pediagenosis: Cardiovascular
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Showing posts with label Cardiovascular. Show all posts
Showing posts with label Cardiovascular. Show all posts

Sunday, October 18, 2020

STRESS TESTING AND NUCLEAR IMAGING

STRESS TESTING AND NUCLEAR IMAGING

STRESS TESTING AND NUCLEAR IMAGING

Stress ECG and stress imaging studies are widely used noninvasive procedures that provide important information on cardiac function and the presence of hemodynamically significant coronary artery disease (CAD). The correct use of stress testing is critically important for the cost-effective management of patients with known or suspected CAD. When the most appropriate procedure is performed, it provides important diagnostic and prognostic information that determines the optimal management strategy to be undertaken for that individual. Stress testing is also used in patients with known CAD to determine exercise “prescriptions” before cardiac rehabilitation (Fig. 10.1).

ECHOCARDIOGRAPHY

ECHOCARDIOGRAPHY

ECHOCARDIOGRAPHY

Echocardiography is a highly reproducible, safe, and widely available noninvasive imaging technique integral to the practice of modern clinical cardiology. With the use of high-frequency ultrasound to image cardiac and great vessel structure and blood flow, this method provides definitive anatomic and hemodynamic information crucial to the diagnosis and management of patients with a wide range of cardiac and vascular conditions. Although often considered a mature imaging technique, the technology and its applications continue to improve.

CHEST RADIOGRAPHY

CHEST RADIOGRAPHY

CHEST RADIOGRAPHY

TECHNICAL ASPECTS

Chest radiography was one of the first clinical studies to use x-rays, which were discovered in 1895 by Wilhelm Conrad Roentgen. X-rays are typically generated by passing a current across a diode, which results in the generation of electrons. The electron beam is aimed at a metal anode, and the resultant interaction produces x-ray photons. The x-ray beam diverges as it exits from the x-ray tube and pro- duces a conical-shaped beam. When x-rays are captured by film or a digital system, the divergence of the beam can lead to geometric distortion, which is a function of the distance from the x-ray source to the object and from the object to the detector. The further an object is from the radiation source, the less geometric distortion and clearer image that will be produced, but higher levels of energy and longer exposure times are required for adequate image production. More energy and longer exposure lead to an increase in radiation expo- sure for the patient. To balance the competing factors of geometric distortion and radiation exposure, 6 feet is considered the standard source-to-image distance for a typical posteroanterior (PA) and lateral chest x-ray. The radiation exposure of a standard PA and lateral chest x-ray at this distance is approximately 3 millirems or approximately 1/100 of the typical annual rate of celestial radiation for an individual. Because ionizing radiation causes a dose-dependent increase in the risk of genetic alteration and malignancy, as low as reasonably allow-able principles of radiation safety are followed to minimize patient exposure.

ELECTROCARDIOGRAPHY

ELECTROCARDIOGRAPHY

ELECTROCARDIOGRAPHY

LEADS

Twelve leads are routinely used to record the body surface ECG: three bipolar limb leads labeled I, II, and III; three augmented limb leads labeled aVR, aVL, and aVF; and six chest leads labeled V1 through V6 (Fig. 7.1). In the bipolar limb leads, the negative pole for each of the leads is different. The chest leads are often referred to as “unipolar leads” because the negative pole is constant. It is created by the left arm, right arm, and left leg electrodes connected together to form a single lead that is referred to as the Wilson central terminal. The positive chest lead is an exploring lead that can be placed anywhere. In children, the routine ECG often includes leads placed on the right side of the chest in positions referred to as V3R and V4R. Similar right-sided chest leads are often used in adults to diagnose right ventricular infarction, and one or more leads placed on the back are sometimes used to diagnose posterior wall infarction.

