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VasoSeal is a purified bovine, absorbable collagen plug currently successfully used to close the femoral arterial puncture site after cardiac catheterization under full anticoagulation. Up to now there has been no experience with potential complications. We observed acute ischemia in the right lower leg of 2/100 patients 36 resp. 24 h after successful closure of the puncture site with VasoSeal. Angiography confirmed acute occlusion of the distal A. poplitea dextra. A 25-mm resp. 50-mm long cylindrical foreign body embolus was removed with a Fogarty-catheter by retrograde indirect embolectomy. Histopathology confirmed a fresh collagen clot with appositional thrombosis.

Background: Cardiac troponin T is a regulatory contractile protein not normally found in blood. Its detection in the circulation has been shown to be a sensitive and specific marker for myocardial cell damage. We used a newly developed enzyme immunoassay for troponin T to determine whether its presence in the serum of patients with unstable angina was a prognostic indicator., Methods: We screened 109 patients with unstable angina (25 with accelerated or subacute angina and 84 with acute angina at rest) for serum creatine kinase activity, creatine kinase isoenzyme MB activity, and troponin T every eight hours for two days after admission to the hospital. The outcomes of interest during the hospitalization were death and myocardial infarction., Results: Troponin T was detected (range, 0.20 to 3.64 micrograms per liter; mean, 0.78; median, 0.50) in the serum of 33 of the 84 patients (39 percent) with acute angina at rest. Only three of these patients had elevated creatine kinase MB activity (two were positive for troponin T, and one was negative). Of the 33 patients who were positive for troponin T, 10 (30 percent) had myocardial infarction (3 after coronary-artery bypass surgery), and 5 of these died during hospitalization. In contrast, only 1 of the 51 patients with angina at rest who were negative for troponin T had an acute myocardial infarction (P less than 0.001), and this patient died (P = 0.03). Thus, 10 of the 11 patients with myocardial infarctions had detectable levels of troponin T; only 1 had elevated creatine kinase MB activity. Troponin T was not detected in any of the 25 patients with accelerated or subacute angina, and none of these patients died., Conclusions: Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial-cell injury than serum creatine kinase MB activity, and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina.

Impaired contractile performance at rest is not necessarily due to irreversible tissue damage but may relate to the "hibernating" myocardium. Hibernating myocardium has been defined as potentially reversible, chronic contractile dysfunction during prolonged, painless ischemia. The extent and time course of functional recovery after restoration of flow is of major importance for clinical decision making. The existence of hibernating myocardium was first documented in patients following bypass surgery. Angiographic studies in patients undergoing coronary angioplasty revealed immediate recovery of global and regional systolic, as well as diastolic, function after revascularization. Subgroup analysis showed an improvement in patients without previous myocardial infarctions and in those with non-Q-wave infarctions, but a benefit was not consistently seen in patients with transmural infarctions. A further improvement of systolic function after 15 weeks suggests a biphasic course of recovery. Prospective studies must clarify whether the potential for improvement in function constitutes an indication for revascularization independent of clinical symptoms.

We prospectively investigated the influence of the cardiovascular risk factors hypercholesterolemia, smoking, diabetes mellitus, and arterial hypertension on the occurrence and extent of restenosis after successful coronary dilatation (PTCA). Of the 103 patients included in the study, control coronary angiography was obtained in 75 (73%) after 173 +/- 117 days. The restenosis rate (82 stenoses), defined as greater than or equal to 50% loss of initial gain in percent diameter stenosis, was 37%. Older age, male gender, and a history of diabetes mellitus were associated with a significantly increased mean extent of restenosis (p less than 0.05). In patients with hypertension, the initial success of dilatation was less than in controls without hypertension (p less than 0.05), and restenosis tended to be enhanced (p = 0.06). The risk of restenosis was unaffected by smoking and the presence of hypercholesterolemia. In spite of the mostly insignificant influence of single cardiovascular risk factors, the extent of restenosis clearly increased with the number of risk factors.

