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Procoagulant activity, thrombin and fibrinolytic system activation have been demonstrated in the first 24-48 h after acute myocardial infarction treated with thrombolytic therapy. Little is known about what happens in the subsequent days, during which the incidence of ischaemic recurrence is high. In 21 patients treated with streptokinase and in 20 patients treated with urokinase we evaluated, with multiple plasma determinations, D-dimer and fibrinogen plasma levels in the first week after myocardial infarction. From the 2nd hour after the beginning of thrombolysis to the 4th day, all patients received intravenous heparin in doses sufficient to raise the partial thromboplastin time to twice its normal level; subcutaneous calcium heparin (12,000 U/day) was subsequently substituted for the intravenous route. Coronary angiography was performed 7 days after infarction. From the basal values 2.22 +/- 1.44 nmol.1(-1) in the streptokinase group and 3.28 +/- 3.05 nmol.1(-1) in the urokinase group, D-dimer rose consistently in the 1st hour after thrombolysis 269.4 +/- 206.7 nmol.1(-1) and 44.5 +/- 35.5 nmol.1(-1) in the streptokinase and urokinase groups, respectively; P < 0.001. After the peak value, which in both groups was reached after 5 h, D-dimer slowly decreased during the study period. It reverted to normal values only in 10/21 patients in the streptokinase group; in the urokinase group normalization was attained in 14/20 patients between the 3rd and 6th days. After withdrawal of i.v. heparin in patients of both groups with TIMI 0 or 1 grade of coronary patency, D-dimer rose to levels four to seven times greater than normal; in patients of both groups with TIMI 2 or 3 grade coronary flow, D-dimer showed a monophasic pattern of progressive normalization (P < 0.05 and P < 0.01 at the 6th and 7th days, respectively, for differences between TIMI 0-1 and TIMI 2-3 groups). After myocardial infarction, thrombolysis is followed by active and persistent fibrin degradation more marked and lasting after streptokinase than after urokinase. When occurring sooner, it is a consequence of plasmin activation induced by thrombolytic agents; later it seems to be related to intracoronary substrate, as suggested by the relationship of plasma elevation of D-dimer with the presence of occluded or suboccluded infarction-related vessels.

The purpose of this study was to investigate whether, to what extent, and through which mechanisms intravenous heparin, administered before and after streptokinase, affects the plasma levels of D-dimer and fibrinogen in myocardial infarction. Data concerning mortality and incidence of coronary recanalization in patients receiving heparin and thrombolytic therapy after acute myocardial infarction are controversial; furthermore, the mechanisms through which heparin acts in combination with thrombolytic therapy are unclear. Thirty-eight patients with acute myocardial infarction treated with streptokinase were considered. Nineteen of them received, immediately before the beginning of thrombolytic treatment, a bolus of heparin (100 U.kg-1 intravenously) and, 2 h later, intravenous heparin in doses raising the partial thromboplastin time to 2-2.5 times the normal value (Group 1); the remaining 19 did not receive anticoagulant treatment (Group 2). Multiple determinations of plasma D-dimer and fibrinogen levels were obtained in all patients before, and in the seven days following thrombolytic treatment. Six hours after streptokinase, fibrinogen decreased from 304 +/- 34 to 61 +/- 34 mg.dl-1 in Group 1 and from 312 +/- 29 to 38 +/- 21 mg.dl-1 in Group 2 (P < 0.02 versus Group 1). The same difference between groups persisted at the 12th and at the 18th hour. D-dimer values, from 0.5 +/- 0.1 microgram.dl-1 in Group 1 and 0.4 +/- 0.1 microgram.dl-1 in Group 2, increased at the 1st hour to 37.2 +/- 36.5 micrograms.dl-1 and 52.2 +/- 39.8 micrograms.dl-1, respectively. A peak value was reached in both groups at the 6th hour, which was followed by a slow decrease.(ABSTRACT TRUNCATED AT 250 WORDS)

Holter monitoring in a 75-year-old man with a VVI pacemaker with rate hysteresis and concomitant quinidine treatment documented the occurrence of several episodes of non-sustained polymorphous ventricular tachycardia, triggered by each first paced beat following the longer escape interval. These arrhythmias disappeared when quinidine was withdrawn or when the pacemaker was reprogrammed without hysteresis. We hypothesize that the association of the different effects produced by hysteresis and quinidine created the electrophysiologic substrate for the observed arrhythmias.

In 16 subjects with paroxysmal supraventricular tachycardia (SVT) we sought a relationship between haemodynamic changes associated with artificially induced arrhythmias and the electrophysiological properties of the related atrioventricular (AV) nodal reentry circuit. In 10 patients (group 1) induced SVT was typical (long AH) and caused a significant fall in cardiac output (-1.720 ml min-1) and arterial systolic pressure (-18 mmHg). In six subjects (group 2), induced SVT was atypical (long HA) and did not significantly alter the output of the heart and systolic pressure, despite the elicitation of similar tachycardia. The opposite AV nodal reciprocation pattern which resulted in a substantial increase in AH/HH in group 1 and in a slight rise of the same variable in group 2, may explain these haemodynamic differences. In fact, atrial and ventricular systoles occurred simultaneously and impeded the ventricular filling in the former group, while a regular subsequence of contraction was maintained in the latter group. In group 2, systolic arterial pressure and cardiac output fell to the same level as in group 1 when right atrial pacing, at a similar rate of SVT, determined an increase of AH/HH similar to that observed during typical tachycardia. Thus, the haemodynamic response to SVT differs significantly between the two types of reciprocating tachycardia, particularly as regards cardiac output and blood pressure, and is mainly influenced by the temporal relationship between atrial and ventricular systole, independent of the rate of contraction. The different conduction velocities of the reciprocating circuit limbs and their interrelation seem to be major determinants of the haemodynamic pattern of SVT.