Biomedical subjects
Publications and source records attributed to B Meier.
An attempt to occlude a fistula between the right coronary artery and the pulmonary trunk with a detachable balloon resulted in balloon dislodgment and occlusion of the right coronary artery. The dislodged balloon could be retrieved by suction with the help of a guiding catheter for coronary angioplasty.
Mycoplasma arthritidis is the causative agent of severe polyarthritis in rats and mice, which resembles human rheumatoid arthritis (RA). Several mechanisms are involved in this disease. M. arthritidis releases substances acting on polymorphonuclear granulocytes (PMNs), i.e. oxygen radical formation stimulating substances (500-3,000 daltons), a chemotactic substance (400 daltons) and an aggregating substance (500 daltons). These products were separated from the cell-free culture supernatant by gel chromatography on Sephadex G-15 and G-10 columns. Isolated membranes of M. arthritidis possesses toxic properties for rats, mice, and chicken embryos. Hemolytic activities for sheep red blood cells and toxic effects on fetal rat skin fibroblasts were detected for this 170,000 dalton substance. Cross-reactivity between M. arthritidis and rat tissues was demonstrated in several investigations with polyclonal and monoclonal antibodies. Polyclonal antibodies against M. arthritidis showed a strong reaction in immunofluorescence tests with rat chondrocytes. In Western blot analysis six corresponding protein bands were observed in M. arthritidis membranes and rat chondrocytes, favoring the idea of several shared epitopes. Monoclonal antibodies were established reacting with M. arthritidis as well as with rat and human chondrocytes in the immunofluorescence test and in the enzyme immunoassay. Cross-reactivity could be observed also on the cellular level. T-cell lines of the OX 19 and W 3/25 type were established that could be stimulated by M. arthritidis antigens and by syngeneic chondrocytes. In the initial stage of the arthritis, toxic processes seem to be predominant that are continued by autoimmune reactions in the progressing disease.
To assess left ventricular diastolic filling in patients with single-vessel coronary artery disease, Doppler-derived transmitral velocity was studied in 22 normal subjects and in 15 patients with isolated proximal stenosis of the left anterior descending coronary artery (LAD) and normal systolic function of the left ventricle. Transmitral velocity was recorded before and after balloon inflation during coronary angioplasty. At baseline the transmitral velocity pattern in patients with LAD stenosis differed from that of normal subjects with a significant (p at least less than 0.05) decrease in the early diastolic filling phase (E area 0.094 +/- 0.022 m in normal subjects vs 0.078 +/- 0.008 m in patients) and an increase in the late diastolic filling phase (A area 0.034 +/- 0.007 m vs 0.042 +/- 0.008 m). Correspondingly the ratio E area/A area decreased (2.7 +/- 0.51 vs 1.9 +/- 0.4) and the ratio A area/total area increased (0.28 +/- 0.04 vs 0.35 +/- 0.05). During coronary occlusion the E area and the ratio E area/A area decreased further, whereas the A area and the ratio A area/total area increased. The results suggest that patients with single-vessel disease and normal systolic function often exhibit an altered pattern of transmitral velocity even in the absence of overt ischemia, and that during acute regional ischemia early diastolic filling is further compromised with compensatory enhancement of the late diastolic filling phase.
Evaluations of drugs for the prevention of restenosis after human coronary angioplasty have been disappointing. Heparin failed to reduce restenosis in a randomized study in Atlanta, Georgia, in patients maintained on heparin for 24 h. A randomized study in the same centre compared acetylsalicylic acid to anticoagulation with coumadin. Restenosis was slightly but not significantly less frequent in patients on acetylsalicylic acid. An American multicentre randomized study comparing a combination of acetylsalicylic acid and dipyridamole to ticlopidine and to placebo revealed no difference in terms of incidence of restenosis. Dipyridamole alone shows no effect against acute or late coronary artery restenosis. Two calcium antagonists (diltiazem and nifedipine) did not significantly diminish restenosis in randomized trials. Neither did a thromboxane A2 inhibitor. Only eicosapentaenoic acid (EPA), an n-3 fatty acid, significantly reduced restenosis in a randomized study using a high dose. But the same compound proved ineffective in a similar study using a somewhat lower dose. Despite scientific evidence for the inefficacy of virtually all tested compounds, I do not know of a single institution that does not continue to discharge its patients after coronary angioplasty on one or several of them.