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) was shown not to be preventable by antiplatelet therapy; residual platelet function under treatment with platelet inhibitors could be one cause of this. Therefore, in a prospective investigation, residual platelet function was assessed in 98 patients treated with acetylsalicylic acid (ASA) on three occasions during the first 3 months after successful PTCA. Control cardiac catheterization was obtained in 75 of these patients (77%) with 82 dilated stenoses 173 +/- 117 days after PTCA. Restenosis, defined as diameter stenosis greater than or equal to 50% at control angiography, occurred in 41% of the dilated vessels, and 43% of patients experienced restenosis in at least one vessel. The in vitro platelet aggregatory response to either ADP (0.5, 1, and 10 microM) or collagen (1 and 5 mg/L) as aggregating agents did not differ between patients with and without restenosis. In addition, neither the collagen-stimulated in vitro synthesis of thromboxane nor the basal or prostaglandin E1-stimulated concentrations of cyclic AMP in platelet-rich plasma (PRP) was different in the two groups. There was no significant correlation between any of the parameters of platelet function assessed and the change in coronary luminal diameter observed between immediately after PTCA and control coronary angiography. The mean dose of ASA ingested during follow-up was also not a determinant of the occurrence of restenosis. Thus, residual platelet function under treatment with ASA as measured in vitro in this study, did not influence the occurrence of restenosis after successful PTCA.

The treatment of delayed coronary occlusion after primary successful percutaneous transluminal coronary angioplasty (PTCA) is more difficult because surgical standby is often not available. The purpose of this study was to assess the therapeutic approaches and outcome of patients with delayed coronary occlusion from 30 to 180 minutes after successful PTCA. A delayed occlusion occurred in 18 (0.9%) (61 +/- 11 years; male n = 14, female n = 4) out of 2065 consecutive patients after PTCA. In 11 patients the dilated stenoses were located in the left descending artery, while seven patients had the stenosis in the right coronary artery. Twelve patients had unstable or postinfarction angina. The time interval between completion of PTCA and the onset of chest pain was 64 +/- 39 minutes. Immediate i.v. nitroglycerin resulted in no relief of the symptoms in any patient. One patient was operated upon at once, and one was given i.v. thrombolysis resulting in pain relief and reversal of ECG changes. The remaining 16 patients returned initially to the catheterization laboratory, where the occluded vessels were opened by mechanical recanalization. Three of them remained in stable condition. Due to impending reocclusion surgery was necessary in four patients and thrombolysis was performed in nine. After thrombolysis the vessel remained open in four patients. The other five needed bypass surgery on the day of PTCA. Myocardial infarction developed in nine patients (maximal CK 673 +/- 488 units/l). In conclusion, delayed occlusion after successful PTCA is a rare complication occurring primarily in patients with unstable angina. Mechanical recanalization opened the occluded vessel in most patients, and myocardial infarction was prevented in 50%.

Unlabelled: The effect of PTCA on chronically impaired, regional wall motion was studied in 40 patients with stable angina and stenoses in the left anterior descending artery. Left-ventricular angiograms were obtained before, 15 min after PTCA and, additionally, in eight patients 15 +/- 5 weeks after PTCA. Left-ventricular ejection fraction and regional myocardial function were assessed by the centerline method. Patients with no (n = 18) or non-Q-wave (n = 12) infarction were compared to patients with Q-wave infarction (n = 10). After PTCA, ejection fraction increased from 54 +/- 8% to 59 +/- 8% (p less than 0.05) and regional function improved significantly (maximal standard deviation before PTCA: 2.8 +/- 0.8; after PTCA: 1.9 +/- 0.9- segments below the first standard deviation before PTCA: 31 +/- 16; after PTCA: 19 +/- 17). The improvements were found in patients with no or non-Q-wave infarction. The benefit on regional function was unchanged at follow-up., Conclusions: PTCA reduced chronic regional myocardial dysfunction in 78% of the patients with stable angina within 15 min. Reversible myocardial dysfunction is most likely related to hibernating myocardium.

The benefit and safety of new angioplasty equipment as compared with the conventional guidewire approach was evaluated in 154 consecutive patients. with chronic, totally occluded coronary arteries. The protocol followed a stepwise design: first, conventional guidewires and low-profile balloons were used, followed by "balloon-on-the-wire" systems (Probe, Ace) or by a shaft-enforced, tip-deflecting catheter (Omniflex). In 97 patients with occlusions of 2 to 12 weeks' duration, recanalization was achieved in 51 patients (53%) with the conventional approach and in 29 patients with the new devices (balloon-on-the-wire [n = 5], Omniflex [n = 24]), thereby raising the success rate to 82%. In 57 occlusions of greater than 12 weeks' duration, the recanalization attempt was successful in 58%, mediated in 16 patients (28%) by the Omniflex catheter and in 5 patients by balloon-on-the-wire systems. There were no life-threatening complications and only 1 (0.6%) emergency bypass operation was necessary. New angioplasty devices are therefore of considerable value in the attempt to improve the results of coronary angioplasty in chronic total occlusions.

