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Primary percutaneous coronary intervention (PCI) decreases myocardial damage in patients with ST-elevation myocardial infarction (STEMI). Cellular reperfusion injury associated with calcium overload may limit myocardial salvage. We previously showed (CASTEMI trial) that caldaret (MCC-135), which modulates myocardial calcium handling when administered before PCI in patients with STEMI, did not change residual left ventricular (LV) function. The aim of this subanalysis was to examine whether caldaret decreases the incidence of LV dysfunction (LV ejection fractionor=30%) in patients with STEMI undergoing primary PCI. Of 387 patients enrolled in the CASTEMI study, 239 had single-photon emission computed tomographic data on days 7 and 30 after the infarct. The incidence of LV dysfunction in patients receiving low- and high-dose caldaret was compared with placebo. At day 30 after the infarct, there was a significant decrease in the incidence of LV dysfunction in patients receiving low and high doses of caldaret versus placebo (8.0%, 6.9% vs 17.5%, p0.05 for the 2 comparisons). This difference was more pronounced in patients with anterior wall MI and Thrombolysis In Myocardial Infarction grade 0/1 flow. In this group, 52% decrease in the incidence of LV dysfunction was observed already on day 7 after the infarct (p = 0.026). The incidence of an LV ejection fractionor=30% was significantly decreased between day 7 and day 30 in patients treated with the 2 doses of caldaret and was unchanged in the placebo group. In conclusion, treatment with intravenous caldaret in patients with STEMI undergoing primary PCI is associated with a significant decrease in the incidence of severe LV dysfunction.

Aims Successful epicardial reperfusion with primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) can paradoxically evoke myocardial reperfusion injury, which may be signalled by temporally associated ventricular arrhythmias (VAs). We correlated reperfusion VA 'bursts' with final infarct size (IS) in patients with restored TIMI 3 flow following PCI for anterior STEMI. Methods and results All 128 anterior STEMI patients with final TIMI 3 flow had continuous 24 h digital 12-lead ECG with simultaneous Holter recording initiated prior to PCI, and Day 7/discharge SPECT imaging IS assessment. Angiography, SPECT imaging, continuous ST recovery, and quantitative rhythm analyses were performed. Reperfusion VA bursts were defined against patient-specific background VA rates and timed as concomitant with or following first angiographic TIMI 3 flow restoration associated withor =50% stable ST recovery; they were then correlated with IS and global left ventricular ejection fraction (LVEF) at Day 7/discharge. Bursts occurred in 81/128 (63%) patients and were significantly correlated with larger IS and worse LVEF (median: 21.0 vs. 10.0%, P0.001; 35.5 vs. 46.5%, P0.001, respectively). In multivariable analyses that adjusted for known predictors of IS, the association of bursts with larger IS remained significant; similar results were seen for worse LVEF. Conclusion Reperfusion VA bursts predict larger IS despite TIMI 3 flow restoration withor =50% stable ST recovery following PCI for anterior STEMI. Well-characterized reperfusion VAs may provide a novel biomarker of reperfusion injury.

Objectives The purpose of this study was to investigate the appropriateness of stenting a functionally nonsignificant stenosis. Background Percutaneous coronary intervention (PCI) of an intermediate stenosis without evidence of ischemia is often performed, but its benefit is unproven. Coronary pressure-derived fractional flow reserve (FFR) is an invasive index used to identify a stenosis responsible for reversible ischemia. Methods In 325 patients scheduled for PCI of an intermediate stenosis, FFR was measured just before the planned intervention. If FFR was ≥0.75, patients were randomly assigned to deferral (Defer group; n = 91) or performance (Perform group; n = 90) of PCI. If FFR was Results There were no differences in baseline clinical characteristics between the 3 groups. Complete follow-up was obtained in 98% of the patients. Event-free survival was not different between the Defer and Perform groups (80% and 73%, respectively; p = 0.52), but was significantly worse in the Reference group (63%; p = 0.03). The composite rate of cardiac death and acute myocardial infarction in the Defer, Perform, and Reference groups was 3.3%, 7.9%, and 15.7%, respectively (p = 0.21 for Defer vs. Perform group; p = 0.003 for the Reference vs. both other groups). The percentage of patients free from chest pain at follow-up was not different between the Defer and Perform groups. Conclusions Five-year outcome after deferral of PCI of an intermediate coronary stenosis based on FFR ≥0.75 is excellent. The risk of cardiac death or myocardial infarction related to this stenosis is

Objectives: The EXhaustion Intervention Trial investigated the effect of a behavioural intervention programme on exhaustion, health-related quality of life (HRQL), depression, anxiety, hostility, and anginal complaints in angioplasty patients who felt exhausted after percutaneous coronary intervention (PCI). Methods: Seven hundred ten patients were randomized into an intervention group and a usual care control group. The group intervention focused on stressors leading to exhaustion and on support of recovery. HRQL (measured by the MacNew questionnaire), exhaustion [measured by the Maastricht Questionnaire and the Maastricht Interview Vital Exhaustion (MIVE)], anxiety (measured by the State-Trait Inventory), and depression (measured by the structured clinical interview for DSM-IV) were assessed at intake and at 6 and 18 months. Presence of anginal complaints was assessed at 18 months. Results: The intervention had a significant beneficial effect on all psychological factors except hostility and on the presence of anginal complaints. The effect of the intervention on exhaustion, as assessed by the MIVE, was modified by a previous history of coronary artery disease (CAD). Gender modified the effect of the intervention on exhaustion and on anxiety, the strongest effect being observed in women. Conclusions: The behavioural intervention improved HRQL and related psychological factors. Somatic comorbidity and a history of CAD limited the effect of the intervention.

Objective The effects of a short intervention on behavioral risk factor modification in patients with coronary artery disease (CAD) on Type A behavior, vital exhaustion, and depression were studied in a randomized controlled trial. Methods Acute myocardial infarction patients or patients who underwent coronary artery bypass grafting (CABG) were randomly assigned to an 8-week multiple risk modification group program ( n =94) or to a control group ( n =90) that received usual care with standard physical exercise training. Patients were assessed before intervention, directly after intervention, and at 9-month follow-up. Results The intervention was effective in reducing hostility and total Type A behavior at postintervention ( P =.01) and at 9-month follow-up ( P =.03). The intervention had no overall impact on vital exhaustion and depression, measured by the Beck Depression Inventory (BDI), whereas we unexpectedly found that the percentage of patients with major depression was reduced in the control group but not in the intervention group. Conclusion The results indicate that a short behavioral intervention for coronary patients can result in relatively large and persistent reductions in cognitive aspects of Type A behavior and hostility, in particular. In view of the unwanted findings on the diagnosis of depression, however, we do not unequivocally advise the intervention to the general population of AMI and CABG patients.

Contains fulltext : 48264.pdf (Publisher’s version ) (Closed access) BACKGROUND: Extreme fatigue is a common complaint in percutaneous coronary intervention (PCI) patients, and is associated with an increased risk for new cardiac events. The objective of the Exhaustion Intervention Trial (EXIT) was to determine whether a behavioral intervention on exhaustion reduces the risk of a new coronary event after PCI. METHODS AND RESULTS: Seven hundred ten consecutive patients, ages 35 to 68 years, who felt exhausted after PCI were randomized into an intervention group and a usual-care group. The intervention was based on group therapy focusing on stressors leading to exhaustion, and on support for recovery by promoting rest and making rest more efficient. One month after PCI, 50% of the patients felt exhausted. The intervention reduced the odds of remaining exhausted at 18 months by 56% in those without a previous history of coronary artery disease (CAD) (OR = 0.44; 95% CI 0.29-0.66), but had no effect on exhaustion in those with a history of CAD (OR = 0.93; 95% CI 0.56-1.55; p = .78). The intervention did not reduce the risk of a new coronary event within 2 years (RR = 1.14; 95%CI 0.82-1.57). Post-hoc analyses suggest that the effect of the intervention was limited by a positive history of CAD, the presence of a chronic, painful condition (especially rheumatism), and by opposite effects on early and late cardiac events. CONCLUSION: A behavioral intervention in PCI patients has a beneficial effect on feelings of exhaustion. It could not be demonstrated that the intervention reduces the risk of a new coronary event within 2 years.

