Advances in Electrocardiograms

Electrocardiograms have become one of the most important, and widely used medical tools for diagnosing diseases such as cardiac arrhythmias, conduction disorders, electrolyte imbalances, hypertension, coronary artery disease and myocardial infarction. This book reviews recent advancements in electrocardiography. The four sections of this volume, Cardiac Arrhythmias, Myocardial Infarction, Autonomic Dysregulation and Cardiotoxicology, provide comprehensive reviews of advancements in the clinical applications of electrocardiograms. This book is replete with diagrams, recordings, flow diagrams and algorithms which demonstrate the possible future direction for applying electrocardiography to evaluating the development and progression of cardiac diseases. The chapters in this book describe a number of unique features of electrocardiograms in adult and pediatric patient populations with predilections for cardiac arrhythmias and other electrical abnormalities associated with hypertension, coronary artery disease, myocardial infarction, sleep apnea syndromes, pericarditides, cardiomyopathies and cardiotoxicities, as well as innovative interpretations of electrocardiograms during exercise testing and electrical pacing

Aerospace medicine and biology: A continuing bibliography with indexes, supplement 130, July 1974

This special bibliography lists 291 reports, articles, and other documents introduced into the NASA scientific and technical information system in June 1974

Potential Predictors of Sudden Cardiac Death in Aortic Valve Disease

Although sudden death continues to claim 15 to 20% of patients with aortic valve disease, the exact cause still remains speculative. It has been the assumption of many workers that these deaths result from ventricular tachyarrhythmias. The major aim of this thesis was therefore to assess the prevalence of ventricular arrhythmias in patients with aortic valve disease and to evaluate their significance by signal-averaged electrocardiography (SAECG). A total of 100 patients, 55 with predominant aortic stenosis (AS) with a mean transaortic gradient of 81+/-27 mmHg, 16 with predominant aortic regurgitation (AR) and 29 with combined AS and AR were studied prior to aortic valve replacement (AVR). Substantial left ventricular hypertrophy was present with a mean echocardiographic left ventricular mass index of 210+/-72 g/m2. Left ventricular systolic and diastolic function were normal in 94% and 61% of patients respectively. Coronary angiography was performed in 89 patients of whom 50 (56%) had chest pain typical of angina pectoris and 21 (24%) had significant coronary artery disease. Angina was present in 20 of these 21 patients (95%). Thus angina could predict the presence of significant coronary artery disease with 95% sensitivity and 54% specificity. In agreement with previous work, this study has shown a high prevalence of complex ventricular arrhythmias. Nonsustained ventricular tachycardia (NSVT) was detected by ambulatory electrocardiographic monitoring in 9 (9%) patients of whom only one had late potentials on SAECG. The frequency of ventricular arrhythmias was not related to the degree of left ventricular hypertrophy or the severity of aortic valve disease. Left ventricular function did not have any effect on ventricular arrhythmias. A high prevalence of complex ventricular arrhythmias was also seen in the early (5 to 7 days post AVR) and late (121+/-24 days post AVR) post-operative periods. The frequency of ventricular arrhythmias was not affected by AVR. In the late post-operative period, 4 patients had NSVT, but none of them had late potentials on SAECG. As with the pre-operative results, there was little to suggest the presence of an arrhythmogenic substrate in these patients in view of the absence of late potentials on SAECG. Furthermore, no sustained ventricular arrhythmias were detected in the 3 study periods. Aortic valve replacement was accompanied by a significant regression in echocardiographic left ventricular hypertrophy in patients with predominant AS and those with combined AS and AR. Of the total 100 patients in this study, 75 were on the cardiac surgical waiting list of whom 60 have already undergone operation. There have been 7 deaths (7%) during the study period, 3 of them occurring suddenly in patients awaiting surgery. Thus, the incidence of sudden death while awaiting operation was 4%. It has been suggested that patients with decreased heart-rate variability have decreased vagal tone, increased sympathetic activity or both and hence are at a higher risk of developing ventricular fibrillation and sudden death. Cardiovascular autonomic function was assessed in 47 patients prior to AVR and repeated in 10 patients 3 months following AVR. Abnormal heart-rate variation during deep breathing was detected in 18 (38%) patients. AVR was not accompanied by any improvement in cardiovascular autonomic function at least in the shortterm . Thus, despite a high prevalence of ventricular arrhythmias in aortic valve disease patients with substantial left ventricular hypertrophy, there was little to suggest the presence of an arrhythmogenic substrate. The potential mechanism of sudden death in these patients could be speculated on the basis of impaired cardiovascular autonomic function

