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The evidence for a systolic BP target of 130 mm Hg is less strong and includes 2 prospective cohort studies 27, 28 ; and the normotensive Appropriate Blood Pressure Control in Diabetes ABCD ; trial 32 ; . In the cohort studies, direct relationships were observed between higher systolic BP levels and death, coronary artery disease, nephropathy and proliferative retinopathy 27, 28 ; . Although this relationship extended to systolic BP as low as 110 mm Hg, the Canadian Diabetes Association Clinical Practice Guidelines Expert Committee did not judge the evidence to be sufficient to recommend a systolic BP target lower than 130 mm Hg. Results of the normotensive ABCD trial also support the systolic BP target of 130 mm Hg 32 ; , but, again, not to a level that justified a Grade A recommendation. Stronger evidence for the optimal systolic BP target awaits completion of the Action to Control Cardiovascular Risk in Diabetes ACCORD ; trial in which thousands of people with diabetes are being randomized to systolic BP targets of 120 mm Hg or 140 mm Hg. Treatment of hypertension If BP cannot be controlled with lifestyle intervention in people with diabetes without nephropathy, any 1 of the following drugs is recommended as the initial choice of therapy, in the following order: ACE inhibitor, ARB, cardioselective beta blocker or thiazide-like diuretic. This recommendation reflects the results of studies that have compared, as a prespecified primary goal, clinically important vascular outcomes in people with diabetes who were randomized to either a drug from the studied class or to placebo 33, 34 ; , or to an active comparator control group 35-37 ; . Because the efficacy of long-acting calcium channel blockers CCBs ; has not been proven in similarly designed trials, but was demonstrated in post-hoc analyses of randomized trials 38 ; , CCBs remain an attractive option for patients unable to use drugs from any of the 4 aforementioned classes. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial ALLHAT ; , 12 000 people with diabetes were randomized to treatment with a CCB, ACE inhibitor, thiazide-like diuretic or alpha-adrenergic blocker 36, 37 ; , and CV outcomes were compared over 5 years. Early termination of the alpha-adrenergic blocker arm occurred because of excess heart failure relative to the diuretic arm 37 ; . This is the reason to avoid alpha-adrenergic blockers, at least as first-line therapy, for the treatment of hypertension. More recently, the primary ALLHAT results were reported 36 ; . No differences were observed in people with diabetes among the 3 remaining drug classes with respect to the primary outcome fatal coronary heart disease or nonfatal myocardial infarction [MI] ; , but a lower rate of prespecified secondary vascular outcomes, including heart failure, occurred among those randomized to the thiazide-like diuretic. Although glycemic control was also worse in this group relative to the ACE inhibitor and CCB groups 36 ; , the lack of differences in the primary outcome, the lower. New insights into the pathogenesis and treatment of diabetic renal disease may emerge from recent advances in proteomics using high-throughput mass spectrometry MS ; of urine. Using a combination of online capillary electrophoresis CE ; and MS we evaluated urinary polypeptide patterns UPP ; in 4 groups of type 2 diabetic patients matched for age, gender and diabetes duration including; 20 normoalbuminuric patients with and 20 without diabetic retinopathy DR ; , 20 microalbuminuric patients with DR and 18 macroalbuminuric patients with DR. Furthermore, changes in UPP during treatment with the angiotensin II receptor blocker candesartan were evaluated in the macroalbuminuric patients in a randomized double-blind, cross-over trial where each patient received treatment with placebo, candesartan 8, 16 and 32 mg daily each for two months. Overall 4551 different polypeptides were found in the samples. UPPs were comparable in normo- with and without DR ; and microalbuminuric patients whereas distinct differences were found in macroalbuminuric patients. Differences in UPP between normo- and macroalbuminuric patients permitted the establishment of a diabetic renal damage DRD ; pattern consisting of 113 polypeptides. Eleven of these polypeptides had been sequenced and identified. Candesartan treatment in macroalbuminuric patients significantly changed 15 of the 113 polypeptides in the DRD pattern towards levels in normoalbuminuric patients. Change in the DRD pattern was not candesartan dosedependent but individual changes correlated with changes in urinary albumin excretion at each dose level. Additional studies to evaluate the predictive value of these polypeptides utilizing samples from longitudinal studies are underway and will be presented as well. CE-MS serves as a fast and sensitive tool for identification of biomarkers. Urinary polypeptide patterns specific for macroalbuminuric type 2 diabetic patients may be used to explore and monitor renoprotective effects of angiotensin II receptor blockade as well as other therapeutic strategies!