The aim of the study was to compare acute and long-term angiographic and clinical outcome of balloon angioplasty and elective stenting in de novo lesions in the body of a saphenous vein graft (SVG). A total of 150 patients, with de novo lesions in SVG, were randomly assigned to balloon angioplasty or elective Wiktor I stent implantation. The angiographic restenosis rate at 6-month follow-up was 32.8% in the balloon group and 19.1% in the stent group (P = 0.069). At 1-year follow-up, target vessel revascularization rate was 31.4% vs. 14.5% (P < 0.05), and event-free survival was 60.0% vs. 76.3% (P < 0.05) for the balloon and stent group, respectively. Elective stent implantation in de novo SVG lesions is associated with a significant lower target vessel revascularization rate and a significant higher event-free survival at 1-year follow-up as compared to balloon angioplasty.

Objective Many patients feel exhausted or depressed before the onset of an acute coronary event, but little is known about the origin of these feelings. We tested the hypothesis that the depressive symptomatology is associated with a reactivation of latent viruses and inflammation of a coronary vessel. Methods A blood sample was drawn and a biopsy sample was obtained from the coronary lesion of 15 exhausted and 15 nonexhausted patients treated with directional coronary angioplasty because of severe angina. Blood samples were analyzed to measure antibody titers against Chlamydia pneumoniae, cytomegalovirus, and the cytokines interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha. The biopsy sample was analyzed for the presence of IL-1beta and TNF-alpha. Results Exhausted/depressed patients had higher antibody titers against cytomegalovirus, higher levels of C. pneumoniae immunoglobulin G, and higher levels of IL-1beta and TNF-alpha. No associations between the mental state of a patient and cytokine mRNA in the biopsy sample were found. Conclusions The findings indicate that the mental state of angioplasty patients is positively associated with serological markers of inflammation. It remains to be seen whether the inflammation causes feelings of exhaustion, whether exhaustion and depression set the stage for inflammation, or whether existing feelings of exhaustion are amplified by the inflammation.

The purpose of this study was to determine the feasibility, safety, and efficacy of elective stenting with heparin-coated Wiktor stents in patients with coronary artery disease. In experimental studies, heparin coating has been shown to prevent subacute thrombosis and restenosis. Recently, a new method of heparin coating was developed, resulting in a more stable and predictable heparin layer on stent devices. This trial constitutes the first in-human use of this coating procedure, applied on the well-known Wiktor stent device. Heparin-coated Wiktor stent implantation was performed in 132 consecutive patients (132 lesions) in a multicenter international trial from September 1996 to February 1997. Forty-three percent of patients had unstable angina, 33% had previous myocardial infarction, and 10% had diabetes mellitus. Patients were followed for 12 months for occurrence of major adverse cardiovascular events, and 96% of the eligible patients underwent quantitative angiographic control at 6 months. Stent deployment was successful in 95.5% of lesions. Minimal lumen diameter increased by 1.67 +/- 0.48 mm (from 1.02 +/- 0.38 mm before to 2.69 +/- 0.37 mm after the stent implantation). Mean percent diameter stenosis decreased from 67.4 +/- 11.3% before to 18.9 +/- 7.7% after the intervention. A successful intervention (

OBJECTIVES How effective and safe is rescue percutaneous transluminal coronary angioplasty [PTCA] compared with primary PTCA, and is it cost effective? BACKGROUND In acute myocardial infarction (AMI), primary PTCA has been shown to be beneficial in terms of clinical outcome. In contrast, the value of rescue PTCA has not been established. METHODS In a retrospective analysis, we compared the angiographic and clinical outcomes of 317 consecutive patients who had rescue PTCA ∼90 min after failed thrombolysis and 442 patients treated with primary PTCA. An estimation of interventional costs was compared with the strategies of primary and rescue PTCA or with the strategy of thrombolysis with rescue PTCA, when indicated. RESULTS Baseline characteristics between primary and rescue PTCA were comparable for most variables. Treatment delay was longer for patients who had rescue PTCA: 240 min. versus 195 min. Coronary patency after PTCA was comparable: 90.2% for rescue PTCA and 91.4% for primary PTCA (p = 0.67, power 71.9%). In-hospital mortality rates were 4.7% and 6.6%, respectively (p = 0.37). Also, the other complications were fairly similar during the in-hospital phase and during one-year follow-up. Predictors of death were age, infarct size, localization of AMI, failed PTCA and left main stem occlusion. The estimated interventional costs during one-year follow-up were $7,377 for primary PTCA and $8,246 for rescue PTCA: difference $869 (11.7%). CONCLUSIONS In this retrospective analysis of 759 patients with AMI, rescue angioplasty early after failed thrombolysis seems to be as effective and safe as primary PTCA. In the present evaluation, interventional costs of primary PTCA are less than those of rescue PTCA (p = 0.0001).

Coronary heart disease (CHD) is still the main cause of death in developed countries. Because of improved treatment, many patients survive the acute phase of a myocardial infarction, which makes secondary prevention of CHD of major importance. Most risk factors responsible for the development and progression of CHD are associated with behavior. Therefore, interventions aimed at behavior change may contribute to risk factor modification and secondary prevention of CHD. The effects of separate risk factor modification efforts by means of randomized, controlled clinical trials of nonpharmacological interventions in patients suffering from CHD are reviewed. Interventions aimed at healthy lifestyles may stimulate smoking cessation rates, reduce elevated serum total and low-density lipoprotein (LDL)-cholesterol concentrations, and favorably modify type A behavior in CHD patients. Moreover, reduction of coronary atherosclerosis has been reported after intensive lifestyle and exercise interventions, whereas exercise and type A interventions may also lead to reduced CHD morbidity and mortality. As for hypertension and obesity, studies aimed at secondary prevention are lacking.

OBJECTIVE—To assess the safety and feasibility of acute transport followed by rescue percutaneous transluminal coronary angioplasty (PTCA) or primary PTCA in patients with acute myocardial infarction initially admitted to a hospital without PTCA facilities. DESIGN—In a multicentre randomised open trial, three regimens of treatment of acute large myocardial infarction were compared for patients admitted to hospitals without angioplasty facilities: thrombolytic treatment with alteplase (75 patients), alteplase followed by transfer to the PTCA centre and (if indicated) rescue PTCA (74 patients), or transfer for primary PTCA (75 patients). RESULTS—Between 1995 and 1997 224 patients were included. Baseline characteristics were distributed evenly. Transport to the PTCA centre was without severe complications in all patients. Mean (SD) delay from onset of symptoms to randomisation was 130 (75) minutes and from randomisation to angiography 90 (25) minutes. Death or recurrent infarction within 42 days occurred in 12 patients in the thrombolysis group, in 10 patients in the rescue PTCA group, and in six patients in the primary PTCA group. These differences were not significant. CONCLUSIONS—Acute transfer for rescue PTCA or primary PTCA in patients with extensive myocardial infarction is feasible and safe. Efficacy of rescue PTCA or primary PTCA in this setting will have to be tested in larger series before this approach can be implemented as "routine treatment" for patients with extensive myocardial infarction. Keywords: myocardial infarction; percutaneous transluminal coronary angioplasty; primary PTCA; rescue PTCA; reperfusion

