Pandora's box is torn asunder.
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Acute Disease↗
Biomedical subjects
A S Jaffe
Publications and source records attributed to A S Jaffe.
Direct comparison of early elevations of cardiac troponin T and I in patients with clinical unstable angina.
BACKGROUND: The aim of this study was to compare the prognostic efficacy of cardiac troponin T (cTnT) and I (cTnI) in patients with clinical unstable angina. METHODS: We studied 74 patients with chest pain at rest, electrocardiographic evidence of myocardial ischemia, and normal (<6.7 ng/mL) values of creatine kinase-MB. cTnT was measured with a commercial assay (cutoff level 0.1 ng/mL) and cTnI with a preliminary research application (cutoff level 3.1 ng/mL). All patients had blood drawn at baseline and 8 hours thereafter. The prospectively defined end point was the proportion of patients identified by each assay as having myocardial damage. RESULTS: cTnT and cTnI were elevated in the same percentage of patients (18 of 74; 24%). Overall, 23 patients had elevations of 1 or both markers. In 13 there were elevations of both. Ten patients had elevations of only one (5 for each marker). In 51 patients, no elevations were present. Death or nonfatal myocardial infarction was more frequent in patients with elevated cTnI (27.7% vs 5.3%; P =.02) than those with normal values. The prognostic influence of cTnT was less (17% vs 8.5%; P =.2). However, the difference between the 2 markers when compared directly was not statistically significant (27.7% vs 17%; P = NS). CONCLUSIONS: These data indicate that both markers identify myocardial damage in equal numbers of patients with clinical unstable angina. Patients with elevations had a worse short-term outcome. The significance of the minor differences in prognostic value will require additional studies.
Aged↗
Resuscitation 2000: the need for improved databases in regard to neurological outcomes.
The Utstein protocol was developed to facilitate the collection of a consistent data base with which to evaluate the success or failure of resuscitative efforts. We urge redrafting of the section on neurological outcomes which should be an essential component of all outcome studies. Once this is accomplished, we believe that the use of this format should be demanded by every editor to whom an article on resuscitation is submitted.
Central Nervous System Diseases↗
Adherence to a prophylactic medication regimen in patients with symptomatic versus asymptomatic ischemic heart disease.
Although angina pectoris is the most common symptom of coronary artery disease, some patients do not experience angina during ischemic episodes. The effects of asymptomatic (silent) heart disease on patient self-management have rarely been studied. Studies of other patient populations with asymptomatic illnesses indicate that patients with silent myocardial ischemia might adhere less well to a prophylactic medication regimen than would those with symptomatic ischemia. Depression, a state associated with poor adherence to medical regimens is more common among patients with symptomatic ischemia. For prevention of thromboembolic events, 37 patients with documented ischemic heart disease who denied having anginal symptoms and 28 patients who reported almost daily symptoms were given a 3-week supply of low-dose aspirin packaged in an unobtrusive electronic adherence monitor. All other medications were provided in standard pill bottles. The symptomatic patients removed their prescribed aspirin on 62.4% of the days; the patients with silent ischemia took their medication on 77.3% of the days. Possible explanations for these results, their clinical implications, and directions for future research are discussed.
Aged↗
Prognostic influence of elevated values of cardiac troponin I in patients with unstable angina.
BACKGROUND: Elevations of the MB isoform of creatine kinase (CK) and cardiac troponin T seem to confer an adverse prognosis in unstable angina. We examined whether this prognostic influence is also present for cardiac troponin I (cTnI), a new and even more specific marker of myocardial injury. METHODS AND RESULTS: We studied 106 patients with the clinical diagnosis of unstable angina showing chest discomfort at rest within 48 hours of admission, ECG evidence of myocardial ischemia, and normal values of total CK over the initial 16 hours of observation. The primary end point was death or nonfatal myocardial infarction (MI) at 30 days; the secondary end point was the incidence of cardiac events at 1 year. Blood was drawn every 8 hours for 3 days. Thirteen patients were excluded because of increased CK-MB mass concentrations within 16 hours of admission (non-Q-wave MI) and 2 because of inadequate blood sampling. Of the remaining 91 patients, 22 had cTnI elevations on admission (n=7) or after 8 hours (n=15). At 30 days, no deaths (0%) and 4 MIs (5.8%) occurred in the 69 patients with normal cTnI compared with 2 deaths (9.1%) and 4 MIs (18.2%) in the 22 patients with elevated cTnI. The combined incidence of death and nonfatal MI was 5.8% and 27.3%, respectively (P=.02). At 1 year, only 68% of patients with elevated cTnI were free of cardiac events, compared with 90% of those without elevations (P=.01). CONCLUSIONS: These data indicate that cTnI is an important prognostic variable in patients with unstable angina. Elevations of cTnI predict an adverse short- and long-term prognosis.