STEM CELL THERAPIES FOR CARDIOVASCULAR DISEASE

STEM CELL THERAPIES FOR CARDIOVASCULAR DISEASE

STEM CELL THERAPIES FOR CARDIOVASCULAR DISEASE

Myocardial infarction and congestive heart failure are the leading causes of morbidity and mortality worldwide, despite great therapeutic achievements in the treatment of cardiovascular diseases. The inability of the heart to regenerate lost cardiac muscle, coupled with a robust fibrotic repair response, contribute to adverse ventricular remodeling and decline in postinjury cardiac function. Consequently, much of the research of the last three decades has focused on reducing the atherosclerotic burden of ischemic heart disease, reperfusion, and addressing the fibrotic changes associated with heart failure. After an ischemic insult and the formation of necrotic myocardium, the process of scar formation from the recruitment of activated cardiac fibroblasts leads to reduced cardiac pump function. However, in recent years, it has been convincingly shown that the heart has the ability to regenerate cardiomyocytes, albeit at a low rate (~0.3%–1% annually). These findings and our better understanding of stem cell biology are paving the way to a new area of research, with the main goal of regenerating cardiac tissue.

Tuesday, October 13, 2020

Autonomic Control Of The Cardiovascular System

Autonomic Control Of The Cardiovascular System


Autonomic Control Of The Cardiovascular System
The autonomic nervous system (ANS) comprises a system of efferent nerves that regulate the involuntary functioning of most organs, including the heart and vasculature. The cardiovascular effects of the ANS are deployed for two purposes.
Shock and Haemorrhage

Shock and Haemorrhage


Shock and Haemorrhage
Cardiovascular or circulatory shock refers to an acute condition where there is a generalized inadequacy of blood flow throughout the body. The patient appears pale, grey or cyanotic, with cold clammy skin, a weak rapid pulse and rapid shallow breathing. Urine output is reduced and blood pressure (BP) is generally low. Conscious patients may develop intense thirst. Cardiovascular shock may be caused by a reduced blood volume (hypovolaemic shock), profound vasodilatation (low-resistance shock), acute failure of the heart to maintain output (cardiogenic shock) or blockage of the cardiopulmonary circuit (e.g. pulmonary embolism).
Pulmonary Hypertension

Pulmonary Hypertension


Pulmonary Hypertension
The mean pressure in the pulmonary artery (mPAP) in a normal resting adult is 16 mmHg. Pulmonary hypertension (PH) is defined as a mPAP exceeding 25 mmHg at rest. The increased PAP can be due to a rise in pulmonary vascular resistance (PVR), increased pulmonary blood flow due to a systemic to pulmonary shunt (Eisenmenger’s syndrome; see Chapter 55) or back pressure from the left heart. PH increases right ventricular afterload, eventually leading to right heart failure.

Friday, October 2, 2020

CARDIOVASCULAR EPIDEMIOLOGY AND RISK PREDICTION MODELS

CARDIOVASCULAR EPIDEMIOLOGY AND RISK PREDICTION MODELS

CARDIOVASCULAR EPIDEMIOLOGY AND RISK PREDICTION MODELS

Cardiovascular epidemiology studies the determinants and distribution of cardiovascular disease (CVD). The overarching goal of CVD epidemiology is to reduce the incidence and prevalence of CVD within the population. Cardiovascular epidemiology has provided vital bidirectional connections between basic mechanistic science and clinical research. Through these types of investigations, our understanding of the extent of CVD and its natural history, mechanisms, and underlying pathophysiology is expanding greatly, which provides opportunities for individual-level therapeutic strategies, as well as population-level approaches to reduce the incidence and burden of CVD.