Saruplase (unglycosylated human-type high molecular weight single-chain urokinase-type plasminogen activator) was given to 1698 patients in the open-label Practical Applicability of Saruplase Study (PASS), which assessed the safety and efficacy of saruplase in the treatment of acute myocardial infarction. Thirty-seven hospitals in Europe participated in the study. All patients received 20 mg saruplase as a bolus followed by an infusion of 60 mg saruplase over 1 hour. Prior to the infusion of saruplase, 62% of the patients received a bolus of 5000 U of heparin, and after saruplase a 24-hour intravenous infusion of heparin was given to 95% of patients. The mean age of the patients was 59 years and 80.1% were male. The median delay from the onset of chest pain to the start of saruplase infusion was 145 minutes. Acute angiography was performed in 8 of the participating 37 centers in 350 patients (20.6%), on average 85 minutes (median) after the start of the saruplase infusion. TIMI 3 flow was obtained in 186 patients (53.1%) and TIMI 2 flow in 61 patients (17.4%). Patency rates were similar for patients with anterior and inferior infarction. ECG signs suggestive of reperfusion were seen in 63% of the patients. In-hospital mortality was low (92 patients; 5.4%), and nonfatal recurrent myocardial infarction was seen in 60 patients (3.5%). Severe bleeding complications occurred in 92 patients (5.4%), 21 of whom (1.2%) needed a blood transfusion. An intracerebral hemorrhage was observed in eight patients (0.5%), and seven patients (0.4%) suffered from a thromboembolic stroke. At discharge 85.9% of the patients were in NYHA functional class I. One-year mortality was low (142 patients; 8.4%). Mortality was high in patients with TIMI 0 or 1 flow at the acute angiography who did not undergo rescue PTCA (9/39; 23.1%), lower in patients with TIMI 0 or 1 flow followed by successful rescue PTCA (7/64; 10.9%), and low in patients with TIMI 2 flow (1/61; 1.6%) or with TIMI 3 flow (2/186; 1.1%). Patency rates and (bleeding) complications did not differ between patients with a body weight greater than or less than 70 kilograms. No antibodies against saruplase were detected in samples from 455 patients. In conclusion, it can be stated that saruplase, given in combination with aspirin and intravenous heparin, can be given safely and effectively to patients with acute myocardial infarction.

OBJECTIVES We sought to study the effect of early infusion of abciximab on coronary patency before primary angioplasty in patients with acute myocardial infarction. BACKGROUND Glycoprotein IIb/IIIa antagonists have proved to be effective in reducing ischemic events associated with coronary angioplasty. The present study explores whether abciximab alone, without administration of thrombolytic therapy, may induce reperfusion in patients with acute myocardial infarction. METHODS In the Glycoprotein Receptor Antagonist Patency Evaluation pilot study 60 patients with less than 6 h signs and symptoms of acute myocardial infarction eligible for primary angioplasty received in the emergency room a bolus of abciximab 250 μg/kg followed by a 12-h infusion of 10 μg/min. All patients were also treated with an oral dose of 160 mg aspirin and 5,000 IU of heparin intravenously. As soon as possible a diagnostic angiography was performed to evaluate the patency of the infarct-related artery. RESULTS The median time between onset of symptoms and the administration of the abciximab bolus was 150 min (range 45 to 345), and the median time between abciximab bolus and first contrast injection in the infarct-related artery was 45 min (range 10 to 150). In 24 patients (40%, 95% confidence interval 28% to 52%) Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 was observed at a median time of 45 min (range 10 to 150) after abciximab bolus; TIMI flow grade 3 was observed in 11 patients (18%, 95% confidence interval 9% to 28%). There was no difference in percentage of TIMI flow grade 2 or 3 between patients who received abciximab within 2.5 h after onset of symptoms or thereafter. CONCLUSIONS Abciximab therapy given in the emergency room in patients awaiting primary angioplasty is associated with full reperfusion (TIMI flow grade 3) in about 20% and with TIMI flow grade 2 or 3 in about 40% of the patients at a median time of 45 min. These figures are higher than those in primary angioplasty trials without such pretreatment. Randomized controlled trials of very early infusion of abciximab, either prehospital or in-hospital, in patients eligible for angioplasty are warranted.

Saruplase, or unglycosylated, single-chain urokinase-type plasminogen activator (scu-PA) selectively activates fibrin-bound plasminogen, and is subsequently converted to its two-chain derivative tcu-PA (urokinase) by plasmin. The efficacy of a 20 mg IV bolus followed by an infusion of 60 mg over 1 hour (standard regimen) has been demonstrated in acute myocardial infarction (AMI). The Bolus Administration of Saruplase in Europe (BASE) study compared the efficacy of standard therapy, single bolus (80 mg), and split bolus (2 × 40 mg at 30-minute intervals) in AMI. In a substudy of BASE, the pharmacokinetics of total u-PA activity (amidolytic activity after plasmin treatment), high molecular weight (HMW) u-PA antigen, and tcu-PA activity were compared in patients receiving standard therapy (n = 4), single bolus (n = 4), or split bolus (n = 5). Total u-PA activity and HMW u-PA antigen were similar. The maximum concentration (Cmax,, mean ± SD) of total u-PA activity was 2.2 ± 0.3 µg/mL after standard therapy, 16.3 ± 3.9 µg/mL after single bolus, and 8.2 ± 1.6 ug/mL after split bolus. The area under the concentration versus time curve (AUC) values of total u-PA activity were 1.7 ± 0.1 µg/mL*h (standard therapy), 4.0 ± 0.9 µg/mL*h (bolus), and 3.0 ± 0.7 µg/mL*h (split bolus). The dominant initial half-lives (t1/2 α) were 7.1 ± 1.1 minutes (standard), 8.8 ± 0.8 minutes (bolus), and 5.1 ± 2.1 minutes (split bolus). Maximum plasma concentrations of of tcu-PA activity were observed at 5.2 ± 7 minutes (standard), 21 ± 10 minutes (bolus), and 42 ± 2 minutes (split bolus). Cmax was lowest after standard therapy (0.6 ± 0.3 µg/mL), highest after bolus (4.2 ± 2.2 µg/mL), and approximately twice as high as standard therapy after split bolus (1.3 ± 0.8 µg/mL). After standard therapy the mean fibrinogen concentration decreased gradually from approximately 300 mg/dL to 70 mg/dL at 90 and 120 minutes. After a single bolus the fibrinogen concentration decreased below the limit of quantification within 30 minutes and remained there for at least 120 minutes. Directly after the second 40 mg dose of the split bolus, the fibrinogen levels had an accelerated and more pronounced decrease to approximately 65 mg/dL at 90 and 120 minutes. A single bolus results in very high early total u-PA activity, which accelerates the appearance of tcu-PA activity and fibrinogen consumption. The pharmacokinetics and hemostatic effects of the split-bolus regimen are more comparable with those of standard therapy.

