Fibrillation clinical presentation

A number of diseases involve deposition of a characteristic amyloid fiber. However, in each of these diseases, the amyloid is derived from a different protein that has changed its conformation (three-dimensional structure) to that of the amyloid repeated p-sheet structure. Once amyloid deposition begins, it seems to proceed rapidly, as if the fibril itself were promoting formation and deposition of more fibrils (a phenomenon called "seeding"). The different clinical presentations in each of these diseases results from differences in the function of the native protein and the site of amyloid deposition. 

HPI DD is a 67-year-old woman who presents to the clinic complaining of headache, dizziness, and "buzzing in her ears." She states that her symptoms have been present for about 4 days. One week prior, the patient was discharged from the hospital for atrial fibrillation Rate control was achieved and she was converted to normal sinus rhythm (NSR). She was placed on a new antiarrhythmic medication to prevent further episodes of AF. PMH Episodic AF, cirrhosis,... 

Antithrombotic therapy is used in myriad CV diseases such as atrial fibrillation, heart failure, valve replacement, peripheral vascular disease, and stroke. This presents an ideal setting for a pharmacist-managed antithrombosis clinic. Today, many institutions have antithrombosis clinics managed by clinical pharmacists this trend continues to grow. 

Frequently, especially in the elderly, a paroxysmal arrhythmia crisis, especially atrial fibrillation, may cause chest pain, which may have anginal characteristics and may be of long duration, in relation with the duration of the arrhythmia. In this case the possibility to be confused with ACS is high. Often, no concurrent coronary atherosclerosis is present, and basically, the impairment of diastolic properties due to the tachycardia may explain the clinical picture. In spite of the presence of severe symptoms, the lack of enzyme-level changes, in the presence of a long-duration thoracic pain and tachyarrhythmia, leads one to suspect that this is not a classical ACS, but rather pain of anginal characteristics and usually not due to ischaemia but to haemodynamic origin. 

Cardiovascular Essential hypertension and electrocardiographic changes are present (ST-segment depression or flattening, T-wave inversion, and U-wave elevation). Clinical arrhythmias include heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, and digitalis-induced arrhythmias. 

Other less frequent complications of lead extraction include arteriovenous fistulas that present either acutely or in the days following the procedure. Pericardial tamponade could be clinically evident several hours after the procedure. Patients undergoing lead extraction should be monitored for at least 24 h in the intensive care unit, with echocardiography performed electively immediately after the procedure and 6 h later to evaluate the pericardial space and tricuspid valve integrity. Life-threatening arrhythmias such as ventricular tachycardia, torsade de pointes, and ventricular fibrillation are rare but possible complications. 

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