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Background. Different common gene variants were related to coronary artery disease (CAD) in many studies. Yet, the relation of these loci to the severity of CAD is not completely elucidated. Methods. We enrolled 520 subjects (315 CAD cases and 205 controls). CAD presence and extension were assessed by coronary angiography (CAG). Genotyping of five SNPs (namely, rs2230806 (1051G > A) in ABCA1 on chromosome 9, rs2075291 (553G > T) in ApoA5 on chromosome 11, rs320 in LPL on chromosome 8 intron (T → G at position 481), rs10757278 (c.22114477A > G), and rs2383206 (c.22115026 A > G) on chromosome 9p21 locus) was performed by allele-specific PCR. The degree and site of arterial lesions were used to classify patients, tested for association with CAD severity, and related to allele dosage. Results. The polymorphisms rs2383206 and rs10757278 showed significant associations with 2- and 3-vessel coronary disease (p =0.003 and 0.006, respectively). The homozygous GG genotypes of rs10757278 was associated with higher frequency of left anterior descending (LAD), right coronary artery (RCA) and left circumflex (LCX) diseases (p =0.002, 0.016 and 0.002, respectively). The GG genotypes of rs2383206 were found in higher percentage in patients with left main (LM) trunk and left circumflex (LCX) diseases ( p = 0.013 and 0.002, respectively). Conclusion. SNPs rs10757278 and rs2383206 allele dosage could predict CAD severity in the Saudi Arab population.

Neda Bogari,1 Anas Dannoun,1 Mohammad Athar,1,2 Osama Elkhateeb,3,4 Massimo Porqueddu,5,6 Reem Allam,7 Francesco Alamanni6 1Department of Medical Genetics, Faculty of Medicine, Umm Al-Qura University, Makkah, Kingdom of Saudi Arabia; 2Science and Technology Unit, Umm Al-Qura University, Makkah, Kingdom of Saudi Arabia; 3Department of Cardiology, King Abdullah Medical City Makkah, Makkah, Kingdom of Saudi Arabia; 4Department of Cardiology, Dalhousie University Halifax, Nova Scotia, Canada; 5Department of Cardiac Surgery, King Fahd Armed Forces Hospital, Jeddah, Kingdom of Saudi Arabia; 6Department of Cardiac Surgery, Monzino Heart Center, University of Milan, Milano, Italy; 7Clinical Pathology Department, Faculty of Medicine, Zagazig University, Sharkia, EgyptCorrespondence: Neda BogariDepartment of Medical Genetics, Faculty of Medicine, Umm Al-Qura University, Makkah, Kingdom of Saudi ArabiaTel + 966 25270000 Ext:5057-4168Fax +966 25272155Email nmbogari@uqu.edu.saReem AllamClinical Pathology Department, Faculty of Medicine, Zagazig University, Sharkia, EgyptEmail rmallam@medicine.zu.edu.egPurpose: Coronary artery disease (CAD) is one of the most important leading causes of morbidity and mortality worldwide. Few studies have been carried out in the Saudi population regarding the association of rs10757278 polymorphism with CAD. This study aimed to investigate the association of the rs10757278 polymorphism with CAD in Saudi population.Materials and Methods: In this case-control study, we recruited 437 patients with CAD and 251 cross-matched healthy controls and performed polymorphism genotyping for rs10757278 using a polymerase chain reaction followed by a restriction fragment length polymorphism analysis.Results: The G allele (OR-1.44; 95% CI: 1.15– 1.80; p=0.001), as GG (OR-2.13; 95% CI: 1.35– 3.36; p=0.0009), in the dominant (OR-1.47; 95% CI: 1.03– 2.10; p=0.03) and recessive mode (OR-1.84; 95% CI: 1.26– 2.70; p=0.001) of inheritance showed a high-risk association. A disease stratified risk analysis was conducted and comparisons were made using an ANOVA analysis. Diabetes showed a risk association (p=0.001). However, a regression analysis confirmed that for the CAD cases, there was an association between the GG genotype and diabetes (p=0.005).Conclusion: The results of this study suggest that the polymorphism rs10757278 is related to a high risk of CAD in a Saudi population.Keywords: coronary artery disease, 9p21, rs10757278, gene polymorphism and Saudi population