To study the safety and efficacy of the thrombolytic agent saruplase as a bolus, the angiographic and clinical outcomes of three bolus regimens were investigated in a pilot study conducted in 192 patients with an acute myocardial infarction and were compared with the standard regimen. Fifty-two patients received a double bolus of 40 mg and 40 mg after 30 minutes, 51 patients a bolus of 80 mg, and 36 patients a bolus of 60 mg. Fifty-three patients received the standard regimen (a bolus of 20 mg and 60 mg IV infusion over 1 hour). At 60 minutes TIMI 2 and 3 flow were, respectively, 9.6% and 61.5% with the 40/40-mg bolus, 15.7% and 51.0% with the 80-mg bolus, 16.7% and 30.6% with the 60-mg bolus, and 7.5% and 54.7% with the standard 20/60-mg infusion. At 90 minutes TIMI 2 and 3 flow improved to 9.6% and 73.1%, 15.7% and 56.9%, 13.9% and 36.1%, and 5.7% and 71.7%, respectively. The primary endpoint, persistent patency (TIMI 2 + 3) at 24–45 hours, was seen in 69.2%, 64.7%, 44.4%, and 67.9% of patients who had no rescue PTCA, respectively. Inclusion in the 60-mg bolus group was prematurely stopped because of their low patency rates. The 40/40-mg bolus group had the highest mortality rate (13.5%), whereas the 60-mg bolus group had no deaths. Other adverse event rates were similar in the four groups. This clinical outcome is highly influenced by rescue PTCA of patients with insufficient TIMI flow. This pilot study indicates that in patients with an acute myocardial infarction, a double bolus of 40/40 mg resulted in the highest patency but also had the highest complication rate. The 80-mg single bolus is an attractive alternative for further evaluation because of its acceptable patency and event profile, and its easy form of administration.

It is difficult to identify characteristics of patients with unstable angina that are predictive of a high likelihood of developing clinical events. However, several features have been recognized. Patients with a clinical history of previous stable exertional angina symptoms who began to experience rest pain appear to be at risk and tend to have more extensively underlying coronary disease. When the ischemic episodes are accompanied by rales, a new or worsening mitral regurgitation murmur, or hypotension, there is a high likelihood of significant coronary artery disease and one should triage these patients to early cardiac catheterization and prompt revascularization. An angiographic feature that carries a high risk is a lesion in the proximal left anterior descending or in the left main coronary artery. Certain typical ECG patterns are very suggestive for a critical narrowing in these coronary arteries. If chest pain and ST-segment changes recur on vigorous medical management, early invasive evaluation should be strongly considered. Even so, the left ventricular function is very important prognostically. According to serologic tests, the level of C-reactive protein and serum amyloid A protein suggesting that there may be active inflammation predicts an early poor outcome. However, these serologic abnormalities do not have much clinical value. An increased platelet activation and a reduced fibrinolytic capacity play a role in the pathogenesis of unstable angina, but thrombolytic therapy does not improve the prognosis in patients with unstable angina.

This study evaluates the feasibility and safety of a 6Fr hydrodynamic thrombectomy catheter, the Hydrolyser, in native coronary arteries and aortocoronary bypass grafts. With use of a conventional contrast injector, saline solution is injected into the narrow lumen of the catheter which makes a 180° bend at the tip. The resultant high-velocity jet (150 km/hour) is directed over a sidehole near the tip into a wide exhaust lumen. As a consequence of the Venturi effect, thrombus is sucked into that sidehole, fragmented, and removed through the wide exhaust lumen into a collection bag. Thirty-one thrombotic lesions were treated in 31 patients. The culprit vessel was a venous graft in 21 patients (15 with Thrombolysis in Myocardial Infarction Trial [TIMI] grade 0 or 1 flow) and a coronary artery in 11 patients (9 with grade 0 or 1 flow). Twenty-six patients had angina New York Heart Association functional class III or IV heart failure and 5 an acute myocardial infarction. In 26 patients, Hydrolyser therapy was the primary treatment, whereas in 5 patients coronary angioplasty preceded Hydrolyser therapy. In 1 patient the Hydrolyser could not reach the lesion. Thrombus was removed in 29 of the 31 patients. Successful reperfusion (TIMI grade 2 or 3 flow) by Hydrolyser therapy alone was achieved in 14 of the 24 patients with TIMI grade 0 or 1 flow before the procedure. Adjunctive therapy (coronary angioplasty, stent, or thrombolysis) was performed in 28 of the 31 patients. At the end of the total procedure 24 patients had TIMI grade 3 flow. Distal embolization during thrombectomy occurred in 2 patients, which led to a non-Q-wave infarction in 1. No patient died or needed emergency coronary bypass due to the Hydrolyser procedure. Thus, thrombectomy using the 6Fr Hydrolyser is feasible and was performed safely in 31 patients. Feasibility and safety of a new hydrodynamic thrombectomy device, the Hydrolyser, was evaluated in thrombus-containing coronary arteries or saphenous bypass grafts in 31 patients. Thrombus could be removed in 29 of the 31 vessels. There were no major adverse events related to the Hydrolyser.

Four hundred seventy-three patients with acute myocardial infarction (AMI) were treated with either saruplase (80 mg/hour, n = 236) or alteplase (100 mg every 3 hours, n = 237). Comedication included heparin and acetylsalicylic acid. Angiography was performed at 45 and 60 minutes after the start of thrombolytic therapy. When flow was insufficient, angiography was repeated at 90 minutes. Coronary angioplasty was then performed if Thrombolysis In Myocardial Infarction (TIMI) trial 0 to 1 flow was seen. Control angiography was at 24 to 40 hours. Baseline characteristics were similar. Angiography showed comparable and remarkably high early patency rates (TIMI 2 or 3 flow) in both treatment groups: at 45 minutes, 74.6% versus 68.9% (p = 0.22); and at 60 minutes 79.9% versus 75.3% (p = 0.26). Patency rates at 90 minutes before additional interventions were also comparable (79.9% and 81.4%). Angiographic reocclusion rates were not significantly different: 1.2% versus 2.4% (p = 0.68). After rescue angioplasty, angiographic reocclusion rates of 22.0% and 15.0% were observed. Safety data were similar for both groups. Thus, (1) early patency rates were high for saruplase and alteplase treatment, (2) reocclusion rates for both drugs were remarkably low, and (3) complication rates were similar. Thus, saruplase seems to be as safe and effective as alteplase.

Department of Human Biology, Maastricht University, The Netherlands.Animal studies suggest that myocardial ischemia/reperfusion causes oxidative stress. We, therefore, examined whether routinely performed percutaneous transluminal coronary angioplasty (PTCA) might be a human ischemia/reperfusion model for oxidative stress-induced lipid peroxidation. Fasting antecubital venous blood was sampled from 13 patients on the morning of PTCA, and 2 d after PTCA. Venous and coronary arterial blood were sampled just before and 10 min after the first balloon inflation. Samples were analyzed for plasma and LDL lipid hydroperoxide levels, in vitro oxidation of LDL, and LDL antioxidant levels. Lipid hydroperoxide levels in plasma and LDL remained unchanged throughout the study. During the first 10 min of PTCA, the lag time during oxidation of LDL in vitro did not change, but the maximum rate of oxidation decreased in venous and arterial samples (Wilcoxon signed rank test: p < .002). At the same time, total tocopherol levels in LDL significantly increased by 6.3% (p = .048) in arterial, but not in venous samples. Total carotenoid levels increased by 3.8% (p = .127) in arterial samples and decreased by 2.9% (p = .040) in venous samples. Forty hours after PTCA, LDL oxidation parameters and LDL antioxidant levels were similar to baseline, except for about 17% lower levels of delta-tocopherol (p = .037) and gamma-tocopherol (p = .014). Our results, therefore, do not support that PTCA in humans is associated with oxidative stress-induced lipid peroxidation.Publication Types: Clinical Trial

Evidence is increasing that a patent culprit artery improves the prognosis of patients with acute myocardial infarction (AMI). Primary percutaneous transluminal coronary angioplasty (PTCA) has shown to be more effective than thrombolytic therapy alone. How effective is rescue PTCA after failed thrombolytic treatment? In a retrospective analysis, 176 consecutive patients with AMI and TIMI 0 or 1 perfusion grade were included. Patients had either rescue PTCA after failed thrombolysis (100 patients) or primary PTCA (76 patients). Angiographic data and in-hospital and 1-year outcome were analyzed. Comparison of baseline data of the two groups showed a higher proportion of long-standing angina and use of nitrates and aspirin in the primary PTCA group. Also, the delay between the onset of pain and PTCA was not significantly different, with a mean of 222 minutes for rescue PTCA and 245 minutes for primary PTCA (p = 0.52). The angiographic outcomes in the rescue PTCA group and the primary PTCA group were identical: The intervention was successful (TIMI 3 flow and residual stenosis

