Jean-Christian Farcot

Mechanism of paradoxic pulse in bronchial asthma.

To elucidate the mechanism of paradoxic pulse in severe bronchial asthma, we performed hemodynamic studies and measured esophageal pressure in nine patients who had status asthmaticus and clinical paradoxic pulse. Two-dimensional echocardiography allowed simultaneous assessment of cyclic changes in right- and left-heart size throughout the respiratory cycle. Esophageal pressure varied from a markedly negative level during inspiration (-24.4 ± 6.5 cm H20) to a positive level during expiration (7.6 ± 6.0 cm H20). Competition between right- and left-heart chambers for pericardial space during inspiration was suggested by the reduced left ventricular cross-sectional area at end-systole (- 24%, p < 0.01) and end-diastole (-32%, p < 0.01), the leftward septal shift, and the increased right ventricular internal diameter at end-systole (42%, p < 0.01) and end-diastole (40%, p < 0.001). Competition for filling, however, could not entirely account for the paradoxic pulse, for systemic and pulmonary pulse pressures were almost (within one cardiac cycle) in phase: both were minimal at inspiration and maximal at expiration. The increase in impedance to right ventricular ejection is another major factor reducing left ventricular preload at inspiration. This reduction in preload was shown to be the predominant mechanism for the decrease in left ventricular stroke output at inspiration.

Usefulness of Two-Dimensional Speckle Tracking Echocardiography for Assessment of Tako-Tsubo Cardiomyopathy

The aim of this study was to characterize left ventricular (LV) systolic function using 2-dimensional strain in Tako-Tsubo cardiomyopathy (TTC). Forty-two women were prospectively studied using 2-dimensional speckle-tracking echocardiography, divided into 3 groups: 14 patients with TTC (group 1), 14 patients with coronary artery disease (group 2), and 14 healthy patients (group 3). In patients with TTC, mean values of systolic peak velocity, strain, and strain rate were significantly lower than those in group 3 (p <0.04), but these values were similar between the basal septum and lateral wall, between the middle septum and lateral wall, and between the apical septum and lateral wall. LV ejection fractions were significantly improved during follow-up (p <0.0001). All values of velocities were significantly increased at day 7 compared with the acute phase (p < or =0.01). This improvement differed between the middle septum and lateral wall (p <0.0001), and values for the middle septum and lateral wall in patients with TTC were not significantly different from those observed in patients with coronary artery disease (p = NS). At 1-month follow-up, no significant difference was noted between patients in groups 1 and 3. In conclusion, 2-dimensional speckle-tracking echocardiography is a reliable tool for assessing circular dysfunction in patients with TTC. Once the acute phase has passed, TTC may mimic the LV systematized dysfunction observed in patients with coronary artery disease and so lead to misdiagnosis. This novel echocardiographic technique can also be used in the follow-up of LV functional recovery.

Triage Patients with Suspected Pulmonary Embolism in the Emergency Department Using a Portable Ultrasound Device

The diagnosis of pulmonary embolism (PE) is difficult, despite validated diagnostic models. We sought to determine the value of a portable ultrasound device for triage of patients with suspected PE referred to the emergency department, using simplified echo criteria. We prospectively studied 103 consecutive patients with suspected PE, referred to our emergency department. After D‐dimer screening, 76 patients were prospectively enrolled in this ultrasound study and underwent helical chest tomography, transthoracic echocardiography, and venous ultrasonography. Among patients with PE (n = 31), a right ventricular dilation was detected in 17 patients (55%), a direct visualization of clot in the lower limbs was present in 18 patients (58%), and 8 patients (26%) had both right ventricular dilation and deep venous thrombosis. The sensitivity and specificity of a combined ultrasound strategy using echocardiography and venous ultrasonography were respectively 87% (95% confidence interval 74% to 96%), and 69% (95% confidence interval 53% to 82%). The sensitivity of this combined strategy was significantly improved as compared to venous ultrasonography alone (P = 0.01) or echocardiography alone (P = 0.005). In patients with dyspnea or with high clinical probability of PE, this combined strategy was particularly relevant with high sensitivities (respectively 94% and 100%). Echocardiography combined with venous ultrasonography using a portable ultrasound device is a reliable method for screening patients with suspected PE referred to an emergency department, especially in patients with dyspnea or with high clinical probability.

