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Pulmonary embolism typically occurs from deep venous thrombosis (DVT). However, not always a DVT can be identified, and 'in situ' generation of pulmonary embolism has been considered, referred to in the literature as 'De novo pulmonary embolism' (DNPE). The objective of the study is to assess risk factors, comorbidities, clinic characteristics and long-term evolution of patients with pulmonary embolism in the absence of an identified source. Retrospective study of 280 patients with pulmonary embolism, 190 pulmonary embolisms with DVT group and 90 (32%) pulmonary embolism without DVT (DNPE group), admitted to an Internal Medicine Department of a tertiary hospital from January 2012 to December 2015. In the DNPE group, segmental and subsegmental arteries were more frequently affected (P = 0.01). As compared with pulmonary embolisms with DVT group: older age, female sex, sedentary lifestyle, diabetes mellitus, arterial hypertension, heart failure, respiratory infections and chronic obstructive pulmonary disease (COPD) were significantly more frequent in DNPE. In multivariate analysis, respiratory infection [odds ratio (OR) 12.2, P < 0.0001], COPD (OR 8.7, P < 0.0001) and female sex (OR 3.0, P = 0.003) were independently associated risk factors. Long-term mortality (median follow-up 15 months) was also higher in DNPE group (34 vs. 16%, P = 0.01). De novo pulmonary embolism occurred in 32% of cases of pulmonary embolisms and was more frequent in female and COPD patients or those with respiratory infections as compared with pulmonary embolisms in which DVT was identified as a source of embolism.

OBJECTIVES Ranolazine improves vascular function in animal models. We evaluate the effects of ranolazine on vascular function and adrenergic response in human saphenous vein. METHODS Rings from 53 patients undergoing coronary artery bypass grafting were mounted in organ baths. Concentration–response curves to ranolazine were constructed in rings precontracted with phenylephrine, endothelin-1, vasopressin, KCl and the thromboxane A2 analogue U-46619. In rings precontracted with phenylephrine, relaxation to ranolazine was tested in the absence and presence of endothelial factors inhibitors, K+ channel blockers and verapamil. The effects of ranolazine on frequency–response and concentration–response curves to phenylephrine were performed in the absence and presence of endothelial factors inhibitors and K+ channel blockers. Endothelial nitric oxide synthase, α1 adrenergic receptor and large conductance Ca2+-activated K+ channel protein expressions were measured by Western blotting. RESULTS Ranolazine (10−9–10−4 M) produced a concentration-dependent relaxation only in rings precontracted with phenylephrine that was reduced by endothelial denudation, NG-nitro-l-arginine methyl ester (10−4 M), charybdotoxin (10−7 M) and verapamil (10−6 M). Ranolazine diminished adrenergic contractions induced by electrical field stimulation (2–4 Hz) and phenylephrine (10−9–10−5 M) that were prevented by tetraethylammonium (10−3 M) and charybdotoxin (10−7 M). Ranolazine significantly decreased α1 adrenergic receptor and increased large conductance Ca2+-activated K+ channel protein expression in the saphenous vein. CONCLUSIONS Ranolazine diminishes the adrenergic vasoconstriction, acting as α1 antagonist, and by increasing large conductance Ca2+-activated K+ channel involvement. The relaxant effects of ranolazine are partially mediated by endothelial nitric oxide, large conductance Ca2+-activated K+ channels and the blockade of voltage-dependent Ca2+ channels.

Introduction and objectives The aim of this study was to compare the in-hospital clinical outcomes of minimally invasive, isolated aortic valve replacement vs median sternotomy. Methods Between 2005 and 2012, 615 patients underwent aortic valve replacement at a single institution, 532 by a median sternotomy (E group) and 83 by a J-shaped ministernotomy (M group). Results No significant differences were found between the E and M groups in terms of age (69.27 [9.31] years vs 69.40 [10.24] years, respectively), logistic EuroSCORE (6.27 [2.91] vs 5.64 [2.17], respectively), size of implanted valve prosthesis (21.94 [2.04] mm vs 21.79 [2.01] mm, respectively), or the incidence of diabetes, hypercholesterolemia, high blood pressure, or chronic obstructive pulmonary disease. Mean cardiopulmonary bypass time was 102.90 (41.68) min for the E group vs 81.37 (25.41) min for the M group (P

