It is important that the medical profession plays a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced and tested in the detection, management, or prevention of disease states. Rigorous and expert analysis of the available data documenting absolute and relative benefits and risks of those procedures and therapies can produce helpful guidelines that improve the effectiveness of care, optimize patient outcomes, and favorably affect the overall cost of care by focusing resources on the most effective strategies.

The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have jointly engaged in the production of such guidelines in the area of cardiovascular disease since 1980. The ACC/AHA Task Force on Practice Guidelines, whose charge is to develop, update, or revise practice guidelines for important cardiovascular diseases and procedures, directs this effort. The Task Force is pleased to have this guideline developed in conjunction with the European Society of Cardiology (ESC). Writing committees are charged with the task of performing an assessment of the evidence and acting as an independent group of authors to develop or update written recommendations for clinical practice.

Experts in the subject under consideration have been selected from all 3 organizations to examine subject-specific data and write guidelines. The process includes additional representatives from other medical practitioner and specialty groups when appropriate. Writing committees are specifically charged to perform a formal literature review, weigh the strength of evidence for or against a particular treatment or procedure, and include estimates of expected health outcomes where data exist. Patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies are considered as well as frequency of follow-up and cost effectiveness. When available, information from studies on cost will be considered; however, review …

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ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

https://www.urgences-serveur.fr/IMG/pdf/TDRV_ESC.pdf

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)

Sleep-related breathing disorders are highly prevalent in patients with established cardiovascular disease. Obstructive sleep apnea (OSA) affects an estimated 15 million adult Americans and is present in a large proportion of patients with hypertension and in those with other cardiovascular disorders, including coronary artery disease, stroke, and atrial fibrillation.1–14 In contrast, central sleep apnea (CSA) occurs mainly in patients with heart failure.15–19 The purpose of this Scientific Statement is to describe the types and prevalence of sleep apnea and its relevance to individuals who either are at risk for or already have established cardiovascular disease. Special emphasis is given to recognizing the patient with cardiovascular disease who has coexisting sleep apnea, to understanding the mechanisms by which sleep apnea may contribute to the progression of the cardiovascular condition, and to identifying strategies for treatment. This document is not intended as a systematic review but rather seeks to highlight concepts and evidence important to understanding the interactions between sleep apnea and cardiovascular disease, with particular attention to more recent advances in patient-oriented research. Implicit in this first American Heart Association/American College of Cardiology Scientific Statement on Sleep Apnea and Cardiovascular Disease is the recognition that, although holding great promise, this general area is in need of a substantially expanded knowledge base. Specific questions include whether sleep apnea is important in initiating the development of cardiac and vascular disease, whether sleep apnea in patients with established cardiovascular disease accelerates disease progression, and whether treatment of sleep apnea results in clinical improvement, fewer cardiovascular events, and reduced mortality.

Experimental approaches directed at addressing these issues are limited by several considerations. First, the close association between obesity and OSA often obscures differentiation between the effects of obesity, the effects of OSA, and the effects of synergies between these conditions. Second, multiple comorbidities, …

Sleep Apnea and Cardiovascular Disease An American Heart Association/American College of Cardiology Foundation Scientific Statement From the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing In Collaboration With the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health)

Idiopathic dilated cardiomyopathy (IDC) is a primary myocardial disease of unknown cause characterized by left ventricular or biventricular dilatation and impaired myocardial contractility1. Depend...

Idiopathic Dilated Cardiomyopathy

The members of the Task Force on Sudden Death dedicate this paper to the memory of our former friend and colleague, Professor Ronald W. F. Campbell. Ronnie spent his life working in the field of sudden cardiac death; he contributed much and helped many. But his own life fell victim to this very problem, sadly illustrating its unexpected nature. With Ronnie’s memory in mind the Task Force has worked diligently to describe the extent of our expanding knowledge in this field, hoping that our small contribution might help to appease his sad and sudden death.

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Task Force on Sudden Cardiac Death of the European Society of Cardiology

Mode of death in idiopathic dilated cardiomyopathy: a multivariate analysis of prognostic determinants.

The incidence and prognostic significance of electrically induced ventricular arrhythmias were prospectively assessed in 42 patients with idiopathic dilated cardiomyopathy. All patients underwent 24-hour, long-term electrocardiographic (Holter) monitoring and 30 were analyzed by a signal-averaging vectorcardiographic procedure at entry into the study. Their response to programmed electrical stimulation during basic right ventricular pacing was investigated using 1 and 2 ventricular extrastimuli. A monomorphic tachycardia was not induced in any patient. In 36 patients (86%) polymorphic ventricular arrhythmias were initiated. Three or more induced consecutive ventricular premature complexes occurred in 9 patients (21%), nonsustained polymorphic ventricular tachycardia in 2 (4.8%) and ventricular fibrillation in 1 patient (2.4%). There was no association between electrically induced polymorphic ventricular arrhythmias and the degree of impairment of left ventricular function. Furthermore, the incidence of induced ventricular arrhythmias was not related to the Lown grade or to the total number of ventricular premature complexes during Holter monitoring. A late potential was detected by the averaged vectorcardiogram in only 1 of the 30 patients. During follow-up (mean 16 ± 7 months) 7 patients died, 5 from chronic congestive heart failure and 2 from sudden cardiac death. No patient had an electrically induced arrhythmia of 3 or more ventricular premature complexes. Thus, in most patients with idiopathic dilated cardiomyopathy, programmed electrical stimulation of the right ventricle with up to 2 extrastimuli fails to reproduce an electrophysiologic correlate to the frequent ventricular arrhythmias.

