Coupled D dimer and fibrinogen levels during thrombolytic therapy of venous thromboembolism.
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Biomedical subjects
Publications and source records attributed to C Thery.
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Fifty patients (38 men) with unstable angina pectoris defined by: pain lasting > 15 minutes+percritical electrocardiographic changes+significant coronary narrowing on coronary angiography (Coro 1) performed within 24 hours, were treated in a double blind protocol with rt-PA (n = 25) 100 mg/90 minutes (10 mg bolus + 90 mg/90 minutes or placebo (n = 25). All received effective intravenous heparin and intravenous nitrates. Calcium antagonists and betablockers were prescribed in half the cases. Aspirin (100 mg orally per day) was prescribed after control coronary angiography (Coro 2) performed 24 +/- 6 hours after starting treatment. Qualitative and quantitative analysis (CAESAR system) was centralised. There were no differences in the angiographic findings between the two groups. Intracoronary thrombosis was observed in 43% (rt-PA) and 44% (placebo) in Coro 1 and in 17% and 28% in Coro 2. The incidence of myocardial revascularisation procedures was similar in the two groups: angioplasty: 12 (rt-PA) and 13 (placebo); coronary bypass surgery: 5 (rt-PA) and 6 (placebo). Seven patients developed myocardial infarction (5 rt-PA, 2 placebo), one of whom died of cardiogenic shock (placebo). Eighteen patients had haemorrhagic complications (14 rt-PA, 4 placebo; p < 0.002) mainly at the puncture sites (12/14, 3/4). Spontaneous haemorrhage occurred in 7/25 (28%) of patients on rt-PA (haematuria 3, gastrointestinal haemorrhage 2, haematuria + gastrointestinal haemorrhage 1, epistaxis 1) and in 1/25 patients on placebo (gastrointestinal haemorrhage) This study shows that intravenous thrombolysis with rt-PA in severe unstable angina pectoris doe not modify the clinical outcome or the angiographic lesions but exposes patients to a high risk of haemorrhagic complications.
Non-valvular atrial fibrillation multiplies the risk of presumed embolic events by a factor of four. The hemorrhagic risk of anticoagulant treatment varies considerably and its prophylactic efficacy was not tested in any randomised trial before the end of 1989. The recommendations of experts at that time recognised that data were inadequate. The publication since of four randomised trials involving 3,049 patients has provided a more objective base for management decisions, highly in favour of the anticoagulation of cases of non-isolated atrial fibrillation in the absence of contraindications.
The effect of intravenous streptokinase therapy on the time course of functional recovery was investigated in a controlled study of 64 patients randomized within 3 hours after the onset of acute myocardial infarction (AMI). Contrast ventriculography was performed 1 to 4 days after AMI and repeated 5 weeks later. Wall motion was analyzed by the centerline method in the central infarct, peripheral infarct and noninfarct regions. In patients with ventriculographic data at the early catheterization, streptokinase-treated patients had less severe hypokinesia in the central infarct region than control patients (-2.9 +/- 0.9 [n = 29] vs -3.4 +/- 0.7 standard deviations below normal [n = 21], p less than 0.05). The benefit of streptokinase was more marked in the peripheral infarct region (-1.5 +/- 0.7 vs -2.1 +/- 0.6, p less than 0.001). As a result, the ejection fraction was slightly higher in treated versus control groups (46 +/- 10 vs 43 +/- 7%, respectively; difference not significant). At 5 weeks, function in the streptokinase and control groups had diverged further because of continued improvement in the streptokinase-treated patients. This study shows that streptokinase benefits left ventricular (LV) function by 1 to 4 days after AMI, earlier than previously reported. The benefit was not limited to the peripheral infarct region, where ischemia might have been less severe, but was also seen in the central infarct region. The implication is that thrombolytic therapy can improve LV function during the period of myocardial stunning, while myocardial function is still recovering.
Ten patients with sick sinus syndrome having repetitive sinus node electrograms during long postpacing pauses were studied during programmed atrial stimulation. Sinus node activity was recorded using a percutaneous catheter electrode. A sinus node electrogram was recorded before the return atrial beat in seven patients; it was similar to the sinus node electrogram observed during postpacing pauses and is clearly identified because sinoatrial conduction time was markedly prolonged following the atrial extra beat. Complete sinoatrial exit block occurred in four patients. (1) Sinus node electrograms were thus validated both during postpacing pauses and during programmed atrial stimulation in most patients with sick sinus syndrome. (2) Sinoatrial conduction time was markedly prolonged after one extrasystole, accounting for supracompensatory atrial return cycles. (3) If it were cumulative following multiple extrasystoles, this effect could constitute the electrophysiologic link between an abnormal response during programmed atrial stimulation and the complete sinoatrial block recorded during the pauses that follow rapid atrial pacing.
