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OBJECTIVES: The purpose of this study was to assess the clinical and angiographic benefits of elective stenting in coronary arteries with a reference diameter of 2.1 to 3.0 mm, as compared with traditional percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: The problems related to small-vessel stenting might be overcome using modern stents designed for small vessels, combined with effective antiplatelet therapy. METHODS: In five centers, 145 patients with stable or unstable angina were randomly assigned to elective stenting treatment with the heparin (Hepamed)-coated beStent or PTCA. Control angiography was performed after six months. The primary end point was the minimal lumen diameter (MLD) at follow-up. Secondary end points were the restenosis rate, event-free survival and angina status. RESULTS: At follow-up, there was a trend toward a larger MLD in the stent group (1.69 +/- 0.52 mm vs. 1.57 +/- 0.44 mm, p = 0.096). Event-free survival at follow-up was significantly higher in the stent group: 90.5% vs. 76.1% (p = 0.016). The restenosis rate was low in both groups (9.7% and 18.8% in the stent and PTCA groups, respectively; p = 0.15). Analyzed as treated, both the MLD and restenosis rate were significantly improved in patients who had stents as compared with PTCA. CONCLUSIONS: In small coronary arteries, both PTCA and elective stenting are associated with good clinical and angiographic outcomes after six months. Compared with PTCA, elective treatment with the heparin-coated beStent improves the clinical outcome; however, there was only a nonsignificant trend toward angiographic improvement.

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The experience in consecutive procedures with 800 recanalization attempts of chronic total coronary occlusions using the Magnum wire was analyzed from a prospectively constituted computerized database. The data confirm that the Magnum wire, generally used as a primary intervention for occlusive angioplasty at our centers, is competitive with conventional systems in this setting.

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The magnum wire is a stiff-shaft, blunt-tip wire constructed for recanalisation during angioplasty. Smaller series have demonstrated superior qualities compared to conventional wires. The purpose of this study was to analyze its feasibility in a larger number of procedures. A single centre database analysis identified the use of Magnum wire during 443 procedures accounting for 26% of all angioplasties from October 1992 to February 1995. There were 347 total occlusions and 222 non-total lesions. Technical success was 69% in total and 90% in non-total lesions, whereas angiographic success was 58% and 75%, respectively. Stents were successfully implanted in 48 lesions; in 29 (8%) total occlusions and 19 (9%) non-total lesions. The total occlusion-related complication rate was 1.7%. Acute closure occurred in 4.1% of non-total lesions. In conclusion, Magnum wire is a feasible tool for angioplasty of total occlusions and severe stenoses. It is a cheap, simple and safe method for recanalisation.

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The majority of patients with serious exercise-induced ventricular arrhythmias have extensive coronary artery disease. These arrhythmias develop, however, only in a minority of patients with angina pectoris. The purpose of the present study was therefore to investigate whether these arrhythmia patients are characterized by any specific "arrhythmogenic" pattern of coronary artery disease. Among 1100 consecutive patients undergoing coronary artery bypass grafting, 30 (2.7%) patients had ventricular tachycardia or fibrillation during preoperative exercise testing. For each of these patients, two matched controls with angina pectoris but no ventricular arrhythmia were selected. All patients underwent angiocardiography by standard techniques. The recordings were blinded and interpreted in random order by an experienced invasive cardiologist. Significant stenosis (> or = 50%) of the main left coronary artery was found in 27% of the case patients compared to 12% of the matched controls (p = 0.069, two-tailed t test); proximal left anterior descending artery stenoses were more frequent in the arrhythmia patients. Although stenosis > or = 75% was only moderately more frequent in the case patients, the difference was highly significant for stenosis > or = 95%, which was seen in 47% of the case patients compared to 22% of the controls (p = 0.015). The difference was even more pronounced for the combination of main left coronary artery stenosis and/or high-grade stenosis (> or = 95%) of the left anterior descending artery. This pattern was seen in 60% of the case patients compared to 28% of the matched controls (p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

