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Middle East Journal of Family Medicine, 2005; Vol. 3 Authors: Abdullah Alsaeedi MD, FRCPC Division of internal Medicine Aljahra Hospital Kuwait Dr. Rashed Alhamdan MD, FRCPC Division of Internal Medicine Aljahra Hospital Kuwait Correspondence: Dr. R. Alhamdan Department of Medicine Aljahra Hospital Kuwait E.mail: ralhamdan yahoo Heart failure is a clinical syndrome characterised by an inability to provide sufficient cardiac output to meet tissue demands at normal ventricular filling pressures 1 ; . The syndrome is a significant health issue in the United States, where almost 5 million people have received the diagnosis of heart failure and about a half million new cases are diagnosed annually. According to estimates, nearly a half billion dollars are spent on drugs for treatment of heart failure every year in the United States 2 ; . This review focuses on the latest advances in the management of acute and chronic heart failure in patients with left ventricular systolic dysfunction. Acute versus chronic heart failure Diminished left ventricular systolic function is distinguishable by an ejection fraction of less than 35% to 40% 1 ; and is usually accompanied by an increase in the left ventricular end systolic and diastolic diameters. In response, the body activates several compensatory mechanisms as it attempts to maintain adequate tissue perfusion. These mechanisms include stimulation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone system, and local vasoregulation 3 ; . Although beneficial in their initial stages, the mechanisms may have a net detrimental effect of left ventricular remodeling coupled with an excessive increase in myocardial oxygen consumption, which results in further deterioration of cardiac function. Heart failure can be divided into acute and chronic forms on the basis of acuity of presentation and severity of signs and symptoms. In the past, both acute and chronic types were viewed primarily as haemodynamic disease and were treated with drugs that improve myocardial contractility inotropic agents ; , optimise volume status diuretics ; , and improve cardiac output through afterload reduction vasodilator agents ; . Although many of these drugs improved short-term symptoms in patients with chronic heart failure, they often failed to produce significant gains in long-term survival. In contrast, drugs that block neurohormonal factors, such as angiotensin-converting enzyme ACE ; inhibitors and beta-blockers, have generally improved not only the symptoms of chronic heart failure but also long-term survival. Treatment of chronic heart failure To optimally tailor therapy for chronic heart failure to an individual patient in the outpatient setting, it is important to categorise the patient's disease into the appropriate New York Heart Association NYHA ; class Table 1 ; . Treatment goals for chronic heart failure include alleviation of symptoms and improvement of quality of life, prevention of progression of myocardial dysfunction, and prolongation of life. The various drugs used in the treatment of heart failure contribute differently to these therapeutic end points. Their differences are outlined in Table 2. A treatment algorithm that integrates the therapeutic options is shown in Figure 1. ACE inhibitors These agents prevent the conversion of angiotensin I to angiotensin II through inhibition of the angiotensinconverting enzyme, which results in diminution of the adverse effects of angiotensin II. Moreover, inhibition of this enzyme prevents the breakdown of bradykinin and enhances kinin-mediated prostaglandin synthesis. In the Studies of Left Ventricular Dysfunction SOLVD ; trial 4 ; , treatment of mild to moderate heart failure NYHA classes II and III ; with enalapril 20 mg day ; was associated with a 16% reduction in allcause mortality compared with placebo 35.2% versus 39.7%; P .0036 ; . Enalapril use also resulted in a 26% decrease in risk of death or hospitalisation for worsening heart failure P .0001 ; . Even patients with reduced cardiac function ejection fraction, 35% ; who are asymptomatic derive significant benefit from treatment with ACE inhibitors i.e. reduction in risk of heart failure and rate of related hospitalisations ; 5 ; . Thus, it is recommended that all patients with heart failure and left ventricular systolic dysfunction receive an ACE inhibitor unless its use is contraindicated. Beta-blockers Once a patient's chronic heart failure is stabilised by an effective dose of ACE inhibitor, beta-blocker therapy should be initiated. Long-term treatment with carvedilol 6 ; , bisoprolol fumarate 7 ; , or long-acting metoprolol 8 ; has been shown in large randomised clinical trials to 22.
