The screening by immunoenzymometric assay (IEMA) of 784 monoclonal antibody (MAb) combinations resulted in the selection of an optimal pair of MAbs for measuring human cardiac troponin I (TnI). Using a one-step IEMA described here, we were able to detect TnI within the range of 0.2-20 micrograms/L in 30 min at room temperature. No cross-reactivity was observed with the skeletal isoforms of troponin up to a concentration of 500 micrograms/L. This assay was used to measure cardiac TnI in the plasma of 43 patients with acute myocardial infarction (AMI). TnI was detected relatively early after the onset of chest pain (4.3 +/- 2.1 h, mean +/- SD); the peak occurred after 12.2 +/- 4.6 h in a population that had undergone fibrinolysis. TnI disappearance was generally observed between 5 and 9 days after the onset of chest pain. No cardiac TnI could be detected in 145 healthy donors or in a control group of 6 patients (with skeletal damage or rhabdomyolysis). This assay allows a specific diagnosis of AMI in its early acute phase, with a high diagnostic specificity and sensitivity.

Long-term endocardial biventricular stimulation via a transseptal approach was safe and effective in this small population. This approach needs to be further compared with conventional epicardial pacing via the coronary sinus.

This article describes a new technique of LV lead insertion, using transseptal catheterization performed through the right internal jugular vein, to obtain a totally endocardial biventricular chronic pacing in end-stage heart failure. Three patients with QRS widening (> 180 ms) linked to complete left bundle branch block (n = 2) or right ventricular pacing (n = 1) were included in this preliminary study. Catheterization was performed under fluoroscopy and transesophageal echocardiography guidance. Transseptal catheterization was achieved by puncture of the right internal jugular vein at the base of the neck and by using a Brockenbrough needle, the tip curve of which was more curved than the standard model. A flexible long sheath was advanced in the left atrium through the interatrial septum and then a unipolar electrode was placed easily in the LV. The proximal tip of the LV lead was tunneled from the neck to the subclavian area and connected to the ventricular channel of a dual (n = 1) or simple (n = 2) chamber pacemaker. Efficient acute sensing (V wave amplitude = 13 +/- 3 m V) and pacing (acute pacing threshold = 0. 7 +/- 0.4 V) were obtained in the three patients. Early loss of capture occurred in two patients requiring lead replacement. Functional status dramatically improved in all three patients. At 6-month follow-up, biventricular pacing was maintained in all patients (mean threshold 1.4 V) who were free of clinical embolic event with oral anticoagulation therapy. This modified technique of jugular transseptal catheterization appears promising for the development of left heart pacing.

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In 20 patients undergoing coronary arteriography, the hemodynamic effects of an experimental preparation of i.v. amiodarone 5 mg kg-1 without Tween 80 (N) (10 patients) were compared with those of the commercial form with Tween 80 (A) (10 patients). Analysis of variance demonstrated differences during the 3 min of injection and for 3 min afterwards: left ventricular systolic pressure decreased from 110 + 11 to 86 +/- 11 mmHg (P = 0.001) after A and from 114 +/- 22 to 106 +/- 19 (P = 0.05) after N (comparison P = 0.01) while related tachycardia was also more pronounced after A (comparison P = 0.001). Left ventricular end diastolic pressure transiently decreased after A while continuously increasing after N (P = 0.05). During the following 30 min both A and N caused similar bradycardia, increase in ventricular filling pressure, vascular resistance and decrease in cardiac and contractility indexes. Amiodarone blood levels were similar after A or N. These data document a significant initial short duration vasoplegia, mainly related to Tween 80, after A, when amiodarone itself after producing a similar very slight effect causes bradycardia, and a moderate and progressive negative inotropic effect. It was concluded that while the experimental form would be of interest, the risk of severe hypotension after i.v. Cordarone can be largely avoided by using a slower rate of infusion, especially in patients with hypovolemic status.