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T Stefenelli

Publications and source records attributed to T Stefenelli.

At least 19 recordsLinked to original sources
PubMed2001

Emergency angioplasty and stent deployment for acute occlusion of an anomalous single coronary artery (all three coronary arteries from one ostium in the right sinus of Valsalva).

A single coronary ostium is traditionally considered to be of little clinical significance. We report a case of a single ostium in the right sinus of Valsalva, giving rise to the right coronary artery, from which the left main coronary artery originated. Sudden death occurred seven days after acute gastrointestinal bleeding and subsequent interruption of aspirin therapy. Acute coronary angiography following successful resuscitation revealed an ascending thrombus in the right coronary artery. The patient underwent a complex percutaneous coronary angioplasty with stent deployment. We conclude that coronary artery disease may lead to severe ischemia with a large area at risk and major complications in patients with coronary anomalies. Patients with acute stent implantation might benefit from platelet aggregation even in cases of recent intestinal bleeding.

Aged↗
PubMed2001

Afterload reduction in severe aortic regurgitation.

This study was designed to assess the effects of afterload reduction in asymptomatic patients with severe aortic regurgitation (AR) and maintained LV function by cine-MRI. We studied 13 patients at baseline and after 0.2 mg/kg Hydralazine (I.V.). Patients were stratified according to the volumetric LV response to acute afterload reduction: Group I comprised patients with improved LV response; Group II comprised patients with unchanged or deteriorated LV response. Baseline LV function and severity of AR were not significantly different between groups. However, regurgitant fraction decreased (50 +/- 12 vs. 36 +/- 9%; P < 0.03) and cardiac output increased (4.9 +/- 1.4 vs. 7.1 +/- 1.6l/minute; P < 0,001) in Group I and remained unchanged in Group II (54 +/- 10 vs. 55 +/- 10%, P = n.s. and 5.5 +/- 1.4 vs. 6.6 +/- 0.9l/minute; P = n.s.) during maximal vasodilation. Beat-to-beat analysis revealed a decrease of left ventricular endsystolic volume index in group I (48 +/- 13 vs. 37 +/- 9 ml/beat; P < 0.05) and no change in group II (61 +/- 20 vs. 62 +/- 20 ml/beat; P = n.s.). In the natural history of chronic AR, the absence of improved LV performance during acute vasodilation using beat-to-beat analysis by MRI may identify patients with more advanced cardiac adaptation to chronic volume overload.

Adult↗
PubMed2001

The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: a cine MRI study.

Cardiac remodeling in case of hypertension induces hypertrophy of myocytes and elevated collagen content and, subsequently, impaired diastolic filling of the left ventricle. The purpose of this prospective study was to evaluate changes of left ventricular (LV) myocardial mass, as well as diastolic filling properties, in hypertensive patients treated with the ACE inhibitor fosinopril. Sixteen hypertensive patients with echocardiographically documented LV hypertrophy and diastolic dysfunction received fosinopril (10-20 mg daily). Measurements of LV myocardial mass and properties of diastolic filling (peak filling fraction (PFF); peak filling rate (PFR)) were performed prior to medication, as well as after 3 and 6 months of therapy using cine magnetic resonance imaging (MRI). Ten healthy subjects served as a control group. LV myocardial mass (g/m2) decreased continuously within 3-6 months of follow-up by 32% (148 +/- 40 vs. 120 +/- 26 vs. 101 +/- 22 g/m2; P < 0.0001/0.005). The extent of regression correlated to the severity of LV hypertrophy at baseline (r = 0.77; P < 0.004). Early diastolic filling increased significantly within 6 months of therapy (PFF (%): 36 +/- 6 vs. 61 +/- 7, P < 0.0001; PFR (mL/second): 211 +/- 48 vs. 282 +/- 48, P < 0.001). Cine MRI can be used to assess the time course of pharmacological effects on cardiac remodeling in the course of hypertension. ACE inhibitor therapy results in a significant reduction of LV mass within 3 months and is accompanied by a normalization of diastolic filling that is completed after 6 months.

Adult↗
PubMed2001

Endothelial dysfunction in patients with polycythaemia vera.

