Cardiac Echinococcus Infection (Hydatid Pericarditis): Symptoms, Diagnosis and Treatment

Cardiac Echinococcus Infection (Hydatid Pericarditis): Symptoms, Diagnosis and Treatment

pediagenosis    July 04, 2026    Comment   

Echinococcus Infection and Hydatid Pericarditis

Cardiac Echinococcus Infection

Even in endemic regions, the heart is rarely affected by Echinococcus disease; the incidence of primary myocardial involvement is less than 2% in human echinococciasis (echinococcosis). The parasitic six-hooked embryo reaches the myocardium through the coronary circulation, having passed through the gastric or intestinal mucosa into the portal circulation, and through both the hepatic and the pulmonary capillary bed. It can establish itself and develop into an echinococcus cyst in almost any part of the myocardium, but cysts are mostly located in the walls of the ventricles (see Plate 6-149). There is a higher incidence of cysts in the myocardium of the left ventricle because its vascular bed is more abundant. The developing parasitic membranous cyst is surrounded by a fibrous sac or capsule, the adventitia. When it grows larger, the cyst may protrude into a cardiac cavity, the pericardial sac, or both, its greater and more prominent part usually projecting toward the pericardium.

ANOMALIES OF THE VENTRICULAR SEPTUM

ANOMALIES OF THE VENTRICULAR SEPTUM

pediagenosis    October 05, 2025    Comment   

ANOMALIES OF THE VENTRICULAR SEPTUM

Ventricular Septal Defects (“MEMBRANOUS”)

Of the anomalies involving ventricular septal defects, those located beneath the aortic valve, the membranous ventricular septal defects, are by far the most common. Not only are these defects frequently seen in association with other cardiac anomalies, but even when occurring as isolated lesions, the membranous VSDs constitute the most important and also the most common type of congenital heart disease. This is not surprising considering the complex embryologic history of the subaortic portion of the ventricular septum. This is the last part of the septum to close, a closure effected by the fusion of components from the embryonic muscular septum, endocardial cushions, and conal swellings. Anomalous development of any one or several of these contributors will lead to a defect of the ventricular septum. There fore, although located in the same general area, membranous VSDs may vary considerably in position and size. Some are found immediately beneath the right and posterior aortic valve cusps; these probably are caused mainly by deficiency of the conus septum and, because of a lack of support for the aortic valve cusps, may lead to prolapse of one or both cusps, causing aortic regurgitation. Other membranous VSDs mainly caused by deficiency of the right limb of the endocardial cushions, or failure of otherwise normally developed endocardial cushions to fuse with the ventricular septum and conus septum, are located a few millimeters away from the aortic valve, leaving a rim of muscular or fibrous tissue. All these defects are located in the general area where the membranous septum is found in the normal heart, and thus are usually rather loosely referred to as “membranous septal defects.”

ANOMALIES OF TRICUSPID VALVE

ANOMALIES OF TRICUSPID VALVE

pediagenosis    October 05, 2025    Comment   

ANOMALIES OF TRICUSPID VALVE

TRICUSPID ATRESIA

Of the congenital tricuspid valve anomalies, only two tricuspid valve atresia and Ebstein’s anomaly are clinically significant. Tricuspid regurgitation and stenosis occurring as isolated lesions are extremely rare. Some forms of septal defects, such as endocardial cushion defects or ventricular septal defects, may involve the tricuspid valve’s medial cusp, rendering this cusp insufficient or allowing for a direct shunt from the left ventricle to the right atrium. Tricuspid valve stenosis usually accompanies pulmonary atresia or severe stenosis when the ventricular septum is intact. Actually, the tricuspid valve in these patients, although small and often with thickened cusps, is normally formed, and the stenosis is a secondary hypoplasia.