Abnormal levels of plasma lipid have been linked to atherosclerosis, strokes and heart conditions. Variations in high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol levels are considered as risk factors for coronary artery disease (CAD). Furthermore, triglycerides are a leading cause of cardiovascular disease. Therefore, measurement of plasma lipid levels is an important mortality predictor. Several factors were associated with irregularity in plasma lipids such as genetic alterations. Recent researches have linked single nucleotides polymorphism (SNP) in ApoA5 gene with these deviations. In this study, we reported the effects of the genetic variant c.553G>T in ApoA5 on the levels of plasma lipids. To explore these effects, a case-control study including 280 male and female subjects (44 of them were assigned as CAD cases while the remaining subjects were categorized as control) was established. All patients in the study were recruited from the western region in KSA. The results have detected minor variations in LDL, HDL and cholesterol levels between CAD patients carrying T allele and CAD patients carrying the WT allele. However, there were no significant effects due to these variations. TG levels in the wild type carriers reached up to 291 mg/dl while T allele carriers, the cases, presented lower levels of TG (170 mg/dl and 71 mg/dl). Although, T allele showed no effects on plasma lipids with the exception of TG levels. We suggest by this study that T allele in this SNP might be considered as a valuable tool in the diagnosis of CAD.

Aims Patients with coronary heart disease (CHD) are at very high risk of recurrent events. A strategy to reduce excess risk might be to deliver structured secondary prevention programmes, but their efficacy has been mostly evaluated in the short term and in experimental settings. This is a retrospective case–control study aimed at assessing, in the real world, the efficacy of a secondary prevention programme in reducing long-term coronary event recurrences after coronary artery bypass surgery (CABG). Methods and results Programme participants (henceforth ‘cases’) were men and women aged Conclusion In a real-world setting, taking part in a structured longstanding secondary prevention programme, in addition to usual cardiology care, meaningfully lowers the risk of coronary recurrences.

Introduction: To our knowledge KFAFH Department of cardiac surgery is one of the few centers performing aortic arch surgery in Saudi Arabia.The optimal strategy for management of the circulation during aortic arch surgery remains controversial and neurologic dysfunction due to cerebral ischemia remains a significant concern. We report our experience on aortic arch surgery performed with Deep or Moderate Hypothermic Circulatory Arrest (DHCA or MHCA) and Antegrade Selective brain Perfusion. Methodology: 21 consecutive patients (pts) underwent aortic arch repair between 2009 and 2017. 9 pts (42.8%) were operated on emergency basis because of type A aortic dissection or impending rupture, 12 pts (57.2%) on elective basis. 7 pts (33.3%) had complete arch replacement and 14 pts (66.6%) had emiarch repair. Axillary cannulation was performed in 15 pts (71.4%), femoral cannulation in 6 pts (28.6%). Our brain protection strategy consisted in DHCA (18–20 C) in 11 pts (52.4%), MHCA (23–25 C) in 10 pts (47.6%). Selective monolateral antegrade perfusion (uSAP) trough axillary artery was performed in 12 pts (57.1%), selective bilateral antegrade perfusion (bSAP) in 9 pts (42.9%). Mean circulatory arrest was 32 ± 15 min, Cerebral oximetry has been employed to monitoring brain perfusion. Results: In-hospital mortality rate was 1 (5%) (type A aortic dissection), no pt had permanent neurological deficit. 3 pts (14.2%) had a temporary neurological deficit, 4 pts renal impairment (19.4%), 1 pt vocal cord paralysis (4.8%), 3 pts bleeding (14.3%). uSAP but not temperature was identified as independent predictor of transient neurological deficit (p 0.05). DHCA was significantly associated to higher blood loss after surgery (p

Background Elevated plasma triglycerides (TGs) are widely used as a major cardiovascular risk predictor and are thought to play an important role in the progression of coronary heart disease (CHD). It has been demonstrated that lipid lowering was associated with lower mortality in patients with CHD. The present study therefore aimed to investigate the consequences of the genetic variant c.553G > T (rs2075291) in apolipoprotein A5 gene to determination of triglycerides levels in CAD patients receiving, atorvastatin, lipid lowering drug. Methods We here report that a recently identified genetic variant, c.553G > T in the APOA5 gene which causes a substitution of a cysteine for a glycine residue at amino acid residue 185(G185C) is also associated with increased TG levels. To investigate theses effects, a case-control study compressing 608 subjects from the same area was performed. Results TG levels in T allele patients were significantly lower than the control GT allele patient (χ2 = 2.382E2a, P-value T variant (rs2075291); in APOA5 gene increases human plasma TG levels. Conclusion Nevertheless, T allele is found to reduce TG levels in CAD patients who are on the cholesterol medication, atorvastatin. Thus, c.553G > T variant can be considered as a significant predicator of hypertriglyceridemia. In addition, it could be used as a hallmark for the diagnosis and prognosis of CAD.

