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As robots become more involved in underwater operations, understanding underwater contact sensing with compliant systems is fundamental to engineering useful haptic interfaces and vehicles. Despite knowledge of contact sensation in air, little is known about contact sensing underwater and the impact of fluid on both the robotic probe and the target object. The objective of this work is to understand the effects of fluidic loading, fin webbing, and target object geometry on strain sensation within compliant robotic fins and beams during obstacle contact. General descriptions of obstacle contact were sought for strain measurements in fins and beams. Multiple phases of contact were characterized where the robot, fluid, and object interact to affect sensory signals. Unlike in air, the underwater structure-fluid-structure interaction (SFSI) caused changes to strain in each phase of contact. The addition of webbing to beams created a mechanical coupling between adjacent beams, which changed contact strains. Complex obstacle geometries tended to make contact less apparent and caused stretch in fins. This work demonstrates several effects of fluidic loading on strain sensing with compliant robotic beams and fins as they contact obstacles in air and underwater, and provides guidance for future work in underwater active sensing with compliant manipulators.

Engineered robotic fins have adapted principles of propulsion from bony-finned fish, using spatially-varying compliance and complex kinematics to produce and control the fin's propulsive force through time. While methods of force production are well understood, few models exist to predict the propulsive forces of a compliant, high degree of freedom, robotic fin as it moves through fluid. Inspired by evidence that the bluegill sunfish (Lepomis macrochirus) has bending sensation in its pectoral fins, the objective of this study is to understand how sensors distributed within a compliant robotic fin can be used to estimate and predict the fin's propulsive force. A biorobotic model of a bluegill sunfish pectoral fin was instrumented with pressure and bending sensors at multiple locations. Experiments with the robotic fin were executed that varied the swimming gait, flapping frequency, stroke phase, and fin stiffness to understand the forces and sensory measures that occur during swimming. A convolution-based, multi-input-single-output (MISO) model was selected to model and study the relationships between sensory data and propulsive force. Subsets of sensory data were studied to determine which sensor modalities and sensor placement locations resulted in the best force predictions. The propulsive forces of the fin were accurately predicted using the linear MISO model on intrinsic sensory data. Bending sensation was more effective than pressure sensation for predicting propulsive forces, and the importance of bending sensation was consistent with several results in biology and engineering studies. It was important to have a spatial distribution of sensors and multiple sensory modalities in order to predict forces across large changes to dynamics. The relationship between propulsive forces and intrinsic sensory measures is complex, and good models should allow for temporal lags between forces and sensory data, changes to the model within a fin stroke, and changes to the model through gait transitions.

Taking into account all the risk factors and blood pressure levels, as indicated by several American and European recommendations available since 1997, is a leading strategy to reduce mortality and morbidity of hypertensive patients. The aim of this study was to quantify how, in 1999. French practitioners applied recommendations on hypertension (HTN), diabetes and hypercholesterolemia in recently diagnosed hypertensive patients and to evaluate whether or not the recommended targets were met. 1639 French GPs and cardiologists included 5831 recently diagnosed (7.5 +/- 3.6 months) hypertensives (57 +/- 12 years of age, M/F = 55/45%). Initial BP was 173 +/- 15/99 +/- 9 mmHg. 56% had no concomitant disease, 36% had either diabetes, dyslipidemia or coronary heart disease, 8% had at least two concomitant diseases. At the time of the study corresponding to 6.3 +/- 3.8 months after initiation of diet and/or medical treatment, their BP was 148 +/- 17/86 +/- 11 mmHg (-25/-19 mmHg). At that time only 37% of patients with stage 2 HTN were encouraged to adopt lifestyle modifications without any medical treatment as recommended by the JNC VI. Among these hypertensives, measurement of plasma cholesterol was performed in only 61%, HDL-C/LDL-C in 26% and blood glucose in 51%. In the patients with dyslipidemia, LDL-C was measured in only 47%. In the 677 diabetic patients only 27% had a glycated hemoglobin measurement. The percentage of patients reaching target BP was 59% as regard DBP < 90 mmHg, 25% as regard SBP < 140 mmHg, and 23% reached both target values of BP. In addition, 30% of patients with dyslipidemia reached the target LDL-C as defined by French recommendations (ANAES 1996) and 30% of the diabetic patients reached the target value for glycemia recommended by ADA (1997). In 1999 in France, a minority of patients reaches the national or international recommended target values for blood pressure, glycemia and plasma LDL-cholesterol. In spite of that, French practitioners do not implement all the available diagnostic tools to improve the treatment of metabolic disorders in hypertensive patients. As a conclusion, to improve the prognosis of hypertensive patients, it is mandatory to raise the awareness of physicians about multiple risk factor management and help them implement the recommendations in their daily practice.

