Acute Myocardial Infarction - Essay Example

?Acute Myocardial Infarction Case Study A 29-year-old female patient was admitted to the internal medicine department with epigastric pain, continuous colic, nausea, and vomiting. The ECG demonstrated an old anterior wall myocardial infarction. The serum creatine phosphokinase (CK) and cardiac troponin T (TnT) levels were normal. Seven days later, the patient had sudden onset orthopnea, followed by respiratory and cardiac arrest. The patient was transferred to the ICU after cardiopulmonary resuscitation. The patient's BP was 80/40 mm Hg; the pulse was 130 bpm. The shock was corrected via the application of the presser and respirator supported ventilation. During the ICU monitoring, an ultrasound system was used on the patient for daily monitoring. Respiration enhanced pain, while leaning forward alleviated and she described left arm radiation. She also complained of nausea, vomiting and diarrhea for the past week. She had no past medical or surgical history (Ashikaga et al, 2007). Cardiac risk factors were active cigarette smoking (2 pack-years), obesity (BMI 33.3 kg/m2) and a sedentary life-style. Usual medication was oral estroprogestative contraception introduced 2 weeks prior to admission and paracetamol. History was inconsistent with past or present drug abuse. Physical examination revealed elevated blood pressure at 160/80 mm Hg and a regular tachycardia at 110 beats per minute. Respiratory frequency, temperature, and oxygen saturation, were however normal. Pulmonary and cardiac auscultation was normal, as well an abdominal examination. A chest X ray was unremarkable. Initial ECG showed sinus tachycardia with anterolateral ST elevation as well as inferior ST depression. Laboratory reports revealed an elevated troponin Ic at 0.69 ?g/l, CK was within normal limits and CRP was slightly elevated at 19 mg/l; the rest of the workup, including a complete toxicological-screen, was normal, and a pregnancy test was negative. Acute Myocardial Infarction Acute Myocardial Infarction (AMI) is considered to be irreparable myocardial cell death ensuing from ischemia. Various diagnostic features aid in determining AMI encompassing sustained regional ST rise through ECG, cardiac enzyme studies etc. The cardiac enzyme studies classifies AMI as Q-wave infarction (previously called transmural) and non Q-wave infarction (previously called subendocardial). Q- wave infarctions are related with atherosclerosis that comprise major coronary artery, it involves the entire width of the cardiac muscles thereby resulting in absolute occlusion blood supply in that region. On the other hand in case of non Q-wave infarctions, only a small area is affected as a result of diminished blood supply either due to obstruction by an atherosclerotic plaque, that may or may not be accompanied by superimposed thrombus. Two chief theories were proposed to understand the AMI (a) hemorrhage turning into a plaque, expansion of the plaque obstructs the lumen (b) removed or injured endothelium above the plaque, causing attachment of the platelet thrombus, resulting in more thrombus formation (Pain Ladder). Epidemiology Acute myocardial infarction is the most common presentation of ischemic heart disease. According to the WHO estimate (2002), 12.6 percent of deaths across the world were attributed to ischemic heart disease, in developed nations as well as it emerged as a third major cause of death in developing nations, after AIDS and lower respiratory infections. In developed nations like United States, deaths from heart disease are more abundant than the mortality from cancer. One in five deaths in the United States is due to coronary attacks. It is reported that >1 million people suffer a coronary attack per year, of these 40 percent die as a result of stroke. Thus, an American dies every minute from a coronary episode pathological state. It also suggests that the patient is not treated of gastritis for a certain time and the patient is subjected to constant stress. In India, cardiovascular disease has emerged as the leading cause of death. Reports states that, one third of the deaths occurred in India (in 2007) were due to cardiovascular disease, the figure increased from one million in 1990, 1.6 million in 2000, to two million by 2010 (Bartolomei et al, 2010). Pathophysiology Established forms of therapy for acute myocardial infarction include hospitalization in a coronary care unit with continuous ECG monitoring, treatment of pain with narcotic analgesics, administration of supplemental oxygen, and attempts to minimize myocardial oxygen demand through attention to the determinants of myocardial oxygen consumption. The use of oxygen is now recognized as a routine measure for all patients with acute coronary syndromes. Oxygen therapy may limit both the size of myocardial injury as well as reduce the ST