1 the only relevant fact is that society that is, drug regulatory authorities ; accepts the increased risk of a xenobiotic that does not treat or prevent a fatal disease. Part A Hospital inpatient deductible for days 1-60 Coinsurance for days 61-90 Coverage for all Medicare-Eligible charges after lifetime reserve days have been used 365 days is maximum lifetime benefit ; First three pints of blood each year unless already paid for under Part B ; Post Hospitalization - Skilled nursing facility coinsurance for days 21-100 Part B Part B Medical deductible per calendar year ; Part B generally 20% coinsurance First three pints of blood each year unless already paid for under Part A and 20% of Medicare-Approved charges for additional units on an outpatient basis 100% fo Medicare Part B excess charges up to maximum limits set by Medicare or state law Foreign Travel Benefit - Medically necessary emergency care beginning during the first 60 days of each trip outside the United States is subject to a 0 calendar year deductible. The benefit pays 80% of billed charges for Medicare eligible expenses , 000 is lifetime maximum benefit ; At Home Recovery Services A NO YES C YES YES D YES YES F YES YES. What happened in the past is a good indicator of what can and likely will ; happen in the future if you take more ototoxic drugs.

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Led to progressive decreases in mean arterial pressure MAP ; over the course of 70 min 123 2 to 96 and 122 3 to 100 8 mmHg; P 0.05, respectively ; . Administration of candesartan at a dose of 0.01 mg kg did not reduce arterial pressure significantly in comparison with rats treated with the saline vehicle alone 117 7 to 114 9 and 112 5 to 111 5 mmHg, respectively ; . Effects of candesartan on arterial pressure responses to bolus doses of ANG II. As shown in Fig. 2, the control responses in arterial pressure to bolus doses of ANG II at doses of 10, 50, 100, and 1, 000 ng were 26 6, 54 and 79 7 mmHg. Candesartan treatment at 10.1 mg kg completely blocked the pressor responses to ANG II up to 1, 000 ng, although there were slight, but not significant, increases in arterial pressure 6 2 mmHg ; in the rats treated with 0.1 mg kg candesartan. After treatment with the highest candesartan dose, the ANG II bolus dose 1, 000 ng ; actually decreased arterial pressure 5 2 mmHg ; , suggesting a slight vasodilatory effect. This vasodilatory effect of ANG II was prevented by treatment with the AT2 receptor blocker PD-123319 ; . Candesartan treatment at 0.01 mg kg markedly attenuated but did not completely block the arterial pressure responses to bolus doses of ANG II to 9 3, and 23 6 mmHg. Effects of candesartan on CRBF responses to bolus of ANG II. As shown in Fig. 3, the control decreases in CRBF to ANG II doses of 10, 50, 100, and 1, 000 ng averaged 47 9, 68 and 82 6%, respectively. The CRBF responses were completely blocked by candesartan at doses of 1 and 0.1 mg kg. Candesartan at a dose of 0.01 mg kg markedly attenuated but did not abolish the decreases in CRBF to ANG.

Drugs 1 ; Diuretics - improve failure as volume overload. However they further GFR and so AT-II, exacerbating the CCF. Thiazides are commonly used in early stages of treatment, or if inadequate use frusamide. They are excellent at reducing symptoms, improving exercise tolerance and quality of life. There is no data as to their effect on prognosis as unethical to give placebo, but probably don't reduce mortality. 2 ; ACE-I - first-line treatment of choice for symptomatic CCF or asymptomatic LVF. ACE-I work in multiple ways, but 2 main ones are inhibition of ACE, causing dec. AT-II prod. which reduces AT-II actions of vasoconstriction, aldosterone prod., vasopressin prod. and sympathetic drive ; , and inhib. kininaseII which breaks down bradykinin so increasing its vasodil., PG prod. and tPA prod. actions ; . Also have local effects on cardiac tissue. ACE-I thus dec. symptoms, decreases progression & dec. mortality ?by altering neuroendocrine levels or remodelling ; . The reduction in mortality is 40% for those in NYHA-IV disease CONSENSUS trial ; but 16% in less severe disease SOLVD trial ; . SAVE trial showed a 19% reduction in mortality in asymptomatic LV dysfcn. post-MI. HOPE trial showed 23% reduced risk of developing HF even if normal LV fcn., in those with risk factors for IHD, esp. DM so should consider long-term ACE-I in these pts. But care if renovascular disease as atherosclerosis in efferent bv affects autoreg. in kidney and this is worsened by vasodil. by ACE-I. Contraindicated if hear renal artery bruit ; . There is no evidence to suggest the use of 1 ACE-I over another, so based on pharmacokinetics. Captopril is required tds while ramipril and lisinopril can be given od, although 1 study has indicated that higher doses are better. AT-II inhib. may be used if cough precludes ACE-I use. These competitively block the AT1 subtype of AT-II recs, inhibiting the vasoconstrictive and proliferative action of ATII. ELITE-II trial compared losartan with captopril in patients with severe HF to show no difference in efficacy or mortality. New Val-HeFT trial showed AT-II valsartan ; and ACE-I work synergistically in severe HF. Can use losartan bd or valsartan or candesartan od. However unpublished data suggests there is a point of XS suppression, and that it is hazardous to give b-blocker, spironolactone, ACE-I AND AT-II inhibitor. 3 ; Spironolactone - competitive antag. of aldosterone rec. Aldosterone stimulates the retention of Na + & H2O causing oedema, excretion of K + & Mg2 + causing arrhythmias, and collagen deposition causing fibrosis of myocardium and vessels and serophene.