EFFECTS OF EXERCISE ON CARDIOVASCULAR HEALTH

EFFECTS OF EXERCISE ON CARDIOVASCULAR HEALTH

EFFECTS OF EXERCISE ON CARDIOVASCULAR HEALTH

Exercise as an intervention for treatment and management of coronary heart disease and many of its associated comorbidities (e.g., diabetes, obesity, hypertension, dyslipidemia) remains one of the most effective, yet poorly used treatments. This chapter outlines the current evidence supporting an active lifestyle, active exercise training, and their impact on various measures of cardiovascular health. It reviews the available data for patients with heart failure, which constitutes one of the largest groups of patients cared for with chronic heart disease, resulting in heavy health care resource utilization. The chapter reviews the evolving wearable and mHealth technologies that may affect our ability to recommend and monitor exercise in the future and may suggest further directions for research.

GENETICS IN PHARMACOLOGY

GENETICS IN PHARMACOLOGY

GENETICS IN PHARMACOLOGY

The genetic role in cardiovascular diseases has been essential, especially in the field of pharmacology. The identification of genetic and epigenetic associations with diseases has led to the development of medications in the prevention and treatment of cardiovascular diseases. An important and novel example is the development of a class of medications called proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. 

GENETICS IN CARDIOVASCULAR DISEASE

GENETICS IN CARDIOVASCULAR DISEASE

GENETICS IN CARDIOVASCULAR DISEASE

This chapter introduces the clinically important principles of genetics and the application of these principles to clinical medicine. It places an emphasis on the genetics of cardiovascular diseases, the role in pharmacology, and future direction. Genetics mutation epigenetics hypertrophic cardiomyopathy long QT syndrome PCSK9 inhibitor.

THE PHYSICAL EXAMINATION

THE PHYSICAL EXAMINATION

THE PHYSICAL EXAMINATION

There are several advantages to obtaining the history of the patient before the physical examination. First, the information gained in the history directs the clinician to pay special attention to aspects of the physical examination. For instance, a history consistent with CHD necessitates careful inspection for signs of vascular disease; a history suggestive of CHF should make the clinician pay particular attention to the presence of a third heart sound. Second, the history allows the clinician to establish a rapport with patients and to assure patients that the clinician is interested in their well-being; clinicians are then allowed to perform a complete physical examination, which is imperative in a complete evaluation. In this light, the therapeutic value of the physical examination to the patient should not be underestimated. Despite the emphasis on technology today, even the most sophisticated patients expect to be examined, to have their hearts listened to, and to be told whether worrisome findings exist or whether the examination results were normal.

Sunday, September 13, 2020

The History and Physical Examination

The History and Physical Examination


The History and Physical Examination
The history and physical examination should allow the clinician to establish the previous probability of heart disease, that is, the likelihood that the symptoms reported by the patient result from heart disease. A reasonable goal is to establish the risk of heart disease in a patient as “low,” “intermediate,” or “high.” One demonstration of this principle in clinical medicine is the assessment of patients with chest pain, in which exercise stress testing to accurately diagnose coronary heart disease (CHD) depends on the previous probability of disease. In patients with a low risk of CHD based on clinical findings, exercise stress testing results in a large number of false-positive test results. Because up to 15% of exercise stress tests produce positive results in individuals without CHD, use of this test in a low-risk population can result in an adverse ratio of false-positive to true-positive test results and unnecessary cardiac catheterizations. Conversely, in patients with a high risk of CHD based on clinical findings, exercise stress testing can result in false-negative test results, which is an equally undesirable outcome, because patients with significant coronary artery disease (CAD) and their physicians may be falsely reassured that no further evaluation or treatment is necessary.
Emphasis is increasing on quantifying previous probability to an even greater degree with various mathematical models. This is a useful approach in teaching and may be clinically feasible in some diseases. However, for most patients with suspected heart disease, categorizing risk as low, intermediate, and high is appropriate, reproducible, and feasible in a busy clinical practice. Therefore obtaining the history and physical examination represents a key step before any testing, to minimize use of inappropriate diagnostic procedures.
A wealth of information is available to clinicians who carefully assess the history of the patient. Key components are assessment of the chief complaint; careful questioning for related, often subtle symptoms that may further define the chief complaint; and determination of other factors that help categorize the likelihood of disease. Major symptoms of heart patients include chest discomfort, dyspnea, palpitations, and syncope or presyncope.
Pain of myocardial ischemia.
FIG 2.1 Pain of myocardial ischemia.

