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Objective: Most women eligible for a trial of labor after a cesarean (TOLAC) undergo an elective repeat cesarean section (ERCS). We hypothesized that this is largely because of poor patient education., Study Design: This was a prospective study of women who presented to our hospital from November 2010 through July 2011 who were candidates for TOLAC. Women filled out a questionnaire prior to their scheduled ERCS or upon admission for TOLAC. A χ(2) and a Student t test were used, as appropriate., Results: The study included 155 women, 87 for TOLAC and 68 for ERCS. Women in both groups demonstrated a lack of knowledge on the risks and benefits of TOLAC and ERCS. When patients perceived their providers as having a preference for ERCS, very few chose TOLAC, whereas the majority chose TOLAC if this was their provider's preference., Conclusion: Candidates for TOLAC appear to know little about the risks and benefits associated with their mode of delivery, and provider preference affects this choice., (Copyright © 2012. Published by Mosby, Inc.)

The aim of this study was to compare the efficacy of a new generation endodontic irrigant, Tetraclean, to the widely used sodium hypochlorite. Tetraclean combines a powerful detergent effect with a strong antimicrobial efficacy, whereas sodium hypochlorite has several drawbacks and is sometimes ineffective in preventing microbial-mediated endodontic failure. The bactericidal activity of both irrigants against Enterococcus faecalis, the most commonly isolated species from root canals of teeth with post-treatment disease, was assessed i) in vitro, according to the European Standard lines for the evaluation of the bactericidal activity of chemical disinfectants, and ii) with an ex vivo model of extracted and decoronated human teeth, infected with E. faecalis and subsequently irrigated with either of the irrigants. Both irrigants display very similar bactericidal activity against E. faecalis in vitro. However, the ex vivo model shows that only in the teeth irrigated with Tetraclean did the bacterial burden gradually drop until no bacteria were detectable a few days post-irrigation. Vice versa, in the teeth irrigated with sodium hypochlorite, the drop in the bacterial burden was rapid but temporary and most of the teeth were colonized again by 48 hours post-irrigation.

Cardiac troponin-T (Tn-T) and troponin I (Tn-I) isoforms are sensitive and specific tests for the diagnosis of acute myocardial infarction. Information is scanty regarding the ability of these markers to discriminate patients with or without reperfusion early after thrombolytic treatment. To this purpose, 64 patients (mean age 63.7 +/- 7.5 years) with acute myocardial infarction, treated with recombinant tissue-type plasminogen activator within 6 hours from the onset of symptoms, were enrolled in the study. Tn-I was determined by immunofluorescency (Dade, Stratus II) at the beginning of thrombolysis, 30 min after therapy (120 min after starting) and every 6 hours in the first 2 days of acute myocardial infarction. At the same intervals, samples for Tn-T (immunoenzymatic methods ELISA), creatin phosphokinase (CK) and CK-MB (biochemical method) were collected. Normal subjects showed values of Tn-I and Tn-T steadily lower than 0.2 micrograms/l. To evaluate reperfusion, for each parameter the time to peak concentration and the ratio (delta) between the levels of the marker 30 min after thrombolysis vs basal, were considered. Coronary angiography was performed in all patients within 4 days, in 48 patients (Group 1) reperfusion (TIMI grade 2-3) of the involved vessel was reached, in 16 (Group 2) reperfusion was absent (TIMI 0-1). In Group 1, at 30 min after the end of thrombolysis, an increase of cardiac Tn-1 of at least 5.5 times compared to baseline, was observed; In-T, CK and CK-MB reached concentrations at least 7-fold greater than basal ones; in Group 2 patients, no significant variation of concentration of all markers was found. Therefore, in order to discriminate between reperfused and non reperfused patients, cut-off values of the ratio delta of 5.5 for Tn-I and of 7 for Tn-T were chosen. By this method, sensitivity for detection of reperfusion was 95, 80, 54 and 56%; specifically 100, 89, 79 and 82%, respectively. In Group 1 Tn-I peaked earlier than other parameters (9.2 +/- 1.7 vs 12.4 +/- 2.4 hours for Tn-T, p< 0.04 and vs 13 +/- 1.7 hours for CK and CK-MB, p<0.03); the peak of each marker showed the following values of sensitivity and specificity for reperfusion: 86 and 89% for Tn-I, 79 and 82% for Tn-T, 78 and 80% for CK, 83 and 80% for CK-MB. The time to peak of troponins, CK and CK-MB is a sensitive index of reperfusion after thrombolytic therapy in acute myocardial infarction; the delta Tn-I is the earliest marker of reperfusion allowing the assessment of efficacy of treatment within 2 hours after its beginning.

