Postoperative non-invasive assessment of pulmonary vascular resistance using Doppler echocardiography.

Non-invasive monitoring of pulmonary vascular resistance (PVR) in postoperative cardiac surgery patients might be useful, particularly for management of pulmonary hypertension. For this purpose, we sought to assess Doppler echocardiography in the intensive care setting. In 73 patients, hemodynamics was measured using both, invasive gold standard (pulmonary artery catheter), and non-invasively by Doppler echocardiography. Four Doppler parameters: (1) tricuspid regurgitant velocity/time-velocity-integral of right ventricular outflow tract (TRV/VTI(RVOT)), (2) tricuspid annular systolic velocity (S'), (3) tricuspid annular strain, and (4) tricuspid annular strain rate, were compared with invasive PVR, using linear regression analysis and receiver-operating-characteristics. Patients without (n = 25, group 1) and patients with elevated left ventricular filling pressure (wedge pressure ≥ 15 mmHg, group 2, n = 48) were compared. Correlations were (1) R = 0.874, P < 0.0001, (2) R = -0.765, P < 0.0001, (3) R = 0.279, P = 0.009, (4) R = 0.378, P = 0.001. TRV/VTI(RVOT) showed prediction of PVR >300 dyn*s*/cm(5) (area-under-curve 0.975, cut-off 0.245, sensitivity 100%, specificity 91%). Strain correlated with PVR in group 2 patients only. TRV/VTI(RVOT) and tricuspid annular systolic velocity (S'), are useful for non-invasive monitoring of PVR in postoperative cardiac surgery patients with or without elevated left ventricular filling pressure. Strain may be used in patients with elevated filling pressure.

Successful management of fulminant pulmonary embolism using a novel portable extracorporeal life support system.

A 46-year-old man presented to the emergency room with pain in his left leg, dyspnea, and general cyanosis. During examination he collapsed and required resuscitation. Under suspicion of pulmonary embolism, a new portable "click 'n run" extracorporeal life support system (LIFEBRIDGE-B(2)T [Medizintechnik AG, Ampfing, Germany]) was implanted by the femoral vessels under resuscitation within 15 minutes of presentation. The patient was stabilized, despite severe decompensation (pH, 6.8), and could be transferred for a computed tomographic scan, which confirmed massive pulmonary embolism. Still connected to the life support system, the patient was transferred to the operating room. After a pulmonary thrombectomy was performed, the patient recovered without any organ dysfunction. A portable emergency extracorporeal life support may change clinical practice in the treatment of patients with severe hemodynamic deterioration at emergency care hospitals.

Evidence for a negative inotropic effect of obesity in human myocardium?

OBJECTIVE: The present study was performed as an attempt to analyze the relationship between body weight and human myocardial performance. As overweight is frequently associated with hypertension, stenosis of epimyocardial coronary arteries and other factors that influence myocardial performance, the experimental model of isolated human atrial myocardium was selected. Atrial contractile performance does neither depend on the extent of stenosis of epicardial coronary arteries nor on the degree of hypertension and its secondary pathology. METHODS: Right atrial muscle preparations (0.5 x 6 mm) of 183 patients undergoing coronary artery bypass surgery were electrically stimulated at optimal length. Active tension (stimulation) and passive resting tension (relaxation) were measured (measurement conditions: 37 degrees C, Krebs-Henseleit solution, optimal length and supramaximal electrical stimulation). The relationship of body weight with the measured parameters was analyzed statistically by using linear regression model and Student's t-test. RESULTS: Active tension (mN/mm2) and passive resting tension (mN/mm(2)) declined significantly with increasing body weight (p < 0.0001). The ratio passive resting tension/active tension correlated significantly with body weight (p < 0.0001). The negative association between body weight and active tension amplitude was more pronounced in women (p < 0.05). The following linear regression was calculated: for men: force = -0.04 x body weight + 8.74 (R = 0.505, p < 0.0001, n = 106); for women: force = -0.08 x body weight + 12.03 (R = 0.717, p < 0.0001, n = 77). CONCLUSION: The experimental data are in accordance with the hypothesis, that obese tissue may exert a direct cardio-depressant effect on electromechanical coupling.