Chest Discomfort
Determining whether chest discomfort results from a cardiac cause is often a challenge. The most common cause of chest discomfort is myocardial ischemia, which produces angina pectoris. Many causes of angina exist, and the differential diagnosis for chest discomfort is extensive (Box 2.1). Angina that is reproducible and constant in frequency and severity is often referred to as stable angina. For the purposes of this chapter, stable angina is a condition that occurs when CAD is present, and coronary blood flow cannot be increased to accommodate for increased myocardial demand. However, as discussed in Chapters 12 through 14, there are many causes of myocardial ischemia, including fixed coronary artery stenoses and endothelial dysfunction, which lead to reduced vasodilatory capacity.

A description of chest discomfort can help establish whether the pain is angina or of another origin. First, characterization of the quality and location of the discomfort is essential (Fig. 2.1). Chest discomfort because of myocardial ischemia may be described as pain, a tightness, a heaviness, or simply an uncomfortable and difficult-to-describe feeling. The discomfort can be localized to the midchest or epigastric area, or may be characterized as pain in related areas, including the left arm, both arms, the jaw, or the back. The radiation of chest discomfort to any of these areas increases the likelihood of the discomfort being angina. Second, the duration of discomfort is important because chest discomfort due to cardiac causes generally lasts minutes. Therefore pain of short duration (“seconds” or “moments”), regardless of how typical it may be of angina, is less likely to be of cardiac origin. Likewise, pain that lasts for hours, on many occasions, in the absence of objective evidence of myocardial infarction (MI), is not likely to be of coronary origin. Third, the presence of accompanying symptoms should be considered. Chest discomfort may be accompanied by other symptoms (including dyspnea, diaphoresis, or nausea), any of which increase the likelihood that the pain is cardiac in origin. However, the presence of accompanying symptoms is not needed to define the discomfort as angina. Fourth, factors that precipitate or relieve the discomfort should be evaluated. Angina typically occurs during physical exertion, during emotional stress, or in other circumstances of increased myocardial oxygen demand. When exercise precipitates chest discomfort, relief after cessation of exercise substantiates the diagnosis of angina. Sublingual nitroglycerin also relieves angina, generally over a period of minutes. Instant relief or relief after longer periods lessens the likelihood that the chest discomfort was angina.
Although the presence of symptoms during exertion is important in assessing CHD risk, individuals, especially sedentary ones, may have angina-like symptoms that are not related to exertion. These include postprandial and nocturnal angina, or angina that occurs while the individual is at rest. As described herein, “rest-induced angina,” or the new onset of angina, connotes a pathophysiology different from effortinduced angina. Angina can also occur in persons with fixed CAD and increased myocardial oxygen demand due to anemia, hyperthyroidism,bor similar conditions (Box 2.2). Angina occurring at rest, or with minimal exertion, may denote a different pathophysiology, one that involves platelet aggregation, which is clinically termed “unstable angina” or “acute coronary syndrome” (see Chapters 20 and 21).
Patients with heart disease need not present with chest pain at all. Anginal equivalents include dyspnea during exertion, abdominal dis- comfort, fatigue, or decreased exercise tolerance. Clinicians must be alert to and specifically ask about these symptoms. Often, a patient’s family member or spouse notices subtle changes in the endurance of the patient or that the individual no longer performs functions that require substantial physical effort. Sometimes, patients may be unable to exert themselves due to comorbidities. For instance, the symptoms of myocardial ischemia may be absent in patients with severe peripheral vascular disease who have limiting claudication. One should also be attuned to subtle or absent symptoms in individuals with diabetes mellitus (including type 1 and type 2 diabetes), which is a coronary risk equivalent as defined by the Framingham Risk Calculator.
When the likelihood that CHD accounts for a patient presenting with chest discomfort or any of the aforementioned variants is considered, assessment of the cardiac risk factor profile is important. The Framingham Study first codified the concept of cardiac risk factors, and over time, quantification of risk using these factors has become an increasingly useful tool in clinical medicine. Cardiac risk factors deter- mined by the Framingham Study include a history of cigarette smoking, diabetes mellitus, hypertension, or hypercholesterolemia; a family history of CHD (including MI, sudden cardiac death, and first-degree relatives having undergone coronary revascularization); age; and sex (male). Although an attempt has been made to rank these risk factors, all are important, with a history of diabetes mellitus being perhaps the single most important factor. Subsequently, a much longer list of potential predictors of cardiac risk has been made (Box 2.3). Multiple risk calculators have since been created, such as the atherosclerotic cardiovascular disease algorithm used by the American College of Cardiology, the American Heart Association cholesterol guidelines, and the Multi-Ethnic Study of Atherosclerosis (MESA), which uses classic risk factors with the addition of a coronary artery calcium score to predict a 10-year risk of CHD.