OBJECTIVES: Increasing degrees of renal impairment are associated with higher rates of morbimortality after coronary artery bypass grafting (CABG). This incremental risk has not been well studied in off-pump procedures (OPCAB). We assessed its impact on OPCAB and on-pump CABG (ONCAB). METHODS: A total of 1769 patients undergoing primary CABG (January 1995 through June 2011) had complete data on glomerular filtration rate (eGFR). 930 patients had Stage 2 renal insufficiency, 330 Stage 3, 27 Stage 4 and 465 normal renal function (Stage 1). Seventeen patients with end-stage disease (Stage 5) were excluded. The OPCAB technique was selectively used in 350 high-risk patients. Preoperative variables and postoperative outcomes were compared among eGFR subgroups and between matched and unmatched OPCAB vs ONCAB groups. RESULTS: Stages 3–4 patients were older (P< 0.0001), with higher prevalence of diabetes (36.8, 35.0, 39.7 and 74.1%, P< 0.01, 1–4 eGFR groups) peripheral arteriopathy (6.0, 9.0, 15.8 and 29.6%, P< 0.0001) and lower left ventricular ejection fraction (LVEF) (GFR-LVEF correlation: Pearson: 0.12, P< 0.0001). On-pump GFR groups had increasingly higher in-hospital mortality (1.0, 1.2, 3.5 and 15.4%, P< 0.0001), but no differences were observed in OPCAB (5.5, 4.8, 5.4 and 7.1%, P= 0.97). Similar trends on in-hospital morbidity were observed in ONCAB vs OPCAB groups: low cardiac output (P< 0.01), pneumonia (P< 0.01) and stroke (P< 0.05). GFR only predicted mortality in ONCAB patients (odds ratio (OR): 0.96, 95% CI: 0.94–0.98; P< 0.01). Patients with higher eGFR stages had statistically more reduced long-term survival, and this pattern was similar in the three treatment groups, also including the OPCAB group, who had the lowest survival in patients with eGFR stage 4. CONCLUSIONS: Patients with low GFR (Stages 3–4) undergoing ONCAB were at increased risk of early morbimortality. In contrast, there were no significant differences in operative morbimortality among eGFR groups in OPCAB patients. This ‘off-pump advantage’ on early outcomes was not observed at the long-term follow-up.

OBJECTIVES: We aim to describe our experience in coronary artery bypass grafting (CABG) with or without cardiopulmonary bypass by comparing intraoperative and postoperative outcomes. METHODS: From January 1993 to June 2013, 3097 patients underwent consecutive emergency and scheduled CABG surgery. A total of 1770 patients underwent on-pump CABG (ONCABG) and 1327 off-pump CABG (OPCABG). A propensity score matching was performed to identify appropriate matched-pair patients; univariable and multivariable logistic regression analyses were performed to assess significant predictors of hospital and 30-day morbidity and mortality composite end-points. Morbidity composite end-point was defined as any renal, pulmonary, cardiovascular and neurological complication that occurred during hospital stay. We collected all-cause mortality data during the study period. RESULTS: We identified 1004 patients in each group. There were no significant differences in thirty day mortality, 2.8 vs 3.8%, in OPCABG and ONCABG, respectively (P = 0.21). Cardiovascular, neurological, respiratory and renal complications were more frequent in the ONCABG group: 13.9 vs 8.7% (P < 0.001), 3.9 vs 2.2% (P = 0.03), 13.5 vs 7.5% (P < 0.001), 7.1 vs 5.3% (P = 0.095), respectively. The long-term all-cause mortality rate was 12.3 vs 12.9% in the OPCABG versus ONCABG group (P = 0.42), respectively. In both uni- and multivariable analysis preoperative renal failure, chronic obstructive pulmonary disease and ONCABG were independent predictors of mortality and morbidity composite end-points. CONCLUSIONS: OPCABG is associated with less postoperative morbimortality and shorter hospital and intensive care unit length of stay. ONCABG resulted as an independent predictor of morbidity and mortality composite end-point. No statistically significant differences were observed in long-term all-cause mortality between groups.

Background We studied the participation of K + channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca 2+ channels on modulation of adrenergic responses by K + channels blockade. Methods Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. Results Iberiotoxin (10 −7 mol/L), an inhibitor of large conductance Ca 2+ -activated K + channels, and charybdotoxin (10 −7 mol/L), an inhibitor of both large and intermediate conductance Ca 2+ -activated K + channels, enhanced the contractions elicited by electrical field stimulation and produced a leftward shift of the concentration–response curve to norepinephrine. In contrast, the inhibitor of small conductance Ca 2+ -activated K + channels apamin (10 −6 mol/L) did not modify the contractile response to electrical field stimulation or norepinephrine. In the presence of the dihydropyridine Ca 2+ -channel blocker nifedipine (10 −6 mol/L), iberiotoxin and charybdotoxin failed to enhance the contractile responses to electrical field stimulation and norepinephrine. Conclusions The results suggest that large conductance Ca 2+ -activated K + channels are activated by stimulation with norepinephrine to counteract the adrenergic-induced contractions of human saphenous vein. Thus, inhibition of these channels increases significantly the contraction, an effect that appears to be mediated by an increase in Ca 2+ entry through L-type voltage-dependent Ca 2+ channels.