Objective In this observational prospective study, we assessed the role of clinical variables and circulating biomarkers in graft occlusion at 18 months to identify a signature for graft occlusion. Methods A total of 330 patients undergoing primary elective coronary artery bypass grafting were enrolled. Blood collection for biomarker assessment was performed before surgery and discharge. Patients were then scheduled to undergo coronary computed tomography angiography at 18 months follow-up, and 179 patients underwent coronary computed tomography angiography 18 ± 2 months postoperatively. Results There were 46 of 503 (9.1%) occluded grafts; of these, 29 (63%) were venous and 17 (37%) were arterial grafts; overall, 43 of 179 patients (24%) had at least 1 occluded graft. Logistic mixed effects model assessing independent factors associated with graft occlusion identified that lower D-dimer levels at baseline (odds ratio [OR], 2.58; 95% confidence interval [CI], 1.36-4.89; P = .00) and total protein content at discharge (OR, 1.09; 95% CI, 1.01-1.19; P = .028) were related to overall graft occlusion at follow-up, along with an arterial graft other than the left internal thoracic artery (OR, 2.92; 95% CI, 1.24-6.9; P = .078); moreover, a venous graft emerged was possibly associated with graft occlusion (OR, 1.51; 95% CI, 0.95-2.39; P = .078). By separately analyzing saphenous vein and arterial grafts, D-dimer levels (OR, 2.67; 95% CI, 1.15-6.2; P = .022 and OR, 2.5; 95% CI, 1.01-7.0; P = .05 for venous and arterial graft, respectively) were still associated with arterial and venous graft occlusion at follow-up. Conclusions We identified D-dimer as a biomarker associated with arterial and venous grafts occlusion. This may help stratify patients at risk of graft failure and identify new molecular targets to prevent this complication.

Background . This study was undertaken to investigate the relations between whole body oxygen consumption (VO 2 ), oxygen delivery (DO 2 ), and hemodynamic variables during cardiopulmonary bypass. Methods . One hundred one patients were studied during cooling, hypothermia, and rewarming. Oxygen consumption, DO 2 , hemodynamics, and DO 2crit were measured at these times. Results . There was a direct linear relation between DO 2 and VO 2 during all three times. No relation between VO 2 and hemodynamics was detected during cooling; during hypothermia, an inverse linear relation with peripheral arterial resistance was found. Finally, during rewarming, there was a direct relation with pump flow rate, and an inverse relation with arterial pressure and arterial resistance. The same relations among the variables were found at delivery levels above or below DO 2crit . Conclusions . During cardiopulmonary bypass there is a direct linear relation between DO 2 and VO 2 ; the relations with hemodynamic variables depend on the phases of cardiopulmonary bypass. This suggests that increasing delivery levels may recruit and perfuse more vascular beds, and higher delivery levels are advisable during perfusion. During rewarming and hypothermia, lower arterial resistances are also desirable to optimize VO 2 .

Although significant advances have been made in the surgical treatment of diseases affecting the descending thoracic aorta, paraplegia remains a devastating complication. We propose the quick, simple clamping technique to prevent spinal cord ischemic injury.From 1983 to 1998, 143 patients had descending thoracic aorta aneurysm repair. We divided the patients into the following three groups according to the surgical technique used: selective atriodistal bypass was used in group 1 (66 patients); simple clamping technique in group 2 (28 patients); and quick simple clamping technique in group 3 (49 patients). Mean aortic cross clamp time was 39+/-13 minutes in group 1, 37+/-11 minutes in group 2, and 17+/-6 minutes in group 3 (p0.01 group 3 versus group 1 and group 2).The overall incidence of paraplegia was 4.8% (7 patients), 4.5% (3 patients) in group 1, 14.3% (4 patients) in group 2, and 0 in group 3 (p0.05 group 3 versus group 2). The overall in-hospital mortality rate was 5.5%. Multivariate logistic regression analysis showed a powerful effect of aortic cross-clamping time as risk factor for both paraplegia (p0.008), with an odds ratio of 1.03 per minute, and in-hospital mortality (p0.001), with an odds ratio of 2.5 per minute. The mean follow-up time was 65 months with a lower overall mortality rate in group 3 than in group 1 and group 2 (p0.05).In descending thoracic aortic aneurysm repair, spinal cord perfusion can be maintained adequately without reimplantation of segmental vessels or use of atriodistal bypass when the aortic cross-clamp time is short (15 to 20 minutes).