The acute hemodynamic effects of 20 mg iv amlodipine were evaluated in a placebo-controlled study in 16 normotensive patients 15 +/- 1 days after an acute myocardial infarction by covariance analysis. Atenolol was given orally for at least 1 week before the study to maintain the heart rate between 50 and 60 beats/min. All patients were given two doses of 10 mg of amlodipine, or 10 ml of a placebo twice, in i.v. infusion lasting 2 minutes each. Hemodynamic data were collected during the control period and 15 minutes after each of the two amlodipine or placebo infusions. At the time of the last measurements, 15 minutes after the second amlodipine or placebo infusion, the plasma amlodipine level was 31 +/- 16 micrograms/l and the plasma atenolol level was 773 +/- 564 mu/l in the amlodipine group versus 795 +/- 916 micrograms/l in the placebo group. There were no chronotropic, dromotropic, or inotropic effects. The main hemodynamic effect was a fall in systemic vascular resistance (1548 +/- 591 dynes.sec.cm-5 to 1176 +/- 526 dynes.sec.cm-5, p = 0.045) with decreases in aortic pressure and in the left ventricular stroke work index. The left ventricular ejection fraction was 51 +/- 12% in the placebo group and 56 +/- 15% in the amlodipine group (ns) during the control period, and did not change after infusion of placebo or amlodipine. Left ventricular compliance seemed to be enhanced by amlodipine, because the end-diastolic left ventricular volume index rose from 82 +/- 11 ml/m2 to 87 +/- 11 ml/m2 (p = 0.026) 15 minutes after the beginning of the second infusion of 10 mg of amlodipine, without any change in end-diastolic left ventricular pressure. Intravenous infusion of 20 mg of amlodipine is well tolerated 15 days after acute myocardial infarction in normotensive patients without deeply depressed left ventricular systolic function and chronically treated with atenolol. The main hemodynamic effects observed are potentially useful for such patients.

This retrospective study was designed to determine the characteristics of myocardial infarction with normal coronary arteries. The files of consecutive patients admitted to hospital for a first infarction in 1992 and 1993 were analysed. Patients younger than 70 years of age, who had undergone coronary angiography during their admission to hospital were selected. A total of 109 infarctions complied with these criteria and 9 of them were associated with angiographically normal coronary arteries. In this series, patients with angiographically normal coronaries tended to be younger than those with at least one stenotic coronary artery (47 +/- 13 years vs 55 +/- 11 years, p = 0.07). The sex ratio did not differ between the two groups. The body mass index of patients with normal coronary arteries was significantly lower (22.9 +/- 3.9 kg/m2 vs 26.3 +/- 3 kg/m2; p = 0.02). These patients more frequently reported a history of phlebitis (3/9 kg/cm2 vs 26.3 +/- 3 kg/cm2; p = 0.02). These patients more frequently reported a history of phlebitis (3/9 vs 2/100). The frequency of anterior and posterior infarctions was virtually the same. Myocardial infarction with normal coronary arteries appears to be less severe, as reflected by the creatine phosphokinase peak (867 +/- 268 IU/l vs 1921 +/- 1389 IU/l), the maximal sum of ST elevation (5 mm vs 16 +/- 12 mm; p = 0.05), the percentage of left ventricular akinesia on angiography (25.5 +/- 4 vs 38.7 +/- 11.8; p = 0.01), and the lower ventricular end-diastolic pressure (11.5 +/- 3.5 mmHg vs 38.7 +/- 11.8 mmHg; p = 0.02). Fewer complications were observed during the acute phase, with no deaths. During the subsequent follow-up, with a median of 2 years, no recurrent infarctions, no cardiac decompensation and no deaths were observed in the group with normal coronary arteries. Two patients presented an episode of angina and one developed a recurrent episode of phlebitis. In the other group of 100 patients, 12 deaths were observed during the acute period, followed subsequently by 2 other deaths, 10 episodes of recurrent angina, 2 recurrent infarctions and 12% of patients developed heart failure. In this series, infarction with normal coronary arteries therefore appears to have a good prognosis, possibly because of more limited myocardial necrosis. No abnormalities of haemostasis or coagulation were observed in these patients.