Reevaluation of direct true lumen cannulation in surgery for acute type A aortic dissection.

BACKGROUND: The optimal mode of arterial cannulation in acute type A aortic dissection is controversial. We retrospectively investigated our experience with direct true lumen cannulation as an alternative to standard cannulation procedures. METHODS: From April 2004 to August 2007, 29 patients (20 men, 9 women; mean age of 63.2 +/- 12.6 years) underwent emergency operation for acute type A aortic dissection with direct true lumen cannulation. After venous drainage into the venous reservoir, the ascending aorta was completely transected in the region between the sinotubular junction and innominate artery. After visual and digital identification of the true lumen, the arterial cannula was directly inserted into the true lumen and secured with a ligature. RESULTS: Mean aortic cross-clamp time was 77.4 +/- 28.3 minutes, and hypothermic circulatory arrest for the distal anastomosis was 10.4 +/- 11.0 minutes. All patients survived the surgical procedure. No surgical problems were observed by applying this strategy. Mean intensive care unit stay was 4.0 +/- 3.5 days. Postoperative mean ventilation time was 43.3 +/- 41.3 hours. One patient had a prolonged postoperative course and required permanent ventilation. Two patients required temporary hemofiltration. Neurologic disorders occurred in 6 patients: 2 had severe cerebral hypoxia, and 4 had temporary hemiplegia under good regression. All patients were alive at discharge. CONCLUSIONS: Direct true lumen cannulation is a promising surgical strategy for emergency operations in type A aortic dissection. It is a simple, quick, and safe method to provide antegrade flow through the true aortic lumen.

The adenosine deaminase inhibitor erythro-9-[2-hydroxyl-3-nonyl]-adenine decreases intestinal permeability and protects against experimental sepsis: a prospective, randomised laboratory investigation.

INTRODUCTION: The treatment of septic conditions in critically ill patients is still one of medicine's major challenges. Cyclic nucleotides, adenosine and its receptors play a pivotal role in the regulation of inflammatory responses and in limiting inflammatory tissue destruction. The aim of this study was to verify the hypothesis that adenosine deaminase-1 and cyclic guanosine monophosphate-stimulated phosphodiesterase inhibition by erythro-9-[2-hydroxyl-3-nonyl]-adenine could be beneficial in experimental endotoxicosis/sepsis. METHOD: We used two established animal models for endotoxicosis and sepsis. Twenty-four male Wistar rats that had been given intravenous endotoxin (Escherichia coli lipopolysaccharide) were treated with either erythro-9-[2-hydroxyl-3-nonyl]-adenine infusion or 0.9% saline during a study length of 120 minutes. Sepsis in 84 female C57BL/6 mice was induced by caecal ligation and puncture. Animals were treated with repeated erythro-9-[2-hydroxyl-3-nonyl]-adenine injections after 0, 12 and 24 hours or 4, 12 and 24 hours for delayed treatment. RESULTS: In endotoxaemic rats, intestinal production of hypoxanthine increased from 9.8 +/- 90.2 micromol/l at baseline to 411.4 +/- 124.6 micromol/l and uric acid formation increased from 1.5 +/- 2.3 mmol/l to 13.1 +/- 2.7 mmol/l after 120 minutes. In endotoxaemic animals treated with erythro-9-[2-hydroxyl-3-nonyl]-adenine, we found no elevation of adenosine metabolites. The lactulose/L-rhamnose ratio (14.3 versus 4.2 in control animals; p = 2.5 x 10(-7)) reflects a highly permeable small intestine and through the application of erythro-9-[2-hydroxyl-3-nonyl]-adenine, intestinal permeability could be re-established. The lipopolysaccharide animals had decreased L-rhamnose/3-O-methyl-D-glucose urine excretion ratios. Erythro-9-[2-hydroxyl-3-nonyl]-adenine reduced this effect. The mucosa damage score of the septic animals was higher compared with control and therapy animals (p < 0.05). Septic shock induction by caecal ligation and puncture resulted in a 160-hour survival rate of about 25%. In contrast, direct adenosine deaminase-1 inhibition resulted in a survival rate of about 75% (p = 0.0018). A protective effect was still present when erythro-9-[2-hydroxyl-3-nonyl]-adenine treatment was delayed for four hours (55%, p = 0.029). CONCLUSIONS: We present further evidence of the beneficial effects achieved by administering erythro-9-[2-hydroxyl-3-nonyl]-adenine, an adenosine deaminase-1 and cyclic guanosine monophosphate-stimulated phosphodiesterase inhibitor, in an endotoxicosis and sepsis animal model. This suggests a potential therapeutic option in the treatment of septic conditions.