Porcelain aorta is associated to significantly increased risk of atheromatous embolization in patients who undergo cardiac surgery. We described three cases in which coronary artery bypass grafting was performed off-pump and the saphenous vein graft was anastomosed proximally to the left common carotid artery. This technique permitted avoidance of ascending aortic manipulation and reduce the risk of atheromatous embolization.

Objectives The aim of this study, undertaken in patients who underwent mitral valve (MV) repair surgery, was to evaluate the feasibility and accuracy of 3-dimensional (3D) transthoracic (TTE) and transesophageal (TEE) echocardiography in the evaluation of MV pathology. Background A pre-operative assessment of MV anatomy is essential to surgical design in patients undergoing MV repair. Although 2-dimensional (2D) echocardiography provides precise information regarding MV anatomy, 3D TTE and 3D TEE could increase the understanding of MV apparatus and individual scallop identification. Methods One-hundred-twelve consecutive patients with severe mitral regurgitation due to MV prolapse underwent a complete 2D and 3D TTE the day before surgery and a complete 2D and 3D TEE in the operating room. Echocardiographic data obtained by the different techniques were compared with surgical inspection. Results Three-dimensional techniques were feasible in a relatively short time (3D TTE: 7 +/- 4 min; 3D TEE: 8 +/- 3 min), with good (3D TTE 55%; 3D TEE 35%) and optimal (3D TTE 21%; 3D TEE 45%) imaging quality in the majority of cases. Three-dimensional TEE allowed more accurate identification (95.6% accuracy) of all MV lesions in comparison with other techniques. Three-dimensional TTE and 2D TEE had similar accuracies (90% and 87%, respectively), whereas the accuracy of 2D TTE (77%) was significantly lower. Conclusions Three-dimensional TTE and TEE are feasible and useful methods in identifying the location of MV prolapse. They were superior in the description of pathology in comparison with the corresponding 2D techniques and should be regarded as an important adjunct to standard 2D examinations in decisions regarding MV repair.

Background This study was undertaken to evaluate the long-term clinical and echocardiographic outcome after aortic valve replacement with the Bravo Cardiovascular Model 400 stentless xenograft. Methods Between February 1992 and January 1994, 67 patients underwent aortic valve replacement with the Bravo 400 bioprosthesis. The valvular pathology was aortic stenosis in 36 patients (53.7%), aortic insufficiency in 17 patients (25.4%), and mixed lesion in 14 patients (20.9%). Mean follow-up time was 9.8 ± 2.73 years and median follow-up time was 11 years. Cumulative follow-up time was 659 patients-years and was 94% complete. Results No early deaths were observed. Overall survival estimates at 11 years were 74.71% ± 5.47%. The actuarial freedom from valve-related death at 11 years was 91.04% ± 3.84%; from cardiac-related death at 11 years it was 87.95% ± 4.29%; and from noncardiac death at 11 years it was 85.14% ± 4.58%. Eleven-year Kaplan-Meier survival of patients younger than 65 years was 90.91% ± 6.13% versus 66.08% ± 7.38% for older patients ( p = 0.0307, log-rank test). The actuarial freedom from all valve-related morbidity and mortality at 11 years was 80.3% ± 5.4%. The mean transvalvular gradient decreased significantly after aortic valve replacement with a corresponding increase in effective orifice area. Left ventricular mass index at 10-year follow-up was 68.5% of the preoperative value. Conclusions The Bravo Cardiovascular Model 400 stentless xenograft has provided good clinical and hemodynamic results up until 11 years of follow-up.