Aged↗
Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates.
BACKGROUND: Endomyocardial biopsy is currently the standard method used to diagnose myocarditis. However, it is invasive and has a low diagnostic yield. Because the histological diagnosis of myocarditis requires the presence of myocyte injury, we sought to determine whether measurement of cardiac troponin I (cTnI), which is a serum marker with high sensitivity and specificity for cardiac myocyte injury, could aid in the diagnosis of myocarditis. METHODS AND RESULTS: To validate this approach, cTnI values were first measured in mice with autoimmune myocarditis. cTnI values were elevated in 24 of 26 mice with myocarditis but were not elevated in any of the control animals (P < .001). Next, cTnI values were measured in the sera from 88 patients referred to the Myocarditis Treatment Trial and were compared with creatine kinase-MB (CK-MB) values measured in the same patients. cTnI values were elevated in 18 (34%) of 53 patients with myocarditis and in only 4 (11%) of 35 patients without myocarditis (P = .01). In contrast, CK-MB values were elevated in only 3 (5.7%) of 53 patients with myocarditis and 0 of 35 patients without myocarditis (P = .27). Thus, elevations of cTnI occurred more frequently than did elevations of CK-MB in patients with biopsy-proven myocarditis (P = .001). Importantly, elevations of cTnI in patients with myocarditis were significantly correlated with < or = 1 month duration of heart failure symptoms (P = .02), suggesting that the majority of myocyte necrosis occurs early, and thus the window for diagnosis and treatment may be relatively brief. CONCLUSIONS: cTnI was superior to CK-MB for detection of myocyte injury in myocarditis, and cTnI elevations were substantially more common in the first month after the onset of heart failure symptoms.
Animals↗
Cardiac troponin I in pediatrics: normal values and potential use in the assessment of cardiac injury.
OBJECTIVE: To establish normal values and determine the impact of congenital or acquired heart disease on serum cardiac troponin I (cTnI). METHODS: Concentrations of cTnI were measured in two groups of children. Group A represented ambulatory pediatric patients with no apparent cardiac disease (n = 120) and patients in stable condition with known congenital or acquired cardiac abnormalities (n = 96); group B was composed of patients admitted to intensive care units with normal echocardiograms (n = 16), with abnormal echocardiograms (n = 36), and those with blunt chest trauma who were thought to have cardiac contusions (n = 7). RESULTS: The cTnI concentrations were generally less than 2.0 ng/ml in group A and frequently below the level of detection for the assay (1.5 ng/ml). There was no statistical difference between the two outpatient subgroups (p = 0.66). Nine intensive care patients had cTnI values greater than 2.0 ng/ml. Six of these patients, all with abnormal echocardiograms, had values less than 7.7 ng/ml. All improved and had subsequent normal cTnI concentrations. None of the three remaining patients (two with systemic illness (trauma and sepsis) and one with severe pulmonary hypertension), all with values greater than 8.0 ng/ml, survived. Three of the four patients with high likelihood of cardiac contusion had cTnI concentrations greater than 2.0 ng/ml (including one patient who died). CONCLUSIONS: Cardiac troponin-I values are generally not elevated in children with stable cardiac disease or general pediatric conditions. In the context of severe acute illness, significant elevation of cTnI may be an indicator of poor outcome. Elevation of cTnI may also have diagnostic value in cases when cardiac contusion is suspected.
Adolescent↗
Prolonged exercise decreases serum leptin concentrations.
Serum leptin and free fatty acid concentrations were determined in two groups of subjects undergoing strenuous exercise: 12 men who fasted overnight and then pedaled a stationary ergometer for 2 hours, and 14 nonfasting ultramarathon runners. Blood samples were collected before exercise, immediately after cessation of exercise, and 6 to 24 hours after the end of the exercise period. Two hours of strenuous pedaling following an overnight fast significantly reduced mean leptin levels by 8.3%; free fatty acids were highly increased and correlated well with the decrease in serum leptin (r = .737, P = .01). After 6 hours of rest and refeeding, leptin concentrations recovered to preexercise levels and free fatty acid concentrations were decreased to less than preexercise levels. A similar decrease in serum leptin levels (12.3%) occurred in subjects who fasted overnight and then for a period corresponding to the cycle exercise period. The prolonged exercise of an ultramarathon significantly reduced leptin concentrations by 32% in comparison to prerace levels; free fatty acid concentrations were highly increased, but did not correlate with the change in serum leptin concentrations (r = .366, P = .20). Leptin and free fatty acid concentrations all trended toward prerace levels in blood samples collected 18 to 24 hours after cessation of racing. The results suggest that the negative energy balance of exercise can reduce serum leptin concentrations, but that the significant decrease occurs only at extremes of severity/duration of the exercise-induced negative balance. The possible physiological role of reduced leptin concentrations in response to energy balance and the role of free fatty acids in mediating the response are discussed.