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The role of myocardial revascularization in the treatment of malignant ventricular arrhythmias is not well defined. Our hypothesis was that in patients with ventricular tachycardia or fibrillation exposed by exercise-induced ischaemia, the acute transient ischaemia plays a principal causal role, and that in these patients surgical myocardial revascularization alone might be an effective treatment. Among 1100 consecutive patients undergoing isolated coronary artery bypass surgery (CABG) 30 patients (2.7%) characterized by ventricular tachycardia or fibrillation at the symptom-limited exercise tests prior to revascularization were studied prospectively. All patients had exercise-induced angina pectoris or ischaemic ST-segment depression preceding at least one of the arrhythmic events. In addition, eight of these 30 patients had experienced syncope during out-of-hospital exertional activities. After surgical revascularization, the 28 patients surviving to hospital discharge were followed for 1.6 to 86 months (mean 29 +/- 29 months) as outpatients and underwent between one to eight exercise tests (mean 2.6 +/- 1.9). One of these patients died suddenly of unknown causes at 14 months, another from cancer at 53 months. Twenty-six patients experienced a total of 34 episodes of ventricular tachycardia before revascularization. Two of these patients, both having residual ischaemia, had arrhythmia recurrences during follow-up; odds ratio (OR) 84.5, 95% confidence interval (CI) 18.7-381.9; P = < 0.010. Exercise-induced ventricular fibrillation occurred in eight patients pre-operatively.(ABSTRACT TRUNCATED AT 250 WORDS)

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Follow-up angiographic study was performed in 86 patients after initially successful Wallstent stent (Medinvent, Lausanne, Switzerland) implantation between April 1986 and October 1990. The stent angiographic restenosis rate was 16% at a mean of 8 months after stenting despite the inclusion of a substantial number of patients at high risk of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Of a total 15 variables analyzed, only suboptimal stent placement was found to be a significant predictor of stent restenosis. Age; gender; baseline New York Heart Association functional class; previous PTCA; indication for stenting; left ventricular ejection fraction; preangioplasty and immediate postangioplasty diameter stenosis severity; stented vessel site, lesional morphology; number, diameter, and length of stents implanted; and the interval between stenting and follow-up angiographic restudy were not significant risk factors of stent restenosis. Our study suggests that intracoronary stent implantation with the Wallstent may be a useful and promising adjunctive option after PTCA, particularly in patients at high risk of restenosis after PTCA. However, because of the significantly enhanced risk of restenosis after suboptimal stent implantation, we strongly recommend the selection and placement of Wallstent stents that adequately cover the entire length of the dilated coronary segment.

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We have used the right gastroepiploic artery as a viable jump graft to the distal right coronary artery in two patients. The first patient was a 37 year-old man with recurrent angina after coronary bypass surgery with three vein grafts eight years previously. The second patient was a man aged 45 with angina in New York Heart Association Class III to IV. In both cases coronary angiography revealed severe triple vessel disease with multiple proximal and distal occlusions or stenosis. Both internal mammary arteries were also used in the two patients to revascularize the LAD and circumflex systems. Thus, a complete revascularization was achieved by use of only viable arteries as conduits. Both patients recovered well and were free from angina. At present only the first patient has had a postoperative angiogram, which showed good patency of the gastroepiploic artery jump graft. If the long-term patency of this type of graft is similar to that of the internal mammary arteries, it is another suitable arterial conduit for revascularization of the ischemic myocardium.

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In previous studies, the peptide secretin has demonstrated the ability to increase cardiac output and peripheral organ flow. In this investigation the mechanisms of the myocardial effects of secretin were studied. The secretin effects on cardiac output, stroke volume and systemic resistance were unaltered after propranolol, whereas the effect on LVdP/dt was reduced and the heart rate effect negligible. Systemic pressure, myocardial blood flow and myocardial oxygen consumption were unchanged by secretin infusion both before and after beta-receptor blockade. Secretin caused reduction of all three end-systolic left ventricular diameters. Thus, an inotropic effect by secretin was confirmed. Beta-receptor blockade reduced the inotropic effect and almost abolished the chronotropic effect, whereas the vasodilating effect was unaltered. The main haemodynamic effect of secretin was caused by activation of receptors other than the beta-adrenergic receptors.