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Table 3. Overview of human studies investigating the effect of statins on endothelial function.
References 1. 2. 3. Kersel, DA, Marsh, NV, Havill, JH, and Sleigh, JW 2001 ; . Psychosocial functioning during the year following severe traumatic brain injury. Brain Injury; 15: 683-696. Nochi, M 1998 ; . "Loss of self" in the narratives of people with traumatic brain injuries: a qualitative analysis. Social Science and Medicine; 46: 869-878. Hibbard, MR, Uysal, S, Kepler, K, Bogdany, J, and Silver, J 1998 ; . Axis I psychopathology in individuals with traumatic brain injury. Journal of Head Trauma Rehabilitation; 13: 24-39. Deb, S, Lyons, I, Koutzoukis, C, Ali, I and McCarthy, G 1999 ; . Rate of Psychiatric Illness 1 Year After Traumatic Brain Injury. American Journal of Psychiatry; 156: 374-378. Bowen, A, Chamberlain, M, Tennant, A, Neumann, V, and Conner, M 1999 ; . The persistence of mood disorders following traumatic brain injury: A 1 year follow-up. Brain Injury; 13: 547-553. Alderman, N in press ; . Irritability and Aggression. In Wilson, BA Ed ; Neuropsychological Rehabilitation Theory and Practice. Swets and Zeitlinger. Tyerman, A and Humphrey, M 1984 ; . Changes in self-concept following severe head injury. International Journal of Rehabilitation Research, 7 1 ; , 11-23. Thomsen, IV, 1974 ; . The patient with severe blunt head injury and his family. A follow-up of 50 patients. Scandinavian Journal of Rehabilitation Medicine; 6: 180-183. Simpson, G, and Tate, R 2002 ; Suicidality after traumatic brain injury: demographic, injury and clinical correlates. Psychological Medicine. 32 4 ; : 687-697. Kim, SH, Manes, F, Kosier, T, Baruah, S and Robinson, 1999 ; . Irritability following traumatic brain injury. Journal of Nervous and Mental Disease; 187: 327-335. Schoenhuber, R and Gentilini, M 1988 ; . Anxiety and Depression after mild head injury: a case control study. Journal of Neurology, Neurosurgery, and Psychiatry; 51: 722-724. Andersson, S, Krogstad, JM and Finset, A 1999 ; . Apathy and depressed mood in acquired brain damage: relationship to lesion localization and psychophysiological reactivity. Psychological Medicine; 29: 447-456. Reitan, RM, and Wolfson, D 1997 ; . Emotional disturbances and their interaction with neuropsychological deficits. Neuropsychology Review; 7: 3-19. Gainotti, G 1993 ; . Emotional and psychosocial problems after brain injury. Neuropsychological Rehabilitation; 3: 259-277. Arciniegas, DB and Topkoff, J 2000 ; . The neuropsychiatry of pathologic affect: An approach to evaluation and treatment. Seminars in Clinical Neuropsychiatry; 5: 290-306. McGrath, J 1997 ; . Cognitive impairment associated with posttraumatic stress disorder and minor head injury: a case report. Neuropsychological Rehabilitation; 7: 231-239. Faby, S 1998 ; . A model for diagnostics in neurological rehabilitation: an answer to "the biopsychosocial disease-consequence model in rehabilitation" of Talo et al. The International Journal of Rehabilitation Research; 21: 113-126. Wilson, BA 2002 ; . Towards a comprehensive model of cognitive rehabilitation. Neuropsychological Rehabilitation; 12: 97-110. 19, for example, bisoprolol fumarate tablets.
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Adco-Bisocor is a highly cardioselective beta-blocker 16 ; that reduces combined mortality and all-cause hospitalisation in elderly patients with chronic heart failure 16, 17 ; . Conditions favouring use 4 ; are angina pectoris 4 ; , heart failure 4, 16, 17 ; . Adco-Bisocor bisoprolol ; should be considered a standard treat and bupropion.
