coreg 10 mg
Although the benefits of beta-blocker therapy for patients with congestive heart failure (CHF) are independent of pretreatment heart rate, patients with chronic systolic heart failure and low resting heart rates are often excluded from beta-blocker therapy. We investigated the effectiveness and cost-effectiveness of prophylactic pacemaker insertion to facilitate beta-blocker use in these patients.
coreg usual dose
Long-term treatment with carvedilol produces greater effects on left ventricular ejection fraction than metoprolol when both drugs are prescribed in doses similar to those that have been shown to prolong life.
coreg normal dosage
The effect of the cardiovascular drug carvedilol on cytosolic free Ca2+ concentrations ([Ca2+]i) and viability has not been explored in human hepatoma cells. This study examined whether carvedilol altered [Ca2+]i and caused cell death in HA59T cells. [Ca2+]i and cell viability were measured using the fluorescent dyes fura-2 and WST-1, respectively. Carvedilol at concentrations >or=1 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 value of 20 microM. The Ca2+ signal was reduced partly by removing extracellular Ca2+. Carvedilol induced Mn2+ quench of fura-2 fluorescence, implicating Ca2+ influx. The Ca2+ influx was sensitive to La3+, econazole, nifedipine, and SKF96365. In Ca2+-free medium, after pretreatment with 1 muM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), carvedilol-induced [Ca2+]i rises were abolished; and conversely, carvedilol pretreatment inhibited a major part of thapsigargin-induced [Ca2+]i rises. Inhibition of phospholipase C with 2 microM U73122 did not change carvedilol-induced [Ca2+]i rises. At concentrations between 1 and 50 microM, carvedilol killed cells in a concentration-dependent manner. The cytotoxic effect of 1 microM (but not 30 microM) carvedilol was fully reversed by prechelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Apoptosis was induced by 30 (but not 1) microM carvedilol. Collectively, in HA59T hepatoma cells, carvedilol induced [Ca2+]i rises by causing Ca2+ release from the endoplasmic reticulum in a phospholipase-C-independent manner and Ca2+ influx via store-operated Ca2+ channels. Carvedilol-caused cytotoxicity was mediated by Ca2+ and apoptosis in a concentration-dependent manner.
typical coreg dosage
To describe the time course over which echocardiographic improvement of systolic function occurred in a cohort of children who presented in acute heart failure, without structural or metabolic abnormality.
coreg renal dosing
Thirty-five patients with IDC were randomly assigned to receive metoprolol or carvedilol in an open-label study. Echocardiographic measurements and circulating levels of tumor necrosis (TNF)-alpha and interleukin (IL)-1beta and IL-6 were obtained at baseline and after 3 months of treatment. The 2 beta-blockers significantly improved the left ventricular ejection fraction and reduced end-diastolic and end-systolic volume. The magnitude of these changes was greater with carvedilol than with metoprolol (respectively P < .001, P < .05, and P < .05). Both treatments induced a significant decrease in the levels of cytokines (for all P < .01), but the decrease in TNF-alpha and IL-1beta was more consistent in the carvedilol group ( P < .01).
coreg 40 mg
The Carvedilol or Metoprolol European Trial (COMET) demonstrated improved survival with carvedilol vs. metoprolol tartrate in patients with heart failure. The benefits of carvedilol in typical clinical practice in the United States are unknown.
coreg 6 mg
The use of ICD devices increased in apparent response to new research evidence, and, at least in part, in response to need. However, this process only involved men; ICD devices are largely underused in women and without apparent relation to need.
coreg dosage forms
Chronic heart failure (CHF) is common, and increases in incidence and prevalence with age. There are compelling data demonstrating reduced mortality and hospitalizations with adrenergic blockade in older patients with CHF. Despite this, many older patients remain undertreated. The aim of the present article is to review the potential mechanisms of the benefits of adrenergic blockade in CHF and the clinical data available from the large randomized studies, focusing particularly on older patients.