Few cases of transcatheter coronary fistula closure have been reported. High flow coronary fistulae are usually treated by surgery. This case report presents a 5.4 liters/min flow coronary fistula percutaneously closed by steel coils. This large flow needed the packing of 25 coils, 10-15 cm long, for its total occlusion.

This study assesses the value of P wave measurements on the surface ECG at implantation, in the prediction of atrial fibrillation in VVI paced patients. From a consecutive series of 320 pacemaker implantations 172 VVI paced patients for symptomatic atrioventricular block (AVB) (n = 126; mean age 69 +/- 14) or sick sinus syndrome (SSS) (n = 56; mean age 68.6 +/- 12) and in sinus rhythm at implantation were used in this study. P wave duration in V1 is correlated with the incidence of atrial fibrillation during 5 years of follow-up. V1 at implantation was significantly longer (114.6 +/- 2.7 msec) in the patients who developed atrial fibrillation than in those who did not (91.9 +/- 2.7 msec) (P < 0.001). Although positive predictive accuracy increases progressively for higher V1 values for AVB and SSS, the negative predictive and diagnostic accuracy of V1 criteria were less in SSS. Application of the Bayes' theorem showed that in SSS the probability to develop atrial fibrillation is 33% for V1 < 110 msec and is for V1 < 90 msec still higher than that reported in DDD paced patients. In the AVB group the probability to develop atrial fibrillation is 8% for V1 < 110 msec and 6% for V1 < 100 msec. It seems, therefore, that atrial stimulation (AAI or DDD) is always indicated in SSS. In AVB with V1 < 100 msec, DDD pacing, if not needed for other indications, apparently does not offer much benefit in the prophylaxis of atrial fibrillation.

The P waves of patients with VVI pacemakers were compared with those of DDD pacemakers at implantation and then regularly for 5 years. A certain number of cardiac pathologies are known to cause P wave changes. The incidence of atrial fibrillation (AF) was much higher in VVI than in DDD patients. In the VVI group, the incidence was much greater in patients paced for sinus node disease than in patients paced for AVB. Analysis of sinus P wave characteristics in 320 patients with VVI pacemakers shows progressive abnormalities of atrial function with time. The expression of this atrial dysfunction is a statistically significant prolongation of the P wave in V1 and dII and of the terminal part of the P wave in V1. The factors responsible for this abnormality and which favours the occurrence of AF are quasi-permanent pacing, the presence of retrograde conduction and an abnormality of atrial activation at the time of implantation.

Amiodarone, an anti-ischaemic and anti-arrhythmic drug, has been the object of numerous studies and seems to be highly effective in the treatment of severe ventricular arrhythmias on dilated cardiomyopathies, as well as of hypertrophic or ischaemic heart diseases. Some studies have shown a decrease in the incidence of sudden death in patients under amiodarone, but most of these studies were conducted on limited series with an insufficiently strict methodology. Contrary to other antiarrhythmic agents, amiodarone seems to be devoid of significant proarrhythmic effect and of depressant effect on cardiac function. Its anti-ischaemic activity has been demonstrated in exercise-induced and spastic angina. The side-effects of amiodarone are mainly extracardiac, and they may be a source of concern when they produce dysthyroidism or pulmonary pathology; however, they can be detected, or even prevented, by careful monitoring. Owing to its mechanism of action and its potential effectiveness, amiodarone deserves to be studied in patients at high risk of sudden death, especially those who suffer from severe ventricular arrhythmia on ischaemic cardiopathy with or without ventricular dysfunction. Three extensive clinical trials have been devised to determine with accuracy the effect of amiodarone on the mortality of patients who have survived a myocardial infarction or present with heart failure. At the end of these trials, it will perhaps be possible to evaluate the influence of a long-term amiodarone treatment on the mortality of patients whose life expectancy is shortened. The results obtained will be weighed against the side-effects of the treatment to obtain a benefit/risk ratio which, for the time being, is imperfectly known.