Patients with polycythaemia vera (PV) are at increased risk of developing arterial and venous thromboembolic complications. We investigated whether endothelium-dependent, flow-mediated vasodilatation (FMD) is impaired in PV patients without clinical evidence of artery disease as observed in patients with conventional cardiovascular risk factors. FMD and endothelium-independent, nitroglycerine-induced vasodilatation (NMD) were assessed using high-resolution ultrasound in the brachial artery of 20 patients with PV and 20 sex- and age-matched control subjects (CTL). FMD was markedly impaired in PV patients compared with CTL (7.6 +/- 2.9% versus 11.6 +/- 5.7%, P = 0.009) whereas NMD was similar in both study groups. The impairment of FMD was independently related to the presence of PV (r = -0.434, P = 0.009) and vessel size (r = -0.107, P = 0.038) but was not related to haematocrit values and platelet counts. The results demonstrate that PV is associated with endothelial dysfunction in the pre-clinical phase of arterial disease. However, the precise mechanisms by which PV leads to this altered vascular reactivity remain unclear.

Adult↗
PubMed2001

Informational contribution of noninvasive screening tests for coronary artery disease in patients on chronic renal replacement therapy.

The prevalence of coronary artery disease (CAD) is high in patients on renal replacement therapy; therefore, reliable noninvasive screening tests are needed. We retrospectively determined the sensitivity, specificity, and positive and negative likelihood ratios (LRs) for a history of chest pain, resting and exercise electrocardiography (ECG), thallium dipyridamole scintigraphy, and echocardiography in 42 patients undergoing chronic hemodialysis and 42 patients after renal transplantation who also underwent coronary angiography. In addition, the prognostic power of each test for the occurrence of a cardiovascular event after angiography (therapeutic intervention, myocardial infarction, or cardiovascular death) was evaluated during a follow-up of 37 months. Forty-three patients had significant CAD on angiography. Angina pectoris had a sensitivity of 65% and specificity of 66%, corresponding to a positive LR of 1.9 and a negative LR of 0.5. A variable number of patients underwent noninvasive tests before angiography. Results were similar in patients undergoing hemodialysis and after renal transplantation and in patients with or without angina pectoris. Exercise ECG could not be performed in the majority of patients, and resting ECG (sensitivity, 67%; specificity, 52%; corresponding to a positive LR of 1.4 and negative LR of 0.6) and scintigraphy (sensitivity, 80%; specificity, 37%; positive LR, 1.3; negative LR, 0.5) in patients on renal replacement therapy were not useful for the diagnosis of CAD. Angina also markedly increased the relative odds for the occurrence of a cardiovascular event during follow-up (relative odds, 4.6) compared with other noninvasive tests. Angina pectoris had the best informational and prognostic value of noninvasive screening methods, but angiography seems to be the only method to clearly document CAD in patients on renal replacement therapy.

Aged↗
PubMed2000

Accumulation of oxidized LDL in human semilunar valves correlates with coronary atherosclerosis.

OBJECTIVE: Recent data indicate that oxidized low-density lipoprotein (ox-LDL) has several proatherogenic effects, e.g. induction of macrophage chemoattractants, adhesion molecules, cytokines, type-1 plasminogen activator inhibitor and platelet-derived growth factor A-chain by smooth muscle cells. Therefore, ox-LDL has been utilized as a marker of oxidative modification of proteins in atherosclerosis. Because heart valves consist of smooth muscle cells, fibroblasts and endothelial cells, and because valvular disease and coronary atherosclerosis could result from similar biological processes, we investigated ox-LDL accumulation in isolated aortic and pulmonary valves and coronary arteries from patients with angiographically proven coronary heart disease (CHD, n = 19), patients with idiopathic congestive heart failure (IDCM = idiopathic dilated cardiomyopathy, n = 20), and transplant donors. METHODS: Masson-Goldner staining and immunohistochemistry utilizing anti ox-LDL and CD68 were performed on paraffin sections of freshly isolated semilunar valves. Data were analyzed by digital image planimetry and by visual scoring of staining intensity. RESULTS: Ox-LDL immunoreactivity was identified in the vascular aspect of the attachment line, in the deep valve stroma, and in the ventricular and vascular endothelium of the semilunar valves, colocalizing with macrophages. Valvular ox-LDL area was significantly increased in CHD-patients (P < 0.03) and IDCM-patients (P < 0.04) compared with controls. More ox-LDL was accumulating in the pulmonary valves than in the aortic valves (P = 0.04) as assessed by area and staining intensity. Valvular ox-LDL area in pulmonary valve and aortic valve was significantly correlated with ox-LDL accumulation in the intimal layer (P < 0.001) and medial layer (P < 0.001) of coronary arteries from the same patients. CONCLUSION: The data suggest that the biological process leading to ox-LDL accumulation in coronary atherosclerosis also involves heart valves. Therefore, accumulation of the oxidative stress marker ox-LDL in heart valves illustrates atherosclerosis as an additional mechanisms accelerating valvular degeneration in these patients.