Adult↗
Transient right but not left ventricular dysfunction after strenuous exercise at high altitude.
OBJECTIVES: We sought to evaluate whether prolonged exercise in ultramarathon runners results in left ventricular (LV) damage. BACKGROUND: Strenuous exercise has been reported to cause LV damage. METHODS: Fourteen runners who completed an ultramarathon at high altitude underwent echocardiography, finger-tip oximetry and blood measurements of cardiac troponin I (cTnI) and creatine kinase, MB fraction (CK-MB) levels before, immediately after and 1 day after the race. RESULTS: At baseline, the echocardiograms showed normal LV and right ventricular (RV) size and function in all subjects, as well as mild tricuspid regurgitation in nine subjects, with normal estimated pulmonary artery systolic pressure (mean 28 mm Hg). At baseline, all oxymetric readings and CK-MB measurements were normal, and cTnI was undetectable. Immediately after the race, the echocardiograms showed the expected augmentation of global and segmental LV function in all subjects. Although the RV was normal in nine subjects, five developed marked RV dilation and hypokinesia, paradoxic septal motion, pulmonary hypertension and wheezing. CK-MB values were elevated in all subjects. In all but one subject cTnI was undetectable. In that subject there was a small elevation in cTnI accompanied by severe RV dysfunction and pulmonary hypertension. At the 1-day follow-up study, the echocardiographic measurements had normalized in all subjects. CONCLUSIONS: In trained athletes, strenuous exercise at high altitude did not result in LV damage. However, wheezing, reversible pulmonary hypertension and RV dysfunction occurred in a third of those completing the race. The incidence and pathogenesis of these findings remain to be determined.
Adult↗
Cardiac troponin I levels are normal or minimally elevated after transthoracic cardioversion.
OBJECTIVES: The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury. BACKGROUND: Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB). METHODS: We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated. RESULTS: Patients received a mean (+/-SD) of 2.1 +/- 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal < or = 0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal < 6.7) in only one patient after cardioversion. CONCLUSIONS: Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.
Aged↗
Time course of lysophosphatidylcholine release from ischemic human myocardium parallels the time course of early ischemic ventricular arrhythmia.
BACKGROUND: We determined the kinetics of the release of lysophosphatidylcholine (LPC) into the coronary sinus of patients undergoing stress tests after coronary artery bypass grafting. The kinetics were consistent with a role for this amphiphile in the pathogenesis of ischemic ventricular arrhythmia, a major cause of sudden death. METHODS: Stress testing was initiated in the operating suite by pacing at a rate of 160 beats/min for 2 min. Ischemia was then induced by clamping the bypass grafts to the anterior wall for a maximal time of 4 min. RESULTS: The pacing procedure induced a prompt but reversible increase in coronary sinus LPC concentration from a baseline of 60.9 +/- 2.5 to 83.8 +/- 5.0 mumol/l via pacing alone, and a further increase to 101.8 +/- 6.7 mumol/l when the grafts were clamped for 2 min (P < 0.01). Six minutes after the cessation of pacing, LPC concentration returned to 67.5 +/- 4.4 mumol/l. CONCLUSIONS: These results demonstrate that severe myocardial ischemia is an agonist for rapid release of LPC from the myocardium. Kinetics of this release paralleled the time-course of early onset of electrophysiologic changes in isolated myocytes and perfused heart preparations in vitro. These results indicate that LPC may have an important role in the pathogenesis of ischemic ventricular arrhythmia in patients.
Aged↗
Troponin, where do we go from here?
The development of new techniques brings new challenges of interpretation and changes in previously standard clinical paradigms, but it also provides an opportunity to markedly enhance our understanding of the processes that lead to cardiovascular pathobiology. The troponins offer great promise as a method for us to further our understanding of the pathogenesis of a variety of cardiac syndromes.
Biomarkers↗
Improved detection of cardiac contusion with cardiac troponin I.
