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Quantifying the scattering effects of pronounced volcano topography on the seismic wavefield is an important component in locating and interpreting volcano seismic sources. In this study, we perform seismic wave simulations to quantify the scattering generated by a 3-D digital elevation map and 1-D velocity model of Arenal volcano, Costa Rica. Full waveform synthetic seismograms were generated using a 3-D elastic lattice method including complex topography. Several different simulations were performed where the source location, source type and topographic models were varied. Synthetic seismograms were calculated for 35 seismic arrays each one comprising nine stations. At each array, the slowness vector of wave propagation is estimated from the time delays between the sensors obtained using the cross-spectral method. Results show that the backazimuth estimated for some arrays, in particular those close to the source, deviate from the true source position suggesting strong topographic effects in these regions. The maximum of the probability density function, obtained by crossing the backazimuths of the remaining arrays, coincides exactly with the true source location. We also compare our synthetic seismograms with array results from a physical field study. The true and calculated location misfit depends largely on the topography, but also on the number of antennas, the distance from the source and the spatial resolution of the antennas. The results show that this kind of study could be undertaken prior to the installation of seismic arrays to select the sites that minimize the topographic effects leading to improved source locations. [ABSTRACT FROM AUTHOR]

Objectives: Recently, direct stenting has been shown in retrospective and randomized studies to be feasible and safe in highly selected patients, with a potential interest to reduce the cost of the procedure and the rate of no-reflow. This randomized pilot study was designed to compare the incidence of no-reflow after direct stenting or conventional stenting after balloon predilation in acute coronary syndrome-related lesions., Methods and Results: Between December 1998 and October 1999, 130 patients in our center with acute coronary syndromes were included in this study and randomized in 2 groups. In group A (n = 65), direct stent implantation was performed without balloon predilation. In group B (n = 65), conventional balloon predilation was carried out before stent implantation. Baseline clinical and angiographic characteristics before the procedure were similar in the 2 groups of patients. No-reflow was observed in 7.7% after direct stenting and in 6.1% after conventional stent implantation (P = not significant). The immediate clinical success rate was similar in the 2 groups. Among the procedural data, only duration of the procedure (shorter in the direct stenting group), the number of balloons used, and the quantity of contrast agent (lower in the direct stenting group) were significantly different between the 2 groups (P <.05). The 6-month clinical outcome was similar in the 2 groups., Conclusion: This randomized study confirms the promising results of previous studies that show the feasibility and the safety of direct coronary stenting in highly selected acute coronary syndrome-related lesions. The major impact of this strategy is the improvement of the cost-benefit ratio, with no major influence on the acute complications and especially on the occurrence of no-reflow in this high-risk population.

The purpose of this study was to assess the feasibility and safety of direct coronary stenting in acute coronary syndromes using 5 Fr guiding catheters by transradial approach. A series of 119 patients with an acute coronary syndrome (unstable angina, n = 55; acute myocardial infarction, n = 45; recent acute myocardial infarction, n = 19) explored by transradial approach and eligible for direct stenting were included. A large proportion of patients (52%) was treated during the procedure by platelet IIb/IIIa receptor blockade. Only Medtronic 5 Fr guiding catheters were used in this study. Direct coronary stenting was attempted in all 119 highly selected patients. Failure of direct stenting was observed in only five cases (3.9%) and the stent successfully retrieved in each case in the 5 Fr guiding catheter. In these five cases, balloon predilation was performed and then the stent implanted successfully. Different stents were used: ACS stent (54%), AVE stent (33%), Velocity stent (10%), Nir stent (3%), with diameter ranging from 2.5 to 4 mm. In four cases, the dilation was finally performed using 6 Fr guiding catheters because the backup of the 5 Fr catheter was considered to be too low (3%). No vascular access site complications occurred in this series of patients. We conclude that direct coronary stenting using transradial approach and 5 Fr guiding catheters yields excellent procedural success rate. In the setting of acute coronary syndromes requiring platelet IIb/IIIa receptor blockade or after failure of thrombolysis, this mini-invasive strategy is very attractive because of the low risk of access site complications., (Copyright 2002 Wiley-Liss, Inc.)

