Support is provided for an approach to feeding vulnerable infants. Enhanced auditory assessment of infant feeding rhythms increases the responsiveness of the feeder and improves infant behavioral and physiological responses.
After beta-blockade, LVEF improved from 30% +/- 11% to 40% +/- 13%. In the whole population, independent predictors of deltaLVEF were nonischemic etiology, baseline LVEF (negative correlation), and baseline heart rate (positive correlation). In ischemic patients, independent predictors of deltaLVEF were absence of history of myocardial infarction, baseline heart rate, and baseline LVEF; whereas in nonischemic patients, independent predictors were baseline LVEF and baseline QRS width (negative correlation). After 1082 days of follow-up, there were 53 cardiovascular deaths and 2 urgent transplantations. Left ventricular ejection fraction improvement (defined as an absolute increase in LVEF > 5%) was an independent predictor of cardiac survival. Patients who had an LVEF < or = 45% after beta-blockade with a deltaLVEF < or = 5% represented a high-risk subgroup.
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To determine the effect of beta blockade on parasympathetic nervous system activity, we assessed RR variability during 24-hour Holter monitoring in 10 patients with congestive heart failure before and after 3 to 4 months of treatment with the beta blocker carvedilol. High-frequency power increased from 26 to 64 ms2, root-mean-square of successive differences in RR interval increased from 14.3 to 23.7 ms2, and percentage of absolute differences >50 ms between successive normal RR intervals increased from 0.8% to 4.7%, all p <0.01, indicating a substantial increase in parasympathetic modulation of RR intervals.
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A 66-year-old white man was referred to the cardiology pharmacotherapy clinic for difficult-to-treat hypertension. His initial office blood pressure (BP) was 152/71 mm Hg on diltiazem and chlorthalidone. After a series of medication adjustments based on serial PRA measurements, the patient achieved his target BP with a regimen that included 3 anti-R angiotensin system medications: carvedilol, valsartan, and aliskiren.
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The clinical use of cisplatin is highly limited by its nephrotoxicity, which has been associated with mitochondrial dysfunction. We investigated the protective effect of carvedilol, an antihypertensive with strong antioxidant properties, against the nephrotoxicity induced by cisplatin in rats. Carvedilol was able to counteract the renal damage by preventing the mitochondrial dysfunction induced by cisplatin. The mitochondrial eletrochemical potential, calcium uptake, respiration and the phosphorylative capacity were preserved by the co-administration of carvedilol. The mechanism of protection probably does not involve alterations in the cellular and sub-cellular distribution of cisplatin. The study suggests that carvedilol is a potential drug for the adjuvant nephroprotective therapy during cisplatin chemotherapy.
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We studied 543 subjects (63% men; age 61.8 ± 14 years) prospectively enrolled in the Vanderbilt AF registry and managed with rate-control strategy. A "responder" displayed adequate ventricular rate control based on the AFFIRM (Atrial Fibrillation Follow-Up Investigation of Rhythm Management) criteria: average heart rate (HR) at rest ≤80 beats/min; and maximum HR during a 6-min walk test ≤110 beats/min or average HR during 24-h Holter ≤100 beats/min.
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The buccal region offers an attractive route of administration for systemic drug delivery. Carvedilol (dose, 3.125-25 mg) is beta-adrenergic antagonist. Its oral bioavailability is 25-35% because of first pass metabolism. Buccal absorption studies of a carvedilol solution in human volunteers showed 32.86% drug absorption. FTIR and UV spectroscopic methods revealed that there was no interaction between carvedilol and polymers. Carvedilol patches were prepared using HPMC, carbopol 934, eudragit RS 100, and ethylcellulose. The patches were evaluated for their thickness uniformity, folding endurance, weight uniformity, content uniformity, swelling behaviour, tensile strength, and surface pH. In vitro release studies were conducted for carvedilol-loaded patches in phosphate buffer (pH, 6.6) solution. Patches exhibited drug release in the range of 86.26 to 98.32% in 90 min. Data of in vitro release from patches were fit to different equations and kinetic models to explain release profiles. Kinetic models used were zero and first-order equations, Hixon-Crowell, Higuchi, and Korsmeyer-Peppas models. In vivo drug release studies in rabbits showed 90.85% of drug release from HPMC-carbopol patch while it was 74.63 to 88.02% within 90 min in human volunteers. Good correlation among in vitro release and in vivo release of carvedilol was observed.
