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Paul Herijgers

Publications and source records attributed to Paul Herijgers.

At least 19 recordsLinked to original sources

Infective endocarditis: changing epidemiology and predictors of 6-month mortality: a prospective cohort study.

AIMS: The aim here is to analyse epidemiology, optimal treatment, and predictors of 6-month mortality in infective endocarditis (IE). METHODS AND RESULTS: A prospective observational cohort study included 193 patients with 203 episodes of definite IE by the modified Duke criteria. Thirty-four percent of episodes involved prosthetic valves. Thirty-three percent of episodes were nosocomial. Forty-three percent included staphylococci, 26% streptococci, and 17% enterococci. At least one complication occurred in 79% of the episodes and 63% had surgical intervention. Six-month mortality was 22%: 33% for staphylococci, 24% for enterococci, and 8% for streptococci. Seventy-four percent of patients with a contraindication to surgery died when compared with 7% with medical treatment without a contraindication and 16% with surgical treatment. In multivariable logistic regression, predictors of 6-month mortality were age (P=0.03), the causative microorganism (P=0.04), and treatment group (P<0.001). CONCLUSION: Compared with older series, we observed more prosthetic valve IE, nosocomial IE, and surgery. Staphylococcus aureus and Enterococcus faecalis were predominant microorganisms. Age, staphylococci, and a contraindication to surgery predicted 6-month mortality. Nearly half of deaths had a contraindication to surgery. Six-month mortality did not differ significantly between patients who received surgical treatment as against those who received medical treatment without a contraindication to surgery.

Adolescent↗

A SERCA2 pump with an increased Ca2+ affinity can lead to severe cardiac hypertrophy, stress intolerance and reduced life span.

Abnormal Ca(2+) cycling in the failing heart might be corrected by enhancing the activity of the cardiac Ca(2+) pump, the sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a (SERCA2a) isoform. This can be obtained by increasing the pump's affinity for Ca(2+) by suppressing phospholamban (PLB) activity, the in vivo inhibitor of SERCA2a. In SKO mice, gene-targeted replacement of SERCA2a by SERCA2b, a pump with a higher Ca(2+) affinity, results in cardiac hypertrophy and dysfunction. The stronger PLB inhibition on cardiac morphology and performance observed in SKO was investigated here in DKO mice, which were obtained by crossing SKO with PLB(-/-) mice. The affinity for Ca(2+) of SERCA2 was found to be further increased in these DKO mice. Relative to wild-type and SKO mice, DKO mice were much less spontaneously active and showed a reduced life span. The DKO mice also displayed a severe cardiac phenotype characterized by a more pronounced concentric hypertrophy, diastolic dysfunction and increased ventricular stiffness. Strikingly, beta-adrenergic or forced exercise stress induced acute heart failure and death in DKO mice. Therefore, the increased PLB inhibition represents a compensation for the imposed high Ca(2+)-affinity of SERCA2b in the SKO heart. Limiting SERCA2's affinity for Ca(2+) is physiologically important for normal cardiac function. An improved Ca(2+) transport in the sarcoplasmic reticulum may correct Ca(2+) mishandling in heart failure, but a SERCA pump with a much higher Ca(2+) affinity may be detrimental.

Animals↗

Type II diabetic mice exhibit contractile dysfunction but maintain cardiac output by favourable loading conditions.

