Images in cardiology. An isolated single coronary artery.
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Biomedical subjects
Publications and source records attributed to U Tebbe.
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BACKGROUND: The VERAS study (VErringerung der Restenoserate nach Angioplastie durch ein Somatostatin-analogon [Prevention of Restenosis Following Angioplasty With a Somatostatin Analogue]) was a placebo-controlled trial to evaluate the effects of octreotide for the prevention of restenosis after coronary angioplasty. Octreotide is a somatostatin analogue with antiproliferative properties on smooth muscle cell growth in vitro that limits myointimal thickening of arteries in balloon injury models. METHODS AND RESULTS: Patients received either octreotide or placebo, starting 1 hour before angioplasty and continued for 3 weeks. The minimal luminal diameters before and after angioplasty and at 6-month follow-up were analyzed with a digital quantitative algorithm. Of the initial 274 patients recruited, 217 (108 in the octreotide group and 109 in the placebo group) could be analyzed after a complete 6-month evaluation: the minimal luminal diameters were 1.67+/-0.57 mm in the octreotide-treated group and 1.66+/-0.64 mm in the placebo group (two-paired P=.70), and the relative losses were 0.16+/-0.22 and 0.13+/-0.21 (two-paired P=.27). The restenosis rates were also identical in both treatment groups: final diameter stenosis > or =50% (34.3% versus 33.9%, two-paired P=1.0), loss of > or =50% of the initial gain (34.3% versus 33.9%, two-paired P=1.0), and absolute reduction of minimal luminal diameter >0.72 mm (29.6% versus 24.8%, two-paired P=.45). Likewise, there was no difference with regard to the incidence of clinical events (death, myocardial infarction, bypass operations, reintervention). Octreotide was well tolerated, with the exception of gastrointestinal side effects, which were three times more common than in the placebo group. CONCLUSIONS: Octreotide did not reduce the angiographically determined restenosis rate or the incidence of major clinical events after coronary angioplasty.
UNLABELLED: Increased QT dispersion, defined as the difference between the maximum and minimum QT interval on the standard 12-lead electrocardiogram is assumed to reflect regional inhomogeneity of ventricular repolarization and has been shown to be associated with an increased risk of arrhythmic events. The purpose of the present study is to examine the influence of amiodarone on QT dispersion in patients with life-threatening ventricular arrhythmias and to evaluate the predictive value of QT dispersion after amiodarone therapy for further arrhythmic events. ECG's were obtained in 47 patients 1-2 days before and 6-8 weeks after amiodarone was started. All patients had coronary artery disease with a mean EF of 34 +/- 14%. The QT interval was measured in each lead of a digitized ECG displayed on a high resolution monitor (250 mm s-1). Amiodarone therapy resulted in a significant increase in the maximal QTc interval (476 +/- 44 to 505 +/- 44 ms, p < 0.001). However, measurement of QT dispersion (70 +/- 34 vs 73 +/- 29 ms) and Qtc dispersion (78 +/- 37 vs 77 +/- 31 ms) revealed no significant difference before and after amiodarone. During a one year follow-up period 26 patients were free of arrhythmic events and 7 patients developed further arrhythmic events. The remaining 14 patients were excluded from the one year follow-up analysis because of drug discontinuation (n = 8), death due to heart failure (n = 1), medical intervention (n = 3) and incomplete follow-up (n = 2). No measure of QT dispersion was predictive of recurrent arrhythmic events during treatment with amiodarone. CONCLUSION: Treatment with amiodarone results in significant QT prolongation without altering QT dispersion. Measurements of QT dispersion were not predictive of amiodarone efficacy in this patient population.
