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1.
Crit Care Med ; 26(12): 1986-90, 1998 Dec.
Article in English | MEDLINE | ID: mdl-9875908

ABSTRACT

OBJECTIVE: To monitor cardiac troponin I (cTnI), a newly developed biochemical index for cardiac damage, in patients during and after coronary artery bypass surgery (CABS) to determine whether the measurement of the serum levels of this marker could be of value in formulating an early diagnosis of Q-wave perioperative myocardial infarction (PMI). DESIGN: Prospective study with sequential measurements of biological markers in a selected surgical patient group. SETTING: University research laboratory and general university hospital (Cardiac Surgery Unit and Anesthesiology and Reanimation Unit). PATIENTS: Forty-two patients undergoing elective CABS without concomitant valvular replacement. INTERVENTIONS: There were no interventions required for this study. However, patients entered into the study had CABS, sequential arterial blood samples, ECG recordings, and echocardiograms performed. MEASUREMENTS AND MAIN RESULTS: Pre-, intra-, and postoperative (up to 48 hrs) measurements of cardiac troponin I, MB-CK, and total creatine kinase, as well as serial electrocardiograms and echocardiograms. Perioperative infarction was assessed as the development of new persistent regional wall motion abnormalities in echocardiography together with electrocardiographic alterations and MB-CK increases. Eight patients had Q-wave PMI. All PMI patients had elevated peak cTnI values (all >9.2 ng/mL), whereas the 34 nonPMI patients had peak values <9.0 ng/mL; therefore, sensitivity and specificity (with a 9.0 ng/mL cut-off value) are 100%. MB-CK measurement peak values did not demonstrate such a high specificity and sensitivity. CONCLUSIONS: Because of its high specificity and sensitivity, serial measurements of cTnI provide a rapid and accurate method for confirming or excluding the diagnosis of perioperative myocardial injury. cTnI evaluation can therefore be used both as an independent prognostic marker for patients undergoing cardiac surgery and as a powerful tool for detecting smaller PMIs often missed with standard PMI diagnostic criteria.


Subject(s)
Coronary Artery Bypass/adverse effects , Myocardial Infarction/diagnosis , Myocardial Infarction/metabolism , Troponin I/blood , Aged , Biomarkers/blood , Creatine Kinase/blood , Echocardiography , Electrocardiography , Female , Humans , Immunoassay , Isoenzymes , Male , Middle Aged , Monitoring, Physiologic , Myocardial Infarction/etiology , Prognosis , Prospective Studies , Reproducibility of Results , Sensitivity and Specificity
2.
J Mol Cell Cardiol ; 29(7): 1877-84, 1997 Jul.
Article in English | MEDLINE | ID: mdl-9236141

ABSTRACT

The aim of our study was to characterize the molecular defect in Italian Marfan patients, thus contributing to the effort of correlating the genotype with the phenotype. In particular, our ultimate goal was to identify the region(s) of the fibrillin 1 (FBN1) gene mainly involved in the health of the heart and of the aorta in terms of the cardiovascular system. We searched for a molecular defect in three patients with classic Marfan syndrome (MFS). The mutations were detected applying heteroduplex analysis to each of the 65 exons of the FBN1 gene amplified by polymerase chain reaction (PCR). Exons containing heteroduplex bands were sequenced directly from PCR products. This study reports the detection of three unique missense mutations in the FBN1 gene in three Italian patients: a 44-year-old adult male and 36-year-old female affected by classic MFS (with all the cardinal manifestations in the cardiovascular, ocular and skeletal systems), and an 11-year-old male affected by infantile (earlier onset) classic MFS. The first two are sporadic cases and present a Cys-->Arg amino acid substitution (T-->C substitution at nucleotide 7729) in exon 62 and a Cys-->Tyr amino acid substitution (G-->A substitution at nucleotide 6695) in exon 54. The third is a familial case which presents a Cys-->Trp aminoacidic substitution (C-->G substitution at nucleotide 3546) in exon 28. Our data confirm that cysteine substitutions in calcium binding epidermal growth factor (cbEGF)-like domains cause severe Marfan phenotype. Exon 24-32 cluster seems to produce an even more severe phenotype. The early characterization may be of clinical relevance for prevention and early surgical treatment of aortic aneurysm or dissection.


Subject(s)
Cardiovascular Diseases/genetics , Marfan Syndrome/genetics , Microfilament Proteins/genetics , Adult , Base Sequence , Child , Female , Fibrillin-1 , Fibrillins , Humans , Male , Mutation , Protein Structure, Secondary
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