Biomedical subjects

Finn T Jensen

Publications and source records attributed to Finn T Jensen.

5 recordsLinked to original sources

PubMed2005

Hemodynamic function of the standard St. Jude bileaflet disc valve has no clinical impact 10 years after aortic valve replacement.

OBJECTIVES: Size mismatch and impaired left ventricular function have been shown to determine the hemodynamic function of the standard St. Jude bileaflet disc valve early after aortic valve replacement (AVR). We aimed to analyse St. Jude valve hemodynamic function and its clinical impact in the survivors of a prospective series 10 years after AVR for aortic stenosis. DESIGN: Forty-three survivors aged 32-90 years from a prospective series attended a follow-up study with Doppler echo and radionuclide cardiography 10 years after AVR for aortic stenosis. Six patients with significant left sided valve regurgitation were excluded from further analysis: they had significantly lower St. Jude valve gradient and left ventricular ejection fraction (LVEF) and larger mass index (LVMi) than 37 without. RESULTS: In the 37 patients without left sided valve regurgitation peak and mean gradients were inversely related to St. Jude valve geometric orifice area (GOA) indexed for either body surface area or left ventricular end-diastolic dimension (LVEDD). The gradients correlated directly with LVEDD but not with LVEF or LVMi. Eleven patients with hypertension had higher peak gradients (31+/-13 versus 22+/-8 mmHg, p<0.05), lower LVEF, and higher LVEDD and LVMi than 26 without. Peak gradient was greater than 35 mmHg in five hypertensive patients with normal LVEF but lesser than 30 mmHg in six with impaired LVEF. Supranormal LVEF and severe size mismatch identified the remaining patients (N=3) with peak gradient above 35 mmHg. In a multilinear regression analysis GOA indexed for LVEDD, hypertension, and LVEF were independently related to peak gradient. CONCLUSION: High gradients of the standard St. Jude bileaflet disc valve 10 years after AVR was primarily related to systemic hypertension and mismatch between valve and left ventricular cavity size. Hypertension and left sided valve regurgitation, but not St. Jude valve gradient or size mismatch, were the dominant determinants of left ventricular hypertrophy and impaired function.

Adult↗

PubMed2004

Predictable changes in left ventricular mass and function during ten years after valve replacement for aortic stenosis.

BACKGROUND AND AIM OF THE STUDY: Left ventricular (LV) hypertrophy is the underlying basis for longevity after aortic valve replacement (AVR) for aortic stenosis (AS). However, a detailed account of changes in LV mass and function in the long term after AVR and identification of the determinants of such changes have not yet been presented. METHODS: Ninety-one unselected consecutive adult patients with AS underwent AVR and were followed up to 10 years, at which time 41 survivors without new mitral disease underwent repeat measurement of LV mass index (LVMi), ejection fraction (LVEF), fast filling fraction (LVFFF), and end-diastolic volume index (LVEDVi). A subgroup comprising 49 patients was also assessed at eight days, three months, and 1.5 years postoperatively. All measurements were analyzed in a longitudinal regression model for repeated measures. RESULTS: LVMi fell from 202 +/- 58 g/m2 (n = 91) via 150 +/- 45 g/m2 (n = 39) at 1.5 years to 139 +/- 40 g/m2 (n = 41) at 10 years in all patients, and to 124 +/- 31 g/m2 (n = 29) in non-hypertensive patients. The LVMi falls were paralleled by improvements in LVEF and LVEDVi. LVFFF was not correlated to LVMi before the 10-year study. The longitudinal model indicated progressive reduction of LVMi to 1.5 years, but no change thereafter. The predictor variables were preoperative LVMi and end-systolic dimension index (high values of both related to high postoperative LVMi), hypertension, and male gender. The model for LVEF indicated a rapid increase to three months, followed by a slight decrease to 1.5 years and further to 10 years, predicted by preoperative LVEF and LVFFF. LVFFF fell sharply by three months, had recovered somewhat at 1.5 years and fully at 10 years, positively related to preoperative LVFFF and inversely to end-systolic chamber radius:wall thickness ration and small-sized prosthetic valves. LVEDVi converged from extreme values over time predicted by preoperative LVEF, but rose with hypertension and coronary artery disease. Hemodynamic function of the prosthetic aortic valve at any of the measurement times had no impact. CONCLUSION: Changes in LV mass and function up to 10 years after AVR for AS were highly predictable. Poorer outcomes were related to preoperative excessive hypertrophy and indices of underlying irreversible myocardial disease and further compromised by hypertension and, to a lesser extent, coronary artery disease. The hemodynamic function of the aortic prosthetic valve did not seem to play a role.

Adult↗

PubMed2003

Evaluation of myocardial iron by magnetic resonance imaging during iron chelation therapy with deferrioxamine: indication of close relation between myocardial iron content and chelatable iron pool.

