[Echocardiography versus cardiac catheterization for surgical indications in the era of DRG: cost-benefit analysis].
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Biomedical subjects
Publications and source records attributed to B Marino.
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The aim of this study was to analyse the risk factors in patients undergoing closed heart commissurotomy (CHC). From 1956 to 1978 a total of 630 patients with severe mitral stenosis underwent CHC at this Institute. The study was performed on a sample of 100 patients. Follow-up was performed using data taken from the Institute archives, questionnaires sent to the doctors in charge, telephone interviews or visits to outpatient clinics by the Institute's medical staff. The mortality rate 30 days after surgery was 2.9%. Re-CHC was necessary in 11 patients after a mean interval of 7.2 years. The overall probability of survival was 83%, 71%, 48% an 33% respectively at 10, 20, 30 and 40 years. Survival free from mitral re-operation at 10, 20, 30 and 40 years was 76%, 39%, 29% and 11% respectively. The probability of incidence for central and peripheral thromboembolism was 38%, 26%, 11% and 4% at 10, 20, 30 and 40 years. Mitral valve replacement surgery (MVR) was performed in a total of 64 patients. Operative mortality was 0.6% (1 patient). The mean duration of follow-up in patients undergoing post-CHC MVR was 10 years. The probability os survival in overall terms and free of cardiac decompensation was 79 and 53% respectively. From this study it is clear the CHC is a surgical procedure that offers excellent long-term results with a low incidence od thromboembolic events, very low costs and a good quality of life. CHC currently represents a valid alternative o mitral valve replacement in selected patients.
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Atrioventricular canal defects (AVCD) constitute the predominant congenital heart defect in Down syndrome. For this reason, a candidate gene involved in atrioventricular canal development was previously searched and excluded in dominant pedigrees of AVCD, using linkage analysis of polymorphisms from chromosome 21. Because of the striking association between 8p deletion and AVCD, a search for an AVCD gene was carried out in two pedigrees of individuals with autosomal dominant AVCD using a set of DNA markers of the 8pter-->q12 region. These two families include affected individuals and subjects who have transmitted the defect but are not clinically affected. Two-point lod scores were significantly negative for all markers at penetrance levels of 90% and 50%. Multipoint analysis excluded the region covered by the markers LPL-D8S262 and 30 cM to either side of this area. This result corroborates heterogeneity of this heart defect and indicates that the genetic basis of familial AVCD is different from AVCD associated to either trisomy 21 or 8p deletion.
We have characterized the extent and the phenotype of total and proliferating cell population of aortic plaques in aged rabbits receiving a long-term low-dose cholesterol hyperlipemic diet, which represents an experimental model of atherosclerosis. For nine months, rabbits received the hypercholesterolemic diet alone or in addition to a treatment with propionyl-L-carnitine (PLC), a derivative of carnitine, an intramitochondrial carrier of fatty acids present in most cell types. We observed that, in both PLC-treated and control hyperlipemic rabbits, the ratio between proliferating macrophage-derived and smooth muscle cells was 2:1. PLC in addition to the hypercholesterolemic diet induced a marked lowering of plasma triglycerides, very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) triglycerides, while plasma cholesterol was slightly and transiently reduced. Moreover, PLC-treated hyperlipemic rabbits exhibited a reduction of plaque thickness and extent, a slight but significant reduction of the percentage of macrophage-derived cells as compared to control hyperlipemic animals and a reduction of the number of both proliferating macrophage- and smooth muscle cell-derived foam cells. Finally, both proliferating and non-proliferating plaque cells expressed large amounts of macrophage colony-stimulating factor protein, in particular macrophage-derived foam cells. These results indicate that a modification of plasma lipemic pattern obtained by a long-term oral administration of PLC was associated with a decrease of plaque cell proliferation and severity of aortic atherosclerotic lesions.