Symptoms suggestive of vascular disease require special attention. Peripheral vascular disease may mask CHD because the individual may not be able to exercise sufficiently to provoke angina. A history of stroke, transient ischemic attack, or atheroembolism in any vascular distribution is usually evidence of significant vascular disease. Sexual dysfunction in men is not an uncommon presentation of peripheral vascular disease. The presence of Raynaud-type symptoms should also be elicited because such symptoms suggest abnormal vascular tone and function, and increase the risk that CHD is present.
Determining whether the patient has stable or unstable angina is as important as making the diagnosis of angina. Stable angina is important to evaluate and treat but does not necessitate emergent intervention. However, unstable angina or acute coronary syndrome carries a significant risk of MI or death in the immediate future. The types of symptoms reported by patients with stable and unstable angina differ little, and the risk factors for both are identical. The severity of symptoms is not necessarily greater in patients with unstable angina, just as a lack of chest discomfort does not rule out significant CHD. The important distinction between stable and unstable coronary syndromes is whether the onset is new or recent, and/or progressive (e.g., occurring more frequently or with less exertion). The initial presentation of angina is, by definition, unstable angina, although for a high percentage of individuals this may merely represent the first recognizable episode of angina. For those with unstable angina, the risk of MI in the near future is markedly increased. Likewise, when the patient experiences angina in response to decreased levels of exertion or when exertional angina has begun to occur at rest, these urgent circumstances require immediate therapy. The treatment of stable angina and acute coronary syndrome is discussed in Chapters 19 to 21.
The Canadian Cardiovascular Society Functional Classification of Angina Pectoris is a useful guide for everyday patient assessment (Box 2.4). Categorizing patients according to their class of symptoms is rapid and precise and can be used in follow-up. Class IV describes the typical patient with acute coronary syndrome.
Physical examination. CHF, Congestive heart failure.
FIG 2.2 Physical examination. CHF, Congestive heart failure.

Finally, it is important to distinguish those patients who have noncoronary causes of chest discomfort from those with CHD. Patients with gastroesophageal reflux disease (GERD) often present with symptoms that are impossible to distinguish from angina. In numerous studies, GERD was the most common diagnosis in patients who underwent diagnostic testing for angina and were found not to have CHD. The characteristics of the pain can be identical. Because exercise can increase intraabdominal pressure, GERD may be exacerbated with exercise, especially after meals. Symptoms from GERD can also be relieved with use of sublingual nitroglycerin. GERD can also result in early morning awakening (as can unstable angina) but tends to awaken individuals 2 to 4 hours after going to sleep, rather than 1 to 2 hours before arising, as is the case with unstable angina. Other causes (see Box 2.1) of angina like pain can be benign or suggestive of other high-risk syndromes, such as aortic dissection or pulmonary embolus. Many of these “coronary mimics” can be ruled out by patient history, but others, such as valvular aortic stenosis, can be confirmed or excluded by physical examination.
The goal of taking the history is to alert the clinician to entities that can be confirmed or excluded by physical examination or that necessitate further diagnostic testing.