Aged↗
PubMed2000

Response of right ventricular function to prostaglandin E1 infusion predicts outcome for severe chronic heart failure patients awaiting urgent transplantation.

BACKGROUND: Selection of patients for urgent heart transplantation who have end-stage heart failure requires objective criteria to distinguish between subjects who may deteriorate clinically and those who can be stabilized. This population appears to differ in terms of right ventricular function, and right ventricular changes in loading may provide prognostic information. To investigate predictive parameters of patients admitted for urgent heart transplantation, we prospectively studied the mechanical performance of the right ventricle during acute afterload reduction. PATIENTS AND METHODS: We studied 68 heart failure patients hospitalized for bridge-to-transplant. The patients underwent right heart catherization at baseline and during prostaglandin E1 infusion. We stratified patients according to clinical outcome: Group A comprised patients who could be weaned from bridging therapy or who were electively transplanted after at least 90 days, and Group B comprised patients who died or who remained unstable and required transplant under urgent conditions. RESULTS: Right ventricular hemodynamics at baseline were comparable in both groups. However, during maximal vasodilatation, with prostaglandin E1 infusion, the right ventricular end-diastolic volume index (EDVI) was significantly reduced in Group A, (-23 ml/m(2) (p < 0.01) vs +12 ml/m(2) (p = n.s. DeltaEDVI in Group B. Reduction of EDVI by less than 10% during prostaglandin E1 infusion has a sensitivity of 89% and a specificity of 70% for clinical deterioration. CONCLUSIONS: The response of right ventricular volumes to prostaglandin E1 may predict the outcome of patients with severe congestive heart failure listed for urgent heart transplantation.

Aged↗
PubMed2000

Effects of successful parathyroidectomy on altered arterial reactivity in patients with hypercalcaemia: results of a 3-year follow-up study.

OBJECTIVE: Serum calcium was found to be an independent, prospective risk factor for myocardial infarction. We have previously shown that altered arterial reactivity in the course of primary hyperparathyroidism, a disease characterized by hypercalcaemia, may predominantly involve the arterial media and not the endothelium as observed in patients with various stages of atherosclerosis. The present study was performed to test whether successful parathyroidectomy can improve vascular reactivity in patients with primary hyperparathyroidism. SUBJECTS AND DESIGN: Endothelium-dependent, flow-mediated and endothelium-independent, nitroglycerin-induced dilatation were assessed by brachial artery ultrasound (7 MHz) in 18 patients with primary hyperparathyroidism (mean +/- SD; age, 55.1 +/- 12.6) prior to and 3 years after successful parathyroidectomy. RESULTS: Parathyroidectomy resulted in significant decreases of PTH (242 +/- 186 vs. 34 +/- 24 ng/l, P = 0. 0001) and serum calcium levels (2.8 +/- 0.3 vs. 2.4 +/- 0.1 mm/l, P = 0.00001) and in an increase of serum phosphate levels (0.78 +/- 0. 23 vs. 1.17 +/- 0.18 mm/l, P = 0.00001). However, normalization of hormone and electrolyte levels did not lead to an improvement of flow-mediated dilatation (12.1 +/- 3.1 vs. 11.0 +/- 5.4&, P = 0.49) or nitroglycerin-induced dilatation (12.5 +/- 3.1 vs. 13.2 +/- 6.8%, P = 0.68) within the follow-up period. No changes were observed with respect to the risk factor profile, vessel size and blood flow. CONCLUSION: These data suggest that restoration of normocalcaemia by parathyroidectomy cannot improve vascular reactivity in patients with primary hyperparathyroidism but may prevent further progression of vascular disease within this period of time.

