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Percutaneous coronary interventions (PCI) of complex coronary lesions in patients with severely depressed left ventricular (LV) function may increasingly constitute an alternative to surgical revascularization. The availability of hemodynamic support devices offers a promising option to reduce PCI-related complications in such high-risk procedures. We report the case of a successful distal left main coronary artery T-stenting supported by the Impella Recover LP 2.5 assist device in a patient with severe LV dysfunction., (Copyright (c) 2008 Elsevier Masson SAS. All rights reserved.)

Introduction: Lutembacher syndrome refers to the rare combination of congenital atrial septal defect and acquired mitral stenosis. This condition is usually treated surgically by mitral valve operation with concomitant closure of the atrial septal defect., Materials and Methods: Between 1993 and 2003, 4 patients with congenital Lutembacher syndrome had percutaneous mitral commissurotomy without closure of the atrial septal defect at our institution. The 4 patients were very symptomatic with right-sided heart failure signs and NYHA functional class III-IV., Results: The procedure was carried out successfully for the four patients. Mitral valve area increased from 0.87 to 1.97 cm2 at mean; left atrial pressure decreased from 28.2 to 12.7 mmHg and the mean valve mitral gradient was reduced from 15.5 to 3.9 mmHg. Functional and clinical improvement was observed in all the cases. During a mean follow up of 55 +/- 29 months, our 4 patients remain pauci symptomatic under medical treatment., Conclusion: The percutaneous treatment of the Lutembacher syndrome is currently a possible alternative to the surgery among patients having an anatomy favourable to the procedure.

ECMO (extracorporeal membrane oxygenation) may be viewed as a prolonged cardiopulmonary bypass allowing for a prolonged cardio-respiratory support. Since its introduction in the 60's, its indication has expanded from acute respiratory failure to acute cardiac failure refractory to conventional treatments. The target group involves mainly those patients presenting with a cardiogenic shock following cardiac surgery or acute myocardial infarction. The advantages of this form of circulatory support, when compared with long-term ventricular assist devices, are its less invasive aspect, its ease of implantation and its reduced cost. However, its main limitation lies in its limited duration of 7 to 10 days, in particular because of hemorrhage complications. Currently, ECMO provides a temporary hemodynamical stability in order to perform an invasive cardiac treatment (coronary bypass or percutaneous dilatation), or to assess the eligibility of the patient for a long-term ventricular assist device, which will enable to wait for the availability of an allograft. The latter scenario is crucial nowadays because of the severe lack of organ donors, which is the leading cause of death among patients waiting for a heart transplant.

The atrio-bi-ventricular pacing has been used for hemodynamic improvement since 1994, and the MUSTIC trial is the first controlled study assessing this concept. It collected 67 patients with severe and stable heart failure with optimised medical therapy, with sinus rhythm and without any traditional indication for pacing. After two periods of three months with blinded randomisation and cross-over, the bi-ventricular pacing mode showed its superiority to the inactive mode concerning all study endpoints, for example with an improvement of the functional capacity of 23% assessed by the 6-minutes-walk test. Thus the MUSTIC trial opens up the way for morbidity and mortality studies.

Purpose: To show that the bispectral index (BIS) is not only a monitor of the depth of anesthesia but that acute decreases of the index may be related to severe cerebral ischemia., Clinical Features: Several clinical observations suggest that an unexplained fall of the BIS may be the result of cerebral ischemia. Somatosensory evoked potentials decreased in parallel to the decrease in BIS during carotid clamping in a 58-yr-old patient undergoing carotid endarterectomy. In a 62-yr-old patient undergoing resection of an aortic aneurysm, the BIS decreased from 40-50% to 8% as the cardiac index and central venous O(2) saturation decreased. The BIS returned to normal values when the low cardiac output was corrected pharmacologically., Conclusion: While the BIS is a well accepted monitor of the depth of anesthesia, several factors, unrelated to anesthesia, can modify the index. Thus, to adjust the level of anesthesia based solely on the BIS could be inappropriate. While the sensitivity and specificity of the BIS for this indication have not been determined, we suggest that the BIS may be useful to detect severe cerebral ischemia.