Dyspnea, Edema, and Ascites
Dyspnea can accompany angina pectoris or it can be an angina! equivalent. Dyspnea can also reflect congestive heart failure (CHF) or occur because of noncardiac causes. The key to understanding the etiology of dyspnea is a clear patient history, which is then confirmed by a targeted physical examination.
Dyspnea during exertion that quickly resolves at rest or with use of nitroglycerin may be a result of myocardial ischemia. It is impottant to establish the amount of activity necessary to provoke dyspnea, the reproducibility of these symptoms, and the duration of recovery. As with angina, dyspnea, as an angina! equivalent or a aecompanying symptom, tends to occur at a given workload or stress e el; dyspnea that occurs one day at low levels of exertion but not pro pted by vigorous exertion on another day is less likel}I to be an angina! equivalent.
In patients with CHF, dyspnea generally reflects i creased left ventricular (LV) filling pressures (Fig. 2.2 ). Although V systolic dysfunction is the most common cause of the dyspnea, dyspnea also occurs in individuals with preserved LV systolic function and severe diastolic dysfunction. However, these two entities present differently, and physical examination can distinguish them. With LV systolic dysfunction, dyspnea tends to gradually worsen, and its exacerbation is more variable than that of exertional dyspnea resulting from myocardial ischemia, although both are due to fluctuations in pulmonary arterial volume and left atrial filling pressures. Typically, patients with LV systolic dysfunction do not recover immediately after exercise cessation or use of sublingual nitroglycerin, and the dyspnea may linger for longer periods. Orthopnea, the occurrence of dyspnea when recumbent, or paroxysmal nocturnal edema provides further support for a presumptive diagnosis of LV systolic dysfunction. Patients with LV diastolic dysfunction tend to present abruptly with severe dyspnea that resolves more rapidly in response to diuretic therapy than does dyspnea caused by LV systolic dysfunction. The New York Heart Association (NYHA) functional classification for CHF ( Table2.1 ) is extremely useful in following patients with CHF and provides a simple and rapid means for longitudinal assessment. The NYHA functional classification also correlates well with prognosis. Patients who are in NYHA functional class I have a low risk of death or hospital admission within the following year. In contrast, the annual mortality rate of those with NYHA functional class IV symptoms exceeds 30%.
As with chest discomfort, the differential diagnosis of dyspnea is broad, encompassing many cardiac and noncardiac causes (Box 2.5). Congenital heart disease, with or without pulmonary hypertension, can cause exertional dyspnea. Patients with significant intracardiac or extracardiac shunts and irreversible pulmonary hypertension (Eisen­menger syndrome) are dyspneic during minimal exertion and often at rest. It is also possible to have dyspnea because of acquired valvular heart disease, usually from aortic or mitral valve stenosis or regurgitation. All of these causes should be easily distinguished from CHD or CHF by physical examination. Primary pulmonary causes of dyspnea must be considered, with chronic obstructive pulmonary disease and reactive airways disease (asthma) being the most common causes. Again, a careful history for risk factors (e.g., cigarette smoking, industrial exposure, allergens) associated with these entities and an accurate physical examination should distinguish primary pulmonary causes from dyspnea due to CHD or CHF.
Peripheral edema and ascites are physical examination findings consistent with pulmonary hypertension and/or right ventricular (RV) failure. These findings are included in the history because they may be part of the presentation. Although patients often comment on peripheral edema, with careful questioning, they may also identify increasing abdominal girth consistent with ascites. Important questions on lower extremity edema include determination of whether the edema is symmetrical (unilateral edema suggests alternate diagnoses) and whether the edema improves or resolves with elevation of the lower extremities. The finding of “no resolution overnight” argues against RV failure as an etiology. In addition, for peripheral edema and ascites, it is important to ask questions directed toward determining the presence of anemia, hypoproteinemia, or other causes. The differential diagnosis of edema is broad and beyond the scope of this chapter.