This study examines the effect of anger and vital exhaustion on recurrent events after percutaneous transluminal coronary angioplasty (PTCA). Data came from 149 patients (123 men and 26 women) who underwent successful PTCA. During 18 months of follow-up, there were 37 recurrent events (25%) for which there was objective evidence of new or progression of coronary disease. The 123 male patients with high anger were significantly more likely to have multivessel disease before PTCA (odds ratio 2.42; p = 0.04), after controlling for standard heart disease risk factors. High-anger male patients also had a threefold increased risk for recurrent events after PTCA (RR 2.94; p = 0.01), which remained marginally significant after accounting for other heart disease risk factors and residual stenosis after PTCA (RR 2.33; p = 0.09). Among female patients, these relations were much weaker and not statistically significant. Among male patients, additional adjustment for vital exhaustion did not change the risk for recurrent events associated with high anger. A composite index of psychosocial risk based on anger and vital exhaustion was significantly related (p = 0.02) to events after PTCA after adjustment for standard heart disease risk factors. These findings add to the growing body of research on the role of psychosocial factors on clinical course in patients with coronary artery disease.

Objectives: To evaluate the expansion ratio of a self-expanding stem over time, and the chronic effect of stent pressure on the vessel wall. Methods: Self-expanding stents, developed by Medtronic Inc. (Minneapolis, MN, USA) and the Rouen group (Letac, Cribier, France), were implanted in 21 normal pig coronary arteries. Animals were sacrificed after recatheterization at 1 day (group I, n = 4), I week (group 2, n = 3), 3 weeks (group 3, n = 5), or 8 weeks (group 4, n = 4). Histological morphometry of the vessel medial and neointimal layers was performed. Changes were related to the, stent diameter and. its force on the vessel wall. Results: The stent expansion ratio gradually increased from 73% to 93% after 8 weeks, which implicates that radial force decreased concomitantly from 0.10 N to 0.03 N. Media compression under the rods ranged from 4l%-66% immediately after stent implantation. The mean compression was unrelated to stent expansion and remained nearly the same (40%-50%) during follow-up. Individual media rod compression ranged from 5%-95%. The neointimal layer on top of the rods increased until the third week after stent implant (neointimal thickness 211 ± 108 μm). The layer significantly decreased at 8 weeks (neointimal thickness 65 ± 9 μm). The cross-sectional neointimal area increased gradually only at the end of the stent during the 8-week follow-up. Conclusions: The self-expanding stent implanted in normal pig coronary arteries reached a gradual relaxation state 8 weeks after implantation due to the persistent radial force. This radial force induces medial wall compression, which was only positively related to the thickness of the neointimal layer at 3 weeks after implant. (J Interven Cardiol 1996;9:45–52)

It has been observed that vital exhaustion, a state characterized by unusual tiredness, increased irritability and feelings of demoralization not uncommonly precedes myocardial infarction in apparently healthy individuals. This observation raised the question as to whether vital exhaustion is a marker of subclinical coronary disease. To answer that question the condition was assessed in 105 male patients (mean age 54.8 year) before and 2 weeks after successful percutaneous transluminal coronary angioplasty (PTCA) by the Maastricht questionnaire. Vital exhaustion was found to be significantly correlated with the number of diseased vessels before PTCA and to decrease significantly after PTCA. However, the association was rather modest (R2 = 0.08) and most patients remained exhausted after PTCA. During a follow-up period of 1.5 years, 32 patients (30%) experienced a new cardiac event (cardiac death, myocardial infarction, coronary artery bypass grafting, repeat PTCA, a new coronary lesion or recurrent angina with documented ischaemia). Univariate and multivariate analyses showed that the number of diseased vessels, hypercholesterolaemia, and vital exhaustion were independently associated with future events. The odds ratios were 3.74 (P = 0.02), 3.08 (P = 0.08) and 3.07 (P = 0.04), respectively. It is concluded that the tiredness preceding a cardiac event is only modestly associated with the extent of coronary artery disease and that a state of exhaustion after PTCA increases the risk for a new cardiac event.

Background A double-blind, placebo-controlled study using anistreplase was performed in 159 patients with unstable angina. All patients had a history of unstable angina combined with typical ECG changes and without evidence of a previous, recent, or ongoing myocardial infarction. The purpose of the present study was to analyze the relationship between the patency of the culprit artery and the behavior of the ischemia-related regional left ventricular (LV) wall motion. Methods and results On entry to the study, all patients received conventional drug therapy: IV nitroglycerin therapy, an oral beta-blocking agent, and a calcium antagonist. Baseline angiography was carried out within 3 h after randomization, a mean of 4.2±3.0 h (range, 1 to 17 h) after the last attack of chest pain. Treatment with trial medication was withheld in 33 cases. Sixty-five patients with coronary artery disease received anistreplase (30 U/5 min)/heparin and 61 patients heparin-only therapy. Angiography was repeated 20.6±4.6 h (mean±SD; range, 12 to 39 h) after the baseline angiographic study. To assess changes in regional myocardial wall motion, the LV wall was divided into seven segments. The ischemia-related coronary artery stenosis was calculated quantitatively and related to the quantitatively assessed mean regional left ventricular ejection fraction (RLVEF) of the ischemia-related segments. In 118 of 126 patients who received trial medication, we found that anistreplase/heparin therapy leads to a significantly (p Conclusion In these patients with unstable angina, the LV wall motion improved both in the treated and the control group at follow-up angiography 1 day later. Improved coronary arterial anatomy was associated with a lesser improvement of the LV contractile function than when worsening of the coronary angiographic appearance occurred. There is no rational explanation of these results. This is a beginning of an effort to elucidate the clinical significance of the stunned and hibernating myocardium in humans.

Saruplase is an unglucosylated single-chain recombinant urokinase-type plasminogen activator. Dose finding studies in patients with acute myocardial infarction indicated that a dose of 80 mg of saruplase, given as a bolus of 20 mg and iv infusion of 60 mg in one hour, led to excellent patency figures.Saruplase is most effective when combined with a bolus of 5000 IU heparin followed by an iv heparin infusion for at least 24 hours.When saruplase is compared to other thrombolytic agents (streptokinase, alteplase, urokinase), it becomes apparent that its profile is excellent. Early patency rates are at least comparable to alteplase. Further reocclusion rates of saruplase after one day are lower than those of streptokinase and alteplase. Patency rates 24-72 hours after start of medication are comparable between saruplase and urokinase.The large database in over 6000 patients shows that saruplase, in comparison to the other thrombolytic agents, is safe. Its bleeding complication rate is significantly lower than streptokinase, and a trend to lower in-hospital mortality is observed when compared to urokinase.Summarizing, when comparing to the presently available thrombolytic agents, saruplase is a fast acting, effective and safe thrombolytic agent.