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The extent of myocardial damage occurring during acute myocardial infarction is time dependent, and there is abundant evidence from most clinical trials that mortality reduction is greatest in patients treated early with thrombolytic agents, although beneficial effects have been shown with treatment initiated up to 12 h after onset of symptoms. All studies on prehospital thrombolysis have conclusively shown the practicability and safety of patient selection and administration of the thrombolytic agent. The accuracy of diagnosis in the prehospital setting was comparable to trials of in-hospital thrombolysis, e.g., in the Myocardial Infarction Triage and Intervention Project (MITI) 98% of the patients enrolled had subsequent evidence of acute myocardial infarction. With regard to time savings, all randomized studies showed positive results. The smallest time gain was observed in the MITI trial: prehospital-treated patients received thrombolytic therapy an average of 33 min earlier than those treated in hospital. In the European Myocardial Infarction Project (EMIP) the difference in time between prehospital and hospital treatment was a median of 55 min. However, none of these trials was able to show a significant short-term mortality difference between the two groups. Only a meta analysis of five randomized studies with a combined median time gain of about 60 min showed a significant 17% reduction in short-term mortality for patients who received thrombolytic therapy in the prehospital phase. In the Grampian Region Early Anistreplase Trial (GREAT), a study performed in a more rural area than other studies, the time gain by prehospital initiation of thrombolysis was a median of 130 min. GREAT was the only study to date reporting a significant mortality benefit for prehospital-treated patients after 3 months and 1 year. In conclusion, prehospital thrombolysis is feasible and safe. Patients with acute myocardial infarction can be correctly identified and treated with thrombolytic agents in the prehospital setting with the same rate of complications as expected for in-hospital thrombolysis, provided basic resuscitation equipment including a defibrillator is available. The results of randomized studies comparing the results of prehospital and in-hospital thrombolysis seem to justify the prehospital institution of thrombolytic therapy, especially in rural areas where transport times to the hospital are long and the expected time gain is largest. The choice of the thrombolytic agent seems to be of minor importance and should follow prehospital practicability (bolus injection) and costs. Aspirin should be given to all prehospital patients with suspected myocardial infarction regardless of thrombolytic therapy.
AIMS: To describe patient characteristics, pre-hospital delay, treatment, complications and outcome in patients with acute myocardial infarction admitted to hospitals in Germany. METHODS AND RESULTS: The study was of prospective observational multicentre design. Those involved were consecutive patients with acute Q-wave myocardial infarction admitted within 96 h of onset of symptoms to 136 German hospitals between July 1992 and September 1994 (n = 14980, median age 66 (quartiles 57, 74) years, 68% male, 48% anterior wall infarction). Median pre-hospital delay was 170 (90, 475) min, with 17% arriving within the first hour and 61% within 4 h of onset of symptoms. The following patient groups had a short pre-hospital delay: males, those aged less than 65 years, those admitted at night or the weekend, those with a previous myocardial infarction, those in need of cardiopulmonary resuscitation, and those with a diagnostic first ECG. The first ECG was diagnostic in 67.6% of cases. Reperfusion therapy was used in 53%, with thrombolytic therapy in 51.6%. Median time from admission to initiation of treatment was 30 (20, 55) min. Respective rates of treatment with aspirin, nitrates, and beta-blockers were 81%, 83%, and 16%. Major complications were cerebral bleeding (0.4%), bleeding requiring transfusions (0.9%), left ventricular rupture (0.6%) and anaphylactic shock (0.1%). Median hospital stay was 20 (13, 26) days. In-hospital death rate was 17.2%. Increased hospital mortality was observed with female gender, an unknown or long pre-hospital delay, a diagnostic first ECG, anterior wall infarction, trauma or major operation within the last 14 days, renal insufficiency and malignoma. CONCLUSIONS: 'Real-life' hospital mortality is much higher than previously reported in clinical trials. To reduce hospital mortality, the efficacy of thrombolysis should be increased by shortening the pre-hospital delay, and the use of concomitant therapy, especially beta-blockers, should be increased.
OBJECTIVE: To evaluate the benefit to risk ratio of thrombolytic treatment in patients with small inferior acute myocardial infarction (AMI). Controlled studies relating the benefit from thrombolysis with initial electrocardiographic features are scarce and of limited sample size. DESIGN: Retrospective study of 728 patients with a first inferior AMI of six hours' duration from the Intravenous Streptokinase in Acute Myocardial Infarction (ISAM) study comparing streptokinase with placebo stratified by the initial sum ST segment elevation (sigma ST) of 0.8 mV or less and greater than 0.8 mV, and 636 patients from the International Joint Efficacy Comparison of Thrombolytics (INJECT) trial comparing double blind streptokinase with reteplase stratified by either sigma ST or the presence of precordial ST segment depression. RESULTS: ISAM study patients with an sigma ST of greater than 0.8 mV had a significant mortality benefit from streptokinase throughout six years, while those with an sigma ST of 0.8 mV or less showed a trend to higher mortality at six months (6.3% streptokinase v 5.1% placebo). Despite significantly smaller infarcts and fewer clinical complications in patients with an sigma ST of 0.8 mV or less (ISAM and INJECT) or the absence of precordial ST segment depression (INJECT) thrombolytic treatment was associated with higher early mortality than in those with initially larger ST segment deviations. CONCLUSION: Thrombolytic treatment in patients with inferior AMI presenting with larger ST segment deviations is associated with improved survival throughout six years. The risk to benefit ratio, however, in terms of early mortality in patients who have an sigma ST of 0.8 mV or less and no precordial ST segment depression may be unfavourable.
