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Beta Blocker Treatment in Heart Failure - Literature review Example

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The review "Beta-Blocker Treatment in Heart Failure" proves that given therapy has immensely aided in managing heart failure predicaments and proved to be a superior alternative due to its evident benefits - decreased transience and hospitalizations rates…
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Beta Blocker Treatment in Heart Failure
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Beta Blocker Treatment in Heart Failure (Literature Review) The Latest studies regarding deployment of Beta Blocker therapy have proved its efficacy in dealing with heart failure (BMC 2011, p.106). This is via prolonging the victims’ survival and reduced hospitalization rates, which is specifically to the individuals who have chronic heart failure (MNT, 2009). Additionally, this therapy has enabled physicians effectively tackle the predicament of ventricular systolic malfunction (Aschenbrenner, 2009, p. 540). However, the therapy does not apply to all individuals who have chronic heart failure, but it is selective, where hospitalized victims cannot qualify1. Since this therapy requires the patients be in a steady state preferably in the class brackets of II or III (SSCTS, 1994). Besides the hospitalized individuals, those who have hypertension, bradycardia or experience intensive heart blockage Beta Blocker cannot be a remedy2 (Bachmakov et al 2009, p. 1082). Since to gain the necessary stability they require optimal dieresis coupled with low doses once their condition starts to improve (Shaw, 2009). In addition, this will entail close monitoring with increased dose in each 2 - 4 weeks while awaiting the victim to attain a heightened tolerated dose (Delgado, 2009, p. 52). The universal goal of this therapy encompasses long duration improvement, instead of immediate management of the predicaments’ symptoms (Baker, Nikolić, & Oconnor, 2009). Hence, enabling the patients get maximum assistance from the medication that may be difficult in attaining with other alternative managements in which they incur more expenses (Gerstenblith & Margolis, 2007). Medical evidence Table 1: Impact of Beta Blockers to All-Cause Mortality Research No. of patients(Functional class) Medicine and average Dose (mg/ day) Follow up duration Mortality comparative reduction (in %) Drug’s Nature (Receptors) Hospitalization reduction (In %) Carvedilol Heart malfunction program 1, 095 (mostly class II or III) Carvedilol, 45 28 weeks 65 Alpha1, beta1 & beta2 29 Bisoprololin, Cardiac deficiency 2,650 (II & III) Bisoprololin, 7.5 1 year & 4 months 34 Beta1-selective 20 Metoprolol 3,991 patients (II or III) Metoprolol, 159 1 year 34 Beta1-selective - The Beta Blocker preference as a remedy for heart malfunction treatment descended from carvedilol study program (Chan, Gold & Nallamothu, 2010, p. 1010). This entailed treating victims of ventricular systolic malfunction besides those who experienced mild impairment, hence having low tolerance to medication (Parker, 1996). According to Carvedilol studies its deployment yielded to 65% reduced mortality and 29% hospitalization rates, besides the drug showing significant improvements among ventricular victims (Foody, 2001). Close examination of the patients approximately averaged seven months coupled with reduced hospitalization (Churchouse, 2009). Bisoprololin study entailed either mild or a moderate patient whose mortality rate equaled that of Metoprolol except the monitoring duration that is longer than the latter (Beebe & Myers, 2010) is. In addition, the study has a reduced hospitality rate by 20% having examined 2,650 patients within a year. All the three studies, their patients fall between II and III functional classes but vary in terms of number, drug capacity and monitoring durations (JCS, 2012). According to the presented data, Metoprolol’s injection per day is higher than Carvedilol and Bisoprolol3. Since the two studies have 7.5 and 45 mg per day respectively while that of Metoprolol’s is 159mg/day (Ferrera et al, 2011). Their effectiveness is evident through their reduction rates where Carvedilol