Search PubMed⌕ Search

Biomedical subjects

A S Jaffe

Publications and source records attributed to A S Jaffe.

At least 19 recordsLinked to original sources

A new simplified immediate prognostic risk score for patients with acute myocardial infarction.

BACKGROUND: Immediate risk stratification of patients with myocardial infarction in the emergency department (ED) at the time of initial presentation is important for their optimal emergency treatment. Current risk scores for predicting mortality following acute myocardial infarction (AMI) are potentially flawed, having been derived from clinical trials with highly selective patient enrollment and requiring data not readily available in the ED. These scores may not accurately represent the spectrum of patients in clinical practice and may lead to inappropriate decision making. METHODS: This study cohort included 1212 consecutive patients with AMI who were admitted to the Mayo Clinic coronary care unit between 1988 and 2000. A risk score model was developed for predicting 30 day mortality using parameters available at initial hospital presentation in the ED. The model was developed on patients from the first era (training set--before 1997) and validated on patients in the second era (validation set-during or after 1997). RESULTS: The risk score included age, sex, systolic blood pressure, admission serum creatinine, extent of ST segment depression, QRS duration, Killip class, and infarct location. The predictive ability of the model in the validation set was strong (c = 0.78). CONCLUSION: The Mayo risk score for 30 day mortality showed excellent predictive capacity in a population based cohort of patients with a wide range of risk profiles. The present results suggest that even amidst changing patient profiles, treatment, and disease definitions, the Mayo model is useful for 30 day risk assessment following AMI.

Aged↗

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. Various cut off concentrations were analysed, but patients were categorised prospectively as having increased or no increased cTnI based on a cut off concentration of 0.6 ng/ml. The main outcome measure was in-hospital mortality. RESULTS: On admission, 14 of the 48 patients (29%) had cTnI concentrations greater than the receiver operating characteristic curve value used to diagnose acute myocardial infarction (> 0.6 ng/ml). Subsequently, six patients developed increases for an overall prevalence of 42% (20 of 42). The prevalence was higher when lower cut off concentrations were used: 73% (35 of 48) at the 99th centile and 60% (29 of 48) at the 10% coefficient of variability. Increased cTnI > 0.6 ng/ml was associated with a slower oxygen saturation (86 (7)% v 93 (4)%, p < 0.0001) and more frequent involvement of the main pulmonary arteries as assessed by spiral computed tomography (100% v 60%, p = 0.022). In-hospital mortality was 36% (5 of 14) of patients with increases > 0.6 ng/ml v 3% (1 of 42) of patients with lower concentrations (p = 0.008). Increased cTnI > 0.6 ng/ml on admission was the most powerful predictor of mortality (p = 0.046). CONCLUSIONS: In high risk patients with acute PE, cTnI was frequently detected on admission. It was the strongest independent predictor of mortality.

Acute Disease↗

Cardiac troponin levels following monitored epileptic seizures.

Cardiac arrhythmia associated with myocardial injury is a proposed mechanism for sudden unexplained death in epilepsy. The authors measured serial cardiac troponin levels in 11 patients after monitored seizures. Using highly sensitive assays and criteria, no troponin elevations were seen, indicating that myocardial injury does not occur during uncomplicated seizures. An elevation in postictal troponin elevations should suggest the presence of cardiac injury secondary to neurocardiogenic mechanisms or primary cardiac factors, prompting further evaluation.

Adult↗

Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients.

The authors investigated whether patients with drug refractory epilepsy have cardiovascular abnormalities that might be related to a high frequency of sudden death. Twenty-three subjects underwent comprehensive cardiovascular evaluations before and during video-EEG monitoring. ST-segment depression occurred in 40% and was associated with a higher maximum heart rate during seizures. These data suggest that cardiac ischemia may occur in these patients.

Adult↗

The chain of survival.

Explore the source record for details and available documents.

Advanced Cardiac Life Support↗

Elevations in cardiac troponin measurements: false false-positives: the real truth.

The development of assays for troponin markers has improved cardiovascular diagnosis. However, because the assays are so sensitive and specific, elevations are often detected in patients without overt coronary artery disease. Some would like to attribute such elevations to biological "false positives." That is rarely the case. There can be analytic false positives but most such elevations are indicative of subtle degrees of cardiac injury, many not related to ischemic heart disease. The spectrum of such increases and their potential etiologies are elaborated in this article.

Biomarkers↗

Cardiac involvement in patients with acute neurologic disease: confirmation with cardiac troponin I.

