Myocardial infarction arrhythmia

YuXC et al. (2001) Cardiac effects of the extract and active components of Radix stephaniae tetrandrae II. Myocardial infarct, arrhythmias, coronary arterial flow and heart rate in the isolated perfused rat heart. Life Sci 68(25) 2863-2872... 

The response-to-injury hypothesis states that risk factors such as oxidized LDL, mechanical injury to the endothelium, excessive homocysteine, immunologic attack, or infection-induced changes in endothelial and intimal function lead to endothelial dysfunction and a series of cellular interactions that culminate in atherosclerosis. The eventual clinical outcomes may include angina, myocardial infarction, arrhythmias, stroke, peripheral arterial disease, abdominal aortic aneurysm, and sudden death. 

Amiodarone (11), a benzofuran derivative, was initially developed as a coronary vasodilator in the early 1960 s [11,12]. Several years later, the efficacy of the compound as an antiarrhythmic agent began to be exploited. The first clinical trials with amiodarone were reported in 1974 [13]. Amiodarone was effective in controlling the tachyarrhythmias of eleven patients with Wolff-Parkinson-White syndrome. Since that time the compound has been studied extensively [14,15]. Recently, in the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), amiodarone was shown to reduce mortality during a mean 18 month period following myocardial infarction (13.8% deaths in placebo group vs. 2.1 % deaths in the treatment group) [16]. 

Coronary atherosclerosis angina pectoris, myocardial infarction, arrhythmia Atherosclerosis of cerebral vessels cerebral infarction stroke... 

Like procainamide, lidocaine is an amide with local anesthetizing action. Lidocaine is usually administered intravenously for short-term therapy of ventricular extrasystole, tachycardia, especially in the severe phase of myocardial infarction, arrhythmia of natural cause, and for arrhythmia that can originate in the heart during surgical manipulations. Synonyms of this drug are lidopen, xylocaine, xylocard, and others. 

Cairns JA, Connolly SJ, Roberts R, et al. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations CAMIAT. Canadian Amiodarone myocardial infarction arrhythmia trial investigators. Lancet. Mar 8 1997 349(9053) 675-682. 

Lidocaine Post-myocardial infarct arrhythmias Ventricular tachycardia... 

Cardiovascular system (angina, myocardial infarction, arrhythmias, arterial hypertension, valvular heart disease)... 

Cardiac arrhythmias are a common problem in clinical practice, occurring in up to 25% of patients treated with digitalis, 50% of anesthetized patients, and over 80% of patients with acute myocardial infarction. Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances for example, early premature ventricular depolarizations can precipitate ventricular fibrillation. In such patients, antiarrhythmic drugs may be lifesaving. On the other hand, the hazards of antiarrhythmic drugs—and in particular the fact that they can precipitate lethal arrhythmias in some patients—has led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason. 

In the European Myocardial Infarction Arrhythmia Trial (EMIAT) amiodarone reduced the risk of dysrhythmic deaths from 8.5 to 4.1% compared with placebo (40). 

In the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT) amiodarone reduced dysrhythmic deaths from 6.0 to 3.3% compared with placebo non-dysrhythmic deaths were not affected (41). 

Other Clinical Indications - The list of clinical indications in which 6-blockers have either been proven efficacious or are now being studied continues to grow. In addition to their now accepted efficacy in angina, myocardial infarction,arrhythmias and hypertension,104 other disease states characterized by excess sympathetic activity such as thyrotoxicosis have been treated with 3-blockers,... 

Pargyline (Eutonyl) Inhibits monoamine oxidase in adrenergic nerves. Inhibits norepinephrine release Because of DANGEROUS effects, is last choice antihypertensive drug. Life-threatening effects (stroke, hypertensive crisis, myocardial infarction, arrhythmias) may occur when taken with foods (fermented products, cheese) and drugs (diet pills, cold remedies) which contain sympathomimetics. 

CV safety issues are a major cause of drug attrition in both the nonclinical and clinical phases of drug discovery and development, and an estimated 45% of drug withdrawals during the postmarketing phase are atttibuted to adverse CV events, such as myocardial infarction, arrhythmia, and cardiac arrest (Laverty et al., 2011 Pierson et al., 2013). 

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

The dmg is effective in the treatment of ventricular arrhythmias, especially those following acute myocardial infarctions (1,2,22). 

Antidepressants Noradrenaline/5-HT transporters Na+, K+ channels l Noradrenaline/ 5-HT reuptake l Na+ currents t K+ currents l Excitability of peripheral and central neurons Cardiac arrhythmia, myocardial infarction, sedation, nausea, dry mouth, constipation, dizziness, sleep disturbance, blurred vision... 