BACKGROUND: Cardiomyopathy in type II diabetes is incompletely understood. The leptin receptor-deficient (db/db) mouse is a well-accepted model of type II diabetes. To date, left ventricular contractility has not been studied in animal models of type II diabetes with in vivo load-independent parameters. AIM: To determine cardiac function in db/db mice in vivo. METHODS: Cardiac function in 12- and 24-week-old db/db and wild-type mice was assessed using a microtip-pressure-conductance catheter. RESULTS: Left ventricular contractile dysfunction, measured by load-independent parameters (preload recruitable stroke work, end-systolic elastance, dP/dt-V(ed)), is present in diabetic mice from age 24 weeks onwards. Despite this contractile dysfunction, the conventional parameters cardiac output, ejection fraction and dP/dt(max) were maintained, which was due to an increased preload and decreased afterload. Ventriculo-arterial coupling was increased and mechanical efficiency significantly reduced in db/db mice. CONCLUSION: Our results demonstrate that, despite impaired cardiac contractility and mechanical efficiency, cardiac output is maintained in db/db mice by favourable loading conditions and that in vivo load-independent measurements are necessary to fully characterize cardiac performance in animal models of pathophysiological states.

Animals↗

Prosthesis-patient mismatch is not clinically relevant in aortic valve replacement using the Carpentier-Edwards Perimount valve.

BACKGROUND: Previous studies have shown that prosthesis-patient mismatch (PPM) results in higher early and late mortality after bioprosthetic aortic valve replacement. Careful selection of stented bioprostheses was recommended to avoid inadequate effective orifice area. We studied the incidence of PPM and its potential effects on clinical outcome in patients undergoing aortic valve replacement using the Carpentier-Edwards Perimount bioprosthesis. METHODS: Independent predictors of early and late mortality and hospital readmission for cardiac reasons were defined in 506 patients (mean age, 73 years; range, 57 to 87 years) by multivariate analysis. Mean follow-up was 6.1 +/- 4.8 years; maximum follow-up was 18.6 years. RESULTS: The incidence of severe PPM (effective orifice area index < 0.65 cm2/m2) was 0.2% and of moderate PPM (effective orifice area index > 0.65 and < 0.85) was 20%. Multivariate analysis revealed that moderate PPM was not an independent predictor of early mortality, late mortality, or hospital readmission for cardiac reasons. Reduction of septal hypertrophy was similar in patients with and without moderate PPM. CONCLUSIONS: The incidence of severe PPM is virtually nonexistent after aortic valve replacement using the Carpentier-Edwards Perimount valve. Moderate PPM is found in 20% of cases and is clinically irrelevant in this population.

Aged↗

Factors influencing calcification of cardiac bioprostheses in adolescent sheep.

OBJECTIVE: We determined the possible effects of age, antimineralization treatments, circulatory implant conditions, prosthesis design, and valve-related structural aspects on valve calcification in adolescent sheep. METHODS: Calcium content was measured by means of atomic absorption spectrometry in bioprostheses implanted in 120 sheep (age <1 year) for a period of 3 or 6 months. RESULTS: Bioprostheses calcified significantly in adolescent sheep, but the extent of calcification was multifactorial. Multivariate analysis of the calcium content reveals that age, mitral or pulmonary implant position, prosthesis design (stented or stentless), structure (porcine or pericardial, wall portion or cusp), and antimineralization treatment are independent factors influencing calcification; implant duration beyond 3 months was not. In juvenile sheep (age 5 months) the wall portion, as well as the cusps of the prosthesis, calcified significantly more than in adolescent sheep (age 11 months). Irrespective of age, the cusps of valves implanted in the mitral position calcified more than those in the pulmonary position. The wall portion of stentless valves calcified more than that of stented valves, and pericardial valves calcified less than porcine valves. The surfactant (Tween 80, No-React, and alpha-amino-oleic acid) and alcohol (ethanol and octanediol) treatment significantly reduced cusp calcification; sodium dodecylsulfate did not. None of the anticalcification treatments was able to prevent wall calcification in stentless porcine valves. CONCLUSION: These findings suggest that tissue valve calcification is determined by many independent factors, which can be identified by using adolescent sheep as a preclinical in vivo model.

Age Factors↗

Simultaneous valve replacement and venous patch repair of superior mesenteric artery aneurysm due to infective endocarditis: a case report.

