Acute Myocardial Infarction

Acute Myocardial Infarction



H. Michael Bolooki, Arman Askari



DEFINITION AND ETIOLOGY


Acute myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Myocardial infarction occurs when myocardial ischemia, a diminished blood supply to the heart, exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms designed to maintain normal operating function and homeostasis. Ischemia at this critical threshold level for an extended period results in irreversible myocardial cell damage or death.


Critical myocardial ischemia can occur as a result of increased myocardial metabolic demand, decreased delivery of oxygen and nutrients to the myocardium via the coronary circulation, or both. An interruption in the supply of myocardial oxygen and nutrients occurs when a thrombus is superimposed on an ulcerated or unstable atherosclerotic plaque and results in coronary occlusion.1 A high-grade (>75%) fixed coronary artery stenosis caused by atherosclerosis or a dynamic stenosis associated with coronary vasospasm can also limit the supply of oxygen and nutrients and precipitate an MI. Conditions associated with increased myocardial metabolic demand include extremes of physical exertion, severe hypertension (including forms of hypertrophic obstructive cardiomyopathy), and severe aortic valve stenosis. Other cardiac valvular pathologies and low cardiac output states associated with a decreased mean aortic pressure, which is the prime component of coronary perfusion pressure, can also precipitate MI.


Myocardial infarction can be subcategorized on the basis of anatomic, morphologic, and diagnostic clinical information. From an anatomic or morphologic standpoint, the two types of MI are transmural and nontransmural. A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. A nontransmural MI is defined as an area of ischemic necrosis that does not extend through the full thickness of myocardial wall segment(s). In a nontransmural MI, the area of ischemic necrosis is limited to the endocardium or to the endocardium and myocardium. It is the endocardial and subendocardial zones of the myocardial wall segment that are the least perfused regions of the heart and the most vulnerable to conditions of ischemia. An older subclassification of MI, based on clinical diagnostic criteria, is determined by the presence or absence of Q waves on an electrocardiogram (ECG). However, the presence or absence of Q waves does not distinguish a transmural from a nontransmural MI as determined by pathology.2


A consensus statement was published to give a universal definition of the term myocardial infarction. The authors stated that MI should be used when there is evidence of myocardial necrosis in a clinical setting consistent with MI. Myocardial infarction was then classified by the clinical scenario into various subtypes. Type 1 is a spontaneous MI related to ischemia from a primary coronary event (e.g., plaque rupture, thrombotic occlusion). Type 2 is secondary to ischemia from a supply-and-demand mismatch. Type 3 is an MI resulting in sudden cardiac death. Type 4a is an MI associated with percutaneous coronary intervention, and 4b is associated with in-stent thrombosis. Type 5 is an MI associated with coronary artery bypass surgery.3


A more common clinical diagnostic classification scheme is also based on electrocardiographic findings as a means of distinguishing between two types of MI, one that is marked by ST elevation (STEMI) and one that is not (NSTEMI). Management practice guidelines often distinguish between STEMI and non-STEMI, as do many of the studies on which recommendations are based. The distinction between STEMI and NSTEMI also does not distinguish a transmural from a nontransmural MI. The presence of Q waves or ST-segment elevation is associated with higher early mortality and morbidity; however, the absence of these two findings does not confer better long-term mortality and morbidity.4



PREVALENCE AND RISK FACTORS


Myocardial infarction is the leading cause of death in the United States and in most industrialized nations throughout the world. Approximately 450,000 people in the United States die from coronary disease per year.5 The survival rate for U.S. patients hospitalized with MI is approximately 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.


The incidence of MI increases with age; however, the actual incidence is dependent on predisposing risk factors for atherosclerosis. Approximately 50% of all MIs in the United States occur in people younger than 65 years. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years.


Six primary risk factors have been identified with the development of atherosclerotic coronary artery disease and MI: hyperlipidemia, diabetes mellitus, hypertension, tobacco use, male gender, and family history of atherosclerotic arterial disease. The presence of any risk factor is associated with doubling the relative risk of developing atherosclerotic coronary artery disease.1



Hyperlipidemia


Elevated levels of total cholesterol, LDL, or triglycerides are associated with an increased risk of coronary atherosclerosis and MI. Levels of HDL less than 40 mg/dL also portend an increased risk. A full summary of the National Heart, Lung, and Blood Institute’s cholesterol guidelines is available online.6



Diabetes Mellitus


Patients with diabetes have a substantially greater risk of atherosclerotic vascular disease in the heart as well as in other vascular beds. Diabetes increases the risk of MI because it increases the rate of atherosclerotic progression and adversely affects the lipid profile. This accelerated form of atherosclerosis occurs regardless of whether a patient has insulin-dependent or non–insulin-dependent diabetes.



