Approaches to Salvage Damaged Heart Tissue after Myocardial Ischemia - Essay Example

?Approaches to salvage damaged heart tissue after myocardial ischemia Introduction Myocardial ischemia is one of the most common health issues which are experienced by individuals with coronary heart disease or cardiovascular disease. Millions of people around the world suffer the effects of myocardial ischemia and its impact on those affected ranges from the mild to debilitating. Regardless of the severity of its impact, the inadequate blood flow to the heart can damage the heart muscles and reduce the capacity of the heart to carry out its normal functions. This paper shall discuss the different pharmacological approaches in salvaging damaged heart tissue after myocardial ischemia. Various medicinal treatment options will be considered for this discussion in relation to how such options can revive or treat the damaged heart. Body There are various medicinal options which can be used in order to salvage damaged heart tissue after myocardial ischemia. The primary goal in salvaging damaged heart tissue is to improve blood flow to the heart muscle or the heart tissue. One of the primary therapies to accomplish this goal is the administration of tPA or tissue plasminogen activator (Fonarow, et.al., 2011). This is primarily a protein which dissolves blood clots. Normally, tPA is found at the endothelial cells of the blood vessels and functions by converting plasminogen to plasmin, which is the enzyme which breaks down blood clots (Sheehan and Tsirka, 2005). In the practice, the synthesized version is administered in order to dissolve blood clots in the system. For any blockage in the coronary blood vessels, the tPA immediately acts to dissolve such blockage in order to help restore tissue reperfusion (Sheehan and Tsirka, 2005). Such reperfusion helps minimize the tissue damage and ischemia. tPA has been used in diseases which present with risks for blood clots, including pulmonary embolism, myocardial infarction, as well as stroke (Mateen and Nasser, 2009). For these diseases, administering tPA the earliest possible time or as soon as symptoms manifest can help ensure the maximum efficacy of the drug. Based on drug protocols, tPA must be administered within the first three hours of the event; after three hours, the negative impact of the drug would likely outweigh its benefits (Mateen et.al., 2010). It is usually administered systematically in order to ensure maximum perfusion. There are different state guidelines or protocols which refer to the best time to administer the drug (Mateen, et.al., 2010). For example, Canada and the US recommend that tPA can be administered up to 4.5 hours after the event (Davis and Donnan, 2009). Studies have been able to indicate that patients may not immediately seek medical help after an event and the administration of the drug 4.5 hours after the event provides more time to administer the drug (Davis and Donnan, 2009). Allowing a longer window for the administration of tPA has been a favourable option in salvaging the damaged heart tissue of myocardial ischemia patients. Much caution is however emphasized on the use of the drug after the time frame because its mechanism of action in dissolving blood clots also presents a haemorrhage risk for the patient (Davis and Donnan, 2009). For myocardial ischemia patients, the tPA Alteplase has been highly recommended. As a tPA, this drug helps dissolve blood clots in ischemia patients and is usually administered intravenously (Gurm, et.al., 2008). The same precautions for other tPAs are indicated for Alteplase as it cannot be administered beyond 4.5 hours from the initial event because of bleeding risks on the patient. Drugs which interfere with the body’s clotting mechanisms can increase the risk of bleeding for patients receiving this drug (Gurm, et.al., 2008). These drugs would include warfarin, aspirin, non-steroidal anti-inflammatory drugs (ibuprofen, naproxen). Aside from bleeding, other side-effects may also include nausea, vomiting, and allergic reactions (De Luca, et.al., 2005). As soon as tPA is administered, blood clots which may be interfering with the blood flow to the heart would immediately be dissolved. As blood flow is restored, the extent of the ischemia is reduced or minimized. As soon as blood flow is restored, reperfusion of the damaged tissue can help salvage the ischemic heart tissues. The study by Lansberg and colleagues (2009) sought to establish reliable and precise estimates on the treatment impact of tPA based on pooled data from all significant studies. This analysis was carried out in order