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Biomedical subjects

T Vrobel

Publications and source records attributed to T Vrobel.

At least 19 recordsLinked to original sources

Evaluation of a proposed panel of cardiac markers for the diagnosis of acute myocardial infarction in patients with atraumatic chest pain.

OBJECTIVE: The purpose of this study was to evaluate retrospectively the efficacy of a proposed panel of three cardiac markers (myoglobin, creatine kinase-MB mass [CK-MB], and cardiac troponin I) in the diagnosis of acute myocardial infarction (AMI) in patients with atraumatic chest pain. DESIGN: A total of 110 patients admitted for the evaluation of atraumatic chest pain were examined. Forty-one of these patients were diagnosed with AMI. RESULTS: Five of the 41 patients with AMI had abnormally elevated myoglobin levels, whereas values of CK-MB and/or cardiac troponin I remained negative. Creatine kinase-MB mass alone had a sensitivity of 92.7%, a specificity of 89.9%, a positive predictive value of 84.4%, and a negative predictive value of 95.0% for the diagnosis of AMI. Cardiac troponin I alone had a sensitivity of 90.2%, a specificity of 95.7%, a positive predictive value of 92.5%, and a negative predictive value of 94.3% for the diagnosis of AMI. Cardiac troponin I is a more specific marker for the diagnosis of AMI than CK-MB, particularly in patients with chronic renal failure who are evaluated for chest pain. The combination of CK-MB and cardiac troponin I increased the sensitivity to 100% and the negative predictive value to 100% and had a specificity of 88.4% and a positive predictive value of 83.7%. The panel was diagnostic for all patients with AMI within 12 hours after admission. CONCLUSIONS: Our preliminary results indicate that this panel is highly effective for evaluation of AMI in patients with atraumatic chest pain. Elevated myoglobin levels were useful in detecting patients at high risk for AMI who initially were not detected with other markers. The combination of CK-MB and cardiac troponin I provided much higher sensitivity and had a much higher negative predictive value for the evaluation of AMI than cardiac troponin I or CK-MB alone. The 100% negative predictive value is particularly important because it indicates that patients with negative CK-MB and cardiac troponin I values 12 hours after admission have a negligible likelihood of AMI.

Aged

Amiodarone pulmonary toxicity.

Of the side effects that complicate amiodarone therapy, pulmonary fibrosis is potentially the most serious. Therefore, the development of techniques to predict the onset of this troublesome reaction would be of great practical value. Reports of 39 patients who developed pulmonary toxicity with amiodarone were evaluated for clues to precipitating factors and information on the response to corticosteroid treatment. The majority of patients were being given maintenance doses greater than 400 mg/day. Patients appeared to improve after withdrawal of amiodarone, both with and without corticosteroid treatment. In addition, a case report is presented of a patient who developed pulmonary changes that disappeared when amiodarone was withdrawn and did not recur when amiodarone was reinstituted. Data from sequential pulmonary function tests and cumulative amiodarone dosage in 35 patients were also examined to determine their value in predicting pulmonary complications. Pulmonary function tests did not appear to be useful in predicting the likelihood of an individual patient's developing pulmonary complications. Although none of the available information identifies the mechanism mediating amiodarone pulmonary toxicity, the frequency of the complication probably can be reduced by timely reductions in maintenance dosage.

Adrenal Cortex Hormones

Hyponatraemia as a marker for high renin heart failure.

The factors that might activate the renin-angiotensin system in treated heart failure were explored. Serum Na+ correlated inversely with plasma renin activity. The degree of congestive heart failure measured by right atrial pressure, pulmonary capillary wedge pressure, cardiac index, and systemic vascular resistance did not correlate with plasma renin activity. Similarly, renal function as measured by blood urea nitrogen, creatinine, and urinary Na+ excretion did not correlate with plasma renin activity. In a prospectively screened group, seven patients with congestive heart failure who were found to be hyponatraemic had plasma renin activities greater than 15 ng/ml per h. Serial determinations in one patient showed plasma renin activity to vary inversely with the serum Na+. It is concluded that serum sodium can be used to identify those patients with congestive heart failure who have a high plasma renin activity. The value of identifying these high renin heart failure patients was seen in their response in four cases to specific therapy with a converting enzyme inhibitor.

Captopril

Role of the renin-angiotensin system in the systemic vasoconstriction of chronic congestive heart failure.

In 15 patients with severe chronic left ventricular failure, plasma renin activity (PRA) ranged widely, from 0.2--39 ng/ml/hr. The level of PRA was unrelated to cardiac output (CO) or pulmonary artery wedge pressure (PWP), but was slightly negatively correlated with mean arterial pressure (MAP) (r = -0.45) and systemic vascular resistance (SVR) (r = -0.40). After infusion of the angiotensin converting enzyme inhibitor teprotide (SQ 20,881) PWP fell from 26.3 +/- 1.3 (SEM) to 20.3 +/- 1.4 mm Hg (P less than 0.001), CO rose from 3.94 +/- 0.23 to 4.75 +/- 0.31 l/min (P less than 0.001), MAP fell from 87.5 +/- 3.8 to 77.9 +/- 4.1 mm Hg (P less than 0.001) and SVR from 1619 +/- 148 to 1252 +/- 137 dyne-sec-cm-5 (P less than 0.001). The fall in MAP and in SVR was significantly correlated with control PRA (r = 0.68 and r = 0.58, respectively). When subjects were divided on the basis of control PRA the hemodynamic response to teprotide was greatest in the high renin group. PRA rose after teprotide (8.7 +/- 3.4 to 37.9 +/- 7.7 ng/ml/hr, P less than 0.05) but plasma norepinephrine fell (619.1 +/- 103.6 to 449.7 +/- 75.7, P less than 0.05). The renin-angiotensin system thus appears to have an important role in the elevated SVR in some patients with heart failure. Chronic inhibition of converting enzyme should be explored as a possible therapeutic approach.

Adult