Palpitations and Syncope
It is normal to be aware of the sensation of the heart beating, particularly during or immediately after exertion or emotional stress. Palpitations refer to an increased awareness of the heart beating. Patients use many different descriptions, including a “pounding or racing of the heart,” the feeling that their heart is “jumping” or “thumping” in their chest, the feeling that the heart “skips beats” or “races,” or countless other descriptions. A history that shows that palpitations began to occur during or immediately after exertion, and not at other times, raises the concern that these sensations reflect ventricular ectopy associated with myocardial ischemia. It is more difficult to assess the significance of palpitations occurring at other times. Supraventricular and ventricular ectopy may occur at any time and may be benign or morbid. As discussed in Chapters 41 and 42, ventricular ectopy is worrisome in patients with a history of MI or cardiomyopathy. Lacking this information, clinicians should be most concerned if lightheadedness or presyncope accompanies palpitations.

Syncope generally indicates an increased risk for sudden cardiac death and is usually a result of cardiovascular disease and arrhythmias. If a syncopal episode is a presenting complaint, the patient should be admitted for further assessment. In approximately 85% of patients, the cause of syncope is cardiovascular. In patients with syncope, assessment for CHD, cardiomyopathy, and congenital or valvular heart disease should be performed. In addition, neurocardiogenic causes represent a relatively common and important possible etiology for syncope. Box 2.6 shows the differential diagnosis for syncope. It is critical to determine whether syncope really occurred. A witness to the episode and documentation of an intervening period are helpful. In addition, with true syncope, injuries related to the sudden loss of consciousness are common. However, individuals who report recurrent syncope (witnessed or unwitnessed) but has never injured themselves may not be experiencing syncope. This is not to lessen the concern that a serious underlying medical condition exists but, instead, to reaffirm that the symptoms fall short of syncope, with its need for immediate evaluation.

 Keywords anginasyncopeheart failureauscultationheart soundshemodynamic maneuvers

CARDIAC NEURAL CREST

CARDIAC NEURAL CREST


CARDIAC NEURAL CREST
The neural crest is a transient population of cells that form from the dorsal ectoderm at the time of neural tube closure (Fig. 1.5). The neural crest population arises through a series of inductive interactions with surrounding tissues around the fourth week of development. 
SEPTATION

SEPTATION


SEPTATION
Atrial septation is initiated when the second heart field derived dorsal mesenchymal protrusion and the myocardial primary atrial septum (or septum primum) extend ventrally into the, yet undivided, common atrium. In the mouse, this process takes place between embryonic day (ED) 9.5 to 10.5; in humans the process occurs around day 30. The space between the leading edge of the atrial septum and the fusing atrioventricular cushions in the atrioventricular canal is the primary atrial foramen. As the primary atrial septum grows toward the mesenchymal atrioventricular cushions, thereby closing the primary interatrial foramen, perforations appear in the upper part of the primary atrial septum. These perforations will eventually coalesce and form the secondary interatrial foramen. As this part of atrial septation process nears completion, the secondary atrial septum (or septum secundum) appears in the space between the primary atrial septum and the left venous valve in the roof of the right atrium. Eventually, the upper part of the primary atrial septum will fuse with the secondary atrial septum, thereby closing off the secondary atrial foramen and completing the atrial septation process. Failure of fusion of the two atrial septa will lead to the congenital defect patent foramen ovale.
CHAMBER FORMATION