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CIBIS II Investigators and Committees: , The Cardiac Insufficiency Bisoprolkl Study II CIBIS-II ; : a randomised trial. Lancet 1999 353 9-13 and isoptin.
Patient Description A 60 year old man presented to the emergency department of the Bnai Zion Medical Center on 1 September 2004 with intense pain and swelling of joints, and said that he was "unable to move." He had a 10 year history of CAD, with angina pectoris and myocardial infarction, as well as hyperlipidemia, and was taking the following medications once a day: bisoprolol fumarate 5 mg, aspirin 100 mg and simvastatin 10 mg. The CAD had been stabile on treatment until 2 months before the emergency room visit when he began to develop new symptoms at rest. Three weeks prior to presentation he underwent percutaneous transluminal coronary angioplasty of the distal left coronary artery with stent insertion. After this procedure he was prescribed clopidogrel 75 mg once daily in addition to his maintenance treatment. Two weeks later he developed widespread pruritus, with appearance of.
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In CIBIS-II, 43% of patients reached the target dose of 10 mg day and 67% the half-target dose of 5 mg [12]. Fifteen percent of patients discontinued the drug. Biskprolol reduced mortality by 34% and hospital admissions for worsening heart failure by 32 and doxazosin.
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Most of the studies were not powered to detect clinically significant differences in drug side-effects, and many reported the composite endpoint of either recurrence of AF or occurrence of a drug-related side-effect or drug withdrawal. 6.1.2. Evidence Statements Sotalol versus Propafenone 1 Two studies 121, 122 found no difference in the proportion maintaining 1 + sinus rhythm at 12 months between sotalol and propafenone. One study 122 also found a similar result when only those subgroups with a history of paroxysmal or persistent AF were considered. One study 123 found propafenone resulted in a lower incidence of side effects or AF recurrence than sotalol 52% versus 81%, respectively; p 0.001 ; . Sotalol versus Amiodarone 3 Three studies 86, 118, 119 found amiodarone to be significantly associated with an increased likelihood of remaining in sinus rhythm compared to sotalol at 12 86, 118, and 24 119 months following cardioversion. A similar result was found in terms of the likelihood of remaining in sinus rhythm without side effects 108, 119 and the monthly incidence of AF recurrence or side-effects 120. One study 86 also found amiodarone to be associated with an increased likelihood of remaining in sinus rhythm compared to sotalol regardless of the duration of AF and whether or not the AF was associated with symptoms. However, the study found no significant difference between the two drugs in those patients with ischaemic heart disease. Sotalol versus Beta-blockers 7 One study 125 found no difference in the percentage of patients with recurrent AF during a mean follow-up period of approximately 8 months between 5 mg day biso0rolol and 160 mg day sotalol 42% versus 41%, respectively ; . There were two cases of proarrhythmia and two cases of bradycardia in the sotalol group and two cases of bradycardia in the bisopr0lol group. Flecainide versus Amiodarone 8 One study 117 of patients with recurrent AF found no significant difference in the efficacy of flecainide and amiodarone over a period of 3 months in terms of the rate of recurrent AF 38% versus 32%, respectively ; . Propafenone versus Amiodarone 9 One study 109 comparing either propafenone or sotalol with amiodarone found amiodarone to be associated with a higher proportion of patients remaining in sinus rhythm after an average follow-up period of 468 days 39% versus 69%, respectively; p 0.001 ; . Sotalol and propafenone were comparable to each other 1 + 2.
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A continuous stream of new drugs and treatments appears on the market. Pharmacological knowledge of the drugs currently available is likely to be outdated within the next five years. New drugs are often marketed aggressively. A critical attitude is therefore needed to review such new treatments and give them a place or not ; in the therapeutic armoury. Failure to inculcate such an attitude and skill in the students will result in their being insufficiently prepared to withstand high-pressure salesmanship in the future.
