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Publications and source records attributed to W Daenen.
A case is reported of recurrent intracerebral abscesses occurring in a patient with isolated drainage of a persistent left superior vena cava to the left atrium without causing cardiac symptoms or arterial desaturation. The diagnosis and therapy are discussed.
Total of 123 patients (mean age: 63.8 +/- 7.3 years, (male/female 65/35 percent) underwent mitral valve surgery combined with coronary artery bypass grafting during a seven year period. Preoperatively 12% of them belonged to NYHA functional class II, 54% to class III, 29% to class IV and 3% was operated under emergency conditions. The mitral valve lesion was most frequently either ischaemic (45%) or rheumatic (33%) in origin. Left ventricle function was moderately decreased in 18% and severely damaged in 3% of the patients as documented by preoperative ventriculography. Coronary surgery was performed in all cases with an average number of distal anastomosis of 2.2 +/- 1.1 per patient. The hospital mortality was 13%. Risk factors for early and late mortality were determined by univariate and multivariate analysis. Advanced preoperative functional class and decreased left ventricular function or ischaemic etiology were identified as significant risk factors for early mortality. The patients were followed for an average of 33 +/- 25 months. The majority of them experienced significant functional improvement postoperatively with 69% belonging to NYHA class I or II. The late survival for the 107 hospital survivors was 94.7% at one year, and 84.7% at five years, respectively. Late survival was independently determined by preoperative functional class or previous myocardial infarction. Freedom from ischemic and valve related complications at five years was 95% and 71.2% respectively. 58.2% of the hospital survivors were in functional class I or II and free of any valve related or ischemic complications at the end of the fifth follow up year.(ABSTRACT TRUNCATED AT 250 WORDS)
Between May 1st 1985 and December 31st 1992, 283 Carpentier-Edwards pericardial valves were implanted in 260 patients in the aortic (n = 196), mitral (n = 41) and both aortic and mitral (n = 23) positions at the Gasthuisberg University Hospital in Leuven, Belgium. Patients undergoing tricuspid valve replacement or mixed replacement with another type of prosthesis were excluded from this study. The mean age was 70 +/- 7 years, there were 121 males and 139 females. The mean follow up was 40.55 months, the total follow up experience 10543 months (878.6 patients years). Hospital mortality was 10.4%, and was not significantly related to the position of the valve: 17.3% +/- 7.88% (n = 23) for double valve replacement, 10.2% +/- 2.16% (n = 196) for aortic valve replacement and 7.3% +/- 4.06% (n = 41) for mitral valve replacement. Hospital mortality was 14.1% +/- 3.27% for those with and 7.48% +/- 2.5% for those without concomitant coronary surgery (p = NS). Survival at 92 months was 63% +/- 6% and was not significantly related to the position of the valve. Not a single patient needed to be reoperated because of primary tissue failure. We conclude that the mid-term durability of this valve is excellent and consider the Carpentier-Edwards pericardial valve as the stented bioprosthesis of choice both in the aortic and mitral positions for the elderly. Because of the older age of our study population and the medium term length of follow up, we were unable to draw any conclusions concerning the incidence of calcific degeneration of this valve.
We reviewed the coronary angiographic findings of 19 patients with a cardiac myxoma, who underwent cardiac catheterization before surgery. Seventeen myxomas were localized in the left atrium and seven had angiographically visible tumor vascularity emerging from atrial branches of the right coronary artery in four patients and the circumflex coronary artery in three. In one patient, we found significant coronary artery disease of the circumflex coronary artery and in another we saw a thrombus-like lesion in the proximal third of the left anterior descending coronary artery. Our results are compared with the findings in two smaller groups of patients with cardiac myxoma who underwent coronary angiography preoperatively. We conclude that the major importance of coronary angiography in patients with cardiac myxomas is to exclude concomitant coronary artery disease before surgery. In a very small minority of patients, a selective coronary angiography is the clue to the diagnosis of cardiac myxoma.