BACKGROUND: The pathogenesis of posterior papillary muscle dysfunction is poorly understood. We hypothesized that papillary muscle perfusion pattern may explain the higher prevalence of posterior papillary muscle dysfunction after myocardial infarction. METHODS AND RESULTS: Twenty patients were monitored by transesophageal echocardiography during coronary surgery. Superselective coronary graft injections of 0.2 to 0.5 mL of sonicated albumin microbubbles were performed to assess graft patency and papillary muscle perfusion. Thirty-five graft injections were analyzed: 13 in the right coronary artery, 15 in an obtuse marginal branch, 1 in the left anterior descending coronary artery, and 6 in the first diagonal branch. The posterior papillary muscle was opacified in 16 patients, 11 from the right coronary artery and 5 from one obtuse marginal branch. In 10 of 16 patients (63%), the papillary muscle was perfused by one vessel, while in 6 of 16 (37%), it was perfused by two vessels. The anterior papillary muscle was opacified in 14 patients. Ten patients (71%) had double-vessel and 4 (29%) had single-vessel supply. In the subgroup of 10 patients with old inferior myocardial infarction, mitral regurgitation was present only among those 6 with single rather than double blood supply (P < .05). CONCLUSIONS: Myocardial infarction may cause papillary muscle dysfunction when the blood supply is provided by one rather than two vessels, as is more frequently the case with the posterior rather than the anterior papillary muscle.
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Tetralogy of Fallot (TF) is a congenital conotruncal heart defect commonly found in DiGeorge (DGS) and velo-cardio-facial (VCFS) syndromes. The deletion of chromosome 22q11 (del22q11) is a well established cause of DGS and VCFS, and it has been demonstrated also in sporadic or familial cases of TF. In order to investigate the prevalence of del22q11 in patients with TF, we analyzed the DNA of 137 consecutive patients with syndromic and isolated TF, using the HD7k probe, which detects hemizygosity for the D22S134 locus. Del22q11 has been detected in 11/26 (42%) syndromic patients. Evidence for hemizygosity was obtained in all patients with DGS and in 8/15 patients with VCFS. None of the 107 patients with isolated TF had del22q11. Our experience suggests that children with TF and del22q11 always present major or minor extracardiac anomalies. These features, including subtle facial dysmorphisms, should be checked routinely in patients with TF and other conotruncal heart defects.
UNLABELLED: Among 41 consecutive children with classic Noonan syndrome, 27 patients (66%) presented cardiac anomalies. Eight patients (19.5%) had a congenital anomaly of the mitral valve consisting of 5 with partial atrioventricular canal defect and 3 with anomalous insertion of the mitral valve on the ventricular septum. Five patients (12%) presented with a significant left ventricular outflow tract obstruction caused by the anterior leaflet of the mitral valve: two cases with atrioventricular canal and three cases with isolated anomalous insertion of the mitral valve. Echocardiography is the best tool for the diagnosis. Cardiac defects of patients with Noonan syndrome may be explained on the basis of anomalies of the extracellular matrix involving cardiac valves including the mitral valve. CONCLUSION: In children with Noonan syndrome and left ventricular hypertrophy a careful echocardiographic assessment of the mitral valve should reveal those in whom the left ventricular outflow tract obstruction is anatomical in nature.