Background The immune rejection has been anticipated as one of the major causes of allograft aortic valve (AAV) degeneration. The purpose of this study was to prospectively serially measure the magnitude and evolution of the recipient anti-HLA class I antibody response up to 6 years from AAV implant and to correlate serologic data with valve performance by means of a concurrent echocardiographic survey. Methods Cryopreserved AAVs were obtained from multiorgan HLA-typed donors. Nineteen patients younger than 50 years (mean age, 43.3 ± 8 years) were prospectively studied. After successful surgery, all AAV recipient underwent at 3 and 6 months and each year postoperatively (mean follow-up, 71.9 months) concomitant serum sample collection and two-dimensional transthoracic echocardiography. The presence of anti-HLA antibodies was tested against a panel of lymphocytes obtained from 30 blood donors. Results Progressive structural valve deterioration was seen in 6 patients (31.5%) of whom 4 (21%) were reoperated. All pretransplant recipients sera were panel-reactive antibody negative. Seventeen patients (89.4%) demonstrated significant panel-reactive antibody levels, which peaked at 6 months postoperatively, declined from 6 to 24 months, and slowly decreased afterward. In 14 of 19 cases (73.6%) donor-specific HLA antibodies were identified. A strong immunization (6-year persistence of panel-reactive antibody > 70% and peak panel-reactive antibody > 80%) was detected in 31.5% and 36.8% of recipients, respectively. Strong immunization was found to be significantly associated with progressive structural deterioration. Conclusions The immune reaction after cryopreserved AAV implantation is a peculiar long-lasting response occurring in the majority of recipients younger than 50 years of age. An association between a sustained and pronounced immunization and an aggressive AAV degeneration was observed.

The aim of this study was to identify the most important variables associated with early and late mortality in patients operated on for type A aortic dissection over a 15-year period. From January 1984 to March 1999, 110 patients underwent surgery for type A aortic dissection. The 88.1% of patients had an acute type A dissection (AD) and 11.8% had a chronic dissection (CD). Cardiac tamponade and shock occurred in 21.8% and 14.5% of the patients, respectively. The location of the primary intimal tear was in the ascending aorta in 70.9% of cases, in the arch in 17.2%, and in the descending aorta in 7.2%. Univariate and multivariate analyses were conducted to identify non-embolic variables independently correlated to in-hospital death. Kaplan-Meier and Cox regression analyses and hazard function for death risk were used to analyze factors influencing overall and surgical survival. The overall in-hospital mortality rate was 20.9% (23/110 patients), being 9% for CD and 21.6% for AD. Emergent procedures had an in-hospital mortality rate of 47.6%, whereas nonemergent operations had an in-hospital mortality rate of 13.7% (p0.01). Univariate analysis revealed 41 preoperative and operative variables, including age (years), age70 years, remote myocardial infarction, cerebrovascular dysfunction, diabetes, preoperative renal failure, shock, cardiopulmonary bypass time (minutes), emergency operation, as factors associated to in-hospital death (p0.05). Stepwise logistic regression analysis for in-hospital death selected as independent predicting variables (p0.05) remote myocardial infarction [p = 0.006, odds ratio (OR) = 1.9], preoperative renal failure (p = 0.031; OR = 0.8), shock (p = 0.001; OR = 3.1), and age70 years (p = 0.007; OR = 1.7). Follow-up ranged from 9 to 172 months (median 78 months), with Kaplan-Meier survivals for all the patients and hospital survivors of 42% and 54% at 10 years, respectively. Cox regression analysis has identified postoperative stroke [relative risk (RR) = 3.7; p = 0.012), intimal tear in the aortic arch (RR = 2.3; p = 0.036), and postoperative renal failure (RR = 4.5; p = 0.007) as independent predictors of reduced survival at follow-up. When this kind of analysis was performed on hospital survivors only, preoperative renal dysfunction (RR = 1; p = 0.013), reoperation (RR = 1.7;p = 0.004) and intimal tear in the aortic arch (RR = 1.2; p = 0.002) emerged as risk factors. The actuarial freedom from reoperation was 85.4% at 5 years. Multiple factors still influence early and late survival after surgery for type A aortic dissection. Preoperative renal impairment both affects early and late outcome. Early postoperative course affects late outcome in hospital survivors. The presence of the intimal tear in the aortic arch has a negative impact on late survival.

Background . The Cosgrove-Edwards Annuloplasty System includes a universally flexible band that corrects mitral annular dilatation via measured plication of the posterior annulus. The purpose of this study was to evaluate midterm clinical and functional results in the first 197 patients receiving this flexible annuloplasty band at mitral valve repair. Methods . From February 1993 to July 1994, 197 consecutive patients with mitral regurgitation had mitral valve repair using this system. Valve disease was degenerative in 73%, rheumatic in 15%, ischemic in 5%, infectious in 2.5%, and other in 4%. Results . Immediately after repair, echocardiographic mitral regurgitation was none or trivial in 92%, 1+ in 5%, and 2+ in 3%. There were no hospital deaths. Late follow-up was available in 195 patients (99%), with 661 patient-years of follow-up available for analysis. Four-year actuarial survival was 93%, freedom from thromboembolism 94%, from endocarditis 98%, and from reoperation 95%. At a mean interval of 18 months, echocardiography in 157 patients demonstrated no or trace mitral regurgitation in 56%, 1+ in 24%, 2+ in 9%, 3+ in 6%, and 4+ in 3%. At a mean of 61 ± 5 months, reconstruction of the mitral annulus from real-time three-dimensional echocardiographic images in 10 patients confirmed preserved nonplanar shape and sphincter mechanism of the mitral annulus. Annular orifice area decreased 28% ± 11% during the cardiac cycle from a mean of 10.1 ± 3.9 cm 2 in diastole to 7.2 ± 2.8 cm 2 in systole. Conclusions . This annuloplasty system is effective for repair of mitral regurgitation secondary to all causes and preserves mitral annular flexibility and function at 5-year follow-up.