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Cirrhosis is the end-stage of chronic liver disease and leads to the development of portal hypertension and its complications such as esophagogastric varices. Non-selective beta blockers (NSBB) are the keystone for the treatment of portal hypertension since the 1980s and, over the decades, several studies have confirmed their beneficial effect on the prevention of variceal (re)bleeding. Pharmacological studies showed effects of gender, sex hormones, oral contraceptives, and pregnancy on cytochrome P450 (CYPs) enzymes that metabolise NSBB, suggesting that gender differences might exist in the effect of NSBB. In this review, we focused on the 35-year knowledge about the use of beta blockers in cirrhosis and potential gender differences. We specifically examined the role of NSBB in pre-primary, primary and secondary prophylaxis of variceal bleeding, compared two commonly used NSBB (i.e., Propranolol and Carvedilol), and present the current controversies about the window of treatment in advanced cirrhosis with a specific focus on gender differences in NSBB effects. NSBB are not currently recommended in pre-primary prophylaxis of varices mainly because of lack of proven efficacy. On the other hand, NSBB are strongly recommended in patient with cirrhosis as primary (as alternative to endoscopic band ligation, EBL) and secondary prophylaxis (in addition to EBL) of variceal bleeding. To date, no studies have focused specifically on the effect of gender on NSBB treatment. Data extrapolated from clinical studies show that gender was neither a risk factor for the development of varices nor associated with a different response to treatment in primary or secondary prophylaxis. According to the available guidelines, no different, gender-based treatment for portal hypertension is recommended.
coreg max dose
The ambulatory blood pressure did not differ in the treatment periods. Losartan significantly reduced albuminuria relative to placebo and carvedilol (27.62+/-17.58 vs. 49.55 +/- 25.33 v. 44.77 +/- 21.9 mg/g creatinine; P < 0.01). A significant but not clinically relevant decrease in hemoglobin level after losartan was observed (losartan: 129 +/- 3.1 g/l, placebo: 134.2 +/- 3.2, carvedilol: 137.1 +/- 3.7; P < 0.001). Serum potassium, creatinine, creatinine clearance, and trough blood cyclosporine levels were unaffected.
coreg starting dose
The interpretation of congestive heart failure (CHF) in '80 was exclusively in haemodynamic terms. In accordance with such a pathophysiologic hypothesis, cardiovascular drugs, mainly positive inotropics and/or vasodilators were experimented with not significative results. From the second half of the 80's the attention starts focusing on the neurohumoral asset, strongly activated in patients suffering from CHF and that was it selves cause of worsening of CHF and responsible for the poor prognosis of these patients, so as to become therapeutic targets and to represent the rationale for using ace-inhibitors (ACE-I), betablockers and angiotensin II receptor blockers (ARBs). Evidence has been provided that these drugs can reduce morbidity and mortality. However, this evidence derives only from studies on general population. In uraemic patients there are no controlled trials dedicated and the nephrological guidelines recommends the use of ACE-I on the hypothesis that they may have similar efficacy than non uremic patients. Among all the medications used to treat CHF in the general population, only betablockers has been shown to be effective in a randomized trial in the dialysis population. Carvedilol was found to improve left ventricular function and decrease hospitalization, cardiovascular deaths and total mortality, remarking that pathophysiology, rationale for using and results may be similar in uremic and non uremic patients suffering from CHF.
coreg cr generic
The baseline LVEF, LVEDV, plasma BNP, and NYHA functional class were similar in both groups. However, there was a greater increase of LVEF (Delta LVEF) with dobutamine infusion during D-QGS in group A than that in group B (12.0% +/- 5.8% vs. 2.7% +/- 4.2%, P < 0.0001). When a cutoff value of 6.6% for Delta LVEF was used to predict the improvement of LVEF by carvedilol therapy, the sensitivity was 86.7%, the specificity was 86.7%, and the accuracy was 86.7%. LVEDV, plasma BNP, and NYHA functional class all showed superior improvement in group A compared with group B.