The management of heart failure that has become refractory to conventional drug treatment is an increasingly frequent problem for clinicians. Peritoneal dialysis, by ultrafiltration, is an effective method to treat refractory oedema, thereby improving the functional symptoms of these patients. The objective of this article is to review the data, of the literature and to define the results and indications of this treatment, which still remains and exceptional modality.

Objectives: This study sought to compare the efficacy of 2-h regimens of alteplase and streptokinase in acute massive pulmonary embolism. The primary end point was immediate hemodynamic improvement, and secondary end points included early clinical efficacy and safety, as well as 1-year clinical outcome., Background: Several thrombolytic regimens have been compared for the past 10 years in randomized studies, showing that 2-h infusion regimens of alteplase or urokinase lead to faster hemodynamic improvement than former 12- to 24-h administration protocols in acute massive pulmonary embolism. Many trials have focused on immediate hemodynamic and angiographic outcomes, but none has addressed long-term follow-up after thrombolysis., Methods: Sixty-six patients with acute massive pulmonary embolism (Miller score > 17 and mean pulmonary artery pressure >20 mm Hg) were randomly assigned to receive either a 100-mg 2-h infusion of alteplase (n = 23) or 1.5 million IU of streptokinase over 2 h (n = 43). In both groups, heparin infusion was started at the end of thrombolytic infusion and adapted thereafter. Total pulmonary resistance was monitored over a 12-h period. Pulmonary vascular obstruction was assessed 36 to 48 h after thrombolytic therapy. One-year follow-up information included death, cause of death, recurrent pulmonary embolism, chronic thromboembolic pulmonary hypertension, stroke and bleeding., Results: Both groups had similar baseline angiographic and hemodynamic characteristics of severity, with maintained cardiac output in 64 (97%) of 66 patients. The results (mean +/- SD) demonstrated that despite a faster total pulmonary resistance improvement observed at 1 h in the alteplase group compared with the streptokinase group (33+/-16% vs. 19 16%, p = 0.006), a similar hemodynamic efficacy was obtained at 2 h when both thrombolytic regimens were completed (38+/-18% vs. 31+/-19%). There was no significant difference in either pulmonary vascular obstruction at 36 to 48 h or bleeding complication rates. One-year event-free survival was similar in both groups, as most events were related to concomitant diseases., Conclusions: These results suggest that a 2-h regimen of streptokinase can be routinely used in patients with massive pulmonary embolism and maintained cardiac output without obviously compromising efficacy or safety.

This prospective nonrandomized study enrolled 16 patients with congestive heart failure [NYHA (New York Heart Association) III and IV] refractory to a maximal well-tolerated drug therapy. The aims were to evaluate if peritoneal ultrafiltration (PUF) could improve clinical conditions and to determine morbidity secondary to resistant congestive heart failure (RCHF) and PUF. There were 16 patients (12 male, 4 female) with a mean age of 65.4 years (56-81 years) and follow-up of 15.6 months (4-33 months). Thirteen patients had RCHF without end-stage renal disease. Patients were classified as NYHA class IV (n = 11) or class III (n = 5). One anuric patient had been on previous hemodialysis and switched to APD. PUF was obtained with a 2-L hypertonic dialysis solution, once a day (n = 7) or every 2 days (n = 4). Clinical improvement was obtained for all the patients. Weight decreased from 72.2 to 66.7 kg with a weekly ultrafiltration of 3.74 L (2.2-6.5 L). Sodium removal was 79 mmol/day (urinary 43%, peritoneal transport 57%). During the follow-up period, 2 patients received a cardiac transplant since 7 died due to cardiac reasons. Mean hospitalization time was 4.4 and 1.20 per patient per day before and after PUF, respectively. Hospitalization was in keeping with either RCHF (36%), dialysis complications (16%), or miscellaneous causes (48%). Our experience showed that a functional improvement and a better quality of life were achieved for all these patients with a low rate of hospitalization.