The functional properties of the endothelium of human thyroid arteries remain unexplored. We investigated the intervention of nitric oxide (NO), prostacyclin (PGI(2)) and endothelium-derived hyperpolarizing factor (EDHF) in the responses to acetylcholine and noradrenaline in isolated thyroid arteries obtained from multi-organ donors. Artery rings were suspended in organ baths for isometric recording of tension. The contribution of NO, PGI(2) and EDHF to endothelium-dependent relaxation was determined by the inhibitory effects of N(G)-monomethyl-L-arginine (L-NMMA), indomethacin, and K(+) channel inhibitors respectively. Acetylcholine induced concentration-dependent relaxation; this effect was not modified by indomethacin and was only partly reduced by L-NMMA, but was abolished in endothelium-denuded rings. The relaxation resistant to indomethacin and L-NMMA was abolished by using either apamin combined with charybdotoxin, ouabain plus barium, or a high-K(+) solution. Noradrenaline induced concentration-dependent contractions which were of greater magnitude in arteries denuded of endothelium or in the presence of L-NMMA.In conclusion, the results indicate that in human thyroid arteries the endothelium significantly modulates responses to acetylcholine and noradrenaline through the release of NO and EDHF. EDHF plays a dominant role in acetylcholine-induced relaxation through activation of Ca(2+)-activated K(+) channels, inwardly rectifying K(+) channels and Na(+)-K(+)-ATPase.

In arteries, agonists such as acetylcholine release an endothelium-derived hyperpolarizing factor (EDHF) that is neither nitric oxide nor prostacyclin.To examine the responses to acetylcholine in segments of forearm veins from patients with chronic renal failure who either had never received dialysis or had undergone long-term dialysis, and to determine the contribution of nitric oxide and EDHF to endothelium-dependent relaxation in veins from patients with chronic renal failure.Isometric tension was recorded in rings of forearm vein from 34 non-dialysed patients, 27 dialysed patients and 14 multiorgan donors (controls).Relaxation in response to acetylcholine was reduced in veins of non-dialysed and dialysed patients. The inhibitors of nitric oxide synthase NG-monomethyl-l-arginine (l-NMMA) and NG,NG-dimethyl-l-arginine (ADMA) reduced by 50% the maximum relaxation in response to acetylcholine in veins from controls and non-dialysed patients; the remaining relaxation was inhibited by 20 mmol/l KCl or by the K+ channel blockers tetraethylammonium chloride, iberiotoxin, charybdotoxin and the combination of barium plus ouabain, but not by apamin or glibenclamide. Relaxation in veins from dialysed patients was inhibited by K+ channel blockade but not by l-NMMA or ADMA.The results demonstrate that the endothelium-dependent relaxation in forearm veins from controls and non-dialysed patients is mediated by release of nitric oxide and EDHF. In contrast, the relaxation in veins from dialysed patients is mediated mainly by EDHF. EDHF-induced relaxation involves activation of large-conductance Ca2+-activated K+ channels.

We studied the relaxant effects of milrinone, an inhibitor of phosphodiesterase 3, and rolipram, an inhibitor of phosphodiesterase 4, on contracted human penile dorsal artery and deep dorsal vein. Vascular rings from 12 multi-organ donors were suspended in organ baths for isometric recording of tension. Both milrinone and rolipram inhibited (100%) the contraction induced by noradrenaline and shifted the relaxation–response curves to the cAMP forming agents prostaglandin E1 and forskolin to the left. The findings indicate that the cAMP pathway appears to be a main determinant of relaxation in human penile vessels.