The authors present a removable vena cava filter that may be introduced percutaneously, is atraumatic to the venous wall, and permits the simultaneous use of thrombolytic therapy. Sixty-five patients were studied: 42 cases of pulmonary embolism with threatening venous thrombosis; 23 cases of phlebitis associated with an ilio-caval thrombus without pulmonary embolism. The filter was introduced 38 times femorally and 27 times by a jugular approach. In 16 cases (24.6%) clots broke loose, were effectively caught by the filter, and were progressively dissolved during thrombolytic therapy. The filter remained in place on average 4.5 +/- 1.2 days. The filter was removed in all cases without provoking the recurrence of pulmonary embolism. Two deaths, not related to pulmonary embolism, occurred during hospitalization. Phlebography, performed in all cases before and after treatment, showed a significant decrease of the phlebographic score (10.88 +/- 0.82 vs 6.77 +/- 0.86, P less than 0.001). The same was observed in 40 patients who underwent a pulmonary angiography before and after treatment (Miller index = 17.04 +/- 0.73 vs 5.49 +/- 0.87, P less than 0.0001). After removal of the filter, no sign of pulmonary embolism was detected on lung scan in the 23 patients with ilio-caval thrombus alone. More than 5 g (100 ml)-1 of haemoglobin was lost by 15.38% of patients. All patients were followed-up for a mean of 7.12 +/- 1.3 months; in no case was there any clinical recurrence of pulmonary embolism. Thus this device allows an effective temporary filtering of the vena cava.(ABSTRACT TRUNCATED AT 250 WORDS)
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The first results of the long-term treatment of chronic heart failure with inotrope positive medications are disappointing, especially in that survival is not prolonged and even a greater mortality is suggested. Is it because of the regular failure of specific medications, of a class of medications or because the overall concept of inotropism stimulation during chronic heart failure should be condemned? The mechanisms of inotropism of normal muscles or muscles in human chronic heart failure are reviewed as well as the various pharmacological means available to stimulate inotropism.
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Within 3 h after the onset of symptoms of myocardial infarction, 64 patients were randomly assigned to receive either a 1-h intravenous infusion of 1,500,000 IU of streptokinase (SK) or a conventional therapy. Infarct size was estimated in CK gram equivalent (CKg) by measurement of CK-MB every 3 hours during a 48-h period. Enzymatic study revealed that myocardial infarction of the SK group was significantly smaller (61.4 +/- 45 vs. 89.4 +/- 56 CKg, p less than .05). Angiograms were performed at early stage and five weeks after myocardial infarction. At first coronary angiogram, the infarct-related vessel was open in 82% in the SK group versus 12% in controls. The SK group had higher global ejection fraction at second angiogram (57 +/- 11% vs. 49 +/- 11%, p less than .02), but differences in regional wall motion were not significant. By analysis according to patency or occlusion of infarct-related vessel, global and regional ejection fractions were significantly better at first and at second angiograms in all patients and in anterior infarctions with a patent infarct-related coronary artery. There was no significant difference for inferior infarction. We conclude that intravenous streptokinase infusion early after the onset of myocardial infarction reduces infarct size and improves left ventricular function, chiefly in anterior infarction. This benefit appears to be closely correlated to patency of infarct-related vessels.
Coxsackie B virus infections are common and frequently asymptomatic. However in young people, they can cause primary congestive cardiomyopathy and complicate previous cardiovascular illnesses. Virus diagnosis is difficult and based mainly on the detection of significant rising or stating high neutralizing antibody titers. A clinical and epidemiological five years study investigated 3,856 sera. 30.2% of the patients had evidence of a significant antibody titer (greater than or equal to 64) to one of the group B Coxsackie viruses; this percentage reaches 34.6% in cardiology and fluctuates from year to year; Coxsackie B2 is predominant (55.9%) in cardiology; coxsackie B1 and B2 antibody responses were detected more frequently than B3, B4 and B5. Coxsackie B6 appears to be uncommon. From these, 66 patients have evidence of coxsackie B virus infections with 60.2% for Coxsackie B2; they include pericarditis (30.3%), acute and chronic congestive cardiomyopathies (19.7%). Moreover it has been suggested that Coxsackie B virus might be responsible for electrocardiographic abnormalities (9.1%), ischemic heart disease and myocardial infarction. Enzyme linked immunosorbent assay (ELISA) and radioimmunoassay with purified antigens (VP1 and VP4) did not appear better than microneutralisation for evaluation of IgM and IgG antibodies. To elucidate the mechanisms of cardiac injury it is refer to viral replication, virus specific and auto-reactive T cells cytotoxic activities.
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A transvenous electrode catheter technique was used for direct recording of bipolar sinus node electrograms during postpacing atrial pauses. Multiple repetitive local sinus node electrograms during atrial quiescence validate sinus node electrograms. Such atrial pauses with sinus node electrograms are due to sinoatrial block; atrial pauses without sinus node electrograms are due to overdrive suppression or improper recording. Eight consecutive patients were prospectively selected on the basis of a corrected sinus node recovery time greater than 1500 msec during diagnostic electrophysiologic evaluation. Six patients had atrial pauses with sinus node electrograms; three patterns of sinus node electrograms during atrial pauses were observed. We conclude that (1) sinus node electrogram recording is of value in understanding the mechanism underlying postpacing atrial pauses; (2) atrial pauses are usually (6/8) caused by sinoatrial block; (3) three patterns of sinus node electrograms are observed, thus making indirect interpretation unreliable.
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Histological study of the sinoatrial node (SAN) was performed in 111 patients in order to estabilsh correlations between the ECG findings and the anatomical lesions. This series includes both patients with sinus rhythm and patients with atrial arrhythmias. The results are as fololows: (a) the amount of nodal cells in the SAN was found to be inversely proportional to the age of the patients (p less than 0.001); (b) normal sinus rhythm was present in some cases with severe fibrosis of the SAN; (c) the present study does not support lesions of the SAN as responsible for atrial fibrillation; (d) chronic sinoatrial block was associated with extensive lesions of the approaches of the AV node or the AV node itself; (e) the auricular tachycardia-bradycardia syndrome was associated in most cases with both lesions of the main feature of the SAN lesion. The pathogenesis of these fibrotic lesions are discussed.