Immune heparin-induced thrombocytopenia is a rare complication of heparin administration. We describe a patient with a previous diagnosis of heparin-induced thrombocytopenia and related contraindications to anticoagulation who underwent urgent off-pump myocardial revascularization with the administration of only antiaggregant therapy.

This study investigates the time-dependent resistance of the endothelium of porcine aortic and pulmonary valves to different periods of warm ischemia (WIT).Twenty-five 9-month-old swine were divided after death into five groups of WIT (0, 6, 12, 24, and 36 hours). Aortic and pulmonary valves were removed and a total of 15 aortic and 15 pulmonary valve specimens were obtained for each WIT interval. Valves were then examined for (1) their viability rate by the trypan blue dye exclusion method at light microscopy (percent of viability compared with 0 hours of WIT); (2) ultrastructural signs of irreversible or reversible ischemic damage by transmission electron microscopy (cell disruption, dilation of endoplasmic reticulum, cytoplasmic edema, nuclear and mitochondrial changes); (3) endothelial function by pharmacologic evaluation of both the endothelial-releasing capacity of prostacyclin and the endothelial-dependent dynamic responses to relaxing (acetylcholine from 1 x 10(-10) mol/L to 1 x 10(-4) mol/L) in aortic and pulmonary valve segments precontracted with norepinephrine (1 x 10(-6) mol/L) and contracting (NG-monomethyl-L-arginine, 1 x 10(-4) mol/L) drugs.Our results showed an endothelial progressive time-dependent ischemic injury, which reached significance after 12 hours of exposure. Viability and functional data indicated that 6 hours of WIT only provoked slight endothelial damage (p0.05 respect to time 0 hours), with signs at transmission electron microscopy consistent with a reversible injury. At 12 hours of exposure, we observed a significant reduction (p0.05) with respect to time 0 of the viability rate of prostacyclin production and of the endothelium-dependent dynamic responses to acetylcholine and NG-monomethyl-L-arginine. These functional impairments, although significant, were not consistent, however, with a complete loss of viability. Transmission electron microscopic observations confirmed the appearance of signs of irreversible injury; nevertheless, some elements were found to be well preserved or presented reversible damage. After 24 hours of WIT, ultrastructural and functional data were consistent with a dramatic decrease compared with controls in endothelial viability and functions (p0.01). Finally, after 36 hours of WIT, there was a subtotal loss of viability, of functions (p0.001) and, at transmission electron microscopic observations, of the endothelial layer of the valves.Our data show that the endothelial cells are resistant to short periods of WIT (up to 6 hours), and suggest that these cells can endure longer exposures, up to 12 hours of warm ischemia. Periods of 24 and 36 hours of WIT provoke progressive irreversible damage.

