Diagnostic approach of valvular myocardial and

pericardial diseaseAmirreza Sajjadieh

Interventional Cardiologist1392/11/13

Myocardial and Pericardial Diseases

Outlines: • Introducation

• Myocardial diseases: 1. - Myocarditis2. - Cardiomyopathy : 4 major types :

1. Dilated.2. Hypertrophic.3. Restrictive.4. Arrhythmogenic right venticular.

• Pericardial diseas:1. acute pericarditis2. pericardial effusion and cardiac tamponade3. constrictive pericarditis.

MYOCARDIAL DISEASES

Introduction Of Myocardial Diseases:

• Although the myocardium is involved in most types of heart disease, the term myocarditis and cardiomyopathy are usually reserved for conditions that primerly affect the heart muscle.

• So we are discussing today Myocardial diseases that is not due to ischaemic, valvular or hypertensive heart disease or a known infiltrative, metabolic/toxic or neuromuscular disorder

Myocardial diseases may be caused by:

1. an acute or chronic inflammatory pathology

(myocarditis)

2. idiopathic myocardial disease (cardiomyopathy).

Myocarditis

• Acute inflammation of the myocardium. • It has many causes:

1. Idiopathic2. Infective3. Viral: Coxsackievirus, adenovirus, CMV, echovirus, influenza, polio, hepatitis, HIV.4. Parasitic: Trypanosoma cruzi, Toxoplasma gondii (a cause of myocarditis in the newborn or

immunocompromised)5. Bacterial: Streptococcus (most commonly rheumatic carditis), diphtheria (toxin-mediated

heart block common)

Cont.causes:

• Spirochaetal: Lyme disease (heart block common),leptospirosis.

• Fungal.

• Rickettsial.

• Toxic.

• Drugs: Causing hypersensitivity reactions, e.g. methyldopa, penicillin, sulphonamides, antituberculous,modafinil.

• Radiation: May cause myocarditis but pericarditis more common.

• Autoimmune: An autoimmune form with autoactivated T cells and organ specific antibodies may occur.

Pathology:

• In the acute phase myocarditic hearts are flabby with focal haemorrhages; in chronic cases they are enlarged and hypertrophied.

• Histologically an inflammatory infiltrate is present.

• lymphocytes predominating in viral causes.

• Polymorphonuclear cells in bacterial causes.

• eosinophils in allergic and hypersensitivity causes.

Clinical features:

• Myocarditis may be an acute or chronic process.

• its clinical presentations range from:an asymptomatic state associated with limited

and focal inflammation. fatigue, palpitations, chest pain, dyspnoea

and fulminant congestive cardiac failure due to diffuse myocardial involvement.

Physical examination:

• includes soft heart sounds.

• a prominent third sound.

• often a tachycardia.

• A pericardial friction rub may be heard.

Investigations:

■ Chest X-ray may show some cardiac enlargement.

■ ECG demonstrates ST- and T wave abnormalities and arrhythmias.

■ Cardiac enzymes are elevated.

■ Viral antibody titres may be increased. However, since enteroviral infection is common in the general population, the diagnosis depends on the demonstration of acutely rising titres.

■ Endomyocardial biopsy may show acute inflammation but false negatives are common by conventional criteria. Biopsy is of limited value outside specialized units.

■ Viral RNA can be measured from biopsy material using polymerase chain reaction (PCR). Specific diagnosis requires demonstration of active viral replication within myocardial tissue.

CARDIOMYOPATHY

• Cardiomyopathies are a group of diseases of the myocardium that affect the mechanical or electrical function of the heart.

• They are not secondary to coronary artery diseases, hypertension, or congenital, valvular or pericardial abnormalities.

• They are frequently genetic and may produce inappropriate ventricular hypertrophy or dilatation and can be primarily a cardiac disorder or part of a multi-system disease.

Four main types:

1. Dilated.

2. Hypertrophic.

3. Restrictive.

4. Arrhythmogenic right venticular.

1. Dilated cardiomyopathy (DCM):• is characterized by dilatation of the ventricular chambers and

systolic dysfunction with preserved wall thickness.

• In about 25% of the patients it is a familial disease.