Background . Sildenafil is currently used in the treatment of erectile dysfunction. However, assessment of direct effects of sildenafil on coronary arteries and on arteries used as coronary grafts is unknown. This study was designed to investigate the effects of sildenafil on contracted human coronary, internal mammary, and radial arteries obtained from multiorgan donors. The observations were extended to forearm veins. Zaprinast was included in this study for comparison. Methods . Segments of left coronary, internal mammary, and radial arteries, and forearm veins were obtained from 16 multiorgan donors. Vascular rings were suspended in organ bath chambers and isometric tension was recorded. Then the effects of sildenafil, zaprinast, and sodium nitroprusside on precontracted vessels were studied. Results . Sildenafil (10 −8 − 3 × 10 −5 mol/L) caused concentration-dependent relaxation in the internal mammary arteries, radial arteries, and forearm veins. In the coronary arteries, sildenafil had a modest relaxant effect. In addition, sildenafil amplified the relaxation induced by sodium nitroprusside in all four vessels. Relaxation was unaffected by the inhibitor of nitric oxide synthase N G -monomethyl-L-arginine (10 −4 mol/L). Compared with zaprinast, sildenafil was eight to ten times more potent in terms of EC 50 values. Conclusions . The direct relaxant effects of sildenafil together with its synergistic interaction with nitric oxide donors should be considered in patients undergoing coronary bypass surgery, patients with low blood pressure, and patients receiving antihypertensive regimes.

Objectives: Plasma levels of endogenous guanidino-substituted analogues of L -arginine are increased in various pathologic conditions. In the present study we determined the effects of some of these compounds on basal and stimulated release of nitric oxide in human internal thoracic and radial arteries. Methods: Rings of human internal thoracic and radial arteries were obtained from 16 multiorgan donors. The rings were suspended in organ baths for isometric recording of tension. Results: N G -monomethyl L -arginine (10 –6 to 10 –3 mol/L) and N G ,N G -dimethyl L -arginine (10 –6 to 10 –3 mol/L) caused concentration- and endothelium-dependent contractions. Maximal force of contractions for N G -monomethyl L -arginine and N G ,N G -dimethyl L -arginine in the internal thoracic artery were 18.0% ± 4.3% and 17.8% ± 3.8%, respectively, of the contraction to 100 mmol/L KCl, and those found in the radial artery were 9.6% ± 2.5% and 9.1% ± 2.4%, respectively. Aminoguanidine (10 –5 to 3 × 10 –3 mol/L) and methylguanidine (10 –5 to 3 × 10 –3 mol/L) produced endothelium-independent contractions. L -Arginine (10 –3 mol/L) prevented the contractions by N G -monomethyl L -arginine and N G ,N G -dimethyl L -arginine but did not change contractions induced by aminoguanidine and methylguanidine. N G -monomethyl L -arginine and N G ,N G -dimethyl L -arginine inhibited, in a concentration-dependent manner, the endothelium-dependent relaxation to acetylcholine in the internal thoracic artery and had little attenuating effect in the radial artery; aminoguanidine and methylguanidine were without effect. Conclusions: The results suggest that the contractions induced by N G -monomethyl L -arginine and N G ,N G -dimethyl L -arginine are due to inhibition of both basal and stimulated nitric oxide production, whereas aminoguanidine and methylguanidine do not affect the synthesis of nitric oxide. An increase in the plasma concentration of N G -monomethyl L -arginine and N G ,N G -dimethyl L -arginine is likely to represent a risk factor for abnormal vasomotor tone in conduit arteries used as coronary grafts. (J Thorac Cardiovasc Surg 2000;120:729-36)

Background —Arginine vasopressin (AVP) not only acts directly on blood vessels through V 1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins. Methods and Results —Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (3×10 −9 mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.87×10 −7 to 1.04×10 −7 mol/L; P 1 vasopressin receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP (10 −6 mol/L) prevented the potentiation evoked by AVP. The selective V 1 receptor agonist [Phe, 2 Orn 8 ]-vasotocin (3×10 −9 mol/L) induced potentiation of electrical stimulation–evoked responses, which was also inhibited in the presence of the V 1 receptor antagonist (10 −6 mol/L). In contrast, the V 2 receptor agonist desmopressin (10 −9 to 10 −7 mol/L) did not modify neurogenic responses, and the V 2 receptor antagonist [d(CH 2 ) 5 , D-Ile, 2 Ile, 4 Arg 8 ]-vasopressin (10 −8 to 10 −6 mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (10 −6 mol/L) did not affect the potentiating effect of AVP. Conclusions —The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V 1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated.