The authors studied 18 patients (15 men, 3 women) with an average age of 67 +/- 8 years with refractory cardiac failure. In order to determine the potential of pacing to raise cardiac output in severe cardiac failure. The average ejection fraction was 26 +/- 6.5%. All patients were in sinus rhythm:resting cardiac output was 3.35 l/min. Two temporary pacing catheters were positioned in the right atrium and at the apex of the right ventricle for dual-chamber mode pacing triggered by the spontaneous P waves. Changes in cardiac output were measured by Doppler echocardiography at different values of atrioventricular delay. Patients were considered to be responders if their cardiac outputs rose by 15%. In 7 patients meeting this criterion, the average increase in cardiac output was 27% (2.99 +/- 0.7 to 3.81 +/- 0.86 l/mn; p < 0.01); all had dilated cardiomyopathies with left bundle branch block and the optimal AV delay was 103 +/- 21 ms (80-140 ms); the duration of diastolic filling increased from 212 +/- 98 to 292 +/- 116 ms (p = 0.02). In the non-responding group (11 patients with an increase of cardiac output of only 3.6 +/- 0.09 to 3.9 +/- 0.92 l/mn; p < 0.01), the underlying disease process was mainly ischaemic. Two predictive factors of efficacy of dual-chamber pacing were identified: a short ventricular filling period (29 +/- 8% of the RR interval in the responders vs 44 +/- 9% in the non-responders; p < 0.01) and the presence of 1st degree atrioventricular block. Dual-chamber pacing could be a valuable method of increasing resting cardiac outputs in a selected group of patients with severe, refractory, cardiac failure.

The physiopathologic role of thrombosis in the genesis of myocardial infarction, began to be suspected early in the 20th century but its logical treatment, thrombolysis, was first used on a large scale only ten years ago. Today, it is well established that short, middle and long-term mortality is correlated to coronary permeability, the delay in the revascularization treatment start-up, its efficacy, its swiftness of action, and to the maintaining of permeability following reperfusion. The importance of time elapse before reperfusion is obtained was demonstrated as early as 1986 by the GISSI study. According to this study, the administration of streptokinase (compared to a conventional treatment) reduced mortality at 21 days respectively by 47%, 23%, and 17%, depending on whether patients were treated within one hour, three hours, or between 3 and 6 hours following the onset of the painful symptoms. One of the major teachings of the GUSTO study, reported at the end of 1993, was the confirmation of the so-called "open artery" theory: mortality at 30 days was of 4.5% among patients whose coronary circulation was restored at the 90th minute, whatever thrombolytic treatment was used, compared to 8.9% when the coronary artery remained occluded. The value of aspirin in preserving coronary permeability following thrombolysis was demonstrated by the ISIS-2 study: mortality at 5 weeks was reduced by 23% in the group of patients randomised to receive only aspirin, while it was reduced by 25% in the group of patients randomised to be treated with streptokinase, and by 42% in the group randomised to receive both aspirin and streptokinase, compared to the group who received neither aspirin nor streptokinase. However, mortality during the first days following randomisation was identical among the groups, with or without aspirin, which suggested its action was rather one of prevention against reocclusion than one of accelerating dissolution of the thrombus. However, in spite of improved therapeutical protocols, a normal flow, which is the major criteria for a reduced mortality, is only obtained at the 90th minute in 54% of the patients who were administered the up-to-date treatment ie aspirin-accelerated t-PA-heparin in combination.(ABSTRACT TRUNCATED AT 400 WORDS)

Antiarrhythmic medications are widely used either at the ventricular or supraventricular level. However, those drugs can induce severe side effects. Actually, antiarrhythmic drugs are paradoxically able to favour the occurrence of new arrhythmias or aggravate the preexisting arrhythmia for which they were indicated. These proarrhythmic effects have been found in 10 to 20% of patients, as evidenced by literature. Moreover, the CAST study showed a significant increase in mortality in patients with non sustained ventricular arrhythmias after myocardial infarction who were treated with either flecainide or encainide, compared to the placebo group. This overmortality seems to be due, in large, to the proarrhythmic effects of antiarrhythmic drugs. Several mechanisms have been evoked, related to the type of antiarrhythmic drug and to the presenting arrhythmia: early post-depolarization due to slow calcium and sodium inward currents in the case of torsades de pointes, facilitation of intraventricular reentries in the case of class 1c antiarrhythmic drugs, facilitation of the ventricular response of atrial arrhythmias. These deleterious effects, that can be very serious, are unpredictable, not toxicity-related and all antiarrhythmic drugs are involved. Their detection appears to be difficult and is based upon ECG, Holter monitoring, treadmill test and possibly electrophysiologic study. The use of antiarrhythmic drugs requires the knowledge of their proarrhythmic effects, the analysis of the benefit-risk ratio--particularly if left ventricular function is impaired--and careful monitoring.