Anomalous origin of the left coronary artery from the pulmonary artery: mid-term results after surgical correction.

OBJECTIVES: Children with anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) are at risk for myocardial infarction and death. This retrospective study shows the mid-term follow-up after the use of aortic implantation and alternative methods to achieve coronary transfer. METHODS: Since 1990 seven consecutive children underwent primary repair of ALCAPA. Age at operation ranged from 2 to 71 months (median 11 months). Operative techniques included ligation (n = 1), intrapulmonary tunnel (n = 1), and aortic implantation (n = 5). One patient with severe mitral valve incompetence underwent additional mitral valve replacement. A 4-month-old patient was successfully treated after the operation with a left heart assist device. RESULTS: One death in the series occurred at 2 weeks after intrapulmonary tunneling. The mid-term results were evaluated in the six survivors with a follow-up mean of 98 months (ranged 58-168). In all surviving patients with two-vessel coronary blood supply, left ventricular end-diastolic volume and left ventricular ejection fraction returned to near normal values 2-12 months postoperatively. The mitral valve incompetence decreased in all patients with a native mitral valve. One patient with coronary ligation showed severe mitral valve regurgitation and received additional mitral valve replacement concomitantly. Six years after primary valve replacement of a 21 mm SJM (Saint Jude Medical) a change of the mechanical valve to a 27 mm valve was necessary because of development of severe stenosis due to growth. CONCLUSIONS: It is always preferable to establish an antegrade flow of oxygenated blood through the coronary arteries and to create a two-coronary artery system. Mitral valve annuloplasty or replacement may be necessary for patients with severe mitral valve incompetence.

Oxidative inhibition of the mitochondrial aldehyde dehydrogenase promotes nitroglycerin tolerance in human blood vessels.

OBJECTIVES: We tested the hypothesis of whether an inhibition of the nitroglycerin (GTN) bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to GTN tolerance in human blood vessels. BACKGROUND: The hemodynamic effects of GTN are rapidly blunted by the development of tolerance, a phenomenon associated with increased formation of reactive oxygen species (ROS). Recent studies suggest that ROS-induced inhibition of ALDH-2 accounts for tolerance in animal models. METHODS: Segments of surgically removed arteria mammaria and vena saphena from patients undergoing coronary bypass surgery were used to examine the vascular responsiveness to GTN and the endothelium-dependent vasodilator acetylcholine. The ALDH-2 activity and expression in these segments were assessed by the conversion of a benzaldehyde or its derivative to the benzoic acid metabolite and by Western blotting technique. RESULTS: In contrast to patients not treated with nitrates (n = 36), patients treated with GTN for 48 h (n = 14) before surgery showed tolerance to GTN and endothelial dysfunction in arterial and venous vessels. In vivo GTN tolerance was mimicked in vitro by incubation of nontolerant vessels with the ALDH-2 inhibitor benomyl. In vivo GTN treatment decreased vascular aldehyde dehydrogenase activity compared with nontolerant vessels and decreased the expression of ALDH-2 in arterial tissue. Incubation of control venous vessels with GTN caused a significant attenuation of aldehyde dehydrogenase activity that was reversed by presence of the sulfhydryl group donor dithiothreitol. CONCLUSIONS: Long-term GTN treatment induces tolerance and endothelial dysfunction in human vessels, associated with an inhibition and down-regulation of vascular ALDH-2. Thus, these findings extend results of previous animal studies to humans.