Management and Care of Acute Coronary Syndromes
Mauricio G. Cohen, M.D., FACC
Atherothrombosis is the leading cause of death worldwide and accounts for 52 percent of all deaths. Over 55 million people worldwide died from atherothrombotic disease in 2000. In 2004, there were 1.6 million of hospitalizations for ACS, 700,000 for UA and 900,000 for myocardial infarction (MI). Of these, about 30 percent presented ST-segment elevation in the electrocardiogram (ECG).
Acute coronary syndromes (ACS) covers a wide spectrum of clinical syndromes ranging from unstable angina (UA) to ST-elevation acute myocardial infarction. The disruption of an atherosclerotic coronary plaque is the pathophysiologic substrate of ACS. The plaque usually has a large core rich in lipids and necrotic material and a thin fibrous cap. In the shoulder region of the plaque, there is an inflammatory infiltrate rich in macrophages and foam cells that release matrix-metalloproteinases that erode and rupture the fibrous cap, exposing the lipid-rich necrotic core to the blood stream. This material is highly thrombogenic, causing platelet activation and aggregation that leads to intracoronary thrombosis and coronary occlusion. Microembolization of platelet aggregates and the release of vasoactive substances, such as endothelin and serotonin, cause microvascular dysfunction with plugging of small capillary vessels at the level of the ischemic myocardium, causing necrosis and the release of myocardial markers. These markers are the mainstay of an ACS diagnosis.
The clinical diagnosis of ACS is based on clinical, electrocardiographic and laboratory findings. ACS patients usually present chest pain in the sternal area that radiates to the jaw, left shoulder and medial aspect of the left arm. Accompanying symptoms may include shortness of breath, profuse sweating, nausea, vomiting, and dizziness.
Through the interview and physical exam, the clinician needs to interpret symptoms in conjunction with other major cardiovascular risk factors including age, gender, diabetes mellitus, hypertension, smoking, and hyperlipidemia, and define whether the patient is at high, intermediate or low likelihood of having actual myocardial ischemia.
The second major element in ACS diagnosis is the ECG. This tool rapidly identifies risks dictating further cardiac management. Identifying shifts in the ST segments is important because it determines prognosis and needs for immediate therapies. ST segment elevation indicates that an epicardial coronary artery is occluded and myocardial muscle cells are dying. Patients without ST elevation do not need emergency therapies and can be managed conservatively without need for emergency cardiac catheterization.
Assessment of cardiac markers is the third element in ACS diagnosis. Elevated cardiac markers confirm the diagnosis of a myocardial infarction. Patients without elevated cardiac markers are labeled as having UA. Patients with elevated troponins benefit from aggressive and early invasive management and the use of potent antiplatelet therapies.
The American College of Cardiology and the American Heart Association have issued guidelines with the objective of improving the use of evidence-based management strategies in ACS patients. These guidelines recommend cardiac catheterization within 48 hours of admission and the use of aspirin, clopidogrel, heparin, betablockers, ACE-inhibitors, statins and glycoprotein IIbIIIa inhibitors.
In ST-elevation ACS patients an epicardial coronary artery is usually completely occluded, therefore rapid treatment time essential and the initial care determines patient outcomes. Reperfusion therapy via fibrinolytic agents or primary PCI needs to be implemented as soon as the diagnosis is established. Primary PCI is more effective and is the preferred reperfusion strategy, but it involves more resources and is available at a minority of sites.
Integrating EMS, emergency departments and cardiologists to minimize the time of diagnosis and treatment of ST-elevation ACS patients will improve guidelines-recommended therapies for ACS patients. Door-to-balloon time (the time between hospital arrival and the first balloon inflation in the culprit vessel), in the case of primary PCI, and door-to-needle time (the time between hospital arrival and the administration of fibrinolytic agent), in the case of fibrinolytic therapy, have become benchmarks of quality of care. Door-to-balloon time should not exceed 90 minutes and door-to-needle time should not exceed 30 minutes.
ACS patients without ST elevation in their ECGs can be stabilized medically during the first 24 to 48 hours without need of emergency cardiac catheterization. The decision to perform PCI or open heart surgery is based on the extent of coronary artery disease and left ventricular function. Patients with more extensive disease and poorer ventricular function usually are referred to by-pass surgery.
Patients presenting without ECG changes and normal cardiac markers are at lower risk and can be triaged to an observation unit. They can remain hospitalized for 23 hours and have their cardiac markers checked every 8 hours. If there are no evolutionary ECG changes, and the cardiac marker levels remain within normal limits, the patient can take a stress test. If the result is negative, then the patients can be discharged safely and their primary physicians can follow up with them.
The discharge process is as important as the initial care. Patients who had stents or surgery or were diagnosed with a heart attack need to be discharged on aspirin, clopidogrel, beta-blockers, statins and ACE-inhibitors. Recommending lifestyle changes are as important as prescribing medication. Patients should be counseled to stop smoking, referred to cardiac rehabilitation and diabetes education programs and begin a heart-healthy diet.
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