The incidence of endocarditis due to Cardiobacterium hominis is probably underestimated because clinical presentations vary greatly and culture of this Gram negative germ is difficult. A 48-year-old man with a past history of post-streptococcic aortic regurgitation was hospitalized twice within 1 week for fever (38 degrees C) and junctional tachycardia which responded to amiodarone. Subsequently, infero-apical necrosis was documented. Based on the result of the laboratory tests, coronary embolism was suspected although 12 blood cultures were negative. The patient recovered well with a standard antibiotic treatment. Fifteen days later, the blood cultures revealed Cardiobacterium hominis. Antibiotic therapy was adapted and aortic valve replacement was programmed. Two months later the patient died from uncontrollable left heart failure. A 63-year-old man who had had mitral valve replacement 10 years earlier for Streptococcus mitis endocarditis was hospitalized for fever (38 degrees C) and a painful left calf. Phlebocavography eliminated deep vein thrombosis and a complete cardiac work-up was inconclusive. Endocarditis was suspected although blood cultures were negative. The patient was given oral penicillin and discharged after one week. Three months later, the patient was again febrile (38 degrees C) and suffered a cerebral vascular event. Fourteen days after blood sampling, cultures revealed Cardiobacterium hominis. The patient's haemodynamic status worsened and valve replacement with atrioplasty was performed. Outcome after 4 years follow-up has been favourable. Endocarditis due to Cardiobacterium hominis, a saprophitic germ of the upper airway and the female genital tract, has been reported in 64 cases in the literature. The clinical picture is often limited to fever and a heart murmur and laboratory tests show an accelerated erythrocyte sedimentation rate and hyperleukocytosis. Inflammatory type anaemia is often found due to the latency of the endocarditis. Complications are frequent and can be fatal due to massive pulmonary emboli, cerebral vascular events or irreversible heart failure. C. hominis is sensitive to amoxycillin and netilmicin. Surgical treatment of the valvulopathy is indicated.

Three distinct forms of rupture of the heart may be identified after myocardial infarction: sudden rupture with massive intrapericardial haemorrhage, and sudden death with clinical signs of electromechanical dissociation; rupture into the pericardium resulting in a false aneurysm, the treatment of which is surgical; subacute rupture which accounts for 30% of cases in which bleeding into the pericardium is slow and/or repeated. Over an 8 year period and in a series of 2,400 consecutive infarcts admitted to the intensive care unit, 10 cases of subacute rupture of the heart were diagnosed. They were 6 men and 4 women, with a mean age of 73.6 years. The clinical presentation was isolated chest pain in 5 cases, syncope alone in 2 cases and the association of pain and syncope in 3 cases. Six patients were in shock on admission. In two cases, shock developed after admission. The infarction was confirmed biologically by a significant elevation of creatinine kinase in 9 out of 10 cases. Transmural infarction was observed in 9 cases: the infarct was electrocardiographically non-transmural in 1 case. Emergency echocardiography showed pericardial effusion in all cases, usually moderate, but sometimes compressive with an intrapericardial echogenic mass suggesting a thrombus. Haemodynamic improvement was obtained by medication allowing cardiac catheterisation which showed adiastole in 3 cases. Coronary angiography was performed in 7 cases. In 5 of the 7 cases, apart from occlusion of the artery presumed to be responsible for the infarct, the coronary vessels were diffusely infiltrated without significant stenosis. Left ventriculography was performed in 7 cases. In 6 of the 7 cases regional akinesis was demonstrated: the 7th case showed dyskinesia of the anterior wall. In two cases, contrast medium was observed to fill the pericardium during ventriculography, indicating myocardial rupture. The diagnosis of subacute rupture, suggested by clinical and paraclinical (particularly echocardiography), was confirmed in 9 cases at surgery and in the 10th case at autopsy. Surgery consisted of repairing the rupture. In the last two cases, biological glue was used to reinforce the surgical repair. The clinical outcome was good after surgery in 6 cases with a follow-up of 5 months to 8 years. The diagnosis of subacute rupture should therefore be made on clinical and echocardiographic criteria, as these results suggest that surgery is often possible, with a good prognosis.