Purpose: The goal of this study was to determine the effects of vasopressin and the selective V 2 -receptor agonist desmopressin on human saphenous veins, with special emphasis on endothelium-mediated responses. Methods: Human saphenous vein segments were obtained from 35 patients undergoing coronary bypass surgery. Paired segments, one normal and the other deendothelized by gentle rubbing, were mounted for isometric recording of tension in organ baths. Concentration-response curves to vasopressin and desmopressin were determined in the presence and in the absence of either the V,-receptor antagonist d(CH 2 ) 5 Tyr(Me)AVP (10 −6 mol/L), the V 1 -V 2 receptor antagonist desGly-d(CH 2 ) 5 D-Tyr(Et)ValAVP (10 −6 mol/L), indomethacin (10 −6 mol/L), or N G -nitro-L-arginine methyl ester hydrochloride (L-NAME, 10 −4 mol/L). Results: In vein rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions with a concentration of vasopressin producing-half-maximal contractions (EC 50 ) of 3.44 × 10 −8 mol/L. The vasopressin V 1 -receptor antagonist (10 −6 mol/L) displaced the control curve to vasopressin 9.86-fold to the right in a parallel manner. In precontracted vein rings previously treated with the V 1 -antagonist (10 −6 mol/L), vasopressin caused endothelium-dependent relaxations. This relaxation was reduced significantly by indomethacin (10 −6 mol/L) and unaffected by the V 1 -V 2 -receptor antagonist (10 −6 mol/L) or by L-NAME (10 −4 mol/L). Desmopressin caused endothelium-dependent relaxations in precontracted vein rings that were inhibited by the mixed V 1 -V 2 -receptor antagonist and by indomethacin, but not by the V 1 -antagonist or by pretreatment with L-NAME. Conclusions: These observations indicate that vasopressin exerts contractile effects on human saphenous vein by V 1 -receptor stimulation. Vasopressin causes dilatation of human saphenous vein only if V 1 -receptor blockade is present. This relaxation appears to be mediated by the release of relaxant Prostaglandins, probably derived from endothelial cells, and is independent of V 2 -receptor stimulation or release of nitric oxide. Desmopressin elicits relaxation that is largely dependent on V 2 -receptor stimulation, which may bring about the release of dilating Prostaglandins from the endothelial cells.

Objective: Development of late significant tricuspid regurgitation (TR) after successful mitral valve replacement (MVR) is not infrequent. The impact of different aetiologies or diverse surgical procedures has not been adequately investigated. We studied the influence of subvalvular preservation techniques during MVR on the incidence of late TR. Methods: A total of 801 patients with grade 2+/4+ preoperative TR underwent MVR without associated tricuspid procedures from January 1994 to August 2008. In 595 patients, only posterior mitral leaflet preservation was performed (group A). In the remaining 206 patients, both anterior and posterior leaflets were retained (group B). Postoperative development of significant TR was defined as a TR increase by more than one grade from preoperative or final TR grade 3+/4+ at follow-up. Results: The global incidence of postoperative significant TR was 8.6%, with higher incidence in females (9.4% vs 6.7%, p = 0.12), rheumatic disease (9.7% vs 6.5%, p = 0.07), patients with previous AF (11.8% vs 3.8%, p < 0.001) and, especially, in group A (10.8% vs 2.4%, p < 0.001). The Maze procedure was protective in patients with AF (the incidence with and without associated Maze was 6.7% vs 13.2%, p = 0.04). Preoperative left-atrial diameters were higher in patients with postoperative development of TR (56 9m m vs 51 12 mm, p = 0.01). Group A (p = 0.04) and preoperative atrial fibrillation (p = 0.001) were significant predictors of late postoperative TR. Late functional TR decreased free survival from chronic heart failure. Conclusions: Several clinical and operative factors are associated with the development of significant TR after MVR. Although early surgical intervention for TR may be recommended in selected patients, complete subvalvular preservation of the mitral valve and routine surgical ablation of atrial fibrillation can significantly reduce its incidence. # 2010 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