Evaluation of myocardial iron during iron chelation therapy is not feasible by repeated endomyocardial biopsies owing to the heterogeneity of iron distribution and the risk of complications. Recently, we described a noninvasive method based on magnetic resonance imaging. Here, the method was used for repeated estimation of the myocardial iron content during iron chelation with deferrioxamine in 14 adult nonthalassemic patients with transfusional iron overload. We investigated the repeatability of the method and the relationship between the myocardial iron estimates and iron status. The repeatability coefficient (2sD) was 2.8 micromol/g in the controls (day-to-day) and 4.0 micromol/g in the patients (within-day). Myocardial iron estimates were elevated in 10 of all 14 patients at first examination, but normalized in 6 patients after 6 to 18 months of treatment. If liver iron declined below 350 micromol/g all but one of the myocardial iron estimates were normal or nearly normal. At start (R2 = 0.69, P =.0014) and still after 6 months of iron chelation (R2 = 0.76, P =.001), the estimates were significantly and more closely related to the urinary iron excretion than to liver iron or serum ferritin levels. In conclusion, our preliminary data, which may only pertain to patients with acquired anemias, suggest the existence of a critical liver iron concentration, above which elevated myocardial iron is present, but its extent seems related to the size of the chelatable iron pool, as reflected by the urinary iron excretion. This further supports the concept of the labile iron pool as the compartment directly involved in transfusional iron toxicity.

Adult↗

PubMed2003

Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile.

BACKGROUND: Previous studies have suggested that regression of hypertrophy may be the underlying determinant of longevity and left ventricular function after valve replacement (AVR) for aortic stenosis (AS). The potential for hypertrophy regression could therefore be related to the preoperative risk profile. METHODS: Ninety-one consecutive patients with AS had a "project" Doppler-echo and radionuclide ventriculography in addition to the standard investigation programme prior to AVR with a disc valve (19-29mm, n=82), a caged ball valve (26-29mm, n=8), or a stented porcine valve (26mm, n=1); 49 (group A) were selected for a serial follow-up study while 42 served as controls (group B). Forty-two group A patients took part in a 1.5-year examination while 47 (26 group A, 21 group B) patients were studied at 10 years. RESULTS: Groups A and B were comparable as regards all pre- and intra-operative data including left ventricular mass index (LVMi). A previously developed preoperative prognostic index (PI) separated the patients into groups with low (n=23), intermediary (n=19) and high risk (n=49) with 10-year survivals of 87%, 58% and 43% (P<0.01). LVMi dropped from 202+/-58g/m(2)preoperatively to 152+/-45g/m(2)(P<0.0001) at 1.5 years, and 139+/-40g/m(2)(P<0.0001) at 10 years (three and six patients, respectively, with paravalvular leak or mitral regurgitation excluded). PI correlated with preoperative (r=0.51, P<0.001), 1.5-year (r=0.46, P<0.01), and 10-year LVMi (r=0.41, P<0.01). Also preoperative left ventricular ejection fraction correlated with the three LVMi measurements. Patients with systemic hypertension had higher LVMi at 1.5 years (193+/-42, n=6 vs 144+/-42, n=33, P<0.05) and 10 years (175+/-39, n=12 vs 124+/-31g/m(2), n=29, P<0.001). Patients with low, intermediary or high PI, excluding those with hypertension, had 1.5-year LVMi of 110+/-35 (n=8), 134+/-43 (n=9) and 164+/-33g/m(2)(n=16; P<0.01), respectively, and 10-year LVMi of 116+/-25 (n=17), 126+/-27 (n=6), and 146+/-41g/m(2)(n=6; P<0.05), respectively. There was no relation between LVMi at 1.5 or 10 years and peak or mean Doppler gradient, prosthetic valve size, or valve size index. CONCLUSIONS: Left ventricular hypertrophy regression for patients who survived up to 10 years after AVR for AS is dependent on the preoperative risk profile indicating that irreversible myocardial disease is the underlying factor. Systemic hypertension is an important factor in its own right.

Aged↗

PubMed2002

Relationship between hepatocellular injury and transfusional iron overload prior to and during iron chelation with desferrioxamine: a study in adult patients with acquired anemias.

The role of iron overload as cause of liver dysfunction has never been studied in detail in patients without concomitant hepatotropic infections who receive multiple transfusions. We therefore investigated the relationship between the extent of hepatocellular injury as reflected by serum levels of aminotransferases (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and several iron status indices in 39 anti-hepatitis C virus-negative (HCV(-)) nonthalassemic patients with transfusional iron overload owing to acquired anemias. In 12 patients, we monitored aminotransferase levels and indices of iron status during iron chelation treatment. Before treatment, elevated aminotransferase activity was seen only at liver iron concentrations more than 300 microM/g. During treatment all aminotransferase values were normal if the liver iron concentration returned below 350 microM/g. At the start of treatment, ALT (R(2) = 0.64, P =.006) and AST activity (R(2) = 0.57, P =.01) were closely related to urinary iron excretion, reflecting the size of the chelatable or the labile iron pool. During treatment, a comparable pattern was seen and the urinary iron excretion was also directly related to the liver iron concentration at concentrations above approximately 400 microM/g. All elevated ALT values were associated with a urinary iron excretion more than 15 mg/24 h. In conclusion, our data suggest the existence of a critical liver iron concentration range, above which hepatocellular injury is seen. The extent of the injury seems to be determined mainly by the size of the chelatable or labile iron pool, supporting the concept of the labile iron pool as the compartment directly involved in iron toxicity. Our findings may be helpful in establishing criteria for safety from complications of transfusional iron overload.

Adult↗