Learning Objectives
Learn the differential diagnosis of ischemic chest pain and the laboratory tests used in the assessment of myocardial injury, including acute myocardial infarction.
Learn the clinical features of congestive heart failure (CHF) and the laboratory tests useful in ruling in and ruling out CHF and monitoring and risk outcomes assessment of patients with this disorder.
Introduction
There are many forms of cardiac disease. This chapter briefly covers the role of biomarkers in acute myocardial infarction (AMI) and congestive heart failure (CHF). The large numbers of other cardiac diseases are not discussed in this chapter because of the relatively minor role of diagnostic clinical laboratory tests in these disorders.
Acute Myocardial Infarction
The term AMI is defined as an imbalance between myocardial oxygen supply (ischemia) and demand, resulting in injury to and the eventual death of myocytes. AMI should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. Such necrosis is most often associated with a thrombotic occlusion superimposed on coronary atherosclerosis. It is now apparent that the process of plaque rupture and thrombosis is 1 of the ways in which coronary atherosclerosis progresses. Total loss of coronary blood flow results in a clinical syndrome associated with an ST-segment elevation MI (STEMI). Partial loss of coronary perfusion, if severe, can lead to necrosis as well, which is generally less severe and is known as non-ST-segment elevation MI (NSTEMI). Both STEMI and NSTEMI are considered type 1 MIs. In instances of myocardial injury with necrosis with a condition other than coronary artery disease (CAD), which contributes to an imbalance between oxygen supply and/or demand (eg, coronary endothelial dysfunction, respiratory failure, hypotension, etc), this MI is a type 2 MI that is secondary to ischemic imbalance. Other ischemic events of lesser severity without myocardial necrosis are designated as angina, which can range from stable to unstable. About 1.7 million patients are hospitalized each year in the United States with an acute coronary syndrome (ACS). Approximately 700,000 patients suffer from an initial AMI annually and another 500,000 from a recurrent AMI. Coronary heart disease causes 20% of all deaths and cardiovascular diseases up to 40%. Historically, most deaths caused by ischemic heart disease have been acute, but as our therapeutic abilities have improved, the disease is slowly becoming a more chronic one.
In many patients with AMI, no precipitating factor can be identified. The clinical history remains of substantial value in establishing a diagnosis. A prodromal history of angina can be elicited in 40% to 50% of patients with AMI. Of the patients with AMI presenting with prodromal symptoms, approximately one third have had symptoms from 1 to 4 weeks before hospitalization; in the remaining two thirds, symptoms predate admission by a week or less, with one third having had symptoms for 24 hours or less. The pain of AMI is variable in intensity, and the discomfort is described as a squeezing, choking, vise-like, or heavy pain. It may also be characterized as a stabbing, knife-like, boring, or burning discomfort. Often the pain radiates down the left arm. In some instances, the pain of AMI may begin in the epigastrium and simulate a variety of abdominal disorders, which often causes AMI to be misdiagnosed as indigestion. In other patients, the discomfort of AMI radiates to the shoulders, upper extremities, neck, and jaw, again usually favoring the left side.
The ideal biomarker of myocardial injury should 1) provide early detection of myocardial injury, 2) provide rapid, sensitive, and specific diagnosis for an AMI, 3) serve as a risk stratification tool in ACS patients, 4) assess the success of reperfusion after thrombolytic therapy, 5) detect reocclusion and reinfarction, 6) determine the timing of an infarction and infarct size, and 7) detect procedural-related perioperative MI during cardiac or noncardiac surgery. In reality, no 1 biomarker is able to 100% cover all these areas. However, cardiac troponin (cTn) does provide the power to be utilized in the majority of these clinical areas. Ruling in AMI requires a test with high diagnostic sensitivity (preferred by the ER physician in the urgent care, emergency setting as to not send anyone home with an AMI), whereas ruling out AMI requires a test with high diagnostic specificity (preferred by the cardiologist following admission to avoid excessive and costly diagnostic evaluations in the non-AMI patient). It is the function of the laboratory to provide advice to physicians about cardiac biomarker/troponin characteristics.
An updated 2012 “Global Task Force for the Third Universal Definition of MI” has codified the role of biomarkers. The advocate that the diagnosis be made from evidence of myocardial injury based on biomarkers of cardiac damage, preferably cardiac troponin (cTn) I or T, in the appropriate clinical situation of ischemic symptoms.
Until 2000, the diagnosis of AMI established by the World Health Organization (WHO) required at least 2 of the following criteria: 1) a history of chest pain, 2) evolutionary changes on the ECG, and/or 3) elevations of serial cardiac biomarkers (total creatine kinase [CK] and CKMB). It was rare for a diagnosis of AMI to be made in the absence of biochemical evidence of myocardial injury. A 2000 ESC/ACC consensus conference, updated in 2007 and most recently in 2012 by the “Global Task Force for the Third Universal Definition of MI,” has codified the role of biomarkers. The advocate that the diagnosis be made from evidence of myocardial injury based on biomarkers of cardiac damage, preferably cTnI or cTnT, in the appropriate clinical situation of ischemic symptoms (Table 9–1). This guideline does not suggest that all increases of cTn should elicit a diagnosis of AMI, but only those associated with the appropriate clinical, ECG, and imaging findings. When cTn increases that are not caused by acute ischemia occur, the clinician is obligated to search for another etiology for the elevation, a number of which are shown in Table 9–2. The initial ECG is diagnostic of AMI in about 30% of AMI patients. Further, the universal classification of different types of myocardial infarction is highlighted in Table 9-3.
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