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To identify the clinical and functional effects of carvedilol, focusing on diastolic function and mitral regurgitation variations.
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Out of 36 patients, 4 did not tolerate the drug and were dropped out. At 6.35 +/- 1 months, the daily dosage of carvedilol was 49.7 +/- 21 mg. The NYHA functional class improved from 1.52 +/- 0.67 to 1.29 +/- 0.53 (p = 0.017), the heart rate markedly diminished from 73.6 +/- 13.3 to 60.8 +/- 10.8 b/min (p < 0.001) and so did Ea (3.35 +/- 0.91 to 2.84 +/- 0.93, p = 0.001). Peripheral resistances and Ees did not change. Therefore, the decrease in the Ea/Ees ratio (2.61 +/- 0.78 vs 2.19 +/- 0.89, p = 0.004) and the related increase in left ventricular ejection fraction (28.8 +/- 5.68 vs 33.3 +/- 7.5%, p < 0.001) were due to the decrease in Ea, while Ees did not vary significantly. Moreover, the Ea reduction was related linearly to the decrease in heart rate (r = 0.46, p = 0.001). There was no change in diuretic or ACE-inhibitor dosing during carvedilol titration. At 14.7 +/- 2 months of follow-up, no further variation occurred, short of a trend toward a slight increase in Ees (1.38 +/- 0.49 to 1.58 +/- 0.65, p = 0.07).
In a single-center, prospective, double-blind, randomized, placebo-controlled study, 39 patients with idiopathic dilated cardiomyopathy were randomized to pentoxifylline 400 mg TID (n=20) or placebo (n=19) if they had a left ventricular ejection fraction <40% after 3 months of therapy with digoxin, ACE inhibitors, and carvedilol. Primary end points were New York Heart Association functional class, exercise tolerance, and left ventricular function. Patients were followed up for 6 months. Five patients died (3 in the placebo group). Patients treated with pentoxifylline had a significant improvement in functional class compared with the placebo group (P:=0.01), with an increment in exercise time from 9.5+/-5 to 12.3+/-6 minutes (P:=0.1). Left ventricular ejection fraction improved from 24+/-9% to 31+/-13%, P:=0.03, in the treatment group.
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Significant progress has been made in the last few years in the management of heart failure. In particular, several trials have given significant results. It has become apparent that heart failure may be prevented in some patients by treatment of risk factors such as coronary artery disease. Experience with angiotensin-converting enzyme (ACE) inhibitors has shown that the survival and symptomatic benefits do last in the long term, and confirm that they are the first-line treatment in heart failure. The results of a number of trials using the angiotensin receptor blockers (ARBs) candesartan, valsartan and losartan are presented and discussed. There is also some experience now in the use of candesartan for patients with heart failure and preserved left ventricular systolic function. The COMET trial compared the beta-blockers carvedilol and metoprolol tartrate, and suggests that there may be differences in clinical effect between beta-blockers. The selective aldosterone receptor blocker eplerenone was evaluated in the EPHESUS trial in post-MI patients with signs of heart failure. Based on these clinical trials, heart failure guidelines are now being updated.
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Thirty-four AA 30-70 years of age with T2DM and PMA despite ACEI therapy were randomized to receive carvedilol or metoprolol in addition to ACEI and any other concurrent therapy. Carvedilol/metoprolol dose was titrated to achieve blood pressure (BP) <130/80 mm Hg. UAE and brachial-artery reactivity were studied at baseline and 12 weeks. We analyzed the effects of addition of beta-blockers and whether there was any difference in response between the two beta-blockers.
Baseline demographic and clinical characteristics were similar in the three groups. The composite end point during follow-up was lower in the patients treated with nebivolol than those treated with metoprolol (14.5 vs. 31.5%; p = 0.03). However, event rates were similar between the patients treated with carvedilol and those treated with the metoprolol (20.3 vs. 31.5%, p > 0.05) and between the patients treated with nebivolol and carvedilol (14.5 vs. 20.3%, p > 0.05).