Dobutamine echocardiography has recently been introduced for use in identification of viable myocardium in patients with acute myocardial infarction and prediction of the response of dysfunctioning myocardial segments to coronary angioplasty. The aim of this study was to evaluate whether this test may be used to predict the early response of dysfunctioning myocardial segments to surgical revascularization. We studied 30 patients with three-vessel disease and chronic, stable angina pectoris during coronary artery bypass grafting (CABG). Patients were monitored by intraoperative transesophageal echocardiography in the transgastric short-axis view at the papillary muscle level. The left ventricle was divided into eight segments; and 240 myocardial segments were analyzed. Percentage of systolic wall thickening (PSWT) was calculated in each segment at baseline (early after pericardiectomy), before bypass during dobutamine infusion (5 micrograms/kg/min), and after separation from cardiopulmonary bypass. Segments showing PSWT < 30% at baseline were considered dysfunctional. Segments showing an increase in PSWT > 10% during dobutamine infusion were considered responders. Segments showing an increase in PSWT < 10% during dobutamine infusion were considered nonresponders. At baseline, 161 (67%) of 240 segments had PSWT < 30% (dysfunctioning segments). During dobutamine, 98 (60%) of these segments increased PSWT > 10% (from 11.3% +/- 7.6% to 24.2% +/- 12.0%, p < 0.01; responder segments), and 63 (40%) increased PSWT < 10% (from 10.2% +/- 4.9% to 8.3% +/- 5.5%, p value not significant [NS]; nonresponder segments).(ABSTRACT TRUNCATED AT 250 WORDS)
The hypothesis that nicorandil might enhance myocardial protection due to cold St Thomas' Hospital (STH) solution ([K+]o 16 mmol/l) through opening of cardiac KATP channels was assessed in isometrically contracting guinea-pig papillary muscles submitted to 120 min of cardioplegic hypoxia followed by 60 min of normothermic reoxygenation. Right ventricular papillary muscles were paced (2 ms, 4 mA) in an organ bath and superfused with oxygenated (O2 content 16 ml/l) Tyrode's solution (37 degrees C). The force-frequency relationship in the range 1600-300 ms cycle length (CL) was studied. Preparations were randomized to receive 120 min cold (20 degrees C), non-oxygenated (O2 content 5 ml/l) STH solution while continuously stimulated at 1600 ms CL, with: (1) saline (No-additive, n = 12); (2) DMSO 1% (Vehicle, n = 8); (3) nicorandil 1 mmol/l (n = 8); (4) nicorandil 1 mmol/l plus glibenclamide 1 mumol/l, the latter also given, before STH solution, in Tyrode's solution for 15 min (n = 8); (5) glibenclamide 1 mumol/l, also circulated, before STH solution, in Tyrode's solution for 15 min (n = 8); (6) nitroglycerin 100 mumol/l (n = 4); in addition, we studied: (7) STH solution with no-additive and no-pacing (n = 4); (8) cold Tyrode's in place of cold STH solution (n = 4). Inotropic state was investigated by measuring: (i) velocity of developed tension (DT), obtained by dividing DT by time to peak tension; (ii) percentage (from precardioplegia values) velocity changes of DT; (iii) log velocity of DT. Post-cardioplegic recovery of contractility (including force-frequency relationship) was assessed in all preparations: (a) 60 min after reoxygenation with Tyrode's solution; (b) after further 15 min superfusion with the positive inotropic agent dobutamine (10 mumol/l). In parallel experiments, action potential duration (APD) 50% changes induced by nicorandil or glibenclamide plus nicorandil in spontaneously beating atrial (n = 4) or electrically driven (1600 ms CL) ventricular (n = 8) tissues during 10 min of STH solution were investigated. Based on force-frequency relationship, at 60 min reoxygenation, in absence of cardioplegia, the lowest recovery of myocardial contractility was seen (stunning). In STH solution, there was moderate to severe stunning, which was unaffected by removing pacing during cardioplegia, or by vehicle or nitroglycerin. In contrast, nicorandil improved recovery of contractility (F = 3.01, P = 0.0106). After dobutamine, nicorandil preparations showed the highest positive inotropic response, which was completely offset by glibenclamide (F = 3.47, P = 0.0046).(ABSTRACT TRUNCATED AT 400 WORDS)