DEFECTS OF THE ATRIAL SEPTUM

DEFECTS OF THE ATRIAL SEPTUM

pediagenosis    September 28, 2025    Comment   

DEFECTS OF THE ATRIAL SEPTUM

ATRIAL SEPTAL DEFECTS

The atrial septum normally consists of two overlapping, closely adjacent components. Each forms an incomplete partition. The right-side component, corresponding to the embryonic septum secundum, is muscular and firm and has a posteroinferior oval-shaped opening, the foramen ovale. The left-side component, derived from the embryonic septum primum, is fibrous and thin and has a somewhat round opening anterosuperiorly, the ostium secundum. Together, the two components act as a one-way flap valve, allowing the flow of blood from right to left (normal before birth) but not from left to right. After birth, with the establishment of pulmonary circulation, the increased amount of blood entering the left atrium elevates the pressure in that chamber, thereby closing the flap valve. In most cases, this functional closure is eventually followed by anatomic closure; that is, the two components of the septum fuse. In the minority of cases where fusion fails, an increase in the right atrial pressure due to congenital cardiac anomalies, or any other condition that elevates right ventricular and right atrial pressure, causes the right atrial blood to flow again into the left atrium. Such a probe-patent foramen ovale, however, should not be considered a form of atrial septal defect; it causes no hemodynamic abnormalities by itself. In ASD there is an abnormal opening in the atrial septum allowing blood to flow either way; a predominantly left-to-right shunt usually exists. With associated anomalies or other conditions tending to increase right atrial pressure, the shunt is always from right to left, as in tricuspid valve atresia, or an initially left-to-right shunt reverses, as occurs after pulmonary vascular changes with pulmonary hypertension.

ENDOCARDIAL CUSHION DEFECTS

ENDOCARDIAL CUSHION DEFECTS

pediagenosis    September 28, 2025    Comment   

ENDOCARDIAL CUSHION DEFECTS

ENDOCARDIAL CUSHION DEFECTS: ANATOMY AND EMBRYOLOGY

The group of anomalies known as the endocardial cushion defects (ECDs) is of interest to not only the cardiologist but the embryologist, pathologist, and surgeon as well. All ECD types are primarily caused by a developmental defect of the atrioventricular endocardial cushions. Normally, the endocardial cushions fuse with each other and bend to form an arc, the convexity of which is toward the atrial side. The atrial septum fuses with the apex of the arc, thus dividing it into two approximately equal parts. The right half contributes to the ventricular septum, the atrioventricular septum, and the medial or septal cusp of the tricuspid valve. The left half of the fused cushions forms the aortic or anterior cusp of the mitral valve.

ANOMALIES OF THE ATRIA

ANOMALIES OF THE ATRIA

pediagenosis    September 24, 2025    Comment   

ANOMALIES OF THE ATRIA

Juxtaposition Of The Atrial Appendages

In juxtaposition of the atrial appendages (auricles), the main bodies of the atria are normally located, but there is levoposition of the right atrial appendage. Instead of being to the right of the arterial trunks, the right atrial appendage crosses behind them to appear on their left, interposing itself between the great arteries and the left atrial appendage. Juxtaposition of the atrial appendages has no functional significance because it causes no hemodynamic disturbance itself. Its presence, however, always indicates the coexistence of other major cardiac anomalies. Transposition of the great vessels and a ventricular septal defect are invariably present, and atresia of the tricuspid valve is common. Plate 5-5 also depicts a double aortic arch.

ANOMALOUS PULMONARY VENOUS CONNECTION

ANOMALOUS PULMONARY VENOUS CONNECTION

pediagenosis    September 24, 2025    Comment   

ANOMALOUS PULMONARY VENOUS CONNECTION

TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION

In patients with anomalous pulmonary venous connection (APVC), all or some of the pulmonary veins fail to communicate with the left atrium, instead discharging blood into major systemic veins or directly into the right atrium. This discussion only considers the isolated forms of APVC. When these occur with other cardiac malformations, the clinical and hemodynamic features are usually modified or are chiefly determined by the complicating defect.

ANOMALIES OF THE GREAT SYSTEMIC VEINS

ANOMALIES OF THE GREAT SYSTEMIC VEINS

pediagenosis    September 24, 2025    Comment   

ANOMALIES OF THE GREAT SYSTEMIC VEINS

CARDIAC VEIN ANOMALIES

Anomalies can involve the large systemic venous trunks because of the complex embryogenesis and tremendous variability of the venous system in general. Abnormal channels almost always empty into other systemic veins and rarely cause functional changes disturbing to the patient, usually discovered incidentally at postmortem examination or during cardiovascular diagnostic or surgical procedures. Venous trunk anomalies may occur as isolated malformations but more often are associated with other cardiovascular anomalies. The presence of an anomaly, if unsuspected, may lead to troublesome or even dangerous situations when total cardiopulmonary bypass techniques are employed.

PHYSICAL EXAMINATION

PHYSICAL EXAMINATION

pediagenosis    September 19, 2025    Comment   

PHYSICAL EXAMINATION

Although many forms are not seen in adult patients, cardiologists often do see simple clues to the diagnosis of certain forms of congenital heart disease (CHD), usually acyanotic or cyanotic and postoperative. Any child with or suspected with CHD should be seen by a pediatric cardiologist at an institution with interventional pediatric cardiologists and cardiac surgeons. Adult patients with CHD should be seen and advised by a pediatric cardiologist or adult cardiologist (prefer ably both) at a surgical center with experts in congenital heart surgery and percutaneous procedures. Many adult patients present with arrhythmias, heart failure, or failure of the original childhood surgery. Occasionally, older patients or patients with anomalous coronary artery disease present with ischemic heart disease symptoms.