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.

In vitro and in vivo studies have shown both an inhibition and an activation of platelets after thrombolysis in acute myocardial infarction. Plasma beta-thromboglobulin, a marker of platelet activity, was evaluated daily during the first week after myocardial infarction in 24 patients who received intravenous streptokinase (group 1) and 26 who did not (group 2). On admission, levels of beta-thromboglobulin, as compared to those in healthy subjects (35 +/- 9 IU/ml), were similarly augmented in group 1 (105 +/- 27 IU/ml) and in group 2 (115 +/- 30 IU/ml); 3 hours later, values averaged 191 +/- 58 IU/ml in group 1 (p < 0.001 vs baseline) and 95 +/- 28 IU/ml in group 2 (not significant vs baseline; p < 0.001 between the two groups). From the second to the seventh day, beta-thromboglobulin augmented in those patients in both groups with postinfarction angina. From day 5 to day 7, patients of group 1 without angina had lower beta-thromboglobulin levels than patients of group 2 who had no symptoms. The lowest levels of platelet activity were observed in group 1 reperfused patients. These data indicate that in myocardial infarction an early platelet activation takes place that is enhanced by thrombolytic treatment; recurrence of angina is associated with persistent activation; in the absence of recurrent angina, thrombolysis can limit late platelet activation.

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)

Extracorporeal ultrafiltration (UF) can improve the clinical condition, as assessed by cardiopulmonary exercise evaluation, of patients with moderate heart failure (HF); the pre-UF level of physical performance above which UF does not induce clinical benefits, is not defined. For this purpose, we studied 29 patients with stable HF in functional class II-III (NYHA), who underwent UF (veno-venous bypass, removal of 1,830 +/- 550 ml of plasma water), regardless their baseline oxygen consumption at peak exercise (VO2p) and at anaerobic threshold (VO2AT). All patients experienced cardiopulmonary exercise tests (cycloergometer, increasing workloads of 25 W every 3 min) before (pre-UF), and 4 days and 3 months following UF. According to VO2 changes following UF 2 groups of patients were identified: in Group I (9 patients) no differences in VO2p and VO2AT were observed, while in Group II (18 patients) VO2p rose by 2.7 ml/min/kg (p < 0.001) at 4 days and 4.5 ml/min/kg (p = 0.04) at 3 months, and VO2AT rose by 1.2 ml/min/kg (p < 0.001) at 4 days and 2.8 ml/min/kg (p = 0.03) at 3 months. In unresponsive patients baseline values of VO2p > or = 18 ml/min/kg and VO2AT +/- 13 ml/min/kg were detected. Pre-UF VO2p inversely correlated with the shift of VO2p (delta VO2p) both at 4 days (r = -0.62, p < 0.001) and at 3 months (r = -0.53, p = 0.005), and pre-UF VO2AT inversely correlated with delta VO2AT at 4 days (r = -0.71, p < 0.001) and at 3 months (r = -0.63, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrafiltration improves the clinical condition of patients with moderate congestive heart failure. Ultrafiltration (1895 +/- 120 ml of plasma water, rate 600 ml/h, veno-venous bypass) was performed in 30 patients with moderate congestive heart failure in stable clinical conditions. The effects of ultrafiltration were assessed through pulmonary function and cardiopulmonary exercise tests performed before and 30 days after the procedure. Vital capacity, forced expiratory volume (1 s) and maximal voluntary ventilation improved as improved exercise performance (increase in oxygen consumption at peak exercise and at anaerobic threshold). Tidal volume at anaerobic threshold and at peak exercise increased by 10% with no changes in respiratory rate. This suggests that ultrafiltration induces changes at the physical characteristics of the lungs probably related to changes in lung water content.

