Medical Radiology - Lazar A.P. 2008

Radiological Examination of the Heart and Blood Vessels
Myocardial and Pericardial Diseases

Myocardial disorders include myocarditis, cardiomyopathies, myocardial dystrophy, coronary artery disease, Cor Pulmonale, and hypertensive Heart disease.

Myocarditis is an inflammatory disease of The Heart Muscle caused by rheumatic fever, diphtheria, typhoid fever, or other bacterial and viral infections. Patients typically report weakness, fatigue, chest pain, and palpitations upon exertion. Objective findings include fever, leukocytosis, elevated ESR, muffled heart sounds, hypotension, and a decreased amplitude of T and P waves on the Electrocardiogram.

Radiologically, the heart appears triangular with a symmetrically increased transverse diameter. Muscle tone is reduced, making the heart appear flattened against the Diaphragm, and the contours along the left and right borders are smoothed out. Fluoroscopy reveals decreased contractility and weakened, superficial, often arrhythmic pulsations along the borders. The transverse diameter of the heart decreases during inspiration and increases during expiration. Ultrasound, CT, and MRI enable precise measurement of myocardial wall thickening.

Cardiomyopathy is a non-inflammatory disease of the heart muscle. It can be triggered by systemic disorders (such as systemic lupus erythematosus, chronic alcoholism, or drug addiction) or remain idiopathic. Cardiomyopathy disrupts myocardial METABOLISM, leading to reduced tonic and contractile function, as well as cardiac enlargement caused by wall thickening (hypertrophic cardiomyopathy) or chamber dilation (dilated cardiomyopathy), ultimately resulting in Heart Failure. These enlarged cardiac dimensions may remain stable for several years or progressively worsen, leading to relative valvular incompetence and dilated cardiomyopathy (or myocardial dystrophy). Myocardial dystrophy refers to cardiomyopathy accompanied by ventricular dilation. It often develops secondary to myocarditis, anemia, hypo- or hyperthyroidism, Diabetes Mellitus, malnutrition, or vitamin deficiencies. Eliminating the underlying cause can halt the progression of myocardial dystrophy.

Clinically, cardiomyopathy manifests as mild dyspnea, palpitations, chest pain, arrhythmias, muffled heart sounds, and functional murmurs, particularly over the cardiac apex. Radiologically, dilated cardiomyopathy presents with marked cardiomegaly and signs of venous congestion and/or pulmonary edema. Echocardiography, CT, and MRI are used to assess the severity and localization of left ventricular wall thickening, detect asymmetric Hypertrophy of the interventricular septum, and quantitatively evaluate myocardial mass in hypertrophic cardiomyopathy.

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Fig. 153. Myocardial infarction on PET: A - with 13N-ammonia, B - with 18F-fluorodeoxyglucose.

1 - Transmural myocardial infarction showing no uptake of either radionuclide;

2 - area of myocardial ischemia showing absent N-13 Ammonia uptake alongside F-18 FDG uptake;

3 - healthy myocardial tissue with normal uptake of both N-13 Ammonia and F-18 FDG.

Coronary artery disease develops due to impaired Coronary Circulation and subsequent myocardial ischemia, clinically manifested as constricting chest pain (angina pectoris). The lumen of the coronary Arteries narrows As a result of atherosclerosis or spasm. Coronary patency is evaluated using coronarography (coronary angiography), which reveals the Location, extent, and nature of stenoses or occlusions in the affected vessels. Irregularities and reduced amplitude of ventricular wall contractions during ischemia can be detected via ultrasound. Perfusion scintigraphy demonstrates decreased ²¹⁰Tl-chloride uptake in the injured heart muscle. Contrast-enhanced computed tomography identifies areas of ischemic myocardium by their low attenuation and delayed enhancement, as well as visualizing narrowed segments of the coronary arteries.

Prolonged spasm of sclerotically narrowed coronary arteries can trigger a myocardial infarction. The Diagnosis is established based on the Clinical presentation, electrocardiography, and serum levels of cardiospecific Enzymes and Myoglobin. In the first few hours following an uncomplicated infarction, chest X-rays may show no abnormalities, though calcifications from prior infarctions are occasionally visible. Sometimes, acute myocardial infarction leads to cardiomegaly, venous pulmonary Hypertension, and pulmonary edema. Within the first two weeks, heart size typically decreases by about a quarter. The location and extent of myocardial damage are determined using ultrasound, MRI, and radionuclide Diagnostics. Sonography reveals impaired contractility in the affected myocardial areas and potential ruptures of the papillary Muscles or interventricular septum. Gadolinium-enhanced Magnetic Resonance imaging detects a reduced concentration of this intravascular paramagnetic agent within the infarct zone. Scintigraphy and PET can identify areas of decreased metabolic activity corresponding to the myocardial infarction (Fig. 153).

Fig. 154. Calcified cardiac aneurysm (arrow) on frontal (A) and lateral (B) radiographs and CT (C).

A potential complication of myocardial infarction is a cardiac aneurysm, which forms when necrotic tissue is replaced by a thin layer of Connective Tissue that bulges outward under intracardiac pressure. Because myocardial infarctions most frequently involve the left ventricular wall, cardiac aneurysms are primarily observed in this region. Radiologically, a left ventricular aneurysm appears as a protrusion of varying size along the left or posterior cardiac border (Fig. 154). A classic fluoroscopic sign of a cardiac aneurysm is paradoxical pulsation—meaning that during ventricular systole, the aneurysm shadow expands rather than contracts. Calcified cardiac aneurysms are best visualized using CT.

Intraventricular thrombosis, another complication of myocardial infarction, can be diagnosed using two-dimensional echocardiography, ventriculography, and MRI.

