Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to assess the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease (CAD) by programmed stimulation. Sixteen inpatients subjected to an electrophysiological investigation because of dizziness or palpitations were given 10 mg of intravenous bisoprolol after basal measurement and were checked again 15 and 45 min after infusion. Eight patients with CAD (seven males and one female; mean age of 60+/-4 years) and eight patients without CAD (five males and three females; mean age of 59+/-4 years) were investigated after washout of prior antiarrhythmic drugs. For coronary patients, the CAD was documented by a history of myocardial infarction or by a confirmatory coronary arteriography. Main outcome measures were parameters of invasive electrophysiological exploration, with measurement of conduction intervals at rest and during pacing and of refractory periods by means of extrastimulus technique. No significant difference was noted at baseline between the two groups except for CSNRT. After infusion of 10 mg of bisoprolol, with the exception of CSNRT (increased in the group without CAD), no significant differences were noted on comparison between coronary and noncoronary patients. Bisoprolol significantly increased the sinus cycle length, SACT, and FRP of the atria. Regarding atrioventricular nodal conduction, bisoprolol significantly increased the AH 100, ERP, and FRP and significantly decreased the Wenckebach point. In the right ventricle, bisoprolol moderately, but significantly, decreased the corrected QT and induced a small, temporary, significant increase in ERP. Bisoprolol appears to be a very potent beta-blocker that is well tolerated at an intravenous dose of 10 mg. Its depressant effects concern mainly the atrial function and the nodal conduction, without significant differences between the two groups of patients. The decrease in QTc may be a favorable aspect regarding its electrophysiologic tolerance especially in the acute phase of myocardial infarction.
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PMID:Study of the electrophysiological properties of intravenous bisoprolol in patients with and without coronary artery disease by programmed stimulation. 1152 22

Bisoprolol is a highly selective beta(1)-adrenoceptor antagonist. Administration of bisoprolol to patients with chronic heart failure is associated with increases in left ventricular function and reductions in heart rate; increases in heart rate variability are also seen. Two major randomised, double-blind, placebo-controlled, multicentre trials have examined the clinical efficacy of bisoprolol in combination with ACE inhibitors and diuretics in patients with stable chronic heart failure (New York Heart Association class III or IV): the Cardiac Insufficiency Bisoprolol Study (CIBIS; n = 641) and CIBIS II (n = 2 647). All-cause mortality (primary endpoint) was significantly lower in bisoprolol than in placebo recipients in CIBIS II (11.8 vs 17.3%) and was reduced by bisoprolol regardless of dosage. All-cause mortality was also lower in CIBIS (16.6 vs 20.9%) although the difference did not achieve statistical significance. In a meta-analysis of CIBIS and CIBIS II (n = 3 288), a relative reduction of 29% in the incidence of all-cause mortality was seen in bisoprolol versus placebo recipients; this analysis also demonstrated that bisoprolol reduces mortality in patients with chronic heart failure regardless of aetiology or severity. In CIBIS II, there were significantly fewer cardiovascular deaths, admissions to hospital for any reason, or cardiovascular deaths or cardiovascular hospitalisations (combined endpoint) in bisoprolol, compared with placebo, recipients (secondary endpoints). Compared with standard treatment alone, the addition of bisoprolol was a cost-effective option in chronic heart failure in UK, French, German and Swedish pharmacoeconomic studies. Bisoprolol is generally well tolerated in patients with chronic heart failure. In CIBIS II, adverse events occurring more commonly in bisoprolol than placebo recipients, regardless of causal relationship with the study medication, included dizziness, bradycardia, hypotension and fatigue. Bisoprolol recipients were less likely than placebo recipients to experience worsening of heart failure, dyspnoea or tachycardia. In both CIBIS and CIBIS II there was no significant difference between bisoprolol and placebo recipients in the incidence of permanent treatment withdrawal. In conclusion, adding the highly selective beta(1)-blocker bisoprolol to a treatment regimen comprising an ACE inhibitor and a diuretic significantly improves survival in patients with stable chronic heart failure and reduces the need for hospitalisation. The use of bisoprolol in this disorder is generally well tolerated and is cost effective. Thus, bisoprolol should be considered a standard treatment option when selecting a beta-blocker for use in combination with ACE inhibitors and diuretics in patients with stable, moderate to severe chronic heart failure.
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PMID:Bisoprolol: a review of its use in chronic heart failure. 1246 13

The life-time risk of developing HF is about 20% (40% if hypertension present). With increasing longevity in the developed world the burden of HF (hospitalisation) is set to increase over the next 10-20 years. CAD and hypertension are the two main causes of HF; CAD (and obesity) in the case of systolic HF and hypertension in the case of diastolic HF (mainly in the elderly). BB have become the corner-stone (alongside ACE-inhibitors) in the treatment of systolic HF. Bisoprolol, metoprolol and carvedilol (on an ACE-inhibitor background) have reduced all-cause death by 34-5%. The presence of intrinsic sympathomemetic activity (xamoterol, bucindolol, nebivolol) diminishes efficacy in the treatment of systolic HF. First-line bisoprolol has proved "non-inferior" to first-line enalapril in reducing all-cause death and is probably superior in reducing sudden death. The main mode of action of BB in treating systolic HF is inhibition of chronic beta-1 stimulation-induced myocardial apoptosis/necrosis/inflammation. The combination of pure beta-1 blockade (low-dose bisoprolol) and pure beta-2 blockade (clenbuterol) may prove invaluable in the treatment of end-stage systolic HF (thus avoiding cardiac transplantation). The appropriate treatment of diastolic HF has yet to be determined. Beta-blockade is effective in the prevention of HF i) in the post-MI period and ii) as first-line agents in the treatment of young/middle-aged hypertension and as second-line agents (to first-line diuretics) in the treatment of elderly systolic hypertension. BB are highly effective in reversing LVH in young/middle-aged hypertensives (LVH pre-disposes to HF in young/middle-aged hypertension) and are (bisoprolol) at least as good as ACE-inhibitors. Choice of BB is important as benefit is not a class-effect. ISA (xamoterol, bucindolol, nebivolol) markedly diminishes efficacy. The choice is between bisoprolol, metoprolol succinate and carvedilol for optimal efficacy. Adverse reactions are associated, mainly, with beta-2 blockade and alpha-blockade. Thus non-selective (e.g. propranolol) or modestly beta-1 selective (e.g. metoprolol, atenolol) are associated with metabolic disturbance, bronchospasm, epinephrine/hypertensive interaction (with cigarette-smoking or insulin-induced hypoglycaemia), while the possession of alpha-blocking activity (e.g. carvedilol) is associated with dizziness and postural hypotension. The possession of beta-2 blockade, particularly if combined with alpha-blockade, is associated with an increased occurrence of sexual dysfunction. Lipophilic BB like propranolol and metoprolol appear in high concentrations in human brain tissue and are associated with side-effects such as insomnia, dreams and nightmares.
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PMID:Beta-blockers and heart failure. 2118 Feb 98