Biomedical subjects
Publications and source records attributed to J L Bonnet.
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The outcome of patients presenting with spasm of normal or subnormal coronary arteries is only known in small series of patients at medium-term. The authors reviewed the outcome of 277 successive patients over an average period of 86 +/- 43 months (12 to 174 months). There were 206 men and 71 women with a mean age of 54 +/- 9 years. Coronary angiography was performed in all cases and did not show any stenosis greater than 50%. Spasm was documented during coronary angiography in 157 cases (57%) by a positive Methergin test after coronary angiography in 113 cases (41%) and by an ECG recording of Prinzmetal angina in 7 cases (2.5%). Nearly all patients (264: 95%) were treated by calcium antagonists. At the end of follow-up, there were: 35 lost to follow-up (12.6%), 20 deaths (7.2%) of which 10 were cardiac (3.6%), 18 myocardial infarctions (6.5%): 11 had repeat coronary angiography which showed one or more new significant (> 70%) coronary lesions in all cases; 109 patients had persistence of chest pain (39%). The severity of symptoms in 52 cases (over one attack of chest pain per month) led to repeat coronary angiography which showed significant coronary disease in 19 cases; 95 patients (34%) were asymptomatic. A multivariate statistical analysis showed hypertension or subnormal appearances on the initial coronary angiography to be significant predictive factors for new coronary events (death, myocardial infarction or angina requiring repeat coronary angiography). The authors conclude that coronary spasm of angiographically normal or subnormal arteries is only well controlled at long-term in 39% of patients not lost to follow-up and is responsible for death or myocardial infarction in 11.6% of cases (nearly 1.5% per year).
The prognosis of thromboembolic disease depends, to a large degree, on the deep venous thrombosis. It is located in the legs in nearly 80% of cases and proximal to the popliteal vein in one out of two patients. It is the cause of recurrence and at longer term, of post-thrombotic disease, the frequency of which contrasts with the rarity of chronic post-embolic cor pulmonale. The deep vein thrombosis is often neglected, either because it has no clinical expression or because the symptoms it causes regress rapidly with treatment. Venous ultrasonography by a skilled operator, a painless and easily repeated investigation, is the method of first intention. When the thrombus is not well visualised, it is necessary to complete the investigation with bilateral phlebocavography in free flow or with a computerised tomography scan if the vena cava is poorly seen. The treatment of the pulmonary embolism depends on its size, its tolerance, the embolic source and sites of embolism. Severe pulmonary embolism may require surgical embolectomy at the outset, during which inferior vena cava interruption should be systematic. When thrombolytic therapy is considered, the implantation of a temporary caval filter should be proposed, especially if the thrombus is "floating" or extends into the inferior vena cava. If pulmonary embolism is associated with a recent proximal venous thrombosis it would seem logical to propose surgical thrombectomy or thrombolysis, at least in young patients. Conversely, distal deep vein thrombosis only requires heparin therapy. Interruption of the inferior vena cava is essential when embolism complicates well-treated deep vein thrombosis or when the thrombosis becomes more extensive despite effective treatment. It is also advisable when pulmonary sequellae are severe, long-term anticoagulant therapy is contra-indicated or when the aetiology of the thromboembolism cannot be determined.
OBJECTIVES: Venous stasis in bedridden patients is recognized as one of the risk factors for venous thromboembolism but the phenomena is known to occur in ambulatory subjects and another cause must be involved. We investigated a series of consecutive ambulatory patients with venous thromboembolism in order to distinguish the particular clinical manifestations and possible aetiologies. METHODS: We compared a retrospective series of 120 consecutive patients with deep vein thromboembolism of the lower limbs and 127 patients with the same disease who had been bedridden at onset. In addition to the physical examination, the aetiological work-up included echography (n = 14), abdominal computed tomography (n = 38) and/or haemostasis studies (n = 61). Mean follow up was 23 +/- 13 months (range 1-45 months). RESULTS: Family history of deep venous thromboembolism was found in 17 patients and recurrence was observed in 50 patients. Phlebitis was on the right in 52 cases, on the left in 47 and bilateral in 17. Proximal locations were more frequent (74%) and pulmonary embolism occurred in one-half of the patients (n = 58). A cause was identified in 61 cases (50.8%): cancer (n = 24, 17 known, 7 previously unknown), dyscrasia (n = 17, protein S or C deficiency (5), increased plasminogen activator inhibitor I (8), circulating anticoagulants (3), hypofibrinogen (1), idiopathic varicose veins (n = 7), pregnancy (n = 5), oral contraceptives (n = 4) and other causes (n = 4). No cause was identified in 59 patients. Pulmonary embolism led to death in 4 cases. Seven patients were lost to follow-up and anticoagulation therapy was taken by 79 (72%) then interrupted in the others 3 to 6 months later. Eighteen patients died, 14 due to the underlying disease, 2 from new cancers and 12 after recurrent thromboembolism. CONCLUSION: Ambulatory venous embolism is as frequent as embolism in bedridden patients and the cause can be observed in 50% of the cases.