Excessive tiredness is one of the most prevalent premonitory symptoms of myocardial infarction and sudden cardiac death. This state is labelled as vital exhaustion and consists of three components: fatigue, increased irritability, and demoralization. Vital exhaustion has been found to be an independent risk-indicator of myocardial infarction in one prospective study and several case-control studies. It is as yet unclear whether the association between vital exhaustion and future myocardial infarction can be explained by confounding of (subclinical) coronary artery disease. Therefore, the present study investigates the predictive value of vital exhaustion for the occurrence of new cardiac events after percutaneous transluminal coronary angioplasty (PTCA), while explicitly controlling for the severity of coronary artery disease. Patients with a successful PTCA were followed during 1.5 years. A new cardiac event was defined as present if one of the following end points occurred: cardiac death, myocardial infarction, coronary bypass surgery, repeat-PTCA, increase of coronary atherosclerosis, or new anginal complaints with documented ischemia. Vital exhaustion was assessed using the Maastricht Questionnaire two weeks after hospital discharge. Participants of the present study were 127 patients (mean age 55.6 +/- 9.1; 105 men, 22 women). Fifteen (35%) of the 43 exhausted patients experienced a new cardiac event, whereas 14 (17%) of the 84 not exhausted patients had a new cardiac event (OR = 2.7; CI = 1.1-6.3; p = .02). Multiple logistic regression analysis revealed that vital exhaustion continued to be of predictive value when other significant risk factors for new cardiac events were controlled for (i.e., severity of coronary artery disease and hypercholesterolemia).(ABSTRACT TRUNCATED AT 250 WORDS)

Excess fatigue and exhaustion are among the most prevalent premonitory complaints of myocardial infarction and sudden cardiac death. These feelings may reflect subclinical heart disease, prolonged psychological tension, or both. The present study investigates to what extent coronary artery disease explains exhaustion. For this purpose, the relationship between the severity of coronary artery disease and exhaustion, and the relief of exhaustion after successful percutaneous transluminal coronary angioplasty (PTCA) is investigated. Patients who had a successful elective PTCA ( N = 120) were evaluated on feelings of exhaustion on admission, 2 weeks after discharge and 6 months after discharge, making use of the Maastricht Questionnaire. Multiple regression analyses were used to investigate to what degree exhaustion on admission and after PTCA was determined by the extent of coronary artery disease and other patient characteristics. Severity of coronary artery disease before PTCA was positively associated with exhaustion and successful PTCA resulted in a significant decrease of exhaustion scores ( P R 2 = 0.04, F = 5.1, P = 0.03). The majority of patients who were exhausted before PTCA remained exhausted after PTCA. Exhaustion was present in 75% of the patients before PTCA and in 65% 2 weeks after PTCA, which indicates that restoration of coronary perfusion by successful PTCA does not substantially reduce the number of exhausted patients. At 6 months, exhaustion was present in 60% of the patients, and there was no difference between patients with and without typical anginal complaints at that time. It is concluded that impaired coronary perfusion can only partially account for the tiredness in patients with CAD and that successful PTCA does not substantially ameliorate feelings of exhaustion.

The aim of this study was to assess the value of the electrocardiogram recorded during chest pain for identifying high-risk patients with 3-vessel or left main stem coronary artery disease (CAD). Therefore, the number of leads with abnormal ST segments, the amount of ST-segment deviation, and specific combinations of leads with abnormal ST segments were correlated with the number of coronary arteries with proximal narrowing of > 70%. Electrocardiograms recorded during chest pain were compared with one from a symptom-free episode. In this retrospective analysis, 113 consecutive patients were included. One-vessel CAD was present in 47 patients, 2-vessel CAD in 22, 3-vessel CAD in 24 and left main CAD in 20. Stratification was performed according to the presence of an old myocardial infarction. The number of leads with ST-segment deviations, and the amount of ST-segment deviation in the electrocardiogram obtained during chest pain at rest showed a positive correlation with the number of diseased coronary arteries. These findings were more marked when the absolute shifts from baseline were considered, because ST-segment abnormalities could be present also in the electrocardiogram obtained during the symptom-free episode. Left main and 3-vessel CAD showed a frequent combination of leads with abnormal ST segments: ST-segment depression in leads I, II and V4-V6, and ST-segment elevation in lead aVR. The negative predictive and positive accuracy of this pattern were 78 and 62%, respectively. When the total amount of ST-segment changes was > 12 mm, the positive predictive accuracy for 3-vessel or left main stem CAD increased to 86%.(ABSTRACT TRUNCATED AT 250 WORDS)

Complications after implantation of articulated Palmaz-Schatz stents in coronary arteries of 3 patients are reported. In 1 patient, embolization of the stent occurred during the acute phase, and in the other 2 patients, we observed restenosis after 4 and 5 months, respectively. Late restenosis was located in the midportion and the distal end of the stent in 1 patient. In the other patient a severe subtotal occlusion was found 1 cm proximal to the stent. These findings suggest that adaptation of the stent delivery system is needed to prevent loss of the stent and scraping of the vessel wall.

Outcome after myocardial infarction (MI) is commonly conceptualized as exercise tolerance, recurrent infarction and return to work. In the present study a relative measure of return to former leisure and social activities (LSA) was tested in 366 myocardial infarction (MI) patients. Next, the hypothesis that psychosocial factors are more important predictors for return to LSA than medical ones, was tested. It appeared that at baseline (3 weeks after MI) 36%, at post-test (3 months after MI) 51% and at follow-up (1 year after MI) 54%, reached former levels of LSA. It could be shown, both in multiple regression analysis and path analysis, that psychological vulnerability at baseline is the most important predictor of return to former LSA. Females, older patients, single patients and patients with angina pectoris showed an unfavorable psychological profile at baseline. It is suggested that more attention should be given to the improvement of the psychological status soon after MI for the categories of patients mentioned.

Aims We sought to define reperfusion-induced ventricular arrhythmias (VAs) more precisely through simultaneous angiography, continuous ST-segment recovery, and beat-to-beat Holter analyses in subjects with anterior ST-elevation myocardial infarction (STEMI) undergoing primary angioplasty [percutaneous coronary intervention (PCI)]. Methods and results All 157 subjects with final TIMI 3 flow had continuous 12-lead electrocardiography with simultaneous Holter recording initiated prior to PCI for continuous ST-segment recovery and quantitative VA analyses. Ventricular arrhythmia bursts were detected against subject-specific background VA rates using a statistical outlier method. For temporal correlations, timing and quality of reperfusion were defined as first angiographic TIMI 3 flow with ≥50% stable ST-segment recovery. Almost all subjects had VAs [156/157 (99%)], whereas VA bursts during or subsequent to reperfusion occurred in 97/157 (62%). The majority of VA bursts (72%) arose within 20 min of reperfusion (95% CI: 26.7, 72), with onset at a median of 4 min post-reperfusion (IQR: 0–43) Bursts comprised a median of 1290 ventricular premature complexes (VPCs) (IQR: 415–4632) and persisted for a median of 105 min (IQR: 35–250). Most background VAs occurred as single VPCs; bursts typically comprised runs of three or more VPCs. Subjects with bursts had higher absolute peak ST segments and more frequent worsening of ST elevation immediately after reperfusion. Conclusion Ventricular arrhythmia bursts temporally associated with TIMI 3 flow restoration and stable ST-segment recovery (reperfusion VA bursts) can be precisely defined in subjects with anterior STEMI and may constitute a unique electric biosignal of myocellular response to reperfusion.

Contains fulltext : 51483.pdf (Publisher’s version ) (Closed access) OBJECTIVE: Macrophage migration inhibitory factor (MIF), a protein secreted by immune cells and the pituitary gland, may be associated with coronary artery disease (CAD) and the mental state of coronary patients. The first origin of MIF suggests positive, the second negative associations. The aim of this study was to explore the direction of the association of MIF with CAD and of MIF with exhaustion, if any. METHODS: Participants were 194 patients who had been recently treated by percutaneous coronary intervention (PCI) and who were exhausted at the start of the study. Half entered a behavioral intervention program. MIF, C-reactive protein, interleukin (IL)-6, IL-1 receptor antagonist, and neopterin were measured in blood collected 6 weeks after PCI (baseline) and 6 and 18 months after baseline. A single measurement of MIF was also available for 129 age- and sex-matched healthy individuals (reference group). RESULTS: At baseline, MIF in patients undergoing PCI was significantly lower than in the reference group (p < .01). New cardiac events occurred twice as often in the lowest quartile than in the highest quartile of MIF concentrations. However, the association was not significant (chi(2) = 2.27; df = 3; p = .52). During follow up, MIF concentrations increased significantly in patients undergoing PCI (p < .001). At 18 months, MIF concentrations were significantly lower in the exhausted patients than in the nonexhausted patients (p = .02). hsCRP, IL-1ra, IL-6, and neopter in concentrations did not change over this time period. CONCLUSIONS: The data are suggestive of a negative association of MIF with CAD and of MIF with exhaustion. The observation that those patients who remained exhausted had lower concentrations of MIF fits into earlier observations that suggested that exhausted coronary patients may be characterized by a hypoactivity of the hypothalamic-pituitary-adrenocortical axis.