elevations in acute myocardial infarction (AMI). After initial stabilization, oxygen therapy can be discontinued for those with uncomplicated acute myocardial infarction (AMI). On the other hand oxygen therapy should be continued for the cases with oxygen saturation < 90% or cases with complications such as pulmonary edema or hypotension (Christman & Lee, 2006). Aspirin should be administered in a dose greater than or equal to 160 mg to all patients (provided they have no known hypersensitivity) with suspected acute coronary syndrome or acute myocardial infarction (AMI). The second International Study of Infarct Survival (ISIS-2) demonstrated that acetylsalicylic acid alone reduced the mortality of evolving acute myocardial infarction by 23%. It is established that Acetylsalicylic acid inhibits platelet aggregation by an almost complete inhibition of thromboxane A2 production. Morphine sulfate given intravenously in 2- 4mg increments is the chosen analgesic agent because of its potency, safety when given intravenously, devoid of myocardial depressant effects, and generally brings minimal hemodynamic changes in the supine patient. Beta-Blockers have been shown to reduce mortality both in the early (hospital) and chronic post-AMI periods. In ISIS-1 atenolol was administered within 12 hours of diagnosis and reduced hospital mortality from 4.3% to 3.7%. Similar results were seen in the MIAMI trial and in TIMI-II, where early intravenous metoprolol (within 2 hours) followed by oral dosing is observed to reduce mortality, reinfarction, and recurrent ischemia. The benefits were evident by day 1 and were sustained throughout the follow-up period. Three large well-done randomized trials have demonstrated that institution of a beta-blocking agent prior to discharge for acute myocardial infarction reduces subsequent mortality to a significant level over the next several years (Abdel-Aty et al, 2004). Studies also indicate that early treatment with inhibitors of the angiotensin-converting enzyme decrease the incidence of future mortality and recurrent acute myocardial infarction (AMI). The only trial that did not demonstrate a mortality benefit used intravenous enalapril, which caused excessive hypotension, especially in the elderly group. Current recommendations are to start treatment within 24 to 48 hours of all AMIs, especially anterior AMIs, with an angiotensin-converting enzyme inhibitor, as tolerated by blood pressure greater than 100 mm Hg. Intravenous angiotensin-converting enzyme inhibitor should be avoided in the acute phase. It is observed that individuals with persistent left ventricular dysfunction received constant benefit from its long-term use (Janket, Baird, Chuang & Jones, 2003). Nitrates are also commonly used in the treatment of acute myocardial infarction (AMI). They are indicated in patients with acute myocardial infarction and congestive heart failure, large anterior acute myocardial infarction, recurrent angina, persistent ischemia, or pulmonary edema. Caution should be used in those with right ventricular infarction, systolic blood pressure less than 90 mm Hg, or bradycardia. Nitrates act by dilating the capacitance veins, and coronary and peripheral arteries. Anginal pain is likely to be relieved by a combination of increasing myocardial blood flow, decreasing ventricular preload, and reducing left ventricular after-load (thus reducing myocardial O2 demand). Intravenous nitrates are preferred because they are easily titrated to effect and systolic blood pressure (Demir et al, 2009). Signs and Symptoms The clinical presentation is usually that of severe, oppressive chest pain accompanied by diaphoresis and lasting from 20 minutes to several hours. Up to 50% of patients have a prodrome of intermittent angina-like pain lasting up to several days, but with the onset at rest (i.e. unstable angina), the prodromal pain could become mild or transient and patients do not seek medical attention. The discomfort of acute myocardial infarction is sometimes epigastric, accompanied by a desire to belch, and often mistaken by both patient and physician for gastrointestinal upset. The pain can occasionally be interscapular, only in the arms, or only in the mandible. Data from the Framingham study, however, showed that acute myocardial infarction can be clinically silent in approximately 25% of patients. Other commonly associated symptoms are dizziness and weakness from low cardiac output, marked diaphoresis from autonomic discharge, and palpitations or syncope from ventricular arrhythmia. Despite relatively typical and severe symptoms in most cases, the average delay from the onset of symptoms to arrival at a hospital is 1 to 3 hours in various studies; during this period, the acute ischemic myocardium is most unstable electrically and ventricular fibrillation is most likely to occur. Further, patient and public