Cor Pulmonale. Circulatory obstruction in the Pulmonary Circulation caused by lung diseases leads to hypertrophy and subsequent dilation of the heart, a condition known as cor pulmonale. Its development can be acute or chronic. Causes of acute cor pulmonale include Pulmonary Embolism, acute Pneumonia, and tension pneumothorax, whereas Chronic cor pulmonale may result from tuberculosis, emphysema, pneumosclerosis, and other chronic pulmonary conditions.

Acute cor pulmonale causes severe microcirculatory disturbances in the myocardium (stasis, hemorrhages), contractures of the right ventricular muscle fibers, and areas of patchy myocyte necrosis, which can prove fatal if the underlying cause is not promptly resolved.

In chronic cases, the reduction in the functional vascular bed and the resulting pulmonary hypertension increase the workload on the right ventricle, prompting hypertrophy of the muscular layer and dilation of the ventricular cavity. The thickness of the right ventricular wall may equal or even exceed that of the left ventricle (whereas the normal ratio is 1:2). In advanced cases, the enlarged right ventricle displaces the right atrium and forms part of the right cardiac border. The left ventricle is also shifted to the left, though overall transverse cardiac enlargement may not be apparent due to a typically low-positioned diaphragm.

Clinically, patients experience precordial pain, dyspnea, tachycardia, muffled heart sounds, and an accentuated second heart sound over the pulmonary trunk. Over time, systemic circulation becomes impaired, leading to hepatomegaly, ascites, and peripheral edema.

Radiologically, acute cor pulmonale manifests as widening of the pulmonary roots, enlargement of the right heart chambers, dilation of the SUPERIOR VENA CAVA, and an elevated right hemidiaphragm. On a standard frontal chest radiograph, chronic cor pulmonale is characterized by a vertical cardiac axis, a mitral configuration, a small transverse diameter, and a relatively increased longitudinal dimension. A prominent pulmonary trunk bulge is visible along the left heart border, accompanied by a pronounced indentation (notch) at the junction with the left ventricle. The right border shows an enlarged lower arc formed primarily by the right ventricle, along with an elevated cardiophrenic angle. The relatively small overall size of the heart in cor pulmonale is attributed to inadequate ventricular filling caused by restricted pulmonary Blood flow. Fluoroscopy reveals hyperactive pulsations of the pulmonary trunk, pulmonary arteries, and lung roots. Deep pulsations of the right ventricle often match the contraction pattern of the left ventricle.

Angiocardiography, echocardiography, CT, and MRI reveal hypertrophy and dilation of the right ventricular cavity, enlargement of the pulmonary infundibulum, and narrowing or deformation of the pulmonary trunk branches. Meanwhile, Doppler Ultrasonography and advanced contrast-enhanced CT and MRI demonstrate reduced blood flow velocity within these vessels.

The Heart in Hypertensive Disease. Hypertension increases the workload on the left ventricle, leading to hypertrophy of its muscular wall and subsequent cavity dilation. Over time, the left ventricle enlarges, and both cardiosclerosis and coronary sclerosis develop.

On frontal chest radiography in the Cytology/cytology/16.html">Early stages of the disease, the heart adopts an aortic configuration: the waist is accentuated, the left ventricular arch projects to the left, and the cardiac apex is submerged into the diaphragm. The shadow of the aorta is widened along its entire course. Left ventricular border pulsations are hyperactive and exhibit a deep amplitude. Ultrasound, CT, and MRI reveal thickening of the left ventricular wall.

Pericarditis is inflammation of the Pericardium. It can be caused by rheumatic fever, tuberculosis, pneumonia, uremia, myocardial infarction, or malignant tumors of the Lungs and Mediastinum. Clinical manifestations include dyspnea, palpitations, chest pain, hypotension, and muffled heart sounds. In dry (fibrinous) pericarditis, a pericardial friction rub can be auscultated in the 3rd and 4th intercostal spaces to the left of the Sternum, whereas in effusive pericarditis, the areas of cardiac dullness expand and the apical impulse disappears. Pericarditis is classified into dry (fibrinous) and effusive (exudative) forms.

Fig. 155. Tuberculous pericarditis on contrast-enhanced computed tomography.

Dry pericarditis may not be visible on conventional radiographs. Occasionally, a shadow of the thickened pericardium can be detected as a stripe along the heart border, measuring about 2 mm in width, along with localized, streaky, or continuous calcification (known as "concretio cordis" or "armored heart"). Thickening and immobility of the pericardium, where the pericardial cavity is partially or completely obscured, can be visualized using ultrasound, CT, and MRI. Pericardial calcification (calcinosis), most commonly resulting from previous tuberculosis, is best detected via CT (Fig. 155).

Exudative pericarditis can be radiographically identified when at least 100–150 ml of fluid accumulates in the pericardial cavity. The heart assumes a trapezoidal shape with an increased transverse diameter, a shortened vascular pedicle, and flattened or obliterated contours along the borders (in cases of massive effusion) (Fig. 156). Pulsatile Movements of the heart are diminished or absent because they are dampened by the accumulated pericardial fluid, whereas aortic pulsation remains preserved. The cardiac silhouette changes shape with positional shifts of the patient and during Respiration. In massive pericardial effusions, the heart takes on a globular shape. During the resorption of the exudate, encysted pericarditis may develop, which appears on radiographs as a distinct shadow projected against the cardiac silhouette.

Ultrasound, CT, and MRI can detect even small amounts of fluid (exceeding 50 ml) and determine its distribution within the pericardial cavity.

Fig. 156. Exudative pericarditis on a posteroanterior chest radiograph of the heart.