Heart transplantation (HT) provides longer survival than that of the natural history in patients with dilated cardiomyopathy (DCM). However, the optimal timing for cardiac transplantation and predictors of mortality in patients with end-stage cardiomyopathy (ESCM) has been poorly defined. The primary purpose of this study focused on the natural history of ambulatory patients with ESCM for HT assessment. Secondly, we tried to determine prognostic factors of individuals with the poorest short-term outcome and the optimal timing for HT in patients with ESCM. Finally, clinical treatment with angiotensin converting-enzyme inhibitors (ACEIs), carvedilol and amiodarone in the prevention of mortality caused by ESCM, were retrospectively evaluated. The short-term outcomes of 119 referral patients with ESCM for four years were observed. The patients had New York Heart Association class III to IV dyspnea at initial assessment for HT. Left ventricular ejection fraction (LVEF) was 17 +/- 6% and cardiac index (CI) was 2.0 +/- 0.6l/min/m2. After optimization of medical treatment, the patients were divided into two major groups according to CI equal to or less than 2.0l/min/m2 and more than 2.0l/min/m2. HTs were accepted in 88 patients and the patients were divided into two groups: medical treatment (group 1, 56 patients) or HT (group 3, 32 patients); HT was not accepted in the other 31 patients (group 2). We studied the probability of the survival curve and prognostic variables of the groups with medical treatment in the follow-up of 12 +/- 9 months. During follow-up, 49 patients were alive without HT. The remaining 38 patients died; 27 patients were in group 1 and 11 patients were in group 2. Eight deaths in group 2 were sudden. The actuarial survival rate among the non-HT population was 73%, 68%, 63 %, and 56 % at 3, 6, 9 and 12 months, respectively. The actuarial survival rate among group 1 was 70 %, 59 %, 55 %, and 52 % at 3, 6, 9 and 12 months, respectively. The actuarial survival rate among group 2 was 87 %, 85 %, 77 %, and 65 % at 3, 6, 9 and 12 months, respectively. A comparison, excluding patients with HT, was performed with those who had survived < 1 year and > or 1 year after assessment, and those who had died. Two parameters were independent predictors of prognosis on univariate and multivariate analysis: total pulmonary vascular resistance (TPR) > or = 14 Wood units (W) and CI < 1.65 l/min/m2 at 6 and 12 months after assessment. Treatment with amiodarone for ventricular tachycardia (VT) showed no convincing role in the prevention of sudden death in our patients. Also, treatment with ACEIs or carvedilol for heart failure was unconvincing to improve the short-term outcome in this study. Our results suggest in properly selected patients that HT should be considered within six months among patients with severe heart failure. Hemodynamic parameters associated with right cardiac function are important determinants of mortality caused by progressive heart failure. Predictors such as CI and TPR may be considered as important markers of mortality in prediction of short-term outcome in patients with ESCM, as other predictors reported in the literature.
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Although metoprolol has been proven to be beneficial in the majority of patients with heart failure, a subset of the remaining patients shows long-term survival without satisfactory clinical improvement.
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Carvedilol has proven to be beneficial in a majority of adult patients with congestive heart failure. Although the experience from adult patients may be extrapolated to older children, symptomatic infants remain a subset for whom dosage, safety and efficacy need to be established. The purpose of this study was to assess whether treatment with carvedilol is efficacious and safe for infants with dilated cardiomyopathy who do not show satisfactory clinical improvement despite treatment with conventional medications.
coreg recommended dosage
1. Patients with unstable angina and non-ST elevation myocardial infarction in associations with diabetes mellitus type 2 are characterized with increased heart rate partly resistant to β-blockers, which indicates worse prognosis of cardiovascular diseases. 2. Prescription of carvedilol in daily dose 12.5 - 25 mg. is inadequate for obtaining HR < 70 bmp. in some patients with acute coronary syndrome and diabetes mellitus. 3. According to heart rate resistance to β-blockers in patients with unstable angina and non-ST elevation myocardial infarction and concomitant diabetes mellitus patients need individual titration of higher doses of carvedilol.
coreg 25mg tab
In rats with an abrupt termination of the chronic continuous ethanol intake, the homogeneity of myocardial repolarization impaired and correlated with the cardiac sympathovagal balance. Carvedilol pretreatment is associated with a reduction in both the QTd and LF/HF ratio, raising the possibility that the cardiac sympathovagal balance shift may be responsible for the impaired homogeneity of myocardial repolarization, and that beta-blocker pretreatment may decrease the mortality risk during alcoholic withdrawal.