Aged↗
PubMed1999

"Overestimation" of catheter gradients by Doppler ultrasound in patients with aortic stenosis: a predictable manifestation of pressure recovery.

OBJECTIVES: This study sought to evaluate whether pressure recovery can cause significant differences between Doppler and catheter gradients in patients with aortic stenosis, and whether these differences can be predicted by Doppler echocardiography. BACKGROUND: Pressure recovery has been shown to be a source of discrepancy between Doppler and catheter gradients across aortic stenoses in vitro. However, the clinical relevance of this phenomenon for the Doppler assessment of aortic stenosis has not been evaluated in patients. METHODS: Twenty-three patients with various degrees of aortic stenosis were studied with Doppler echocardiography and catheter technique within 24 h. Using an equation previously validated in vitro, pressure recovery was estimated from peak transvalvular velocity, aortic valve area and cross-sectional area of the ascending aorta and compared with the observed differences between Doppler and catheter gradients. Doppler gradients were also corrected by subtracting the predicted pressure recovery and then were compared with the observed catheter gradients. RESULTS: Predicted differences between Doppler and catheter gradients due to pressure recovery ranged from 5 to 82 mm Hg (mean +/- SD, 19 +/- 16 mm Hg) and 3 to 54 mm Hg (12 +/- 11 mm Hg) for peak and mean gradients, respectively. They compared well with the observed Doppler-catheter gradient differences, ranging from -5 to 75 mm Hg (18 +/- 18 mm Hg) and -7 to 48 mm Hg (11 +/- 13 mm Hg). Good correlation between predicted pressure recovery and observed gradient differences was found (r = 0.90 and 0.85, respectively). Both the noncorrected and the corrected Doppler gradients correlated well with the catheter gradients (r = 0.93-0.97). However, noncorrected Doppler gradients significantly overestimated the catheter gradients (slopes, 1.36 and 1.25 for peak and mean gradients, respectively), while Doppler gradients corrected for pressure recovery showed good agreement with catheter gradients (slopes, 1.03 and 0.96; standard error of estimate [SEE] 8.1 and 6.9 mm Hg; mean difference +/- SD 0.4 +/- 8.0 mm Hg and 1.1 +/- 6.8 mm Hg for peak and mean gradients, respectively). CONCLUSIONS: Significant pressure recovery can occur in patients with aortic stenosis and can cause discrepancies between Doppler and catheter gradients. However, pressure recovery and the resulting differences between Doppler and catheter measurements may be predicted from Doppler velocity, aortic valve area and size of the ascending aorta.

Adult↗
PubMed1998

Impairment of endothelium-independent vasodilation in patients with hypercalcemia.

OBJECTIVE: Patients with primary hyperparathyroidism (PHPT) and/or hypercalcemia are at increased risk for myocardial ischemia. Whether PHPT is associated with altered endothelium-dependent dilation, vascular smooth muscle cell function, or both is unknown. This study was performed to test the hypothesis that endothelium-dependent, flow-mediated dilation (FMD) and/or endothelium-independent, nitroglycerin-induced dilation (NMD) is impaired in the preclinical phase of vascular disease in patients with PHPT. METHODS: Twenty-six PHPT patients (mean +/- SD; age 55 +/- 15 y, serum calcium 3.00 +/- 0.37 mmol/l, serum phosphate 0.79 +/- 0.21 mmol/l, iPTH 249 +/- 262 pg/ml) with no evidence of coronary artery disease (CAD) as well as 26 normocalcemic control subjects (CTL; age 51 +/- 12 y) were studied. FMD following reactive hyperemia and NMD after 0.8 mg nitroglycerin (NTG) were assessed in the brachial artery by using high resolution ultrasound (7 MHz). RESULTS: NMD was impaired in PHPT patients compared to CTL (11.9 +/- 3.9% vs. 15.6 +/- 5.7%; p = 0.012). FMD was similar in both study groups (11.6 +/- 4.6% vs. 12.6 +/- 4.9; NS). The ratio of FMD to NMD was significantly different between PHPT patients and CTL (0.98 +/- 0.19 vs 0.81 +/- 0.25, p = 0.0009). On multiple stepwise regression analysis serum calcium was independently associated with the FMD/NMD ratio (r = 0.34, p = 0.017). CONCLUSIONS: Endothelium-independent vasodilation is impaired in PHPT patients without clinical evidence of coronary artery disease compared to normocalcemic CTL, while endothelium-dependent dilation was similar in both study groups. Thus, altered arterial reactivity in the course of PHPT may predominantly involve the arterial media and not the endothelium as observed previously in patients with various stages of atherosclerosis.