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The half-century old prescription drug law created new jobs at the same rabies vaccine that's used for cancer. Charbonnel B1, Massin P2 1 Hotel Dieu Hospital, Nantes, France, 2 Lariboisiere Hospital, Paris, France Objective: DIRECT consists of three randomised, double blind, placebo controlled, parallel group studies and is designed to determine the effects of blocking the AT1 receptor on retinopathy in normoalbuminuric patients with Type 1 DT1 ; and Type 2 DT2 ; diabetes. Methods: Standardised investigations at enrolment included BP measurement, HbA1c and serum lipids. Retinopathy was assessed yearly using seven-field stereo photographs according to ETDRS protocol, and graded centrally. At randomisation, treatment with 16 mg candesartan or matching placebo was initiated, and increased to 32 mg after one month. Results : 5 231 patients were randomised globally, 1 421 and 1 905 patients in studies in DT1 patients, respectively and 1 905 patients in the study in DT2. HbA1c showed mean values of 8.1 8.5 8.2 % for the 3 studies. In DT1 secondary prevention study 49% of the patients had level 20 in at least one eye, and 9 % had level 43 47. In DT2 patients, 17 % had level 43 47 and the remainder less severe retinopathy. Significant correlation with retinopathy levels at baseline was found with duration of diabetes p 0.0001 ; , HbA1c p 0.0001 ; , and SBP p 0.003 ; in both DT1 and DT2 patients. DBP was significantly correlated with retinopathy level in DT1 patients p 0.001 ; . Conclusion: As the prevalence of diabetes is increasing worldwide and is predicted to double within the next 20 years, this programme will generate information on our ability to prevent the occurrence of microalbuminuria and will also assess the ability of candesartan to prevent the onset or progression of diabetic retinopathy and clomiphene.

Table 2 Oral Antihypertensive Agents 24 ; Name ACE inhibitors Benazepril Captopril Enalapril Fosinopril Lisinopril Moexipril Peridopril Quinapril Ramipril Trandolapril ARBs Candesartan Eprosartan Irbesartan Losartan Telmisartan Valsartan Antiadrenergic Agents Clonidine Transdermal ; Doxazosin Guanabenz Guanfacine Methyldopa Prazosin Reserpine Terazosin -Blockers * Acebutolol Atenolol Betaxolol Bisoprolol Carteolol Carvediolol Labetalol Metoprolol extended release ; Nadolol Penbutol Pindolol Propanolol extended release ; Timolol Calcium Channel Blockers Dihydropyridines Amlodipine Felodipine Isradipine extended release ; Nicardipine extended release ; Nifedipine extended release ; Nisoldipine Trade Name s ; Lotesin Capoten Vasotec Monopril Zestril Prinivil Univasc Aceon Accupril Altace Mavik Atacand Teveten Avapro Cozaar Miscardis Diovan Catapres Catapres-TTS Cardura Wytensin Tenex Aldomet Minipress Serpasil Hytrin Sectral, Monitan 1 ; Tenormin 1 ; Kerlone 1 ; Zerbeta 1 ; Cartrol Coreg 1 2 ; Trandate, Normodyne 1 2 ; Lopressor, Betalov 1 ; Toprol XL 1 ; Corgard 1 2 ; Levatol 1 2 ; Visken 1 2 ; Inderal 1 2 ; Inderal LA 1 2 ; Blocadren 1 2 ; Norvasc Plendil, Renedil DynaCirc DynaCirc CR Cardene Cardene SR Procardia, Adalaf Procardia XL, Adalaf CC Sular Initial Dose mg ; 10 qd bid 25 bid tid 5 qd bid 10 qd 10 7.5 qd bid 4 qd 10 bid 2.5 qd bid 12 qd 16 600 qd 150 qd 50 qd 0.1 bid 1 qwk 0.1 mg ; 1 qhs rarely used 1 qhs 250 bid tid 1 bid tid 0.050.1 qd 1 qhs 200 bid 2550 qd 510 qd 2.55.0 qd 2.5 qd 6.25 bid 100 bid 2550 bid 50100 qd 2040 qd 20 qd bid 2040 bid 6080 qd 10 bid 2.55.0 qd 2.55 qd 2.5 bid 510 qd 20 tid 30 bid 10 tid 3060 qd 20 qd 000 d 40 d 0.25 d 20 d 1, 200 d 100 d 20 d 400 d 450 d 450 d 320 d 80 d 640 d 640 d 60 d 120 d 120 d 120 d 120 d 60 d Maximum Dose mg ; 80 d 450 d 40 d 800 d 300 d 100 d 80 d 320 d 2.4 d 2 qwk 0.3 mg ; 16 d. We found no differences in baseline haemodynamic values between the six groups of animals Table 1 ; . The administration of enalaprilat and candesartan induced a significant reduction of MAP at 70 min in groups ENA-CTRL, CANDCTRL, compared with the placebo group CTRL. This MAP reduction was similar in enalaprilat and candesartan treated animals. For animals in the haemorrhagic shock groups HS, ENAHS and CAND-HS withdrawal of 4.0 0.3 ; ml [mean, SEM ; ] blood resulted in a 50% reduction of CO. This haemorrhage volume amounts to 17.4% of the calculated total blood volume according to: 19 blood volume 7.46 ml per 100 g body weight. HR was minimally affected, MAP values showed a significant reduction by 4050 and clozaril.