to establish the impact of tPA in the 3-4.5 hour period after the event or the onset of the stroke (Lansberg, et.al., 2009). The outcome measures included mortality as well as extent of the ischemia. Based on the meta-analysis, tPA treatment within the 3 to 4.5 hour period was linked with a higher, more favourable outcome for patients suffering from myocardial infarction (Lansberg, et.al., 2009). The degree of ischemia has registered less extensive and more salvageable levels with the timely use of tPA. All in all, the authors concluded that use of tPA within the 3 to 4.5 hour period following the incident helps ensure efficacy of the drug in reducing the impact of the ischemia and in helping to salvage damaged heart tissue (Lansberg, et.al., 2009). Aside from the tPA, glycoprotein IIb/IIIa inhibitors can also interfere with the aggregation of platelets by blocking the glycoprotein receptors found in the platelets (Valgimigli, et.al., 2012). These are usually administered systematically together with aspirin and heparin. They act quickly, within minutes after the administration of the drug (Valgimigli, et.al., 2012). Various studies have indicated that glycoprotein IIb/IIIa inhibitors like abciximab and eptifibatide reduce the size of the blood clot or the blockage in the coronary arteries, ultimately assisting in blood flow and in managing damage to the heart tissues (Valgimigli, et.al., 2012). For patients who are already at risk for ischemia or who have had a history of MI, these glycoproteins have been known to decrease the risk of ischemia and also improve survival for patients who have unstable angina (Bhatt, 2008). Very much like tPA, glycoproteins also present a risk for bleeding. These patients have therefore to be closely monitored for possible signs of hemorrhage (Bhatt, 2008). Eptifibatide has been known to have a shorter acting time as compared to abciximab; nevertheless, both drugs manifest with similar efficacy. The use of abciximab as a coronary intervention for acute myocardial ischemia was evaluated in a study by Ferenczi and colleagues (2008). The authors discussed that at 30 days, a 12 hour infusion of abciximab helps prevent reinfarction. The authors then set out to assess whether abciximab features a major advantage in relation to increased life-years and in salvaging damaged heart caused by ischemia (Ferenczi, et.al., 2008). The authors identified four randomized controlled trials using abciximab for MI therapy where life years were measured including prevention of reinfarction. The study revealed that based on various trials, the benefit of abciximab to the patient in relation to gain in years increases (Ferenczi, et.al., 2008). The favourable rates are based on the prevention of reinfarction as well as the prevention of the persistent impact of ischemia. The overall goal in administering abciximab is to ensure continued blood flow and to limit the impact of the blockage. The favourable use of abciximab was also highlighted in the study by Iversen and colleagues (2011) where the authors set out to assess the impact of abciximab among patients with diabetes mellitus with acute coronary syndrome from a percutaneous coronary intervention registry. From about 5,000 patients with ACS who went thru PCI, about 600 had diabetes (Iversen, et.al., 2011). Outcome measures for the patients included mortality, revascularization, and myocardial infarction. There was a marked reduction in revascularization, mortality as well as MI among patients included in the study. Findings suggested that abciximab given to patients with diabetes during PCI helps reduce the impact of infarction, reducing mortality rates, as well as damage to heart from ischemia (Iversen, et.al., 2011). When compared with those who did not receive abciximab, the results were very much relevant. The administration of anticoagulants is also an effective means of salvaging damaged heart tissue for patients who have suffered a myocardial ischemia (Linkins, et.al., 2010). Since the coagulation of the blood and subsequent lodging of such coagulated blood in the smaller coronary arteries is the cause of the ischemia, the administration of anticoagulants is one of the effective interventions which can be used in order to reduce the impact of the ischemia and allow for reperfusion of the damaged heart tissue (Anzai, et.al., 2012). Anticoagulants such as heparin and warfarin prevent the formation of blood clots by inhibiting the formation or action of clotting factors (Konstam, 2009). Heparin inhibits the formation and development of blood clots as it inhibits clotting factors which make platelets clump with