Sulotroban, a sulphonamide derivative, causes an inhibition of platelet aggregation by blocking thromboxane A2 receptors. We tested the effects of Sulotroban (4 x 800 mg per day) on acute events during and recurrence rate after coronary angioplasty, and compared it with placebo in a double-blind randomized fashion. The follow-up protocol included regular compliance control by pill count, stress testing, and coronary angiography at 6 months. Restenosis was defined as a loss of 50% of the initial gain in luminal diameter. A total of 107 patients were randomized. There were no differences between the groups in terms of age, sex, artery distribution, or left ventricular function. Primary success per vessel was 86% for the Sulotroban group (50/58), and 88% for the placebo group (51/58). Complications occurred in nine patients (8%): five emergency bypass operations and three myocardial infarctions. There were no differences between the centers, or the study groups. The study protocol was completed for 57 patients. There was one death in the placebo group. Restenosis was found in 65% of patients in the Sulotroban group (19/29) and 61% of patients in the placebo group (17/28) (ns). If all patients were included on an intention to treat basis, regardless of primary success and compliance with the protocol, the recurrence rate was 57% in the Sulotroban group (20/35), compared with 56% in the Placebo group (20/36) (ns). This randomized, double-blind study failed to show that Sulotroban is superior to placebo in preventing acute problems during, or restenosis after, coronary angioplasty.
Percutaneous pulmonary valvuloplasty has been used successfully in the treatment of pulmonary valve stenosis for several years, but reports on long-term results are still sparse. We have performed pulmonary valve balloon dilatation procedures 23 times in 22 patients since February 1985; the age of the patients ranged from 2 days to 22 years. Three patients did not benefit from the procedure, in two instances because the pulmonary valve was dysplastic and once because of severe associated infundibular stenosis. These patients subsequently underwent surgery. In the other 19 patients the initial transvalvular gradient of 35 to 160 mm Hg (mean 81 mm Hg) was markedly reduced (to values ranging from 10 to 60 mm Hg, mean 31 mm Hg) rendering surgery unnecessary. There were no complications. The patients have been followed up for periods ranging from 2 months to 3 years and all are asymptomatic. Repeat measurements of the transvalvular gradient were carried out either by recatheterization or by echo Doppler 4 months to 3 years after the procedure; we have not observed restenosis and the mean gradient remained unchanged compared to the measurements immediately after valvuloplasty. Pulmonary regurgitation was uncommon and indeed appears to be less prominent than after surgical valvotomy. Thus, percutaneous valvuloplasty now appears to be the preferred treatment for pulmonary valve stenosis and open heart surgery can be avoided in most cases.
A randomised trial of 367 patients with acute myocardial infarction was performed to determine whether an invasive strategy combining thrombolysis with recombinant tissue-type plasminogen activator (rTPA), heparin, and acetylsalicylic acid, and immediate percutaneous transluminal coronary angioplasty (PTCA) would be superior to a noninvasive strategy with the same medical treatment but without immediate angiography and PTCA. Intravenous infusion of 100 mg rTPA was started within 5 h after onset of symptoms (median 156 min). Angiography was performed 6-165 min later in 180 out of 183 patients allocated to the invasive strategy; 184 patients were allocated to the non-invasive strategy. Immediate PTCA reduced the percentage stenosis of the infarct-related segment, but this was offset by a high rate of transient (16%) and sustained (7%) reocclusion during the procedure and recurrent ischaemia during the first 24 h (17%). The clinical course was more favourable after non-invasive therapy, with a lower incidence of recurrent ischaemia within 24 h (3%), bleeding complications, hypotension, and ventricular fibrillation. Mortality at 14 days was lower in patients allocated to non-invasive treatment (3%) than in the group allocated to invasive treatment (7%). No difference between the treatment groups was observed in infarct size estimated from myocardial release of alpha-hydroxybutyrate dehydrogenase or in left ventricular ejection fraction after 10-22 days. Since immediate PTCA does not provide additional benefit there seems to be no need for immediate angiography and PTCA in patients with acute myocardial infarction treated with rTPA.
The Monorail balloon catheter is distinctly different from other current balloon catheters: the guidewire passes through the balloon itself, exits the catheter proximal to the balloon, and runs alongside its small shaft (3 French) through the guiding catheter. Monorail coronary angioplasty was attempted in 61 patients on 73 lesions with balloons from 2.0 to 3.7 mm. Angiographic success was obtained in 66 lesions (90%). For 15 lesions, balloon exchanges were needed. In three lesions, the Monorail balloon failed to cross the lesion, while a standard balloon succeeded; two lesions could not be crossed with any balloon. Vessel occlusion occurred in four patients: two had emergency surgery without infarct (one died suddenly 4 days later and one had a stroke 1 day later), one was recanalized with a standard balloon, and one had a myocardial infarct. Continuous infusion of urokinase was used until patient 3 in whom problems with the delivery system led to cardiocerebral air embolization (with complete recovery). No thrombotic complications were observed in the subsequent 58 patients with only a bolus of 10,000 U of heparin. The Monorail balloon facilitates contrast injections and balloon exchanges but appears more difficult to pass through tight lesions. Omission of the previously recommended infusion with a thrombolytic agent proved safe.