Background. We investigated the effects of cryopreservation and antibiotic treatment on endothelium-dependent vasomotor properties of human internal mammary arteries (IMAs). Methods. Sixty IMA specimens from routine coronary artery bypass grafting procedures were randomly assigned to six groups. Group I (controls) were immediately tested after harvest. Remaining groups were prepared according to a stepwise design: group II, 6 hours of warm ischemia; group III, 6 hours of warm ischemia + 24 hours at 4°C (without antibiotics); group IV, 6 hours of warm ischemia + 24 hours of 4°C antibiotic disinfection; group V, 6 hours of warm ischemia + 24 hours at 4°C (without antibiotics) + cryopreservation; and group VI, 6 hours of warm ischemia + 24 hours of 4°C disinfection + cryopreservation. The IMA specimens were cut into rings and the tension of vascular smooth muscle was recorded. The IMA rings were contracted with norepinephrine (3 × 10 −6 mol/L) and tested with cumulative concentrations of acetylcholine (from 1 × 10 −9 to 1 × 10 −5 mol/L), contracted with endothelin-1 (from 1 × 10 −11 to 1 × 10 −6 mol/L), and contracted with the nitric oxide-synthase inhibitor N G -monomethyl-l-arginine (1 × 10 −4 mol/L). Rings were also tested for their capacity to generate 6-keto-prostaglandin F 1 (the stable metabolite of prostacyclin), and endothelial cell viability rate was finally evaluated with the trypan blue dye exclusion method. Results. Our results show that a complete cryopreservation protocol does not significantly modify ( p > 0.05) the relaxant activity to acetylcholine in norepinephrine-precontracted IMA rings (controls; 90.2% ± 4.2% vs group VI, 77.1% ± 6.2%) or the vasoconstrictor response induced by endothelin-1 (controls, 62.6% ± 2.8% versus group VI, 73.7% ± 4.8%) and N G -monomethyl-l-arginine (controls, 22.4% ± 1.5% versus group VI, 18.9% ± 1.9%). Furthermore, IMA cryopreservation does not significantly modify ( p > 0.05) the endothelial release of prostacyclin either in basal conditions (−20% versus controls) or during pharmacologic intervention with acetylcholine (−18% versus controls), endothelin-1 (−17% versus controls), and N G -monomethyl-l-arginine (−18% versus controls). Conclusions. We conclude that the IMA endothelial function does not seem significantly injured by any of the current steps of disinfection and cryopreservation.

The case of a 66-year-old female patient with a tumor located in the right ventricular outflow tract is reported. Histologic examination of an intraoperative biopsy revealed that the tumor was an intracardiac ectopic thyroid. We performed conservative surgery with partial resection of the mass. After 5 years, the patient is asymptomatic and leading a normal life. The authors examine the relation between the embryologic development of the primitive heart and the thyroid primordium and suggest the hypothesis of ectopic thyroid location in the right- or left-ventricular outflow tract.

Background— Only a few studies have focused the attention on the relation between elevated anti– Chlamydia pneumoniae (CP) antibodies and the detection of CP in the arterial wall. The aim of our study is thus to investigate the relationship between immune response to CP and detection of CP in the aortic walls of patients with abdominal aortic aneurysm. Methods and Results— A specimen of aortic wall was obtained from 102 consecutive patients who underwent abdominal aneurysm repair. The possible presence of CP was studied by polymerase chain reaction and confirmed by nonradioactive DNA hybridization. Antibody response to CP was studied (IgG, IgA titers). We found 33 patients (32.4%) with CP DNA+. No correlation between CP DNA detection and antibody titers was found (IgG P =0.52, IgA P =0.66). High correlation between IgG and IgA titer was observed ( P Conclusions— CP antibody titers are not associated with the presence of CP in the aortic wall of patients with abdominal aortic aneurysm.

The case of a patient with an intracardiac ectopic thyroid is reported. A cardiac tumor was found in a 66-year-old woman and was diagnosed by two-dimensional echocardiography. An intraoperative biopsy was performed, and the mass was recognized as an ectopic thyroid and treated with a conservative surgical approach because of the size, location, and relationship to adjacent structures. The 60-month follow-up shows normal echocardiographic images and the good clinical status of the patient.

BACKGROUND Previous studies have shown that defibrotide, a polydeoxyribonucleotide obtained by depolymerization of DNA from porcine tissues, has important protective effects on myocardial ischemia, which may be associated with a prostacyclin-related mechanism. The purpose of this study was to investigate the direct effects of defibrotide (given in cardioplegia or after ischemia) on a model of rat heart recovery after cardioplegia followed by ischemia/reperfusion injury. METHODS Isolated rat hearts, undergoing 5 minutes of warm cardioplegic arrest followed by 20 minutes of global ischemia and 30 minutes of reperfusion, were studied using the modified Langendorff model. The cardioplegia consisted of St. Thomas' Hospital solution augmented with defibrotide (50, 100, and 200 microg/mL) or without defibrotide (controls). Left ventricular mechanical function and the levels of creatine kinase, lactate dehydrogenase, and 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha; the stable metabolite of prostacyclin) were measured during preischemic and reperfusion periods. RESULTS After global ischemia, hearts receiving defibrotide in the cardioplegic solution (n = 8) manifested in a concentration-dependent fashion lower left ventricular end-diastolic pressure (p < 0.001), higher left ventricular developed pressure (p < 0.01), and lower coronary perfusion pressure (p < 0.001) compared to the control group. After reperfusion, hearts receiving defibrotide in the cardioplegic solution also had, in a dose-dependent way, lower levels of creatine-kinase (p < 0.01), lactate dehydrogenase (p < 0.001), and higher levels of 6-keto-PGF1alpha (p < 0.001) compared to the control group. Furthermore, when defibrotide was given alone to the hearts at the beginning of reperfusion (n = 7), the recovery of postischemic left ventricular function was inferior (p < 0.05) to that obtained when defibrotide was given in cardioplegia. CONCLUSIONS Defibrotide confers to conventional crystalloid cardioplegia a potent concentration-dependent protective effect on the recovery of isolated rat heart undergoing ischemia/reperfusion injury. The low cost and the absence of contraindications (cardiac toxicity and hemodynamic effects) make defibrotide a promising augmentation to cardioplegia.