The enantiospecific procedure for assaying carvedilol includes the extraction of the drug from plasma or urine with diisopropylether after alkalization of the sample with pH 9.8 buffer. After evaporation of the org. solvent a chiral derivatization is performed using S-(+)-naproxen chloride. The HPLC separation of the diastereomeric amides is possible on a silica gel stationary phase with a mixture of n-hexane, dichloromethane, and ethanol as mobile phase. Detection of the products is performed by fluorescence measurement at 285/355 nm. Preliminary pharmacokinetic studies after i.v. infusion of racemic compound to healthy volunteers showed that the concentrations of the R-(+)-enantiomer exceeded those of the S-(-)-enantiomer. Overall, both carvedilol enantiomers exhibited a high clearance with preference for the S-enantiomer. The difference was even more expressed after p.o. dosage indicating a stereoselective first-pass effect with higher extraction of the levorotatory enantiomer, which is more potent with respect to beta-adrenoceptor antagonistic activity.
Coronary flow reserve (CFR) is the maximal increase in coronary blood flow (CBF) above its resting level for a given perfusion pressure when coronary vasculature is maximally dilated. Normally, hyperaemic CBF reaches values at least 2- to 3-fold greater than resting CBF. Reduction of CFR is mainly due to epicardial coronary artery stenosis or to coronary microvascular dysfunction. CFR can be determined by several techniques that measure CBF itself (e.g. positron emission tomography) or CBF velocities (Doppler methods) from which coronary flow velocity reserve is calculated. Hyperaemic coronary vasodilation can be obtained by pharmacological agents (e.g. adenosine and dipyridamole), but also by the cold pressure test. Long-term antihypertensive treatment induces significant improvement of CFR, which is parallel to the regression of left ventricular (LV) hypertrophy. First- and second-generation beta-adrenergic receptor antagonists (beta-blockers) have shown contradictory influences on CFR. This can be explained by the interaction of the effects on CBF at rest, generally reduced by these drugs, and after hyperaemia, when minimal coronary resistance appears to be either increased or reduced. Third-generation beta-blockers (e.g. carvedilol and nebivolol), which have vasodilating capacity, improve hyperaemic CBF. This occurs as a result of a reduction in minimal resistance, which can be attributed to alpha-adrenergic blockade and/or to a nitric oxide-mediated effect. This improvement is clearly beneficial in patients with coronary artery disease and indicates an improved coronary microvascular function. Changes of CFR due to vasodilating beta-blockers improve microvascular angina pectoris or silent ischaemia in patients without epicardial artery stenosis, and are also helpful in predicting the response or the further improvement of LV function to treatment.
coreg with alcohol
The proportion of patients with new AF episodes who were prescribed oral rate or rhythm control medications decreased modestly from 2002 through 2011. The use of digoxin decreased by >50%, and amiodarone decreased by 17%. Rate control remains the dominant strategy for treating new AF.
This study investigated the role of adrenergic receptor genetics on transplant-free survival in heart failure (HF).
To compare three stimuli which activate human neutrophils with different signal transduction mechanisms, in order to better localize the effect of the beta-adrenoceptor antagonist carvedilol (CARV) on superoxide generation (O2*-) and myeloperoxidase release (MPO). The effect of CARV [0.1-100 micromol/l] on O2*- generation and MPO release from isolated human neutrophils was studied after specific receptor activator N-formyl-methionyl-leucyl-phenylalanine (fMLP) and nonreceptor phorbol-12-myristate-13-acetate (PMA) and calcium ionophor (A23187) stimuli.
coreg normal dose
AT1-alpha1-receptor crosstalk, involving inositol phosphates, sensitizes HCMAs to alpha1-adrenoceptor agonists. Our results suggest that, in the presence of an increased sympathetic tone, carvedilol provides AT1 receptor blockade via its alpha1-adrenoceptor blocking effects. This could explain the favorable effects of carvedilol versus metoprolol.
coreg overdose death
Beta-blockers (BB) are under prescribed in elderly heart failure (HF) patients. We analysed predictors of BB treatment in relation to age in community patients seen at an HF clinic with nurse specialist support.
coreg generic carvedilol
Metastatic adenocarcinoma in bilateral cerebellopontine angles (CPA) is rare. We report a case and review the current literature in order to enhance recognition of metastatic adenocarcinoma in the cerebellopontine angle. A 44-year-old man was referred to the hospital with rightsided diminished hearing for 7 weeks, left-sided facial palsy for 2 weeks, and left-sided sensorineural hearing loss for 1 week. On Magnetic Resonance Imaging (MRI) two tumors in bilateral CPAs were detected. The left-sided tumor was resected and histopathological examination revealed an adenocarcinoma. Many investigations could not find the primary tumor. One should be careful with middle-aged or elderly patients with sudden progressive deficits in the VIII < sup > th < /sup > or VII < sup > th < /sup > cranial nerves, particularly in bilateral CPA.