This study is an investigation of the long-term effects of VVI pacing on the atrium as derived from the evolution of P wave characteristics of 285 patients. The occurrence of left and right atrial disease is demonstrated as well as the evolution of left atrial hypertrophy in some cases. A comparison is made with DDD pacing and special attention is given to the progression to atrial fibrillation.

Intravenous nicardipine, 5 mg, was administered in two comparable groups of eight patients with chronic coronary artery disease but no clinical signs of heart failure. One group had received no previous treatment and served as a control group, and the other had received long-term treatment with large oral doses of propranolol. Blood concentrations of nicardipine were higher, and the area under the plasma concentration curve was greater in the group previously treated by propranolol. The total clearance of nicardipine was decreased in patients taking propranolol, without a change in the half-life of the drug. Typical hemodynamic responses, namely, a decrease in aortic pressure and in arterial resistances, were greater and more lasting in patients previously treated orally by propranolol. Filling pressure remained stable in both groups. The nicardipine infusion did not induce signs of dromotropic or inotropic negative effects in either group. The greater and more lasting hemodynamic effects of nicardipine in the group previously treated orally by propranolol do not seem to be related to an overall hemodynamic action of propranolol, but are probably due to higher nicardipine plasma levels, and may be caused by a decrease in hepatic blood flow induced by propranolol, with a consequent decrease in nicardipine clearance and by a smaller nicardipine volume of distribution in the propranolol group.

Left ventricular filling may be studied non-invasively by Doppler echocardiographic recording of transmitral blood flow. This study reports the variations in this flow induced by changing cardiac preload by administering trinitrin or by vascular filling in 27 patients undergoing catheterisation. Left ventricular end diastolic pressure (LVEDP) was measured by the pig-tail catheter used for ventriculography. Transmitral flow was recorded by pulsed Doppler using the apical view. The parameters studied were those of the early diastolic E wave and the end diastolic A wave. The hemodynamic and echocardiographic measurements were performed under basal conditions, after trinitrin and after vascular filling. Trinitrin was given to 14 patients and led to a fall in LVEDP from 17.6 +/- 4.5 to 6.7 +/- 1.4 mmHg (p less than 0.001). The amplitude of the mitral E wave decreased and the E/A ratio fell from 0.93 +/- 0.37 to 0.71 +/- 0.32 (p less than 0.001). Thirteen patients underwent vascular filling which increased LVEDP from 10.9 +/- 5 to 27 +/- 4 mmHg (p less than 0.001). The mitral E wave increased and the E/A ratio rose from 0.96 +/- 0.32 to 1.27 +/- 0.23 (p less than 0.01). The patients received trinitrin and then underwent vascular filling. The LVEDP decreased from 16 +/- 3.9 to 8 +/- 2.9 mmHg (p less than 0.001) and then rose to 28.3 +/- 3.5 mmHg (p less than 0.001). The E/A ratio fell after trinitrin from 0.91 +/- 0.40 to 0.58 +/- 0.30 (p less than 0.01) and then rose to 1.42 +/- 0.60 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Infarct size (IS) was estimated from serial total creatine phosphokinase (CK) changes in 82 patients with acute myocardial infarction (MI). Anteroseptal and inferior MI involved a relatively small mass of myocardium (16.0 +/- 6.4 and 24.7 +/- 10.0 CK-g-eq respectively); anteroapical and inferoposterior MI had an average IS of 35.9 +/- 15.9 and 32.8 +/- 13.8 CK-g-eq respectively (NS); extensive anterior and inferoposterolateral MI had an average IS of 57.8 +/- 20.1 and 51.1 +/- 11.5 CK-g-eq respectively (NS). Left ventricular failure (LVF) correlated with estimated IS and not with location of the infarct. In patients with an IS ranging from 30 to 50 CK-g-eq, the incidence of LVF was 33%. In patients with an IS greater than 50 CK-g-eq, the incidence of LVF was 65%. Out of the 6 patients who died, 3 had an IS greater than 60 CK-g-eq. 3 groups of patients could be identified from the duration of the CK release time: in group I (mean = 20 +/l h; n = 61), infarct size was highly correlated with peak CK activity (r = 0.93); in group II (mean = 39 +/- 7 h; n = 17) the correlation between IS and peak CK activity was poor (r = 0.59) and might indicate a gradual necrosis; in group III (n = 4) patients with reinfarction showed a second peak on the descending limb of the CK activity curve. Follow-up information was available in 96% of the 76 survivors. At the end of the follow-up (18.1 +/- 10.8 mth) IS was not significantly different in patients with LVF (42.7 +/- 17.5 CK-g-eq) and in those without LVF (34.7 +/- 19.7 CK-g-eq).

