Infarction atrial

The atrial infarction occurs because an atrial branch, taking off usually from the RCA or LCX, is involved by occluded artery. 

Figure 10.5 Lead II of a patient with acute inferior Ml. to atrial infarction extension. Atrial arrhythmias, frequent...

Figure 10.6). However, no signs are present in the chronic phase that suggests the presence of atrial infarction. 

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... 

Recommended if patient is at high-risk of systemic thromboembolism (anterior wall infarction, heart failure, left ventricular thrombus, atrial fibrillation, previous embolism)... 

Bileaflet mechanical valve and either atrial fibrillation, myocardial infarction, left atrial enlargement, endocardial damage, or low ejection fraction... 

Warfarin has been the primary oral anticoagulant used in the United States for the past 60 years. Warfarin is the anticoagulant of choice when long-term or extended anticoagulation is required. Warfarin is FDA-approved for the prevention and treatment of VTE, as well as the prevention of thromboembolic complications in patients with myocardial infarction, atrial fibrillation, and heart valve replacement. While very effective, warfarin has a narrow therapeutic index, requiring frequent dose adjustments and careful patient monitoring.15,29... 

Structural abnormalities such as atrial-septal aneurysm Myocardial infarction... 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

The predominant mechanism of AF and atrial flutter is reentry, which is usually associated with organic heart disease that causes atrial distention (e.g., ischemia or infarction, hypertensive heart disease, valvular disorders). Additional associated disorders include acute pulmonary embolus and chronic lung disease, resulting in pulmonary hypertension and cor pulmonale and states of high adrenergic tone such as thyrotoxicosis, alcohol withdrawal, sepsis, or excessive physical exertion. 

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. 

In studies involving atrial and ventricular biopsies in sheep and humans, Messina et al. [84] isolated a cardiac progenitor cell that was c-Kit and capable of self-proliferating into a large number of cells. The authors also showed that human CSCs could participate in infarct repair in the murine model. 

Contraindications Phenylephrine HCl injection should not be used with patients with severe hypertension, ventricular tachycardia or fibrillation, acute myocardial infarction (Ml), atrial flutter or fibrillation, cardiac arrhythmias, cardiac disease, cardiomyopathy, closed-angle glaucoma, coronary artery disease, patients who have a known hypersensitivity to phenylephrine, sulfites, or to any one of its components. 

Procainamide is effective against most atrial and ventricular arrhythmias. However, many clinicians attempt to avoid long-term therapy because of the requirement for frequent dosing and the common occurrence of lupus-related effects. Procainamide is the drug of second or third choice (after lidocaine or amiodarone) in most coronary care units for the treatment of sustained ventricular arrhythmias associated with acute myocardial infarction. 

Procainamide INa (primary) and IKr (secondary) blockade Slows conduction velocity and pacemaker rate prolongs action potential duration and dissociates from INa channel with intermediate kinetics direct depressant effects on sinoatrial (SA) and atrioventricular (AV) nodes Most atrial and ventricular arrhythmias drug of second choice for most sustained ventricular arrhythmias associated with acute myocardial infarction Oral, IV, IM eliminated by hepatic metabolism to /V-acetylprocainamide (NAPA see text) and renal elimination NAPA implicated in torsade de pointes in patients with renal failure Toxicity Hypotension long-term therapy produces reversible lupus-related symptoms... 

Propranolol 13- Adrenoceptor blockade Direct membrane effects (sodium channel block) and prolongation of action potential duration slows SA node automaticity and AV nodal conduction velocity Atrial arrhythmias and prevention of recurrent infarction and sudden death Oral, parenteral duration 4-6 h Toxicity Asthma, AV blockade, acute heart failure Interactions With other cardiac depressants and hypotensive drugs... 

Cardiovascular Effects. No studies were located regarding cardiovascular effects of various forms of aluminum following intermediate- or chronic-duration oral exposure in humans. Acute-duration oral exposure to aluminum phosphide has been shown to cause tachycardia, hypotension, cardiovascular electrocardiographic abnormalities, subendocardial infarction, and transient atrial fibrillation in persons who either ingested it accidentally or in suicide attempts (Chopra et al. 1986 Khosla et al. 1988). However, toxicity was probably due to the formation of highly toxic phosphine gas rather than to aluminum exposure. 

Preliminary report effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N EnglJ Med 1989 321 (6) 406—412. Donovan KD, et al. Intravenous flecainide versus amiodarone for recent-onset atrial fibrillation, Am J Cardiol 1995 75( 10) 693—697. 

Pedersen OD, Bagger H, Kober L, Torp-Pedersen C. Trandolapril reduces the incidence of atrial fibrillation after acute myocardial infarction in patients with left ventricular dysfunction. Circulation 1999 100 376-380. 

At total of 75% of cardiac emboli reach the brain. Non-valvular atrial fibrillation with thrombus formation within the left atrial appendix or the left atrium is the most common reason for cardiac emboli (Ferro 2003). Cardio-embolic infarcts within the MCA territory carry a high risk for hemorrhagic transformation after reperfusion. Hemor-... 

Therapeutic uses Lidocaine is useful in treating ventricular arrhythmias arising during myocardial ischemia, such as that experienced during a myocardial infarction. The drug does not markedly slow conduction and thus has little effect on atrial or AV junction arrhythmias. 

In acute MI, the ISIS-1 study [88] was organized to assess the effects of early beta-blockade with atenolol on cardiovascular mortality during the first week following infarction and after long-term (mean 20 months) follow-up. There was a 15% reduction in vascular deaths, especially in the early phase of MI. The difference in early mortality was mainly due to a reduction in electromechanical dissociation in the presence of atenolol. In this regard, atenolol is usually given by intravenous injection or infusion to treat cardiac arrhythmias, and it should be noted that atenolol induced atrial fibrillation in half of the so-predisposed patients [89]. 

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