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A 47-year-old woman was admitted via emergency department due to dyspnea NYHA Fc II-III aggravated for 2 months after upper respiratory infection. Her height and body weight were 161 cm / 67 kg. Initial vital signs were 110/70 mmHg - 112 BPM - 24/min - 36.5°C. Chest PA showed cardiomegaly and pulmonary congestion (Figure 1). B-natriuretic peptide level was markedly increased (2002 pg/mL, normal range ≤ 100 pg/mL). The echocardiographic examination showed severely dilated LV cavity (61/72 mm) and severe LV systolic dysfunction (EF 28%) with normal left ventricular wall thickness (9/11 mm) (Figure 2). She was initially treated with dobutamine and parenteral diuretics. After hemodynamic stabilization with body weight reduction of 4 kg with heart failure medication with diuretics, ACE inhibitors and beta blocker (Carvedilol 3.125 mg bid), she was discharged. At the time of discharge, her blood pressure was 90/74 mmHg and pulse rate was 107 BPM.After 2 years of follow up, her left ventricular systolic function was completely normalized (24/46/73%). Left ventricular wall thickness showed mild hypertrophy (11/12 mm) but apical segments showed akinesia. (Figure 3 ECG and chest PA, Figure 4 Echocardiography). Her blood pressure was recovered to the normal range of 132/70 mmHg and pulse rate was 72 BPM. Her heart failure medication was carvedilol (6.25 mg twice daily) and losartan (100 mg once daily)After 1 year of follow up (Year 3), her blood pressure increased to hypertensive range (150/100 mmHg) and pulse rate was 84 BPM. Nifedipine GITS 30 mg was added to the heart failure medication. Diabetes mellitus was newly developed. Despite diet control, her blood glucose levels were continuously increased (HbA1C levels 7.2%), therefore, oral hypoglycemic agents were intensified with metformin and sitagliptin. As heart failure signs disappeared and glycemic control was difficult, beta blocker was discontinued and antihypertensive regimen was changed to singly pill combination of valsartan 160 mg / amlodipine 5 mg. During follow up, blood pressure control was marginal (136/84 mmHg) and pulse rate was high (86 BPM), so low dose pure beta-1 antagonist (bisoprolol 2.5 mg once daily) was added. Then her blood pressure and pulse rate remained stable (102/70 - 122/80, 72 - 84 BPM)However, for two years' follow up (Year 5), her glycemic levels were continuously aggravated (HbA1C levels 9.3%) despite intensive oral glycemic agent treatment (full dose metformin + sitagliptin + sulfonylurea). Blood pressure and pulse rate were continuously increased (152/88 mmHg, 104 BPM). Indapamide SR 1.5 mg once daily was added and beta blocker dose was increased (Carvedilol 25 mg twice daily). Echocardiographic evaluation showed normal left ventricular size and systolic function (25/47 mm, 72%). Left ventricular wall thickness (8/7 mm) and wall motion were normalized (Figure 5 and 6).After 2 year of follow up (Year 8), insulin treatment was started in endocrinology department because of failure of glycemic control with oral hypoglycemic agents (HbA1C 9.4% with full dose metformin + sitagliptin + sulfonylurea + pioglitazone). As blood pressure control was fair (114/80 mmHg, 84 BPM), carvedilol was discontinued due to hyperglycemia. Then blood pressure and pulse rate were increased to 144/86 mmHg -103 BPM.Incidentally, she was examined abdominal CT due to microscopic hematuria (3+) and found 7.0 x 6.9 cm sized lobulating mass in right adrenal gland suggesting pheochromocytoma. 24 hour urine metanephrine (> 20000 pg/mL, normal range 90 - 930 pg/mL) and normetanephrine (16877 pg/mL, normal range 100 - 230 pg/mL) levels were markedly elevated. Plasma renin activity (26.7 ng/mL/hr, normal range 1 - 2.5 ng/mL/hr) and aldosterone level (23.5 ng/dL, normal range 3 - 16.0) were also elevated. MRI showed 7.1 x 6.7 cm mass in right adrenal gland with good enhancement, internal cystic change and suspicious focal hemorrhage, consistent with pheochromocytoma (Figure 7).After sympathetic blockade with alpha agonist (Doxazosin), the mass was removed by unilateral adrenalectomy. Pathologic evaluated showed 6.5 × 6.0 × 5.5 cm of pheochromocytoma with moderate risk of malignancy (Figure 8 - 11).After surgical removal of pheochromocytoma (Year 9), diabetes mellitus was completely disappeared and blood pressure was controlled with single antihypertensive medication (Valsartan 80 mg once daily, 110/67mmHg - 90 BPM).