Determinants of prognosis in idiopathic dilated cardiomyopathy as determined by programmed electrical stimulation

Echocardiographic evaluation of patients with clinically suspected arterial emboli

Two-dimensional transesophageal echocardiography was used to measure aortic valve orifice area in 24 patients with aortic valve stenosis (AS) and 15 patients without aortic valve disease. Using transesophageal echocardiography, orifice area could be measured in 20 of 24 patients with AS. With transthoracic echocardiography, orifice area could be determined in only 2 of 24 patients. In patients with AS, orifice area determined by transesophageal echocardiography was 0.75 +/- 0.34 cm2 and that calculated with Gorlin's formula was 0.75 +/- 0.32 cm2. In normal aortic valves, orifice area was 3.9 +/- 1.2 cm2 by transesophageal echocardiography. A good correlation was demonstrated between aortic valve orifice area determined using transesophageal echocardiography and calculated orifice area using Gorlin's formula in patients with AS: r = 0.92, standard error of estimate = 0.14 cm2. The absolute difference between orifice area measured with both methods ranged from 0.0 to 0.4 cm2 (mean 0.09 +/- 0.1). In 4 patients orifice area could not be determined with transesophageal echocardiography. The orifice could not be identified in 2 patients because an appropriate cross-sectional view of the aortic valve could not be achieved and in 2 patients with pinhole stenosis (aortic valve orifice area 0.3 cm2). These data show that aortic valve orifice area can be measured reliably using 2-dimensional transesophageal echocardiography.

Determination of aortic valve orifice area in aortic valve stenosis by two-dimensional transesophageal echocardiography

In the Federal Republic of Germany, approximately 10,000 to 20,000 persons die of pulmonary embolism (PE) each year. The mortality of treated PE is about 8% as compared with 18 to 35% in nondiagnosed PE. Massive PE is detected in only about 15 to 30% of the patients while, on the other hand, in 30 to 80% of those in whom PE is suspected the pulmonary angiogram may be normal. On use of pulmonary ventilation-perfusion scintigraphy, in 30 to 40% of the cases, both false negative as well as false positive findings have been described. ROLE OF ECHOCARDIOGRAPHY IN PATIENTS WITH ACUTE PULMONARY EMBOLISM. With echocardiographic imaging, the right heart as well as the central vessels in the proximity of the heart, in particular the pulmonary arteries, can be visualized. In addition to direct detection of right-sided-intraluminal thrombi, echocardiographic diagnosis is based predominantly on indirect signs, such as evidence of an acute cor pulmonale with dilatation of the right atrium and ventricle, the central pulmonary vessels and the inferior vena cava which, however, are relatively unspecific and may also be found in the presence of other diseases. Echocardiographic changes in acute pulmonary embolism can only be expected in the presence of increased pressure in the pulmonary circulation, that is, when at least a 30%-reduction in the cross-sectional area of the pulmonary vascular bed can be found. This can be documented in 60 to 70% of patients with acute PE. According to the literature and our own studies, of a total of 284 patients 84% had dilatation of the right ventricle, 70% paradoxic or hypokinetic motion of the interventricular septum in 102/141 patients there was dilatation of the right pulmonary artery. These changes regressed rapidly after therapeutic intervention. In about 30% of the patients a reduction in the left ventricular dimensions can be seen. Paradoxic septum motion and a decrease in the closing amplitude (EF-slope) of the anterior mitral leaflet can be seen. The extent of dilatation of the right ventricle and the right pulmonary artery correlate with the extent of the angiographic severity of acute PE provided that there is no marked preexisting left ventricular function impairment. NONINVASIVE ESTIMATION OF THE PRESSURE INCREASE IN THE PULMONARY CIRCULATION. On use of Doppler echocardiography, most patients with acute cor pulmonale have tricuspid regurgitation. This enables through determination of the systolic RV-RA pressure gradient an estimation of the systolic right ventricular pressure and, accordingly, the pulmonary artery pressure. In our experience, a systolic acceleration time in the pulmonary artery of less than 90 to 95 ms is

Hofmann T

Papers

Mode of death in idiopathic dilated cardiomyopathy: a multivariate analysis of prognostic determinants.

Determinants of prognosis in idiopathic dilated cardiomyopathy as determined by programmed electrical stimulation

Echocardiographic evaluation of patients with clinically suspected arterial emboli

Determination of aortic valve orifice area in aortic valve stenosis by two-dimensional transesophageal echocardiography

Echocardiography in the diagnosis of lung embolism