We investigated the mechanisms involved in the regulation of salt and water metabolism in patients with congestive heart failure (CHF). Extracorporeal ultrafiltration was utilized as a nonpharmacologic method for withdrawal of body fluids. In 32 consecutive patients with CHF (NYHA class II to IV) and different degrees of water retention, 24-hour diuresis and natriuresis were inversely best correlated with the combination of circulating renin, aldosterone, norepinephrine, and renal perfusion pressure (RPP). Fluid removal (600 to 5,000 ml) at a rate of 500 ml/h, until right atrial pressure decreased to 50% of baseline, caused variable humoral, circulatory, and diuretic effects that were mainly related to the extent of fluid retention. In fact, in 10 patients (Group 1) with overhydration refractory to drug therapy and with urinary output less than 1,000 ml/24 h (mean 370 ml), soon after the procedure, plasma renin (-39%), aldosterone (-50%), and norepinephrine (-47%) were reduced and RPP was increased (+ 16%), and in the subsequent 24 hours, diuresis was increased by 493%; in 9 patients (Group 2) whose baseline urinary output exceeded 1,000 ml/24 h (mean 1,785 ml), renin increased by 40%, norepinephrine, aldosterone and RPP each decreased by 12%, and diuresis remained unchanged; in 13 patients (Group 3) with a daily urinary excretion as in Group 2 and without overhydration, RPP decreased (-7%), renin (+ 196%), aldosterone (+ 170%), and norepinephrine (+ 52%) increased, and diuresis decreased by 45%. There was an overall correlation (p < 0.0001) between the combination of changes in these circulatory and hormonal variables and changes in diuresis and natriuresis with ultrafiltration.(ABSTRACT TRUNCATED AT 250 WORDS)

Objectives: The aim of this study was to evaluate whether ultrafiltration is beneficial in patients with moderate congestive heart failure., Background: Ultrafiltration is beneficial in patients with severe congestive heart failure., Methods: We studied 36 patients in New York Heart Association functional classes II and III in stable clinical condition. Eighteen patients (group A) were randomly selected and underwent a single session of ultrafiltration (venovenous bypass, mean [+/- SEM] ultrafiltrate 1,880 +/- 174 ml, approximately 600 ml/h) and 18 (group B) served as control subjects., Results: Two patients in group A and three in group B did not complete the 6-month follow-up study. In group A, soon after ultrafiltration there were significant reductions in right atrial pressure (from 8 +/- 1 to 3.4 +/- 0.7 mm Hg, pulmonary wedge pressure (from 18 +/- 2.5 to 10 +/- 1.9 mm Hg) and cardiac index (from 2.8 +/- 0.2 to 2.3 +/- 0.2 liters/min). During the follow-up period, lung function improved, extravascular lung water (X-ray score) decreased and peak oxygen consumption (ml/min per kg) increased significantly from 15.5 +/- 1 (day -1) to 17.6 +/- 0.9 (day 4), to 17.8 +/- 0.9 (day 30), to 18.9 +/- 1 (day 90) and to 19.1 +/- 1 (day 180). Oxygen consumption at anaerobic threshold (ml/min per kg) also increased significantly from 11.6 +/- 0.8 (day -1) to 13 +/- 0.7 (day 4), to 13.7 +/- 0.5 (day 30), to 15.5 +/- 0.8 (day 90) and to 15.2 +/- 0.8 (day 180). These changes were associated with increased ventilation, tidal volume and dead space/tidal volume ratio at peak exercise. The improvement in exercise performance was associated with a decrease in norepinephrine at rest, a downward shift of norepinephrine kinetics at submaximal exercise and an increase in norepinephrine during orthostatic tilt. None of these changes were recorded in group B., Conclusions: In patients with moderate congestive heart failure, ultrafiltration reduces the severity of the syndrome.