Radiological and especially scintigraphic methods are important tools in diagnosis finding, diagnosis evaluation, risk stratification and therapy control in patients with coronary artery disease. The major task is to document or exclude myocardial perfusion defects. Within this framework, thallium scintigraphy and radionuclide ventriculography occupy a definite place for non-invasive evaluation. The decision for revascularisation (bypass surgery, angioplasty) and the evaluation of the risk frequently depends on the results of the scintigraphic methods. Conventional radiological techniques and computer tomography are helpful in differential diagnosis of acute chest pain syndromes.

A computer program has been devised to automate rationalization of peptide fragmentation patterns. The program systematically generates all possible linear amino acid sequences which might be attributable to a peptide with a known amino acid composition. The generated sequences are then searched to find those that most closely match the spectrum of an unknown sequence.

Intracoronary thrombi were found in 20 of 52 patients (38%) who had coronary angiography because of treatment-resistant unstable angina. Unrelated to the angiographic finding, eight patients (15%) sustained a myocardial infarction, and two died during their hospital stay. Only one patient (5%) with and six patients (19%) without intracoronary thrombi were stabilized and discharged from hospital. The remaining patients either had an aortocoronary bypass (n = 31) or transluminal balloon angioplasty (n = 13). These findings underline the importance of intracoronary thrombus formation in the pathogenesis of treatment-resistant unstable angina.

Unlabelled: Eleven patients with chronic heart failure (NYHA stage III or IV) were given dobutamine infusions over 7 days, mean dose 6.2 +/- 2.2 micrograms/kg X min. The patients were pretreated with digitalis, diuretics, and vasodilators. Haemodynamic parameters were measured prior to infusion, 30 minutes and 7 days thereafter as well as 24 hours after the end of therapy. Before and after the 7-day therapy a two-dimensional echocardiogram was taken. In four patients, the protocol had to be discontinued prematurely for technical or medical reasons., Results: Arterial blood pressure, body weight, fractional shortening and end-diastolic diameter of the left ventricle were not changed significantly. Cardiac index rose acutely and returned to initial values after 7 days. Total peripheral resistance, which was initially significantly reduced, again rose after infusion over 7 days. Permanent reduction in pulmonary artery wedge pressure, even one day after the end of therapy, was observed in three patients showing a left-ventricular end-diastolic wall thickness greater than 7 mm. However, in patients whose wall thickness was less than 7 mm, there was a rise in pulmonary artery wedge pressure accompanied by a fall in cardiac index even below initial values.

1 The study was designed to elucidate further the mechanism by which beta-adrenoceptor antagonism with pindolol relieves the symptoms of angina pectoris in patients with coronary heart disease. 2 Pindolol administration was associated with an elevated threshold for angina pectoris and improved myocardial lactate metabolism during supraventricular pacing. 3 This beneficial effect of pindolol was independent of changes in myocardial blood flow and was not mediated by haemodynamic effects. 4 The results suggest that in angina pectoris, in addition to the recognized beneficial effects of beta-adrenoceptor blockade, the actions of pindolol also result from, as yet, poorly described phenomena such as redistribution of myocardial blood flow or metabolic effects.

Valvuloplasty was recently introduced as a palliative treatment of calcific aortic stenosis in elderly patients. Embolisation of valvular material has not been described as complication yet. We describe the detachment of a large calcific fragment resulting in acute, severe aortic incompetence in a 76-year-old patient. During immediate operative valve replacement the calcific embolus was recovered from the abdominal aorta.

Thirty-six patients with glomus jugulare tumors have been managed over a 13-year period using various combinations of skull base surgery and irradiation therapy. The data resulting from this study are presented; the techniques of diagnosis and treatment are reviewed. We conclude that irradiation therapy alone is a satisfactory form of treatment for elderly and poor-risk patients; preoperative x-ray therapy followed by skull base surgery is an effective treatment for younger patients.