Ischaemia has been the suggested mechanism of simultaneous left bundle branch block and chest pain on effort with normal coronary angiography. This hypothesis is very controversial and was not the mechanism in the two new cases of this syndrome. The two patients in whom effort pain and left bundle branch block were observed had been treated for paroxysmal supraventricular tachycardia with flecaine. Withdrawal of the anti-arrhtymic resulted in the disappearance of this syndrome. In these cases, the ischaemic mechanism could be excluded without ambiguity. The flecaine was the only cause of rate-related LBBB by slowing conduction in the left bundle branch with no effects on coronary reserve. It would seem that LBBB alone was the cause of chest pain. The absence of coronary artery disease was confirmed in the first patient and the diagnosis was highly improbable in the second.
Left ventricular pseudo-false aneurysm is caused by a discrete rupture of the myocardial wall which remains circumscribed within the wall itself, realising a cavity joined to the left ventricle by a narrow neck. It is an extremely rare complication of myocardial infarction. Two cases diagnosed in vivo by left ventriculography are reported. Their diagnosis and precise locations were confirmed by transoesophageal echocardiography. In the first case, the pseudo-false aneurysm was situated in the interventricular septum and, in the second, in the antero-lateral wall. The natural history of asymptomatic pseudo-false aneurysms is unknown. The advanced age of the patients and the possibility of regular follow-up by transoesophageal echocardiography were the main reasons for surgical abstention in these particular cases.
The anti-angina efficacy of the continuous (C) transdermal application of nitroglycerin may lessen or disappear over the course of time. Pharmacological tolerance, which is probably responsible, might be prevented by intermittent (I) application. However few studies have compared the C and I methods. The effects of transdermal patches containing 10 mg, applied for 24 hours/day and for 15 hours/day for one week were evaluated in twelve patients. Exercise tests were performed before and 4 hours after the initial application and after one week of each type of treatment prescribed in random order with a 7 day wash-out between each treatment phase. Plasma nitroglycerin concentrations were measured at the same time. Total work and ischemia and angina thresholds after 4 hours application all increased significantly in comparison with baseline values. All these values persisted after one week of I treatment. With C treatment they decreased though remained significantly above baseline values with the exception of angina thresholds. I treatment appeared significantly better than C treatment regarding ischemia threshold (3,974.7 kpm v. 3,037.5-p < 0.01). Plasma nitroglycerin levels were the same during each treatment phase. These results suggest that the anti-ischemic efficacy of transdermal patches persists after one week of treatment, though with superiority of intermittent treatment. Continuous treatment tends to induce pharmacodynamic tolerance since there was no difference in plasma nitroglycerin levels.