BACKGROUND: Peripheral mycotic aneurysm development is a rare systemic complication of infective endocarditis. CASE REPORT: We report on a case of a mycotic aneurysm of the superior mesenteric artery in a 66-year-old man with infective endocarditis of the mitral valve. After the mitral valve was replaced by a mechanical valve, a laparotomy was performed. The mycotic aneurysm was excised and the vessel was repaired by sewing an autologous venous patch at the neck of the aneurysm. Five years after the operation, the patient is doing fine, with a normal morphology and patency of the superior mesenteric artery. CONCLUSION: Our case demonstrates that simultaneous valve surgery and repair of a superior mesenteric artery mycotic aneurysm by sewing a vein patch in the neck of the artery is a viable treatment option.

Aged↗

Survival benefits of intensive insulin therapy in critical illness: impact of maintaining normoglycemia versus glycemia-independent actions of insulin.

Tight blood glucose control with insulin reduces morbidity and mortality of critically ill patients. However, the relative impact of maintaining normoglycemia and of glycemia-independent actions of insulin remains unknown. We therefore independently manipulated blood glucose and plasma insulin levels in burn-injured, parentally fed rabbits over 7 days to obtain four study groups: two normoglycemic groups with either normal or elevated insulin levels and two hyperglycemic groups with either normal or elevated insulin levels. We studied the relative impact of glycemia and glycemia-independent effects of insulin on survival; myocardial contractility in an open chest preparation; endothelial function in isolated aortic rings; and liver, kidney, and leukocyte function in a rabbit model of critical illness. Mortality was significantly lower in the two normoglycemic groups independent of insulin levels. Maintaining normoglycemia, independent of insulin levels, prevented endothelial dysfunction as well as liver and kidney injury. To increase myocardial systolic function, elevated insulin levels and prevention of hyperglycemia were required concomitantly. Leukocyte dysfunction was present in the two hyperglycemic groups, which could in part be rescued by insulin. The results suggest that the observed benefits of intensive insulin therapy required mainly maintenance of normoglycemia; whereas glycemia-independent actions of insulin exerted only minor, organ-specific impact.

Acetylcholine↗

Matrix metalloproteinases and atrial remodeling in patients with mitral valve disease and atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is associated with extracellular matrix remodeling involving atrial fibrosis and atrial dilatation. Angiotensin II mediated pathways and matrix metalloproteinases (MMPs) have been implicated in these processes. Our aim was to study atrial structural remodeling and the expression of the angiotensin receptor subtypes and MMPs and their inhibitors (TIMPs) in patients with mitral valve disease with and without AF. METHODS AND RESULTS: Biopsies from right and left atrial appendages (RA and LA) were taken from patients undergoing CABG (n=9, all in sinus rhythm (SR)) or mitral valve surgery (MVS; n=19; 9 with permanent AF and 10 in SR). Patients with MVS and AF had significantly larger atria (versus MVS and SR: p=0.02; versus CABG: p<0.01). The MVS patients had significantly more fibrosis than the control CABG group. Fibrosis was increased in both the AF and SR MVS groups in the LA, but only in the MVS-AF group in the RA. These AF patients had significantly more tricuspid regurgitation than SR patients. MMP-1 was down-regulated in LA of MVS patients (p=0.02) independent of the underlying rhythm (SR or AF; p=0.95). In RA biopsies, MMP-1 was down-regulated only in the MVS and AF group. MMP-9 was down-regulated in the MVS patients compared to CABG both in the RA and LA, and without a difference between the SR and AF groups. Protein expression of AT-1, AT-2, MMP-2, TIMP-1, -2 and -4, TNF-alpha, and TNF-alpha-converting enzyme did not differ significantly between the 3 groups. CONCLUSIONS: Concordant changes between MMP-expression and fibrosis during mitral valve disease, both in LA and RA, suggest involvement of MMPs in structural atrial remodeling. AF itself did not contribute to altered fibrosis or MMP-expression in the LA. The association between AF and RA changes may be precipitated by greater hemodynamic load due to tricuspid regurgitation in these patients.