education are needed to make at-risk patients well-informed about the symptoms and aware of the danger of delay in seeking attention. Physicians must also be prepared to deal with false alarms in emergency rooms and some ultimately unnecessary hospital admissions (Grabczewska, Bialoszynski & Kubica, 2007). When a complete database is available (history, ECG, and serum enzymes) the diagnosis is usually not difficult, but the pain is sometimes atypical or even absent in 25% of acute myocardial infarction patients. Other diseases that should be considered in the differential diagnosis are acute pericarditis, mitral valve prolapsed, acute pulmonary embolism, aortic dissection (which can cause acute myocardial infarction by occluding the coronary ostium), stable angina, unstable angina, variant (Prinzmetal’s) angina, costochondritis and other chest wall pain, esophageal spasm, biliary disease, cervical root compression, and psychosomatic pain. Acute pulmonary embolism can occasionally be particularly difficult to distinguish from acute myocardial infarction because it can produce visceral pain, acute decrease in cardiac output, an autonomic response to this decrease, and ECG changes, all of which can resemble those of acute myocardial infarction (AMI). The presenting physical signs can be surprisingly few. Either hypotension from low cardiac output or hypertension from sympathetic discharge can be present. Similarly, either bradycardia from vagal discharge (common in inferior infarction) or heart block or tachycardia from reduced stroke volume or sympathetic stimulation can be observed. In a few patients, pulmonary congestion can be manifested by tachypnea, dyspnea, rales, or even frank pulmonary edema with frothy sputum. Examination of the heart is often normal; some patients, though, might have an S3 gallop, a murmur of mitral regurgitation caused by papillary muscle dysfunction, or a pericardial bulge reflecting dyskinetic myocardium (left ventricular wall moving outward with systole) (Gullu, Sav & Kamel, 2005). Clinical Presentation Patients with uncomplicated acute myocardial infarction are hospitalized for 3 to 7 days. Near the end of the hospitalization, it has become accepted practice in patients who did not receive early coronary angiography to perform a low-level exercise test to look for symptoms or signs of ischemia at a low workload. Provided that patients with severe left ventricular dysfunction or severe congestive heart failure, or patients manifesting myocardial ischemia at rest or on minimal activity are excluded, the low-level exercise test can be performed safely. Some studies have shown a markedly increased risk for a future coronary event in patients who exhibit ischemia in the form of angina or ST-segment depression, or hemodynamic instability (lack of adequate heart rate or blood pressure increase) on the low-level exercise test. Thus, it has become accepted practice to recommend coronary angiography in patients exhibiting symptoms of myocardial ischemia either spontaneously or on the low-level exercise test following acute myocardial infarction (AMI). Such patients generally have multivessel coronary artery disease, and well-controlled clinical trials in this subgroup of patients have been performed to demonstrate that coronary artery bypass surgery or percutaneous coronary intervention improves outcome compared with medical therapy (Homoncik, Gessl, Ferlitsch, Jilma, & Vierhapper, 2007). Laboratory Findings Live 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 trickle into the blood stream, which could be detected by a blood sample analysis. These values vary depending on the assay used in each laboratory. Given the insight 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 an appropriate situations. The real value of biomarkers such as troponin lies in the diagnosis and prognosis of NSTEMI (Margolis, Adami, Luo, Ye, & Weiderpass, 2007). Diagnosis Various parameters determine the clinical predisposition of the patient. These factors are history of the patient, cardiac risk factors, and data procured from ECG. It is therefore, existence or nonexistence of stretched ST elevation by ECG is significant in determining the need to obtain medical or catheter-based coronary reperfusion. The present American Heart Association/ American College of Cardiology guidelines promotes establishment of revascularization therapy that is required to be given within 30 minutes as soon as the individual is presented with thrombolytic agents or within 60 minutes by percutaneous coronary revascularization (Pain Ladder, Abdel-Aty et al, 2004). Patients witnessing protracted ischemic chest pain, who do not undergo ST elevation, hospitalization, anti-ischemic and antithrombotic procedures as explained, are established to regulate for acute myocardial infarction (AMI) based on sequential methods undertaken by cardiac