Digital angiography provides a convenient means to quantify the progression of a contrast medium bolus injected into a coronary artery throughout the myocardium, which in turn yields information on myocardial perfusion. Sixteen patients presenting a single critical proximal stenosis (estimated diameter reduction greater than 80%) on either the left anterior descending coronary artery (LAD) or the left circumflex coronary artery (LCX) were studied. First, 12 consecutive end-diastolic images of an ECG-triggered intracoronary injection of 4 ml of iopamidol were acquired on 60 degree left anterior oblique projection under basal conditions. This was repeated 30 s after intracoronary injection of 12 mg of papaverine. For each image sequence, a densogram was computed in each pixel by fitting a curve through its 12 consecutive intensity values. The 'time of maximal pixel opacification' (TMAX) and the 'mean ascending time' (TMAT), expressed in cardiac cycles, were determined from each curve. Two myocardial regions of interest (ROI) were defined for each patient, one in the perfusion bed of the LAD, the other in the bed of the LCX. The mean values of TMAX and TMAT in each ROI were computed, at rest and during hyperemia. At rest, the mean values of TMAX and TMAT obtained from the ROI associated to the stenosis artery were not significantly different from the values obtained in the ROI associated with the intact artery. During hyperemia, a significant decrease of the mean TMAX and TMAT was observed in the normally perfused regions (p less than 0.001). The rest to hyperemia ratios of both TMAX and TMAT mean values were considered to be indices of coronary flow reserve.(ABSTRACT TRUNCATED AT 250 WORDS)
The average restenosis rate reported so far in the literature is just below 30%. Although restenosis correlates well with the recurrence of symptoms, the two factors are not identical. The incidence of myocardial infarction during the first 2 years after coronary angioplasty is 4% and the incidence of death is 2%. These two cardiac events are rarely the first symptom of restenosis. Restenosis, therefore, is not primarily a life threatening disease but still deserves prompt evaluation and correction. Restenosis is stenosis-related rather than patient-related. Thus, restenosis rate per patient increases with the number of lesions or arteries treated. Restenosis rates vary considerably with centres. Serial analyses of restenosis rates at individual centres revealed that the restenosis rates remained constant at a centre-specific level. Differences in case selection and particularities in data definition and analysis may account for both these observations. There is no sound evidence that procedural factors (balloon size, number, duration, or pressure of inflations, etc.) or drug regimens are capable of reducing the recurrence rate. All risk factors for restenosis identified so far are difficult to influence. Extinguishable factors such as smoking seem of little importance in this particular problem. Efforts to find ways of reducing restenoses after coronary angioplasty are commendable and necessary. Their chance of success, however, is small. 'Old customers' will continue to represent 20-30% of the clientele for coronary angioplasty. Their risk for failure and complications is small, but they do carry a considerable risk of restenosis.
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A sample of 190 male and female "high school" students completed a sleep questionnaire for the first time when they were 10 to 14 years old. The survey was repeated five times at 2 year intervals. Ninety-three subjects answered the questionnaire each time. Subjective sleep need was assessed by the indicated wish for more sleep. The wish for more sleep was very pronounced, varying between 54.3% and 74.5% across the years. Individual consistency, however, was low since only 14.5% of the adolescents indicated the wish for more sleep in each survey, emphasizing the state dependency of this variable. Within each total sample, subjects with the wish for more sleep (MSL) and with sufficient sleep (SSL) were compared. Subjective sleep need was consistently validated by a syndrome of morning-tiredness. In the last two surveys, there was reduced time in bed (TIB) on weekdays in MSL subjects and longer TIB during vacation in surveys 2 through 5. Furthermore, MSL subjects more often showed irregular sleep habits. The previous sleep history of the MSL subjects in the last survey indicated that concomitants of the wish for more sleep were already experienced earlier in adolescence. The desired sleep duration of these subjects was 1.7 h longer than their current sleep on weekdays, an amount they had not obtained on weekdays since early adolescence. It is concluded that a substantial proportion of the adolescents seem to have had difficulties adapting to the general sleep time reduction occurring in adolescence.
In 500 consecutive procedures of elective coronary angioplasty attempted at a centre with a primary success of 86%, one or more major acute complications occurred in 34 cases (6.8%). Twenty four patients (4.8%) sustained an acute myocardial infarction (in six this was despite emergency coronary artery bypass surgery) and two patients (0.4%) had emergency coronary bypass without myocardial infarction. Ventricular fibrillation was a complication without sequelae in five (1.0%) patients; one (0.2%) patient died because of refractory ventricular fibrillation and ensuing electromechanical dissociation. "Benign" coronary artery rupture occurred in one (0.2%) patient, and one (0.2%) patient had elective coronary surgery to retrieve the tip of a fractured guide wire after an otherwise successful angioplasty. Despite a low mortality, coronary angioplasty is associated with major complications in about one of 14 procedures; the complication is usually acute myocardial infarction caused by occlusion of the vessel.
