Evaluation of guidelines for the use of telemetry in the non-intensive-care setting.
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To determine if the American College of Cardiology (ACC) cardiac monitoring guidelines accurately stratify patients according to their risks for developing clinically significant arrhythmias in non-intensive-care settings, we conducted a prospective cohort study of 2,240 consecutive patients admitted to a non-intensive-care telemetry unit over 7 months. Sixty-one percent of patients were assigned to ACC class I (telemetry indicated in most patients), 38% to class II (telemetry indicated in some), and 1% to class III (telemetry not indicated). Arrhythmias were detected in 13.5% of the class I patients, 40.7% of the class II patients, and 12% of the class III patients (p <.001). Telemetry detected an arrhythmia resulting in transfer to an intensive care unit in 0.4% of the class I patients, 1.6% of the class II patients, and none of the class III patients (p =.006). Telemetry led to a change in management for 3.4% of the class I patients, 12.7% of the class II patients, and 4% of the class III patients (p <.001). When patients with chest pain as the reason for admission were moved from class I to class II and patients with arrhythmias as the reason for admission were moved from class II to class I, more arrhythmias and more clinically significant arrhythmias occurred in class I patients and the trends from class I to class III were more consistent with the purpose of the guidelines. These findings indicate that when the ACC guidelines are reexamined, consideration should be given to changing them so they are more useful in non-intensive-care settings. (+info)
Contrasting inotropic effects of endogenous endothelin in the normal and failing human heart: studies with an intracoronary ET(A) receptor antagonist.
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BACKGROUND: Endothelin-1 (ET-1) is a potent positive inotrope in vitro, but its physiological effects on intrinsic myocardial contractile function in humans in vivo are unknown. Plasma ET-1 levels are elevated in heart failure, and ET-1 may be involved in the pathophysiology of this condition. However, its effects on contractile function of the failing human heart are also unknown. METHODS AND RESULTS: A specific ET(A) receptor antagonist, BQ123, was infused (40 nmol/min, 16 minutes) into the left coronary artery in 8 patients with atypical chest pain (normal left ventricular inverted question markLV function and coronary arteries) and 8 patients with nonischemic dilated cardiomyopathy (DCM) who were undergoing diagnostic catheterization. In normal subjects, BQ123 rapidly induced a significant reduction in LV dP/dt(max) (-270+/-71 mm Hg/s after 16 minutes; P<0.05) and in LV dP/dt at a developed pressure of 40 mm Hg (LV dP/dt(40)) (-179+/-54 mm Hg/s; P<0.05). In DCM patients, however, BQ123 caused no reductions in LV dP/dt(max) (62+/-49 mm Hg/s after 16 minutes) or LV dP/dt(40) (83+/-51 mm Hg/s;P<0.05 compared with normal subjects). BQ123 had no effect on heart rate, LV relaxation, LV end-diastolic pressure, right atrial pressure, or pulmonary pressure in either patient group. CONCLUSIONS: Endogenous ET-1 has a tonic positive inotropic effect in normal subjects, independent of effects on the peripheral vasculature and unmasked by inhibition of ET(A) receptors. However, the effect of short-term ET(A) blockade in DCM patients was opposite to that in normal subjects, which suggests that ET-1 may cause negative inotropic effects in the failing heart. (+info)
Odynophagia in a woman with known coronary artery disease and ischemia on electrocardiogram.
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Esophageal intramural hematoma can mimic other causes of chest pain. When the patient is known to have coronary artery disease, the diagnosis may be difficult. Moreover, the course may be complicated and may harm the patient if antiplatelet drugs, thrombolytics, and anticoagulants are used. The presence of odynophagia should alert the clinician to the possibility of an esophageal origin, even in a patient with known coronary artery disease. We present a case in which early recognition of the clinical presentation prevented potential iatrogenic complications. (+info)
Relationships between homocysteine, factor VIIa, and thrombin generation in acute coronary syndromes.
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BACKGROUND: It has been suggested by clinical, epidemiological, and experimental in vitro studies that homocysteine potentiates thrombin generation. This prothrombotic effect however has not previously been demonstrated in patients presenting with acute coronary syndromes (ACS). METHODS AND RESULTS: Patients with ACS (n =117) presenting with confirmed acute myocardial infarction (MI) (n =57) or unstable angina pectoris (UAP) (n =60) were consecutively recruited together with patients (n =18) in whom the presenting chest pain was not of cardiac origin (NCP), included as controls. Plasma samples were collected on admission and before clinical intervention. Homocysteine was assayed by high performance liquid chromatography, and both Factor VIIa and prothrombin fragment F1+2 were analyzed by ELISA. There were significant elevations in F1+2 in MI (P<0.001) and UAP (P=0.003), and modest elevations in Factor VIIa in UAP (P<0.05) compared with NCP but no differences in homocysteine levels among those groups. On dividing patients with ACS into quartiles of homocysteine, there was a stepwise increase in F1+2 (P<0.0001) and of Factor VIIa (P<0.05). There were significant correlations in ACS between homocysteine and F1+2 (r=0.46, P<0.0001), homocysteine and Factor VIIa (r=0.24, P<0.01), and F1+2 and Factor VIIa (r=0.41, P<0.0001). There was no correlation between homocysteine and either F1+2 (r=-0.15, P=0.57) or Factor VIIa (r=0. 22, P=0.37) in the NCP patients. CONCLUSIONS: Elevated plasma homocysteine is associated with and may cause elevated Factor VIIa and thrombin generation in patients presenting with ACS. These findings suggest an explanation for the prothrombotic effect of homocysteine in ACS. (+info)
Should we establish chest pain observation units in the UK? A systematic review and critical appraisal of the literature.