90 DOES THE AVAILABILITY OF ADRENAL VEIN SAMPLING AFFECT THE DIAGNOSIS OF THE ADRENOCORTICAL PATHOLOGY UNDERLYING PRIMARY ALDOSTERONISM? RESULTS OF THE PAPY STUDY G.P. Rossi, G. Bernini, B. Fabris, C. Ferri, C. Ganzaroli, G. Giacchetti, C. Letizia, M. Maccario, F. Mallamaci, M. Mannelli, G. Palumbo, D. Rizzoni, E. Rossi, F. Mantero Padua, Italy ; 91 SELECTIVE ALDOSTERONE BLOCKER, EPLERENONE INCREASES CARDIAC ANGIOTENSIN 2 EXPRESSION IN SALT-SENSITIVE HYPERTENSION Y. Takeda, A. Zhu, T. Yoneda, M. Usukura, H. Takata, N. Oda, Y. Yamamoto Kanazawa, Japan ; 92 REDUCED mRNA AND PROTEIN CONTENT OF REGULATOR OF RHO GUANINE NUCLEOTIDE EXCHANGE FACTOR IN BARTTER'S AND GITELMAN'S SYNDROMES. RELEVANCE FOR THE PATHOPHYSIOLOGY OF HYPERTENSION L.A. Cal, E. Pagnin, M. Sartori, A.C. Pessina, A. Semplicini Padua, Italy ; 93 PREVALENCE OF PRIMARY ALDOSTERONISM AMONG HYPERTENSIVE PATIENTS P. Preti, A. Mugellini, A. Rinaldi, M. Destro, G. Marasi, L. Corradi, R. Fogari Pavia, Italy ; 94 ALDOSTERONE RENIN RATIO IS USEFUL TEST FOR PRIMARY ALDOSTERONISM J. Kos, A. Kovac * , I. Pecin, M. Baresic, T. Zeljkovic-Vrkic, M. Laganovic, D. Kuzmanic, B. Jelakovic Zagreb, * Slavonski Brod, Croatia ; 95 COMPARISON BETWEEN EARLY AND DELAYED SYSTEMIC TREATMENT WITH CANDESARTAN OF RATS AFTER ISCHEMIC STROKE S. Kaiser, F. Hagemann, J. Brdon, Y. Zhao, J. Culman, P. Gohlke Kiel, Germany ; 96 INHIBITION OF THE RENIN-ANGIOTENSIN SYSTEM DOES NOT REDUCE PLATELET ACTIVITY AT REST OR DURING STRESS IN ESSENTIAL HYPERTENSION J.H. Schwieler, N.H. Walln, T. Kahan, J. Nussberger * , P. Hjemdahl Stockholm, Sweden; * Lausanne, Switzerland ; 97 ATORVASTATIN INHIBITS ACE INDUCTION IN DIFFERENTIATING HUMAN MACROPHAGES F. Fyhruist, O. Saijonmaa Helsinki, Finland ; 98 REGULATION OF ANGIOTENSIN CONVERTING ENZYME BY NICOTINE IN HUMAN ENDOTHELIAL CELLS O. Saijonmaa, F. Fyhrquist Helsinki, Finland ; 99 RENIN-ANGIOTENSIN SYSTEM POLYMORPHISMS AND ANTIHYPERTENSIVE RESPONSE TO ITS BLOCKERS A. Mayor-Olea, A. Reyes-Engel, F.J. Aranda-Lara, M.J. Gaitan, G. Callejon, M. Ruiz, P. Aranda Malaga, Spain ; 100 HYPERKALEMIA AND BLOCKADE OF RENIN-ANGIOTENSIN SYSTEM IN CHRONICALLY HEMODIALYZED PATIENTS L. Zibar, J. Barbic, J. Milas-Ahic, M. Jakic, A. Galcic Osijek, Croatia ; 101 SIGNIFICANCE OF A LIPOPHILIC ANGIOTENSIN II RECEPTOR BLOCKER IN A PROTECTIVE EFFECT AGAINST VASCULAR REMODELING: COMPARISON OF TELMISARTAN VERSUS LOSARTAN S. Takai, D. Jin, M. Muramatsu, K. Yoshikawa, M. Miyazaki Takatsuki, Japan ; 102 PRELIMINARY FINDINGS ON URINARY PROSTASIN, A POSSIBLE MARKER OF ALDOSTERONE-DEPENDENT EPITHELIAL SODIUM CHANNEL RENAL ACTIVATION O. Olivieri, A. Castagna, G. Sabaini, L. Chiecchi, P. Guarini, P.G. Righetti Verona, Italy. Table 2. Familial Adenomatous PolyposisAssociated Gastrointestinal Tract and Extracolonic Manifestations and clozapine.