The purpose of this investigation was to define cardioversion success rates, frequency of complications of cardioversion, and current treatment practices in elderly patients (aged > or = 65 years) with atrial fibrillation (AF). The results were compared with those in younger patients (aged < 65 years). The investigation was a prospective multicenter observational study with 61 participating cardiology clinics. Consecutive patients in whom cardioversion of AF was planned had to be prospectively registered. Of 1,152 patients registered, 570 (49.5%) were < 65 years old (group 1) and 582 (50.5%) were > or = 65 years (group 2). The overall success rate of cardioversion on an intention-to-treat basis was 76.1% in group 1 and 72.7% in group 2 (p = 0.18). In multivariate analysis, left atrial size and New York Heart Association functional class before cardioversion were identified as predictors of success (p < 0.001, respectively; p = 0.025). These clinical factors were not equally distributed between the age groups: Left atrial size was larger in the elderly than in younger patients (44.0 +/- 6.4 mm vs 42.8 +/- 6.4 mm; p = 0.006) and a New York Heart Association functional class > or = II was more prevalent in group 2 than in group 1 (48.6% vs 29.6%; p < 0.001). The overall complication rates were not significantly different between the 2 groups (4.2% in group 1 vs 5.3% in group 2; p = 0.37). The frequency of patients who were adequately anticoagulated for cardioversion was 56.9% in age group 1 and 39.6% in age group 2 (p < 0.001). In chronic AF the same trend for age-dependent underuse of anticoagulation was observed. Age itself was not a predictor of cardioversion success and did not predispose to higher complication rates. Therefore, cardioversion should be considered in older patients with the same criteria and emphasis as in younger patients. Anticoagulation and antithrombotic medication is underused for cardioversion and in treating chronic AF, especially in elderly patients.
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The aim of the study was to compare in a single trial, using identical methodology, the pharmacokinetic properties and the effect on the hemostatic system of saruplase (unglycosylated scu-PA) and urokinase (glycosylated tcu-PA). Twenty-four patients with an acute myocardial infarction were either treated with saruplase (n = 12; 20 mg IV bolus followed by a 60 mg infusion for 60 minutes) or urokinase (n = 12; 1.5 million IU IV bolus followed by 1.5 million IU infusion for 60 minutes). Blood samples from saruplase-treated patients were analyzed for u-PA antigen and total u-PA and tcu-PA activities; those from urokinase-treated patients for u-PA antigen and tcu-PA activity. The effect of treatment on, including recovery of, plasma alpha2-antiplasmin, fibrinogen, and plasminogen was examined in both groups. The total clearance of urokinase (179 +/- 55 ml/min) is about half that of saruplase (406 +/- 154 ml/min), and the mean residence time of urokinase (59.1 +/- 22.5 minutes) is nearly twice that of saruplase (28.3 +/- 7.8 minutes), which results in a slower elimination of urokinase from plasma. Whether differences in the pharmacokinetic behavior of the unglycosylated saruplase and the glycosylated urokinase observed in this study are due to the difference in glycosylation or to other factors is not resolved. The systemic effect of saruplase on alpha2-antiplasmin, fibrinogen, and plasminogen is similar to that of urokinase, although retarded.