In patients receiving circulatory assistance by intra-aortic counter-pulsion for myocardial infarction, angiography may be carried out by the retrograde femoral route. It should include left ventriculography makes it possible to assess the number of segments which contract and to draw a correlation between the kinetics of a segment and its vascularisation. Vascular studies should be carried out at the time of maximum effect of the pump, i.e. from the 18th hour onwards. Indications for angiography are as follows: isolated or mechanical cardiogenic shock, early recurrence of infarction, refractory left ventricular failure and persistent arrhythmias. In cardiogenic shock and refractory left ventricular failure, the coronary lesions are diffuse. All our patients died. By contrast, in the group with early recurrence of infarction or persistent arrhythmias surgical treatment is often possible.

Twenty-one patients with postinfarction angina (2 to 15 days after acute myocardial infarction) unresponsive to medical therapy were treated by intra-aortic balloon pumping (IABP). Anginal pain and electrocardiographic (ECG) ST-segment changes were prevented in all patients. Coronary angiograms were obtained during IABP without complication and confirmed severe coronary artery disease. Of the four nonoperated patients, three had reinfarction and two died of cardiogenic shock. Seventeen patients underwent aorta-coronary bypass grafting, associated with aneurysmectomy in two patients and closure of a ventricular septal defect in one. Sixteen patients survived the operation. All survivors are in clinically improved condition and 14 are pain free from 9 to 28 months postoperatively, but three have mild heart failure.

In twenty chronic hemodialyzed patients a hemodynamic study was carried out just before dialysis at bed rest and during sitting bicycle exercise. At bed rest, cardiac index (mean +/- standard deviation = 5.2 +/- 1.1/mn/m2) and pulmonary wedge pressure (17.4 +/- 6.8 mmHg) were increased. At the highest level performed (60 ou 90 W) cardiac index increased in all patients and reached on average normal values as compared to normal sedentary subjects, but heart rate less increased than in normal subjects during maximum effort. These data suggest that these patients had no patent heart failure. Pulmonary wedge pressure was more increased in hypertensive patients (20.7 +/- 6.7 mmHg) than in normotensive patients (13.3 +/- 4.4 mmHg). Since cardiac index was similarly increased in both groups of patients the higher values of pulmonary wedge pressure in hypertensive patients could be related to either an increase in total blood volume, or a reduction in left ventricular compliance or an increase in cardiopulmonary blood volume.

The first case of atrioventricular block located in His bundle observed during oral treatment with bepridil is reported; the block subsided when the drug was discontinued and reappeared when it was reintroduced. Electrophysiological studies performed with bepridil have shown that, as could be foreseen from its beneficial or undesirable effects, this calcium antagonist has some properties of Vaughan Williams' class I antiarrhythmic agents and alters subnodal conduction. Clinical studies indicate that in therapeutic doses this alteration has little or no significance, but it may reach clinical expression when latent of patient pre-existing disorders of conduction within or below His bundle are present.

