Long-term prognosis of patients with clinical unstable angina pectoris without elevation of creatine kinase but with elevation of cardiac troponin i levels.
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Biomedical subjects
Publications and source records attributed to Allan S Jaffe.
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BACKGROUND: Survival is poor in patients with acute myocardial infarction (MI) who also have severe renal disease. Less is known about the outcome of acute MI in patients with mild to moderate renal insufficiency. OBJECTIVE: To compare outcomes after acute MI in patients with varying levels of renal disease and in patients without renal failure. DESIGN: Retrospective cohort study. SETTING: Academic medical center. PATIENTS: 3106 total patients admitted with acute MI and end-stage renal disease (n = 44), severe renal insufficiency (creatinine clearance < 0.59 mL/s [<35 mL/min]) (n = 391), moderate renal dysfunction (creatinine clearance > or = 0.59 mL/s [<35 mL/min] but < or =0.84 mL/s [< or =50 mL/min]) (n = 491), mild chronic renal insufficiency (creatinine clearance > 0.84 mL/s [>50 mL/min] but < or =1.25 mL/s [< or =75 mL/min]) (n = 860), or no renal disease (n = 1320). MEASUREMENTS: Clinical characteristics, treatment strategies, and short- and long-term survival were compared after patients were stratified by creatinine clearance. RESULTS: In-hospital mortality rates were 2% in patients with normal renal function, 6% in those with mild renal failure, 14% in those with moderate renal failure, 21% in those with severe renal failure, and 30% in those with end-stage renal disease (P < 0.001). Compared with patients without renal disease, similar adjusted trends were present for postdischarge death in patients with end-stage renal disease (hazard ratio, 5.4 [95% CI, 3.0 to 9.7]; P < 0.001), severe renal insufficiency (hazard ratio, 1.9 [CI, 1.2 to 3.0]; P = 0.006), moderate renal dysfunction (hazard ratio, 2.2 [CI, 1.5 to 3.3]; P < 0.001), and mild chronic renal insufficiency (hazard ratio, 2.4 [CI, 1.7 to 3.3]; P < 0.001). Patients with renal failure received adjunctive and reperfusion therapies less frequently than those with normal renal function (P < 0.001). Postdischarge death was less likely in patients who received acute reperfusion therapy (odds ratio, 0.7 [CI, 0.6 to 0.9]), aspirin (odds ratio, 0.7 [CI, 0.5 to 0.8]), and beta-blocker therapy (odds ratio, 0.7 [CI, 0.6 to 0.9]). CONCLUSION: Patients with renal failure are at increased risk for death after acute MI and receive less aggressive treatment than patients with normal renal function.
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We present the case of a 43-year-old male who was initially evaluated for angina pectoris and dyspnea. His CK, CK-MB, and cTnI were all elevated following a blood transfusion and he underwent coronary arteriography, which demonstrated no luminal obstructions. After several months, he was transferred to Mayo Clinic where diagnoses of fulminant cardiac amyloidosis and systemic multiple myeloma were established. The cTnI remained elevated despite normalization of the CK and CK-MB. Despite aggressive treatment, the patient died. Postmortem analysis demonstrated amyloid cardiac deposition including involvement of the coronary microvasculature. Electron microscopy revealed myocyte compression injury from amyloid infiltration. We believe this is the first report of elevated troponin I in a patient with cardiac amyloidosis. The electron microscopy in our case confirms cardiac damage as the mechanism for cTnI elevation. This observation strengthens our knowledge about the specificity of cTnI for the detection of cardiac injury.
Depression increases the risk of cardiac mortality and morbidity in patients with coronary heart disease (CHD), but the mechanisms that underlie this association remain unclear. This review considers the evidence for several behavioral and physiological mechanisms that might explain how depression increases the risk for incident coronary disease and for subsequent cardiac morbidity and mortality. The candidate mechanisms include: (1). antidepressant cardiotoxicity; (2). association of depression with cardiac risk factors such as cigarette smoking, hypertension, diabetes, and reduced functional capacity; (3). association of depression with greater coronary disease severity; (4). nonadherence to cardiac prevention and treatment regimens; (5). lower heart rate variability (HRV) reflecting altered cardiac autonomic tone; (6). increased platelet aggregation; and (7). inflammatory processes. Despite recent advances in our understanding of these potential mechanisms, further research is needed to determine how depression increases risk for cardiac morbidity and mortality.
BACKGROUND: The European Society of Cardiology and American College of Cardiology guidelines for redefinition of myocardial infarction suggest that the cutoff value for diagnosis of acute myocardial infarction (AMI) be the 99th percentile of the reference population at a level measured with imprecision (coefficient of variation) > or =10%. No current commercially available troponin assay meets this requirement. Accordingly, questions have been raised about how to implement cutoff values from the guidelines. The Clinical Outcomes Utilizing Revascularization and Aggressive druG Evaluation (COURAGE) trial asked for recommendations concerning the use of troponin assays for the trial. METHODS: Cutoff values for the various assays were obtained from package inserts or from direct communication with manufacturers. RESULTS: The cutoff value with > or =10% imprecision was above the 99th percentile of the reference range for all assays. For the present, we suggest that this value be used for clinical and clinical trial purposes. It will account for analytic variability and individual biological changes. We provide recommendations for clinical practice and clinical trials concerning how to make the diagnosis of AMI in patients with ischemic symptoms and patients who undergo percutaneous coronary intervention and coronary artery bypass surgery. CONCLUSIONS: This is a first attempt to define cutoff values on the basis of the European Society of Cardiology and American College of Cardiology guidelines. These criteria will provide increased consistency until assays improve to allow full implementation of the guidelines.