Evaluation of pulse wave analysis to assess coronary artery disease

Conventional risk factors for cardiovascular disease, such as age, gender, hyperlipidaemia and hypertension are useful clinical markers of coronary artery disease (CAD) in asymptomatic patients or those without a prior history of atherosclerosis. In patients referred for a cardiology opinion, modification of risk factors by lifestyle changes and cardiac medications as well as confounding co-morbidities limit the value of these markers. Patients are often referred for diagnostic coronary angiography to determine the presence and severity of CAD, stratify the risk of future events and determine appropriate management. Despite the use of a variety of tests to best identify those requiring angiography, up to half of all patients referred do not have significant disease. Pulse wave analysis (PWA) is a novel method to derive indices of central (aortic) blood pressure and arterial stiffness. Pressure waveforms are obtained non-invasively from the radial artery using a simple tonometry method and have been shown to correlate with clinical outcomes and cardiovascular events in selected populations. This thesis will explore, for the first time, the clinical potential for PWA as a non-invasive marker of CAD in an unselected contemporary cohort of patients referred for elective coronary angiography. The main hypotheses tested are first that PWA is a suitable tool for clinical use, including those with cardiac and non-cardiac co-morbidities and second that abnormalities of PWA are independent predictors of the presence and severity of CAD. Data have been derived from a prospective, protocol-driven, multi-centre cohort of 550 patients recruited from 2006-8. Results suggest that PWA has a useful clinical role in stratifying the risk of coronary disease. PWA variables were independent of conventional blood pressure measurement and superior to baseline risk factors, biomarkers and other non-invasive tests

Aerospace Medicine and Biology: A continuing bibliography with indexes, supplement 159

This bibliography lists 257 reports, articles, and other documents introduced into the NASA scientific and technical information system in September 1976

Clinical studies of the renin-angiotensin-aldosterone system and cardiac autonomic regulation in man

The work embodied in this thesis was designed to explore the interaction between the renin -angiotensin -aldosterone system (RAAS) and the autonomic nervous system. It was stimulated by the observations that the neurohormonal suppression of the RAAS by ACE inhibitors in chronic heart failure (CHF) is inadequate, and that high residual levels of circulating aldosterone have been shown to have detrimental autonomic modulating effects independent of angiotensin II in experimental models.The effects of aldosterone blockade with spironolactone therapy were examined in CHF patients already established on ACE inhibitors. It was observed that spironolactone has beneficial parasympathomimetic properties, improving heart rate variability and reducing heart rate, particularly during the early morning hours of the day when ACTH -induced aldosterone secretion is maximal. The interaction between the RAAS and the parasympathetic tone was explored further in a series of normal volunteer studies. Although the effects of ACE inhibitors are well recognised, not much is known about the parasympathomimetic properties of direct angiotensin II or aldosterone receptor antagonism. In this thesis, it was demonstrated that losartan, an angiotensin II receptor antagonist, and enalapril, an ACE inhibitor, were equally effective in improving the vagally-mediated baroreflex response in salt depleted normotensive subjects. It was also demonstrated that direct intravenous aldosterone administration impaired the baroreflex response to vasopressor agents in healthy subjects.The observed vagomimetic effects of aldosterone blockade may have important therapeutic implications, suggesting the possibility that spironolactone may have anti -ischaemic or anti -arrhythmic properties. However, aldosterone blockade did not appear to have any significant impact on either autonomic tone or ischaemic events when administered to patients with ischaemic heart disease but preserved LV function. The reasons for the latter remain unclear but may reflect differences in disease -state (less neurohormonal activation, and a larger proportion of these patients was established on beta -blockers -which may influence autonomic tone - and only a minority was taking concomitant ACE inhibitors, compared to the CHF cohort). In CHF however, spironolactone was shown to improve QT dispersion, a surrogate marker of arrhythmic activity and sudden cardiac death. Mechanisms in which aldosterone may contribute towards dispersion of the QT intervals on the electrocardiogram are probably multifactorial. Aldosterone increases cardiac afterload (by increasing vascular tone and potentiating vascular smooth muscle hypertrophy) and it is demonstrated that cardiac afterload would increase QT dispersion through mechano- electrical feedback. Vagal tone modulation itself however did not contribute towards QT dispersion.These studies demonstrate how inextricably linked the RAAS and the autonomic nervous system is. In particular, the detrimental autonomic effects of aldosterone in CHF have been highlighted. The findings of these studies highlight possible mechanisms and provide valuable insights as to why further therapeutic mileage is gained by the addition of an aldosterone antagonist in CHF patients who have already been established on ACE inhibitors