Adult↗
PubMed1997

Urinary apo(a) discriminates coronary artery disease patients from controls.

Increased plasma lipoprotein (a) (Lp(a)) levels are associated with premature cardiovascular diseases and stroke. Since Lp(a) immune reactivity is found in urine we compared urinary apolipoprotein (a) (apo(a)) with plasma Lp(a) levels in 116 patients suffering from angiographically proven coronary artery diseases with that of 109 controls. Urinary apo(a) investigated by immuno blotting, revealed a distinct apo(a) fragmentation pattern with molecular weights between 50 and 160 kDa. Apolipoprotein B however was not secreted into urine. Lp(a) and apo(a) were measured by a fluorescence immuno assay. Within single individuals, urinary apo(a) levels correlated significantly with creatinine (Rho, 0.98; P < 0.0005). Medians and 25/75 percentiles of urinary apo(a) in coronary artery disease (CAD) patients were 5.70, 3.25 and 10.35 microg/dl and in controls 2.64, 1.43 and 3.50 microg/dl respectively. At cut-off levels of 30 mg/dl for plasma Lp(a) and 10 microg/dl of urinary apo(a) respectively, both paramenters showed comparable sensitivities (33.8% vs. 26.7%), yet the specificity (76.1% vs. 91.7%) and the positive predictive value (60.0% vs.76.4%) of urinary apo(a) were much higher. In receiver-operating characteristic plots, urinary apo(a) was much more sensitive at high specificities i.e. greater than 60% as compared to Lp(a). Urinary secretion of apo(a) fragments normalized to creatinine is stable in a given individual and significantly associated with coronary artery disease.

Apolipoproteins A↗
PubMed1997

Time course of regression of left ventricular hypertrophy after successful parathyroidectomy.

BACKGROUND: We have shown that primary hyperparathyroidism may induce myocardial hypertrophy that is reversible after successful parathyroidectomy. The present study was designed to assess the time course of regression of left ventricular hypertrophy without further effects of drug treatment or disease states. METHODS: We performed echocardiographic studies in 16 patients with primary hyperparathyroidism and normal resting blood pressure, normal systolic left ventricular function, no evidence of valvular disease, and without any current medication before parathyroidectomy, as well as during intermediate and long-term follow-up after successful parathyroidectomy. RESULTS: Eleven patients (69%) had end-diastolic wall thickness of the interventicular septum and/or posterior wall greater than 11 mm on baseline echocardiogram. After surgical removal of the inciting disease and an average of 12.5 and 45.7 months of follow-up with normocalcemia and normal parathyroid hormone levels a prolonged regression of left ventricular hypertrophy was observed (interventricular septum, -0.68 mm at 12.5 months and -1.69 mm at 45.7 months; p = 0.02; posterior wall, -0.46 mm at 12.5 months and -2.24 mm at 45.7 months; p = 0.02). CONCLUSIONS: We conclude that the removal of the cause of myocardial hypertrophy by successful parathyroidectomy leads to a prolonged reversal of hypertrophy. The progressive reduction of left ventricular wall thickness is not completed within 12 months.

Aged↗
PubMed1997

Urinary excretion of apo(a) in patients after kidney transplantation.