Hypertension


High blood pressure (BP) has consistently been associated with an increased risk of MI. This risk is associated with systolic and diastolic hypertension. The control of hypertension with appropriate medication has been shown to reduce the risk of MI significantly. A full summary of the National Heart, Lung, and Blood Institute’s JNC 7 guidelines published in 2003 is available online.7



Tobacco Use


Certain components of tobacco and tobacco combustion gases are known to damage blood vessel walls. The body’s response to this type of injury elicits the formation of atherosclerosis and its progression, thereby increasing the risk of MI. A small study in a group of volunteers showed that smoking acutely increases platelet thrombus formation. This appears to target areas of high shear forces, such as stenotic vessels, independent of aspirin use.8 The American Lung Association maintains a website with updates on the public health initiative to reduce tobacco use and is a resource for smoking-cessation strategies for patients and health care providers.



Male Gender


The incidence of atherosclerotic vascular disease and MI is higher in men than women in all age groups. This gender difference in MI, however, narrows with increasing age.



Family History


A family history of premature coronary disease increases an individual’s risk of atherosclerosis and MI. The cause of familial coronary events is multifactorial and includes other elements, such as genetic components and acquired general health practices (e.g. smoking, high-fat diet).



PATHOPHYSIOLOGY AND NATURAL HISTORY


Most myocardial infarctions are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists for more than 20 minutes, irreversible myocardial cell damage and cell death will occur.


The development of atherosclerotic plaque occurs over a period of years to decades. The two primary characteristics of the clinically symptomatic atherosclerotic plaque are a fibromuscular cap and an underlying lipid-rich core. Plaque erosion can occur because of the actions of matrix metalloproteases and the release of other collagenases and proteases in the plaque, which result in thinning of the overlying fibromuscular cap. The action of proteases, in addition to hemodynamic forces applied to the arterial segment, can lead to a disruption of the endothelium and fissuring or rupture of the fibromuscular cap. The loss of structural stability of a plaque often occurs at the juncture of the fibromuscular cap and the vessel wall, a site otherwise known as the shoulder region. Disruption of the endothelial surface can cause the formation of thrombus via platelet-mediated activation of the coagulation cascade. If a thrombus is large enough to occlude coronary blood flow, an MI can result.


The death of myocardial cells first occurs in the area of myocardium most distal to the arterial blood supply: the endocardium. As the duration of the occlusion increases, the area of myocardial cell death enlarges, extending from the endocardium to the myocardium and ultimately to the epicardium. The area of myocardial cell death then spreads laterally to areas of watershed or collateral perfusion. Generally, after a 6- to 8-hour period of coronary occlusion, most of the distal myocardium has died. The extent of myocardial cell death defines the magnitude of the MI. If blood flow can be restored to at-risk myocardium, more heart muscle can be saved from irreversible damage or death.


The severity of an MI depends on three factors: the level of the occlusion in the coronary artery, the length of time of the occlusion, and the presence or absence of collateral circulation. Generally, the more proximal the coronary occlusion, the more extensive the amount of myocardium that will be at risk of necrosis. The larger the myocardial infarction, the greater the chance of death because of a mechanical complication or pump failure. The longer the period of vessel occlusion, the greater the chances of irreversible myocardial damage distal to the occlusion.


STEMI is usually the result of complete coronary occlusion after plaque rupture. This arises most often from a plaque that previously caused less than 50% occlusion of the lumen. NSTEMI is usually associated with greater plaque burden without complete occlusion. This difference contributes to the increased early mortality seen in STEMI and the eventual equalization of mortality between STEMI and NSTEMI after 1 year.



SIGNS AND SYMPTOMS


Acute MI can have unique manifestations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. An asymptomatic MI is not necessarily less severe than a symptomatic event, but patients who experience asymptomatic MIs are more likely to be diabetic. Despite the diversity of manifesting symptoms of MI, there are some characteristic symptoms.



• Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax

• Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back

• Associated dyspnea or shortness of breath

• Associated epigastric discomfort with or without nausea and vomiting

• Associated diaphoresis or sweating

• Syncope or near syncope without other cause

• Impairment of cognitive function without other cause

An MI can occur at any time of the day, but most appear to be clustered around the early hours of the morning or are associated with demanding physical activity, or both. Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) before the infarct.



DIAGNOSIS


Identifying a patient who is currently experiencing an MI can be straightforward, difficult, or somewhere in between. A straightforward diagnosis of MI can usually be made in patients who have a number of atherosclerotic risk factors along with the presence of symptoms consistent with a lack of blood flow to the heart. Patients who suspect that they are having an MI usually present to an emergency department. Once a patient’s clinical picture raises a suspicion of MI, several confirmatory tests can be performed rapidly. These tests include electrocardiography, blood testing, and echocardiography.