Data on 32 consecutive patients undergoing resection of a cardiac myxoma over a 20-year period (1971-1991) was analyzed. The mean age of the patients was 57 +/- 11 years (range 36 to 78). All myxomas were located in the left atrium except one right ventricular tumor. Ten of the atrial resections were performed with only an endocardial cuff while a full thickness atrial septum cuff was removed in 21 cases. One patient, operated under emergency conditions, died 11 days later as a result of cardiac and pulmonary failure (hospital mortality 3.1%). Late follow-up (mean 6.4 +/- 4.4 years) shows excellent results. All patients are alive and well. No recurrences have been found. In this series, good long-term results were obtained by simple excision of cardiac myxomas. This finding supports the theory that recurrence is mainly confined to patients with familial presentation and/or myxoma complex.
The surgical relief of complex multilevel left ventricular outflow tract obstruction remains a challenging surgical problem. We present a new operation which combines the concepts of aortoventriculoplasty, extended aortic root replacement and the use of a pulmonary autograft. Four patients underwent this operation without mortality and morbidity. All patients were in sinus rhythm and showed excellent function of the autograft valve at early follow-up. This operation might present a more durable or even a definitive solution in the management of complex left ventricular outflow tract obstructions.
Two cases of orthostatic dyspnea and arterial desoxygenation, as a postpneumonectomy complication, are reported. In one patient, echocardiography and cardiac catheterization revealed the presence of an atrial septal aneurysm, which has never been described in association with the platypnea-orthodeoxia syndrome. The other case illustrates that, despite actual technical possibilities, clinical suspicion remains a prerequisite for proper diagnosis of the entity.
A total of 647 consecutive patients underwent valve replacement with a Björk-Shiley Monostrut valve (Shiley, Inc., Irvine, Calif.) from January 1, 1984, through December 31, 1988. A total of 135 patients (20.8%) had had a previous cardiac correction. Overall hospital mortality was 6.8%. Preoperative functional class, cardiopulmonary bypass time, aortic crossclamping time, and cause of valve replacement influenced in-hospital mortality significantly (univariate analysis). The median follow-up was 30 months. Overall actuarial survival was 81% +/- 4% at 6 years. Univariate and multivariate regression analysis showed that preoperative functional class, total cardiopulmonary bypass time, size of mitral prosthesis, and pure mitral insufficiency significantly influenced total mortality after valve replacement. Additional coronary bypass grafting and redo valve replacement did not. The actuarial rate of freedom from thromboembolism was 86% +/- 4% at 6 years. There were no cases of valve thrombosis. Patients having a thromboembolic event showed a higher probability of late death after native valve replacement.
To determine whether morphologic structures or abnormal flow patterns predispose to pathologic proliferation of subvalvular tissue, 26 patients (mean age 19.8 +/- 10.3 years) were studied greater than or equal to 6 months after operation for isolated discrete subvalvular aortic stenosis. The aortic root diameter and the mitral-aortic separation were measured with sector echocardiography. Flow patterns in the left ventricular outflow tract of these patients and control subjects were evaluated with a color flow mapping system optimized for the detection of turbulence. All control subjects had laminar flow throughout systole in the left ventricular outflow tract. By contrast, turbulence originating well below the site where the shelf had previously been resected was observed in 20 (77%) of the 26 patients. In 16 of these 20 patients turbulence was caused by a ridge, which in 13 patients could be identified as the offshoot of a ventricular band. In four patients the turbulence was caused by malalignment of the muscular and membranous septum, resulting in protrusion of the muscular septum into the outflow tract. Except for the latter four patients, the aortic root diameter was 84 +/- 10% of values predicted by body surface area, with values in six patients falling below the third percentile (p less than 0.01). The mitral-aortic separation was 9.7 +/- 3.5 mm, values in 21 patients falling above the 97th percentile (p less than 0.001). These data support the theory that discrete subvalvular aortic stenosis may be caused by a chronic flow disturbance, preferably in a small and long outflow tract. Left ventricular bands, if reaching the outflow tract, may be a factor.(ABSTRACT TRUNCATED AT 250 WORDS)
Two patients with generalized ochronosis developed cardiovascular symptoms related to cardiac ochronosis with aortic valvular stenosis. One patient with a transvalvular pressure gradient of 150 mm Hg underwent emergency aortic valve replacement. The other patient with a transvalvular pressure gradient of 96 mm Hg underwent successful elective aortic valve replacement. Cardiac ochronosis is a rare disease that might be encountered, with the typical signs, during an elective, planned cardiac operation. The most frequent presenting feature of this disease seems to be aortic valvular stenosis.