• Sporadic DCM can be caused by multiple conditions:

■ myocarditis – Coxsackie, adenoviruses, erythroviruses, HIV, bacteria, fungae, mycobacteria, parasitic (Chagas’ disease)

■ toxins – alcohol, chemotherapy, metals (cobalt, lead, mercury, arsenic)

■ autoimmune. ■ endocrine. ■ neuromuscular.

Clinical features:• DCM can present with:• heart failure.• cardiac arrhythmias.• conduction defects.• thromboembolism. • sudden death.

• Increasingly, evaluation of relatives of DCM patients is allowing identification of early asymptomatic disease, prior to the onset of these complications.

• Clinical evaluation should include a family history and construction of a pedigree where appropriate.

Investigations:

• ■ Chest X-ray demonstrates generalized cardiac enlargement.

• ■ ECG may demonstrate diffuse non-specific ST segment and T wave changes. Sinus tachycardia, conduction abnormalities and arrhythmias are also seen.

• ■ Echocardiogram reveals dilatation of the left and/or right ventricle with poor global contraction function.

• ■ Cardiac MR may demonstrate other aetiologies of left ventricular dysfunction (e.g. previous myocardial infarction) or demonstrate abnormal myocardial fibrosis. Cardiac MR is also useful for identifying myocardial thrombus .

• ■ Coronary angiography should be performed to exclude coronary artery disease in all individuals at risk (generally patients > 40 years or younger if symptoms or risk factors are present).

• ■ Biopsy is generally not indicated outside specialist care.

2. Hypertrophic cardiomyopathy (HCM)

• It is characterized by marked vantricular hypertrophy in the absence of an alternate cause (e.g. aortic stenosis or hypertension).

• Usually with disproportionate involvment of the interventricular septum.

• The hypertrophic non-compliant vantricles impair diastolic filling, so that stroke volume is reduced.

• Most cases are familial, autosomal dominant and caused by mutation in genes coding for proteins that regulate conraction, e.g troponin and B-myosin.

Clinical features:Symptoms:• ■ many are asymptomatic and are detected through family screening of an

affected individual or following a routine ECG examination.

• ■ chest pain, dyspnoea, syncope or pre-syncope (typically with exertion), cardiac arrhythmias and sudden death are seen.

• ■ sudden death occurs at any age but the highest rates (up to 6% per annum) occur in adolescents or young adults.

■ dyspnoea occurs due to impaired relaxation of the heart muscle or the left ventricular outflow tract obstruction that occurs in some patients.

■ If a patient develops atrial fibrillation there is often a rapid deterioration in

clinical status due to the loss of atrial contraction and the tachycardia – resulting in elevated left atrial pressure and acute pulmonary oedema.

Signs:• ■ double apical pulsation (forceful atrial

contraction producing a fourth heart sound).• jerky carotid pulse because of rapid ejection

and sudden obstruction to left ventricular outflow during systole

• ■ ejection systolic murmur due to left ventricular outflow obstruction late in systole.

• ■ pan-systolic murmur due to mitra regurgitation.

• ■ fourth heart sound (if not in AF).

Investigations:

• ■ ECG abnormalities of HCM include left ventricular hypertrophy, ST and T wave changes, and abnormal Q waves especially in the infero-lateral leads.

• ■ Echocardiography is usually diagnostic and in classical HCM there is asymmetric left ventricular hypertrophy (involving the septum more than the posterior wall), systolic anterior motion of the mitral valve, and a vigorously contracting ventricle.

• ■ Cardiac MR can detect both the hypertrophy but also abnormal myocardial fibrosis.

• ■Genetic analysis, where available, may confirm the diagnosis and provide prognostic information for the patient and relatives.

Treatment:

• The management of HCM includes treatment of symptoms and the prevention of sudden cardiac death in the patient and relatives.

• Risk factors for sudden death:• ■ massive left ventricular hypertrophy (> 30 mm on

echocardiography).

• ■ family history of sudden cardiac death (< 50 years old).

• ■ non-sustained ventricular tachycardia on 24-hour Holter monitoring.

• ■ prior unexplained syncope.

• ■ abnormal blood pressure response on exercise (flat or hypotensive response).

• patients with two or more risk factors should be assessed for implantable cardioverter- defibrillator (ICD).

• In patients in whom the risk is less, amiodarone is an appropriate alternative.

• Chest pain and dyspnoea are treated with B-blockers and verapamil.