leads the lot, despite its mg/day capacity being half of the Metoprolol’s (159mg/day) (Khan, 2007, p. 5). Bisoprololin bears the lowest mg/day, but its examination period is longer than the other two studies. Hence, implying slow medication effect, though, it has the same percentage reduction rate as Metoprolol (34%) (Irwin & Rippe, 2008). The researcher’s study is evident in presenting diverse comparisons amid the three Beta Blockers, where the leading in its effectiveness is Carvedilol. This is due to its receptor’s nature since it has Alpha1, beta1 & beta2 contrary to the other Beta Blockers. Carvedilol nature prompts it to have less follow up period; an aspect that credit the researcher’s work as valid. The study is valid besides its statistics where in the real application supports the same trend as the researcher has argued and elaborated in the table. Systolic Dysfunction Treatment This syndrome is a mechanical malfunction of the heart where due to its muscles’ interference it yields to reduced injection fraction (Barry, 2011). Principally, the heart is incapable of impelling oxygenated blood as necessitated for efficient circulation. Its impact reveals itself via hemodynamic and physiologic deviations coupled with low cardiac yield (Roberts, 2009). Consequently, the phenomenon leads to the reduction of ventricular performance that may prolong due to the absence of early recognition and become chronic (Churchouse, 2009). Beta Blockers normally cancels this activation of neurohormonal mechanisms by making the left heart muscles less stiff and facilitate efficient blood propelling (Wiysonge, 2008). Clinical Data Trials Table 2: Beta Blocker agents’ assessment Agent Receptors Vasodilating characteristics Bisoprololin Beta1-selective None Metoprolol Beta1-selective None Carvedilol Alpha1, Beta1 and Beta2 Evident The data presented depicts the three agents having Beta1 selective except Carvedilol, which has additional of Alpha1 and Beta2 (Nakamura et al, 2011, p.1100). Finally, the above two components does not depict any Vasodilating attributes except Carvedilol (Olsen et al 1995). Table 3: Bisoprololin Mortality Trials (year 1994 & 1999) Trial Features Cardiac Insufficiency Bisoprolol Study (CIBIS) - 1994 Cardiac Insufficiency Bisoprolol Study II (CIBIS II)- 1999 Patients 640 2,650 Average Age 60 61 sex Male: 83% Female: 17% Male: 80% Female: 20% Origin Not depicted Not depicted Injection quantity (Less than..) 40 35 New York malfunction classification II: none III: 95% IV: 5% II: none III: 83% IV: 17% Initial Dose (mg/day) 1.25 1.25 High target (mg/day) 5 10 Follow up duration 2 years 1.25 years End point Death Death Outcomes Death rate: Placebo - 20% Bisoprololin- 16% Death rate: Placebo -17% Bisoprololin: 12% Comments Insignificant mortality gain Death rate lesser than anticipated Great death rate Insignificant death rate variations The 1994 data compares death rates made by two medications on patients, which comprise placebo, Bisoprololin whose percentages are 20% and 16% respectively4 (Lacet, 1997). Dosage titration from 1.25 to 5 mg/day according to the data did affect the expected study outcome. However, Bisoprololin injection yielded to a significant hospitalization reduction rate in New York, hence being beneficial (Vitale, 2011, p. 705). CIBIS-II was extra powerful in identifying death benefit meant for Bisoprololin therapy (Gorell & Mulley, 2009). Conversely, the data monitoring halted early due to the already attainment of anticipated results. This is due to the recognizable gap amid patients receiving placebo and Bisoprololin (Field, 2009). Besides, there was a decreased death rate of 42% irrespective of the others, whose causes were miscellaneous. The study all through the two follow up periods does not indicate significant mortality rate, which implies the improvements of its application is minimal. Possible deductions due to these results might due to utilizing similar and unchanging 1.25mg/day. In addition, amid the placebo and Bisoprololin it depicts increasing gap comparing with initial study year (1994), which might be the reason to “Great death rate.” However, the study despite its minimal advancements according this data, it has immensely assisted in