Fetal Circulation and Changes at Birth

Fetal Circulation and Changes at Birth

pediagenosis    September 19, 2025    Comment   

Fetal Circulation and Changes at Birth

The primary vascular concept of prenatal circulation is the requirement that the intraembryonic circulation of blood bypass the nonfunctioning lungs and liver (see Plate 4-18). The placenta (villous chorion) serves the role of these organs with gas and metabolic exchange between maternal and fetal blood. The airway in the lungs is filled with amniotic fluid, and pulmonary vascular resistance is high. The lungs only receive enough blood to nourish the tissues, and pulmonary venous blood flow into the left atrium is minimal. The plan for the prenatal circulation also requires that it convert the postnatal pattern soon after the first breath of the newborn. Two lung shunts (and a liver shunt) and the design of the interatrial septum serve these needs.

Development of Major Blood Vessels

Development of Major Blood Vessels

pediagenosis    September 19, 2025    Comment   

Development of Major Blood Vessels

The early embryonic vascular system is plexiform (intercalating). Preferential flow related to the development of organ systems, however, leads to enlargement of certain channels in the plexus. This expansion is brought about in part by the fusion and confluence of adjacent smaller vessels and by the enlargement of individual capillaries. Thus a number of vascular systems develop. As the embryo grows, new organs appear; others are transient and disappear. The various vascular systems are also continuously modified to satisfy changing needs.

Initially, the arteries and veins consist simply of endothelial tubes and cannot be distinguished from each other histologically. In later development, typical vessel walls are differentiated from the surrounding mesenchyme. The final pattern of the vascular system is genetically determined and varies with the animal species. Variations are, however, extremely common in both arterial and venous patterns, and local modifications occur in cases of abnormal development of organs.

Formation of Cardiac Septa

Formation of Cardiac Septa

pediagenosis    September 11, 2025    Comment   

Formation of Cardiac Septa

At the close of the preceding phase of development, the heart completely occupies the pericardial cavity. Blood flows in a single path through the sinus venosus and atrium, through an atrioventricular canal into the left ventricle, though an interventricular canal above the free edge of the primordial interventricular septum into the right ventricle, then out the bulbus cordis and truncus arteriosus. The stage is now set for the septation of the heart, which lasts about 10 days. No major changes occur in the external appearance of the heart. The formation of the various cardiac septa occurs more or less simultaneously; for descriptive purposes, however, it is necessary to consider their development separately.

Formation of the Heart Loop

Formation of the Heart Loop

pediagenosis    September 11, 2025    Comment   

Formation of the Heart Loop

At the beginning of the next phase of development, the heart, as described earlier, is essentially a straight tube with a caudal venosus end and cranial arterial end. It lies within the pericardial cavity and is attached posteriorly only by the dorsal mesocardium.

Formation of the Heart Tube

Formation of the Heart Tube

pediagenosis    August 18, 2025    Comment   

Formation of the Heart Tube

ONE-SOMITE AND TWO-SOMITE STAGES

As the primitive, bilaterally symmetric cardiovascular system appears, shaping of the embryo during the fourth week profoundly influences the relative position of the cardiac portion of this system. The trilaminar embryonic disc folds into a cylinder, and the amnion tucks around the embryo on each side. The amnion also envelops the head end of the embryo as the ectodermal tube of the forebrain rapidly increases in size in a cranial and ventral direction. The result is a 180-degree sagittal plane rotation of the cardiogenic mesoderm and oropharyngeal membrane, which were originally cranial to the neural plate and the developing neural tube. The heart is now caudal to the oropharyngeal membrane rather than cranial, and the heart locates dorsal to the developing pericardial cavity (see Plate 4-3).

