Inflammatory aneurysm of the ascending aorta mimicking intramural hemorrhage.
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Biomedical subjects
Publications and source records attributed to R Jenni.
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BACKGROUND: Pressure gradients calculated from echo-cardiography after aortic valve replacement are commonly much higher than would be expected from in vitro measurements. METHODS: The mean, peak-to-peak, and maximal gradients across bileaflet aortic prostheses (St. Jude Medical) were measured invasively in 52 patients at high and low heart rate, cardiac index, and stroke volume. One week after operation the gradients were calculated from a standard transthoracic echocardiogram (delta p = 4v2(2)). In a second study 3 to 12 months later, gradients were calculated using the standard, simplified Bernoulli equation, and with the equation considering subvalvular flow velocities (delta p = 4(v2(2-)v1(2)). Invasive and echocardiographic measurements were matched and compared. RESULTS: Invasively measured mean gradients for 21 to 29-mm valves ranged from 7.4 +/- 4.9 to 4.3 +/- 1.6 mm Hg at systolic flow rates from 11.3 +/- 0.7 to 16.2 +/- 1.8 L.min-1.m-2. Mean echocardiographic gradients were 15.1 +/- 4.5 to 7.5 +/- 2.2 mm Hg (p < 0.001) with the standard method, and 10.5 +/- 1.9 to 5.6 +/- 1.5 mm Hg when considering the subvalvular flow velocity (p < 0.001). CONCLUSIONS: Mean gradients across bileaflet prostheses are generally low, even in small valves and with high systolic flow. The correlation of the invasive in vivo with in vitro gradients is good. Standard echocardiography overestimates gradients across bileaflet heart valves and high gradients are not due to valve dysfunction. Gradients obtained by echocardiography considering the subvalvular flow velocity correlate better to invasively measured and in vitro gradients.
BACKGROUND: Small aortic orifice primarily resulted in heart prosthesis mismatch in a significant number of patients. The Hemodynamic Plus (HP) series of St. Jude Medical heart valves represents an interesting innovation, allowing a larger valve orifice area with an equivalent tissue annulus diameter. METHODS: Hemodynamic characteristics of the 21-mm HP St. Jude Medical valve were prospectively compared with those of the standard 21-mm and 23-mm St. Jude Medical valves in three groups of 22 patients. Patients were selected from a database to be rigorously matched for age, sex, body surface area, functional class, underlying lesion, native valve opening area, left ventricular function, and preoperative peak and mean valve gradients. Postoperative evaluation (follow-up ranging from 3 to 24 months; mean, 11.5 months) included clinical examination and echocardiographic studies. RESULTS: There was no operative mortality or significant perioperative complications. Short-term clinical follow-up was marked by a complete absence of valve-related complications. Presently, all but 1 patient in the 21-mm HP group and 2 in the 21-mm standard group are in New York Heart Association functional class I. Doppler echocardiography-derived mean and maximal pressure gradients were significantly lower in the 21-mm HP group (8.1 +/- 1.9 and 16.4 +/- 3.4 mm Hg) than in the 21-mm standard group (13.4 +/- 3.9 and 21.2 +/- 4.3 mm Hg; p = 0.002 and p = 0.0004, respectively), confirming the better hemodynamic performance already described in in vitro studies. Pressure gradients did not differ significantly between the 21-mm HP and the 23-mm standard groups. The 21-mm HP valve demonstrated the highest performance index; 0.66 +/- 0.08, compared with 0.49 +/- 0.09 for the 21-mm standard valve (p < 0.001) and 0.59 +/- 0.07 for the 23-mm standard valve (p < 0.001). CONCLUSIONS: In vivo hemodynamic performance of the 21-mm HP valve corresponds closely to that of the 23-mm standard valve and is substantially better than that of the 21-mm standard valve. The 21-mm HP St. Jude Medical valve demonstrates excellent hemodynamic characteristics and can be recommended in normal-sized adult patients with narrow aortic root. This valve will minimize the need for aortic annulus enlargement.