each other (Brieger, et.al., 2011). It is also administered systematically or subcutaneously. It is usually administered along with aspirin and antiplatelet agents (Iqbal, et.al., 2012). Patients who have suffered from major heart attacks or damage of heart muscles also have the risk of developing blood clots in their ventricles. The anticoagulant action of this heparin is very fast and is often dependent on dose (Iqbal, et.al., 2012). As with the earlier pharmacological remedies indicated above, bleeding is also a side-effect of heparin with intracranial bleeding being one of the more significant risks. With higher doses, the risk for bleeding is also increased (Schindler, 2009). It is therefore important for patients using heparin to undergo regular blood testing for APPT in order to measure anticoagulation. The levels must be in the safe neutral levels in order to avoid abnormally high APPT levels which may indicate excessive anticoagulation and therefore a higher risk of bleeding (Schindler, 2009). In a paper by Tateno and colleagues (2003), the authors discussed that heparin assists in angiogenesis. They then set out to assess the impact of combined treatment with heparin and exercise on myocardial ischemia in the chronic stage of Kawasaki disease. This study was carried out on 7 patients who experienced blocked coronary artery and stress-induced myocardial ischemia (Tateno, et.al., 2003). Heparin, administered intravenously was given in order increase hepatocyte growth factor. During patient observations, no new infarctions were seen and no hemorrhagic complications were observed. The findings were able to establish that using heparin coupled with exercise treatments in the span of ten days had major significant effects on reducing the impact and occurrence of myocardial ischemia (Tateno, et.al., 2003). This therapy would therefore be highly recommended for patients with coronary artery blockage in the chronic stage of Kawasaki disease. Beta-blockers have also been recommended as a means of managing myocardial ischemia. They work by mainly blocking B1 and B2 receptors; by inhibiting the impact of norepinephrine and epinephrine, these beta blockers decrease the heart rate and decrease the blood pressure by also dilating the blood vessels (Bristow, et.al., 2009). Under such conditions, the impact of the ischemia is reduced and the damage to the heart tissue can be salvaged. In a study by Rajeev and Wong (2009), beta-blockers help reduce the impact and occurrence of myocardial infarction among patients having noncardiac surgery. Based on 16 randomized controlled trials which were chosen for this study, ten trials were established to have utilized beta-blockers in the postoperative period. The authors revealed that the incidence and impact of myocardial ischemia was reduced with the administration of beta-blockers (Rajeev and Wong, 2009). The meta-analysis revealed that in the preoperative and postoperative period for non-cardiac surgeries, the administration of beta blockers have been useful in significantly reducing the impact of ischemia on the patient, reducing its occurrence and ensuring that high blood pressure or abnormal heart rhythm would be prevented (Rajeev and Wong, 2009). Conclusion Based on the above studies and discussion, there are various approaches which can be applied in order to salvage damaged heart tissue after myocardial ischemia. The salvaging of damaged heart tissue after myocardial ischemia refers to the management and the reduction of the impact of the ischemia. The importance of facilitating blood flow and reperfusion of ischemic area is therefore emphasized in the management of ischemia. Dissolving blood clots and preventing the formation of the blood clots is essential to this process, hence, the administration of tPA, anticoagulants, and glycoprotein IIb/IIIa inhibitors. The important consideration for these drugs is their administration in the earliest time possible; preferably, within 3-4.5 hours after the event. Beyond such ideal time, the drug causes a higher hemorrhagic risk which would make the administration of the drug counterproductive. Moreover, the patients administered with these drugs have to be monitored for adverse effects, which primarily include bleeding. Regardless of such adverse risk, with the efficient administration of these drug therapies, damaged heart tissue in myocardial ischemia can be salvaged, thereby eventually ensuring favourable patient outcomes. 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Glycoprotein IIb/IIIa inhibitors, in therapeutic advances in thrombosis. Oxford: Blackwell Publishing Ltd. Read More