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Mortality in heart failure patients not receiving ACE inhibitors. J Coll Cardiol. 2002; 40: 1414-21. Pitt B, Poole-Wilson PA, Segal R. Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomized trial. The Losartan Heart Failure Survival Study ELITE II. Lancet. 2000; 355: 1582-7. Swedberg K, Pfeffer M, Granger C et al. Candesartan in heart failure: assessment of reduction in mortality and morbidity CHARM ; : rationale and design. J Card Fail. 1999; 5: 276-82. Foody JM, Farrell MH, Krumholz HM. Beta-blocker therapy in heart failure. JAMA. 2002; 287: 883-9. CIBIS-II Investigators and Committees. The Cardiac Insufficiency Bisoprolol Study II CIBIS-II ; . Lancet. 1999; 353: 9-13. CIBIS investigators and Committees. A randomized trial of beta-blockade in heart failure: the Cardiac Insufficiency Bisoprolol Study CIBIS ; . Circulation. 1994; 90: 1765-73.

We are experiencing a terrible crisis in the tort arena as pertains to medical malpractice issues. The Board needs to do all it can to ensure that our policyholders are well represented. We need to be doing all we can to provide the best coverage at the best rate. Many physicians are going to be put out of business by high premiums or the fact that they just can't get coverage." He would also like to help educate the Texas Medical Association about medical liability issues. "We would make the membership of the TMA, which brought TMLT into existence, understand the complexity of the problems the Trust has to deal with and represent." Robert I. Parks, MD The TMLT Board of Governors welcomes the experience of another newly elected member, Robert I. Parks, Jr, MD, an anesthesiologist from Dallas. Dr. Parks graduated from the University of Texas Southwestern Medical School at Dallas in 1972. He completed his internship at Baylor University Medical Center and Parkland Memorial Hospital in Dallas and his residency in anesthesiology, 1973-75, at Parkland Memorial Hospital. Dr. Parks served in the United States Air Force, 1975-77 in Biloxi, Mississippi at the USAF Medical Center Keesler. In 1977, he returned to Dallas to start private practice at Baylor University Medical Center where he continues practice today. Dr. Parks has been active in his specialty society, both at the state and national levels. He has served the Texas Society of Anesthesiologists as president, 1992-93. He has been an alternate delegate, 1984-91, delegate, 1991-present, and a member of the Board of Directors, 1999 to present, to the American Society of Anesthesiologists. Working with TMLT management on Trust issues is not a new experience for Dr. Parks, who has been a TMLT policyholder for 8 years. He has been a member of the TMLT claims review committee since 1998. He has also served as president of the medical staff at Baylor University Medical Center in 1999, and chairman of the medical board at Baylor University Medical Center, in 2000. He is currently serving as the physician representative to the Baylor Health Care System Board of Trustees, a sevenhospital system. Dr. Parks sits on the Board of Directors of the Baylor Heart and Vascular Hospital in Dallas. Dr. Parks' experience on the claims review committee prompted his interest in serving on the TMLT Board of Governors. "Interaction with board members at case review conference convinced me of the sincerity, character, integrity and resolve of these members to fairly represent Robert I. Parks, MD the physicians of Texas in their quest to lower TMLT premiums through risk management and tort reform." During his board term, Dr. Parks would like to focus on achieving medical liability reform and bringing risk management education to more physicians. "I would like to strengthen TMLT's relationship with the TMA to lead to tort reform that will pass the constitutionality test. I also hope to expand the successful risk management program by continuing the regional seminars, but also find new marketing methods to reach those physicians who thus far have not participated." Dr. Parks would also like to see a greater understanding develop between policyholders and board members. "I would like to accomplish more face-to-face explanations to policyholders why rates are exploding and why the Board must act in its fiduciary function of keeping TMLT a viable company." The TMLT Board of Governors will face difficult decisions for the Trust in 2002. The Board and TMLT management are working together closely and intelligently to steer the Trust through the stormy waters of a medical liability crisis that is driving up premiums to an unprecedented level, and that is forcing physicians to consider whether they can continue to practice medicine in Texas. If you are seeking ways to help solve the medical liability crisis, please contact your county medical society, the Texas Medical Association, or TMLT for information on how you can have an impact and combivir. This document will address issues related to 10 major DMARDs that are used in day-to-day clinical practice. Although cyclophosphamide is rarely used in the treatment of RA, this drug is not discussed, as it will be one of the major drugs.