Diagnostic Procedures


The first diagnostic test is electrocardiography (ECG), which may demonstrate that a MI is in progress or has already occurred. Interpretation of an ECG is beyond the scope of this chapter; however, one feature of the ECG in a patient with an MI should be noted because it has a bearing on management. Practice guidelines on MI management consider patients whose ECG does or does not show ST-segment elevation separately. As noted earlier, the former is referred to as ST elevation MI (Fig. 1) and the latter as non-ST elevation MI (Fig. 2). In addition to ST-segment elevation, 81% of electrocardiograms during STEMI demonstrate reciprocal ST-segment depression as well.


image

Figure 1 Twelve-lead electrocardiogram showing ST-segment (V1 to V4) elevation myocardial infarction.


(Courtesy of Dr. Donald Underwood, Cleveland Clinic Foundation)


image

Figure 2 12-lead electrocardiogram showing non-specific ST-segment and T-wave changes as might be seen in non-ST segment elevation myocardial infarction.


(Courtesy of Dr. Michael Bolooki, University of Minnesota)



Laboratory Tests


Living myocardial cells contain enzymes and proteins (e.g., creatine kinase, troponin I and T, myoglobin) associated with specialized cellular functions. When a myocardial cell dies, cellular membranes lose integrity, and intracellular enzymes and proteins slowly leak into the blood stream. These enzymes and proteins can be detected by a blood sample analysis. These values vary depending on the assay used in each laboratory. Given the acuity of a STEMI and the need for urgent intervention, the laboratory tests are usually not available at the time of diagnosis. Thus, good history taking and an ECG are used to initiate therapy in the appropriate situations. The real value of biomarkers such as troponin lies in the diagnosis and prognosis of NSTEMI (Fig. 3).


image

Figure 3 Typical rise and fall of cardiac biomarkers following myocardial infarction.



Imaging


An echocardiogram may be performed to compare areas of the left ventricle that are contracting normally with those that are not. One of the earliest protective actions of myocardial cells used during limited blood flow is to turn off the energy-requiring mechanism for contraction; this mechanism begins almost immediately after normal blood flow is interrupted. The echocardiogram may be helpful in identifying which portion of the heart is affected by an MI and which of the coronary arteries is most likely to be occluded. Unfortunately, the presence of wall motion abnormalities on the echocardiogram may be the result of an acute MI or previous (old) MI or other myopathic processes, limiting its overall diagnostic utility.



TREATMENT


The goals of therapy in acute MI are the expedient restoration of normal coronary blood flow and the maximum salvage of functional myocardium. These goals can be met by a number of medical interventions and adjunctive therapies. The primary obstacles to achieving these goals are the patient’s failure to recognize MI symptoms quickly and the delay in seeking medical attention. When patients present to a hospital, there are a variety of interventions to achieve treatment goals. “Time is muscle” guides the management decisions in acute STEMI, and an early invasive approach is the standard of care for acute NSTEMI.4



Medical Options



Antiplatelet Agents


The use of aspirin has been shown to reduce mortality from MI. Aspirin in a dose of 325 mg should be administered immediately on recognition of MI signs and symptoms.4,9 The nidus of an occlusive coronary thrombus is the adhesion of a small collection of activated platelets at the site of intimal disruption in an unstable atherosclerotic plaque. Aspirin irreversibly interferes with function of cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes, aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion. This effect benefits all patients with acute coronary syndromes, including those with amyocardial infarction. Aspirin alone has one of the greatest impacts on the reduction of MI mortality. Its beneficial effect is observed early in therapy and persists for years with continued use. The long-term benefit is sustained, even at doses as low as 75 mg/day.


The Clopidogrel and Metoprolol in Myocardial Infarction Trial/Second Chinese Cardiac Study (COMMIT-CCS 2) trial evaluated the use of clopidogrel versus placebo in patients who were taking aspirin but not undergoing reperfusion therapy. It demonstrated a benefit in favor of clopidogrel when used with aspirin.10 The Clopidogrel as Adjunctive Reperfusion Therapy—Thrombolysis in Myocardial Infarction 28 (CLARITY-TIMI 28) study compared clopidogrel versus placebo in patients receiving fibrinolytics within 12 hours of STEMI and showed a benefit in favor of clopidogrel as well.11 The current recommendations for antiplatelet agents is summarized in Table 1.


Table 1 Antiplatelet Medications























Treatment Modality Aspirin Clopidogrel
Medical management 75-162 mg/day indefinitely Optional: 75 mg/day × 1 month
Bare Metal stent 162-325 mg/day × 1 month, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 month
Sirolimus eluting stent
(Cypher)		 162-325 mg/day × 3 months, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 year
Paclitaxel eluting stent
(Taxus)		 162-325 mg/day × 6 months, then 75-162 mg/day indefinitely 300 mg loading dose,* then
75 mg/day × 1 year

* Note: No loading dose in patients older than 75 years.

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Jul 18, 2017 | Posted by in GENERAL SURGERY | Comments Off on Acute Myocardial Infarction

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