Acute Coronary Syndrome - Essay Example

Acute Coronary Syndrome Name University Acute Coronary Syndrome Pathophysiology In most patients, the pathogenesis of acute coronary symptom syndromes begins with the rupture of the atherosclerotic plaque with the development of superimposed thrombus (Srikanth & Ambrose, 2012). This results in the interruption or limitation of coronary blood flow. The formation of thrombus comes about as a result of fundamental changes in thrombin and platelets; thrombin changes fibrinogen to fibrin, hence activating platelets and activates more platelets into the already platelet-rich thrombus. In patients suffering from acute coronary syndromes, the platelets have a short survival time, and they release various substances that cause thrombosis, including β-thromboglobulin, platelet factor 4 and formation of thromboxanes (Madder et al., 2013). These factors lead to the aggregation of platelets at the location of plaque rupture, forming a thrombus. After the activation of thrombin-induced platelets, coagulation factors converge on the activated platelet surface where they undergo activation by coagulation factors. According to necropsy studies, between 66% and 75% of acute coronary syndromes result from thrombosis (Falk, Nakano, Bentzon, Finn, & R, 2013). The process of atherosclerosis actually begins several years before the symptoms can manifest. This minor inflammation of the intima of medium-sized is caused by risk factors such as genetics, diabetes, high cholesterol, smoking, and blood pressure (Tian et al., 2013). As atherosclerosis progresses, it causes the slow and steady thickening of the inner walls of coronary arteries. Over years, this may lead to the narrowing of the lumen of the artery. Atherosclerosis that leads to acute coronary syndrome tends to develop around the proximal sections of the major coronary arteries, particularly at the at arterial bifurcation sockets that influence flow in the artery (Madder et al., 2013). The gradual atherosclerotic progression may be interjected by cycles of rapid progression resulting from either plaque haemorrhage or asymptomatic plaque disruption that forms a non-occlusive intraluminal thrombus (Falk et al., 2013). As the arterial intima thickens, it demands a continued supply of blood. This supply normally comes from the adventitia into the media and intima, supplying the required nutrients. The endothelial integrity of these blood vessels is not always intact because they are thin-walled. Falk et al. (2013) found that the rupture of these vessels may acutely enlarge the plaque size due to the deposited blood. Due to the lipid-rich nature of the red cell membrane, haemorrhage tends to increase the inflammatory and lipid cell content in the plaque. As the volume of the plaque reaches 40%, the lumen of the artery begins to narrow, which then leads to acute coronary events (Srikanth & Ambrose, 2012). In the case of asymptomatic plaque disruption, the atherosclerotic plaque is formed of cellular debris, inflammatory cells, smooth muscle cells, cholesterol ester and varied amounts of cholesterol. An excess of inflammatory cells move into the arterial wall and cause the fibrous cap to weaken. This can cause the cap to tear, making the thrombogenic lipid core be exposed to blood; hence, forming an intraluminal coronary thrombus (Falk et al., 2013). This thrombus may grow and develop to near or complete coronary obstruction and an acute coronary event. Pharmacological Management The initial treatment of acute coronary syndromes should begin with the relief of pain. There is a connection pain and sympathetic activation as it causes vasoconstriction, leading to an increase in the workload of the heart. In the initial management of ACS, intravenous morphine is most preferred. Antiplatelet/Anticoagulant Therapy Antiplatelet therapy should begin immediately after an acute event to reduce the risk of thrombosis by preventing the release and coagulation of platelets. The most common antiplatelet therapies in relation to this condition include aspirin, glycoprotein IIb/IIIa inhibitors, receptor antagonists, and adenosine diphosphate P2Y12[Che13]. The antiplatelet drugs currently being used target the GPIIb/IIIa receptor (tirofiban, abciximab, eptifibatide), phosphodiesterase (cilostazol and dipyridamole), the P2Y12 ADP receptor (clopidogrel, ticagrelor, ticlopidine, and prasugrel), and the cyclo-oxygenase/thromboxane pathway (ASA) (Fitchett & Théroux, 2011). Aspirin should be given on a daily basis. However, other nonsteroidal anti-inflammatory medications should not be administered because they are