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The aim of the present study was to determine the effect of i.v. inosine on myocardial substrate uptake and function in the in situ dog heart. Inosine was infused i.v. at a rate of 5 mg kg min-1 in eight closed-chest pentobarbital anaesthetized dogs. Inosine caused a 46% decrease (P less than 0.01) in plasma free fatty acids (FFA), a 15% decrease (P less than 0.05) in plasma glycerol, an 18% decrease (P less than 0.05) in plasma glucose and a 46% increase (P less than 0.01) in blood lactate. This was associated with a 55% decrease (P less than 0.01) in myocardial FFA uptake and a 72% increase in lactate uptake, while glucose uptake remained unchanged. These metabolic changes were associated with a five-fold increase (P less than 0.05) in arterial insulin. Inosine caused an 18% increase (P less than 0.01) in myocardial blood flow without changing MVO2. There was a 33% increase (P less than 0.01) in LV dP/dtmax, a decrease in LVEDP from 4.9 +/- 0.9 (mean +/- SEM) to 0.9 +/- 0.3 mmHg (P less than 0.05) and a 24% decrease (P less than 0.01) in systemic vascular resistance. Inosine caused a transient 38% increase (P less than 0.05) in pulmonary vascular resistance. In conclusion, in addition to a positive inotropic effect and vascular effects inosine was found to cause release of insulin and to shift myocardial metabolism towards increased uptake of carbohydrates relative to FFA.

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Secretin, a 27-amino acid peptide with both vasodilating and inotropic properties, was investigated according to its effects on peripheral flow distribution in acute ischemic left ventricular failure accomplished by embolization of the left coronary artery in anesthetized dogs. Electromagnetic monitoring of renal, carotid, femoral and superior mesenteric artery flow was used. During the induction of heart failure a general reduction of flow with preponderance of that of the carotid and femoral arteries occurred. The secretin infusion caused increases in renal flow by 58%, carotid flow by 63%, femoral flow by 50% and superior mesenteric flow by 34%. The corresponding reductions in arterial resistances were 33, 35, 31 and 24%, respectively. Compared to levels before induction of failure, restoration of flow in all arteries as well as cardiac output was achieved, with exception of renal flow that was 25% higher. The arterial pressure was not altered and a modest inotropic effect of secretin was confirmed. It was concluded that in acute left ventricular failure secretin caused a general distribution of the increased cardiac output in the arteries investigated with a preponderance of renal artery flow.

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This study describes the effects of beta-receptor blockade on systemic hemodynamics and regional blood flows during acute ischemic heart failure in dogs. Depression of left ventricular (LV) function was induced by embolization of the left main coronary artery and was evidenced by a significant increase in LV end-diastolic pressure (LVEDP) and decrease in LV dP/dtmax and in cardiac output. Measurements of femoral, renal, mesenteric, and carotid blood flows showed a redistribution of cardiac output during failure. Femoral blood flow decreased to a greater extent than did cardiac output, carotid blood flow decreased in proportion to cardiac output, whereas mesenteric and renal blood flows were moderately reduced in relation to the decrease in cardiac output. Administration of 0.125 mg of propranolol intravenously (i.v.) significantly decreased the performance of the failing left ventricle. Reductions in cardiac output were accompanied by reductions in the peripheral circulations. The decrease in flow was evenly distributed in the femoral, mesenteric, and carotid vascular beds, while there was a relative preservation of renal blood flow. When the dose of propranolol was increased to 0.5 mg/kg, there were no further significant hemodynamic alterations.