Significance of S-T segment elevations in acute myocardial ischemia: Evaluation with intracoronary electrode technique

A method is described for measuring intracoronary S-T segment elevations in the closed chest, a technique that appears to provide more reliable measurements of myocardial ischemia. Electrodes were inserted through intracoronary balloon catheters that were placed within a coronary artery and its adjoining vein both proximal and at several points distal to a coronary occlusion. Intracoronary arterial and adjacent venous electrocardiograms produced equivalent tracings. The intracoronary S-T segment elevations after coronary occlusion resembled those recorded from the epicardial surface but were free of artifacts noted in open chest studies. Study of progressive alterations of the intracoronary S-T segment after proximal occlusion of the left anterior descending coronary artery in 18 closed chest dogs revealed a peak segment elevation of 3.2 +/- 0.6 mv within 5 minutes, followed within 2 to 3 hours by spontaneous reduction by more than 40% of the S-T elevation over the occluded zone. In 44% of these animals, the S-T elevation decreased spontaneously to less than 1 mv, and in 22% it decreased to the preocclusion control level within 2 hours of occlusion. This spontaneous decrease in S-T elevation was frequently followed by a secondary increase and then S-T segment fluctuations. Reperfusion of the left anterior descending coronary artery after 30 to 60 minutes of occlusion generally led to a prompt reduction in S-T elevation. In some cases S-T elevations persisted up to 14 hours of occlusion, were reduced after reperfusion and exhibited a renewed pronounced increase after subsequent reocclusion of the left anterior descending coronary artery. During the 1st hour after occlusion, the early S-T segment elevation followed by spontaneous reduction reduction generally corresponded temporally with the derangements in myocardial lactate extraction and potassium loss. However, after 1 hour of occlusion no clear-cut correlation could be established between S-T fluctuations and changes in hemodynamic or myocardial metabolic measurements. We conclude that the new closed chest intracoronary electrocardiographic S-T technique might be of use for monitoring the early ischemic myocardial derangements and to assess benefits or drawbacks of treatment in both the experimental animal and man. Correspondence of S-T segment elevation with lactate and potassium alterations in the coronary-occluded region in the 1st hour after occlusion indicates that S-T segment elevation might represent an index of early myocardial ischemia. The spontaneous S-T changes that follow coronary occlusion must be taken into consideration when investigators utilize S-T segment modification as a sign of effectiveness of treatment.

Methylprednisolone treatment in acute myocardial infarction: Effect on regional and global myocardial function

The effects of methylprednisolong treatment on acute myocardial ischemia were studied in nine closed chest dogs. After 1 hour of proximal occlusion of the left anterior descending coronary artery, an intravenous bolus injection (50 mg/kg body weight) of methylprednisolone was administered and its effects studied during an additional 2 hours of occlusion. After 2 hours of treatment the following significant mean alterations from levels after 1 hour of occlusion were noted: an increase of 16.7% in heart rate and decreases of 23% in left ventricular end-diastolic pressure, 32% in stroke volume, 14% in cardiac output and 37% in stroke work. Peak systolic pressure, maximal rate of rise of left ventricular pressure (dP/dt), left ventricular end-diastolic volume, systemic vascular resistance and coronary sinus blood flow changed less than 10%. Ejection fraction and regional cardiac wall motion were not improved. Metabolic dysfunction of the coronary-occluded myocardium, revealed by regional lactate as well as potassium derangements, persisted throughout the 2 hour treatment period. Comparison of these results with equivalent data from an untreated series of nine dogs with 3 hours of occlusion demonstrated no improvement in the treated series. Methylprednistone failed to restore regional cardiac metabolic and mechanical function, and treatment was associated with a further rise in S-T segment elevations. Administration of methylprednisolone after 1 hour of proximal left anterior descending coronary occlusion apparently does not reverse cardiac dysfunction in the first 2 hours of treatment.