Doppler echocardiographic parameters of LV diastolic function (isovolumic relaxation time, E wave velocity, ratio of E/A wave velocities, mitral valve pressure half time) were compared to catheter data in 35 patients (average age 67 years) with pure or dominant aortic stenosis (mean gradient: 65 +/- 30 mmHg). The isovolumic relaxation time was prolonged in most patients (m = 103 +/- 23 ms) and seemed uninfluenced by any haemodynamic parameter. There was a positive correlation between pressure half time and ejection fraction (r = 0.41, p = 0.02) and a negative correlation with pulmonary capillary pressure (r = -0.61, p < 0.01). The E and E/A ratio were negatively correlated with the ejection fraction (r = -0.41 and -0.52) and positively correlated with pulmonary capillary pressure (r = 0.46 and 0.62). The Doppler parameters were independant of the patients' age, severity of stenosis and degree of left ventricular hypertrophy. Patients with normal pulmonary capillary pressure (< 15 mmHg, N = 19) had abnormal diastolic filling with low E wave velocities (71 +/- 28 cm/s) and E/A ratios (0.9 +/- 0.6) and prolonged half pressure times (96 +/- 37 ms). Conversely, patients with high pulmonary capillary pressures (> 15 mmHg, N = 16) had normal or high E wave velocities (107 +/- 31 cm/s) and E/A ratios (1.5 +/- 0.6) and normal or shortened isovolumic relaxation times (62 +/- 22 ms).(ABSTRACT TRUNCATED AT 250 WORDS)
Myocardial infarction (MI) is the result of acute coronary occlusion and the prognosis depends on the infarct size. In experimental studies, infarct size is reduced by early coronary reperfusion which may be obtained by intravenous thrombolytic therapy. This simple, rapid and widely used technique is the clinical treatment of choice. The diagnosis of MI must be confirmed by clinical and electrocardiographic findings. The clinical history is important because the value of reperfusion when started after the 6th hour after the onset of chest pain is questionable. However, it is often difficult to determine the beginning of MI when preceded by unstable angina. Contraindications to thrombolytic therapy must be carefully excluded irrespective of the thrombolytic agent because of the risk of haemorrhage. This must be weighed up against the risk of the MI itself. Therefore, age is not a systematic exclusion criterion. The choice of thrombolytic is based on the efficacy, mode of administration and cost. Heparin therapy at effective doses is associated in all cases to prevent reocclusion. Aspirin is given orally. The association of a calcium inhibitor or a betablocker may also be considered. Reperfusion and ischaemia may give rise to arrhythmias and haemodynamic changes which have to be rapidly corrected. Haemorrhagic complications during thrombolysis are treated according to the severity and time of onset by blood transfusion sometimes associated with a plasmin inhibitor. Reocclusion is an indication for emergency coronary angioplasty but in some cases repeat thrombolytic therapy may be beneficial. When the MI is extensive, rapid transfer to a cardiological centre with catheter facilities is advisable.(ABSTRACT TRUNCATED AT 250 WORDS)
Late recanalisation of the infarct Related Artery is possible and may cause post-infarction angina. This was observed in 7 male patients who had complete occlusions of an artery with collateral circulation in the immediate post-infarction period. After a symptom-free period of 17 months, angina recurred and repeat angiography showed recanalisation of the occluded artery with regression of the collateral circulation resulting in myocardial ischemia. Myocardial revascularisation was then required.
Ten patients with acute myocardial infarction were studied by magnetic resonance imaging (MRI) with injection of a paramagnetic contrast agent: Gadolinium-DOTA (Gd-DOTA). The time interval between the onset of symptoms and MRI was 8 to 12 days. The site of infarction was determined in all cases by Thallium 201 scintigraphy (hypofixation) and selective ventriculography (segmental wall anomalies): anterior (6 cases), inferior (4 cases). MRI was performed with a 0.5 Tesla CGR Magniscan by the multiple spin technique. A series of tomographic sections was recorded immediately after intravenous injection of 0.4 mmol/Kg of Gd-DOTA. Recent myocardial infarction with parenchymal oedema gives an enhanced transmural signal: only 3 patients had a sufficiently contrasted image on the 1st spin echo. After Gd-DOTA, 7 patients had significantly increased contrast on this echo and in all excellent contrast between infarcted and healthy myocardium was obtained in 9 of the 10 patients. There was excellent correlation concerning the site of infarction between Thallium scintigraphy and left ventriculography. The intensity of signal and T2 relaxation time of different myocardial segments was studied by the regions of interest technique: the ratio of signal intensity of infarcted/healthy myocardium was 1.3 before and 1.7 after Gd-DOTA on first spin echo images. The mean T2 was 54.1 +/- 9 ms in healthy and 82 +/- 28 ms in infarcted myocardium. After Gd-DOTA, both values decreased and tended to equalize.(ABSTRACT TRUNCATED AT 250 WORDS)
