3,959 research outputs found
Anion-channel blockade with alinidine: a specific bradycardic drug for coronary heart disease without negative inotropic activity
In 14 patients undergoing cardiac catheterization for suspected coronary artery disease, alinidine, 0.6 mg/kg, was administered intravenously to determine its effects on left ventricular (LV) function, coronary blood flow and myocardial oxygen consumption. To assess effects independent of changes in heart rate (HR), measurements were made at spontaneous and matched pacing HRs. At spontaneous HR, alinidine decreased HR from 70 +/- 2 to 61 +/- 3 beats/min (p less than 10(-6]. Peak rate of LV pressure decreased from 1,652 +/- 92 to 1,371 +/- 80 mm Hg/s (p less than 10(-5] and Vmax decreased from 47 +/- 3 to 41 +/- 2 s-1 (p less than 10(-4]. Coronary sinus blood flow decreased from 109 +/- 9 to 89 +/- 7 ml/min (p less than 0.01) and myocardial oxygen consumption from 10.9 +/- 1.0 to 9.0 +/- 0.8 ml O2/min (p less than 0.05). At a matched pacing HR of 98 +/- 3 beats/min before and after alinidine administration, peak rate of LV pressure decreased from 1,984 +/- 124 to 1,793 +/- 106 mm Hg/s (p less than 10(-4] and Vmax from 60 +/- 5 to 56 +/- 4 s-1 (p less than 0.02). Coronary sinus blood flow and myocardial oxygen consumption were not significantly changed at matched pacing HRs. The time constant of the first 40 ms of LV isovolumic relaxation was prolonged by alinidine only during spontaneous HR. Thus, alinidine results in a bradycardia-dependent decrease in myocardial oxygen consumption. It has negative inotropic properties independent of changes in HR and so is not a pure bradycardia-specific agent
Frontiers in interventional cardiology
n more than 20 years since the first percutaneous coronary revascularization procedures, the field of interventional cardiology has proliferated beyond all expectations. Now more than 1 million procedures are performed worldwide each year. Stenting has revolutionized the field, which previously relied on balloon dilatation in the majority of patients. With 50% of patients now undergoing stent implantation, the groundwork is laid for further important advances. In this article, we discuss the 4 most important new advances in the field of interventional cardiology: platelet inhibition, prevention of restenosis, stent evolution, and angiogenesis
Drug-eluting stents: current issues
Early stent thrombosis occurs in about 1% to 1.5% of patients with drug-eluting stents, very similar to the rate with bare-metal stents. Late stent thrombosis is more of a concern with drug-eluting stents, with an incidence of at least 0.35%. I would urge caution if you feel you have to stop antiplatelet therapy in patients with drug-eluting stents. While neointima formation peaks at 6 months and then may actually regress with bare-metal stents, it continues to grow with drug-eluting stents--although this process appears to plateau by 4 years with sirolimus. With the others, we have to wait and see. We still don't know the best drug-eluting stent. Trials are under way to compare stents with surgery, and the future brings the arrival of a number of exciting new devices and approaches that are now entering clinical trials
Intracoronary Blood Flow Velocity and Transstenotic Pressure Drop in an Awake Human Being During Coronary Vasodilation
The pressure drop over a coronary stenosis and the intracoronary Doppler blood flow velocity were measured at rest and during coronary vasodilation. We report the first observation that confirms the validity of fluid dynamic equations to describe the hemodynamics of a coronary stenosis based on quantitative arteriography in a human being. (J Interven Cardiol 1988:1:1) Copyrigh
Who was thrombogenic: the stent or the doctor?
In 1986, when pioneers such as Jacques Puel and Ulrich Sigwart implanted the first coronary Wallstents, no guidelines were available to determine the treatment after stenting. From the experience acquired with mechanical prosthetic heart valves, it was inferred that chronic anticoagulation with coumarins was indicated. When the first cases of subacute occlusion were encountered, the anticoagulation regimen was further reinforced. The use of heparin, dextran, or thrombolytic agents during the procedure followed by warfarin, aspirin, sulphinpyrazone, and dipyridamole did not eliminate subacute thrombosis, which occurred in 18% of the first 117 stents implanted and was responsible for a higher incidence of hemorrhagic complications and prolonged hospital stay
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