The treatment of chronic heart failure has made remarkable progress over the past ten years. Recent advances in our understanding of the pathophysiologic mechanisms involved in heart failure syndrome have led to changes in our approach to the treatment of children. The goals of the therapy have shifted from purely hemodynamic manipulation to a combination of hemodynamic and neurohumoral modulation. As for adults, three therapeutic classes have recently emerged: conversion enzyme inhibitors, spironolactone and beta-blockers. Pediatricians know that a child is not a small adult and we have to think about heart failure on the basis of etiology, the age of the patient, and circulatory physiology and maturation.

Late responsive DDD pacemakers are the most technically advanced devices presently available. These pacemakers are particularly useful in patients with chronotropic insufficiency when the sinus node is incapable of accelerating during exercise. The latest pacemakers have two sensors to reproduce optimal physiological sinus acceleration. The aim of this study was to analyse the performances of a new rate responsive pacemaker with a double activity and respiratory sensor, the interaction of which is automatically controlled by a sophisticated algorithm, in 12 patients (8 men and 4 women) with a mean age of 75 +/- 7 years. Analysis was based on the performance of the sensors used singly or in association: during three exercise stress tests with measurement of the VO2 max; during everyday activities using the data archived by the pacemaker and the answers to a simplified questionnaire on quality of life. The results showed that during exercise stress testing with measurement of VO2 max, the best performances were obtained with the double sensor or the respiratory sensor compared with the activity sensor alone, suggesting that these two sensors are more effective in intense exercise. This tendency was also observed in the analysis of the memory bank of the pacemaker which showed that the total duration of the faster heart rates was greater with the two sensors. On the other hand, the quality of life was not significantly different, whichever sensor was studied. Longer scale trials are necessary to appreciate the real value of these new double sensor pacing devices and to identify the best indications for their usage.

The authors report the first intramyocardial transplantation of autologous skeletal myoblasts in a patient with severe ischaemic cardiac failure. The encouraging result after eight months' follow-up underlines the potential of this new approach.

Cardiac failure has become a major but underestimated public health problem. The EPICAL study in France confirmed the severity of this condition. In addition to the neuro-hormones, the role played by inflammatory cytokines in the progression of the disease has been emphasized. The importance of the "genetic background" in the development and evolution of cardiac failure has been demonstrated (deletion or prospective polymorphism). From the therapeutic point of view, besides the hopes raised by multisite pacing, the betablockers and spironolactone have been shown to provide major functional improvement and prolonged survival, and they take their place with the angiotensin converting enzyme inhibitors in our pharmacological arsenal. Cellular transplantation is associated with encouraging pre-clinical results which open up a new field of interest. Finally, global management, including physical rehabilitation and patient education by plury-disciplinary teams, provides medical and economic benefits. The year 1999 has been particularly rich in the field of cardiac failure from the basis of fundamental research to the organisation of health care.

Sudden death accounts for about 35% of the mortality of cardiac failure and its incidence does not decrease with the use of angiotensin converting enzyme inhibitors. Non-sustained ventricular tachycardia on Holter monitoring, late ventricular potentials and tachycardia induced by programmed ventricular stimulation have no formal predictive value of sudden death, underlining the varied character of the mechanisms underlying sudden death during cardiac failure. Sustained ventricular tachycardia degenerating to ventricular fibrillation is only one of the rhythmic factors implicated together with inaugural ventricular fibrillation, bradyarrhythmias and electromechanical dissociation. The underlying cardiac disease plays a role in the initiation of the fatal arrhythmia. In coronary artery disease, recurrent acute ischaemia is the principal trigger factor in patients who often have triple vessel disease. This explains the fact that classic markers of arrhythmia in the post-infarction period, which are only the reflection of the arrhythmogenic substrate of ventricular tachycardia, usually due to reentry around the fibrous scar of the infarct, are not valid in patients with progressive ischaemic cardiomyopathy. The most effective antiarrhythmic treatment in this type of patient is the prevention of ischaemia, when possible. In primary dilated cardiomyopathy, the mechanism underlying sudden death could be different at each stage. In NYHA Stages I and II, ventricular tachyarrhythmias could play a major part in unexpected sudden death in patients whose stable haemodynamic status suggested a more prolonged survival. The value of an implantable defibrillator would seem to be proved in this group of patients, at least in secondary prevention. In Stages III and IV, ventricular arrhythmias only indicate the degree of ventricular dysfunction and sudden death may follow bradyarrhythmias and electromechanical dissociation due to the precarious haemodynamic status.