P 0.009 ; , largely due to a 24% reduction in hospitalizations in valsartan group. There was also significant improvement in NYHA class, ejection fraction, signs, and symptoms of heart failure and quality of life. At the time of randomisation, 93% patients were taking beta-blockers. Patients receiving valsartan alone without addition of beta-blockers or ACE inhibitor ; faired better than when valsartan was added to ACE inhibitors and beta-blockers. The worst outcome was seen in patients receiving all the three. Valsartan was well tolerated. Addition of Valsartan to a patient already receiving ACE inhibitors and Beta-blockers was found to increase mortality, which is indeed a cause of concern as most patients with CHF are likely to be on them. However, Valsartan as monotherapy was beneficial and attenuation of the benefit was seen if ACEI or beta-blocker was added. CHARM Candesartan in Heart failure Assessment of Reduction in Mortality and Morbidity ; .38 This ongoing multicentric, randomized, placebo-controlled trial has enrolled 7572 patients with NYHA class II-IV heart failure, and includes patients with ejection fractions both greater and less than 40%. The less than 40% ejection fraction group is divided into ACE inhibitor combination ; -treated and ACE inhibitorintolerant groups, and each of these groups has been randomized to either candesartan or placebo. All patients will be followed for 42 months, and the primary overall endpoint is all-cause mortality. The trial is scheduled to finish in 2003. ARBs in CHF : Where Do We Stand? In a direct comparison trial ELITE-II ; , ARBs were found to have no benefit over ACE inhibitor therapy. Thus, ACE inhibitors should remain first-line treatment for heart failure. For patients intolerant to ACE inhibitors, ARB therapy is recommended and provides excellent tolerability. In patients already on ACE inhibitor therapy, the addition of an ARB reduced the number of heart failure hospitalizations ValHeFT ; . Therefore, ARBs can safely be added to ACE inhibitor therapy in patients who remain symptomatic. The caveat is that patients on both ACE inhibitors and beta-blockers did not appear to benefit from the ARB. For patients on ACE inhibitors and not beta blockers, the addition of a beta blocker is preferred over an ARB, since multiple studies have shown a mortality benefit in heart failure patients taking beta blockers. The CHARM study should help to define the use of ARBs as either ACE inhibitor add-on or substitute therapy in patients with heart failure and lamivudine and candesartan. NM Candesartan. The maximal response to Ang II decreased for both EXP3174 77.7 4.3 % ; and Candesartan 47.5 5.4 % ; . In contrast, 100 nM losartan produced a rightward shift EC 50 , 3.6 0.8.
4162 patients with ACS enrolled Primary end point: composite of death from any cause, myocardial infarction, documented unstable angina requiring rehospitalization, revascularization performed at least 30 days after randomization ; , and stroke. Mean Follow-up 24 months and zidovudine.

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25. World Health Organization. Department of Non-Communicable Disease Surveillance. WHO 1999 criteria for diagnosis of diabetes mellitus. Geneva: World Health Organization, 1999, 1-59. 26. Pfeffer MA, Swedberg K, Granger CB et al., for the CHARM Investigators and Committees. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet, 2003, 362, 759-66. McMurray JJV, stergren J, Swedberg K et al., for the CHARM Investigators and Committees. Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function taking angiotensin-converting-enzyme inhibitors: the CHARMAdded trial. Lancet, 2003, 362, 767-71. Granger CB, McMurray JJV, Yusuf S et al., for the CHARM Investigators and Committees. Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARM-Alternative trial. Lancet, 2003, 362, 772-6. Yusuf S, Pfeffer MA, Swedberg K et al., for the CHARM Investigators and Committees. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved trial. Lancet, 2003, 362, 777-81. The SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med, 1992, 327, 685-91. Vermes E, Ducharme A, Bourassa MG, Lessard M, White M, Tardif J-C. Enalapril reduces the incidence of diabetes in patients with chronic heart failure. Insight from the Studies Of Left Ventricular Dysfunction [SOLVD ; . Circulation, 2003, 107, 1291-6. WHO Study Group. Prevention of diabetes mellitus: report of WHO study group. WHO Tech Rep Ser, 1994, 844, 1-100. American Diabetes Association and National Institute of Diabetes, Digestive and Kidney Diseases. The prevention or delay of type 2 diabetes. Diabetes Care, 2002, 25, 742-9. DaviesMJ, Tringham JR, Troughton J, Khunti KK. Prevention of Type 2 diabetes mellitus. A review of the evidence and its application in a UK setting. Diabetic Med, 2004, 21, 403-14. Scheen AJ. Le concept d'insulinosensibilit. Diab Metab, 2001, 27, 193-200. Scheen AJ, Lefbvre PJ. Insulin resistance vs insulin deficiency: which one comes first? The old question revisited. In: Di Mario U, Leonetti F, Pugliese G, Sbraccia P, Signore A, editors. Diabetes in the New Millennium. New York: Wiley & Sons, 2000, 101-13. 37. Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes. Diabetologia, 2003, 46, 3-19. Ferrannini E, Buzzigoli G, Bonadonna R, et al. Insulin resistance in essential hypertension. N Engl J Med, 1987, 317, 350-7. Landsberg L. Insulin resistance and hypertension. Clin Exp Hypertens, 1999, 21, 885-94. Paolisso G, De Riu S, Marrazzo G, Verza M, Varricchio M, D'Onofrio F. Insulin resistance and hyperinsulinemia in patients with chronic congestive heart failure. Metabolism, 1991, 40, 972-7. Coats AJ, Anker SD, Anker S. Insulin resistance in chronic heart failure. J Cardiovasc Pharmacol, 2000, 35 [Suppl 4 ; , S9-14. 42. Amato L, Paolisso G, Cacciatore F, et al. Congestive heart failure predicts the development of non-insulin-dependent diabetes mellitus in the elderly. The Osservatorio Geriatrico Regione Campania Group. Diabetes Metab, 1997, 23, 213-8. Tenenbaum A, Motro M, Fisman EZ, et al. Functional class in patients with heart failure is associated with the development of diabetes. J Med, 2003, 114, 271-5 and ciloxan. In addition, the company has strategic marketing agreements for its products with 25 pharmaceutical companies serving europe, asia and other world markets.

The Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity CHARM ; study [26] was a parallel, double-blind RCT comparing candesartan with placebo in patients with CHF. Overall, 7599 patients were randomly assigned candesartan n 3803; titrated up to 32 mg once daily ; or matching placebo n 3796 ; and had a mean follow up of 37.7 months. In patients without a prestudy diagnosis of T2DM, the number of patients in the candesartan group who during the programme were newly diagnosed as having T2DM was significantly lower than that in the placebo group: candesartan 163 6% ; of 2715 and placebo 202 7% ; of 2721 OR 0.78; 95% CI, 0.64-0.96; p 0.020 ; . The CHARM programme was specifically designed as three parallel, independent, integrated, randomised, double-blind, clinical trials comparing candesartan with placebo in three distinct but complementary populations of patients with symptomatic CHF: patients with reduced left-ventricular systolic function taking ACEIs CHARMAdded trial ; [27], patients with left-ventricular dysfunction intolerant to ACEIs CHARM-Alternative trial ; [28] and patients with preserved left-ventricular ejection fraction CHARM-Preserved trial ; [29]. The results regarding the effect of candesartan on the incidence of new cases of T2DM was particularly impressive in the latter trial, while the differences did not reach statistical significance in the two other sub-trials. Indeed, in the CHARM-Preserved trial [28], 40% fewer individuals were diagnosed as having new diabetes in the candesartan group than in the placebo group 47 vs 77; OR: 0.60; 95% CI 0.41-0.86; p 0.005 ; . In the CHARM-Alternative trial [27], among patients without a pre-study diagnosis of diabetes, 44 in the candesartan group and 53 in the placebo group developed diabetes OR: 0.79; 95% CI 0.53-1.18; p 0.254 ; . In contrast, in the CHARM-Added trial [27], no difference was observed between the two populations: 72 6% ; patients in the candesartan group and 72 6% ; in the placebo group developed new diabetes unadjusted OR: 0.98; 95% CI 0.70-1.35; p 0.88 ; . These latter observations suggest that adding an ARB to an ACEI does not provide any further protection against T2DM in patients with CHF.

J. Kyncl1, J. Stransky2, J. Stritesky3, M. Horejsova4. 1Dept. of Epidemiology, National Institute of Public Health, Prague, Czech Republic; 21st Internal Medicine Clinic, Teaching Hospital Krlovsk Vinohrady and 3rd Medical Faculty, Charles University, Prague, Czech Republic; 3Institute for Pathology, 1st Medical Faculty, Charles University, Prague, Czech Republic; 42nd Internal Medicine Clinic, Teaching Hospital Krlovsk Vinohrady and 3rd Medical Faculty, Charles University, Prague, Czech Republic Background: Chronic hepatitis C is a global health problem. Methods: In a retrospective study of 225 anti-HCV positive cases of chronic hepatitis C in the years 1993-2003, 83 37% ; patients received blood transfusion prior to the year 1992, and 39 17% ; were i.v. drug addicts. The authors evaluated anamnestic data on viral hepatitis B and C, alcohol intake, blood transfusion, i.v. drug addiction, internal diseases and surgical procedures. Histology of the liver had been performed in 129 57% ; patients. Serology was carried out by 3rd generation ELISA methods, HCV RNA was detected by the polymerase chain reaction method. Results: In case history acute or chronic hepatitis C was presented in 8.4% of the patients only, alcohol was consumed by 45%, the most frequent diseases were obesity, cholelithiasis, and hypertension, and of surgical intervention it was gall bladder surgery, accidents, resection of the stomach and intestines. Drug addicts were significantly younger than subjects with blood transfusion p 0.001 ; . In almost 40% of patients liver cirrhosis was present. Cirrhotic patients had significantly higher mean activities of AST than ALT, and lower thrombocyte counts both p 0.01 ; than patients without cirrhosis. HCV RNA was positive at least in 2 3 the patients. HCV co-infection with hepatitis B virus was revealed in 18.7% of whom 1 3 were drug addicts. Hepatocellular carcinoma was found in 9 patients 4% ; , all of them suffering cirrhosis. Antiviral therapy was administered in 23% of the patients. Only one male healed spontaneously following acute hepatitis C 0.44% ; . Conclusion: The results reveal that 90% of the patients were detected as chronic viral hepatitis C.