Regional and global myocardial effects of intravenous and sublingual nitroglycerin treatment after experimental acute coronary occlusion

The consequences of sublingual and intravenous nitroglycerin treatment after acute coronary occlusion were studied in 18 closed chest dogs. Intravenous (0.1 mg/min) or sublingual (0.4 mg/15 min) nitroglycerin therapy was instituted 1 hour after occlusion and the effects were observed over a period of 2 hours. Hemodynamics and global and regional cardiac function were measured in both the coronary occluded and nonoccluded segments of the left ventricle before and during coronary occlusion, and after administration of nitroglycerin. A similar nine dog control series was used to establish the significance of the measured effects of nitroglycerin. Intravenous nitroglycerin therapy after 1 hour of occlusion resulted in a marked increase in heart rate (37 +/- 12 [mean +/- standard error of the mean] percent), reduction of systolic blood pressure (9 +/- 3%), decrease in left ventricular end-diastolic and end-systolic volumes (32 +/- 5% and 34 +/- 5%), increase in coronary sinus flow (64 +/- 24%) and decrease in left ventricular stroke work (29 +/- 8%). Sublingually administered nitroglycerin produced similar trends but much less pronounced effects. However, intravenous or sublingual administration of nitroglycerin provided no improvement or caused further deterioration in ischemic region lactate extraction and potassium loss. The left ventricular ejection fraction, which was severly depressed after 1 hour of occlusion, changed minimally after administration of nitroglycerin, and there was no evidence of any correction of regional left ventricular akinesia or dyskinesia. Whereas mean systemic vascular resistance changed minimally as a result of nitroglycerin therapy, it increased 19 +/- 8% during a corresponding period of an untreated coronary occlusion series suggesting that nitroglycerin prevented an anticipated increase. Postocclusion S-T segment elevation in the electrocardiogram persisted after treatment. Our data corroborated that nitroglycerin reduced left ventricular volumes and increased coronary sinus flow; however, these improvements were accompanied by persisting metabolic and mechanical derangements in the ischemic region.

Derangements of myocardial metabolism preceding onset of ventricular fibrillation after coronary occlusion

To determine alterations in myocardial metabolism and and hemodynamics that occur within the first 30 minutes after coronary arterial occlusion, before the onset of ventricular fibrillation, measurements were compared in two series of dogs. Series A, 90 dogs that did not manifest ventricular fibrillation after coronary occlusion, were considered a control group. Series B consisted of 28 dogs that had ventricular fibrillation within 30 minutes after occlusion. All had similar comprehensive measurements completed preceding the onset of ventricular fibrillation. The animals in series B (subseuqnt fibrillation) had significantly higher heart rates before and after coronary occlusion. In this series cardiac metabolism of the occluded segment judged by transmyocardial lactate extraction, potassium balance, sodium/potassium ratio and blood pH because grossly more abnormal after coronary occlusion than in series A. In 5 animals whose measurements were obtained within 5 minutes of the onset of ventricular fibrillation, a sudden massive lactate production, potassium loss and increased acidosis of the occluded portion supervened minutes before the onset of the fatal arrhythmia. Animals with ventricular fibrillation had higher intracoronary S-T segment elevation that persisted until the onset of ventricular fibrillation. Measurements of abnormal hemodynamic function (left ventricular end-diastolic pressure, peak systolic pressure and first derivative of left ventricular pressure [DP/dt]) were not associated with an increased incidence of ventricular fibrillation. The study indicates that animals that manifest ventricular fibrillation within 30 minutes after coronary occlusion have higher preocclusion heart rates, a more severe metabolic disorder of the coronary occluded segment and more persistent intracoronary S-T segment elevation compared with animals that do not manifest ventricular fibrillation.