Bio Markers in Cardiovascular Disease

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okinase MD, MHS To print for Windows press 'Ctrl+p' on your keyboard. s in the diagnosis of cardiovascular diseases. ers. in therapeutic decision-making. arkers; congestive heart failure triuretic peptide; CAD = coronary artery disease; CPK/CK = creatine (phospho)kinase; LMW = low molecular weight (heparin); proBNP ar pathophysiology, biomarkers have emerged as key players in diagnosis, risk stratification, and therapeutic decision-making in y complaint of chest pain or dyspnea. These symp
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  kinase  D, MHS o print for Windows press 'Ctrl+p' on your keyboard. in the diagnosis of cardiovascular diseases.rs.n therapeutic decision-making.rkers; congestive heart failureriuretic peptide; CAD = coronary artery disease; CPK/CK = creatine (phospho)kinase; LMW = low molecular weight (heparin)roBNPr pathophysiology, biomarkers have emerged as key players in diagnosis, risk stratification, and therapeutic decision-making icomplaint of chest pain or dyspnea. These symptoms are often nonspecific, and diagnosis can be difficult. Biomarker testingians care for their patients. In this lesson, we summarize the current data on three common biomarkers used in cardiovascular B-Type Natriuretic Peptidein natriuretic peptide, is released predominantly from ventricular myocytes in response to increased wall tension. Catecholaminsized as a prohormone that is enzymatically cleaved into the biologically active BNP and the N-terminal proBNP (NT-proBNPheral vasodilation, and inhibition of the renal angiotensin aldosterone and sympathetic nervous systems. Clearance of BNP occd. Both BNP and NT-proBNP markers are used in clinical practice and provide similar diagnostic and prognostic information.cardial systolic and diastolic dysfunction can result in BNP elevation. This elevation extends across the spectrum of coronarycoronary syndrome (ACS). BNP elevation can occur with ischemia in the absence of myonecrosis. Patients with stable coronaing. 1 With coronary angioplasty, BNP elevation is observed after balloon inflation independent of intracardiac filling pressure cpg/mL has a sensitivity of 71% and a specificity of 69% and may be helpful as an adjunctive early marker in patients without sroBNP levels are higher due to a longer plasma half-life; a cut-off at 300 pg/mL yields similar diagnostic performance. In patised mortality independently of left ventricular function. 4 BNP elevation even in troponin-negative patients predicts increasedfunction. 5 However, the role of BNP in determining therapeutic strategy is unclear; BNP elevation did not predict any significa  and risk of death or recurrent myocardial infarction in patients with acute coronary syndrome in both troponin-positive and troe of Cardiology Foundation. 5  in heart failure, particularly for its ability to discriminate between decompensated heart failure and pulmonary disease in dyspdictive value of 79%, and negative predictive value of 89% (Fig 2). 6 Use of BNP in the initial diagnostic phase has been shownn a concomitant favorable reduction of unnecessary hospitalization, hospital length of stay, and total cost of treatment.  r BNP in distinguishing heart failure from other causes in patients with dyspnea. The area under the curve is 0.91. Reproducedindependently predicts higher risk of mortality and adverse cardiac events. 8 During treatment of decompensated heart failure (odynamic parameters, and a discharge BNP level greater than 350 pg/mL is a poor prognostic marker for death or rehospitalizsmall, randomized trial showed that outpatient heart failure therapy titrated by BNP measurements yielded better outcomes thaen, and in patients with renal disease, and are lower in obese patients. 12,13 Although the Breathing Not Properly trial showed en has been seen in other disease states, such as cor pulmonale, pulmonary embolism, primary pulmonary hypertension, acute r ful in ruling out decompensated heart failure, interpretation of elevated values (as with all biomarker testing results) needs to bTroponinpractice in 1989, and multiple subsequent studies have demonstrated its superior sensitivity and tissue-specificity in the clinicaety of Cardiology broadened the definition of acute MI to include biomarker elevation, particularly that of cardiac troponin, inte coronary syndrome, except in the setting of renal failure (as discussed below), have similar diagnostic and prognostic value.al CK-MB levels. 18 This prognostic information is independent of patient age and degree of ST-segment deviation 19,20 and ident bus formation and perpetuation that is a direct result of atherosclerotic plaque rupture with subsequent platelet activation and twith increased severity of angiographic findings (visible thrombus, complex lesion characteristics, and thrombolysis in MI floct than these lesion characteristics. 21 Traditional therapies targeting this pathologic process consisted of aspirin and unfractiona  rombin generation by targeting factor Xa and a more predictable dose-response relationship that obviates the need for routine ld that, while all patients derived short-term (6-day) benefit from use of a LMW heparin, only troponin-positive patients had aW heparin was shown to be superior to unfractionated heparin in the reduction of mortality and major adverse cardiovascular efrom enoxaparin vs unfractionated heparin treatment in troponin-positive patients, this benefit was not seen in the troponin-nection; RR = relative risk; UR = urgent revascularization. Reproduced with permission from American College of Cardiology Fation at the site of plaque rupture. The CAPTURE study showed that patients with ACS given both heparin and abciximab hadonin levels, troponin-positive patients treated with abciximab had a lowering of cardiac risk to that of troponin-negative patiental benefit when tirofiban or lamifiban was added to aspirin and heparin among patients who were troponin-positive, with no sigrevascularization derived the most benefit. Troponin-positive patients, even after receiving aspirin, heparin, and clopidogrel (6nhibitor treatment; this benefit was not seen in troponin-negative patients (Fig 4). 28 In patients with ACS that did not proceed t
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