Aims To examine the safety and efficacy of intravenous caldaret in patients with large acute ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). Methods and results STEMI patients ( n =387) with ≥10 mm summed ST-deviation on electrocardiogram were randomized to receive a 48 h infusion of caldaret 57.5 mg [lower dose (LD)], caldaret 172.5 mg [higher dose (HD)], or placebo, starting before PCI. Both HD and LD were well tolerated. In 247 patients with pre-PCI TIMI 0/1, there was no effect of HD or LD on single photon emission computed tomography infarct size or ejection fraction assessed at Day 7 and Day 30. Subgroup analyses suggest that future work in patients with anterior MI might be warranted. Conclusion This first human experience with caldaret prior to direct PCI for large STEMI shows a good safety profile. No evidence of efficacy was discerned. Subgroup analyses in anterior MI patients showed some effects in endpoints studied, however, these findings require confirmation in a further study if a drug effect is to be established.

A 49-year-old female patient with a history of coronary artery disease was seen in our hospital because of a recurrent pseudoaneurysm of the left ventricle (LV). In 1993, she suffered from an anteroseptal wall myocardial infarction complicated by a ventricular septal rupture requiring surgical closure of the defect with a patch. In 1995, a large pseudoaneurysm of the LV apex originating from the site of the old ventriculotomy was diagnosed …

Contains fulltext : 48049.pdf (Publisher’s version ) (Closed access) Chronic inflammation is one of the main underlying mechanisms in the development of coronary artery disease (CAD). We investigated the prognostic value of inflammatory markers for cardiac events occurring more than 6 months after percutaneous coronary intervention (PCI), i.e. late cardiac events, furthermore we investigated the temporal stability of these markers. Exhausted patients (234) recently treated by successful PCI were studied. Serum samples collected about 6 weeks after PCI (baseline), 6 and 18 months after baseline were analyzed for CRP, IL-6, tumour necrosis factor (TNF-alpha), IL-10, IL-1ra, IL-8 and neopterin. In the mean cardiac follow-up of 24 months, 25 late cardiac events occurred. Cox proportional hazards analysis was used to determine the prognostic value. Elevated concentrations of IL-6 at baseline and 6 months later increased the risk of late cardiac events (RR 3.9, CI 1.7-9.0, p 0.00 and RR 3.6, CI 1.6-8.5, p 0.00). Elevated concentrations of CRP and IL-10 at baseline also increased the risk of late cardiac events (RR 2.5, CI 1.1-5.7, p 0.04 and RR 2.5, CI 1.1-5.6, p 0.03) as did IL-1 receptor antagonist at 6 months (RR 2.6, CI 1.1-6.1, p 0.04). Temporal stability was high for most markers, but highest for IL-6. These results support the assumption that chronic inflammation is a pathophysiological mechanism in the development of CAD.

Serum cholesterol changes after an 8-week behavior modification program for patients with coronary artery disease (CAD) were studied in a randomized controlled clinical trial. Acute myocardial infarction (AMI) or coronary artery bypass grafting (CABG) patients were randomly assigned to the intervention (N = 94) or to usual care (N = 90). After 9 months’ follow-up the intervention was effective in reducing total cholesterol and LDL cholesterol levels, particularly in patients with high baseline lipid levels. After correcting for changes in dose of statins during follow-up, effects were weakened, but for patients with high baseline cholesterol levels favorable effects remained. In these patients, the intervention group showed a decline of total cholesterol and LDL cholesterol levels of 20% and 29%, respectively, compared to a 12% and 19% reduction in the control group (p < .01). These effects could not be explained by changes in dietary fat consumption. An unexpected finding was a lower increase in HDL cholesterol in the intervention group than in the control group.

Plasminogen activator therapy for acute myocardial infarction is limited by lack of achievement of early, complete, and sustained reperfusion in a substantial proportion of patients. Many phase II trials have supported the potential of combined fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition for improving reperfusion. We did a randomised, open-label trial to compare the effect of reteplase alone with reteplase plus abciximab in patients with acute myocardial infarction.16588 patients in the first 6 h of evolving ST-segment elevation myocardial infarction were randomly assigned standard-dose reteplase (n=8260) or half-dose reteplase and full-dose abciximab (n=8328). The primary endpoint was 30-day mortality, and secondary endpoints included various complications of myocardial infarction. Analysis was by intention to treat.At 30 days, 488 (5.9%) of patients in the reteplase group had died, compared with 468 (5.6%) in the combined reteplase and abciximab group (odds ratio 0.95 [95% CI 0.83-1.08], p=0.43). There were fewer deaths or non-fatal reinfarctions with the combination than with reteplase alone, and there was less need for urgent revascularisation and fewer major non-fatal ischaemic complications of acute myocardial infarction. On the other hand, there were more non-intracranial bleeding complications in the combination group. The rates of intracranial haemorrhage and non-fatal disabling stroke were similar.Although combined reteplase and abciximab was not superior to standard reteplase, the 0.3% absolute (5% relative) decrease in 30-day mortality fulfilled the criteria of non-inferiority. Combination therapy led to a consistent reduction in key secondary complications of myocardial infarction including reinfarction, which was partly counterbalanced by increased non-intracranial bleeding complications.

OBJECTIVE—To investigate the value of non-invasive reperfusion indices in acute myocardial infarction, avoiding the possible need for acute coronary angiography and subsequent angioplasty. DESIGN—In a prospective angiographic study, seven potential ECG or clinical markers of reperfusion were analysed in 230 patients with acute myocardial infarction. In all patients two 12 lead ECGs were used: the ECG on admission and the ECG immediately before coronary angiography. Non-invasive markers of reperfusion determined just before coronary angiography were prospectively correlated to thrombolysis in myocardial infarction (TIMI) flow. Data analysis correlated these non-invasive indices with coronary flow (analysis A: TIMI 2-3 v TIMI 0-1 flow; analysis B: TIMI 3 v TIMI 0-2 flow). RESULTS—A sudden decrease in chest pain was the most common sign of reperfusion (36%), followed by reduction in ST segment elevation by ⩾ 50% (30%), and the development of a terminal negative T wave (20%) in the lead with the highest ST segment elevation. Reduction in ST segment elevation by ⩾ 50% and the appearance of an accelerated idioventricular rhythm (AIVR) had the highest positive predictive value for reperfusion. For analyses A and B, the positive predictive values were 85% and 66% for resolution of ST segment elevation, and 94% and 59% for AIVR, respectively. The presence of three or more non-invasive markers of reperfusion predicted TIMI 3 flow accurately in 80% of cases. CONCLUSIONS—The prospective use of non-invasive indices of reperfusion is simple, practical, and can be of value in assessing coronary patency in patients admitted with acute myocardial infarction. Using these indices, discrimination between TIMI 0-1 and TIMI 2-3 flow can be made with good accuracy. However, TIMI 3 flow cannot be determined reliably. The use of such non-invasive indices depends on the goal of reperfusion. Keywords: reperfusion indices; acute myocardial infarction

In 7 of 43 patients in whom a sustained ventricular tachycardia could be induced during programmed electrical stimulation by a single ventricular premature stimulus, an identical tachycardia could also be initiated by a single atrial premature stimulus. This phenomenon was observed only in those patients in whom the ventricular tachycardia could be induced by a single ventricular extrastimulus having a prematurity index (ratio between the longest ventricular premature stimulus interval resulting in tachycardia and the duration of the basic cycle length of the paced ventricular rhythm) above 54%. No single instance of initiation of ventricular tachycardia by atrial premature stimuli was observed in patients with a ventricular prematurity index below 54% or requiring more than one consecutive ventricular extrastimulus to have tachycardia initiated. Other features of patients showing initiation of ventricular tachycardia by atrial premature stimuli were a right bundle branch block configuration of the QRS complex during tachycardia in all seven patients and a relatively slow rate during tachycardia. In one patient ventricular tachycardia was terminated by a conducted atrial premature stimulus.

