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BACKGROUND: Optimal anti-thrombotic therapy for acute coronary syndromes (ACS) should suppress pro-thrombotic activity at the site of plaque rupture. We sought to determine whether platelet reactivity is increased in blood in the immediate vicinity of a ruptured plaque and is apparent even when blood is obtained by sampling from a catheter placed proximal to the lesion. METHODS: Blood was obtained from a catheter placed in the aorta and from the same catheter after engaging the culprit coronary artery. Platelet reactivity was determined with the use of flow cytometry by surface expression of P-selectin. RESULTS: In preliminary studies we demonstrated that a marker of thrombin activity, fibrinopeptide A, was similarly increased in blood taken from the coronary sinus and coronary arterial ostium of patients with ACS. Subsequently blood was obtained from the aorta and coronary arterial ostium through a coronary guide catheter for assessment of platelet reactivity in 23 subjects with ACS and 22 subjects with stable angina. The percentage of platelets expressing P-selectin in response to 0.2 microM adenosine diphosphate (ADP) was greater in coronary arterial samples from patients with ACS (aorta=6.1+/-1%, coronary artery=8.8+/-1.6%, p=0.02) compared with that in patients with stable symptoms (aorta=6.9+/-1.2, coronary artery=6.5+/-1.4, p=NS). CONCLUSIONS: Coronary arterial blood obtained from the ostium through a coronary guide catheter can be used to determine whether thrombin activity and platelet reactivity are increased in the immediate vicinity of a ruptured atherosclerotic plaque. The simplicity of the approach developed should facilitate its use in future studies designed to determine the impact of optimal suppression of platelet reactivity and the pro-thrombotic state before coronary interventions on short- and long-term clinical outcomes.

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Replacing the mitral valve with a pulmonary autograft is an important option at the disposal of surgeons working in areas where lifelong anticoagulation is impractical. In this article we describe the technique of this operation as it has evolved through our experience with 51 patients operated on since July 1997.

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BACKGROUND: Platelet activation is pivotal in the pathogenesis of complications after percutaneous coronary interventions (PCI). We previously reported substantial interindividual variability in activation of glycoprotein (GP) IIb/IIIa in response to a low concentration of ADP. We assessed GP IIb/IIIa activation prospectively to determine whether this could differentiate patients at low risk from those at high risk for complications early and late after PCI. Methods and Results-- A total of 112 patients undergoing PCI were studied. Platelet reactivity was determined with the use of flow cytometry. Patients were classified into high and low platelet reactivity groups on the basis of extent of activation of GP IIb/IIIa in response to 0.2 micromol/L ADP. The median value was used for differentiation. The incidence during 90-day follow-up interval of a composite end point (myocardial infarction, urgent revascularization, or repeat revascularization) was determined in each group. Follow up was completed in all 112 patients. The 2 groups were similar with respect to diverse clinical characteristics. Nevertheless, the incidence of the composite end point occurred in 26.8% of the high and 7.1% in the low platelet reactivity group (P=0.01). The difference in the composite end point was most striking during the 30- to 90-day interval after PCI (16.7% versus 1.9%; P=0.02). Repeat revascularization was more frequent in those with increased platelet reactivity (17.9% versus with 3.6%, P=0.029). CONCLUSIONS: Prospective assessment of platelet GP IIb/IIIa activation permits stratification of patients into low- and high-risk groups with respect to adverse events after PCI.