Coronary angiography followed by percutaneous transluminal coronary angioplasty and/or intracoronary streptokinase infusion was performed in 50 patients 288 +/- 162 min after the onset of symptoms of acute myocardial infarction. Subocclusion of the infarct-related vessel was found in 5 patients, all of whom had angioplasty of the residual stenosis. Recanalization was achieved in 37 patients (success rate 82%). There was no procedure-related death. One patient died 4 days after the intervention. Control coronary angiography 5 +/- 2 months after the procedure in 35 of 42 patients with recanalization documented recurrence of stenosis or reocclusion in 8 (23%). Comparison of preintervention and control angiograms in 33 patients showed an increase in left ventricular ejection fraction from 55 +/- 8 to 61 +/- 13%, p less than 0.001, in patients with collaterals to the infarct-related vessel and/or recanalization within 180 min after the onset of pain, and from 55 +/- 9 to 59 +/- 8%, nonsignificant, in patients with recanalization later than 180 min and without collaterals. At follow-up 7 +/- 4 months after the procedure, 1 patient had died and 36 (86%) were asymptomatic. Good long-term results can be achieved at a reasonable risk by coronary angioplasty with or without thrombolysis in evolving myocardial infarction. Left ventricular function is better preserved in patients with collaterals and/or early recanalization.
To assess the potential of coronary collateral circulation to protect myocardium after occlusion of a coronary vessel, the mean coronary wedge pressure, the angiographic grade of collateral channels, and the left ventricular function were studied in 47 consecutive patients with mechanical recanalization of totally occluded coronary arteries. Coronary wedge pressure measurements were obtained 39 +/- 51 days (range, 2 hours to 361 days) after the presumed time of occlusion. The patients were divided into two groups: 31 with a coronary wedge pressure more than 30 mm Hg (group 1) and 16 with a coronary wedge pressure of or less than 30 mm Hg (group 2). Patients in group 1 had a significantly higher mean global left ventricular ejection fraction than those in group 2 (63 +/- 9% vs. 49 +/- 7%, p less than 0.001). Regional left ventricular function (artery-related area change) was also superior in group 1 compared with group 2 (47 +/- 11% vs. 36 +/- 10%, p less than 0.01). Global left ventricular function was significantly correlated to coronary wedge pressure (r = 0.51, p less than 0.001) but not to the angiographic presence of collaterals. The data suggest that a high coronary wedge pressure is associated with improved left ventricular function after coronary artery occlusion and that coronary wedge pressure more accurately reflects the physiological role of collaterals than their angiographic presence.
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The experimental and early clinical experience with percutaneous valvuloplasty using trefoil and bifoil balloon catheters (Schneider Shiley) and a long introducer sheath with a new back-up wire are reported. The trefoil balloon consists of three and the bifoil balloon of two angioplasty balloons mounted in parallel on a single catheter. Inflated, they form a rosette allowing for some blood flow through the spaces between the individual balloons. These small balloons are more pressure tolerant than one large balloon. The hemodynamic advantage of these balloons compared to single balloons could be demonstrated in animal experiments (healthy valves and surgically created stenoses). In 31 consecutive patients with trefoil-bifoil balloon valvuloplasty, there was no inhospital mortality. The results of trefoil valvuloplasty in twelve patients with pulmonary stenosis compared favorably to those of patients treated with single balloons. There were no technical failures or complications. There were two unsatisfactory results (severely dysplastic valve). In the aortic valve, the results with calcified stenoses were satisfactory at first but disappointing during follow-up. There were no technical failures but one of nine patients suffered an embolic myocardial infarction. In the mitral valve, there were two failures (one deficient equipment, one stroke during balloon positioning). In one case, insufficient balloon size led to an inadequate result. One patient needed surgical drainage for a pericardial tamponade. In two patients, mitral regurgitation was significantly increased. A 17F long sheath was developed to further facilitate balloon valvuloplasty. It guides the balloon catheter across the valve (and across the septum in case of the mitral valve), stabilizes it during inflation, and serves as a second pressure line to continuously monitor the transvalvular pressure gradient. It prevents bleeding at the puncture site during the intervention and presumably reduces the trauma to the artery. Because of its thrombogenic potential, heparinization of the patients is essential. The largest balloon accepted by the sheath is a 2 X 19 bifoil balloon which was the reason to use a bifoil balloon in some mitral valves. Trefoil balloons put in place through a long sheath provide some theoretical advantages over conventional single balloons introduced over guidewires that need to be evaluated by larger clinical studies. Although they do not prevent circulatory collapse during initial inflation in tight stenoses, they permit transvalvular flow when fully unfolded.