Absence of a Major Arrhythmogenic Role for Cyclic AMP. Journal of Molecular and Cellular Cardiology (1986) 18, 375-387. We examined the mechanism whereby beta-adrenoceptor antagonism exerts an antiarrhythmic effect in early myocardial ischaemia. Ligation of the anterior descending coronary artery in the anaesthetized open-chest pig resulted in severe transmural anteroseptal ischaemia. Blood flow in the mid-ischaemic zone 20 min after ligation was decreased to 5.7 +/- 0.7% of the preligation control value. Epicardial ST-segment deflections of 6.7 +/- 0.4 mV were recorded over this zone. A distinct phase of ventricular arrhythmias was evident about 10 to 30 min after ligation. A high incidence of ventricular fibrillation (14/16 pigs) was associated with a circumstantial increase in levels of cyclic AMP in ischaemic tissue. Twenty minute values were: 1.10 +/- 0.06, P less than 0.05 v. the non-ischaemic tissue level of 0.86 +/- 0.05 nmol/g. Propranolol 3 mg/kg IV, metoprolol 20 mg/kg IV or sotalol 10 mg/kg IV were given between 30 min prior to and 10 min after ligation. Adequate beta-adrenoceptor antagonism by each agent could be proven. Metoprolol decreased the incidence of ventricular fibrillation (2/13, P less than 0.0005 v. control group), while propranolol or sotalol did not. All three beta-antagonists decreased tissue levels of cyclic AMP prior to ligation. However, the temporary increase in ischaemic tissue after ligation could not be prevented. Furthermore, cyclic AMP in ischaemic tissue 20 min after ligation was higher in the metoprolol group than in the propranolol or sotalol group (0.94 +/- 0.04 v. 0.81 +/- 0.02 P less than 0.05, and 0.79 +/- 0.03 nmol/g P less than 0.01, respectively). Blood flow in the mid-ischaemic zone of the metoprolol group was increased to 8.6 +/- 0.6% of preligation control value (P less than 0.0001 v. control group). In contrast, blood flow in the mid-ischaemic zone of the propranolol or sotalol group was decreased. Metoprolol also reduced epicardial ST-segment deflections over the mid-ischaemic zone to 3.5 +/- 0.2 mV (P less than 0.0001 v. control group). ST-segment deflections in the propranolol group were increased. The mechanism whereby metoprolol prevented ventricular fibrillation may be explained by a decrease in the severity of ischaemia but not in terms of changes of tissue levels of cyclic AMP.

Cardiovascular changes have been noted to occur during movement from the operating room or recovery room (RR) to the intensive care unit (ICU). This study examined blood pressure changes and related variables during transport from the RR to the ICU in 135 postoperative acoustic tumor patients. Although there was no significant change in blood pressure values from the RR to the ICU, patients with pre-existing hypertension and elevated RR blood pressures were noted to have an increased frequency of postoperative complications. In addition, a relationship was noted between administration of halothane and frequency of postoperative complications. Results highlight the need for nurses not only to monitor, but also closely control postoperative blood pressure in this population.

Phonetically balanced work lists were mechanically coupled onto the ossicular chain of anesthetized guinea pigs by piezoelectric-type drivers and the resulting cochlear microphonic (CM) recorded on magnetic tape. Similar recordings of the CM resulting from free field tympanic membrane stimulation by hi-fi speakers were also obtained. The recordings were compared by conventional discrimination testing. In discrimination testing of all the raw recordings, listeners achieved essentially perfect scores. Addition of masking noise sufficient to reduce mean discrimination scores to 65-70% revealed no significant discrimination differences. When piezoelectrically initiated, CM-derived lists were compared with similar lists passed through hearing aids in an anechoic chamber, the preference of a panel of listeners for the quality of mechanically coupled speech was significantly higher. Mechanical-acoustical displacement equivalency at normal physiological levels and freedom from mechanical-electrical artifact were demonstrated by measurement of ossicular chain displacement by a fiber optic lever displacement transducer.

Prenalterol, a beta 1 selective agonist, exerts a positive inotropic action in animal studies as well as in human volunteers and is effective when administered orally. To assess its immediate haemodynamic and myocardial metabolic effects, we studied the response to prenalterol (50 and 100 micrograms kg-1 given intravenously by cardiac catheterization) in 15 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 l min-1 m2 (mean +/- S.D.) (P less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1335 +/- 411 mmHg s-1 (P less than 0.001); left ventricular end-diastolic pressure fell from 25 +/- 6 to 17 +/- 7 mgHg (P less than 0.001); coronary sinus blood flow increased from 113 +/- 39 to 148 +/- 55 ml min-1 (P less than 0.01); myocardial oxygen consumption was augmented from 12.7 +/- 3.9 to 16.4 +/- 5.8 ml min-1 (P less than 0.001); and heart rate increased slightly (from 76 +/- 12 to 86 +/- 14 beats min-1; (P less than 0.05)). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate and myocardial arteriovenous oxygen difference, and no patients developed angina, ECG changes or ventricular arrhythmias. Infusion of prenalterol effectively improved haemodynamic function and cardiac metabolism in cardiomyopathy. Therefore this agent deserves further investigation to evaluate its possible role for the long-term therapy of patients with chronic heart failure.