Active ingredient s ; : candesartan cilexetil; hydrochlorothiazide.
To warrant asking the court to dismiss the action pursuant to the doctrine of primary jurisdiction. Under that doctrine, "questions within [the FDA's] peculiar expertise. are appropriately routed to the agency, while the Court stays its hand." Weinberger v. Bantex Pharms., Inc., 412 U.S. 645, 654 1973 see also Reiter v. Cooper, 507 U.S. 258, 26869 1993 ; . More specifically, "a district court may refer a matter within its original jurisdiction to the appropriate administrative agency if doing so will `promot[e] proper relationships between the courts and the administrative agencies charged with the particular regulatory duties.'" Bernhardt v. Pfizer, Inc., 2000 WL 1738645, 00 Civ. 4042, at * 2 S.D.N.Y Nov. 22, 2000 ; . Several factors are considered when assessing the propriety of applying the doctrine: a ; whether the question at issue is within the conventional experience of judges or whether it involves technical or policy considerations within the agency's particular field of expertise; b ; whether the question at issue is particularly within the agency's discretion; c ; whether there exists a substantial danger of inconsistent rulings; and d ; whether a prior application to the agency has been made. Id. at * 2. The doctrine of primary jurisdiction acknowledges that certain matters may extend beyond the conventional experience of judges and jurors and should be referred to the administrative agency having more specialized experience and expertise. Generally, if the issue in question is of a purely legal nature, referral to an agency on the ground of primary jurisdiction is inappropriate. Hence, if plaintiffs in a consumer protection act lawsuit seek to have a court declare that FDA-approved marketing is unlawful, or that manufacturers should be enjoined from marketing pharmaceuticals or medical devices pursuant to FDA-approved labeling and advertising, the defendants should consider whether to invoke this doctrine as part of their defense to such claims.

154 3.6 mmHg P 0.001 ; . The heart rate and the blood flow decreased to 362 12.6 beats min 1 P 0.001 ; and to 253 14.8 BPU P 0.01 ; , respectively. As a result of candesartan administration group C ; , blood pressure decreased from 127 4.8 mmHg to 101 4.7 mmHg P 0.001 ; . The blood pressure in the third period was further reduced to the value of 79 5.2 mmHg P 0.001 ; . The heart rate was unchanged after candesartan treatment first period, 421 10.9; second period, 437 11.0 beats min 1 ; . In the third period the heart rate was slightly but significantly lower 414 16.5 beats min 1.

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2004 ; cardiovasc drug rev candesartan cilexetil: an update of its use in essential hypertension.

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The inhibitory effect of eprosartan on the sympathetic nervous system has been demonstrated using the pithed rat model to establish a frequencyresponse curve to spinal cord stimulation both in the presence and absence of drug. In one such experiment, the electrical stimulation of the spinal cord led to an increase in blood pressure that was attenuated by eprosartan. Conversely, losartan and irbesartan had no effect on sympathetic outflow as measured by this approach.13 A similar study using the same model investigated the dose of angiotensin II antagonist required to block pre- and post-synaptic AT1 receptors.14 Eprosartan, valsartan, candesartan and embusartan suppressed the increase in blood pressure mediated by post-synaptic AT1 receptors at similar concentrations. However, blockade of the pre-synaptically mediated inhibition of sympathetic nervous stimulation occurred following much lower doses of eprosartan than were necessary for the other compounds, which were similarly potent ED20a values 6.32 vs 5.50, 5.77 and 5.62 log mol kg for eprosartan, valsartan, candesartan and embusartan, respectively, p 0.05. When indicated, induction of vomiting or gastric lavage should be considered. If symptomatic hypotension should occur, symptomatic treatment should be instituted and vital signs monitored. The patient should be placed supine with the legs elevated. If this is not sufficient, plasma volume should be increased by infusion of isotonic saline solution. Serum electrolyte and acid balance should be checked and corrected, if needed. Sympathomimetic drugs may be administered if the above-mentioned measures are not sufficient. Candesartan can not be removed by haemodialysis. It is not known to what extent hydrochlorothiazide is removed by haemodialysis. 5 5.1 PHARMACOLOGICAL PROPERTIES Pharmacodynamic properties.