To investigate whether carvedilol is associated with improved survival compared with metoprolol succinate.
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In Japan, when pharmaceutical companies launch a new drug, they are obligated to conduct a post-marketing survey to evaluate the safety and efficacy of the drug in accordance with Good Post-Marketing Surveillance Practice under Article 14.4 (re-examination) of the Pharmaceutical Affairs Law at contracted medical institutions. We report the results of a drug use survey, which we conducted as a post-marketing survey.
In patients with left ventricular dysfunction after acute myocardial infarction treated with ACE inhibitors, carvedilol had a beneficial effect on ventricular remodeling, which may, in part, mediate the substantial clinical beneficial effects of carvedilol in this patient population.
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Autonomic assessment fidelity was significantly higher with the P&S Method as validated by comparison with previously known physiology of the cardiovascular system.
Although our study is underpowered, the findings suggest that carvedilol is probably not superior to EVL in preventing first variceal bleed in patients with viral cirrhosis.
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The primary outcome was a composite measure of heart failure outcomes in patients receiving carvedilol (low- and high-dose combined) vs placebo. Secondary efficacy variables included individual components of this composite, echocardiographic measures, and plasma b-type natriuretic peptide levels.
The natriuretic peptide (NP) system is one of the most important systems regulating blood pressure and body-fluid homeostasis. The biological activities of the system are determined by the NPs and the receptors, which are comprised of three subtypes: NP-AR and NP-BR related to biological activities and NP-CR related to the clearance of NP. We focused our studies on the receptor subtypes. In hypertensive rats (SHR-SP/Izm, DOCA/salt), NP-AR was upregulated and NP-CR was downregulated. The ACE inhibitor derapril, but not the Ca2+ blocker manidipine, normalized the upregulated NP-AR, but the effect was completely abolished by the bradykinin beta 2-receptor antagonist, suggesting that bradykinin regulates the vascular NP-AR. The AT1 antagonist TCV-116, but not manidipine, reversed the downregulated NP-CR. Ang II decreased NP-CR in cultured aortic smooth muscle cells. These results suggest that upregulation of NP-AR and downregulation of NP-CR with the increased plasma NPs counteract hypertension by enhancing the action of NP. A beta-blocker (carvedilol) potentiated the hypotensive action of NPs by increasing plasma NPs and enhancing the vascular response to NPs via downregulation of the vascular and lung NP-CR. The newly found mode of actions could be related to its anti-heart failure effect. In genetically hyperglycemic Wistar fatty rats, vascular NP-BR and NP-AR were upregulated. Since plasma ANP and vascular CNP were significantly increased, the local CNP/NP-BR system as well as the systemic ANP/NP-AR system may play an important role in counteracting vascular remodeling in diabetes mellitus. All these observations provide in vivo evidence for the pathophysiological significance of the receptor subtype of the NPs.
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Orthogonal ECG parameters and those of 24-h blood pressure monitoring (BPM) were examined before and after antihypertensive treatment with different drugs in 95 hypertensive patients aged 47 +/- 1 years. Of them, 14 patients received trandolapril+verapamil SR for 2 months, 13 patients--candesartan for 3 months, 25 patients--ramipril for 5 months, 26 patients--carvedilol for 4 months, 10 patients--atenolol for 8 months, 7 patients--doxasozine for 5 months.
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Fasting blood sugar and glucose tolerance tests were evaluated.
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ES was significantly decreased by beta-blocker therapy. According to the change in ES, DCM patients were classified into three groups, patients who improved, patients showing no change and patients who deteriorated. In the improvement and no-change groups, beta-blocker therapy induced a reduction in left ventricular dimensions and an associated increase in ejection fraction. However, in the deterioration group, left ventricular dimensions and ejection fraction were unchanged. There was a significant relationship between the change in left ventricular dimension at end-diastole and the change in ES.