Aged↗

Increased cardiac expression of tissue inhibitor of metalloproteinase-1 and tissue inhibitor of metalloproteinase-2 is related to cardiac fibrosis and dysfunction in the chronic pressure-overloaded human heart.

BACKGROUND: Alterations in the balance of matrix metalloproteinases (MMPs) and their specific tissue inhibitors (TIMPs) are involved in left ventricular (LV) remodeling. Whether their expression is related to interstitial fibrosis or LV dysfunction in patients with chronic pressure overload-induced LV hypertrophy, however, is unknown. METHODS AND RESULTS: Therefore, cardiac biopsies were taken in 36 patients with isolated aortic stenosis (AS) and in 29 control patients without LV hypertrophy. Microarray analysis revealed significantly increased mRNA expression of collagen types I, III, and IV and transcripts involved in collagen synthesis, including procollagen endopeptidase and lysine and proline hydroxylases, in AS compared with control patients. Collagen deposition was greater in AS than in control patients and was most pronounced in AS patients with severe diastolic dysfunction. Cardiac mRNA expression of TIMP-1 and TIMP-2 was significantly increased in AS compared with control patients (mRNA transcript levels normalized to GAPDH: TIMP-1, 0.67+/-0.1 in AS versus 0.37+/-0.08 in control patients; TIMP-2, 9.5+/-2.6 in AS versus 1.6+/-0.4 in control patients; P<0.05 for both) but did not differ significantly for MMP-1, -2, or -9. Cardiac TIMP-1 and -2 transcripts were significantly related to the degree of interstitial fibrosis and proportional to diastolic dysfunction in AS patients. CONCLUSIONS: Cardiac expression of TIMP-1 and TIMP-2 is significantly increased in chronic pressure-overloaded human hearts compared with controls and is related to the degree of interstitial fibrosis.

Aortic Valve Stenosis↗

Interleukin-6 causes myocardial failure and skeletal muscle atrophy in rats.

BACKGROUND: The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. METHODS AND RESULTS: The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 microg x kg(-1) x d(-1), in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, -10%, P=NS; -15%, P=0.0561; and -15% P<0.05; and in the gastrocnemius, -9%, P=NS; -9%, P=NS; and -18%, P<0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 microL; moderate dose, 123 microL; and high dose, 137 microL, P<0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; P=0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; P<0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; P<0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL x min(-1) x g(-1); moderate dose, 0.21 mL x min(-1) x g(-1); and high dose, 0.23 mL x min(-1) x g(-1); P=0.037). In vitro recombinant human IL-6 administration did not cause any alterations in diaphragm force or endurance capacity. CONCLUSIONS: IL-6 clearly caused ventilatory and peripheral skeletal muscle atrophy, even after short-term administration. Blood flow redistribution, resulting from the myocardial failure induced by IL-6, was likely responsible for this muscle atrophy, because IL-6 did not exert any direct effect on the diaphragm.

Animals↗

Effect of free radical scavengers on myocardial function and Na+, K+-ATPase activity in stunned rabbit myocardium.

OBJECTIVES: The role of reactive oxygen species (ROS) in the mechanism of myocardial stunning was investigated. MATERIAL AND METHODS: Isolated Langendorff-perfused rabbit hearts were subjected to 15 min normothermic ischemia followed by 10 min reperfusion with Krebs-Henseleit solution+/-mannitol or histidine. RESULTS: In hearts reperfused without free radical scavenger the left ventricular developed pressure as well as its maximal positive and negative first derivatives (+dP/dt, -dP/dt) was significantly depressed, whereas end diastolic pressure (LVEDP) increased when compared to preischemic values. Treatment with mannitol had little protective effects, whereas singlet oxygen scavenger histidine significantly improved the recovery of LVEDP and -dP/dt. Sarcolemmal Na+, K+-ATPase activity (control, 400+/-41 nmol Pi.min-1.mg-1) was depressed in untreated stunned hearts (260+/-27 nmol Pi.min-1.mg-1), but was almost completely recovered in hearts pretreated with histidine (364+/-27 nmol Pi.min-1.mg-1). The inhibition of Na+, K+-ATPase was only slightly prevented by mannitol (302+/-29 nmol Pi.min-1.mg-1l). CONCLUSIONS: The results suggest that ROS-induced inhibition of Na+, K+-ATPase activity is involved in the mechanism of postischemic contractile dysfunction and support the view that singlet oxygen may be one of the major causes of oxidative injury during ischemia and reperfusion.