Many of the recommendations presented in this consensus report are summarized in Figure 2. All patients with known or suspected heart failure should undergo a detailed history and physical examination. Other causes for the symptoms and/or clinical signs indicative of heart failure should be excluded. Routine biochemical tests, as well as a standard chest x-ray and ECG, should be performed on all patients with heart failure. Precipitating or aggravating causes of heart failure should be eliminated. Patients with potentially surgically correctable lesions, such as constrictive pericarditis, valvular disease or left ventricular aneurysm, should be referred for cardiological evaluation and the appropriate surgery. Patients with ischemic induced heart failure should be assessed for possible revascularization by either angioplasty or bypass surgery. Pending clinical findings and the degree of systolic or diastolic dysfunction present, determined by noninvasive tests, the panel made recommendations concerning the choice of various therapeutic agents. These clinical guidelines have been developed for practising physicians who manage patients with heart failure. The process by which consensus recommendations were developed by the Canadian Cardiovascular Society was based on the principle that guidelines have the best chance of succeeding if they are developed by those who will be using them. Strategies that ensure physicians are aware of the current guidelines, and that their implementation leads to measurable improvement in the diagnosis and management of patients with heart failure must be developed. Consensus reports represent an ongoing process which is subject to revision when further conclusive evidence is obtained by ongoing and future clinical trials.

