrochlorothiazide"
ANNEX I SUMMARY OF PRODUCT CHARACTERISTICS 1 1. NAME OF THE MEDICINAL PRODUCT CoAprovel 150 mg/12.5 mg tablets. 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each tablet contains 150 mg of irbesartan and 12.5 mg of hydrochlorothiazide. Excipient with known effect: Each tablet contains 26.65 mg of lactose (as lactose monohydrate). For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM Tablet. Peach, biconvex, oval-shaped, with a heart debossed on one side and the number 2775 engraved on the other side. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Treatment of essential hypertension. This fixed dose combination is indicated in adult patients whose blood pressure is not adequately controlled on irbesartan or hydrochlorothiazide alone (see section 5.1). 4.2 Posology and method of administration Posology CoAprovel can be taken once daily, with or without food. Dose titration with the individual components (i.e. irbesartan and hydrochlorothiazide) may be recommended. When clinically appropriate direct change from monotherapy to the fixed combinations may be considered: . CoAprovel 150 mg/12.5 mg may be administered in patients whose blood pressure is not adequately controlled with hydrochlorothiazide or irbesartan 150 mg alone; . CoAprovel 300 mg/12.5 mg may be administered in patients insufficiently controlled by irbesartan 300 mg or by CoAprovel 150 mg/12.5 mg. CoAprovel 300 mg/25 mg may be administered in patients insufficiently controlled by CoAprovel 300 mg/12.5 mg. Doses higher than 300 mg irbesartan/25 mg hydrochlorothiazide once daily are not recommended. When necessary, CoAprovel may be administered with another antihypertensive medicinal product (see sections 4.3, 4.4, 4.5 and 5.1). -
Hypertension and Cardiac Arrhythmias: a Review of the Epidemiology, Pathophysiology and Clinical Implications
Journal of Human Hypertension (2008) 22, 380–388 & 2008 Nature Publishing Group All rights reserved 0950-9240/08 $30.00 www.nature.com/jhh REVIEW Hypertension and cardiac arrhythmias: a review of the epidemiology, pathophysiology and clinical implications K-H Yiu and H-F Tse Division of Cardiology, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China Hypertension is commonly associated with cardiac cular ectopy and sudden cardiac death. Recent arrhythmias in patients with and without concomitant prospective clinical trials reveal that antihyper- cardiovascular disease. Experimental and epidemiolo- tensive therapy may delay or prevent the occurrence gical studies have demonstrated potential links of cardiac arrhythmias and sudden cardiac death in between hypertension and atrial and ventricular arrhyth- patients with hypertension. Although antihypertensive mias, although the underlying pathophysiological me- agents that block the renin–angiotensin–aldosterone chanism remains unclear. Nonetheless, the importance system appear to protect against cardiac arrhythmias, of hypertension as a cause of atrial and ventricular this needs to be confirmed by current ongoing clinical arrhythmias is not well recognized. In particular, trials. the occurrence of left ventricular hypertrophy is a Journal of Human Hypertension (2008) 22, 380–388; strong predictor for the development of AF, ventri- doi:10.1038/jhh.2008.10; published online 13 March 2008 Keywords: atrial fibrillation; arrhythmia; sudden cardiac death Introduction Epidemiology Concomitant cardiac arrhythmias are commonly Atrial fibrillation seen in patients with hypertension, although the Atrial fibrillation is the most common sustained mechanism of this association is unclear. The arrhythmia in adults and is associated with an contribution of hypertension to the development of increased risk for cardiovascular morbidity, mortality atrial and ventricular arrhythmias is unrecognized and stroke.1,2 The incidence of AF increases with age; and thus undertreated. -
Monteplase/Nadolol 1345 Moxisylyte Is Given As the Hydrochloride but the Dose May Be Tion Half-Life Is 2 to 3 Hours and Is Prolonged in Renal Pharmacopoeias