Beta-Blockers Choices: Bisoproool starting dose 1.25mg once daily; target dose10mg once daily ; Studies show that beta-blockers improve overall survival in stable symptomatic heart failure: NNT 2210 increasing to NNT 14 in patients with severe HF11 to prevent one death per year. In patients taking a low dose ACEi, the addition of a beta-blocker produces a greater improvement in symptoms and reduction in death than an increasing the ACEi to target dose.3 Since low blood pressure identifies patients with worse outcome, the absolute benefit of treatment is greatest amongst these patients.7 Beta-blockers should always be initiated at a low dose and carefully titrated upwards `start low, go slow'.12 Clinical responses are often not apparent in the first 2 or 3 months of treatment, and transient deterioration may occur during this period.3 The evidence for using beta-blockers for heart failure surpasses even ACEi, 13 as safe to initiate14 with acceptable levels of tolerability.15 Diuretics Prescribed for most patients who have evidence of fluid retention.2, 3, 7 Diuretics improve symptoms breathlessness ; and exercise performance, producing symptomatic benefits more rapidly than any other drug for HF, 2 however, they should not be used alone in the treatment of HF.2, 3, 7, 10 There is no direct evidence that loop and thiazide diuretics confer prognostic benefit in patients with HF.16 Regular review is essential with a flexible approach that uses the minimum dose to maintain `dry weight' so avoiding electrolyte disorders, gout and renal dysfunction.17 In patients with severe heart failure, particularly in the presence of chronic renal impairment, oedema may persist despite increased doses of fruosemide. In such cases either combining with a thiazide diuretic e.g. metolazone ; `double nephron blockade' or switching from furosemide to bumetanide, which has better gastric adsorption, may be beneficial.16 When faced with decreasing renal function, most clinicians opt to reduce or stop the ACEi, when the most appropriate action may be to reduce the diuretic.18 Aldosterone receptor antagonists spironolactone ; . Plasma aldosterone levels may be elevated by 20-fold in patients with heart failure.19 Spironolactone 12.5-50mg ; is recommended in addition to ACEi, beta-blockers and diuretics in advanced heart failure NYHA III IV ; to improve survival and morbidity.20 Angiotensin II Receptor Blockers ARBs ; Choice: Candesartan starting dose 4 8mg once daily: target dose 32mg once daily ; . ARBs are possible alternatives in patients who truly cannot tolerate ACE inhibitors.2, 3, 7 A meta-analysis showed that, when compared to placebo, ARB's non-significantly reduce the rate of death and hospitalisation among patients not taking an ACEi.21 The CHARM study showed that patients, who could not tolerate ACEi, reported a significant decrease in the risk from death for cardiovascular causes or hospitalisation vs placebo.22 Studies combining ACEi and ARBs have also recently published. Val-HeFT combined valsartan with an ACEi in patients with heart failure showed that whilst treatment significantly reduced the number of hospitalisations, improved quality of life, and LVEF, the mortality rate was similar in both groups.23 In contrast, in the combination arm of CHARM, candesartan significantly reduced the composite endpoint of cardiovascular death or hospitalisation for heart failure.24 Given the extensive clinical experience with ACEi and the lower cost of available generics, ACEi remain the logical first line therapy.25 The role of ARBs as an adjunct to ACEi remains to be defined however they may be used as an alternative in patients genuinely intolerant to ACEi.2, 3, 7 Digoxin: Is recommended for 1 ; worsening or severe heart failure due to LV systolic dysfunction despite ACE inhibitor, beta-blocker and diuretic therapy. 2 ; Patients with atrial fibrillation with any degree of heart failure.2 Calcium Channel Blockers: Both felodipine26 and amlodipine27 have been studied in patients with heart failure. Long-term data shows a neutral effect on survival, consequently these agents can be considered for treating concomitant hypertension or angina.2, 25 Link to References mbpct.nhs medman preguid documents and cefaclor and bisoprolol.
