Role of angioplasty in myocardial infarction management strategies: a review

Article Abstract:

Percutaneous transluminal coronary angioplasty (PTCA) is rarely warranted in the care and treatment of acute myocardial infarction (MI). Since only 15 percent of American hospitals are equipped and staffed for 24-hour expert emergency PTCA, it is seldom an option for primary intervention. The thrombolytic, or clot-dissolving, drugs have become the standard primary treatment for acute MI, and emergency angioplasty does not significantly improve on their record. Even with drug therapy 20 to 25 percent of patients still have occluded arteries, but the significance of this for mortality rates is not known. The use of PTCA to ''rescue'' these patients has had modest results in opening the arteries of about half of the treated patients, but it had no demonstrable benefit on mortality or left ventricular function. Drug therapy is more effective, especially since complications were frequent with PTCA. Another goal proposed for PTCA is greater myocardial salvage after drug therapy, but two studies found that there was no benefit to PTCA, and there were more complications with the intervention. PTCA was also considered for the prevention of reocclusion, which occurs in 10 percent to 15 percent of successfully reperfused arteries, but it does not seem to be effective in this regard either. When routine angioplasty (18 to 24 hours after thrombolytic treatment) was considered, the invasive treatment again showed no significant advantage. Only in those patients who suffered from spontaneous or recurrent ischemia (a transient decrease in blood flow to the heart) did PTCA have a favorable impact, reducing the frequency of ischemia. In a small subgroup of patients who have circulatory insufficiency after MI, indicating a poor prognosis, PTCA may help, along with circulatory assist devices. PTCA is advised only in cases of persistent coronary occlusion, clinical instability (such as shock or electrical instability), and documented recurrent ischemia. In almost all cases, PTCA does not improve the outcomes expected with thrombolytic therapy, and often causes complications. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Angioplasty

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Dysrhythmias and blood pressure changes associated with thrombolysis

Article Abstract:

Acute myocardial infarction (AMI; heart attack) continues to result in high rates of illness and death, despite improved care and technological and therapeutic advances. One of the most recent therapeutic innovations is the administration of intravenous and intracoronary thrombolytic (clot-dissolving) medications. (When intracoronary drugs are administered, they are injected into the heart.) The goals of thrombolytic treatment are to interrupt the process of infarction (tissue injury due to inadequate blood flow) before the damage is irreparable, and to permit restoration of blood flow in the blocked coronary vessels. Dysrhythmias (abnormal heart rhythms) frequently occur in association with the administration of thrombolytic agents. The frequency, timing, and characteristics of the dysrhythmias and blood pressure effects associated with administration of the thrombolytic agent tissue-type plasminogen activator (TPA) were studied in 41 heart attack patients. This review showed that dysrhythmias, principally sinus bradycardia, occurred in approximately 80 percent of cases treated with TPA. Changes in mean arterial blood pressures (MAP) were significantly different in patients with dysrhythmias than in those without dysrhythmias. The greatest changes in MAP occurred in patients with blockages of the left anterior descending coronary artery. The effects of prior medication (given before TPA) on some of the patients and the small sample size are cited as limitations of this study. (Consumer Summary produced by Reliance Medical Information, Inc.)

Risk factors, Physiological aspects, Blood pressure, Tissue plasminogen activator, Arrhythmia, Thrombolytic therapy

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Overview: rationale of thrombolysis in treating acute myocardial infarction

Article Abstract:

Acute myocardial infarction (AMI), a heart attack, occurs when the blood vessels in the heart suddenly become blocked or plugged. This inhibits the normal flow of blood and cuts off the oxygen supply to the heart muscle. Since no tissue can survive for prolonged periods of time without oxygen, the affected part of the heart muscle begins to die shortly after an AMI occurs. In the 1950s, thrombolytic agents were developed for treating patients with AMI. These drugs were found to be capable of dissolving blood clots (thrombi) and reopening blocked blood vessels. In the 1960s and 1970s, clinical studies were performed to determine if streptokinase (a thrombolytic drug) could improve mortality after AMI. The results of these studies were inconclusive and largely ignored by the rest of the medical community. The first convincing evidence that thrombolytic drugs are useful for treating patients with AMI came in 1976. A doctor in the Soviet Union demonstrated that streptokinase could unclog a totally blocked artery following an infarction. More recently, studies have shown that thrombolytic agents, streptokinase and recombinant tissue plasminogen activator, reduce mortality in patients with AMI when treatment is started within six hours of the infarction. Currently, studies are being performed to determine if thrombolytic agents are effective in improving mortality following different types of myocardial infarction. (Consumer Summary produced by Reliance Medical Information, Inc.)

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