Renal carcinoma accounts for 3% of malignant urological tumors. The existence of tumor thrombus in the venous system is more infrequent, and, despite it was believed until recently its presence worsened the diagnosis of the disease, currently it is accepted that in the absence of metastatic or lymph node disease, surgery is the treatment of choice and potentially curative for these tumors.Between June 2003 and November 2007 eight patients with renal disease and venous thrombus underwent surgery; two of them wereT3c and six T3b; in five of them surgery was carried out in association with the heart surgery team in our centre. Three of them underwent surgery with extracorporeal circulation. Mean patient age was 56 years.Tumor thrombus was grade I in one patient, grade II in 4 patients, grade III in one patient, and grade IV in two patients. In all patients with tumor gradeor = III, as well as two with grade II, surgery was performed in conjunction with the department of heart surgery. The operation with extracorporeal circulation, deep hypothermia, cardioplegia, and antegrade and retrograde brain perfusion was performed in grades III and IV. Midline incision was performed, with or without sternotomy, depending on the level of the thrombus. Hemorrhage was the most frequent perioperative complication.It is essential to know the exact level of the cephalic extreme of the tumor thrombus to design the proper surgical strategy; for that, we can use MRI, CT scan or ultrasound. Therefore, surgical approach, multidisciplinary cooperation and use of extracorporeal circulation will depend on such extension of the thrombus and concurrent factors of the patient. A good surgical strategy, as well as early surgery may avoid the use of venous filters preoperatively.Venous wall invasion seems to be related with a greater incidence of lymph node disease, but these patients are candidates to intention-to-cure radical surgery. Thrombus level is not a prognostic factor per se, but it should be taken into consideration for surgical planning. After radical surgery survival rates achieved are similar to those of tumors without venous thrombus.

We present a simple technique for facilitating accurate polytetrafluoroethylene chordal height adjustment in surgical repair of myxomatous mitral valve disease. This approach is based on the annulus as the reference level. The artificial chordae are first fixed to the corresponding papillary muscle. Each chordal pair is then attached to the free edge of the prolapsed leaflet, and subsequently, the leaflet edge is also attached to the adjacent annulus by temporary fixing sutures. As a result, the leaflet is gently folded. Finally, the polytetrafluoroethylene suture is knotted during proper apposition of the free edge of the leaflet to the annulus.

Subvalvular preservation is beneficial in patients undergoing mitral valve replacement, especially in degenerative mitral regurgitation. Its feasibility and benefit is less evident in rheumatic disease. Our aim was to study the impact of preservation techniques in rheumatic patients and determine risk factors for mortality.Five hundred sixty-six rheumatic patients undergoing mitral valve replacement between 1996 and 2006 have been included. One hundred fifty-six patients had complete excision of the subvalvular apparatus (group 1), 248 had preservation of the posterior leaflet (group 2), and 162 had total chordal preservation (group 3). Echocardiography was performed preoperatively, at discharge, at 1 year, and at late follow-up.Reduction of ventricular volume was greater in groups 2 and 3, especially if previous mitral regurgitation or mixed disease were present. In mitral stenosis, valve resection caused postoperative increase of volume. Ventricular ejection and pulmonary hypertension had better outcome with valve preservation. Valve resection was associated with late mortality (hazard ratio, 2.64; p0.05), and complete chordal preservation was protective (hazard ratio, 0.31; p = 0.13). Actuarial survival (130 months) was better in group 3: 77.18% +/- 0.04%, 85.38% +/- 0.03%, and 93.22% +/- 0.02%, respectively (p0.01 group 1 versus group 3). Group 1 exhibited more low cardiac output syndrome (p0.01) and more patients in New York Heart Association functional class III and IV at last follow-up: 17.8% versus 3.9% and 2.0% (p0.001).Complete chordal preservation is possible in a large percentage of rheumatic patients. Greater decrease of ventricular volume is obtained for mitral regurgitation. In mitral stenosis, subvalvular preservation may avoid postoperative ventricular dilatation. Consequently, ventricular ejection, pulmonary hypertension, and clinical outcomes may improve with time.

Nowadays atrial fibrillation is usually treated simultaneously with cardiac procedures, and new cryo-systems have been developed for performing easier and faster intraoperative ablation. However, the old cryode designs can still be useful in surgical practice and represent a more cost-effective method. In this article we present a technique using old-fashioned cryodes for intraoperative treatment of atrial fibrillation and comment on its advantages and limitations.

We measured cyclic GMP formation and relaxation response to sildenafil given either alone or in combination with sodium nitroprusside (SNP) in pulmonary arteries obtained from 13 multi-organ donors. Sildenafil (10(-9)-10(-4) M) caused concentration-dependent relaxations and amplified the relaxation induced by SNP. Relaxation was unaffected by endothelium removal or by pre-treatment with the inhibitor of nitric oxide synthase L-NMMA (10(-4) M). SNP (10(-7) M) caused elevation of cyclic GMP levels that was potentiated by sildenafil (10(-6) M). Thus, the enhancement of SNP-induced relaxation by sildenafil is mainly due to an increase in cyclic GMP accumulation.