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OBJECTIVES: The chest pain observation unit (CPOU) has been developed in the United States to allow rigorous assessment of patients presenting with chest pain, thus expediting their discharge if assessment is negative. This review aims to examine the evidence for effectiveness and economic efficiency of the CPOU and to explore whether data from the United States can be extrapolated to the UK. METHOD: Search of the literature using Medline and critical appraisal of the validity of the data. RESULTS: Five studies comparing outcomes of CPOU care with routine practice showed no significant difference in objective measures including mortality or missed pathology. Eleven studies described outcomes of a cohort of CPOU patients. Follow up was comprehensive and demonstrated no clinically significant evidence of missed pathology. Nine studies comparing CPOU costs with routine care demonstrated impressive cost savings that were more modest when randomised comparisons were made. CONCLUSION: CPOU care is safe and costs are well defined. There is no strong evidence that a CPOU will improve outcomes if routine practice is good. Cost savings have been shown when compared with routine care in the United States but may not be reproduced the UK. (+info)
Safety and prognostic value of early dobutamine-atropine stress echocardiography in patients with spontaneous chest pain and a non-diagnostic electrocardiogram.
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AIMS: To risk stratify and shorten hospital stay in patients with spontaneous (resting) chest pain and a non-diagnostic electrocardiogram (ECG). METHODS AND RESULTS: The study comprised 102 patients (mean age 58+/-12 years, 67 men) with spontaneous chest pain and a non-diagnostic ECG. Forty-three patients had suspected coronary artery disease and 59 had known (but of unknown actual significance) coronary artery disease. All patients underwent serial creatine kinase enzyme measurements, continuous ECG monitoring for at least 12 h and early dobutamine-atropine stress echocardiography in patients with negative creatine kinase enzymes and normal findings at ECG monitoring. Dobutamine-atropine stress echocardiography was considered positive in patients with new or worsening wall thickening abnormalities. Patients with negative dobutamine-atropine stress echocardiography were discharged after the test. In-hospital and 6 month follow-up events noted were cardiac death, non-fatal myocardial infarction, unstable angina, and coronary artery bypass surgery or angioplasty. Thirteen patients had evidence of evolving myocardial infarction by elevated creatine kinase enzymes, or unstable angina by ECG monitoring. In the remaining 89 patients, dobutamine-atropine stress echocardiography was performed after a median observation period of 31 h (range 12-68 h). During dobutamine-atropine stress echocardiography no serious complications (death, non-fatal myocardial infarction, sustained ventricular tachycardia or ventricular fibrillation) occurred. Dobutamine-atropine stress echocardiography results were of poor quality in three, non-diagnostic in six, negative in 44 and positive in 36 patients. In the 80 patients with diagnostic dobutamine-atropine stress echocardiography, variables associated with in-hospital events (n=7) were history of exertional angina (P<0. 005), chest pain score (P<0.005), stress-induced angina (P<0.001) and positive dobutamine-atropine stress echocardiography (P<0.005). Variables associated with follow-up events (n=11) were history of exertional angina (P<0.05), chest pain score (P<0.001), stress-induced angina (P<0.01) and positive dobutamine-atropine stress echocardiography (P<0.01). At multivariate analysis the only significant predictor of events was positive dobutamine-atropine stress echocardiography (P<0.01). CONCLUSION: Early dobutamine-atropine stress echocardiography may safely distinguish between low- and high-risk subsets for subsequent cardiac events in patients with spontaneous chest pain and a non-diagnostic ECG. (+info)
Chest pain, enzymes and hypothyroidism.
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Hypothyroidism is a common disorder and when presenting with classical symptoms and signs is easy to recognise. However, hypothyroidism may present in a manner suggestive of an acute myocardial infarction with an elevated creatine kinase and electrocardiographic abnormalities. We report a case of severe hypothyroidism presenting as a cardiac event whose symptoms and signs dispersed following treatment with thyroxine. (+info)
Abnormal myocardial phosphorus-31 nuclear magnetic resonance spectroscopy in women with chest pain but normal coronary angiograms.
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BACKGROUND: After hospitalization for chest pain, women are more likely than men to have normal coronary-artery angiograms. In such women, myocardial ischemia in the absence of clinically significant coronary-artery obstruction has long been suspected. Most methods for the detection of the metabolic effects of myocardial ischemia are highly invasive. Phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopy is a noninvasive technique that can directly measure high-energy phosphates in the myocardium and identify metabolic evidence of ischemia. METHODS: We enrolled 35 women who were hospitalized for chest pain but who had no angiographically significant coronary-artery obstructions and 12 age- and weight-matched control women with no evidence of heart disease. Myocardial high-energy phosphates were measured with 31P-NMR spectroscopy at 1.5 tesla before, during, and after isometric handgrip exercise at a level that was 30 percent of the maximal voluntary grip strength. We measured the change in the ratio of phosphocreatine to ATP during exercise. RESULTS: Seven (20 percent) of the 35 women with chest pain and no angiographically significant stenosis had decreases in the phosphocreatine:ATP ratio during exercise that were more than 2 SD below the mean value in the control subjects without chest pain. There were no significant differences between the two groups with respect to hemodynamic variables at rest and during exercise, risk factors for ischemic heart disease, findings on magnetic resonance imaging and radionuclide perfusion studies of the heart, or changes in brachial flow during the infusion of acetylcholine. CONCLUSIONS: Our results provide direct evidence of an abnormal metabolic response to handgrip exercise in at least some women with chest pain consistent with the occurrence of myocardial ischemia but no angiographically significant coronary stenoses. The most likely cause is microvascular coronary artery disease. (+info)