Appendiceal carcinoid tumor most often presents as appendicitis. In most cases, it is found incidentally during appendectomies and its diagnosis is rarely suspected before histological examination. Appendiceal carcinoid tumor can be managed by simple appendectomy and resection of the mesoappendix, if its size is
BACKGROUND: Heart transplantation (HT) from donation after circulatory death (DCD) has yet to achieve wide clinical application despite the encouraging resultsreported recently. In this study we describe 2 cases of successful adult DCD HT performed at our institution using an original protocol. METHODS: Our local abdominal DCD protocol was updated to allow DCD heart procurement, and was accepted by the institutional ethics committee. The main features of the protocol include: pre-mortem insertion of peripheral venoarterial extracorporeal membrane oxygenation cannulas; thoracoabdominal normothermic regional perfusion (NRP) by clamping the 3 aortic arch vessels to exclude cerebral circulation; and in-situ heart resuscitation. The retrieved hearts were directly transplanted into recipients located in an adjoining operating room. RESULTS: The procurement warm ischemic time was 25 minutes for the first donor, and 26 minutes for the second donor. The cold ischemic time was 16 minutes for the first recipient and 17 minutes for the second recipient. The suture time was 30 minutes for the first recipient, and 53 minutes for the second recipient. Both recipients were easily weaned off cardiopulmonary bypass in sinus rhythm and inotropic support. Post-operative evaluation of cardiac function was excellent and the patients were subsequently discharged home. CONCLUSIONS: Transplantation of hearts from DCD donors is now a clinical reality.NRP is a useful tool for resuscitation, reperfusion, and preservation of transplanted hearts. It also offers the opportunity to assess the function and viability of organs before transplantation. However,due to ethical issues, some may object to ante-mortem intervention.
Morimont P, Lambermont B, Ghuysen A, Gerard P, Kolh P, Lancellotti P, Tchana-Sato V, Desaive T, D'Orio V. Effective arterial elastance as an index of pulmonary vascular load. Am J Physiol Heart Circ Physiol 294: H2736-H2742, 2008. First published April 18, 2008 doi:10.1152/ajpheart.00796.2007.-The aim of this study was to test whether the simple ratio of right ventricular (RV) endsystolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (E a), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism-or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) ϭ Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea ء (PV) ϭ (Pes Ϫ Pla)/SV]. Thus Ea ء (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.hemodynamics; pulmonary hypertension; right ventricle; ventriculoarterial coupling IN CURRENT CLINICAL practice, pulmonary arterial load [or right ventricular (RV) afterload] is usually expressed as the mean pulmonary vascular resistance, computed as the ratio of the pressure drop through the pulmonary circulation [difference between mean pulmonary arterial pressure (PAP mean ) and left atrial pressure (Pla)] to the mean pulmonary blood flow [cardiac output (CO)]. Such an evaluation ignores the pulsatile nature of both pressure and flow. Although oscillatory components of the pulmonary arterial load are low, and mean resistance may be a valuable index of the pulmonary vascular load, the pulsatile nature of the load may be prominent in numerous pathological situations. Wave reflections play an important role and should be taken into account in pulmonary hypertension resulting from several pathological conditions, like pulmonary embolism and septic shock (1,2,5,14). In this way, the pulmonary arterial impedance spectrum, which is defined in the frequency domain, provides a more precise and complete description of the pulmonary vascular load (12, 17). However, be...
In the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency.
In acute pulmonary embolism, right ventricular (RV) failure may result from exceeding myocardial contractile resources with respect to the state of vascular afterload. We investigated the adaptation of RV performance in a porcine model of progressive pulmonary embolism. Twelve anesthetized pigs were randomly divided into two groups: gradual pulmonary arterial pressure increases by three injections of autologous blood clot (n=6) or sham-operated controls (n=6). Right ventricular pressure-volume (PV) loops were recorded using a conductance catheter. Right ventricular contractility was estimated by the slope of the end-systolic PV relationship (Ees). After load was referred to as pulmonary arterial elastance (Ea) and assessed using a four-element Windkessel model. Right ventricular-arterial coupling (Ees/Ea) and efficiency of energy transfer (from PV area to external mechanical work [stroke work]) were assessed at baseline and every 30 min for 4 h. Ea increased progressively after embolization, from 0.26+/-0.04 to 2.2+/-0.7 mmHg mL(-1) (P<0.05). Ees increased from 1.01+/-0.07 to 2.35+/-0.27 mmHg mL(-1) (P<0.05) after the first two injections but failed to increase any further. As a result, Ees/Ea initially decreased to values associated with optimal SW, but the last injection was responsible for Ees/Ea values less than 1, decreased stroke volume, and RV dilation. Stroke work/PV area consistently decreased with each injection from 79%+/-3% to 39%+/-11% (P<0.05). In response to gradual increases in afterload, RV contractility reserve was recruited to a point of optimal coupling but submaximal efficiency. Further afterload increases led to RV-vascular uncoupling and failure.
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