Ventilatory effects of long‐term treatment with pindolol and metoprolol in hypertensive patients with chronic obstructive lung disease.

Lammers, J.-W. J.; Folgering, H.T.M.; Herwaarden, C.L.A. van

doi:10.1111/j.1365-2125.1985.tb05062.x

Cited by 33 publications

(15 citation statements)

References 13 publications

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“…Medical subject heading (MeSH) terms "respiratory tract diseases" and "adrenergic beta-antagonists" yielded 227 studies, 18 of which addressed the review objectives (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Key word searches "chronic obstructive lung disease" and "beta adrenergic receptor blocking agent" or "[beta-blocker name]" identified 2 further studies (23,24).…”

Section: Methodsmentioning

confidence: 99%

Heart Failure and Chronic Obstructive Pulmonary Disease

Hawkins¹,

Petrie²,

MacDonald³

et al. 2011

Journal of the American College of Cardiology

129

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The combination of heart failure and chronic obstructive pulmonary disease presents many therapeutic challenges. The cornerstones of therapy are beta-blockers and beta-agonists, respectively. Their pharmacological effects are diametrically opposed, and each is purported to adversely affect the alternative condition. The tolerability of beta-blockade in patients with mild and fixed airflow obstruction likely extends to those with more severe disease. However, the evidence is rudimentary. The long-term influence of beta-blockade on pulmonary function, symptoms, and quality of life is unclear. Low-dose initiation and gradual up-titration of cardioselective beta-blockers is currently recommended. Robust clinical trials are needed to provide the answers that may finally allay physicians' mistrust of beta-blockers in patients with chronic obstructive pulmonary disease. Beta-agonists are associated with incident heart failure in patients with pulmonary disease and with increased mortality and hospitalization in those with existing heart failure. These purported adverse effects require further investigation. In the meantime, clinicians should consider carefully the etiology of dyspnea and obtain objective evidence of airflow obstruction before prescribing beta-agonists to patients with heart failure.

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Section: Methodsmentioning

confidence: 99%

Heart Failure and Chronic Obstructive Pulmonary Disease

Hawkins¹,

Petrie²,

MacDonald³

et al. 2011

Journal of the American College of Cardiology

129

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“…It has been suggested that non-selective beta blockers with ISA may be preferable to other nonselective antagonists in patients with bronchial obstruction and may behave as though beta1 selective [19][20][21][22]. However, beta blockers with ISA may inhibit the access of betae-agonist bronchoditator drugs to the respirator5, beta receptors, thus inhibiting their effects [23][24][25].…”

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confidence: 99%

Comparative effects of celiprolol, propranolol, oxprenolol, and atenolol on respiratory function in hypertensive patients with chronic obstructive lung disease

Fogari

Zoppi

Tettamanti

et al. 1990

Cardiovasc Drug Ther

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The aim of the study was to compare the pulmonary effects of four beta-blockers with different ancillary properties: propranolol (non-beta 1 selective without ISA), oxprenolol (non-beta 1 selective with ISA), atenolol (beta 1 selective), and celipropol (beta 1 selective with mild beta 2-agonist and alpha 2-antagonist activity) in hypertensive patients with chronic obstructive lung disease. Ten asthmatic patients, all males, aged 50-66 years were studied. Entry criteria were a) DBP greater than or equal to 95 mmHg and less than or equal to 115 mmHg; b) FEV1 less than 70% of the theoretical values; c) FEV1 increase of at least 20% after salbutamol inhalation (200 micrograms). After a 2-week washout period on placebo, each patient received propranolol (80 mg/day), oxprenolol (80 mg/day), atenolol (100 mg/day), and celiprolol (200 mg/day) for 1 week, according to a randomized, cross-over design. At the end of the washout and of each treatment period, airway function, assessed by FEV1, FVC, and FEV1%, was evaluated by spirometry both in the basal condition and after salbutamol inhalation. Unlike propranolol and oxprenolol, which significantly reduced FEV1 and inhibited the bronchodilator response to inhaled salbutamol, atenolol and celiprolol did not significantly affect respiratory function and did not antagonize salbutamol effects. Celiprolol more closely approached placebo in its respiratory effects than did atenolol, although the differences were not statistically significant.

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“…When a β-adrenoceptor blocker is really necessary in hypertensive patients with COPD (for instance, in the presence of myocardial infarction, congestive heart failure, cardiac arrhythmia, and thyrotoxicosis), a β 1 -adrenoceptor-selective blocker is preferred in combination with bronchodilator agents [6, 12]. In fact, the available evidence suggests that cardioselective β-blockers given to patients with COPD do not produce a significant short-term reduction in airway function or in the occurrence of COPD exacerbations [13].…”

Section: Discussionmentioning

confidence: 99%

Comparative Effects of a Two-Week Treatment with Nebivolol and Nifedipine in Hypertensive Patients Suffering from COPD

Cazzola

Matera²,

Ruggeri

et al. 2004

Respiration

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Background: It has been suggested that the antihypertensive agent nebivolol, a β₁-adrenoceptor-blocking agent that modulates the endogenous production of nitric oxide, is preferable to ‘conventional’ β₁-blockers in hypertensive patients with airway dysfunction. Objectives: Since β₁-blockade by nebivolol is larger after repeated dosing than after a single oral intake, we have explored its effect on pulmonary function after a 2-week treatment in hypertensive patients with mild to moderate COPD. Methods: A single-blind crossover design was used. Twenty patients with COPD as selected above and with a diastolic blood pressure of 95–110 mm Hg after 1 week of placebo run-in were entered into the two 2-week active treatment periods with either 5 mg nebivolol (n = 10) or 30 mg nifedipine gastrointestinal-transport-system (GITS) (n = 10) taken for a period of 2 weeks. After a further 1-week washout, subjects were crossed-over to receive the other drug for 2 additional weeks. At each visit, changes in spirometric indexes and the interaction with the bronchodilator effect of salbutamol were investigated. Moreover, systolic and diastolic blood pressure (BP) together with heart rate were manually measured in order to evaluate the cardiovascular effects of the different treatments. Throughout the study, patients recorded symptoms. Results: Similar and significant reductions in systolic and diastolic BP were observed with both treatments. The impact of nifedipine on FEV₁ was not significant (p > 0.05), while that of nebivolol was slight. The maximum response to salbutamol was slightly decreased with either nebivolol or nifedipine GITS. Day-to-day airway obstruction control, interpreted from patient recordings of symptom scores and inhaler use, was similar with both treatments. Conclusions: Our pilot study suggests that the use of nebivolol in hypertensive patients with stable mild to moderate COPD was safe during a 2-week trial. Evaluation of longer time periods, larger patient numbers with more severe COPD or during exacerbations is warranted.

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Ventilatory effects of long‐term treatment with pindolol and metoprolol in hypertensive patients with chronic obstructive lung disease.

Cited by 33 publications

References 13 publications

Heart Failure and Chronic Obstructive Pulmonary Disease

Heart Failure and Chronic Obstructive Pulmonary Disease

Comparative effects of celiprolol, propranolol, oxprenolol, and atenolol on respiratory function in hypertensive patients with chronic obstructive lung disease

Comparative Effects of a Two-Week Treatment with Nebivolol and Nifedipine in Hypertensive Patients Suffering from COPD

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