Monteplase/Nadolol 1345 Moxisylyte is given as the hydrochloride but the dose may be tion half-life is 2 to 3 hours and is prolonged in renal Pharmacopoeias. In Eur. (see p.vii), Jpn, and US. expressed in terms of the base. Moxisylyte hydrochloride impairment. Moxonidine is about 7% bound to plasma Ph. Eur. 6.2 (Nadolol). A white or almost white crystalline 45.2 mg is equivalent to about 40 mg of moxisylyte. proteins. It is distributed into breast milk. powder. Slightly soluble in water; freely soluble in alcohol; prac- In the management of peripheral vascular disease, the usual tically insoluble in acetone. oral dose is the equivalent of 40 mg of moxisylyte four times dai- USP 31 (Nadolol). A white or off-white, practically odourless, ly increased if necessary to 80 mg four times daily. It should be Uses and Administration crystalline powder. Soluble in water at pH 2; slightly soluble in withdrawn if there is no response in 2 weeks. Moxonidine is a centrally acting antihypertensive water at pH 7 to 10; freely soluble in alcohol and in methyl alco- Moxisylyte has been used locally in the eye to reverse the my- structurally related to clonidine (p.1247). It appears to hol; insoluble in acetone, in ether, in petroleum spirit, in trichlo- driasis caused by phenylephrine and other sympathomimetics. It act through stimulation of central imidazoline recep- roethane, and in benzene; slightly soluble in chloroform, in dichloromethane, and in isopropyl alcohol. has also been used orally in benign prostatic hyperplasia, al- tors to reduce sympathetic tone, and also has alpha - though such use has been associated with hepatotoxicity; the 2 doses used in prostatic hyperplasia were generally higher than adrenoceptor agonist activity. -
“Captopril” [Mesh
BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) Open Heart PubMed: 1. (“dose comparison” OR “dose” OR “low dose” OR “high dose” OR “dosage*”) 2. (“captopril” [mesh] OR “Benazepril” OR “Enalapril” [mesh] OR “Enalapril” OR “Cilazapril” [mesh] OR “Cilazapril” OR “Delapril” OR “Imidapril” OR “Lisinopril” [mesh] OR “Lisinopril” OR “Moexipril” OR “Perindopril” [mesh] OR “Perindopril” OR “Quinapril” OR “Ramipril” [mesh] “Ramipril” OR “Spirapril” OR “Temocapril” OR “Trandolapril” OR “Zofenopril” OR “Enalaprilat” [mesh] OR “Enalaprilat” OR “Fosinopril” [mesh] OR “Fosinopril” OR “Teprotide” [mesh] OR “Teprotide” OR “Angiotensin-Converting Enzyme Inhibitors” [mesh] OR “Angiotensin-Converting Enzyme Inhibitors” OR “Angiotensin Converting Enzyme Inhibitors” OR “Inhibitors, Kininase II” OR “Kininase II Antagonists” OR “Kininase II Inhibitors” OR “Angiotensin I-Converting Enzyme Inhibitors” OR “Angiotensin I Converting Enzyme Inhibitors” OR “Antagonists, Angiotensin- Converting Enzyme” OR “Antagonists, Angiotensin Converting Enzyme” OR “Antagonists, Kininase II” OR “Inhibitors, ACE” OR “ACE Inhibitors” OR “Inhibitors, Angiotensin-Converting Enzyme” OR “Enzyme Inhibitors, Angiotensin-Converting” OR “Inhibitors, Angiotensin Converting Enzyme” OR “Angiotensin-Converting Enzyme Antagonists” OR “Angiotensin Converting Enzyme Antagonists” OR “Enzyme Antagonists, Angiotensin-Converting”) 3. (“Heart failure” [mesh] OR “heart failure” OR “Cardiac Failure” OR “Heart Decompensation” OR “Decompensation, Heart” OR “Heart Failure, Right-Sided” OR “Heart Failure, Right Sided” OR “Right-Sided Heart Failure” OR “Right Sided Heart Failure” OR “Myocardial Failure” OR “Congestive Heart Failure” OR “Heart Failure, Congestive” OR “Heart Failure, Left-Sided” OR “Heart Failure, Left Sided” OR “Left-Sided Heart Failure” OR “Left Sided Heart Failure” OR “chronic heart failure” OR "chronic heart" OR (CHF)) 4. -
Update on Rilmenidine: Clinical Benefits
AJH 2001; 14:322S–324S Update on Rilmenidine: Clinical Benefits John L. Reid Rilmenidine is an imidazoline derivative that appears to consistent with a reduction in long-term cardiovascular lower blood pressure (BP) by an interaction with imida- risk, as would recently described actions on the heart zoline (I1) receptors in the brainstem (and kidneys). Ril- (reducing left ventricular hypertrophy) and the kidney menidine is as effective in monotherapy as all other first- (reducing microalbuminuria). Although no data are yet Downloaded from https://academic.oup.com/ajh/article/14/S7/322S/137317 by guest on 28 September 2021 line classes of drugs, including diuretics, -blockers, available from prospective long-term outcome studies, angiotensin converting enzyme (ACE) inhibitors, and cal- rilmenidine could represent an important new develop- cium antagonists. It is well tolerated and can be taken in ment in antihypertensive therapy and the prevention of combination for greater efficacy. Sedation and dry mouth cardiovascular disease. Am J Hypertens 2001;14:322S–324S are not prominent side effects and withdrawal hyperten- © 2001 American Journal of Hypertension, Ltd. sion is not seen when treatment is stopped abruptly. Recently, in addition to a reduction in BP, this agent Key Words: Blood pressure, rilmenidine, imidazoline, insu- has been shown to improve glucose tolerance, lipid risk lin resistance, metabolic syndrome, microalbuminuria, ventricu- factors, and insulin sensitivity. These changes would be lar hypertrophy, end-organ damage. n spite of major developments during the past 50 included in the treatment choice of several key outcome years, there is still no single ideal antihypertensive trials (Veterans Administration [VA] trials and European I drug. -