• Family members should be screened for evidence for evidence of disease by ECG and echocardiography.

Restrictive cardiomyopathy

• In this rare condition, ventricular filling is impaired because the ventricles are 'stiff' .

• This leads to high atrial pressures with atrial hypertrophy dilatation later atrial fibrillation.

Restrictive cardiomyopathy

Aetiology:1. Amyloidosis is the most common cause of

restrictive cardiomyopathy in the UK. 2. other forms of infiltration (e.g. glycogen

storage diseases), idiopathic perimyocyte fibrosis .

Restrictive cardiomyopathy

Clinical features :1. Dyspnoea.2. fatigue .3. embolic symptoms are the presenting features. NB : Restriction to ventricular filling (especially

right) results in persistently elevated venous pressures, consequent hepatic enlargement, ascites, and dependent oedema.

Restrictive cardiomyopathyInvestigations:

1. Chest X-ray: may show pulmonary venous congestion. The heart can be normal or show cardiomegaly and/or atrial enlargement.

2. ECG usually has low-voltage and ST segment and T wave abnormalities.

3. Echocardiogram shows symmetrical myocardial thickening and often a normal systolic ejection fraction, but impaired ventricular filling.

4. Cardiac catheterization and haemodynamic studies help distinction from constrictive pericarditis.

5. Endomyocardial biopsy in contrast with other cardiomyopathies is often useful in this condition and may permit a specific diagnosis such as amyloidosis to be made.

PERICARDIAL DISEASES

Pericardial disease

The pericardium acts as a protective covering for theheart. It consists of two separate layers, the inner visceralpericardium and the outer parietal pericardium. The visceral pericardium reflects back upon it self at the levelof the great vessels to join the parietal pericardium, thusforming a sac. The pericardial sac contains up to 50 mLof pericardial fluid in the normal heart, although this is a potential space for fluid to collect. The pericardium serves to lubricate the surface of the heart, prevents deformation and dislocation of the heart and acts as a barrier to the spread of infection.

Presentations of pericardial disease include:

• acute pericarditis.• a pericardial effusion and cardiac

tamponade• constrictive pericarditis.

1-acute pericarditis

• This refers to inflammation of the pericardium. Classically, fibrinous material is deposited into the pericardial space and pericardial effusion often occurs.

• Acute pericarditis has numerous aetiologies Most commonly in the UK, it is due to viral infection and myocardial infarction, although in many

• cases the cause is unknown.

Type • Viral pericarditis: The most common viral causes areCoxsackie B virus and echovirus. Viral pericarditis isusually painful but has a short time course and rarelylong-term effects. • Post-myocardial infarction pericarditis: occurs in about 20%

of patients in the first few days following MI.. It may be difficult to differentiate this pain from recurrent angina when it occurs early (day 1-2 post- infarct) but a good history of the pain and serial ECG monitoring is helpful.

• Pericarditis may also occur later on in the recovery phase after infarction.

• Uraemic pericarditis: is due to irritation of thepericardium by accumulating toxins. It can occur in 6-10% of patients with advanced renal failure if dialysis isdelayed. • Bacterial pericarditis :may rarely occur with septicaemia or

pneumonia or it may stem from an early postoperative infection after thoracic surgery or trauma or may complicate endocarditis.

• Staphylococcus aureus is a frequent cause of purulentpericarditis in HIV patients. This form of pericarditis,especially staphylococcal, is fulminant and often fatal.

• Other endemic infectious pericarditis includes:mycoplasmosis and Lyme pericarditis which are ofteneffusive and require pericardial drainage. The diagnosisis based on serological tests of pericardial fluid andidentification of organisms in pericardial or myocardialbiopsies.

• Tuberculous pericarditis: usually presents with chronic low-grade fever, parti cularly in the evening, associated with features of acute pericarditis, dyspnoea, malaise, night sweats and weight loss.

• Fungal pericarditis: is a common complication of endemic fungal infections, such as histoplasmosis and coccidioidomycosis but may be also caused by Candida albicans, especially in immunocompromised patients, drug addicts or after cardiac surgery.