Purpose: We investigated the mechanisms involved in the regulation of salt and water metabolism in patients with congestive heart failure (CHF). Extracorporeal ultrafiltration was utilized as a nonpharmacologic method for withdrawal of body fluid., Patients, Methods, and Results: In 32 consecutive patients with CHF (New York Heart Association functional class II to IV) and different degrees of water retention, 24-hour diuresis and natriuresis were inversely best correlated with the combination of circulating renin, aldosterone, norepinephrine, and renal perfusion pressure (RPP, mean aortic pressure minus mean right atrial pressure). Fluid withdrawal (600 to 5,000 mL) at a rate of 500 mL/h, until right atrial pressure decreased to 50% of baseline, caused variable humoral, circulatory, and diuretic effects that were mainly related to the extent of fluid retention. In fact, in 10 patients (Group 1) with overhydration refractory to drug therapy and with urinary output less than 1,000 mL/24 h (mean, 370 mL), soon after the procedure, plasma renin (-39%), aldosterone (-50%), and norepinephrine (-47%) were reduced and RPP was increased (+16%), and in the subsequent 24 hours, diuresis was increased by 493%; in 9 patients (Group 2) whose baseline urinary output exceeded 1,000 mL/24 h (mean, 1,785 mL), renin increased by 40%, norepinephrine, aldosterone, and RPP each decreased by 12%, and diuresis remained unchanged; in 13 patients (Group 3) with a daily urinary excretion as in Group 2 and without overhydration, RPP decreased (-7%), renin (+196%), aldosterone (+170%), and norepinephrine (+52%) increased, and diuresis decreased by 45%. There was an overall correlation (p < 0.0001) between the combination of changes in these circulatory and hormonal variables and changes in diuresis and natriuresis with ultrafiltration., Conclusions: It appears that in CHF, (1) retention of sodium and water results from an interaction of hormonal and hemodynamic (primarily RPP) alterations that may exert a reciprocal positive feedback; (2) depending on the presence and severity of fluid retention, the response to withdrawal of body fluid may vary from neurohumoral activation and restriction of diuresis to neurohumoral depression and extreme potentiation of salt and water excretion; (3) refractory CHF requires the interruption of the humoral-hemodynamic vicious circle, and ultrafiltration is able to accomplish that.

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 congestive heart failure (CHF), hemofiltration is associated with an obvious decrease in circulating norepinephrine. This method was used for investigating the mechanisms whereby plasma norepinephrine is increased in chronic CHF. In 23 cases of advanced CHF, hemofiltration (2,983 +/- 1,228 ml) lowered plasma norepinephrine by 515 +/- 444 pg/ml. This effect was prompt, persisted or became greater in the next 24 hours. It was not associated with significant changes in cardiac output, aortic pressure or systemic vascular resistance. It did not appear to depend on variations in parameters related to the sympathetic activity, such as plasma renin, right atrial, wedge pulmonary artery and renal perfusion pressures, and was independent of duration and amount of hemofiltration. These observations did not support the concept that the norepinephrine decrease was the main consequence of a neural sympathetic inhibition. Hemofiltration increased diuresis by 606 +/- 415 ml; changes were prompt and correlated inversely (r = -0.7; p less than 0.01) with those in plasma norepinephrine. The same unknown mechanism of the increased urinary output might potentiate the norepinephrine removal from the blood by the kidney, or hemofiltration and the augmented diuresis might result in a regression of congestion of lungs and kidneys, leading to an improved extraction of norepinephrine. In CHF, a relation may exist between fluid retention and norepinephrine and in advanced stages, circulating norepinephrine, although strikingly increased, is devoid of important cardiovascular effects. At these stages, plasma norepinephrine is probably unreliable as an index of the sympathetic neural activity.