Background We recently reported that endothelium-dependent relaxation is impaired in forearm veins from patients with chronic renal failure. However, assessment of responses to norepinephrine remains controversial. We examined the contractile response to norepinephrine in forearm veins from patients on chronic hemodialysis and the role of nitric oxide (NO), prostanoids, and Ca 2+ -activated K + channels in this response. Methods Isometric contraction curves were obtained in rings of forearm vein from 21 dialyzed patients and 12 multiorgan donors in response to norepinephrine (1 nmol/L to 10 μmol/L) or KCl (5 to 100 mmol/L). Results Veins from uremic patients were markedly less responsive to norepinephrine (7.6 ± 0.6 g) and KCl (6.0 ± 0.3 g) than those from organ donors (12.0 ± 0.7 g and 10.4 ± 0.5 g, respectively, P N G -monomethyl- l -arginine (100 μmol/L), an inhibitor of NO synthase, or indomethacin (10 μmol/L), an inhibitor of prostacyclin synthesis, increased the response to norepinephrine in veins from control subjects but not in veins from dialyzed patients. Additional blockade of Ca 2+ -activated K + channels did not correct the hyporesponsiveness. In veins incubated in Ca 2+ -free solution containing either 100 mmol/L KCl or 1 μmol/L norepinephrine, addition of calcium chloride (0.1 to 30 mmol/L) elicited contractile responses that were significantly lower in veins from dialyzed patients. Conclusions The results demonstrate that norepinephrine-mediated contractions of forearm veins are markedly decreased in dialyzed patients. Endothelium-derived relaxing factors are not involved in this effect. The reduced contractile response is most likely caused by a decreased calcium entry through voltage- and receptor-dependent calcium channels.

Objective: We studied the intervention of nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) in mediating responses to acetylcholine in thyroid arteries from euthyroid and methimazole-treated (MT) patients. Design and methods: Branches of the superior thyroid artery were obtained from 19 euthyroid patients and 17 MT patients (euthyroid at the time of surgery) undergoing total thyroidectomy or hemithyroidectomy. Artery rings were suspended in organ baths for isometric recording of tension. Results and conclusions: Acetylcholine caused endothelium-dependent relaxation of greater magnitude in arteries from MT patients (pD2 (−log EC50) values were 7.68±0.19 in euthyroid and 8.17±0.26 in MT patients, P l-arginine (l-NMMA). This reduction was higher in arteries from MT patients (50±6%) as compared with euthyroid patients (36±6%) (P + channels using apamin combined with charybdotoxin or high K+ solution abolished the relaxation resistance to l-NMMA and indomethacin. The maximal contraction response to noradrenaline (as a percentage of the response to 100 mM KCl) was lower in MT than in euthyroid patients (57±10 and 96±8 respectively, P < 0.05). The hyporesponsiveness to noradrenaline in arteries from MT patients was corrected by l-NMMA. The results indicate that: (i) thyroid arteries from MT patients show an increased relaxation response to acethylcholine and a decreased contraction response to noradrenaline due to overproduction of NO; (ii) EDHF plays a prominent role in acetylcholine-induced relaxation through activation of Ca2+-activated K+ channels; (iii) the abnormal endothelium-dependent responses in arteries from MT patients are not corrected by medical treatment.

Background Atrial fibrillation is one of the most common complications of cardiac surgery. Beta blockers have been demonstrated to decrease the incidence of postoperative atrial fibrillation. Preliminary investigations reporting sotalol and atenolol to be effective in preventing postoperative atrial fibrillation are encouraging, but no studies have been conducted comparing both drugs. Methods A total of 253 consecutive eligible patients (66 ± 8 years; mean ± standard deviation) scheduled to undergo cardiac surgery were enrolled in this study. Patients were randomized in a prospective open manner 1.5:1 to atenolol group (50 mg/daily; 153 patients) or sotalol group (80 mg twice daily; 100 patients). Results Atrial fibrillation occurred in 44/253 patients (17.45%). A significant difference was found in the occurrence of atrial fibrillation in the atenolol group (34 patients, 22%) compared with those receiving sotalol (10 patients, 10%; p = 0.013). Therapeutic efficiency and efficacy was 12% and 54%, respectively. Stepwise logistic regression analysis revealed that age more than 68 years old (odds ratio=2.72; 95% confidence interval [CI] = 1.37–5.41; p = 0.004), the use of β-adrenergic agents (odds ratio=2.74; 95% CI=1.5–5; p = 0.001), and sotalol (odds ratio=0.46; 95% CI=0.23–0.95; p = 0.035) were independently associated with development of atrial fibrillation. Conclusions Oral low-dose sotalol provides a considerable reduction in the occurrence of atrial fibrillation. A selective approach based on clinical risk prediction should decrease the occurrence of atrial fibrillation after cardiac surgery.

