Nicholas L. DePace

Two dimensional echocardiographic detection of intraatrial masses

With two dimensional echocardiography, a left atrial mass was detected in 19 patients. Of these, 10 patients with rheumatic mitral stenosis had a left atrial thrombus. The distinctive two dimensional echocardiographic features of left atrial thrombus included a mass of irregular nonmobile laminated echos within an enlarged atrial cavity, usually with a broad base of attachment to the posterior left atrial wall. Seven patients had a left atrial myxoma. Usually, the myxoma appeared as a mottled ovoid, sharply demarcated mobile mass attached to the interatrial septum. One patient had a right atrial angiosarcoma that appeared as a nonmobile mass extending from the inferior vena caval-right atrial junction into the right atrial cavity. One patient had a left atrial leiomyosarcoma producing a highly mobile mass attached to the lateral wall of the left atrium. M mode echocardiography detected six of the seven myxomas, one thrombus and neither of the other tumors. Thus, two dimensional echocardiography appears to be the technique of choice in the detection, localization and differentiation of intraatrial masses.

Cardiac autonomic testing and treating heart disease. "A clinical perspective".

Background Coronary heart disease (CHD) is a major health concern, affecting nearly half the middle-age population and responsible for nearly one-third of all deaths. Clinicians have several major responsibilities beyond diagnosing CHD, such as risk stratification of patients for major adverse cardiac events (MACE) and treating risks, as well as the patient. This second of a two-part review series discusses treating risk factors, including autonomic dysfunction, and expected outcomes. Methods Therapies for treating cardiac mortality risks including cardiovascular autonomic neuropathy (CAN), are discussed. Results While risk factors effectively target high-risk patients, a large number of individuals who will develop complications from heart disease are not identified by current scoring systems. Many patients with heart conditions, who appear to be well-managed by traditional therapies, experience MACE. Parasympathetic and Sympathetic (P&S) function testing provides more information and has the potential to further aid doctors in individualizing and titrating therapy to minimize risk. Advanced autonomic dysfunction (AAD) and its more severe form cardiovascular autonomic neuropathy have been strongly associated with an elevated risk of cardiac mortality and are diagnosable through autonomic testing. This additional information includes patient-specific physiologic measures, such as sympathovagal balance (SB). Studies have shown that establishing and maintaining proper SB minimizes morbidity and mortality risk. Conclusions P&S testing promotes primary prevention, treating subclinical disease states, as well as secondary prevention, thereby improving patient outcomes through (1) maintaining wellness, (2) preventing symptoms and disorder and (3) treating subclinical manifestations (autonomic dysfunction), as well as (4) disease and symptoms (autonomic neuropathy).

The Progression of Autonomic Dysfunction in Chronic Disease

Normally, when we are born, we are born with as healthy an ANS as we will have: our resting response is in the middle of the gray area on the baseline response plot. When we are no longer breathing, there is no power in either ANS branch: our resting response is at the bottom left corner of the baseline response plot. The middle diagonal line connecting the two points, the perfect balance line, turns out to be the slowest path from birth to death. This means that the ANS will decline, even if we live a “perfectly healthy life.” As will be demonstrated, chronic disease accelerates this decline. Fortunately, as has been demonstrated in the previous chapter, establishing and maintaining proper balance for the individual can return the patient to a “normal” decline, slowing the progression of autonomic dysfunction as much as possible, minimizing morbidity and mortality risk. Note that the progression plots are not from numbers of patients followed from birth; they are composite plots from large populations of subjects covering the ages. Albeit balance has become the key to promoting and maintaining health and minimizing morbidity and mortality risk. These plots demonstrate the difference between normal aging balance and disease balance.

Clinical Autonomic Dysfunction

Clinical autonomic dysfunction : , Clinical autonomic dysfunction : , کتابخانه دیجیتال جندی شاپور اهواز

Improved Patient Outcomes by Normalizing Sympathovagal Balance: Differentiating Syncope—Precise Subtype Differentiation Leads to Improved Outcomes