associated with increased risk of cardiac events. A single 300mg dose should be administered and trailed by a daily dose of 75mg. Aspirin acts as an inhibitor, inhibiting the activation of platelet by obstructing cyclo-oxygenase-1 and preventing of thromboxane A2 formation, which occurs in the acute phase of myocardial infarction. Studies have revealed the effectiveness of aspirin at this phase. Administering 162.5mg of enteric-coated aspirin on a daily basis for a month showed a great reduction in mortality rates (Smith et al., 2015). The first tablet should be crushed to enable rapid antiplatelet effect. Aspirin should, however, be given early enough to increase its effectiveness. Patients with known hypersensitivity, blood dyscrasia, or bleeding peptic ulcer should, however, not be given aspirin. For such patients, clopidogrel 300mg should be considered as an alternative. A P2Y12 inhibitor such as ticagrelor or clopidogrel should be administered alongside aspirin for twelve months in patients who have undergone either ischemia-guided or early invasive strategy (Smith et al., 2015). Apart from antiplatelet treatment, parenteral anticoagulation is recommended with unfractionated heparin, bivalirudin, fondaparinux, or enoxaparin. For patients without contraindications, a high-intensity statin is advised. Angiotensin-converting enzyme inhibitors also need to be administered continually with a left ventricular ejection ≤40 percentage or stable chronic kidney disease, or hypertension, diabetes, unless contraindicated. Patients who are under percutaneous coronary intervention need to be given a P2Y12 inhibitor such as ticagrelor, prasugrel, or clopidogrel (Smith et al., 2015). Management of STEMI Once in the hospital, management should proceed to acute ST-elevation myocardial infarction (STEMI). The additional pharmacological interventions include: Clopidogrel: there are many benefits of using clopidogrel alongside aspirin in the management of STEMI. Actually, many emergency departments in hospitals administer clopidogrel 300mg during the initial standard treatment of acute coronary syndromes. A dose of 150 mg should be given for at least one week followed by 75 mg daily (Fitchett & Théroux, 2011). Heparin: STEMI patients are also given unfractionated heparin (UFH), but low molecular weight heparin (LMWH) can be given as an alternative. Recent studies suggest that LMWH are the best antithrombin to administer to STEMI patients who have been given aspirin and thrombolysis (Cheng, 2013). Statins: according to recent studies such as Smith et al. (2015), the application of statin therapy within 24 hours after an acute event is associated with considerably lower rate of mortality and early complications. Statin is the most recommended HmG–coenzyme A reductase inhibitor. Further studies suggest that statin use is beneficial irrespective of a patient’s cholesterol level. Beta-blockers: Currently, studies are being conducted on the feasibility of beta-blockers during acute phase after myocardial infarction. It has been found that they have the potential to relieve pain, reduce arrhythmias incidences and limit infarct size (Cheng, 2013). Nevertheless, beta-blockers have not gained widespread use in this area. These studies, however, have shown that the use of beta-blockers during the early phase reduces the risk of ventricular fibrillation and reinfarction. It is, however, recommended that beta-blockers be used only when the patient is haemodynamically stable. β-blockers have been shown to reduce the sinus node rate, myocardial contractility, AV node conduction velocity as they prevent catecholamines from affecting the β-receptors found in the myocardium. Overall, β-blockers help reduce the myocardial oxygen demand and decrease cardiac work rate (Smith et al., 2015). Renin-Angiotensin System Inhibitors: the use of angiotensin-converting enzyme (ACE) inhibitors has shown the ability to reduce mortality within 30 days after an acute event. Trials have shown that the treatment is safe and tolerated among patients. However, it should be noted that ACE inhibitors should be administered only to patients who have experienced heart failure or have compromised left ventricular function in the acute phase after an MI. Current Pharmacological Research Deciding on the best combination of anticoagulants and antiplatelet agents is still a big challenge for medical professionals. The challenge remains severe for patients who undergo an acute coronary syndrome event and are at risk of experiencing long-term anticoagulation; that is patients with atrial fibrillation, mechanical heart valves, or