ABSTRACT
Antithrombotic therapy in acute coronary syndrome without ST-segment elevation should be initiated with aspirin 100 mg/day (loading dose 250-500 mg) and Clopidogrel 75 mg/day (loading dose 300 mg). In addition, anticoagulation with unfractionated heparin or low molecular weight heparin should be started. A GP IIb/IIIa receptor blocker can be given either upfront (Eptifibatide/Tirofiban) or directly in the cathlab preceding PCI (Abciximab). Aspirin should be given in the chronic phase lifelong, Clopidogrel for at least nine months. An invasive strategy is recommended in high-risk patients within 48 hours.
Subject(s)
Angina, Unstable/diagnosis , Angina, Unstable/therapy , Anticoagulants/therapeutic use , Coronary Disease/diagnosis , Coronary Disease/therapy , Fibrinolytic Agents/therapeutic use , Myocardial Infarction/diagnosis , Myocardial Infarction/therapy , Acute Disease , Angina, Unstable/drug therapy , Angina, Unstable/surgery , Coronary Disease/drug therapy , Coronary Disease/surgery , Decision Support Techniques , Humans , Myocardial Infarction/drug therapy , Myocardial Infarction/surgery , Patient Care Management/methods , Practice Patterns, Physicians' , Risk Assessment/methods , Syndrome , Treatment OutcomeABSTRACT
BACKGROUND: Various functional polymorphisms of the cholesteryl ester transfer protein ( CETP) gene influence CETP activity and the concentration of high-density lipoprotein (HDL) cholesterol. Beside other functional variants mainly the promoter polymorphism CETP/C-629A is currently discussed as a risk factor of coronary artery disease (CAD). We evaluated in a large case-control study the impact of various CETP genotypes and haplotypes on HDL concentration and the prevalence of CAD. METHODS AND RESULTS: In 1214 patients with documented CAD as well as 754 population controls we determined the CETP/C-629A, TaqIB, I405V, R451Q, and A373P polymorphisms. All genotypes have an impact on the HDL concentration; univariate genotype and haplotype analyses demonstrate a significant effect of A-allel carriers on the elevation of HDL concentration. In addition, among all genotypes determined, the C-629A polymorphism is associated with the prevalence of CAD in a codominant fashion. Homozygous A-allel carriers reveal a relative risk of 0.6 (95% CI 0.44-0.82; P = 0.005) compared to the wild type. Adjustment for classical risk factors did not alter this association significantly, whereas after controlling for HDL concentration no independent significance between CETP/C-629A genotype and prevalence of CAD was observed anymore. CONCLUSION: CETP genotypes have an significant but moderate impact on systemic HDL-cholesterol concentration. The A-allel of the CETP/C-629A polymorphism is associated with a reduced CAD risk. This risk reduction is probably mediated by elevated HDL-concentration. Whether genotyping of the CETP/C-629A polymorphism provides information over and above that obtained by HDL-cholesterol measurement has to be further investigated in various prospective studies.
Subject(s)
Carrier Proteins/genetics , Cholesterol, HDL/blood , Cholesterol, HDL/genetics , Coronary Artery Disease/epidemiology , Coronary Artery Disease/genetics , Genetic Predisposition to Disease/epidemiology , Glycoproteins/genetics , Risk Assessment/methods , Case-Control Studies , Cholesterol Ester Transfer Proteins , Comorbidity , Coronary Artery Disease/blood , Female , Genetic Testing/methods , Genetic Variation , Humans , Male , Middle Aged , Phenotype , Polymorphism, Genetic , Prevalence , Risk FactorsABSTRACT
The most important symptoms in bradycardia are vertigo, dizziness and syncopy due to diminished cerebral blood sypply. Cardial symptoms are cardiac insufficiency and angina pectoris. By means of ECG, especially Holter-ECG, carotid sinus massage, atropin test and invasive methods (atrial stimulation, His-bundle ECG) sinu-nodal dysfunction, carotid sinus syndrome, bradyarrhythmia absoluta and AV-block can be diagnosed. Pharmacological treatment is only useful in acute situations. For symptomatic bradyarrhythmias the implantation of a Pacemaker is the therapy of choice. Individual treatment of the various types of bradyarrhythmia and the patients special needs is possible through the evolution of pacemaker technology.