Cardiac myxoma is the most common heart neoplasm in adults, comprising about 50% of all primary cardiac tumorsJ This neoplasm is most prevalent between the third and the sixth decades of life, 2 with women predominating, it can be associated with skin myxoma, mucocutaneous pigmentation, myxoid mammary fibroadenomatous neoplasms, and endocrine neoplasmsJ Farah 3 reported that this tumor seemed to be frequent in family members, suggesting an autosomal dominant mode of inheritance. Cardiac myxoma may be found in all cardiac chambers and on any of the heart valves. It is usually single but may be multiple. Myxomas occur three times more often in the left atrium than in the right and much less frequently in the ventricleJ 6 Of those rare ventricular myxomas, fewer than 5% develop in the right ventricle. L 6 In general, myxomas are round, polypoid, sessile, or pedunculated, and they vary in size from 1 to 15 cm in diameter. Histologically, the neoplasms consist of a basophilic mucoid matrix populated by groups of elongated spindle cells. Syncytial multinucleate giant cells are often present] Myxomas seem to be similar to embryonic endocardial cushion tissue, which may be multipotential endocardial tissue. Clinical summary. A 56-year-old woman was admitted in October 1995 with a diagnosis of an anterior mediastihal mass, which had been detected on a routine chest x-ray film. An echocardiogram and computed tomographic scan suggested that the mass arose from the thymus. A thoracoscopic examination revealed that the mass was in an epicardial location, appearing to be connected to the anterior wall of the right ventricle. Subsequently the patient was admitted for surgical treatment. She was free of symptoms and her physical examination showed no abnormalities. Results of electrocardiographic, biochemical, and hematologic studies were within normal limits. A transesophageal echocardiogram confirmed the presence of an intrapericardial anterior mediastinal mass compressing

Background . In the present study, the endothelium-dependent antithrombotic and dynamic properties of porcine aortic (AoV) and pulmonary valves (PuV) were investigated. Methods . Fifteen fresh AoV and 15 fresh PuV were obtained from 25 9-month-old swines. The valves were examined for endothelial function by pharmacologic evaluation (with and without endothelium) of both the endothelial-releasing capacity of prostacyclin and the endothelial-dependent dynamic response to relaxing (acetylcholine from 10 −10 mol/L to 10 −4 mol/L in AoV and PuV segments precontracted with norepinephrine [3 × 10 −6 mol/L]) and contracting (endothelin-1, from 10 −11 mol/L to 10 −5 mol/L; and N G -monomethyl-l-arginine, 10 −4 mol/L) drugs. The ultrastructural integrity of the endothelial valve layer was also examined with transmission electron microscopy. Results . Acetylcholine caused potent relaxation in both AoV and PuV specimens with, but not in those without, endothelium. Endothelin-1 produced a concentration-dependent tension increase in AoV and PuV with and without endothelium. However, the intrinsic activity of the peptide significantly increased in tissues without endothelium. N G -monomethyl-l-arginine evoked a progressive increase in resting tension of the preparations, but the AoV and PuV without endothelium were less sensitive to the inhibition of the nitric oxide generation. Aortic and pulmonary valves with an intact endothelium showed a spontaneous ability to release prostacyclin. The basal release of this lipidic autacoid significantly decreased in cardiac valves without endothelium. This phenomenon was observed in both basal conditions, and under stimulation with the aforementioned drugs. Transmission electron microscopy showed the perfect preservation of endothelial cells in all the preparations examined. Conclusions . Valvular endothelium of AoV and PuV seems to have similar antithrombotic and dynamic functions of vascular endothelium, actively participating in valvular homeostasis.