Carvedilol in the failing heart

Lombardi, William; Gilbert, Edward M.

doi:10.1002/clc.4960241202

Cited by 10 publications

(3 citation statements)

References 61 publications

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“…This property does not result from a direct effect on PTP (these drugs are not specific inhibitors of PTP opening unlike CsA) but might partly contribute to the anti-ischaemic effects of these drugs. This is the case for the anaesthetic propofol that is frequently used for cardiac surgery [15,137] or the β-adrenoceptor blocking agent carvedilol (Coreg™, Roche Biosciences) [138,139].…”

Section: Permeability Transition Porementioning

confidence: 99%

Prevention of cell damage in ischaemia: novel molecular targets in mitochondria

Morin¹,

Papadopoulos²,

Tillement³

2002

Expert Opinion on Therapeutic Targets

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Ischaemia results in a decrease of blood supply to an organ. It may be sudden or progressive, partial or complete. In any case, the lack of oxygen induces a decrease in ATP generation followed by a reduction of cellular energy-dependent processes. When ischaemia is followed by a reperfusion, the efflux of oxygen in an anoxied organ promotes an excess of reactive oxygen species (ROS) generation, which impairs the restoration of ATP synthesis. Both effects induce cellular alterations that can lead to cell death in both necrotic and apoptotic forms. As ATP synthesis and ROS generation both occur in mitochondria, they are obvious targets for pharmacological interventions aiming to prevent or block deleterious effects induced by a lack of oxygen. Different approaches may be used according to the state of the pathological process under investigation. In general, prevention of the ischaemic process is more successful than the cure of the following reperfusion state. This review summarises pharmacological strategies designed to improve cellular protection before or during ischaemia-reperfusion acting via the mitochondria and highlights promising new mitochondrial targets to be considered for future therapies.

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Section: Permeability Transition Porementioning

confidence: 99%

Prevention of cell damage in ischaemia: novel molecular targets in mitochondria

Morin¹,

Papadopoulos²,

Tillement³

2002

Expert Opinion on Therapeutic Targets

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“…Phase II trials of β-blockers, typically lasting 3–6 months, demonstrated that β-blocker treatment in heart failure results in improvements in right heart hemodynamics, reversal of ventricular remodeling (as evidenced by reductions in left ventricular volumes, increases in right and left ventricular ejection fraction, decreases in left ventricular mass and favorable effects upon left ventricular geometry), and improvements in heart failure symptoms [46]. Prospective, randomized, placebo-controlled outcome trials of carvedilol, bisoprolol and metoprolol succinate in heart failure have shown significant reductions in mortality and hospitalizations, as well as an improvement in patient well-being [47,48,49,50].…”

Section: Effects Of β-Blocker Therapy In Heart Failurementioning

confidence: 99%

Beta-Adrenergic Receptors, from Their Discovery and Characterization through Their Manipulation to Beneficial Clinical Application

Wachter

Gilbert²

2012

Cardiology

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118

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β-Adrenergic receptors (β-AR) are central to the overall regulation of cardiac function. From the first proposed receptor/transmitter concept to the latest clinical β-blocker trials β-AR have been shown to play an important role in cardiac disease and heart failure in particular. This study provides a historical perspective, reviews the latest discoveries and beliefs, and discusses the current clinical practices of β-AR and their modulation with their associated guanine-nucleotide regulatory protein/adenylylcyclasesignal transduction pathways.

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“…P hase II trials of b-blockers, typically lasting 3 to 6 months, demonstrated that b-blocker treatment in patients with heart failure (HF) results in improvements in right heart hemodynamics, reversal of ventricular remodeling (as evidenced by reductions in left ventricular [LV] volumes, increases in right and LV ejection fraction (LVEF), decrease in LV mass, and favorable effects on LV geometry), and improvements in HF symptoms. 1 Prospective, randomized, placebo-controlled outcomes trials of carvedilol, bisoprolol, and metoprolol succinate in HF patients have shown significant reductions in mortality and hospitalizations, as well as an improvement in patient wellbeing. [2][3][4][5] Premature termination of these trials because of the superior efficacy of these agents compared with placebo limited the duration of post-trial followup to <18 months (US Carvedilol Heart Failure Study, 2 5 10.4 months).…”

mentioning

confidence: 99%

Carvedilol Produces Sustained Long‐Term Benefits: Follow‐Up at 12 Years

MacGregor

Wachter²,

Munger³

et al. 2009

Congestive Heart Failure

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The authors measured long-term outcomes of patients who initiated carvedilol between 1990 and 1992 to test the hypothesis that carvedilol produces sustained benefits in heart failure patients. The study population consisted of 57 patients who completed a carvedilol placebo-controlled phase II trial. Patients were given open-label carvedilol and were titrated to the maximum dose. Patients were assessed by serial multigated acquisition, echocardiography, and symptom scores. Survival was assessed for all patients and censored as of January 1, 2004. Survival for ischemic vs nonischemic patients was compared using the log-rank test and further compared using Cox regression, controlling for covariates. Etiology of heart failure was ischemic in 15 patients and nonischemic in 42 patients. Median follow-up was 12.9 years. Resting left ventricular ejection fraction (LVEF) and heart failure symptom scores improved at 4 months of treatment and were sustained at 24 months. Left ventricular internal diameter in systole (LVIDS) and left ventricular internal diameter in diastole decreased significantly at 4 and 8 months, respectively, and LVIDS continued to improve at 24 months. Overall mortality was 43% in nonischemic patients and 73% in ischemic patients. In a multivariate analysis, ischemic etiology and baseline LVEF were significant predictors of mortality. Carvedilol produces sustained improvements in left ventricular remodeling and symptoms. Long-term survival is good, particularly in nonischemic patients.

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Carvedilol in the failing heart

Cited by 10 publications

References 61 publications

Prevention of cell damage in ischaemia: novel molecular targets in mitochondria

Prevention of cell damage in ischaemia: novel molecular targets in mitochondria

Beta-Adrenergic Receptors, from Their Discovery and Characterization through Their Manipulation to Beneficial Clinical Application

Carvedilol Produces Sustained Long‐Term Benefits: Follow‐Up at 12 Years

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