Detecting cardiac injury in patients with chest trauma is difficult because the level of the MB isoenzyme of creatine kinase (MBCK) can be elevated from skeletal muscle injury alone. However, the level of cardiac troponin I (cTnl) is not elevated by skeletal muscle injury. To determine whether its measurement would improve the ability to detect cardiac injury in patients with blunt chest trauma, 44 patients were studied. Serial echocardiograms and serial blood samples were obtained. Six patients had evidence of cardiac injury by echocardiography; all had elevations of MBCK and cTnl. One patient had elevations of both MBCK and cTnl with only a pericardial effusion. Twenty-six of the 37 patients without contusion had elevations of MBCK; none had elevations of cTnl. The ratio of MBCK to total creatine kinase improved specificity at the expense of sensitivity. Measurement of cTnl accurately detects cardiac injury in patients with blunt chest trauma and should facilitate the diagnosis and management of such patients.
Case-Control Studies↗
Rationale for the use of conjunctive anticoagulation during thrombolysis.
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Blood Coagulation↗
Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction.
Criteria for the retrospective diagnosis of acute myocardial infarction rely heavily on increases in lactate dehydrogenase (LD) isoenzymes. However, increases of LD isoenzyme activities are not specific for myocardial injury. Recently, increased concentrations of cardiac troponin I (cTnI) have been shown to be highly specific for myocardial damage and to have sensitivity comparable with that of creatine kinase MB isoenzyme for detecting cardiac injury. Furthermore, increases of cTnI persist in plasma for at least several days. The present study was designed to determine the relative sensitivities of cTnI and LD isoenzymes over time for the diagnosis of infarction. The results indicate that cTnI values are at least as sensitive as LD isoenzymes: 90% of patients with myocardial infarction had above-normal concentrations of cTnI on the 4th day after admission to the coronary care unit. Criteria based on cTnI should improve the accuracy of retrospective diagnoses of acute myocardial infarction.
Animals↗
Association of depression with reduced heart rate variability in coronary artery disease.
Decreased heart rate (HR) variability is an independent risk factor for mortality in cardiac populations. Clinical depression has also been associated with adverse outcomes in patients with coronary artery disease (CAD). This study tests the hypothesis that depressed patients with CAD have decreased HR variability compared with nondepressed CAD patients. Nineteen patients with angiographically documented CAD and either major or minor depression were compared with a sample of nondepressed CAD patients according to age, sex, and smoking status. All patients underwent 24-hour Holter monitoring, and the standard deviation of all normal-to-normal intervals was used as the primary index of HR variability. HR variability was significantly lower in depressed than nondepressed patients (90 +/- 35 vs 117 +/- 26 ms; p < or = 0.01), even after adjusting for relevant covariates. Thus, decreased HR variability may help explain the increased risk for cardiac mortality and morbidity in depressed CAD patients.
Aged↗
Myocardial injury in critically ill patients. A frequently unrecognized complication.
OBJECTIVE: To determine the incidence and effect of unrecognized cardiac injury in critically ill patients. DESIGN: Prospective, blinded, single-center study. SETTING: The medical and respiratory intensive care unit of an academic health center. PATIENTS: Two hundred nine patients (224 admissions). MAIN OUTCOME MEASURES: Daily measurement of levels of cardiac troponin I, a sensitive, highly specific, and long-lived marker of myocardial injury. Concurrently, signs and symptoms potentially related to myocardial ischemia were tabulated by blinded investigators. All clinical evaluation and management decisions were made by the physicians responsible for the care of the patient. RESULTS: Thirty-two (15%) of the 209 patients had evidence of myocardial damage based on elevated levels of cardiac troponin I. Only 12 (37%) of these 32 patients were diagnosed as having acute myocardial infarction by the intensive care unit staff. Cardiac damage was unrecognized in the other 20 (63%). Unrecognized cardiac injury was more common in young patients and in blacks. Mortality in patients with myocardial injury that was recognized (42%) or unrecognized (40%) was higher than in those without myocardial injury (15%) (P < .001). Patients with cardiac injury were more frequently hypotensive (75% vs 50%; P = .007) and in need of mechanical ventilation (66% vs 27%; P < .001) and had longer intensive care unit stays (5.3 vs 3.1 days; P < .007) than patients without cardiac injury. CONCLUSION: The incidence of myocardial injury defined by elevated levels of cardiac troponin I was unexpectedly high and associated with increased morbidity and mortality. Clinically, it was often unrecognized.
Adult↗
What is the true periprocedure myocardial infarction rate? Does anyone know for sure? The need for clarification.
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Angioplasty, Balloon, Coronary↗