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OBJECTIVES: In an effort to find a suitable mitral substitute for our young rheumatic patients who cannot follow a proper anticoagulation regimen for life, we resorted to an old concept reported by one of the authors (D.N.R.) in 1967. This report summarizes our experience with the Ross-mitral operation to date. METHODS: Between 19 June 1997 and 27 June 2000, 43 patients with rheumatic valve disease underwent the Ross-mitral operation. Two patients were excluded because of graft stenosis detected at the end of the procedure for which the autograft had to be sacrificed. Of the remaining 41 patients 29 were female, and the age range was 12--57 years (median 39 years). The autograft was incorporated within a Dacron tubing, with a pericardial collar attached to its proximal end. The conduit was sutured distally to the excised mitral annulus; the pericardium was attached proximally to the atrial wall in 36 patients, and was used simply to cover the Dacron tubing in five patients. The pulmonary artery was replaced with a pulmonary or aortic homograft, or with a pulmonary xenograft. RESULTS: There were two hospital fatalities from a cerebrovascular accident and a lung injury, and two postoperative myocardial infarctions. There were five late deaths, two due to bacterial endocarditis, one due to excessive bleeding at reoperation for a paravalvular leak, and two not related to the procedure. A phenomenon of 'autograft stenosis' occurred intraoperatively in four recent consecutive patients that probably resulted from our use, for the first time, of softer Dacron tubing material. This was repaired in two of the four patients. Echocardiography confirmed excellent functioning of all 34 autografts of surviving patients up to 36 months postoperatively (mean follow-up 18.2 months). Two patients remain in functional Class III status, one due to left heart failure following myocardial infarction, and the other due to recurrent tricuspid insufficiency. CONCLUSIONS: We believe that the mitral pulmonary autograft is a worthwhile alternative to mechanical prostheses in developing countries.

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OBJECTIVES: The goal of this study was to evaluate the difference in the respiratory change from expiration to inspiration (%E) between pulsed Doppler mitral inflow (MV) and pulmonary venous flow (PV) velocities in patients with constrictive pericarditis (CP) and to describe the influence of atrial fibrillation (AF). BACKGROUND: The difference in %E between MV and PV velocities as well as the influence of AF on %E has not been well described. METHODS: Pulsed-wave Doppler transesophageal echocardiography (TEE) was performed with respiratory monitoring in 31 patients with CP and sinus rhythm (SR) and in 10 patients with CP and AF. The MV early (E) and late diastolic (A) velocities and their velocity time integral (VTI) as well as PV systolic (S) and diastolic (D) velocities and their VTI were measured. RESULTS: Regardless of the cardiac rhythm: 1) The MV-E velocity and E-VTI as well as PV-D velocity and D-VTI significantly decreased from expiration to inspiration; 2) the %E in PV-D velocity (27% in SR and 35% in AF) and D-VTI (38% in SR and 45% in AF) was significantly greater than that in MV-E velocity (18% in SR and 15% in AF) and E-VTI (21% in SR and 19% in AF), respectively; 3) the PV S/D and S/D-VTI significantly increased from expiration to inspiration. CONCLUSIONS: A significant respiratory variation was observed in both MV and PV velocities in CP, not only in patients with SR but also in those with AF. Moreover, the %E was greater in the PV velocities than it was in the MV velocities. Evaluation of the %E in the PV velocities using TEE can be a sensitive diagnostic strategy for evaluation of patients with CP, even in patients with AF.

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BACKGROUND: After exposure of platelets to abciximab and tirofiban in vitro, we have observed variable inhibition of fibrinogen binding and a lack of inhibition of alpha-granule degranulation. DESIGN: To determine whether such changes occur with treatment, platelet reactivity was assayed in blood from 50 patients receiving abciximab or tirofiban. METHODS: Platelet reactivity was determined before and during steady-state infusions of abciximab (0.125 microg/kg/min) or tirofiban, with either the PRISM-PLUS dosage (0.1 microg/kg/min) or the RESTORE dosage (0.15 microg/kg/min). Fibrinogen binding and P-selectin expression were determined by flow cytometry after stimulation of platelets with ADP (0.2 or 1 microM) or thrombin-receptor agonist peptide (TRAP, 25 microM). RESULTS: Both dosages of tirofiban and abciximab reduced fibrinogen binding in response to 0.2 microM ADP comparably. However, fibrinogen binding in response to 1.0 microM ADP or 25 microM TRAP was inhibited to a greater extent by the RESTORE dosage of tirofiban and abciximab than by the PRISM-PLUS dosage of tirofiban (P< 0.05). Furthermore, only the RESTORE dosage of tirofiban and abciximab reduced P-selectin expression in response to ADP. Inhibition with each regimen varied markedly between patients. CONCLUSIONS: The RESTORE dosages of tirofiban and abciximab each inhibit fibrinogen binding and alpha-granule degranulation similarly. However, substantial interindividual variation in inhibition of fibrinogen binding is evident.