A 69-year-old male patient is described who presented with angina and congestive heart failure 12 years after his aortic valve had been replaced by a bioprosthesis for aortic stenosis. The aortogram showed massive dilatation of the aortic root. Coronary angiography demonstrated a displaced and narrowed left main and circumflex coronary artery. The patient died suddenly before his scheduled elective operation. At autopsy the left main and circumflex coronary artery were patent but severely compressed by extensive dilatation of the aortic root, predominantly of the left sinus of Valsalva. His sudden death was most likely due to external constriction of the left coronary artery with subsequent ischemia and ventricular fibrillation.
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BACKGROUND: Pharmacological and direct-current cardioversion of atrial fibrillation are often performed interventions. Little is known about results and complications of cardioversion in daily practise. PATIENTS AND METHODS: Demographic, procedural and outcome data from patients with cardioversion of atrial fibrillation were collected in a prospective, multicenter registry of 61 hospitals. RESULTS: Between July 1994 and December 1994 1152 patients with a mean age of 64 +/- 11 years were registered on an intention-to-treat basis. 62% were male. The most prevalent underlying disorders were coronary artery disease (34.7%), valvular heart disease (18.1%), and cardiomyopathy (6.9%). 16.4% of patients had lone atrial fibrillation. New onset atrial fibrillation was reported in 21%, paroxysmal in 32% and chronic in 47% of patients. The mean duration of atrial fibrillation was 7 +/- 26 weeks (range 1 day to 7 years, median 5 days). In 3.8% of patients no cardioversion attempt was made and follow-up was not possible in another 5.5%. 19.2% of patients cardioverted spontaneously. Direct current cardioversion was attempted in 39.7% and pharmacological cardioversion in 31.8% of patients. Cardioversion was successful (sinus rhythm at discharge) in 96.4% of spontaneous cardioversion, in 73.1% of direct current cardioversion and in 84.4% of pharmacological cardioversion. Success of cardioversion was significantly related to duration of atrial fibrillation, NYHA functional class and left atrial diameter (p < 0.001). In 55 (4.8%) cases complications were reported of which 14 were fatal. Five cases of sudden death occurred, all of which were related to quinidine therapy for pharmacological cardioversion. Five cases of embolism were reported. Two were not associated with cardioversion attempts and 3 occurred within 24 hours after successful direct current cardioversion. Two of these patients were effectively anticoagulated at the time of cardioversion. A total of only 62% of patients with atrial fibrillation of more than 48 hours duration were anticoagulated for cardioversion with coumadine or i.v. heparin. CONCLUSIONS: The main risks of cardioversion are fatal proarrhythmic events in pharmacological attempts to restore sinus rhythm. The risk of embolism is despite low rates of effective anticoagulation low.
This retrospective analysis reviewed 183 patients with acute myocardial infarction who were given front-loaded recombinant tissue-type plasminogen activator (rt-PA) and r-hirudin (HBW 023) in 1 of 4 dose groups (bolus dose of 0.07, 0.1, 0.2, or 0.4 mg/kg, followed by an infusion of 0.05, 0.06, 0.1, or 0.15 mg/kg/hour over 48 hours). Activated partial thromboplastin time (aPTT) levels were determined at baseline and at 4, 8, 12, 16, 20, 24, 32, 40, and 48 hours. Of the 178 patients with r-hirudin treatment for > or = 12 hours, anticoagulation was optimal in 55.1% (all aPTTs > 2 x baseline), suboptimal in 33.7% (lowest aPTT > 1.5 but < 2 x baseline), and inadequate in 11.2% (> or = 1 aPTT but < 1.5 x baseline). Optimal anticoagulation was observed more frequently in the higher dose groups (dose 1, 15%; dose 2, 44.4%; dose 3, 63.4%; dose 4, 73.4%; p for trend < 0.0001). Patency (according to Thrombolysis in Myocardial Infarction trial grade 2 or 3) of the infarct artery after 36 to 48 hours was higher in the group with optimal anticoagulation compared with those with suboptimal or inadequate anticoagulation: 97.9%, 88.4%, and 85%, respectively (p = 0.03 optimal vs suboptimal or inadequate anticoagulation). In conclusion, r-hirudin in a dose of 0.1 or 0.15 mg/kg/hour achieves an optimal anticoagulation in about 63% or 74% of patients, which is associated with an enhanced patency 24 to 48 hours after rt-PA. A subsequent study revealed that this effective anticoagulation may be accompanied by an increased risk of severe bleeding complications after thrombolysis.