Comparison of methods to identify individuals at increased risk of cardiovascular disease in Italian cohorts.

Background And Aims: Guidelines for the primary prevention of cardiovascular disease recommend the use of risk-assessment methods to identify high risk patients who can benefit from lifestyle changes and/or drug treatment. Although all these risk-prediction methods are based on the same principle, they produce different risk estimates. The aim of this study was to compare the most recent and widely used cardiovascular risk-prediction methods and the respective guidelines when applied to Italian cohorts.

Increased cardiac troponin I on admission predicts in-hospital mortality in acute pulmonary embolism.

Background: To investigate the frequency of cardiac troponin I (cTnI) increases in patients with pulmonary embolism (PE) and to assess the correlation between this finding, the clinical presentation, and outcomes.

Methods: Consecutive patients admitted to the coronary care unit with acute PE were prospectively enrolled between January 2000 and December 2001. cTnI was sequentially determined.

Serum cardiac troponin I levels and ECG/Echo monitoring in breast cancer patients undergoing high-dose (7 g/m(2)) cyclophosphamide.

High-dose cyclophosphamide (HD-CTX) is largely employed in high-dose chemotherapy (HD-CHT) protocols. HD-CTX dose-limiting toxicity expresses itself as cardiac toxicity which is fatal in a minority of patients. The pathophysiology of HD-CTX-associated cardiotoxicity is still poorly understood.

[Assessment of cardiotoxicity of high dose cyclophosphamide with electrocardiographic, echocardiographic, and troponin I monitoring in patients with breast tumors].

Background: High-dose cyclophosphamide is the nucleus for virtually all high-dose chemotherapy protocols. Non-hematologic dose-limiting toxicity is represented by acute cardiomyopathy, even fatal in a minority of patients. The pathophysiology of such a cardiotoxicity is still poorly understood.

Cardiac troponin I as diagnostic and prognostic marker in severe heart failure.

Background: Cardiac cell death has been shown to occur in heart failure and has been implicated as one of the mechanisms responsible for progression of the disease. Cardiac Troponin I (cTnI) represents a highly sensitive marker for myocardial cell death. Based on previous studies reporting that cTnI may be detected in patients with heart failure, we evaluated the clinical correlates and prognostic implications of detectable cTnI in a consecutive series of patients with severe heart failure.

External Quality Assessment of stat test intralaboratory turnaround times. Pilot study from the Members of the Working Group for the Standardization and Promotion of Turnaround Time Control under the Auspices of the Comitato Italiano per la Standardizzazione dei Metodi Ematologici e di Laboratorio.

We describe procedures, results and prospects of a pilot program in External Quality Assessment (EQA) of the stat test intralaboratory turnaround times. Our goals are to promote quality by systematic monitoring and comparison of performances by laboratories, continuous investigation into the state of the art of the processes from receipt of sample to transmission of results and creation of a data base for standardization of measures and definition of consensus values for turnaround time. Of 30 laboratories invited to participate, 25 took part, agreeing to record times of arrival and transmission for all determinations of three analytes (blood hemoglobin, serum/plasma potassium and plasma prothrombin time) for seven consecutive days and to continue for one or more further periods of seven days as necessary if there were less than 300 determinations for each analyte.

Detectable serum troponin I in patients with heart failure of nonmyocardial ischemic origin.

Cardiac troponin I, a specific and sensitive marker of myocardial damage, was detected in the blood of 6 of 26 patients studied in our Heart Failure Clinic. In these patients functional class, ventricular function, and prognosis were significantly worse than in those without detectable troponin I. This study suggests that troponin I may represent the biochemical marker of myocardial damage occurring in severe heart failure.

[Troponin T, Troponin I and CK-MB (mass) in the detection of periprocedural myocardial damage after coronary angioplasty].

The development of methods for the detection of circulating CK-MB mass, cardiac troponin T (cTn-T) and troponin I (cTn-I) has increased the diagnostic potential in the identification of myocardial damage. Coronary angioplasty (PTCA) represents a widely accepted revascularization procedure and a clinical model of induced ischemia. Using these new biochemical markers, we evaluated the incidence and the clinico-procedural correlates of minor myocardial damage (MMD) in a series of patients treated with PTCA in our Department.

Troponin T, troponin I and creatine kinase-MB mass after elective coronary stenting.

Objective: To assess whether and to what extent elective coronary stenting is associated with biochemical evidence of minor myocardial damage (MMD), as defined by the detection of abnormal post-procedural serum levels of one more among the following markers of ischaemic injury: creatine kinase (CK)-MB mass, troponin T (Tn-T) and troponin I (Tn-I).

Methods: Nineteen elective procedure of coronary stenting were compared with a matched group of 25 conventional percutaneous transluminal coronary angioplasty (PTCA) procedures performed in our laboratory from March to June 1995. Cases with evolving or recent (< 2 weeks) myocardial infarction, chronic total occlusions and dilation of saphenous vein grafts were excluded.