Intravenous nicardipine, 5 mg, was infused over 5 minutes in 2 comparable groups of 8 patients with chronic coronary artery disease but no clinical signs of heart failure. Eight patients had received no previous treatment and served as a control group; 8 other patients had received long-term treatment with large doses of propranolol. The hemodynamic responses to nifedipine were similar in the 2 groups, but was greater in patients taking propranolol. At 10 minutes, systemic vascular resistance decreased by 47% in patients taking propranolol and by 39% in the control group; mean aortic pressures decreased by 25% and 10%; heart rate increased by 23% and 19%; and cardiac index increased by 45% in both groups. At 20 minutes, left ventricular end-systolic volume index decreased by 20% in patients taking propranolol and 15% in the control patients; angiographic stroke index increased by 19% and 8%; left ventricular ejection fraction increased by 22% and 11%; and mean circumferential fiber velocity increased by 46% and 32%. Intravenous nicardipine infusion (5 mg) did not induce negative inotropic effects in patients with chronic coronary heart disease, and no evidence of congestive heart failure was seen, even in patients receiving large doses of propranolol. Nicardipine counteracted the potential deleterious effects of propranolol; increased peripheral vascular resistance and left ventricular stroke work and decreased cardiac output.

Obstructive calcification of the thoracic aorta appears as acquired coarctation of the aorta. The case we present is of note because it presented as a dilated cardiomyopathy. The diagnosis, suspected on chest X-ray, was confirmed by catheterization, aortic angiography and thoracic computer tomography. The patient underwent aortic endarterectomy, but died in the post-operative period. Review of the literature shows that the pathogenesis of the condition remains unclear.

Coronary arteriography is the only examination by which the diagnosis of single coronary artery may be made in vivo by demonstrating the presence of an entire coronary system arising from a common trunk. The discovery may be made under two distinct sets of circumstances: 1 degree Coronary ischaemia in a young subject. Arteriography confirms the diagnosis and the customary 2 degrees Coronary ischaemia in an older individual. Arteriography shows atherosclerotic lesions in a single coronary artery. The severity of the condition is related to the proximal character of the stenoses. The most logical therapeutic approach is aorto-coronary bypass if the quality of the distal network as seen at arteriography makes it possible.

To assess the influence of postinspiratory apnea on the measurement of the left ventricular volumes, contrast ventriculography was performed on 19 patients during spontaneous breathing and then in postinspiratory apnea. Data obtained were similar for end diastolic volumes (81 +/- 29 ml/m2 vs. 83 +/- 25; NS), end systolic volumes (35 +/- 20 ml/m2 vs. 34 +/- 19; NS), systolic index (46 +/- 13 ml/m2 vs. 49 +/- 12; NS), and ejection fraction (0.57 +/- 0.11 vs. 0.59 +/- 0.12; NS). Postinspiratory apnea suppressed the overlapping of the left ventricle with abdominal viscera in 15 of 17 patients. Diaphragmatic immobility permitted the assessment of regional left ventricular function in all 19 patients. However, pressures recorded in inspiratory apnea can no longer be compared to a transmural pressure, and, to assess ventricular compliance, intrapleural pressure must be measured simultaneously. We conclude that left ventricular volume assessment by contrast ventriculography is not disturbed by inspiratory apnea. This maneuver improves the quality of the images and allows a better evaluation of left ventricular segmental function. Spontaneous breathing can be recommended to simplify left ventricular compliance study.

The effects of arteriovenous fistulae (AVF) on cardiac output (CO) and cardiac filling pressures were studied at rest and during exercise in 16 chronic hemodialysis patients. After the occlusion of the AVF, average CO fell but cardiac filling pressures remained unchanged, seven patients had a drop in CO greater than or equal to 1.0 l/min (group A) and nine patients had a drop in CO less than or equal to 0.9 l/min (group B). At rest, average CO was higher in group A than in group B, but cardiac filling pressures were the same in group A and in group B. During maximal exercise, average CO and cardiac filling pressures were the same in both groups.