CHAMBER FORMATION


CHAMBER FORMATION
During the time of cardiac looping, at approximately 3 weeks of development, the arterial and venous poles of the heart decrease or cease cell division. At the same time, cardiomyocytes at two distinct locations within the intervening tissue reinitiate cell proliferation. This localized expansion of cardiomyocytes gives rise anteriorly to the atria and posteriorly to the left ventricle, with the area separating the two regions giving rise to the atrioventricular canal. Studies in chickens and mice demonstrated that the atria grow not only through proliferation but also by the recruitment of cells to the venous pole of the heart. The left ventricle and the atria are largely derived from a common pool of progenitors termed the first heart field (Fig. 1.4). In contrast, the second heart field gives rise to the dorsal mesenchymal protrusion and primary atrial septum, which are tissues that are critically important for atrioventricular septation, the outflow tract, and the right ventricle. A con- served role for the second heart field is supported by the observations that abnormalities that affect the expansion of the second heart field are associated with congenital heart disease in mouse models and humans, including atrial and atrioventricular defects, as well as outflow tract abnormalities.
LOOPING OF THE LINEAR HEART TUBE

LOOPING OF THE LINEAR HEART TUBE


LOOPING OF THE LINEAR HEART TUBE
As a consequence of its formation, differentiation, and rudimentary functionality, the linear heart tube is mostly postmitotic. During the fourth week of human gestation, growth and elongation of the linear heart tube occur by means of contribution and division of second heart field cells at both the sinus venosus and truncus arteriosus (posterior and anterior poles, respectively). Concurrently, an embryo-wide genetic program breaks the final axis of symmetry the left-right axis. Asymmetrical intercellular signaling on the left side of the embryo governs the migration and division of second heart field cells in the lengthening heart tube, leading to two major morphological cardiac asymmetries. First, the entire linear heart tube displaces to the right and rotates 90 degrees about its anterior-posterior axis, so that the original ventral surface of the linear tube is now the left side of a C-shaped tube (Fig. 1.3). Second, asymmetrical mitotic expansion of the second heart field contributions leads to localized “ballooning” of the primitive atrial and ventricular regions of the heart tube, transforming the C-shaped tube into an S-shaped heart (Fig. 1.3).
FORMATION OF THE PRIMITIVE LINEAR HEART TUBE

FORMATION OF THE PRIMITIVE LINEAR HEART TUBE


FORMATION OF THE PRIMITIVE LINEAR HEART TUBE
Even before gastrulation has completed, the internalized bilateral cardiac precursor pools continue to migrate in response to signaling cues from neighboring tissues. Remaining as cohesive epithelia, the heart fields move anteriorly and ventrally between 15 and 20 days of development, fusing at the embryonic midline to form the transient cardiac crescent (Fig. 1.1). Proper midline fusion of the bilateral cardiac primordia is essential for development of the heart. Several cardiac transcription factors are required for this process, and loss of function of any one of them causes extensive defects in further morphogenesis, including cardia bifida in severe cases.

Friday, September 11, 2020

 Tricuspid Valve Operations

Tricuspid Valve Operations

 Tricuspid Valve Operations
Abstract
Tricuspid valve surgery has evolved from an almost ignored valve in the past to an important valve that is critical to address at the time of left valve intervention. The incidence of tricuspid regurgitation associated with left valvular disease is quite significant and most common in conjunction with mitral valve disease; however, association with aortic valve pathology is not uncommon. Most commonly, tricuspid regurgitation is functional or secondary to dilation of the annulus, as a consequence of right ventricle dilation secondary to pulmonary hypertension. However, organic (rheumatic, endocarditis, or degenerative in origin) is not uncommon. The purposes of this chapter are to shed light on the anatomy of the tricuspid valve, and elucidate the etiology and pathogenesis of tricuspid valve disease, mainly tricuspid valve regurgitation, with a special focus on secondary tricuspid valve regurgitation. Indications for surgery as well as different surgical approaches (including different repair techniques and valve replacement) to correct tricuspid valve regurgitation are discussed in detail. A transcatheter approach for tricuspid valve repair or replacement is attractive, desirable, and beneficial to this high-risk population as an alternative to surgery.

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