enzymes. It is evident that the abolished myocardial cells discharge their enzymatic contents into the bloodstream. Presence of such enzymes in the serum serves as a diagnostic tool. The presence of Creatine phosphokinase (CPK) could be easily detected in a few hours after the beginning of the symptoms ad provide the max outs at 12 to 24 hours. CPK is completely excreted through kidneys within 48 to 72 hours. An isozyme, CPK-MB enhances the precise and appropriate verification of acute myocardial infarction (AMI). There occurs a double rise in entire CPK combined with CPK-MB percentage characteristically larger than 5% to 7% of the entire CPK. On the other hand, a discrete ascend over the standard value of CPK-MB mass by radioimmunoassay associates extremely through myocardial necrosis, this could serve as a novel troponin assays (Pain Ladder). Detection of the serum LDH level serves as a useful diagnostic tool for those patients who do not try to find therapeutic concern for numerous days after the appearance of symptoms. In order to determine the extra prognostic significance an LDH1/ LDH2 isozyme reversal is measured. Cardiac troponins offer the advantage of higher specificity (Pain Ladder). In the present era, cardiac troponin T (cTn-T) and cardiac troponin I (cTn-I) are used in clinical follow up. They are the most imperative markers as very small cTn-T and no cTn-I are formed by skeletal muscle or by any other tissues and hence they serve as the most definite markers to detect myocardial necrosis. It is reported that the troponins make their first manifestation in the serum around 3 hours after the onset of infarction and reaches the maximum within 12 to 24 hours putting a benefit of enduring 7 to 14 days. Thereby, preventing the requirement for quantifying LDH (Squizzato, Gerdes, Brandjes, Buller & Stam, 2005). Associated Disease Abnormalities of AMI could be detected by means of imaging of the heart by echocardiography, radionuclide SPECT, or MRI. An alternative imaging modality exploited in AMI is technetium 99m pyrophosphate scanning. In this procedure, the pyrophosphate forms a complex along with the calcium in the bone. The similar kind of method of uptake is observed in infaracted myocardial cells as they accumulate large quantity of calcium in their mitochondria, and therefore could respond to the technique. The technology could be exploited with those cases displaying uncharacteristic history and a previous ECG abnormality that prevents an analysis (Pain Ladder). Treatment Treatment of acute myocardial infarction (AMI) encompasses anticipation and management of mortal ventricular fibrillation to an destructive interventional advancement intended to re-institute myocardial perfusion as well as reducing myocardial necrosis. It is to be noted that it is more frequent indicator of coronary thrombosis. Major advances to reinstate myocardial blood involves: emergent coronary bypass graft surgery, thrombolytic therapy, and percutaneous coronary intervention (Pain Ladder). It is established that emergency bypass surgery is executed in chosen patients displaying satisfactory morbidity and mortality. It is also established that intravenous management of thrombolytic agents, or an amalgamation with antiplatelet agents, results in diminishing the mortality and impediments of AMI. In the present era the most accepted care is thrombolytic therapy or percutaneous coronary intervention for cases displaying ST elevation in 12 hours of the appearance of symptoms (Pain Ladder; Warren-Gash, Smeeth & Hayward, 2009). Thrombolytic therapy works well for acute myocardial infarction (AMI). This is displayed by means of trials worth for streptokinase (SK), anistreplase (APSAC), tissue plasminogen activator (t-PA), and recombinant plasminogen activator (r-PA) (Pain Ladder). Studies encompassing GISSI and ISIS-2, established the effectiveness of SK versus placebo also demonstrate that acetylsalicylic acid is necessary in combination with SK therapy. In order to procure the mortality benefit early therapy is prerequisite. With modifications in the treatment regimen, it nowadays come into view that front-loaded t-PA is superior to SK or APSAC. GUSTO-I randomized 41,021 patients for (a) SK and subcutaneous heparin, (b) SK and intravenous heparin, (c) t-PA and intravenous heparin, and (d) t-PA and SK and intravenous heparin (Pain Ladder). Moreover GUSTO-III has since demonstrated equal efficacy for r-PA and t-PA (Hampton, 1997). Prevention Correctable cause of cardiogenic shock is right ventricular infarction, which often requires intravascular volume overexpansion to right atrial pressures greater than or equal to 10 mm Hg to achieve an adequate cardiac output. Ventricular septal rupture and papillary muscle rupture each occur in 1% to 3% of hospitalized acute myocardial infarction patients and generally result in cardiogenic