Pulmonary emboli can cause severe hemodynamic and respiratory disorders whose physiopathologic mechanisms need to be well understood to ensure appropriate treatment. In previously healthy subjects only massive obstructions (greater than 50%) have dangerous effects due to the very large functional reserve of the pulmonary vascular bed. The same is not always true where there are previous anomalies of pulmonary circulation. In man, vascular obstruction appears to be primarily mechanical, although the presence of emboli may also trigger the release of vasoconstrictor mediators. In the animal it is accepted that these mediators may play an important role, in particular by increasing the critical closing pressure in pulmonary microcirculation. Apart from resistance to continuous bloodflow, the vascular obstruction may accentuate a number of dynamic phenomena specifically obstructing the passage of a pulsatile flow. The aggregate obstacles to right ventricular ejection are known by the term pulmonary artery impedance. Gas exchanges can be disturbed by a wide variety of mechanisms. Arterial hypoxemia chiefly results from maldistribution of the ventilation/perfusion ratio and, in severe forms associated with a fall in cardiac output, from diminution of the partial oxygen pressure of mixed venous blood. The right auricular pressure increase may sometimes contribute to hypoxemia by causing reopening of a permeable ductus Botalli with onset of right-left shunt. This possibility should be considered if oxygen administration does not correct hypoxemia. The dead space effect is not always in relation to the size of the vascular obstruction due to hypocapnic bronchoconstriction in the hypoperfused areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac transplantation is theoretically the optimal final treatment of terminal cardiac failure but the indications, especially in the emergency situation, should be carefully considered. Sympathomimetic agents are of limited use in patients with severe cardiac failure partly because of the down regulation of the myocardial beta-receptors. The phosphodiesterase inhibitors, represented by enoximone, are valuable because of their action on the cardiac muscle (inotropic and lusitropic) and their direct systemic vasodilator effect. Enoximone can be administered by intravenous bolus resulting in a rapid onset of action (peak at 30 minutes) with a prolonged effect due to its hepatic metabolites. The authors' experience in this indication dates over 5 years and over 50 patients were included. A preliminary study in 34 patients with cardiac failure resistant to betamimetic drugs, referred to the intensive care unit for urgent cardiac transplantation, or, in the absence of a donor, circulatory assistance is reported. A Swan Ganz catheter and radial artery canula were inserted for haemodynamic monitoring and enoximone was administered in an intravenous bolus over 15 minutes every 8 hours in addition to sympathomimetic agents. A haemodynamic improvement was observed after the 30th minute in 30 patients. The cardiac index increased from 1.82 to 2.67 l/mn/m2 and the pulmonary capillary pressures decreased from 30.8 to 18.9 mmHg. Systemic arterial resistances fell from 2,170 to 1,520 dynes.s.cm-5. No haemodynamic improvement was observed in 4 patients who were treated by mechanical ventricular assistance. After investigations to detect contra-indications to cardiac transplantation, 12 of the 30 patients remained candidates for cardiac transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Early catheterisation was performed in 27 patients with an acute inferior myocardial infarction less than 3 days old complicated by signs of low output with right ventricular dysfunction. All patients had hemodynamic criteria of adiastole (PCP = 14.9 +/- 31 mmHg and LVEDP = 14.1 +/- 4.7 mmHg) with low cardiac output (CI = 1.41 +/- 0.32 l/min/m2). An atropine resistant bradycardia was characteristic (HR = 65 +/- 17.2/min) due to advanced or complete AV block (11 cases), sinoatrial block (3 cases, one with right atrial standstill) or sinus/parasinus rhythm (13 cases) inappropriate to the severity of their hemodynamic state. Although the prognosis based on the discriminating linear function FI = -0.427 + 0.00121 LVW - 0.00125 TPR was initially poor and predicted the death of 21 out of the 27 patients at one month, the outcome was usually favourable and only 8 patients died during the first month. Fifteen patients were treated by temporary endocavitary RV pacing. As the heart rate was increased from 53.8 +/- 11.2 to 92.4 +/- 4.9/min, the CI rose from 1.35 +/- 0.26 to 1.85 +/- 0.46 l/min/m2 (p less than 0.001) with a fall in SI from 26.7 +/- 8.3 to 20.1 +/- 5.6 ml/beat/m2 (p less than 0.005). The results were even further improved in 3 cases by sequential A-V pacing. The observed hemodynamic improvement continued during the period of pacing providing volumic expansion maintained LVEDP above 10 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular monitoring in pediatrics was previously limited by inappropriate material. Following M.M. Pollack's publication, bedside cardiovascular catheterization in children have been developed and used for the last 8 years. These techniques allow the survey and the treatment of latent or patent hemodynamical disturbances with objective data. We describe these invasive techniques and their indications in pediatric intensive care.

Low cardiac output after cardiopulmonary bypass is not uncommon. This per- and postoperative cardiac depression is accompanied by an impairment of renal function, which recovers with the improvement of the low cardiac output. These two correlated failures may become resistant to cardiotonic and diuretic drugs. Indeed the fluid balance is strongly disturbed, although venous pressure is only moderately increased. The only possible treatment could be water withdrawal. Nine patients are reported, all suffering from cardiac and renal failure after cardiopulmonary bypass. They were successfully treated with the method of continuous ambulatory peritoneal dialysis. This method allowed us to stop all intravenous cardiac drugs within 36 h, whilst diuresis reappeared together with a better efficacy of diuretic drugs. This beneficial haemodynamic effect of water withdrawal is discussed. This phenomenon may be related to an influence of right ventricular filling on the left ventricle. Low cardiac output may occur as a result of septal displacement, especially if there is concomitant myocardial suffering. Withdrawing a small volume of water may have modified the septal displacement, and improved cardiac output. Continuous ambulatory peritoneal dialysis was simple and well tolerated; it seemed to have contributed to the haemodynamic recovery of all the nine patients.

The extent of myocardial and coronary lesions, the failure of the mechanisms regulating coronary blood flow, and the inadequacy of adrenergic stimulation account for the difficulties in managing cardiogenic shock as a complication of acute myocardial infarction. Except in cases of hypovolemia, excessive bradycardia, the only adequate treatment is IABP. However, long-term survival is observed only in patients undergoing surgery for a mechanical complication after control of the cardiogenic shock. Finally, the causes of the post-CPB low output syndrome and the principles of their management are discussed.