During the past 20 years intracardiac electrophysiologic studies have proven to be of great help in diagnosing site of origin and mechanism of clinically occurring tachycardia [1, 2]. By closely examining the 12-lead electrocardiogram (ECG) from these patients against the background of information derived from intracardiac electrophysiologic studies we have markedly improved the diagnostic abilities of the 12-lead ECG. In fact, we have reached the stage that an intracardiac study is often unnecessary for diagnostic purposes when a 12-lead electrocardiographic recording of the clinically occurring tachycardia is available [3-9].

OBJECTIVES This study was performed to assess whether angiography six months after coronary balloon angioplasty or stent implantation has an influence on clinical management and one-year outcome. BACKGROUND The Benestent II study randomized 827 patients to balloon angioplasty or stent implantation. A subrandomization was undertaken allocating patients to six-month clinical follow-up (CF) or clinical and angiographic follow-up (AF). METHODS Seven hundred and six patients (349 CF and 357 AF) had no intercurrent angiography, so that restenosis and disease progression elsewhere remained unknown until the time of six-month follow-up. These two groups, which were well matched at enrolment, were compared with respect to symptoms, medication and major cardiac events defined as death, myocardial infarction and need for revascularization at six and 12 months. RESULTS At six-month follow-up, 53 (15%) of the CF and 76 (21%) of the AF patients had stable angina (p = 0.041), while 5 (1%) and 4 (1%) had symptoms of unstable angina. At 12-month follow-up, 44 (13%) patients in both groups had stable angina, and only 1 patient in the CF group had unstable angina. Seventy-seven patients (27 CF and 50 AF; p < 0.01) had major cardiac events between 6 and 12 months. Of the 349 patients in the CF group, 21 underwent repeat percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery between 6 and 12 months, compared with 44 of the 357 patients in the AF group (relative risk 2.05 [1.24 to 3.37], p = 0.003). CONCLUSIONS Patients who had AF six months after balloon angioplasty or stent implantation experienced more repeat revascularization procedures than those who had CF. They also had significantly more angina at six-month follow-up but this may be due to bias.

Background Intracoronary ultrasound (ICUS) imaging is potentially suitable to identify lesions at high risk of restenosis after percutaneous transluminal coronary angioplasty (PTCA), but it has not been studied systematically. Methods and Results We recruited 200 patients in whom ICUS studies were performed after successful PTCA and related their ICUS parameters to 6-month follow-up quantitative coronary angiography. This was performed in 164 patients (82%), yielding 170 lesions for analysis. The overall incidence of a ≥50% diameter stenosis at follow-up (categorical restenosis) was 29.4%. Quantitative ICUS parameters were weakly but significantly related to follow-up minimal luminal diameter on quantitative coronary angiography (lumen area: R 2 =.36, P =.0001; vessel area: R 2 =.29, P =.0002; plaque area: R 2 =−.18, P =.021; percent obstruction: R 2 =−.15, P =.05), but categorical restenosis was not significantly related to these parameters ( P =.63, .77, .38, and .08, respectively). There were no significant predictors of restenosis in ICUS parameters of plaque morphology: eccentric versus concentric ( P =1.0), plaque type (hard, soft, or calcific, P =.98), or the number of calcified quadrants ( P =.41). There were no significant predictors of restenosis in two predefined types of vessel-wall disruptions: (1) rupture: presence ( P =.79), depth (partial versus complete, P =.85), or extent in quadrants ( P =.6), and (2) dissection: presence ( P =.31), depth ( P =.82), or extent ( P =.38). Conclusions Qualitative ICUS parameters after PTCA did not predict restenosis. A larger lumen and vessel area and a smaller plaque area by ICUS were associated with a larger angiographic minimal lumen diameter at follow-up, but these parameters were not significantly related to categorical restenosis.

Sequential electrocardiograms from admission to 36 hours in 358 patients with acute myocardial infarction (AMI) from the Pro-urokinase In Myocardial Infarction trial were assessed. The electrocardiogram was also examined at discharge in 69 of 358 patients. Patients underwent acute angiography, after which angioplasty was performed in most patients with impaired flow. The sum of the ST-segment deviation and Q- and R-wave voltages, and the QRS score were calculated and used for further evaluation. Development of Q waves, loss of R waves, and QRS score were completed within the first 9 hours after onset of AMI and remained stable thereafter. Reperfused patients had earlier stabilization and less severe electrocardiographic (ECG) abnormalities than nonreperfused patients. ST-segment elevation had already stabilized after 5 hours, was unchanged at 36 hours, and had significantly decreased at discharge. No significant ECG and clinical outcome differences were found between the Thrombolysis In Myocardial Infarction trial (TIMI) 2 and TIMI 3 patients. A 23.3% gain in ECG-estimated infarct size was found in the reperfusion group compared with a 12.0% gain in the nonreperfused group (p = 0.08). In summary, as early as 9 hours after onset of AMI, QRS changes were already complete. Thereafter, QRS morphology was stable. Thus, a QRS-based estimation of infarct size can be made as early as 9 hours after AMI. A similar ECG outcome for patients with TIMI 2 and 3 flow was found, which was significantly different from patients with TIMI 0 to 1 flow.

Objectives. The presence of thrombus formation and type of coronary artery lesion were determined in patients with unstable angina and correlated with the angiographic findings and clinical outcome.Background. Some previous studies have suggested that thrombus formation and lesions are predictive of the angiographic and clinical findings. This was evaluated in a retrospective analysis of 159 patients participating in the placebo-controlled Unstable Angina Study Using Eminase (UNASEM) trial on the effect of thrombolysis in unstable angina.Methods. Patients without a previous myocardial infarction who presented with a typical history of unstable angina in the presence or abnormal findings on the electrocardiogram indicative of ischemia were included in the study. After baseline angiography, study medication (anistreplasc or placebo) was given to 126 of 159 patients. Thirty-three patients did not receive medication because of significant main stem disease or normal coronary arteries or for other reasons. Angiography was repeated after 12 to 28 h.Results. Quantitative angiography showed a significant decrease in diameter stenosis in the anistreplase-treated group compared with the placebo-treated group (decrease 11% vs. 3%, p = 0.008). No differences in clinical outcome were found when thrombolytic treatment was compared with placebo (p = 0.98). Neither the presence nor absence of thrombus formation (p = 0.98) nor the type of lesion (p = 0.96) was related to the changes in diameter stenosis or to clinical outcome (p = 0.90 and p = 0.77, respectively). The power of these analyses to detect a 20% difference varied between 56% and 74%.Conclusions. In this selected group of patterns with unstable angina, type of coronary artery lesion and the presence or absence of thrombus formation does not predict clinical outcome.