Animals↗

Pericardial synovial sarcoma: 14-year survival with multimodality therapy.

We report a case of recurrent primary synovial sarcoma of the pericardium. Reverse transcriptase-polymerase chain reaction analysis for t(X,18) demonstrated the presence of the chimeric transcript SYT/SSX. Because of the rarity of this entity, optimal therapy is unknown. The prognosis of this tumor is very poor in previous reports. In this report, we present a case with five recurrences treated by a combination of surgery, chemotherapy, and radiotherapy. The patient survives now for more than 14 years, the longest reported survival of a primary synovial sarcoma of the pericardium.

Adult↗

Endothelial activation through brain death?

BACKGROUND: Brain death induces myocardial dysfunction and multifocal microscopic myocardial necrosis in dogs; however, the pathogenetic pathways between brain death and cardiac damage remain incompletely understood. We hypothesized that brain death might induce a propensity toward coronary vasospasms, possibly by endothelial dysfunction. We therefore studied the effect of serotonin and acetylcholine on tension generated by isolated coronary artery segments from control and brain dead dogs. METHODS: Coronary segments were isolated 1 hour after brain death that was induced by the inflation (15 ml saline) of an extradurally placed balloon or from sham-operated time-matched controls. Studied were the effect of serotonin on isometric tension, with and without pre-constriction with prostaglandin F(2alpha) (PGF(2alpha)), and the effect of acetylcholine after pre-constriction. RESULTS: Coronary segments from brain dead dogs exhibited severe vasoconstriction when serotonin (10(-7), 10(-6), and 10(-5) mol/liter) was administered, a reaction that was barely detectable in control segments. After pre-construction with PGF(2alpha), serotonin caused only significant vasodilation in a concentration of 10(-5) mol/liter, unlike in control segments where 10(-6) mol/liter had already induced a highly significant vasodilation. The reaction on acetylcholine was identical in both groups. CONCLUSION: Brain death induces changes in coronary vasoreactivity in dogs, with a highly increased sensitivity for the vasospastic effects of serotonin. It is, however, not merely caused by aspecific endothelial dysfunction, as evidenced by the normal reaction on acetylcholine. These alterations in coronary artery properties might contribute to the myocardial damage seen after brain death.

Acetylcholine↗

A new model to test the calcification characteristics of bioprosthetic heart valves.

BACKGROUND: Tissue degeneration and calcification are the two chief obstacles to the successful application of bioprosthetic heart valves. To enable the study of the durability of bioprosthetic heart valves and the efficacy of anti-calcification treatment, it has become necessary to develop animal models. The aim of this study is to validate a new model for implantation in the pulmonary position. METHODS: Three juvenile sheep underwent implantation of Carpentier-Edwards pericardial valves in the pulmonary position (experimental group). These three valves were compared with three Carpentier-Edwards pericardial valves in the aortic position in patients which had been explanted due to primary tissue failure (clinical group). The valves were analyzed. RESULTS: The findings of macroscopic, X-ray and light microscopic examination were very similar between the two groups. Scattered irregular calcification was seen near the commissures and at the base of the cusps in both groups. Quantitative calcium content analysis showed that calcification of the cusps had progressed to almost the same degree in both groups (experimental group, 3.7+/-0.2 micro g/mg dry tissue; clinical group, 4.3+/-0.3; p>0.05). In the experimental group, calcification in the commissural area of the cusp was pronounced (6.5+/-1.0). In the clinical group, calcification had also progressed in the commissural area of the cusp (6.0+/-1.5), and extended to the base area of the cusp (6.6+/-1.2). CONCLUSIONS: This model is promising for preclinical evaluation of bioprosthetic heart valves. The degree of calcification is not significantly different between our experimental results after three months of implantation in sheep and clinical results after 10 years of implantation in elderly patients. However, the pattern of calcification is somewhat different between the two groups.