Twenty-four elderly patients (79 +/- 7 years) with long-standing calcified aortic stenosis have been divided in two comparable groups of 12. The first group was treated with 19 mm balloon percutaneous transluminal valvuloplasty, where the balloon diameter was always smaller than the aortic anulus diameter. Peak-to-peak aortic valve gradient decreased from 76 +/- 32 mmHg to 30 +/- 19 (P less than .05), and the aortic valve area, calculated by Gorlin formula, increased from 0.40 +/- 0.17 cm2 to 0.57 +/- 0.17 (P less than .05). The second group was treated with a trefoil 25 mm balloon, always larger than the aortic anulus diameter. In this second group, peak-to-peak aortic valve gradient decreased from 73 +/- 34 mmHg to 23 +/- 15 (P less than .05), and aortic valve area increased from 0.47 +/- 0.14 cm2 to 0.88 +/- 0.36 (P less than .05), increasing thus more than in group I (P less than .05). Clinical tolerance to balloon inflation was not the same according to individual patients but was similar between the two groups; complications were comparable in the two groups. These results suggest that aortic valvuloplasty by trefoil balloon larger than aortic anulus can provide wider aortic valve area without increasing complication rate.

In the search for any deleterious hemodynamic effects of the acute administration of intravenous diltiazem (0.25 mg/kg), in patients on beta blockers, studies were performed in two comparable groups of eight patients with chronic coronary heart disease without clinical signs of heart failure. In the first group, with no previous treatment, the only significant variations observed were a decrease in systemic vascular resistance (p less than 0.01) and an increase in cardiac index (p less than 0.01), which were noted only at 5 minutes. In the second group, receiving long-term oral doses of 120 to 240 mg/day of propranolol, at 5 minutes, despite a slight decrease in peak positive first derivative of left ventricular pressure (p less than 0.05), cardiac index and systolic index increased (p less than 0.05 and p less than 0.01) with decreases in systemic vascular resistance (p less than 0.01) and mean blood pressure (p less than 0.05); at 15 minutes, systemic vascular resistance was still decreased (p less than 0.05) and cardiac index and systolic index were still increased (p less than 0.05). In conclusion, intravenous administration of diltiazem (0.25 mg/kg) to patients with chronic coronary heart disease and no evidence of congestive heart failure, who were receiving propranolol, was safe and prevented, in these patients, the potential deleterious effects of beta blockers, that is, increased peripheral vascular resistance and decreased cardiac output.

Twenty-eight brachial arteriovenous fistulae (AVF) flows were assessed by the Stewart and Hamilton method by bolus dye injection. These measurements were divided in two groups: a first group with dye injection into the AVF artery and a second group with dye injection into the efferent vessel of the AVF in close proximity. The increase and the decrease of dye concentration were regular and the circulation occurred very late in both groups. Reproducibility was assessed by the usual index: the mean of the differences between two successive measurements of each series related to the first of these two and expressed as a percentage, m(Qn - Qn - 1)/Qn%. In the two groups, the reproducibility index was at 10.1%, similar to the index applied to Grimby's results, measuring successive cardiac output by dye bolus injection at 9.8%. Theoretical criteria of validity of the Stewart and Hamilton method were checked for all measurements. Even when the duration of the measurement was very short, arteriovenous flow fulfilled the criteria of validity in the same way as cardiac output. Two AVF flows were measured successively at both injection sites with no difference between the obtained values. The same reproducibility of the efferent vessel injection site group suggests that an arterial puncture is not necessary for a correct assessment of AFV flow.

A patient with a large posterior ventricular septal defect complicating an acute inferior myocardial infarction is reported. Because of medically intractable biventricular failure, temporary circulatory assistance was initiated using intraaortic balloon pumping. Emergency coronary angiography, ventriculography, and subsequent operation were carried out. Operative repair involved closure of the septal defect with the use of a Dacron patch, infarctectomy, and aortocoronary bypass grafting and resulted in long-term survival of the patient.