previous venous thromboembolism. The current procedures recommend the use of a vitamin K antagonist to the prevailing antiplatelet therapy that targets a universal normalized ratio of 2.0 to 3.0 (Deepak, Bhatt, David, & Robert, 2014). Current research focuses on the Optimal Antiplatelet and Anticoagulant Therapy in Patients with Oral Anticoagulation and Coronary Stenting (WOEST) (Dewilde et al., 2013). The WOEST trial studied the administration of clopidogrel alone versus clopidogrel plus aspirin therapy alongside oral anticoagulants. The study revealed that the combination of clopidogrel and aspirin reduced thrombotic events just as much as clopidogrel alone. However, the latter manifested increased risk of bleeding. Clinical trials are being conducted on to help medical professionals find the optimal strategy for patients that need the combination of antiplatelet and anticoagulant treatments. The PIONEER AF-PCI research (evaluating one strategy of oral vitamin K antagonist and two strategies of rivaroxaban in ACS patients with atrial fibrillation who have undergone PCI) is studying two different rivaroxaban treatment strategies and one vitamin K antagonist treatment strategy with various combinations of DAPT in those who have suffered atrial fibrillation and have undergone PCI. Another study, the RE-DUAL PCI study, is ongoing. It aims at evaluating the impact on dabigatran (at two doses) alongside antiplatelet therapy contrasted with warfarin combined with antiplatelet therapy (Deepak, Bhatt, David, & Robert, 2014). Potential Relevance the Findings to a Paramedic As reviewed above, there are various pharmacological strategies for the management of ACS. In the event of an acute event, response time is critical to reduce the chances of mortality. Antiplatelet and anticoagulant therapies should be administered as soon as possible to try to reverse thrombosis. However, the challenge for paramedics who respond to such distress class is that there are various antiplatelet and anticoagulant agents in the market, and they all react differently to patients. As such, it is required that the medical history of the patient is known before administering certain medication. For example, Smith et al. (2015) state that other than aspirin, other nonsteroidal anti-inflammatory medications should not be administered to victims of ACS because they are associated with increased risk of cardiac events. Further studies have found that aspirin should not be given to those who have known hypersensitivity, blood dyscrasia, or bleeding peptic ulcer. Instead, clopidogrel 300mg is recommended for such patients. It is evident that the decisions made by the paramedic regarding the patient are critical when a patient’s life is at stake. A wrong split-second decision can lead to loss of life. Patients who suffer ACS have a high chance of survival if thrombolysis is given within 12 hours after an attack (Tataris, Mercer, & Govindarajan, 2014). This suggests that respnsibility to provide thrombosis rests largely on the paramedics. The paramedic, therefore, must diagnose the condition rightly for effective medication to be given and to reduce mortality. However, acute coronary symptoms are very difficult to diagnose in an out-of-hospital setting. Misdiagnosis by a paramedic can result in poor patient outcomes, and even increased mortality. It is clear that introducing more antithrombotic drugs to the management of ACS can increase the risk of serious bleeding. However, with the right dosage combination, antithrombotic treatment is useful for the right patient. This is a major challenge in the field of paramedics as there are several approved and recommended therapies, and several of combinations on the usage of antithrombotic drugs, yet there is limited clinical evidence that compares their combinations. While many risk factors for bleeding and ischemic events are useful when allocating antithrombotic therapy, this information may not always be available to the paramedic, especially when the patient is unstable and medical history cannot be retrieved immediately. It is, therefore, important for research scientists to investigate and develop pathways that target thrombosis that does not lead to excess bleeding; for example, drugs could target platelet adhesion. This may result in disassociating more potent effectiveness from bleeding. It is imperative to note that currently, no antithrombotic has been proven to achieve this task in experimental trials. As for now, paramedics will continue to weigh various patient characteristics whenever offering thrombosis. References Che13: , (Cheng, 2013), Read More