BACKGROUND: Coronary artery enlargement has been previously described in left ventricular hypertrophy. OBJECTIVES: We sought to assess coronary artery dimensions and their relation to left ventricular muscle mass in primary and secondary hypertrophy. METHODS: Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary angiography in 52 patients: 12 control subjects and 40 patients (13 with hypertrophic cardiomyopathy, 12 with dilated cardiomyopathy and 15 with aortic valve disease). As a measure of left ventricular hypertrophy, angiographic left ventricular mass and equatorial cross-sectional muscle area were determined. RESULTS: Cross-sectional area of both the left and right coronary arteries is increased in left ventricular hypertrophy (p < 0.05 vs. values in control subjects). There is a curvilinear relation between left coronary artery size and left ventricular muscle mass (r = 0.76) or cross-sectional muscle area (r = 0.75). However, normalization of coronary cross-sectional area for left ventricular muscle mass or muscle area shows insufficient enlargement of the coronary arteries in both primary and secondary hypertrophy. CONCLUSIONS: 1) Coronary artery size increases as left ventricular mass increases in both primary and secondary hypertrophy. 2) The enlargement of left coronary cross-sectional area is independent of the cause of the increase in left ventricular mass. 3) The size of the coronary arteries is inappropriate with regard to left ventricular hypertrophy. Thus, the stimulus for growth of the coronary arteries is not influenced by the underlying disease but appears to depend on the degree of left ventricular hypertrophy.
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Myxomas are the most common primary cardiac tumors. They may simulate infective endocarditis but are rarely infected. Currently, 17 infected left atrial myxomas have been reported in the literature [1, 7, 8, 10, 11]. We present a patient with infected left atrial myxoma combined with mitral valve endocarditis, treated by excision of the myxoma and mitral valve reconstruction.
Pseudoaneurysm formation after aortic homograft replacement in patients with active endocarditis is a common observation and usually occurs at the site of a former abscess or paravalvular leak in case of prosthetic valve endocarditis. A 53-year-old man with prosthetic endocarditis underwent aortic valve homograft replacement and developed a pseudoaneurysm at the right and noncoronary aortic sinus which was documented by Doppler echocardiography. Follow-up examination ten months after operation unexpectedly revealed a complete obliteration of the previously echo free space between the homograft and the native aortic root and, thus, spontaneous obliteration of the pseudoaneurysm.
The diagnosis of acute type-A aortic dissection is predominantly based on the demonstration of an intimal tear or a dissection membrane. We describe another pathogenetic mechanism in a patient with the typical features of acute aortic dissection with pericardial tamponade, and a giant aneurysm of the ascending aorta. However, no dissection membrane, rupture site, or intimal tear could be demonstrated by transesophageal echocardiography, intraoperatively, or histologically. The histological work-up showed an extreme form of cystic medial necrosis with intramural hemorrhages consistent with a leaking aneurysm. Hence, in a patient with a symptomatic aneurysm of the aortic root and pericardial tamponade, obvious intimal dissection or rupture does not always have to be present echocardiographically or intraoperatively. A different presentation can occur in the setting of an extreme medial necrosis, where blood leaks through the aortic wall causing intramural hemorrhages with intimal leaks invisible to the surgeon's or echocardiographer's eye. This process is clinically indistinguishable from type-A aortic dissection.
Papillary fibroelastomas are rare and benign heart tumors. We present two cases with these lesions. A young female patient with cerebral infarction was operated to resect the tumor on the mitral valve and the valve was successfully repaired. Another male patient had a history of bradycardia. On examination, coronary stenosis and a tumor in the left ventricle was found. Tumor excision combined with aorto-coronary artery bypass grafting was performed. Echocardiography proved to be highly effective to diagnose these tumors. Because of the potential cerebral and coronary embolization, these tumors should be excised. Surgical results are good.