Syncope is difficult to definitively diagnose, even with tilt-table testing and beat-to-beat blood pressure measurements, the gold-standard. Both are qualitative, subjective assessments. There are subtypes of syncope associated with autonomic conditions for which tilt-table testing is not useful. Heart rate variability analyses also include too much ambiguity. Three subtypes of syncope are differentiated: vasovagal syncope (VVS) due to parasympathetic excess (VVS-PE), VVS with abnormal heart rate response (VVS-HR), and VVS without PE (VVS-PN). P&S monitoring (ANSAR, Inc., Philadelphia, PA) differentiates subtypes in 2727 cardiology patients (50.5% female; average age:u200957 years; age range: 12–100 years), serially tested over four years (3.3 tests per patient, average). P&S monitoring noninvasively, independently, and simultaneously measures parasympathetic and sympathetic (P&S) activity, including the normal P-decrease followed by an S-increase with head-up postural change (standing). Syncope, as an S-excess (SE) with stand, is differentiated from orthostatic dysfunction (e.g., POTS) as S-withdrawal with stand. Upon standing, VVS-PE is further differentiated as SE with PE, VVS-HR as SE with abnormal HR, and VVS-PN as SE with normal P- and HR-responses. Improved understanding of the underlying pathophysiology by more accurate subtyping leads to more precise therapy and improved outcomes.

Autonomic Dysfunction Versus Neuropathy

Unfortunately the “autonomic neuropathy” has inherited the misperception that it is not treatable. While this may be true due to a lack of sufficient information, it is no longer the case. This then begs the question, when does autonomic dysfunction become autonomic neuropathy. While neuropathy may now be treatable, given more information, it still leaves the physician with few therapy options. Autonomic dysfunction has more therapy options but is asymptomatic. In this chapter, we will discuss a recent study to highlight the difference between autonomic neuropathy and dysfunction, and provide another approach to differentiating stages of autonomic decline. There is actually two schools of thought: five stages of decline or six. The six stages of decline include a brief second stage which is early in the progression. It is not often observed. However, it may provide the insight needed to understand the etiology of high BP or hypertension secondary to many chronic diseases.

Medical Specialties’ View of Autonomic System Measurements

This short chapter presents the seminal articles that provide the basis for the patients for whom Autonomic Assessment is recommended. The articles are from the medical leadership, including the American Academy of Family Practitioners, American Academy of Neurology, American Diabetes Association, and American Heart Association. The articles identify which diseases or disorders lead to autonomic neuropathy. We know that autonomic neuropathy is late in the progression and leaves few therapy options. We know that autonomic dysfunction is treatable, but is asymptomatic. Therefore, the leadership articles lead to the conclusion that the disease or disorder itself is the “symptom” indicating the need for autonomic assessment. This avoids the issue of screening. So, as long as the patient has been diagnosed with a chronic condition that is identified in the literature as leading to autonomic neuropathy, then they are recommended for periodic Autonomic Assessment.

Introduction to Parasympathetic and Sympathetic Monitoring

This introductory section starts with a review of the “Old School” information commonly taught in medical school, including the anatomy of the autonomic nervous system (ANS) and its two branches, the parasympathetic and sympathetic nervous systems; the biochemistry of the ANS; general physiology associated with the two ANS branches; and methods of measuring the ANS. Measuring the ANS includes older noninvasive measures and the newer method to be the basis of this book. This section concludes by answering the “So What?” question behind the development of a newer method of measuring the ANS, specifically, a general introduction to why it is important to specifically measure the parasympathetic and sympathetic nervous systems, independently (in a mathematical sense) and simultaneously. The newer method removes many of the assumptions and approximations required by the older methods, improving specificity, sensitivity, reliability, and repeatability and thereby improving patient outcomes.

General Autonomic Disorders

This chapter discusses “general” autonomic disorders. These are autonomic disorders that may be present regardless of the primary disease or disorder or age or stage. Included is the association between autonomic dysfunction and inflammation. Recent evidence indicates that the two are linked and that treating one helps to relieve the other. The etiology of inflammation may provide additional insight into the processes contributing to the progression of autonomic dysfunction.

Cardiovascular Autonomic Neuropathy: Risk Factor or Risk Indicator

This chapter discusses some more recent articles regarding risk factors and inflammation. There is a significant body of evidence that associates cardiovascular autonomic neuropathy (CAN) with most risk factors and with inflammation. It is known that CAN is associated with increased morbidity and mortality risk. The associations with traditional and nontraditional, as well as modifiable and nonmodifiable, risk factors, including inflammation, have historically made CAN a difficult diagnosis, especially since the perception has been that CAN is not treatable. This chapter concludes by explaining that this perception is not correct and discusses, generally, possible treatment modalities. Within the community of P&S monitoring, CAN has become an important diagnosis to document as early as possible to help avoid increased morbidity and mortality risk that leads to greater medication loads and hospitalization rates, causing greater healthcare costs.