BACKGROUND: Increased plasma Lipoprotein (a) (Lp(a)) levels are strongly associated with premature cardiovascular disease and stroke. The kidney is purported to play an important role in apo(a) catabolism. Therefore we investigated plasma Lp(a) levels in relation to kidney function and urinary apo(a) excretion. METHODS: One hundred and sixteen kidney transplant patients with normal or impaired renal function and 109 age- and sex-matched healthy controls were investigated. Plasma Lp(a) and urinary apo(a) levels were determined immunochemically and all other parameters were determined by routine laboratory methods. RESULTS: Transplant recipients were found to have significantly elevated total cholesterol and LDL-C values, but equal HDL-C values compared to controls. Plasma Lp(a) values were higher and urinary apo(a) excretion was lower in transplant recipients compared to controls, independent of renal function. When the patient group was subdivided into 'normal' and 'impaired creatinine clearance', only the latter group secreted less apo(a) than normal controls. CONCLUSION: These data suggest that urinary apo(a) excretion is reduced in transplant recipients with impaired excretory graft function, which may contribute to the elevation of plasma Lp(a) levels in these patients.

Aged↗
PubMed1997

Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up.

Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.

Aged↗
PubMed1996

Rapid adaptation of myocardial calcium homeostasis to short episodes of ischemia in isolated rat hearts.

Short episodes of ischemia and reperfusion (ischemic preconditioning) have been shown to attenuate the detrimental rise in intracellular free Ca2+ ([Ca2+]i) caused by subsequent sustained ischemia. The purpose of this study was to investigate the detailed time course of [Ca2+]i during such short episodes of ischemia and reperfusion. [Ca2+]i was measured at a high time resolution by surface fluorometry and indo-1 in isolated perfused rat hearts during three episodes of 5 minutes of ischemia followed by 5 minutes of reperfusion. We found that the rise in systolic [Ca2+]i was significantly smaller during the second (191% +/- 67%) and third (194% +/- 75%) episodes of ischemia than during the first episode (289% +/- 75%, P < 0.05 vs both subsequent episodes). This attenuated rise in systolic [Ca2+]i was preserved during perfusion with low extracellular Na+ (105.5 mmol/L [Na+]o). During short episodes of ischemia and reperfusion, [Ca2+]i rises less during the second and third ischemic episode than during the first episode. Thus one transient ischemic stimulus led to a rapid adaptation of [Ca2+]i homeostasis to subsequent ischemic conditions. Such a rapid adaptation might be an important mechanism of the ischemic preconditioning phenomenon in protecting against ischemic injury.

Adaptation, Physiological↗
PubMed1996

Assessment of myocardial injury by serum tumour necrosis factor alpha measurements in acute myocardial infarction.

Clinical and experimental data have shown that after acute myocardial infarction there is a significant release of tumour necrosis factor alpha. Therefore, an attempt was made to correlate changes in serum tumour necrosis factor alpha concentrations with indices of infarct extent in patients with acute myocardial infarction. In 50 patients with acute myocardial infarction, blood samples for evaluation of tumour necrosis factor alpha and alpha-hydroxybutyrate-dehydrogenase were collected every 6 h until 120 h after admission. Infarct extent was estimated by clinical parameters such as the occurrence of heart failure and rhythm disturbances, by enzymatic methods such as cumulative release of alpha-hydroxybutyrate-dehydrogenase and imaging techniques, by late resting single photon emission tomography--201 thallium scintigraphy--using an extent score and by echocardiography using a wall motion index. The maximum change in serum tumour necrosis factor alpha after infarction (delta TNF) was calculated by subtracting tumour necrosis factor alpha concentration on admission from peak tumour necrosis factor alpha concentration. The average peak tumour necrosis factor alpha level was observed 84 h after admission (median: 12 pg.ml-1). Between the 72nd and the 96th h no significant changes in tumour necrosis factor alpha values were observed. Analysis of the data showed that larger delta (TNF) values were found to be associated significantly with signs of heart failure (P = 0.003), the presence of rhythm disturbances (P = 0.001), increased enzymatic infarct extent indicated by cumulative release of alpha-hydroxybutyrate-dehydrogenase (r = 0.74; P < 0.001), large myocardial perfusion defects measured with 201 thallium scintigraphy (r = 0.80; P < 0.001), and a considerable number of left ventricular wall motion abnormalities (r = 0.57; P < 0.001). In conclusion, delta (TNF) is a reliable method of assessing damage severity in the myocardium after acute myocardial infarction. As only two blood samples are necessary within 84 h, the method may be one of the more convenient for the assessment of infarct size in clinical practice.

Adult↗