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Myocardial distribution of cardioplegic solution infused by combined antegrade/retrograde routes was assessed with myocardial contrast echocardiography in 18 patients with chronic stable angina and three-vessel disease undergoing elective coronary artery bypass grafting. Overall myocardial opacification was significantly greater in retrograde than in antegrade cardioplegia (77.7% +/- 13.4% versus 59.1% +/- 15.7%; p = 0.0009). The difference was affected by collateral circulation, as pointed out by the significant interaction between coronary collateral circulation and percent of myocardial opacification after antegrade and retrograde cardioplegia (p = 0.002). When we performed multiple comparisons, in patients with good collaterals the opacification difference between antegrade and retrograde cardioplegia was not statistically significant (66.4% +/- 10.2% versus 76.0% +/- 15.2%; p = not significant), whereas in patients with poor collaterals myocardial opacification during retrograde cardioplegia was significantly greater (44.3% +/- 15.0% versus 81.2% +/- 9.0%; p < 0.02). During antegrade cardioplegia, patients with poor collaterals showed a lower degree of myocardial opacification than patients with good collaterals (44.3% +/- 15.0% versus 66.4% +/- 10.2%; p < 0.01). Our results show that retrograde cardioplegia in patients undergoing elective coronary artery bypass grafting offers no advantage over antegrade cardioplegia when collateral circulation is well developed. On the other hand, conventional aortic root infusion may not provide adequate myocardial protection in the subset of patients with significantly narrowed or occluded coronary arteries and poor collaterals.
Cardiopulmonary bypass (CPB) produces hemodynamic and inflammatory disorders involving changes in vascular permeability and regional blood flow and alterations of coagulation and complement systems. It has been reported that an abnormal release of vasoactive substances during CPB, like bradykinin or nitric oxide, could play a role. The aim of this study was to investigate the changes in nitric oxide (NO) release occurring in patients undergoing CPB, under both hypothermic and normothermic conditions. Forty patients (mean age 61.4 +/- 8.4 years) undergoing coronary bypass surgery were studied. In 20 patients (group A) systemic hypothermic CPB and antegrade cold intermittent crystalloid cardioplegia were used. The remaining 20 cases (group B) underwent surgery under systemic normothermic CPB and with antegrade warm blood intermittent cardioplegia. Nitric oxide was measured as the nitrite plasma level (NPL) by the Gries reaction. The time course of changes in NPL were obtained by collecting five whole blood samples: before CPB, 10 and 30 min after the start of CPB, and 10 and 60 min after the end of CPB. Although there were no significant variations of NPL shortly after the start of CPB (10 min after), values measured 30 min after CPB commencement and 10 min after the end of CPB showed a significant increase (P < 0.0001) in both groups. Considering the two groups separately, NPL changes seemed to be similar, so independent of temperature; however, in group B higher values of NPL were measured during (30 min) and after (60 min) CPB (P < 0.0001). In conclusion, during CPB there is a progressive increase, independent of temperature in NO release.
It is reported that the mortality rate for combined coronary bypass grafting and mitral valve replacement is greater than for either isolated operation. To evaluate the effects of various predicting factors we analyzed the results of 67 consecutive patients undergoing combined mvr and CABG. The mean age was 61.3 +/- 7 years. There were 55 males and 12 females and the mean follow-up was 59.4 +/- 7 months. The hospital mortality rate was 13.4% (9/67). Preoperative NYHA functional class (p<0.05), left-ventricular motion score (increased scores indicating impaired function, (p<0.05), and aortic cross-clamp time (p<0.05) were associated with hospital mortality. There was no significant relationship of age (>60), cause of mitral valve disease, severity of mitral regurgitation, number of grafts, or previous myocardial infarction with hospital mortality. There were 7 late deaths, and survival at five years was 76.1%. Although there was a trend for preoperative NYHA class and aortic cross-clamp time to be associated with late survival, the only factor significantly related to late survival was global wall-motion score (p<0.05). Severity of mitral regurgitation and cause of mitral valve disease have been reported as being related to late survival, but we have found no such relationship. Our results indicate that both hospital and late mortality are strongly correlated with preoperative left ventricular function.