chronic heart failure therapy. Table 4: Metoprolol Mortality Trials (1993 & 1999) Trial Features Metoprolol in Dilated Cardiomyopathy (MDC) - 1993 Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)- 1999 Patients 383 3991 Average Age 50 64 sex Male: 73% Female: 25% Male: 78% Female: 22% Origin Not depicted White: 95% Blacks: 5% Injection quantity (Less than..) 40 40 New York malfunction classification II: 47% III: 47% IV: 4% II: 42 III: 55% IV: 3% Initial Dose (mg/day) Metoprolol Titrate 10 Metoprolol Succinate: 12.5 - 25 High target (mg/day) 100 – 150 (Twice daily) 200 Follow up duration 1 – 1.5 years 1 year End point Death and need for transplant Death Outcomes Death rate: Placebo – 20.1% Metoprolol titrate 12.9% Death rate: Placebo -11% Metoprolol succinate: 7.2% Comments Medication advanced clinical status & reduced need for transplant Stagnant Death rate Early termination the research Medication reduced sudden deaths. The 1993 data exemplifies how patients who used Metoprolol titrate had an improved life, work out capacity and injection fraction (AAP, 2000. The two entities amid them they lack great differences, where there was a decreased death rate prompted by strong urge for heart transplant in MDC category (Metra et al, 2007). The second research culminated earlier due to utter death rate, which ranged 7.2% compared with those having 11% annually. The increased mortality emanated from the study’s sole endpoint, which did not include need for transplant, besides other related maladies (Foresi et al, 2010, p. 180). The study utilizes varying titration reagents, which results to varied durations. The initial duration was 1.5 years, compared to the final 1-year timeframe. This implies that the altered Metoprolol succinate from Metoprolol titrates had a significant contribution in varying the results, dosage (100-150 to 200). Hence, the comparison is not viable and bears some flaws, since the study’s element in each aspect are varying, besides the therapy showing improved effectiveness. Table 5: Carvedilol Mortality Trials Trial Features U.S Carvedilol Program Patients 1,094 Average Age 58 sex Male: 77% Female: 24% Origin Not depicted Injection quantity (Less than..) 35 New York malfunction classification II: 53% III: 44% IV: 3% Initial Dose (mg/day) 3.125 – 6.25 High target (mg/day) 25 – 50 (Twice daily) Follow up duration 1 – 1.5 years End point Exercise tolerance Quality life Illness progression Outcomes No advancement both in quality life and exercise tolerance 48% illness reduction Death Rate: Placebo – 7.9% Carvedilol - 3.3% Comments Research halted early due to the outcome Evident benefit in the entire groups Comparing carvedilol with other agents has high mortality advantage5 (Messerli, Bangalore, Yao & Steinberg, 2009). Since, its death rate is insignificant apart from the patients not having the heightened risk hospitalization. In addition, this investigation halted earlier than what numerous researchers had anticipated, hence being the best than others (Endo & Matsumoto, 2008). The study compares the Carvedilol effectiveness with a known placebo whose capability is high, hence acting as a gauge. Carvedilol manages to have 3.3% against the placebo whose rating is 7.9% (Messerli, Bangalore, Yao & Steinberg, 2009). The study’s argument rests on comparing a known simulated substance possessing high strength meant to gauge Carvedilol’s effectiveness. This may pose some weaknesses, since the placebo may have varied concentrations while under study, which would depict diverse results. However, the Carvedilol’s capability is evident via its effectiveness in Systolic Dysfunction therapy (McGavin & Keating, 2002). Discussion Beta Blockers therapy have immensely aided in managing heart failure predicaments and proved to be a superior alternative due t its evident benefits (McGavin & Keating, 2002). These encompass decreased transience and hospitalizations rates. Initially, the thought of proposing Beta Blockers as a remedy for chronic heart failure emanated with “Carvedilol research program” (Beebe & Myers, 2010). The researchers observed how the drug aided in improving state of patients having left ventricular systolic dysfunction besides those who had similar mild (Class II & III) impairments. Carvedilol showed reduced rates having a mortality of 65% and hospitalization 29% respectively. Other Beta Blockers similarly showed their trends, though, differed due to their distinct properties (Beebe & Myers, 2010). Bisoprolol statistics showed a reduced mortality, hospitalization rates of 34% and 20% respectfully. Metoprolol Beta Blocker showed 34% mortality rate reduction similar to Bisoprolol (McGavin & Keating, 2002). Among the three Beta Blockers, Carvedilol is the most effective due to its composition that comprises of Alpha1, Beta1 & Beta2, contrary to the other two, which have Beta1-selective and lack significant vasodilating characteristics. Hence, having high rates in both mortality and hospitalization, which prompts numerous medical practitioners prefer its application (McGavin & Keating, 2002). However, Beta Blockers have selective trends in their applications. This implies that patients to qualify for the beta Blockers’ therapy ought to have one’s predicament be in certain functional class, probably II & III as necessitated by their effectiveness (Cruickshank, 2010). Additionally, the patients’ ventricular ejection fraction should not exceed 40% besides having stable circulation (Beebe & Myers, 2010). This is critical in ensuring the remedy does not develop negative predicaments against the ailing person. Beta Blockers, its application requires that the patients start with low dosing prior having high and powerful dosing for better tolerable state and ensure good management of the disease (Cruickshank, 2010). Beta Blocker therapy normally bear grievous effects that may render the patient succumb to worse predicaments. For illustartion, abrupt discontinuation leads to circulatory deterioration characterized by electrophysiologic unsteadiness6. Further common side effects entail, Bradycardia Decreased blood pressure Fatigue Cold hands and feet Dizziness and frequent headaches Insomnia Chronic chest pains High triglycerides Depression References 1997. Randomised, placebo-controlled trial of carvedilol in patients with congestive heart failure due to ischaemic heart disease. Australia/New Zealand Heart Failure Research Collaborative Group.  Lancet.  ;349:375–80. 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Effect of short-acting beta blocker on the cardiac recovery after cardiopulmonary bypass 2011, Journal Of Cardiothoracic Surgery(JCS), 6, 1, pp. 99-103, viewed 16 April 2012. Endo, M., & Matsumoto, N. 2008. Beta blockers: new research. New York, Nova Science Publishers. Ferrera, R, Hadour, G, Tamion, F, Henry, J, Mulder, P, Richard, V, Thuillez, C, Ovize, M, & Derumeaux, G. 2011, Brain death provokes very acute alteration in myocardial morphology detected by echocardiography: preventive effect of beta-blockers, Transplant International: Official Journal Of The European Society For Organ Transplantation, 24, 3, pp. 300-306, viewed 16 April 2012. Field, J. M. (2009). The textbook of emergency cardiovascular care and CPR. Philadelphia, Wolters Kluwer/Lippincott Williams & Wilkins. Pp. 74-75. Print. Foody, J. M. 2001. Preventive cardiology: strategies for the the prevention and treatment of coronary artery disease. Totowa, NJ, Humana Press. Pp.250-251. Print. Foresi, A, Cavigioli, G, Signorelli, G, Pozzoni, M, & Olivieri, D 2010, Is the use of beta-blockers in COPD still an unresolved dilemma?, Respiration; International Review Of Thoracic Diseases, 80, 3, pp. 177-187, viewed 16 April 2012. Gerstenblith, G., & Margolis, S. 2007. Coronary heart disease. Baltimore, Md, Johns Hopkins Medicine. Pp. 47. Print. Gorell, A. H., & Mulley JR, A. G. 2009. Primary care medicine office evaluation and management of the adult patient. Philadelphia, PA, Lippincott Williams $ Wilkins, a Wolter Kluwer business. Pp. 250-251. Print Irwin, R. S., & Rippe, J. M. 2008. Irwin and Rippes intensive care medicine. Philadelphia, Wolters Kluwer/Lippincott Williams & Wilkins. Pp. 341-347. Print. Keating, G, & Jarvis, B 2003, Carvedilol: a review of its use in chronic heart failure, Drugs, 63, 16, pp. 1697-1741, viewed 17 April 2012. Khan, M. I. G. 2007. Cardiac drug therapy. Totowa, N.J., Humana Press. Pp. 146-147. Print. 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