Hemofiltration is a method suitable for rapid substraction of plasma water that generally allows reduction of circulating levels of norepinephrine. Using that non-pharmacological approach we investigated the mechanisms involved in the metabolism of the hormone as well as the hemodynamic correlates of a prompt and great fall of the sympathetic neurotransmitter in patients with chronic refractory congestive heart failure (CHF). In 23 patients with CHF, hemofiltration of 2983 +/- 1228 ml of plasma water (in 5 +/- 2 hours of treatment) increased urinary output by 606 +/- 415 ml in the day of the procedure as well as sodium excretion by 53 +/- 38 mEq/24 h; simultaneously, a mean fall in plasma norepinephrine concentration by 515 +/- 444 pg/ml was observed. These effects were prompt and persisted or even rose in the next 24 and 48 hours, not being related to changes in plasma renin activity, right atrial, wedge pulmonary artery and renal perfusion pressures and to the amount and duration of hemofiltration. Our data did not clarify the mechanism involved in the increase of the diuresis and for its coupling with the fall in plasma norepinephrine. Nevertheless, we found a strong and statistically significant correlation (r = 0.7; p less than 0.01) between percent changes from baseline values of norepinephrine and diuresis. It is therefore suggested that the same, still unknown, mechanism which increased urinary output also potentiated norepinephrine removal by the kidney: or that water reabsorption from extravascular spaces (triggered by hemofiltration and continued by increased diuresis) resulted in regression of organ congestion leading to an improved clearance of norepinephrine by different organs.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty patients with long-standing (mean 30 days) type I atrial flutter (AF) were treated with overdrive atrial pacing. To evaluate the effect of pretreatment with disopyramide (DISO), the study population was divided into 3 groups of 10 patients each: no therapy (Group A); intravenous DISO (maximum dose 250 mg in 1 hour) (Group B), oral DISO (400 mg/day for 4 days) (Group C). The mean cycle length of AF was 215 +/- 24 ms in Group A, 222 +/- 28 in B and 224 +/- 11 in C (NS). After DISO, AF cycle length increased to 287 +/- 24 in Group B (p less than 0.001) and to 264 +/- 29 in C (p less than 0.001). Overdrive pacing was performed from a maximum of 3 atrial sites up to the shortest paced cycle of 150 ms. Reversion to sinus rhythm (SR) occurred in 20% of patients in Group A, 70% in B and 50% in C. In all these cases SR was obtained with paced cycle length that was 70-90% of the baseline cycle length. Pacing was performed from a mean number of 2.1 sites per patient in Group A, 1.2 in B and 2.0 in C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration of atrial flutter to a faster form of AF occurred in 3, 3 and 4 patients, respectively. The administration of DISO prior to overdrive atrial pacing improves the rate of conversion to SR and allows an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. The administration of DISO is beneficial when overdrive atrial pacing is performed for the treatment of long standing AF in patients with organic heart disease.

Long-lasting (mean 30 days) type I atrial flutter was treated with overdrive pacing in 30 patients (mean age 69 years) with organic heart disease. To evaluate the effect of pretreatment with disopyramide, the study population was divided in 3 groups of 10 patients each: group A, no disopyramide therapy; group B, intravenous disopyramide (maximum dose 250 mg in 1 hour); and group C, oral disopyramide (400 mg daily for 4 days). There were no differences in baseline cycle length of atrial flutter among the 3 groups before drugs were given. The stimulation protocol included overdrive atrial pacing up to the shortest paced cycle of 150 ms performed at a maximum of 3 atrial sites. Reversion to sinus rhythm occurred in 2 patients in group A, 7 in group B (p less than 0.01) and 5 in group C. Pacing was performed from a mean number of 2.1 sites/patient in group A, 1.2 in group B and 2.0 in group C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration to a faster form of atrial flutter occurred in 3, 3 and 4 patients, respectively, and reversion to sinus rhythm occurred in all patients who had intravenous disopyramide and in 1 who took the drug orally. The administration of disopyramide before overdrive pacing improved the rate of conversion to sinus rhythm and allowed an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. Disopyramide is beneficial when overdrive atrial pacing is performed for the treatment of long-standing atrial flutter in patients with organic heart disease.