OBJECTIVES: The purpose of the present study in patients with severe aortic stenosis was to assess the prevalence of absent left ventricular hypertrophy (LVH) (determined according to mass criteria), to identify predictors of absent LVH, and to assess short-term left ventricular adaptation and prognosis after aortic valve replacement. METHODS: Left ventricular mass (LVM) was determined by echocardiography in 109 men and 101 women with severe aortic stenosis (mean pressure gradient < or = 50 mm Hg). LVH was defined as LVM > or = 109 g/m2 in women and LVM > or = 134 g/m2 in men. RESULTS: One hundred and eighty nine patients showed LVH (group 1) (90%; mean (SD) age 65 (14) years), and 21 showed no LVH (group 2) (10%, age 57 (21) years P = 0.02 for difference in age). Twelve (6%) of those without LVH had increased relative wall thickness (that is, > or = 0.45 with LV concentric remodelling) and nine (4%) showed no macroscopically detectable hypertrophic adaptation. The following variables were associated with the absence of LVH: low body surface area, low body mass index, and increased cardiac index. 76/210 patients were followed up a mean of six months after aortic valve replacement. The frequency of adequate ventricular adaptation to the decreased afterload after aortic valve replacement was higher in patients with LVH than in those without. Mortality six months after aortic valve replacement was lower, but not significantly, in patients with LVH (7.6%) than in those without LVH (12.5%, P = 0.10). CONCLUSIONS: A tenth of patients with severe aortic stenosis did not develop LVH according to mass criteria; 4% of the patients did not have any macroscopic signs of myocardial adaptation to the pressure overload despite longstanding disease. Small body size was independently associated with lack of LVH according to mass criteria. Six months after aortic valve replacement, ventricular adaptation was more often adequate in patients with LVH than in those without.
To determine whether insulin-like growth factor I (IGF-I) has systemic cardiovascular effects in humans, 60 micrograms/kg IGF-I or saline were injected sc in a cross-over, randomized, double blind fashion into eight healthy male volunteers. Cardiac function and performance were evaluated by echocardiography and exercise test. In parallel, the metabolic effects of IGF-I during exercise were investigated. IGF-I improved cardiac performance with a significant increase in stroke volume and cardiac output by 14% and 18% (P < 0.03 and P < 0.04), respectively. Ejection fraction increased by 9% after IGF-I treatment (P < 0.05). Heart rate was not significantly increased at rest or during exercise. Systolic blood pressure was slightly increased by IGF-I, whereas diastolic blood pressure was slightly decreased, resulting in a continuous increase in the blood pressure amplitude at rest and during exercise, but without reaching statistical significance. Maximal exercise duration and peak oxygen consumption were not changed. Exercise was uneventful, without pathological changes on electrocardiogram records. Glucose levels were unchanged, whereas insulin and C peptide levels were decreased by IGF-I at rest. During exercise, insulin levels were further decreased, and the insulin-sparing effect of exercise resulted in a further enhancement of tissue sensitivity to insulin. GH levels were suppressed by IGF-I treatment at rest, but were still stimulated by exercise. In conclusion, IGF-I has positive inotropic effects in man. Further investigation of the potential role of IGF-I in cardiac conditions such as heart failure appears to be warranted.
Coronary artery fistula is a very rare congenital malformation with abnormal coronary-cameral communication that may involve any chamber and any or all coronary artery branches. We present our experience with 11 consecutive patients [mean age 16.6 years, ranging from 4 to 64 years]; 9 of them were treated surgically, spontaneous closure of the fistula was observed in one patient and one patient is still under observation. Fistulas originated from the right coronary artery in 4 patients and drained either into the right [n=3] or into the left system [n=1]. In 9 patients, the fistulas originated from the left coronary system and the fistulous communication developed with the right cardiac structures only. In 2 patients both coronary arteries were involved in the pathological drainage and 2 patients were demonstrated to have multiple drainage from the left coronary artery. Additional congenital cardiac malformations were found in 2 patients. Surgical closure of the fistula was successful in all operated patients [in one case treatment was possible without cardiopulmonary bypass]. Simple ligation of the fistula was performed in 1 patient, intracardiac closure of the fistula was combined with different reconstructive procedure in the other patients. Neither hospital mortality nor severe complications occurred. Mean follow-up interval was 39.4 months and all patients except one were in NYHA I. In presence of symptoms of congestive heart failure, significant left-to-right shunt and arrhythmias, elective closure of coronary fistula is generally accepted, whereas indication is more controversial in asymptomatic patients.