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Infusion of the peptide secretin augments cardiac output due to vasodilating and inotropic properties. The aim of this investigation was to study how the increased cardiac output is distributed in the peripheral circulation. Before, during and after 15 min infusion of secretin 64 CU kg-1 h-1 flow changes in renal, carotid, femoral and the superior mesenteric arteries were measured by means of electromagnetic flowmetry in anaesthetized dogs. Cardiac output and stroke volume increased by 41 and 27%, respectively, whereas the total systemic resistance fell 35%. The LVdP/dt increased by 35%. After 5 min infusion, renal and carotid flows increased by 62 and 50%, respectively, whereas the femoral flow was only slightly elevated and the superior mesenteric flow unchanged. Both the femoral and the superior mesenteric flow gradually augmented and at the end of the infusion flow was substantially elevated in all four arteries. The study demonstrated that the increased cardiac output by secretin was distributed to all the four arteries, although a preponderance of flow to the renal circulation was indicated. This flow profile may be regarded as favourable in the management of low output conditions.

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Acute ischemic left ventricular (LV) failure in eight closed-chest, anesthetized dogs was induced by embolization of the left coronary artery with 50 micron polystyrene microspheres until LV end-diastolic pressure reached 25.2 +/- 1.4 mm Hg. Cardiac output was reduced by 33%, LVdP/dt by 32% and mean arterial pressure fell substantially. Plasma secretin increased significantly during the induction of failure. Infusion of secretin, 16 clinical units X kg-1 X hr-1 caused a persistent increment in LV performance, due to arteriolar dilation as well as a modest inotropic effect. Heart rate was elevated slightly and LV end-diastolic pressure unchanged. Mean arterial pressure was unchanged initially, but decreased slightly at the end of the infusion period. Myocardial oxygen consumption was unaltered. It is concluded that secretin may be well suited for the treatment of acute LV failure.

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Acute ischaemic left ventricular failure was induced in closed-chest anaesthetized dogs by injection of 50 microns plastic microspheres into the left main coronary artery. This effected a 33% decrease in cardiac output. Dopamine and high doses of insulin restored cardiac output, and these agents in combination raised cardiac output to 34% above pre-ischaemic levels. Total body oxygen consumption was calculated at the various levels of cardiac output, and was found to remain essentially unchanged. Inotropic agents, then, may result in overperfusion with respect to oxygen demand.

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The effects of acute ischaemic heart failure on renal blood flow and the influence of dopamine at low dose range and high doses of insulin were examined. Acute left ventricular (LV) failure was induced in dogs by injection of 50-micron plastic microspheres into the left main coronary artery. The dogs showed signs of severely depressed LV function. Cardiac output was decreased to a significantly greater extent than renal blood flow, and while total peripheral resistance was significantly increased, there were no significant changes in renal vascular resistance. The results indicate different sympathetic discharge to the various vascular beds during acute ischaemic heart failure. Dopamine at low dose range and high doses of insulin were found to improve myocardial contractility and to reduce renal vascular resistance and increase renal blood flow.

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This study describes the effects of high doses of insulin on systemic haemodynamics and regional blood flows during acute ischaemic heart failure in dogs. Left ventricular (LV) dysfunction was induced by embolization of the left main coronary artery, and was evidenced by a significant increase in LV end-diastolic pressure and decrease in LVdP/dtmax and cardiac output. Measurements of femoral, renal, mesenteric and carotid blood flows showed a redistribution of cardiac output during failure. Femoral blood flow decreased to a greater extent than cardiac output, but carotid blood flow decreased in proportion to cardiac output, while mesenteric and renal blood flows were moderately reduced in relation to the decrease in cardiac output. Administration of 300 IU of fast-acting insulin significantly improved the performance of the failing left ventricle. Cardiac output was raised to levels observed before failure. The greatest increases in peripheral flow occurred in the femoral and carotid vascular beds, while the least occurred in the mesenteric and renal vascular beds. These observations indicate that insulin at high dose levels significantly improves peripheral circulation by positive inotropic and vasodilatating effects. There was a tendency to favour femoral and carotid vascular flows, but not at the expense of renal and visceral flows. Beta receptor blockade blocked neither the systemic nor regional haemodynamic effects of insulin.