BACKGROUND: Patients with acute neurologic illness often manifest findings suggestive of cardiac injury. Their proper interpretation is unclear. Accordingly, we conducted a blinded evaluation to assess the incidence of cardiac injury determined by elevations of cardiac troponin I (cTnI) in patients presenting within 24 hours of a neurologic event and to determine their short- and long-term prognostic effect. METHODS: Blood samples for measurement of cTnI levels were obtained on hospital admission and daily for 3 days and were run by immunoassay. Extensive clinical evaluations including electrocardiograms and echocardiograms were obtained from all patients; daily follow-up evaluations were performed. The clinical electrocardiographic, echocardiographic, and biochemical data were analyzed independently by blinded observers. RESULTS: Peak levels of cTnI were elevated (> or =0.4 microg/L) in 17 patients (19%) (mean + SD, 2.5 + 2.7 microg/L). All patients with elevated cTnI levels had clinical, electrocardiographic, or echocardiographic evidence of cardiac injury except those (n = 5) with minor elevations. One-year mortality was 29% (23/80). Early death (< or =30 days) accounted for 44% of total mortality (n = 10) and was significantly higher in patients with elevated cTnI levels (Wilcoxon P =.01; odds ratio, 6. 4). This difference was less marked by 1 year (Wilcoxon P =.07). CONCLUSIONS: There is a substantial prevalence of myocardial injury in patients with acute neurologic illness. Cardiac injury in this population, as in others, seems to adversely affect prognosis.

Acute Disease↗

Elevated cardiac troponin levels predict the risk of adverse outcome in patients with acute coronary syndromes.

BACKGROUND: Elevations of cardiac troponin T or I are predictive of adverse outcomes in patients with acute coronary syndromes. However, odds ratios (ORs) vary substantially between studies. This investigation refines these values by means of a meta-analysis. METHODS: Twenty-one studies were suitable. ORs were calculated for short-term (30 days) and long-term (5 months to 3 years) follow-up in patients with ST-segment elevation (ST upward arrow), in those without ST-segment elevation (no ST upward arrow), and in patients with unstable angina. The primary end point was a composite of death or nonfatal myocardial infarction. RESULTS: A total of 18,982 patients were included. At 30 days, the OR for death or myocardial infarction was 3.44 (95% confidence interval [CI], 2.94-4.03; P <. 00001) for patients with positive troponin. In the ST upward arrow group, troponin elevations carried a 2.86-fold (95% CI, 2.35-3.47; P <.0001) higher risk during short-term follow-up, which was maintained long term. The no-ST upward arrow patients with troponin elevations manifested a 4.93-fold (95% CI, 3.77-6.45; P <.0001) increase of adverse outcomes. The OR for patients with unstable angina and positive troponin was 9.39 (95% CI, 6.46-13.67; P <.0001). For cardiac death alone, the results were similar. CONCLUSIONS: Patients with acute coronary syndromes who have troponin elevations show a substantial increase in risk during short and long-term follow-up.

Angina, Unstable↗

2001--a biomarker odyssey.

It is a time of transition in the area of biomarkers. Confusion is rampant, progress immense and the challenges invigorating. Better diagnosis is possible if we progress in a rational way and avoid the chaos so often characteristic of transitions by relying on the science of the discipline to keep us on track.

Biomarkers↗

Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease.

BACKGROUND: Although it is now well established that psychiatric depression is associated with adverse outcomes in patients with coronary heart disease (CHD), the mechanism underlying this association is unclear. Elevated heart rate (HR) and plasma norepinephrine (NE), possibly reflecting altered autonomic nervous system activity, have been documented in medically well depressed psychiatric patients, and this pattern is associated with increased risk for cardiac events in patients with CHD. The purpose of this study was to determine whether autonomic nervous system activity is altered in depressed CHD patients. METHODS: HR, plasma NE, and blood pressure (BP) were measured in 50 depressed and 39 medically comparable nondepressed CHD patients at rest and during orthostatic challenge. RESULTS: Resting HR (p = .005), and the change from resting HR at 2, 5, and 10 min after standing (p = .02, .004, and .02, respectively), were significantly higher in the depressed than in the nondepressed patients. There were no differences between the groups in NE or in BP at rest, or in standing minus resting change scores at any time during orthostatic challenge (p < .05). CONCLUSIONS: Depression is associated with altered autonomic activity in patients with CHD, as reflected by elevated resting HR and an exaggerated HR response to orthostatic challenge. Previously reported differences in NE levels between depressed and nondepressed patients were not replicated.

Aged↗