ABSTRACT
The efficacy of coronary angioplasty in the treatment of acute myocardial infarction was assessed in a low volume centre. Between January 1994 and May 1999, 148 consecutive patients (mean age 59 years, 81% men) with acute myocardial infarction, admitted within 12 hours, were included in this retrospective analysis. On admission, 14% of patients were in cardiogenic shock. The average time between the onset of chest pain and arrival at hospital was 244 +/- 183 mins. Reperfusion (TIMI 3 flow) was obtained on average 111 +/- 60 mins after arrival at hospital and 81 mins after informing the on-call team. After angioplasty, residual stenosis < 50% was obtained in 91% of cases. TIMI 3 flow was obtained in 85% of cases (TIMI 2 + 3 in 93% of cases). Over the years, the delay before treatment decreased and the results of angioplasty improved. In the last 79 patients, residual stenosis < 50% was obtained in 95% of cases, TIMI 3 flow in 87% of cases (TIMI 2 + 3 in 97% of cases). The stenting rate increased from 16% before 1997 to 61% thereafter. The hospital mortality was 4%. Direct or salvage angioplasty in the first 12 hours of myocardial infarction in some low volume centres may be carried out safely with intervention times and success rates comparable to those reported in the literature.
Subject(s)
Angioplasty, Balloon, Coronary , Myocardial Infarction/therapy , Acute Disease , Adult , Aged , Aged, 80 and over , Chest Pain , Female , Follow-Up Studies , Humans , Male , Middle Aged , Myocardial Infarction/physiopathology , Retrospective Studies , Shock, Cardiogenic/physiopathology , Time FactorsABSTRACT
The effects of frovatriptan and sumatriptan on internal carotid and coronary vascular haemodynamics were investigated and compared in conscious dogs. Frovatriptan and sumatriptan (0.1 - 100 microg kg(-1)) induced a transient increase in external coronary artery diameter (eCOD) of up to 2.9+/-1.2 and 1.8+/-0.6%, respectively (both P:<0.05). This was followed by a prolonged and dose-dependent decrease in eCOD of up to -5.2+/-1.2 and -5.3+/-0.9% (both P:<0.05), with ED(50) values of 86+/-21 and 489+/-113 micromol kg(-1), respectively. In contrast, only a decrease in the external diameter of the internal carotid artery was observed (-6.0+/-0.6 and -6.2+/-1.4%, both P:<0.05, and ED(50) values of 86+/-41 and 493+/-162 micromol kg(-1), respectively). Frovatriptan was thus 5.7 fold more potent than sumatriptan at the level of both large coronary and internal carotid arteries. After endothelium removal by balloon angioplasty in coronary arteries, the initial dilatation induced by the triptans was abolished and delayed constriction enhanced. The selective antagonist for the 5-HT(1B) receptors SB224289 dose-dependently blocked the effects of sumatriptan on large coronary and internal carotid arteries whereas the selective antagonist for the 5-HT(1D) receptors BRL15572 did not affect any of these effects. In conclusion, frovatriptan and sumatriptan initially dilate and subsequently constrict large coronary arteries in the conscious dog, whereas they directly constrict the internal carotid artery. The vascular endothelium modulates the effects of these triptans on large coronary arteries. Finally, 5-HT(1B) but not 5-HT(1D) receptors are primarily involved in canine coronary and internal carotid vasomotor responses to sumatriptan.