BACKGROUND: In patients with a univentricular heart, the chronic ventricular volume overload is acutely abolished by the creation of a Fontan circuit. This results in an immediate reduction of the ventricular cavity size but also in an inappropriate degree of ventricular wall thickness, at least in the early postoperative period. The implications for the diastolic properties of the ventricle are poorly understood. METHODS AND RESULTS: A chronic volume overload through a modified Blalock-Taussig shunt was created in 10 mongrel dogs. Six weeks later, the shunt was occluded percutaneously with a detachable balloon. The left ventricular end-diastolic dimension and posterior wall thickness were measured with transcutaneous echocardiography. Digitized high-fidelity pressure tracings were used to determine the time constant of isovolumic pressure decay, tau. The isovolumic relaxation time (A2-MVO) and time to minimal left ventricular pressure (A2-LVPmin) were recorded. All variables were followed up to 1 month after occlusion of the shunt. One hour after occlusion, there was an incomplete return to baseline values of the echocardiographic left ventricular dimension (+12 +/- 8% of baseline value, p < 0.01). Despite a 31 +/- 14% (p < 0.001) increase of the posterior wall thickness after removal of the volume overload, tau or ventricular relaxation showed no change from control values. In contrast, the early filling wave was blunted, suggesting diminished ventricular suction. A2-MVO (p < 0.01) and A2-LVPmin (p < 0.05) lengthened well above baseline values for up to 1 week after occlusion of the shunt. Over the following month, the volume-induced hypertrophy regressed, and indexes of early ventricular filling resumed control values. CONCLUSIONS: We conclude that early after removal of a chronic volume overload, the resultant increase of wall thickness is not associated with impaired relaxation but that viscosity and inertia caused by the increased mass-to-volume ratio will impair early ventricular filling.
Pulmonary embolectomies were performed in 30 patients from January 1973 until December 1991 in the University Hospital of Leuven. There was an 80% hospital survival. The late follow-up showed no recurrent pulmonary emboli. The preoperative haemodynamic status was the most important predictor for survival. Patients, under cardiopulmonary resuscitation or in profound cardiogenic shock before surgery, had a survival of only 50% while all other patients survived. Angiography, performed in only 23% of the cases, remained the most important diagnostic tool until the advent of transthoracic and transoesophageal echocardiography. Thrombolysis is an acceptable alternative in the stable patient, but pulmonary embolectomy is life-saving in the haemodynamically unstable patient and when thrombolysis is contraindicated.
Lymphoproliferative diseases may occur as a complication of severe immunosuppression. In our own center two out of 46 heart transplant recipients, receiving a cyclosporin A containing immunosuppressive regimen, presented with this complication and are reported here. Hepatic involvement and an occult small bowel localisation, which only became evident after a chemotherapy-induced small bowel perforation, illustrate the predilection of posttransplant lymphoproliferations for extranodal sites. Both cases represent the extremes of a spectrum of post-transplant lymphoproliferations ranging from polyclonal benign lesions to monoclonal malignant lymphomas. Their B-cell origin was pathologically established, but in none of the two reported cases the previously postulated role of Epstein-Barr virus in the pathogenesis could be confirmed by serological tests. Severe immunosuppression played a major role in the pathogenesis of these disorders, as suggested by concomitant opportunistic infections occurring in both cases. The lymphoproliferation diagnosed in the polyclonal stage was reversible after reduction of the immunosuppressive therapy, without subsequent graft rejection. This observation underscores the importance of early recognition of lympho-proliferative disorders in organ transplant patients, allowing a prompt and successful reduction of the immunosuppressive therapy. Overwhelming opportunistic infections, occurring in the patient treated with cytotoxic drugs, illustrate the inherent risks of such an approach in an already severely immunosuppressed population.