Between May 1991 and February 1992, 31 consecutive patients were included in a prospective study, the aims of which were to determine the criteria of early coronary revascularisation after intravenous thrombolysis in the acute phase of myocardial infarction. The rise in serum myoglobin, the ST segment elevation, accelerated idioventricular rhythm and the evolution of chest pain were analysed. All patients underwent coronary angiography. Twenty-six were revascularized and 5 remained with coronary occlusion. Two types of serum myoglobin curves were demonstrated. Those with a sudden , decrease and a well defined peak in the first 4 hours were specific for revascularisation and easily identified (Group A: 16 patients). The graphs with a progressively rising slope to a peak after the 4th hour were observed in patients with coronary occlusion, but also in 10 patients with recanalized arteries (Group B). No significant difference was demonstrated with regards to the clinical and coronary angiographic parameters between patients in Group A and Group B. On the other hand, the time between the onset of chest pain and peak myoglobin was shorter in Group A (298 +/- 81 min) than in recanalised patients in Group B (380 +/- 54 min) (p < 0.05). The difference in the profile of the serum myoglobin could therefore reflect restoration of arterial flow in myocardial cells which had not suffered the same period of ischemia. ST segment elevation may increase, decrease of remain stable at 120 minutes in patients revascularised and those remaining occluded. In 9 patients, the ST elevation increased compared with the initial electrocardiogram .(ABSTRACT TRUNCATED AT 250 WORDS)

Five to ten per cent of survivors of acute myocardial infarction die within two years. The majority of these deaths are sudden and are attributed to a lethal ventricular arrhythmia. This is usually ventricular tachycardia degenerating to ventricular fibrillation. These post-infarction tachycardias are generally due to reentry. They require an anatomic arrhythmogenic substrate, a zone of delayed conduction. This can be detected as late potentials on signal averaged ECG. The triggering of a significant ventricular arrhythmia by ventricular stimulation is closely correlated to the occurrence of a severe ventricular arrhythmia in the months following infarction. Programmed ventricular stimulation could, therefore, help to identify patients requiring close follow-up and/or preventive antiarrhythmic therapy, but cannot be offered to all patients because of its invasive nature. Seventy nine post-infarction patients were studied prospectively. All underwent coronary angiography, signal averaging electrocardiography, and programmed ventricular stimulation at least 15 days after infarction. Fifty five patients had at least one criterion of late potentials (QRS duration > or = 110 ms and/or amplitude of the last 40 ms < 27 microV and/or duration of potentials of under 40 microV > 37 ms). Twenty four patients had no late potentials. The results of programmed stimulation were estimated to be positive when sustained or unsustained monomorphic ventricular tachycardia was triggered, and negative when ventricular fibrillation, ventricular flutter unsustained polymorphic ventricular tachycardia or no arrhythmia could be induced. Programmed ventricular pacing triggered 15 significant events, 17 unsustained polymorphic ventricular tachycardias, 13 ventricular flutters and 11 ventricular fibrillations. The exploration was negative in 23 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The frequency of cardiac lesion in patients with other signs of Lyme disease has been estimated at 8 percent. The usual manifestation of myocardial involvement is a varying degree of atrioventricular block or more diffuse signs of myocarditis. Autopsy or intramyocardial biopsy provides a histological diagnosis of myocarditis. Microscopy shows a diffuse lympho-plasmocytic infiltrate with presence of macrophages in the myocardium, associated with a varying number of necrotic myocytes. Structures resembling spirochetes have been found in some cases. Exceptionally, the cardiac lesion may be isolated, presenting as an acute atrioventricular block and/or an acute myocarditis; in such cases the diagnosis of cardiac lesion caused by Lyme disease is made on serological grounds. We report the case of a 30-year old man admitted for acute myocarditis which turned out to be totally regressive. Intramyocardial biopsy showed interstitial congestion associated with inflammatory lympho-histiocytic infiltrates and eosinophilic polymorphonuclears; the myocardial fibres in contact with these infiltrates appeared to be altered. The diagnosis of Lyme disease was subsequently confirmed by serological tests. Patients with myocarditis caused by Lyme disease must be treated with antibiotics. Recent reports have demonstrated the presence of spirochetes in the myocardium of patients with dilated cardiomyopathy, suggesting that the spirochete Borrelia burgdorferi might be associated with, or play a part in, the subsequent occurrence of dilated cardiomyopathy.