Diltiazem and Nifedipine could be synergic. The aim of this study was to investigate the benefits of their association. Eighteen patients, 15 men and 3 women, average age 61 +/- 6 years, with stable angina on effort, were studied. Eight patients had single vessel disease and 10 patients had multivessel disease. The patients underwent a randomised double-blind trial with 4 successive treatment periods each lasting one week: placebo; 360 mg/day of Diltiazem; 60 mg/day of Nifedipine; 180 mg/day of Diltiazem with 30 mg/day of Nifedipine. The benefits were evaluated clinically, by exercise stress testing and with drug plasma concentrations at the end of each sequence. The results at the end of the 3 treatment periods were significantly better than with placebo. Diltiazem was significantly better than Nifedipine with respect to the development of angina during exercise testing (1 patient compared with 7 patients) and to maximum load (118.3 +/- 33.3 watts compared with 105.9 +/- 35.4 watts) (p less than 0.05). The association of the two drugs did not give better results than Diltiazem alone. Compared with placebo, the total duration of exercise testing and the duration of 1 mm ST depression were significantly longer during the 3 treatment sequences but there were no significant differences between each of them. Secondary effects were significantly more common with Nifedipine (7 patients) and with the drug association (9 patients) than with Diltiazem alone (3 patients) or placebo (1 patient). Plasma concentrations of Diltiazem were 328 +/- 35 ng/l with the 360 mg/day dosage and 137 +/- 52 ng/l with the 180 mg/day dosage.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic pericarditis can take the form of localised annular bands constricting the atrioventricular grooves, the pulmonary infundibulum and, rarely, the atria. The authors report two cases of pericardial bands surrounding the ventricles and involving the atrioventricular groove resulting in a biloculation of the left ventricle. One case was complicated by adiastole and one by mitral regurgitation due to involvement of the posterior mitral leaflet. Magnetic resonance imaging gave precise definition of these bands and of their extension into the myocardium. This investigation was a valuable complement before surgery of the localised constriction.
ELTs (endless loop tachycardias) are a common occurrence associated with DDD pacing. In order to detect and treat ELTs, an innovative automatic pacemaker algorithm was devised and evaluated. The basic principle of the algorithm rests on the relative stability of the ventriculoatrial conduction time (VACT) during ELTs. ELTs are suspected when the VACT remains stable and adheres to certain programmable limits referred to as VACT stability (16 or 31 msec); it is confirmed when the VACT remains stable after a programmable shortening of the AV delay (AVD) value, referred to as AVD shortening (47 or 63 msec). Ninety-one patients, 54 males and 37 females, were implanted with such an algorithm-specific device between January 10 and September 9, 1989. The reasons for implantation were as follows: 55 patients were implanted for AV block, 31 for sinus node dysfunction, and 2 for carotid sinus syndrome. Pacing parameters were programmed to favor ELT initiation (long AVD, short postventricular atrial refractory period [PVARP] and high atrial sensitivity) followed by basic programming of the algorithm (VACT stability set at 16 msec and AVD shortening set at 47 msec. Once this was done, a 24-hour Holter recording was obtained. Eighty-eight patients were thus analyzed, three being excluded from the final report due to the poor quality of the Holter tracings. In 43.2% of the sampling (38 patients), multiple episodes of ELT were identified, exhibiting a mean rate of 120 beats/min. In 26 of 38 cases (68.4%), the rate of ELT was found to be slower than the upper rate limit (URL).(ABSTRACT TRUNCATED AT 250 WORDS)
Doppler echocardiographic examinations were performed in 146 patients with normal and 42 patients with pathological (31 regurgitations and 11 obstructions) mitral valve prostheses confirmed by catheterisation and/or surgery. The maximum and mean transprosthetic gradients and pressure half times (PHT) were calculated from continuous wave Doppler recordings and regurgitant signals were searched for by continuous and pulsed wave Doppler. In the group of normal mitral valve prostheses, the mean gradients and PHT were very variable even within the subgroups of the same type and size of prosthesis. The best haemodynamic profile was observed with the St Jude prosthesis (mean gradient = 5 +/- 2 mmHg, PHT = 90 +/- 22 ms, p less than 0.05 vs other prostheses). Minimal mitral regurgitation was detected in 12 per cent of bioprostheses and 20 per cent of mechanical prostheses. No