In a prospective study, platelet aggregation in platelet-rich plasma after ADP stimulation (0.5, 1.0 and 10 mumol/l) and collagen (1 and 5 micrograms/ml) was measured in 36 patients with coronary heart disease, 18 with angina at rest during the eight hours preceding the time of blood sampling, and 18 patients with stable, exercise-dependent angina, matched for age and sex. In addition, c-AMP was determined, before and (as a measure of platelet adenylate cyclase activity) after stimulation of this enzyme by prostaglandin E1 (10 mumol/l for 30 sec). There were no differences between all the tested ADP and collagen concentrations with regard to platelet aggregation. c-AMP levels were also similar. Thus, in patients with unstable angina there was no evidence for generalized hyperaggregation of platelets in comparison with control subjects who had stable exercise-dependent angina.

Unstable angina describes a clinical syndrome bridging the gap between stable angina and acute myocardial infarction. By definition, patients with angina of new onset, of a crescendo pattern, and with angina at rest are included in this high-risk group. The underlying pathogenetic mechanisms are complex and include initial atherosclerotic plaque rupture, release of vasoactive substances, and intracoronary thrombus formation. The currently established medical approach of the acute phase consists of heparin for anticoagulation and nitrates combined with beta-blockers for the relief of pain. Calcium antagonists are indicated, if anginal symptoms persist. The effect of thrombolytic therapy is still under investigation. Angina refractory to medical treatment and angina at rest are associated with a particularly unfavorable prognosis and prompt early catheterization. The long-term prognosis of the patient is markedly improved by chronic platelet inhibitory treatment with aspirin.

Our experience in surgical treatment of 105 patients with cerebellopontine angle tumors is reported. Major emphasis is placed on a combined surgical approach and use of the CO2 laser. Our approach to diagnosis is also emphasized, as is the method we have used in compiling and collecting the data resulting from the study. Postoperative results and complications are reported and discussed.

We hypothesized that the antiarrhythmic efficacy of propranolol during acute myocardial ischemia could be dose related. Propranolol was administered in two equally divided doses 30 min before and 10 min after ligation of the anterior descending coronary artery (CAL) in anesthetized open-chest pigs. Only the lowest dose of propranolol, i.e., 0.1 mg/kg intravenously (i.v.) (plasma level 22 +/- 2 ng/ml) decreased the incidence of ventricular fibrillation (VF), i.e. 3 of 12 versus 16 of 20 in control group (p less than 0.01). VF incidence with propranolol 0.5 or 3 mg/kg was 4 of 6 and 8 of 9, respectively (both NS vs. control group). Propranolol 0.1 mg/kg did not change left ventricular (LV) blood flow. Propranolol 3 mg/kg reduced blood flow in the peripheral ischemic myocardium to 13.2 +/- 1.2 versus 19.2 +/- 1.4 ml/100 g/min in control group (p less than 0.01), and in the midischemic zone to 4.4 +/- 0.5 versus 7.0 +/- 0.9 ml/100 g/min in control group (p less than 0.001). Propranolol 0.1 mg/kg prevented a disparity of levels of cyclic AMP from arising between ischemic and non-ischemic myocardium, whereas propranolol 3.0 mg/kg did not. Furthermore, LV mechanical function was suppressed by propranolol 3 mg/kg. Only the lowest dose of propranolol (i.e., 0.1 mg/kg) decreased the incidence of VF in this model.

Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore, urinary excretion of their major metabolites, 2,3-dinor-thromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1 alpha, was studied in 16 patients presenting with prolonged angina at rest. The 10 patients whose condition did not improve under vigorous antianginal treatment within 48 hours exhibited higher thromboxane metabolite excretion than did the 6 patients who responded to therapy (2,208 +/- 1,542 versus 609 +/- 312 ng/g creatinine; p less than 0.001). Elevated values were also found in four of eight patients with sustained postinfarction angina. Enhanced thromboxane metabolite excretion was frequently associated with angiographic evidence of thrombus formation. When nine patients were restudied in a stable phase after 11 +/- 5 months, thromboxane metabolite excretion was consistently normal or high normal. Excretion of prostacyclin metabolites was not depressed in any patient but correlated weakly with thromboxane (r = 0.41). Thus, enhanced thromboxane production as an index of platelet activation may identify patients with active thrombus formation who could benefit most from platelet inhibitory treatment.