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.

The relation between the occurrence of repolarisation abnormalities after right ventricular pacing and spontaneous arrhythmias was investigated in 16 patients in whom the sick sinus syndrome was suspected. All patients had normal QRS complexes and T waves in the electrocardiogram before pacing and required atrial stimulation and His bundle recording for diagnostic purposes. Patients were randomised into a study group or a control group. In the eight patients in the study group right ventricular pacing was performed for 12 hours, and was followed by inversion of the T wave in surface leads II, III, aVF, and V2-V5 and lengthening of the QTc interval. The frequency and complexity of ventricular arrhythmias increased after pacing in six patients who had ventricular extrasystoles in the baseline Holter recording. As the configuration of the T wave became normal the frequency of ventricular extrasystoles returned to baseline values. In the control group of eight patients ventricular pacing was not performed after the electrophysiological study and no changes were seen in T wave configuration and in the frequency of spontaneous arrhythmias. These results suggest that the post-pacing repolarisation abnormalities reflect abnormal electrical properties of the ventricle and that in some cases they lead to increased electrical instability.

Eight subjects with the Lown-Ganong-Levine syndrome were studied by means of His bundle recordings during sinus rhythm and during atrial pacing. During sinus rhythm in all cases, the A-H interval was lesser than the mean value observed in 10 control subjects. Atrial pacing at rates up to 190/min produced three types of responses. Four patients showed an initial increment in A-H interval, followed by a plateau response at higher rates. One patient showed an initial increment and a plateau response in A-H interval at low and intermediate rates, followed by a sudden and conspicuous increment at higher rates, indicating conduction of impulse through the A-V node, due to refractoriness of the by-pass tract. Three patients showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. The possible mechanisms for the different types of response are discussed.

Identification of high-risk subgroups of patients after acute myocardial infarction (AMI) is essential for evaluation of targeted preventive strategies. A case-control study was performed in 250 post-AMI patients to examine whether an episode of ventricular fibrillation (VF) during the in-hospital period modifies the long-term prognosis for patients with either an anterior or an inferior AMI. After identification of 70 patients with an anterior AMI and 55 patients with an inferior AMI, all complicated by VF and discharged alive, we selected 125 additional patients who had an AMI not complicated by VF (control subjects). To minimize the potential sources of differences in outcome, cases and controls were matched for the following variables: sex (all men), age (same +/- 2 years), coronary care unit (same), epoch of AMI (same +/- 3 months), and site of AMI (same). Left ventricular dysfunction and prior AMI were present in only a few patients. Patients receiving either acute or long-term treatment with beta-adrenergic blocking agents were not included. The average follow up was 59 months (range 12 to 120). The cumulative mortality during the first 5 years for the patients with inferior AMI without VF (6%, 11%, 13%, 13% and 13%) was modest and not significantly different from that of inferior AMI complicated by VF (6%, 11%, 20%, 20%, and 26%). In contrast, a striking difference appeared when the cumulative mortality of patients with anterior AMI without VF (9%, 13%, 17%, 27%, and 29%) was compared with that of patients with anterior AMI complicated by VF (32%, 40%, 46%, 49% and 54%) (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