Early Intraembryonic Vasculogenesis

Early Intraembryonic Vasculogenesis

pediagenosis    August 18, 2025    Comment   

Early Intraembryonic Vasculogenesis

Presomite stage (1.5-mm embryo) at approximately 20 days

PRESOMITE STAGE

Although not the first organ system to make its appearance in the embryo, the cardiovascular system reaches a functional state long before the other systems, and doing so while still in a relatively primitive state of development. The vascular system grows from a simple, bilaterally symmetric plexus into an asymmetric, complex system of arteries, veins, and capillaries a necessarily dynamic process involving the formation of new vessels and temporary detours, rerouting of the bloodstream, and the disappearance of previously dominant channels or even of entire vascular subsystems. The vascular system needs to enlarge as the embryo grows, adapting to marked changes in embryonic shape and developmental changes in other organ systems. While hard at work, the heart also must grow and differentiate from a simple tube into a complex, four-chambered organ with sets of valves. Finally, because the very young embryo is tiny compared to the mass of extraembryonic (placental) tissue, which the young heart also supplies with blood, this heart is relatively enormous compared with its relative size in the adult. Describing the development of the cardiovascular system first requires review of the intraembryonic coelom (“body cavity”) formed by the confluence of small, initially isolated spaces that appear in the lateral mesoderm and cardiogenic mesoderm. The spaces fuse together and form the single, horseshoe-shaped intraembryonic coelom that extends the length of the embryo in the lateral mesoderm on each side, communicating across the midline cranially in the cardiogenic mesoderm. Later in development, a communication develops on each side between the caudal ends of the intraembryonic coelom and the extraembryonic coelom. The formation of the coelom separates the lateral mesoderm into two layers: the parietal layer in contact with the ectoderm and the visceral layer in contact with the endoderm. The ectoderm with its parietal layer of lateral plate mesoderm is called somatopleure; endoderm with its visceral mesodermal layer is called splanchnopleure.

EARLY EMBRYONIC DEVELOPMENT

EARLY EMBRYONIC DEVELOPMENT

pediagenosis    August 18, 2025    Comment   

EARLY EMBRYONIC DEVELOPMENT

In humans, as in most other primates, fertilization takes place in the distal part of the uterine tube, near its fimbriated end, about 12 to 24 hours after ovulation. The fertilized ovum, or zygote, is transported to the uterus by rhythmic contractions of the tube, aided by the action of the cilia of the epithelium. During this passage down the uterine tube, which takes about 4 days, the zygote executes a number of cell divisions and, on reaching the uterus, consists of a clump of blastomeres, the morula, which has not increased appreciably in size from the zygote.

CARDIAC MAGNETIC RESONANCE IMAGING

CARDIAC MAGNETIC RESONANCE IMAGING

pediagenosis    August 17, 2025    Comment   

CARDIAC MAGNETIC RESONANCE IMAGING

Cardiac magnetic resonance imaging (MRI) does not use radiation and is based on fundamental principles related to the presence of water in all tissues. Since two protons are contained in a water molecule, when put in a magnetic field, they can be aligned. If the magnetic field is turned off, the photons can return to their original position and generate a radio signal that can be detected and quantitated for an image. The images obtained can help assess ventricular function, aortic disease, ischemic heart disease, cardiomyopathies, pericardial disease, valvular heart disease, cardiac masses, congenital heart disease, pulmonary vascular disease, and coronary artery bypass grafting. In the near future, electrophysiologists will be using cardiac MRI to evaluate atrial morphology before atrial fibrillation ablation therapy (see Plates 3-20 and 3-21).

COMPUTED TOMOGRAPHIC ANGIOGRAPHY

COMPUTED TOMOGRAPHIC ANGIOGRAPHY

pediagenosis    August 17, 2025    Comment   

COMPUTED TOMOGRAPHIC ANGIOGRAPHY

Computed tomographic angiography (CTA) is a 3D image reconstructed from multiple slices of tomographic images of a particular body part (e.g., brain, chest, blood vessels, abdomen, pelvis, joints). CTA of the heart includes the coronary arteries. Because CT studies are created by computer processing, the images can be seen in multiple planes, and ventricles, atria, veins, and arteries can be easily delineated. Pulmonary CTA can reveal emboli in both right and left pulmonary arteries and some subdivisions, as well as in the main pulmonary artery (see Plate 3-19).

VENTRICULOGRAPHY

VENTRICULOGRAPHY

pediagenosis    August 17, 2025    Comment   

VENTRICULOGRAPHY

MEASUREMENT OF LEFT VENTRICULAR FUNCTION USING VENTRICULOGRAPHY

In ventriculography a catheter (usually pigtail) is introduced into the ventricle and radiopaque contrast material injected (see Plate 3-17). The ventricle is then visualized by fluoroscopy/cine as it contracts and relaxes, to assess ventricular wall motion and calculate ejection fraction (EF; normal ≥55%). Ejection fraction is calculated by the formula EF = SV/EDV, where SV is stroke volume and EDV end-diastolic volume.

Myocardial Perfusion Imaging

Myocardial Perfusion Imaging

pediagenosis    August 17, 2025    Comment   

Myocardial Perfusion Imaging

Use of myocardial perfusion imaging (MPI or MPS) is preferable to “stress nuclear imaging,” but both terms are used interchangeably. In general, images at peak stress and at rest reflect changes in the distribution of the radiopharmaceutical if ischemia is present (see Plate 3-16; SPECT, single-photon emission tomography). Indications for MPI are as follows :