The Effect of Moxonidine on Plasma Lipid Profile and on LDL Subclass
Journal of Human Hypertension (1999) 13, 781–785 1999 Stockton Press. All rights reserved 0950-9240/99 $15.00 http://www.stockton-press.co.uk/jhh ORIGINAL ARTICLE The effect of moxonidine on plasma lipid profile and on LDL subclass distribution MS Elisaf, C Petris, E Bairaktari, S-A Karabina, C Tzallas, A Tselepis and KC Siamopoulos Department of Internal Medicine, University of Ioannina Medical School, Greece Moxonidine is a new antihypertensive agent whose cant decrease in both systolic and diastolic blood ,mechanism of action appears to involve specific stimu- pressure (from 147 ؎ 10 to 131 ؎ 11 mm Hg, P Ͻ 0.001 ,lation of imidazoline receptors resulting in an inhibition and from 98 ؎ 4.5 to 86 ؎ 5 mm Hg, P Ͻ 0.001 of the activity of the central and peripheral sympathetic respectively). No significant change in plasma lipid pro- nervous system. The drug seems to behave neutrally file was observed after moxonidine administration. with respect to plasma lipid parameters. However, there Additionally, no change in the susceptibility of LDL sub- are no data on the effects of moxonidine on the low- classes to copper-induced oxidative modification was density lipoprotein (LDL) subclass pattern or on the LDL noticed. Finally, drug therapy was not followed by any oxidation susceptibility, both of which are known to play change in either LDL phenotype or in mass and compo- a prominent role in the pathogenesis of atherosclerosis. sition of the three LDL subfractions. We conclude, that Thus, we undertook the present study to examine the unlike other antihypertensive drugs, such as beta-block- influence of moxonidine on the LDL subspecies profile ers which may predispose to expression of a relatively and their susceptibility to copper-induced oxidative atherogenic lipoprotein subclass pattern, moxonidine modification in 20 hypertensive patients (11 men, 9 does not affect either plasma lipid parameters or lipo- women) aged 38–61 years. -
Interaction of the Sympathetic Nervous System with Other Pressor Systems in Antihypertensive Therapy
Journal of Clinical and Basic Cardiology An Independent International Scientific Journal Journal of Clinical and Basic Cardiology 2001; 4 (3), 185-192 Interaction of the Sympathetic Nervous System with other Pressor Systems in Antihypertensive Therapy Wenzel RR, Baumgart D, Bruck H, Erbel R, Heemann U Mitchell A, Philipp Th, Schaefers RF Homepage: www.kup.at/jcbc Online Data Base Search for Authors and Keywords Indexed in Chemical Abstracts EMBASE/Excerpta Medica Krause & Pachernegg GmbH · VERLAG für MEDIZIN und WIRTSCHAFT · A-3003 Gablitz/Austria FOCUS ON SYMPATHETIC TONE Interaction of SNS J Clin Basic Cardiol 2001; 4: 185 Interaction of the Sympathetic Nervous System with Other Pressor Systems in Antihypertensive Therapy R. R. Wenzel1, H. Bruck1, A. Mitchell1, R. F. Schaefers1, D. Baumgart2, R. Erbel2, U. Heemann1, Th. Philipp1 Regulation of blood pressure homeostasis and cardiac function is importantly regulated by the sympathetic nervous system (SNS) and other pressor systems including the renin-angiotensin system (RAS) and the vascular endothelium. Increases in SNS activity increase mortality in patients with hypertension, coronary artery disease and congestive heart failure. This review summarizes some of the interactions between the main pressor systems, ie, the SNS, the RAS and the vascular endothelium including the endothelin-system. Different classes of cardiovascular drugs interfere differently with the SNS and the other pressor systems. Beta-blockers, ACE-inhibitors and diuretics have no major effect on central SNS activity. Pure vasodilators including nitrates, alpha-blockers and DHP-calcium channel blockers increase SNS activity. In contrast, central sympatholytic drugs including moxonidine re- duce SNS activity. The effects of angiotensin-II receptor antagonist on SNS activity in humans are not clear, experimental data are discussed in this review.