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This study describes the effects of a wide range of plasma concentrations of insulin on systemic haemodynamics and free fatty acids (FFA) and the effect of a high dose of insulin on regional blood flows in the femoral, carotid, mesenteric and renal arteries. Insulin was infused in 10 dogs at rates of 4, 8, 16, 32, 64 and 128 IU/kg/h, and the experiments were concluded with a bolus injection of 300 IU. Plasma glucose concentrations were kept constant during the experiments. A dose-related increase in maximum rate of left ventricular pressure rise, stroke volume and cardiac output, and decrease in total peripheral resistance was found with insulin infusion rates up to 64 IU/kg/h. Heart rate and mean aortic blood-pressure were unchanged. The maximum antilipolytic effect was obtained at an infusion rate of 16 IU/kg/h. Insulin was given as a bolus dose of 300 IU in 6 dogs. Blood-flow was increased in all vascular beds, but insulin caused a redistribution of cardiac output. The greatest increases occurred in the femoral and carotid vascular beds, and the least occurred in the renal bed. Mesenteric blood-flow was increased in proportion to cardiac output. The results suggest that insulin exerts combined positive inotropic and vasodilating effects at high dose levels, which result in improved regional perfusion. It may be a potentially useful clinical agent with special benefit under circumstances where enhanced cerebral blood-flow is of importance.

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Acute ischaemic heart failure was induced in 13 dogs by coronary embolisation. Severe dysfunction of the left ventricular (LV) performance was shown by a significant increase in LV end-diastolic pressure and significant decreases in maximum rate of LV pressure rise (LVdP/dtmax), stroke volume and cardiac output. 300 IU of fast-acting insulin was injected as a bolus dose in 7 dogs 90 min after the embolisation procedure. This was followed by infusion of glucose and potassium to maintain normal blood levels. After 15 min, insulin had significantly improved the performance of the failing left ventricle. Total peripheral resistance was decreased. Myocardial blood flow was significantly increased while myocardial oxygen consumption was unchanged. After beta receptor blockade with propranolol 0.5 mg kg-1 given intravenously, the improvement in cardiac performance was reduced, heart rate decreased, and a concomitant decrease in myocardial blood flow and oxygen consumption was recorded. Compared with values before treatment, the net effect of combined insulin and beta receptor blockade was unchanged LVdP/dtmax, LV end-diastolic pressure and cardiac output, significantly increased stroke volume and decreased heart rate, and moderately reduced total peripheral resistance and mean aortic blood pressure. Myocardial blood flow was unaltered, while myocardial oxygen consumption was significantly reduced. In the control group of 6 dogs propranolol was given before insulin, and similar haemodynamic alterations were found.

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Acute ischemic heart failure was induced in eight dogs by coronary embolization. Severe depression of the left ventricular (LV) performance was evidenced. At 15 min after the embolization procedure, dopamine was infused at a dosage sufficient to increase the maximum rate of LV pressure rise (LVdP/dtmax) by approximately 50%. The significant improvement in cardiac performance was obtained at unaltered myocardial oxygen consumption (MVo2). Dopamine infusion was concluded, and after a stabilization period 300 IU of insulin was injected. This was followed by the infusion of glucose and potassium to maintain levels. Insulin significantly improved the performance of the failing left ventricle at unaltered MVo2, but to a lesser extent than did dopamine. Additional dopamine infusion further significantly improved cardiac performance. The net effect of insulin and dopamine in combination as compared with dopamine alone was a significantly greater increase in stroke volume and cardiac output due to a more pronounced decrease in total peripheral resistance. Dopamine increased arterial concentrations and myocardial uptake of free fatty acids (FFA). The net metabolic effect of insulin and dopamine in combination as compared with dopamine alone was a shift in myocardial substrate uptake from FFA to carbohydrates.

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