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JB: What music were you into as a teenager? JM: In 1993 I discovered club music and started to get into stuff that wasn't played on the radio. The genre was not that important, though. My brother and I listened to a lot of U2 and Pearl Jam, then grunge later and, of course, hip-hop, mainly old school. That's what I started with when I bought turntables. JB: Which other musicians have been really important influential in your development? JM: All artists who don't take their work toooo seriously. JB: Your track `Zdarlight' is huge for lots of DJs. Do you feel any connections with the house scene? JM: It works very well in that scene too. But the contemporary house scene's ended up plain and boring, way too hi-fi the old tracks were tight though ; . These days I think people into the music, not just the parties, have switched to the electro thing. JB: How strong is the electro scene right now? JM: I think pure electro is vanishing again. It was another trend, like many others, sneaking into the clubs and the mainstream. But of course it's left its fingerprints. You can also see electro as the second biggest club scene next to house. If you do, it's a big one and still on the rise. JB: You've done many remixes in a short time. How do you manage? JM: We just do it, but don't look in our hard disk where everything is saved. Cosmic chaos! Remixes rarely take us more than one evening. Sometimes we do three or four versions; that takes longer of course. Our best trick is to create a Digitalism song out of the original. Who needs a second original anyway? Yes, our schedule is becoming busier and busier, so the fees are rising, of course!" JB: Many people think you're French because you're signed to Parisian imprint Kitsun; what does it feel like being on a flash label? JM: It feels very comfortable as we know that the guys at Kitsun appreciate good things. They're stylish, addicted to art, proper music fashion lovers. If you insist on certain standards you might get labelled as snobbish, but that's just because you like quality! They told us, "Franz Ferdinand do rock music to make people dance, Digitalism do dance music to make people rock, " Bless them. JB: You're being compared to Daft Punk when they started. How are you coping with all the attention? JM: We are upgrading and Digitalism updating ourselves a lot, learning to be professional. Also we redirect this outside energy into a lot of our ideas. JB: So are you ready to go public? JM: I guess so. When I look back this was something that had to happen. I need my audience. I have something to say. For more, check out kitsune.
1. Heart and Stroke Foundation of Canada. The changing face of heart disease and stroke in Canada 2000. Ottawa, Canada, 1999. 2. No authors listed. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. The Long-term Intervention with Pravastatin in Ischaemic Disease LIPID ; Study Group. N Engl J Med 1998; 339: 1349-57. HPS Heart Protection Study Collaborative Group. MRC BHF Heart Protection Study of cholesterol lowering with simvastatin in 20, 536 high-risk individuals: A randomised placebo-controlled trial. Lancet 2002; 360: 7-22. The Metoprolol CR XL Randomised Intervention Trial in Congestive Heart Failure MERIT-HF ; Study Group. Effect of metoprolol CR XL in chronic heart failure: Metoprolol CR XL Randomised Intervention Trial in Congestive Heart Failure MERITHF ; . Lancet 1999; 353: 2001-7. Packer M, Coats AJ, Fowler MB, et al. Carvedilol Prospective Randomized Cumulative Survival Study Group. Effect of carvedilol on survival in severe chronic heart failure. N Engl J Med 2001: 344; 1651-8. No authors listed. The Cardiac Insufficiency Visoprolol Study II CIBIS-II ; : A randomised trial. Lancet 1999; 353: 9-13. Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med 1996; 334: 1349-55. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000; 342: 145-53. Mathiesen ER, Hommel E, Giese J, Parving HH. Efficacy of captopril in postponing nephropathy in normotensive insulin dependent diabetic patients with microalbuminuria. BMJ 1991; 303: 81-7. Giatras I, Lau J, Levey AS. Effect of angiotensin-converting enzyme inhibitors on the progression of nondiabetic renal disease: A metaanalysis of randomized trials. Angiotensin-Converting-Enzyme Inhibition and Progressive Renal Disease Study Group. Ann Intern Med 1997; 127: 337-45. Fallen E, Cairns J, Dafoe W, et al. Management of the postmyocardial infarction patient: A consensus report revision of the 1991 CCS Guidelines. Can J Cardiol 1995; 11: 477-86. Ryan TJ, Antman EM, Brooks NH, et al. 1999 update: ACC AHA guidelines for the ganagement of patients with acute myocardial and cefuroxime.
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