Occurs when the volume of extracellular fluid is significantly diminished. Examples include hemorrhage, fluid loss caused by burns, diarrhea, vomiting, or excess diuresis Occurs when the heart is unable to deliver an adequate cardiac output to maintain perfusion to the vital organs. Examples include as the result of an acute myocardial infarction, ventricular arrhythmias, congestive heart failure (CHF), or severe cardiomyopathy. 

These dm are primarily used in the treatment of hypertension (see the Summary Drug Table Adrenergic Blocking Drugs also see Chap. 39) and certain cardiac arrhythmias (abnormal rhythm of the heart), such as ventricular arrhythmias or supraventricular tachycardia They are used to prevent reinfarction in patients with a recent myocardial infarction (1—4 weeks after MI). Some of these dm have additional uses, such as the use of propranolol for migraine headaches and nadolol for angina pectoris. 

Adverse reactions include transitory stinging on initial instillation, blurring of vision, mydriasis, increased redness, irritation, discomfort, and increased IOP. Systemic adverse reactions include headache, browache, palpitations, tachycardia, arrhythmias, hypertension, myocardial infarction, and stroke. 

Systemic anaphylaxis in man is frequently accompanied by electrocardiographic alterations ischemic ST waves, arrhythmias and atrial fibrillation [6-11]. Anaphylactic reactions after insect stings can lead to coronary spasm or acute myocardial infarction [12, 13]. Myocardial infarction can also occur as a consequence of idiopathic... 

While epinephrine is usually well tolerated in young and healthy individuals, there may be problems in elderly patients with cardiac arrhythmia or previous myocardial infarction episodes [31-33]. Pharmacological effects of epinephrine include rapid rise in blood pressure, pallor, anxiety, tachycardia, headache and tremor as well as vertigo. Most commonly these effects occur after intravenous injection or after overdosing epinephrine. Cardiac arrhythmia or pulmonary edema may develop in serious cases [33, 34]. 

Cardiovascular Effects. In one case study, a woman who had accidentally consumed about 20 mL of trichloroethylene was reported to have suffered a myocardial infarction within 2 hours of ingestion (Morreale 1976). In two other case studies, men who ingested 350 and 500 mL of trichloroethylene had ventricular arrhythmias that persisted for up to 3 days (Dhuner et al. 1957). The arrhythmias were described as ventricular tachycardia with extrasystoles from different ventricular foci. Cardiac arrhythmia was also reported in a women who drank an unknown amount of trichloroethylene (Perbellini et al. 1991). 

Increased oxygen demand secondary to increased heart rates and blood pressure has been hypothesized to lead to myocardial infarction (especially in patients with fixed coronary disease) and/or ventricular arrhythmias. In patients with no history of cardiac disease, cocaine is thought to induce acute isehemie complications via vasospasm of the coronaries (Ascher et al. 1988). In addition, Virmani et al. (1988) have reported a 20 percent incidence of myocarditis thought to be secondary to accumulated microvascular injuries. 

One eritical factor that has been neglected in considering mechanisms of cardiac fatalities is the timeframe for various types of toxicities. For example, a majority of cocaine-related fatalities and near fatalities reported from emergency rooms are attributed to one or more types of cardiac ischemic or hypertensive episodes (Isner et al. 1986). Thus, these studies may discount the cocaine-induced arrhythmias and conduction defects as important direct causes of fatalities. Yet, if coroner reports are used as data sources (Virmani et al. 1988 Wetli and Wright 1979 Mittleman and Wetli 1984), there are great numbers of deaths in which pulmonary effusion and lack of evidence for coronary occlusion, acute myocardial infarction, or... 

Treatment of sinus bradycardia is only necessary in patients who become symptomatic. If the patient is taking any med-ication(s) that may cause sinus bradycardia, the drug(s) should be discontinued whenever possible. If the patient remains in sinus bradycardia after discontinuation of the drug(s) and after five half-lives of the drug(s) have elapsed, then the drugs(s) can usually be excluded as the etiology of the arrhythmia. In certain circumstances, however, discontinuation of the medication(s) may be undesirable, even if it may be the cause of symptomatic sinus bradycardia. For example, if the patient has a history of myocardial infarction or HF, discontinuation of a (3-blocker is undesirable, because (3-blockers have been shown to reduce mortality and prolong life in patients with those diseases, and the benefits of therapy with... 

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