This is the first study demonstrating that carvedilol blocks HERG potassium channels. The biophysical data presented in this study with a potentially antiarrhythmic effect may contribute to the positive outcome of clinical trials with carvedilol.
It is not surprising that there has been a search for compounds that combine two useful antihypertensive properties. The expectation is that one such product will offer a simple once-a-day control of blood pressure in a large portion of the population who require drug therapy for their disease. The major disadvantages of the first drug in this class, labetalol, are its poor and variable bioavailability, its relatively short duration of action, and its ability to produce postural hypotension. Attempts to improve the pharmacokinetic deficiencies have given rise to adimolol, which has a prolonged action of up to 90 h in single-dose studies. Of more immediate clinical interest are carvedilol, celiprolol, and dilevalol, each of which appear to have a different mechanism of producing vasodilation. Dilevalol, one of the four isomers of labetalol, is said to form approximately 25% of racemic labetalol. In the pithed rat, both labetalol and dilevalol behave as competitive nonselective beta-blocking drugs but dilevalol, unlike labetalol, shows weak alpha-blocking activity yet produces a dose-dependent fall that is blocked by propranolol, indicating that the drug has a vasodilator action presumably mediated by a beta 2-agonist effect on beta-adrenoceptors. The presence of beta 2-adrenoceptor agonism of this degree makes this drug extremely interesting. Possible advantages include the ability to produce falls in peripheral resistance without significant postural hypotension, and beneficial metabolic effects and effects on plasma lipids compared with traditional beta-adrenoceptor blocking agents that tend to raise blood sugars, interfere with insulin release, lower HDL levels, and raise LDL triglycerides.
The aim of this study was to synthesis the conjugated chitosan by covalent attachment of thiol moieties to the cationic polymer, mediated by a carbodiimide to improve permeation properties of chitosan. Thioglycolic acid was covalently attached to chitosan by the formation of amide bonds between the primary amino groups of the polymer and the carboxylic acid groups of thioglycolic acid. Hence, these polymers are called as thiomers or thiolated polymers. Conjugation of chitosan was confirmed by Fourier transform-infrared and differential scanning calorimetric analysis. Matrix type transdermal patches of carvedilol were prepared using the different proportions of chitosan and chitosan-thioglycolic acid conjugates (2:0, 1.7:0.3, 1.4:0.6, 1:1, 0.6:1.4 and 0.3:1.7) by solvent casting technique. Prepared matrix type patches were evaluated for their physicochemical characterization followed by in vitro evaluation. Selected formulations were subjected for their ex vivo studies on Wistar albino rat skin and human cadaver skin using the modified Franz diffusion cell. As the proportion of conjugated chitosan increased, the transdermal patches showed increased drug permeation. The mechanism of drug release was found to be nonFickian profiles. The present study concludes that the transdermal patches of carvedilol using conjugated chitosan with different proportions of chitosan were successfully developed to provide improved drug permeation. The transdermal patches can be a good approach to improve drug bioavailability by bypassing the extensive hepatic first-pass metabolism of the drug.
normal coreg dosage
Plasma N-BNP and adrenomedullin were measured in 297 patients with chronic ischemic (LV) dysfunction before randomization to carvedilol or placebo, added to established treatment with a converting enzyme inhibitor and loop diuretic (with or without digoxin). The patients' clinical outcomes, induding mortality and heart failure events, were recorded for 18 months.
coreg 5 mg
Although patient characteristics and outcomes differed between users of non-benefit and benefit drugs, misclassification of drug exposure did not meaningfully bias estimates of all-cause mortality and hospitalization after covariate adjustment in our study.