Background The objective of this study was to characterize the neurogenic contraction and relaxation of the human gastroepiploic artery and to determine whether the responses are mediated by nitric oxide (NO) from neural or endothelial origin. Methods Rings of human gastroepiploic artery were obtained from 18 patients (12 men, 6 women) undergoing gastrectomy. The rings were suspended in organ baths for isometric recording of tension. We studied the contractile and relaxant responses to electrical field stimulation. Results In arteries under resting conditions, electrical field stimulation (2 to 8 Hz) caused frequency-dependent contractions that were of greater magnitude in arteries denuded of endothelium and blocked by tetrodotoxin (10−6 mol/L). The inhibitor of NO synthesis NG-monomethyl- l -arginine (L-NMMA, 10−4 mol/L) increased contractile responses only in arteries with endothelium. In preparations contracted with norepinephrine in the presence of guanethidine (10−6 mol/L) and atropine (10−6 mol/L), electrical stimulation induced frequency-dependent relaxations. This neurogenic relaxation was prevented by L-NMMA (10−4 mol/L) and tetrodotoxin (10−6 mol/L), but was unaffected by removal of the endothelium. Conclusions The results provide functional evidence that NO is released by autonomic nerves of the human gastroepiploic artery. We hypothesize that the release of NO from both endothelial and neurogenic origin may modulate resistance of the human gastroepiploic artery. Dysfunction in any of these sources of NO should be considered in some form of vasospasm.

Objective: We investigated the potentiating effect of U-46619, a synthetic analogue of thromboxane A2 (TXA2), on the adrenergic responses in human saphenous vein. Methods: Saphenous vein rings were obtained from 35 patients undergoing coronary artery bypass surgery. The rings were suspended in organ bath chambers for isometric recording of tension. Results: U-46619 (10−10–3×10−7 mol/l) produced concentration-dependent and endothelium-independent contractile responses. U-46619 (10−10 mol/l) potentiated the contractions elicited by electrical stimulation and potassium chloride, and produced leftward shifts of the concentration–response curve for noradrenaline. The TXA2 receptor antagonist SQ-30741 (10−8 mol/l) prevented the potentiation evoked by U-46619. The dihydropyridine calcium antagonist nifedipine (10−6 mol/l) did not affect the potentiation of electrical stimulation and noradrenaline induced by U-46619, but abolished the potentiation of U-46619 on KCl-induced contractions. Conclusions: U-46619 facilitates sympathetic neurotransmission and potentiates constrictor effects of noradrenaline in human saphenous veins through stimulation of TXA2 receptors. These effects are independent of calcium entry through dihydropyridine calcium channels.

Objectives. To investigate the effects of sildenafil on human penile blood vessels and evaluate the interaction of sildenafil with neurogenic-mediated responses. Sildenafil is currently used in the treatment of erectile dysfunction. Methods. Penile dorsal arteries and deep dorsal veins were obtained from 14 multiorgan donors. Vascular rings were suspended in organ bath chambers, and the isometric tension was recorded. We then studied the effects of sildenafil on precontracted vessels and the neurogenic (noradrenergic and nitrergic) responses. Results. Sildenafil (10 −9 to 3 × 10 −6 M) caused concentration-dependent relaxation and amplified the relaxation induced by sodium nitroprusside. Relaxation was unaffected by the inhibitor of nitric oxide synthase N G -monomethyl- l -arginine (10 −4 M). Compared with zaprinast, sildenafil was 8 to 10 times more potent in terms of the median effective concentration (EC 50 ) values. Electrical field stimulation of the vessels under resting tension caused frequency-dependent contractions that were attenuated in the presence of sildenafil. When penile vessels were contracted after blockade of norepinephrine release with guanethidine (10 −6 M), electrical stimulation induced frequency-dependent, nitric oxide-dependent relaxations that were enhanced by sildenafil. Conclusions. These results indicate that the relaxation of human penile arteries and veins induced by sildenafil involves inhibition of noradrenergic contraction, enhancement of neurogenic nitric oxide-mediated relaxation, and inhibition of smooth muscle contraction.

Kent bundles are seldom visualized at operation, but, in the patient described, the pathway was subepicardial, running superficial to the right coronary artery. This was probably why radiofrequency ablation failed. When this unusual pathway course is encountered, the epicardial approach should be used at operation.