The analgesic, hemodynamic and respiratory effects of buprenorphine (0.3 mg i.v.) were monitored in 15 coronary care unit-admitted patients presenting with myocardial infarction who were in functional class I according to the Killip classification. At the time of the study, 8 of them had unequivocal precordial pain (group 1); the remaining 7 were painfree (group 2). The agent showed a prompt and potent analgesic action. It also induced a slight decrease in mean aortic pressure associated with a reduction in systemic vascular resistance and an increase in cardiac index, a rise in the pulmonary arterial pressure and arteriolar resistance and right atrial pressure, a reduction in arterial pO2 and pH and an increase in pCO2. Tension-time-indices of the left and right ventricles varied in parallel with variations in aortic and pulmonary artery pressure, respectively. These responses were probably unrelated to analgesia since they were similar in groups 1 and 2. Changes in systemic circulation were such as to possibly decrease the contractile effort and the oxygen need of the left ventricle and the size of infarction. On the contrary, the rise in pulmonary arterial pressure imposes a hemodynamic burden on the right ventricle that, depending on the patient's condition, may assume clinical importance. It is felt that the use of buprenorphine in myocardial infarction should be restricted to uncomplicated and selected cases.

The administration of class IA antiarrhythmic drugs facilities termination of atrial flutter by overdrive pacing. To investigate the electrophysiologic determinants of this effect, changes in the cycle length, the effective refractory period and the excitable gap of spontaneous type I atrial flutter were studied in 11 patients given intravenous disopyramide (3 mg/kg in 1 hour). After drug infusion, the cycle length of atrial flutter increased from 238 +/- 26 to 298 +/- 38 ms (+25%; p less than 0.001) and the effective refractory period prolonged from 169 +/- 19 to 192 +/- 25 ms (+14%; p less than 0.01). The excitable gap prolonged from 62 +/- 16 to 96 +/- 27 ms (+55%; p less than 0.001). Atrial flutter was terminated by overdrive pacing (mean cycle 203) in 10 of 11 patients; in 1 patient atrial fibrillation resulted after high rate stimulation. In the setting of an anatomically defined reentry circuit, as in type I atrial flutter, the administration of disopyramide prolongs both cycle length and refractory period. The finding of an increased excitable gap suggests that the drug exerts its prominent effect by depressing conduction velocity. A wider excitable gap allows easier penetration of the stimulus in the reentry circuit and accounts for the beneficial effects of type IA antiarrhythmic drugs on the termination of atrial flutter by overdrive pacing.

Hemofiltration has been suggested as a new therapeutic tool in refractory heart failure. In this study, 11 patients with primary or ischemic heart disease in New York Heart Association class IV, in whom there was no response to medical treatment, were subjected to hemofiltration. The pathophysiologic adjustments promoted by subtraction of plasma water were investigated, and guidelines for an appropriate use of this procedure in heart failure are provided. Fluid was removed from plasma at a rate of 500 ml/hour until either normalization of the right atrial pressure (which was increased in all cases) was achieved or the hematocrit exceeded 50 percent. According to these criteria, the duration of treatment ranged from four to six hours and the total amount of fluid removed was 2,000 to 3,000 ml. In each case, hemofiltration promoted relief of dyspnea and of clinical and radiographic evidence of lung congestion and pleural effusion, and substantially reduced the dependent edema and abdominal girth. These effects were paralleled by progressive decrease of the right (-70 percent) and left (-45 percent) ventricular filling pressures and of the pulmonary arterial pressure and arteriolar resistance, without significant variations in heart rate, aortic pressure, cardiac index, and systemic vascular resistance. Changes in the right atrial and wedge pulmonary pressures are interpreted as reflecting a combined effect of a decrease in pressure on the outside of the heart due to fluid reabsorption (from lung interstitial spaces and pericardial, pleural and abdominal cavities) and of intravascular volume subtraction. The arterial partial pressure of oxygen was raised, the partial pressure of carbon dioxide and pH were unchanged, and urinary output was substantially enhanced by the procedure. The study indicates that: hemofiltration may be a short-term treatment for refractory cardiac insufficiency with overhydration; a filtration rate of 500 ml/hour is effective and safe; and the central venous pressure may be a reliable guide to volume subtraction.