Two new automated, highly sensitive methods for the measurement of C-reactive protein (CRP) were compared using blood samples from active and retired health care workers (116 males, 114 females). The regression equation was y=1.115x-0.0267 forthe Kamiya K assay immunoturbidimetric method (x) vs. the Behring BNII nephelometric method (y) with medians (IQR) of 0.156 (0.081 to 0.276) and 0.150 (0.060 to 0.240) mg/dl, respectively. Significant differences in hsCRP values between males and females were observed (p=0.013 and p=0.0018 for Behring and Kamiya methods, respectively). This gender difference in CRP levels was confirmed by analysis of serum samples from 1,114 individuals (639 males and 475 females) obtained through Mayo Medical Laboratories reference services, which represents participants from across the United States. The gender difference, which was confirmed (p<0.0001), was independent of age differences as assessed by multiple regression analysis. The observed gender differences have important implications for the establishment of cut-off points for cardiovascular risk stratification.
OBJECTIVES: Clinical depression is a risk factor for cardiac mortality in patients with coronary heart disease. High QT interval variability is a risk factor for arrhythmic events, including sudden cardiac death. The purpose of this study was to determine whether depression is associated with increased QT variability in patients recovering from myocardial infarction. METHODS: Twenty patients with major depression recovering from a recent myocardial infarction were matched with 20 nondepressed post-myocardial infarction patients on age and sex, and all underwent 24-hour Holter monitoring. RESULTS: There were no differences between groups on average heart rate, heart rate variability, or other electrocardiographic measures. However, the QT interval showed significantly greater variability in the depressed than in the nondepressed group, especially at midnight and at 6:00 AM. CONCLUSIONS: Depressed post-myocardial infarction patients may be at greater risk for sudden cardiac death as a result of abnormalities in ventricular repolarization. More work is needed to determine the clinical and prognostic significance of QT variability in these patients.
OBJECTIVE: Prevalence estimates of depression in hospitalized patients with congestive heart failure (CHF) differ considerably across studies. This article reports the prevalence of depression in a larger sample of hospitalized patients with CHF and identifies demographic, medical, psychosocial, and methodological factors that may affect prevalence estimates. METHODS: A modified version of the Diagnostic Interview Schedule was administered to a series of 682 hospitalized patients with CHF to determine the prevalence of DSM-IV major and minor depression; 613 patients also completed the Beck Depression Inventory. Medical, demographic, and social data were obtained from hospital chart review, echocardiography, and patient interview. RESULTS: In the sample as a whole, 20% of the patients met the DSM-IV criteria for a current major depressive episode, 16% for a minor depressive episode, and 51% scored above the cutoff for depression on the Beck Depression Inventory (>or=10). However, the prevalence of major depression differed significantly between strata defined by the functional severity of heart failure, age, gender, employment status, dependence in activities of daily living, and past history of major depression. For example, the prevalence ranged from as low as 8% among patients in New York Heart Association class I failure to as high as 40% among patients in class IV. CONCLUSIONS: The prevalence of depression in hospitalized patients with CHF is similar to rates found in post-myocardial infarction patients. However, it is considerably higher in certain subgroups, such as patients with class III or IV heart failure. Further research is needed on the prognostic importance and treatment of comorbid depression in CHF.
OBJECTIVE: The Enhancing Recovery in Coronary Heart Disease study was a multicenter clinical trial in which patients with depression and/or low perceived social support after an acute myocardial infarction were randomly assigned to an intervention consisting of cognitive behavior therapy and, in some cases, sertraline, or to usual care. There was no difference in survival between the groups. A possible reason why the intervention failed to affect survival is that too many patients with mild, transient depression were enrolled. Another is that some patients died too soon to complete the intervention. This analysis evaluates whether there was a difference in late (ie, > or =6 months after the myocardial infarction) mortality among initially depressed patients who had a Beck Depression Inventory score > or =10 and a past history of major depression, and who completed the 6-month post-treatment assessment. It also examines the relationship between change in depression and late mortality. METHODS: Out of the 1,165 (47%) of the Enhancing Recovery in Coronary Heart Disease study participants who met our criteria, 57 died in the first 6 months, and 858 (409 usual care, 449 intervention) completed the 6-month assessment. Cox regression was used to analyze survival. RESULTS: The intervention did not affect late mortality. However, intervention patients whose depression did not improve were at higher risk for late mortality than were patients who responded to treatment. CONCLUSIONS: Patients whose depression is refractory to cognitive behavior therapy and sertraline, two standard treatments for depression, are at high risk for late mortality after myocardial infarction.