shock. These can be corrected surgically, although with a high operative mortality. When hypovolemia, right ventricular infarction, and rupture of the septum or papillary muscle have been excluded, acute left ventricular dysfunction involving 40% or more of the left ventricle is the likely cause of the cardiogenic shock. Temporary improvement in hemodynamic status can be obtained with the use of a mechanical support device such as the intraaortic balloon; by inflating in diastole and deflating in systole this balloon can reduce left ventricular afterload and increase coronary perfusion pressure. The intraaortic balloon alone, however, is rarely sufficient. The best chance for short-term survival is conferred by early cardiac catheterization with primary angioplasty of the culprit stenosis for early reperfusion. In patients who undergo such treatment successfully, several weeks after recovery significant residual ischemia should be treated by appropriate means to favorably impact on long-term survival (Zarich, Luciano, Hulford & Abdullah, 2006). Complications The most common complication of acute myocardial infarction is ventricular arrhythmia, which occurs in some form in more than 90% of patients in the first 72 hours following the onset of the infarction. Premature ventricular beats are almost universal; more complex forms, such as couplets, triplets, and non-sustained ventricular tachycardia, are also commonly seen early after acute myocardial infarction (AMI). The value of treatment for these rhythms when asymptomatic has not been demonstrated; however, ventricular tachycardia (or ventricular fibrillation), when hemodynamic ally destabilizing, must be treated aggressively, with intravenous lidocaine and direct current cardio-version. Accelerated idioventricular rhythm also occurs relatively commonly in those with acute myocardial infarction (AMI). It must be distinguished from ventricular tachycardia (on the basis of a rate between 50 and 110 beats per minute) because the former is generally benign and requires no treatment. Case Study Solutions The clinical picture indicated a stable condition of anterior wall myocardial infarction, where mostly the left heart is impaired. Any transfusion quantity should be restricted based on stable BP. This is because the strength of a ventricular contraction of patients with an impaired left heart is attenuated and inadequate for creating an adequate stroke volume. This results in inadequate cardiac output, causing ventricular end-diastolic pressure and volumes to increase. Restricted transfusion quantity can release heart burden and be beneficial for myocardial recovery. There were no per procedural Complications. Post-procedure ECG demonstrated partial ST-segment resolution. A treatment of lifelong aspirin, one-year Clopidogrel, atorvastatine, metoprolol and lisinopril were initiated. The patient remained symptom free and was discharged on day five for cardiac rehabilitation. A 3-month control echocardiography was consistent with a slightly diminished ejection fraction at 50% and anteroseptal, as well as anterolateral, akinesia. A complementary laboratory workup showed that cholesterol and triglyceride levels were within limits but HDL-cholesterol was low at 0.75 mmol/l (normal 1.0–2.2 mmol/l). Complete immunological and thrombophilia workup were unremarkable. An additional transoesophageal echocardiography showed no patent foramen ovale (Pain Ladder). References Abdel-Aty, H., Zagrosek, A., Schulz-Menger, J., Taylor, A. J., Messroghli, D., Kumar, A., Gross, M., Dietz, R., Friedrich, M. G. (2004). Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation, 109(20), 2411–2416. Ashikaga, T., Nishizaki, M., Fujii, H., Niki, S., Maeda, S., Yamawake, N., Kishi, Y., Isobe, M. (2007). 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Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Pral Surg Oral Med Oral Pathol Oral Radiol Endod, 95(5), 559-569. Margolis, K. L., Adami, H. O., Luo, J., Ye, W., Weiderpass, E. (2007). A prospective study of oral contraceptive use and risk of myocardial infarction among Swedish women. Fertil Steril, 88(2), 310-316. Pain Ladder. Available at http://painladder.com/index.php/chest-pain/acute-myocardial-infarction. [Accessed on 1st Aug 2011]. Squizzato, A., Gerdes, V. E., Brandjes, D. P., Buller, H. R., Stam, J. (2005). Thyroid diseases and cerebrovascular disease. Stroke, 36(10), 2302-2310. Warren-Gash, C., Smeeth, L., Hayward, A. C. (2009). Influenza as a trigger for acute myocardial infarction or death from cardiovascular disease: a systematic review. Lancet Infect Dis, 9(10), 601-610. Zarich, S., Luciano, C., Hulford, J., Abdullah, A. (2006). Prevalence of metabolic syndrome in young patients with acute MI: does the Framingham Risk Score underestimate cardiovascular risk in this population? Diab Vasc Dis Res, 3(2), 103-107. Read More