correlations were found between the mean pressure gradient or PHT and the size of the prostheses. Regular Doppler echocardiographic follow-up over 2.4 years was obtained in 25 patients and showed a remarkable stability of the Doppler parameters in 17 patients whereas prosthetic valve dysfunction was diagnosed in the other 8 cases. In the group of pathological mitral valve prostheses, regurgitation (N = 31) was associated with a high early diastolic pressure gradient (20.2 +/- 8 mmHg) and a normal or shortened PHT (84 +/- 28 ms). Obstructed prostheses (N = 11) had high mean pressure gradients (17 +/- 5 mmHg) and increased PHT (195 +/- 53 ms). All cases of obstruction were correctly identified by the Doppler but 4 prosthetic valve regurgitations were missed or underestimated (4 mechanical prostheses).(ABSTRACT TRUNCATED AT 250 WORDS)
Doppler echocardiography was performed in 112 patients with normal aortic valve prostheses and 13 patients with dysfunction (3 obstructions, 10 regurgitations) confirmed at catheterisation and/or surgery. The maximum and mean transprosthetic pressure gradients were measured in all patients by continuous wave Doppler. The prosthetic valve surface area was calculated by applying the continuity equation in the last 67 patients and compared with the effective surface area deduced from hemodynamic studies in the literature: --There was a great variability in the values of mean pressure gradient and prosthetic valve area within each group and with each size of prosthesis in patients with normal valves. No significant difference was observed between the gradients of different prostheses. However, for a given size, the St Jude Medical prosthesis had larger calculated surface areas than the other prostheses. The Doppler valve surface area did not differ significantly from the area measured invasively for the different categories of prostheses, and it increased with the size of the prosthesis. Mild aortic regurgitation was observed in 16 per cent of bioprostheses and 30 per cent of mechanical prostheses. The three cases of obstruction were characterised by a high mean pressure gradient (59 +/- 16 mmHg, p less than 0.01 vs normal prostheses) and a reduced Doppler surface area (0.7 +/- 0.2 cm2, p less than 0.005 vs normal prostheses) and were correctly diagnosed by Doppler echocardiography. Eight of the ten prosthetic regurgitations were correctly quantified by Doppler. Cardiac Doppler coupled with echocardiography is a very valuable method of non-invasive assessment of aortic valve prostheses.(ABSTRACT TRUNCATED AT 250 WORDS)
A prospective randomized study was undertaken in 50 patients treated with intravenous thrombolysis (streptokinase, tissue plasminogen activator, association of the two thrombolytics) for acute myocardial infarction to determine the best time to perform percutaneous transluminal coronary angioplasty (PTCA). Coronary angiography was carried out 24 to 72 hours after thrombolysis. This investigation allowed identification of the patients in whom PTCA was technically feasible. These patients were then divided into two groups: Group A: early PTCA (24-72 hours) and Group B: delayed PTCA (8-10 days). During the hospital period, the patients were prescribed heparin therapy and aspirin. Recurrent ischemia (RI) was investigated and treated by PTCA. The criteria of success of strategies A and B were a primary success of PTCA and no RI during the hospital period. Coronary angiography was performed in 108 successive patients of whom 50 were included for the comparative trial, 25 in Group A and 25 in Group B. In group A, PTCA was successful in 24 cases and there were 2 incidents of RI (6 hours and 12 days). In Group B, 4 episodes of RI were observed in the 24 hours following coronary angiography: after 10 days, 15 of the 20 patients with uncomplicated courses underwent PTCA; 1 patient refused consent, 2 regressions of stenosis and 3 asymptomatic reocclusions were observed. A primary success of PTCA was obtained in 13 of the 15 patients. There was no statistically significant difference between the results of the strategies adopted in Groups A and B. A therapeutic success was obtained in 22 of the 25 patients in Group A, and 19 of the 25 patients in Group B.(ABSTRACT TRUNCATED AT 250 WORDS)
Based on a 19-month experience of intravenous thrombolysis performed at home during the acute phase of myocardial infarction, we feel it is a realistic procedure, since it did not result in too many unnecessary calls: in 648 calls which seemed attributable to a coronary emergency by the Emergency Medical Services, this diagnosis was ruled out in 119 instances (18.4%) and confirmed in 529 instances (81.6%); diagnostic errors were not too frequent: 3.8 p. cent of false positive and 5.8 p. cent of false negative; it was not very hazardous: one death only from cardiogenic shock; it permitted to save time by decreasing by 30 minutes the start of the treatment; it avoided excessive costs by using already established structures.