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BACKGROUND AND AIM OF THE STUDY: The study aim was to alert surgeons embarking on mitral replacement with the pulmonary autograft to the possibility of graft stenosis resulting from kinking of the Dacron tube support. METHODS AND RESULTS: After having used old-style Dacron tubing for pulmonary autograft support in 32 patients, a change was made to a softer variety. This, together with routine retention of the posterior subvalvular apparatus, resulted in Dacron tube angulation and autograft stenosis detected at intraoperative echocardiography in four consecutive patients, This sequela was corrected in one patient by re-adjusting the pericardial collar, and in another by severing the retained chordae. However, in two patients it was necessary to sacrifice the autograft and replace it with a mechanical prosthesis. When the reason for the complication was identified, and a return to the use of a firmer Dacron material instigated, this phenomenon disappeared and surgery was completed in the final three patients, without mishap. CONCLUSION: The use of a newer soft Dacron tubing to support the pulmonary autograft in mitral replacement might result in autograft stenosis. Thus, a firm-type Dacron should be used for this operation.

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Clinical heart failure with normal systolic function is suggestive of diastolic dysfunction. This can result from myocardial or pericardial disorders. Myocardial disorders are a broad range of pathologies leading to restrictive physiology. Amyloidosis is a prototype of restrictive cardiomyopathy leading to diastolic dysfunction. Pericardial disorders leading to diastolic heart failure are usually in the form of constrictive physiology. Differentiation between restrictive and constrictive pathologies is often difficult and require careful attention to hemodynamic and Doppler echocardiographic features.

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OBJECTIVE: To review our early experience with left ventricular volume reduction surgery (the Batista operation) in the management of patients with end-stage heart failure. METHODS: Between December 1996 and April 1998, 10 patients (9 males, mean age 32yr) with advanced symptomatic cardiomyopathy underwent left ventricular volume reduction surgery at Damascus University Cardiovascular Surgical Center. The cause of cardiomyopathy was idiopathic in three patients, valvular in four, ischemic in two, and viral myocarditis in one patient. Concomitant procedures included aortic valve replacement in four patients, mitral valve repair in six patients, and coronary artery bypass grafting in two patients. RESULTS: All patients survived the procedure. Echocardiography prior to discharge documented significant improvement in ejection fraction in all but two patients. Mean follow-up was 7.6 months. After discharge, three patients developed progressive congestive heart failure to which they subsequently succumbed, and two more patients died suddenly late postoperatively. Only two patients continue to show both clinical and echocardiographic evidence of improvement. CONCLUSION: Left ventricular volume reduction surgery cannot be freely advocated until better means are found to identify patients who will benefit from the procedure, and proper prophylaxis against fatal postoperative complications can be afforded.

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BACKGROUND AND AIM OF THE STUDY: For long-term substitution of the mitral valve, mechanical prostheses require life-long anticoagulation which is impractical in developing countries, xenografts degenerate early in our young population, and mitral homografts have not yet been established as being suitable. We therefore returned to an original concept first reported by one of the authors (D.N.R.) in 1967. METHODS: Between July 1997 and November 1998, 22 patients (mean age 40.3 years; range: 28 to 57 years) with rheumatic mitral valve disease unsuitable for reconstruction were subjected to excision of their pulmonary valve in the standard fashion of the Ross procedure. The inverted autograft was incorporated in a 2.5 cm-long Dacron conduit, with a pericardial collar attached to its proximal end. The distal end of the autograft-conduit was sutured to the annulus of the excised mitral valve, and the proximal end incorporating the pericardial collar was attached to the adjacent atrial wall. In this way all prosthetic material was covered. The right ventricular outflow was reconstructed with a pulmonary homograft in 17 patients, with an aortic homograft in two, and with a porcine pulmonary xenograft in three. RESULTS: One patient developed a fatal cerebrovascular accident, probably related to an incorrectly placed pericardial collar with rough surface exposed to the blood flow. In a second patient the autograft had to be replaced six weeks after operation due to bacterial endocarditis contracted in the operating room. Echocardiography confirmed excellent function of the remaining autografts up to 16 months postoperatively (mean follow up 8.3 months). CONCLUSIONS: We believe the pulmonary autograft to be a valid option for mitral valve replacement in our patients.