OBJECTIVES: The management of hepatic venous outflow obstruction, usually known as Budd-Chiari syndrome, remains complex despite a variety of treatments. METHODS: We present the results from 16 patients with Budd-Chiari syndrome who underwent dorsocranial liver resection and direct hepatoatrial anastomosis over a 10-yr period. The inferior caval vein was occluded in 10 patients. RESULTS: Operative mortality was 12.5% (2/16). During a mean follow-up of 7.2 yr, three patients required reoperation, two of whom had veno-occlusive disease. The late mortality was 14% (2/14). Clinical status improved in terms of: abdominal pain, 81 versus 14%; lower limb edema, 56 versus 14%; hematemesis, 19% versus 0%; hepatomegaly, 94 versus 36%; esophageal varices, 56 versus 7%; splenomegaly, 56 versus 21%; and ascites, 87 versus 29%. Mean serum bilirubin (micromol/l) fell from 40.2 to 27.1 (p = 0.005), and serum albumin remained unchanged. A patent hepatoatrial anastomosis was demonstrated in 10/12 survivors. The actuarial survival rate was 74.2% at 5 and 10 yr. CONCLUSIONS: Thus, in patients with outflow obstruction of the major hepatic veins, transcaval dorsocranial liver resection and direct hepatoatrial anastomosis recreate an adequate hepatic runoff. Moreover, this procedure is appropriate for patients with occlusion of the inferior caval vein, obviates or defers the need for liver transplantation, and prevents recurrence of thrombosis.
The results of surgical procedures for termination of Wolff-Parkinson-White (WPW) Syndrom were assessed in 59 patients undergoing operation between January, 1980 and December, 1993. All cases of WPW were refractory to medical treatment and 14 of 58 patients had one or several syncopes, and 4 of them had to be reanimated. The surgical treatment of these patients was a dissection of an accessory atrioventricular pathway. 15 patients required additional heart operation. A total of 60 accessory pathways were diagnosed preoperatively, 64 were located intraoperatively. The reoperation rate was 3% (2 patients) due to persistent WPW. Incidence of total AV block after the operation was 7% (4 patients). In the late postoperative stage, 12 patients developed supraventricular tachycardias, but none of these cases required a surgical treatment. The actuarial survival rate after 10 years was 100% and after 14 years 96%. We conclude that surgical dissection of accessory pathways offers a good alternative in cases of unsuccessful catheter ablative procedure or in cases of additional heart operation.
Late cardiac tamponade is a very severe condition that presents with subtle signs and symptoms within days or weeks after cardiac surgery. In a consecutive series of 3782 patients, 33 developed this complication, mostly due to overdosage of anticoagulants or to unsafe combination of 2 anticoagulation regimen. Diagnosis can be difficult and is best confirmed by echocardiography; in patients with primary uneventful recovery and sudden cardiocirculatory deterioration, intensive work-up should be performed to exclude or confirm the suspicion of late pericardial tamponade. The treatment of late pericardial tamponade should not be delayed and consists in subxyphoidal drainage. Re-sternotomy might be necessary to assume complete decompression of the heart in case of well-localized and posterior tamponade and/or organized pericardial fluid. Since this complication can happen in any patient transferred to peripheral hospital for postoperative recovery after cardiac surgery, we believe that this complication should be recognized very early and should be treated, in case of necessity, by general surgeons. Usually, no active bleeding is found at revision.
The purpose of the present study in patients with severe aortic stenosis was to assess prevalence, predictors and course after aortic valve replacement in patients without left ventricular hypertrophy according to echocardiographic mass criteria (LVH). 90% had LVH compared with 10% without. The following variables were associated with absence of LVH: younger age, low body surface area, and increased cardiac index. In patients with LVH, ventricular adaptation following aortic valve replacement was adequate more often than in those without. Six-month mortality following aortic valve replacement was insignificantly lower in patients with LVH (7.6%) than in those without it (12.5%, p = 0.10).
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