carvedilol coreg dosage
Heart failure (HF) is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricles to fill with or eject blood. The approach to pharmacologic treatment has become a combined preventive and symptomatic management strategy. Ideally, treatment should be initiated in patients at risk, preventing disease progression. In patients who have progressed to symptomatic left ventricular dysfunction, certain therapies have been demonstrated to improve survival, decrease hospitalizations, and reduce symptoms. The mainstay therapies are angiotensin-converting enzyme (ACE) inhibitors and beta-blockers (bisoprolol, carvedilol, and metoprolol XL/CR), with diuretics to control fluid balance. In patients who cannot tolerate ACE inhibitors because of angioedema or severe cough, valsartan can be substituted. Valsartan should not be added in patients already taking an ACE inhibitor and a beta-blocker. Spironolactone is recommended in patients who have New York Heart Association (NYHA) class III to IV symptoms despite maximal therapies with ACE inhibitors, beta-blockers, diuretics, and digoxin. Low-dose digoxin, yielding a serum concentration <1 ng/mL can be added to improve symptoms and, possibly, mortality. The combination of hydralazine and isosorbide dinitrate might be useful in patients (especially in African Americans) who cannot tolerate ACE inhibitors or valsartan because of hypotension or renal dysfunction. Calcium antagonists, with the exception of amlodipine, oral or intravenous inotropes, and vasodilators, should be avoided in HF with reduced systolic function. Amiodarone should be used only if patients have a history of sudden death, or a history of ventricular fibrillation or sustained ventricular tachycardia, and should be used in conjunction with an implantable defibrillator [corrected]. Finally, anticoagulation is recommended only in patients who have concomitant atrial fibrillation or a previous history of cerebral or systemic emboli.
coreg 25 mg
The aim of a multicenter, randomized open trial (the Diastolic Heart Failure Assessment Study in Tohoku District, DIAST) is to evaluate the safety and prognostic efficacy of the multiple action non-selective beta-blocker carvedilol in 160 patients with DHF (left-ventricular ejection fraction > or =50%). The target dose of carvedilol is 10 mg twice a day and the mean follow-up is estimated to be 2 years. The primary endpoints are to evaluate (1) all-cause mortality or hospitalization, (2) cardiovascular mortality or hospitalization and (3) worsening heart failure. The secondary endpoints are to assess (1) cardiovascular events, (2) the individual components of the above combined endpoints, (3) the duration of hospitalization, (4) the functional class and exercise capacity and (5) the safety and tolerability. All patients' data are processed using an original registration system on an internet homepage. Several substudies to assess neurohumoral factors, heart rate variability, oxidative stress and sleep apnea will clarify the pathophysiology of DHF.
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The validated method is successfully applied to determine propranolol, metoprolol and carvedilol in human urine samples obtained from the patients who received these drugs.
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A 109-year-old woman was hospitalized with myocardial infarction in the geriatric long-term care ward of our hospital. Her medical history was unknown, and she was receiving only peroral 20 mg/day furosemide. Her medical records at another hospital revealed that she had been given a previous diagnosis of myocardial infarction of the anteroseptal wall of the left ventricle by a cardiovascular specialist approximately 10 years previously. Although treatment with cardiovascular drugs such as an angiotensin II receptor blocker, aspirin, and spironolactone had been started, it was discontinued because of her hospital transfer and change in her attending physician. Because of aggravation of the symptoms of cardiac failure caused by infection, treatment with the angiotensin-converting enzyme inhibitor temocapril (1 mg/day), spironolactone (12.5 mg/day), aspirin (100 mg/day), and a beta-adrenoceptor blocker carvedilol (2 mg/day) was tentatively initiated. Consequently, her B-type natriuretic peptide (BNP) level improved and her condition stabilized. She finally died of old age. Both inappropriate sharing of patient information among medical facilities and restrictions on medical care in Japanese health care system for the elderly may lead to improper and/or inadequate medical treatment for elderly patients. Although little evidence is available to support medical care for centenarians, treatment which is based on a thorough understanding of their physiological characteristics enables us to improve their quality of life.
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The VE/Vco(2) slope was lower in carvedilol- compared with bisoprolol-treated patients (29.7 +/- 0.4 vs 31.6 +/- 0.5, P = .023, peak oxygen consumption adjusted) and with patients not receiving beta-blockers (31.6 +/- 0.7, P = .036). Maximum end-tidal CO(2) pressure during the isocapnic buffering period was higher in patients treated with carvedilol (39.0 +/- 0.3 mm Hg) than with bisoprolol (37.2 +/- 0.4 mm Hg, P < .001) and in patients not receiving beta-blockers (37.2 +/- 0.5 mm Hg, P = .001).