Aged↗

Recurrence of mitral valve regurgitation after mitral valve repair in degenerative valve disease.

BACKGROUND: Durability assessment of mitral valve repair for degenerative valve incompetence is actually limited to reoperation as the primary indicator, with valve-related risk factors for late death as a secondary indicator. We assessed serial echocardiographic follow-up of valve function as an indicator of the durability of mitral valve repair. METHODS AND RESULTS: In 242 patients who had undergone mitral valve repair for degenerative valve incompetence, echocardiographic follow-up of valve function, rate of reoperation, survival, and clinical outcome was studied. At 8 years after repair, clinical outcome was excellent, survival was 90.9+/-3.2%, freedom from reoperation was 94.2+/-2.3%, and freedom from anticoagulation bleeding and thromboembolic events was 90.4+/-2.7%. However, freedom from non-trivial mitral regurgitation (>1/4) was 94.3+/-1.6% at 1 month, 58.6+/-4.9% at 5 years, and 27.2+/-8.6% at 7 years. Freedom from severe mitral regurgitation (>2/4) was 98.3+/-0.9% at 1 month, 82.8+/-3.8% at 5 years and 71.1+/-7.4% at 7 years. The linearized recurrence rate of non-trivial mitral regurgitation (>1/4) was 8.3% per year and of severe mitral regurgitation (>2/4) was 3.7% per year. Inadequate surgical techniques (chordal shortening, no use of annuloplasty ring or sliding plasty) could only partially explain recurrence of regurgitation. In selected patients who did not have these risk factors, linearized recurrence rates were 6.9% per year and 2.5% per year, respectively. CONCLUSIONS: The durability of a successful mitral reconstruction for degenerative mitral valve disease is not constant, and this should be taken into account when asymptomatic patients are offered early mitral valve repair.

Disease-Free Survival↗

Modified stentless porcine valve enhances accelerated cuspal calcification in the juvenile sheep model.

OBJECTIVE: Stent mounting of any bioprosthesis, induces a loss of mobility and reduces the effective valve orifice. By contrast, for stentless procedures, the higher surgical technicality remains a major obstacle for many surgeons. In an attempt to facilitate the insertion of the stentless porcine aortic valve (Toronto SPV), we tried to alter the design by lowering the invasive profile at the depth of the sinuses on both coronary sites. This could theoretically facilitate the implant of the modified stentless valve with an easygoing single layer suture at the challenging subcoronary level and make it more attractive for every surgeon. METHODS: Modifications of the standard model were done by lowering the profile at the depth of the sinuses on both coronary sites, whether by plication or excision of the protruding porcine aortic wall at the nadir of each coronary sinus. Nine juvenile sheep underwent implantation of stentless porcine aortic valves in pulmonary position: 3 standard Toronto SPV, 3 plicated Toronto SPV and 3 excised Toronto SPV. In each series, valves were explanted after 3 months. Valves were analyzed. RESULTS: The cusps of standard Toronto SPV were perfectly functioning and pliable, without visible calcification after three months. The calcium content of the cusps was less than those in the plicated and excised Toronto SPV (2.4 +/- 0.7 microg/mg versus 10.8 +/- 5.9 and 6.7 +/- 3.4 microg/mg). In the plicated and excised valves, calcification of the cusp was more pronounced in the commissural region (3.9 +/- 1.9, 29.0 +/- 16.7, 13.8 +/- 9.5 microg/mg in the standard, plicated and excised Toronto SPV, respectively). On the other hand, the aortic wall from the plicated Toronto SPV had more calcium than that from the other groups (53.6 +/- 6.3, 41.2 +/- 7.1, 45.2 +/- 7.4 microg/mg in the plicated, standard and excised Toronto SPV, respectively). CONCLUSIONS: The modification of stentless porcine valve enhanced accelerated cuspal calcification in the commissural region. It accentuated that the correct implantation technique for stentless procedures is extremely important in order to prevent early degeneration.