Arabogalactane sulphate of quinidine (AGSQ) is a slow release preparation of quinidine. The aim of this study was to compare the plasma levels of quinidine obtained by different preparations of AGSQ (AGSQ I, II and III) and to determine which was best suited to therapeutics. The "in vitro" study showed different amounts of quinidine liberated in 6 hours, 34% with AGSQ I, 58% with AGSQ II and 100% with AGSQ III. The plasma quinidine levels were studied after administration of a dose corresponding to 330 mg quinidine base, morning and evening for 7 consecutive days to 27 hospitalised patients; 7 received AGSQ I, 11 received AGSQ II 5, received AGSQ III and 4 quinidine sulphate. The delay in reaching a steady state was 24 hours for the quinidine sulphate 36 hours for AGSQ I, 48 hours for AGSQ II and 60 hours for AGSQ III. The average plasma level on the 7th day (Cee) was 2.74 +/- 0.71 microgram/ml, 2.62 +/- 0.74 microgram/ml and 3.29 +/- 0.72 microgram/ml respectively. The plasma quinidine levels were maintained between toxic and therapeutic levels (3,5 and 1,7 microgram/ml) only with AGSQ II by suppressing the peak observed 1 hour administration of quinidine sulphate. An excellent correlation (r = 0,984) was observed between the plasma quinidine 6 hours after ingestion and the Cee. A blood test during the steady state, 6 hours after ingestion of the drug, is useful in adjusting the dosage. These results suggest that AGSQ II is the preparation best suited for therapeutic usage although it does not give the best relative bioavailability of the drug.

Forty patients with chronic atrial fibrillation, apparently unrelated to any overt heart disease, were randomly allocated to two groups after restoration of sinus rhythm by direct current shock. The patients in group A were given 4 daily doses of quinidine polygalacturonate, while those in group B were given 2 daily doses of a long-acting quinidine preparation, quinidine arabogalactan sulphate. The percentage of early relapses (within the first month following DC shock) was not significantly different in the two groups: 44-4% in group A and 35% in group B (P greater than 0-50). On the other hand, there were fewer late relapses with long-acting quinidine. After 18 months of treatment, 27-8% of patient in group A remained in sinus rhythm, compared with 61% in group B (P less than 0-05). The average amount of quinidine actually ingested by the patients in group A was smaller than that in group B. However, this could not entirely account for the difference observed in the incidence of relapse since with short-acting quinidine the proportion of patients remaining in sinu rhythm was similar whether the dose was decreased or not. The incidence of gastrointestinal side-effects was the same in the two groups and there were no seriou complications that could be attributed to treatment. It is concluded that long-acting quinidine preparations are more effective than conventional quinidine in preventing late relapses of atrial fibrillation.

Forty-two patients with cardiogenic shock (CS) secondary to myocardial infarction were treated with intra-aortic balloon pumping (I.A.B.P.). In 14 patients C.S. was associated with ventricular septal defect (V.S.D.) and in four with mitral regurgitation (M.R.) secondary to rupture of the posterior papillary muscle. All patients were resistant to conventional medical therapy. Shock was reversed in 20 of the 24 patients in C.S. without mechanical complications. After 24 to 48 hours of I.A.B.P., cardiax index (C.I.) increased from 1.38 to 2.00 L./min./M2, systolic arterial pressure (S.A.P.) from 83 to 96 mm. Hg, urinary output (U.O.) from 10 to 56 ml. per hour, and pulmonary wedge pressure (P.W.P.) decreased from 22 to 16 mm. Hg. Three patients treated with I.A.B.P. alone survived more than 1 year; of the 13 patients who were balloon dependent, four have undergone emergency surgical procedures and two were long-term survivors. In all patients with mechanical complications, I.A.B.P. resulted in significant clinical and hemodynamic improvement. P.W.P. decreased from 19 to 15 mm. Hg, and U.O. increased from 13 to 38 ml. per hour while S.A.P. remained unchanged. In patients with V.S.D. the pulmonary/systemic flow ratio (P/S) declined from 3.5 to 2.8; in patients with M.R., "V" wave amplitude decreased by 8 mm. Hg. Emergency surgery was performed in 10 patients with V.S.D. and in three patients with M.R. and there were eight long-term survivors (13 to 27 months). It is concluded that I.A.B.P. is an effective means of supporting the circulation in C.S. Of the 42 patients with C.S. treated by combining I.A.B.P. and emergency surgery, 13(31%) were long-term survivors (20 +/- 6 months).