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BACKGROUND: We report our early experience with partial left ventriculectomy done by a group of cardiac surgeons in the Asia-Pacific region. METHODS: Partial left ventriculectomy was done in 48 patients (mean age, 43 years) with advanced symptomatic cardiomyopathy. The origin of cardiomyopathy was idiopathic in 30 patients, valvular in 10, ischemic in 3, peripartum in 3, sarcoidosis in 1, and viral myocarditis in 1. Procedures performed on the mitral valve were repair with Alfieri method in 8 patients, ring annuloplasty in 2, and replacement in 25. RESULTS: Seventy-seven percent of patients required myocardial support for weaning from cardiopulmonary bypass, and the overall in-hospital mortality rate was 27%. Mean follow up was 6.5 months (range, 1 to 18 months), and patient survival at 1, 3, and 6 months after discharge was 91%, 88%, and 84%, respectively. Sixty-five percent of survivors with idiopathic and valvular disease achieved significant and sustained improvement in ventricular contractility and symptoms, but there were no clear symptomatic benefits from partial left ventriculectomy in patients with cardiomyopathy from other causes. Most cases of late recurrence of heart failure symptoms (90%) appeared to be related to the development of progressive mitral incompetence. CONCLUSIONS: After partial left ventriculectomy left ventricular function improved in patients with idiopathic and valve related cardiomyopathies. Late deterioration was related to the development of significant mitral valve incompetence postoperatively, hence definitive mitral valve repair or replacement at the time of the partial left ventriculectomy procedure is advised.

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Between October 1978 and June 1993, 24 consecutive operations for atrial myxoma were performed on 23 patients at the Damascus University Cardiovascular Surgical Center, using the biatrial approach. Fifteen of the patients were female; ages ranged between 4 and 71 years. Nineteen patients had symptoms of left and 3 of right atrioventricular obstruction. One patient presented with a cerebrovascular accident, and another with recurrent emboli to the lower extremities. Ten patients had constitutional manifestations. Diagnosis was established preoperatively in all patients by echocardiography with or without angiocardiography. Twenty-one patients had left atrial myxoma, 1 of whom had a double lesion. Two patients had right atrial myxoma; in 1 of them it extended to the left atrium. This last patient had the only recurrence in the series, which was removed 7 years after the initial operation. All tumors were excised with a wide margin of full-thickness septum. Four patients had concomitant mitral valve reconstruction. There was no hospital mortality, and follow-up did not reveal any other complication related to the operation.

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Four patients with echinococcosis of the heart are presented. The diagnosis was suspected or established before operation by serology, echocardiography and cardiac catheterization. The sites affected were the right and left atria, left ventricular apex and interventricular septum. The right and left atrial cystic masses simulated atrial myxoma, with brain embolization from the latter. The cyst in the interventricular septum was discovered on routine echocardiography in a patient with disseminated hydatidosis. All patients successfully underwent excision of their cysts under temporary cardiopulmonary bypass, and are doing well up to 2 years and 8 months afterwards on medical therapy.

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During a period of 6 years and 5 months, a group of 26 men and 16 women between 53 and 80 years of age underwent combined coronary artery bypass and mitral valve replacement. All patients were catheterized preoperatively, and hemodynamic and surgical variables were noted. In accordance with the variables, operative mortality was evaluated and compared among subgroups. Eight patients died, and the factors found to adversely change successful treatment were instability of ischemia, advanced New York Heart Association functional class, severe mitral regurgitation, associated aortic regurgitation, extensive coronary artery disease, the extent of left ventricular dysfunction as estimated by left ventricular end-diastolic pressure and ejection fraction, and elevated pulmonary vascular resistance. Prolonged operative time was also significant. The only variable that did not seem to influence mortality was the pathology type of mitral valve involvement. Analysis of our data confirms the high risk of coronary artery by pass combined with valve replacement for mitral regurgitation reported by others, and it appears advisable at present to exercise caution in recommending combined coronary artery by pass and mitral valve replacement in patients with extensive coronary artery disease and advanced left ventricular dysfunction. Pre-and postoperative utilization of afterload reduction, with the use of circulatory assist devices, may prove effective in some patients, and deserves special evaluation.

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