Cardiac troponin I and creatine kinase-MB mass to rule out myocardial injury in hospitalized patients with renal insufficiency.

Serum cardiac troponin I measurement is preferred to creatine kinase-MB mass for the diagnosis of acute myocardial infarction in patients with renal insufficiency. Unexplained increases in cardiac troponin I in this population requires further evaluation and close follow-up.

Regulation of regional norepinephrine spillover in heart failure: the effect of angiotensin II and beta-adrenergic agonists in the forearm circulation.

BACKGROUND: Prejunctional receptors for angiotensin II (A-II) and norepinephrine (NE) have been reported to facilitate NE release. If operative in patients with congestive heart failure (CHF), such receptors could participate in positive feedback cycles amplifying sympathoactivation. METHODS AND RESULTS: A-II and isoproterenol (ISO) would increase regional NE spillover via facilitation of presynaptic release of NE in the forearm circulation of patients with chronic stable CHF. A-II, ISO, and nitroprusside (NP) were sequentially infused into the brachial arteries of 10 patients with chronic stable CHF, which was attributed to dilated cardiomyopathy. Forearm blood flow (FBF) was measured via plethysmography and regional spillover of NE was measured by using the isotope dilution method of Esler. A-II (5 ng/min) produced a nonsignificant decline in FBF (1.87+/-0.14 to 1.46+/-0.1 mL/100 g/min, P = .07) and did not change regional NE spillover (418+/-128 to 409+/-121 ng/min). ISO increased FBF from 1.6+/-0.12 to 4.3+/-0.7 mg/100 g/min (P < .001). Regional NE spillover increased from 337+/-86 to 856+/-300 ng/min (P < .001). Venous NE and regional extraction of NE did not change. NP increased FBF from 2.0+/-0.3 to 6.3+/-1.2 mL/100 g/min (P < .001; P = NS v change with ISO) and also increased regional NE spillover (301+/-99 to 712+/-288 ng/min, P < .001; P = NS v change with ISO). As with ISO, venous NE and extraction of NE were not altered. CONCLUSIONS: Mild vasoconstrictor infusions of A-II do not increase regional NE spillover in the forearm circulation of patients with CHF. The beta-adrenergic agonist ISO does increase regional spillover, but the effect seems to be primarily related to flow rather than presynaptic stimulation of NE release. These data argue against an important positive feedback loop involving A-II and NE on sympathoactivation, at least with the dosages of the agonists studied and in the limb circulation in chronic stable CHF.

Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle.

Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.

Cardiac troponin I and T concentrations in patients with cocaine-associated chest pain.

Patients with cocaine-related chest pain with electrocardiographic (ECG) abnormalities are often admitted to rule out acute myocardial infarction (AMI). Cardiac troponin I and T should be superior to measurement of creatine kinase (CK)-MB for detecting cardiac injury in patients with coexisting skeletal muscle injury. We prospectively evaluated 19 consecutive patients with acute chest pain related to cocaine use who were hospitalized to rule out AMI. The admission ECG was abnormal in 16 of 19 patients. Total CK and CK-MB were elevated during the hospital course in 14 and 3 patients, respectively. Cardiac troponin I and cardiac troponin T levels were within normal limits in all patients demonstrating that recent myocardial injury did not occur. Clinically, no patient had an AMI. Cocaine-induced thoracic skeletal muscle injury or transient cocaine-induced coronary vasospasm should be considered as alternative sources of chest pain in these patients.