Damage to blood corpuscles seems to be related to the magnitude and exposure time of the turbulent shear stresses (TSS). According to in vitro studies the critical TSS level for lethal erythrocyte and thrombocyte damage is 150-400 N/m2, for exposure times within physiological ranges. To study the distribution of TSS in the human ascending aorta, a hot-film anemometer needle probe was used to register blood velocities at 41 evenly distributed measuring points in the cross-sectional area 5-6 cm downstream of the aortic annulus. Measurements were made in the ascending aorta after normal aortic valves (prior to coronary bypass surgery), after stenotic aortic valves, and after implantation of either St. Jude Medical or Starr Edwards Silastic Ball valves. Three-dimensional visualization of velocity profiles were performed and Reynolds normal stresses (RNS) were calculated within 50-ms overlapping time windows in systole. By coordinating the mean RNS for each time window and for all 41 measuring points, 2-dimensional color-coded mapping of the RNS distribution was made. Based on the velocity profiles and the RNS distribution a relative blood damage index (RBDI) was calculated to incorporate the magnitude and exposure time for RNS in the entire cross-sectional area into one parameter. Turbulent shear stresses were estimated by using a previously determined correlation equation between RNS and TSS. After normal aortic valves, RNS was below 4 N/m2.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac valve replacement was performed on 76 patients with acute or subacute native infective endocarditis. The 30-day mortality/5-year survival (%/% +/- SE) was 18/67 +/- 7, after aortic valve replacement (n = 50), 6/82 +/- 10 in the mitral group (n = 18) and 38/63 +/- 17 after double valve replacement (n = 8): NS/NS. In patients with destruction and/or abscess of the anulus (DESAB), which was commonest in the aortic group, the corresponding figures were 31/48 +/- 10, compared with 10/81 +/- 6 in the other patients (p less than 0.05/less than 0.01). Atrioventricular block and complete bundle branch block were commoner in the former group. When the time from onset of fever to operation was 1-6 months (n = 50), the 5-year survival was 79 +/- 6% compared with 51 +/- 10% (p less than 0.05) when that time was less than 1 month (n = 14) or greater than 6 months (n = 12). Logistic regression analysis showed NYHA class III-IV and DESAB to be independent risk factors in 30-day mortality, which was 3.8% when neither, and 46.2% when both of these factors were present (p less than 0.01). Cox regression analysis identified NYHA class IV (p less than 0.0001), calcified mitral valve or anulus (p = 0.001), DESAB (p = 0.01), male gender (p = 0.02), supraventricular arrhythmia (p = 0.04) and vegetations on the diseased valve (p = 0.05) as independent determinants of overall long-term mortality. Patients with none (n = 6), any one (n = 16), any two (n = 28), any three (n = 20), any four (n = 6) or any five (n = 2) of these risk factors (none had 6) had respective 30-day/5-year survival rates (% +/- SE) of 100/100, 94 +/- 6/94 +/- 6, 89 +/- 6/85 +/- 7, 75 +/- 10/43 +/- 13, 67 +/- 9/17 +/- 15 (at 1 year) and 0/0 (p less than 0.0001). Identification of independent risk factors permitted stratification of the patients into subgroups with prognosis ranging from 100% 5-year survival to 0% 30-day survival. Surgical treatment of native infective endocarditis should be undertaken before cardiac disability is advanced or infective destruction of the anulus, notably of the aortic valve, becomes evident.
In 26 patients with left ventricular aneurysm and ventricular tachycardia and/or ventricular fibrillation following myocardial infarction, coronary angiography, left ventriculography and electrophysiologic examination were performed preoperatively. Surgery in all cases consisted of aneurysmectomy and mapping-guided endocardial resection of the area found to be the arrhythmogenic center. Four patients died peroperatively or during the postoperative hospital stay. The 22 survivors were followed up for 3-48 (mean 22) months postoperatively. There were no late deaths. Repeated electrophysiologic studies were performed in 18 of the survivors. Freedom from ventricular tachycardia and fibrillation was achieved in 21 patients, 17 after surgery alone and four after combined surgical and medical treatment. The remaining patient still has ventricular tachycardia despite combined treatment.
A postoperative follow-up study of 21 cases of discrete membranous subvalvular aortic stenosis is presented. The age at operation was 6-47 (mean 16) years, and the follow-up time 0.6-16 (mean 6.7) years. Preoperatively most patients were in NYHA function class II or III and had high peak systolic pressure gradient, left ventricular hypertrophy and/or cardiothoracic index greater than 0.50. At follow-up all but six patients were in NYHA class I, the Doppler-estimated peak systolic gradient was 0-36 (mean 18) mmHg, the cardiothoracic index unchanged and the mean left ventricular hypertrophy score had declined from 4.3 to 2.3. Of 13 patients without aortic regurgitation preoperatively, eight had regurgitation at follow-up (group I) and five did not (group II). The interval to follow-up was significantly longer and the preoperative peak systolic gradient was greater in group I than in group II. Aortic regurgitation may develop even after surgical relief of discrete membranous subvalvular aortic stenosis, possibly associated with high preoperative pressure gradient and time from operation. Regular postoperative Doppler echocardiography is therefore recommended.
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