Animals↗

Remote preconditioning lessens the deterioration of pulmonary function after repeated coronary artery occlusion and reperfusion in sheep.

PURPOSE: We investigated whether remote organ preconditioning (RPC) can preserve pulmonary function following repeated myocardial ischemia/reperfusion in a model mimicking multi-vessel off-pump coronary artery bypass (OPCAB) revascularization. METHODS: Nine sheep (Group-RPC) underwent RPC by three episodes of five-minute occlusion and five-minute reperfusion of the iliac artery. Five sheep (Group-C) were time-matched controls. Afterwards, ten-minute occlusion and reperfusion of the left anterior descending, the first diagonal and the left circumflex coronary arteries were performed consecutively. Hemodynamic and respiratory parameters and arterial blood gases were measured until 120 min after the final coronary reperfusion. Anesthesia was maintained with halothane in oxygen and nitrous oxide. Animals were ventilated with a tidal volume of 15-20 mL.kg(-1) in a non-rebreathing system, and a respiratory rate 14-16 min, with 5-cm H(2)O positive end expiratory pressure after thoracotomy. RESULTS: Repeated coronary occlusion and reperfusion was associated in this experimental model with an increase in pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) and a decrease in PaO(2) and PaO(2)/FIO(2) in Group-C. After 120 min reperfusion, PaO(2) and PaO(2)/FIO(2) in Group-RPC were higher (192 +/- 69 mmHg and 241 +/- 78 vs 115 +/- 54 mmHg and 129 +/- 64, P < 0.05), while PVR and PAP were lower than in Group-C. At 120 min of reperfusion, PaO(2) and PaO(2)/FIO(2) were inversely correlated with PVR (P < 0.01). CONCLUSIONS: RPC by transient occlusion of the iliac artery improves lung gas exchange after repeated coronary artery occlusion and reperfusion mimicking OPCAB surgery, and preserves low PVR in sheep.

Analysis of Variance↗

Continuous retrograde blood cardioplegia is associated with lower hospital mortality after heart valve surgery.

OBJECTIVE: Myocardial preservation studies comparing blood and crystalloid cardioplegia techniques were almost exclusively performed on patients undergoing coronary bypass, and they were unable to show a difference in hospital mortality. We investigated possible factors, including cardioplegia techniques, influencing hospital mortality in patients undergoing cardiac valve surgery. METHODS: We evaluated hospital mortality in 1098 consecutive patients undergoing cardiac valve surgery by using a multivariate logistic regression with propensity score balancing of the groups. In 25% of the patients, multiple valve or Bentall procedures were performed, and in 46% of all patients, coronary bypass grafting was associated with valve surgery. A first cohort of 504 consecutive patients were operated on by using single-shot antegrade cold crystalloid cardioplegia, and a second cohort of 594 patients were operated on by using continuous retrograde cold blood cardioplegia. RESULTS: After correction for patient-related and operative risk factors, lower hospital mortality was found in patients who received retrograde blood cardioplegia (P =.020). The odds ratio of in-hospital death when using blood cardioplegia was 0.44 (95% confidence interval, 0.22-0.88). Further predictors of hospital mortality were age, advanced New York Heart Association functional class, cardiopulmonary bypass time, reoperation, active endocarditis, and renal failure. CONCLUSIONS: This study shows that continuous retrograde blood cardioplegia is associated with lower hospital mortality in heart valve operations.

Adult↗