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A patient with calcified aortic valve disease secondary to ochronosis and alkaptonuria is presented. Urgent aortic valve replacement was necessary. The cardiovascular complications of this disease are reviewed.
From January 1, 1980, through December 31, 1985, 473 patients underwent valve replacement with an Ionescu-Shiley valve. Overall hospital mortality was 7.8%. Major associated procedures and preoperative New York Heart Association (NYHA) Classes IV and V influenced hospital mortality significantly. The mean follow-up was 2.6 +/- 1.3 years. Late mortality was 5.9%. Overall actuarial survival was 81% at 5 years. A chief cause of reoperation was cusp rupture of a mitral prosthesis in 5 patients (all after aortic and mitral valve replacement). The overall actuarial reoperation-free incidence was 93% at 5 years. Thromboembolic (TB) phenomena occurred at a linear incidence of 1.4 +/- 0.3% per patient-year or an actuarial thromboembolism-free incidence of 92% at 5 years. Univariate and multivariate analyses showed that postoperative NYHA Class, rhythm at follow-up, and anticoagulant therapy significantly influenced the incidence of TE phenomena.
A case of excessive serous leak through a modified polytetrafluoroethylene Blalock-Taussig shunt is presented. This relatively rare complication was treated successfully with fibrin glue and collagen fleece.
The cardioprotective effect of the addition of the slow calcium-channel blocker nifedipine to cardioplegic solution was tested in two double-blind placebo controlled randomized studies. The first study included 24 patients undergoing aortic-coronary bypass grafting, and the second included 24 patients undergoing aortic valve replacement. Nifedipine at a dose of 200 micrograms/L or placebo was added to St. Thomas' Hospital cardioplegic solution. The following markers of ischemia were used: adenosine triphosphate and its catabolites, creatine phosphate and inorganic phosphate, determined in transmural left ventricular biopsy specimens taken before, at the end of, and after aortic cross-clamping; hemodynamic recovery 15 minutes after cessation of cardiopulmonary bypass; clinical outcome in terms of the incidence of arrhythmias, low cardiac output, positive inotropic support immediately after operation, and follow-up at 15 months. The main difference between the two studies was that myocardial temperature during cross-clamping remained constant at 14 degrees C in coronary bypass grafting but increased to 25 degrees C in valve operations despite the application of the same amounts of cardioplegic solutions. This lower temperature resulted in better preservation of high-energy phosphates in coronary bypass operations as compared to the placebo group having valve replacement operations. According to analysis of variance, a drug effect could be demonstrated only in the aortic valve replacement study: Accumulation of breakdown products of the adenine nucleotide pool was less in the nifedipine group than in the placebo group (p less than 0.05). Adenosine triphosphate decreased only to 84% in the nifedipine group and to 72% in the placebo group. Despite this adenosine triphosphate-sparing effect, weaning from cardiopulmonary bypass was more difficult in the nifedipine group. Left ventricular stroke work index 15 minutes after bypass was decreased to 72% of the prebypass value in the nifedipine group (t test, p less than 0.01) and only to 86% in the placebo group (p = NS). In contrast, after the patients were admitted to the intensive care unit, the incidence of low cardiac output tended to be lower in the nifedipine group than in the placebo group: 33% versus 58% (p = NS). In conclusion, ischemia-induced degradation of nucleotides as it occurs when myocardial cooling is inadequate can be prevented by the addition of nifedipine to the St. Thomas' Hospital cardioplegic solution. This effect, however, is not associated with an improved clinical outcome.