• Malignant pericarditis. :Carcinoma of the bronchus,

• carcinoma of the breast and Hodgkin's lymphoma are the most common causes of malignant pericarditis. Leukaemia and malignant melanoma are also associated with pericarditis.

etiology• Infectious pericarditisViral (Coxsackievirus, echovirus, mumps, herpes, HIV)Bacterial (staphylococcus, streptococcus,pneumococcus, meningococcus, Haemophilu influenzae, mycoplasmosis,

borreliosis, Chlamydia)TuberculousFungal (histoplasmosis, coccidioidomycosis, Candida)• II. Post-myocardial infarction pericarditisAcute myocardial infarction (early)Dressler's syndrome (late)• III. Malignant pericarditisPrimary tumours of the heart (mesothelioma) Metastaticpericarditis (breast and lung carcinoma, lymphoma,leukaemia, melanoma)

• IV. Uraemic pericarditis• V. Myxoedematous pericarditis• VI. Chylopericardium• VII. Autoimmune pericarditisCollagen-vascular (rheumatoid arthritis, rheumatic fever,systemic lupus erythematosus, scleroderma)Drug-induced (procainamide, hydralazine, isoniazid,doxorubicin, cyclophosphamides)• VIII. Post-radiation pericarditis• IX. Post-surgical pericarditisPostpericardiotomy syndrome• X. Post-traumatic pericarditis• XI. Familial and idiopathic pericarditis

Clinical features

• Pericardial inflammation produces sharp central chest

• pain exacerbated by movement, respiration and lyingdown. It is typically relieved by sitting forward.

• It may be referred to the neck or shoulders. • The main differential diagnoses are angina• and pleurisy.

The classical clinical sign is• a pericardial friction rub occurring in three phases corresponding to atrial

systole, ventricular systole and ventricular diastole. It may also be heard as a biphasic 'to and fro' rub.

• The rub is heard best with the diaphragm of the stethoscope at the lower left sternal edge at the end of expiration with the patient

leaning forward.

• There is usually a fever, leucocytosis or lymphocytosis when pericarditis is due to viral or bacterial infection, rheumatic fever or myocardial infarction.

• Large pericardial effusion can compress adjacent bronchi and lung tissue and may cause dyspnoea.

• Investigations• ECG is diagnostic. There is concave-upwards (saddle-shaped)

• ST elevation .These changes evolve over time, with resolution of the ST elevation, T wave flattening/inversion and finally T wave normalization.

• The early ECG changes must be differentiated from ST• elevation found in myocardial infarction .

• Sinus tachycardia may result from fever or haemodynamic• embarrassment, and rhythm and conduction

• abnormalities may be present if myocardium is involved.

• Cardiac enzymes should be assayed as they may be• elevated if there is associated myocarditis

• Chest X ray, echocardiograms and radionucleotide• scans are of little value in un complicated acute

• pericarditis.

ECGs associated with pericarditis. (a) Acute pericarditis. Note the raised ST segment, concave

upwards (arrow), (b) Chronic phase of pericarditis :associated with a pericardial effusion. Note the T

wave flattening and inversion and the alternation of the QRSamplitude (QRS alternans).

(c) The same patient after evacuation of the pericardial fluid. Note that the QRS voltage has increased and the T waves have returned to normal.

2-Pericardial effusion and cardiactamponade

• A pericardial effusion is a collection of fluid within the potential space of the serous pericardial sac as in the figure

• commonly accompanying an episode of acute pericarditis.

• When a large volume collects in this space, ventricular filling is compromised leading to embarrassment of the circulation. This is known as cardiac tamponade.

Chest X-ray showing a pericardial effusion,the heart appears globular.

Chest X-ray showing a peric ardialcalcification (arrow).

Valvular Heart Disease

Types

• Mitral Stenosis• Mitral Regurgitation• Mitral Valve Prolapse• Aortic Stenosis• Aortic regurgitation• Tricuspid valve is affected infrequently

– Tricuspid stenosis – causes Rt HF– Tricuspid regurgitation –causes venous overload

Rheumatic Heart Disease

• Inflammatory process that may affect the myocardium, pericardium and or endocardium

• Usually results in distortion and scarring of the valves

Rheumatic Heart Disease, cont.

• Subjective symptoms– Prior history of rheumatic fever– General malaise– Pain – may or may not be present

• Objective symptoms– Temperature – Murmurs– Dyspnea– polyarthritis

Rheumatic Heart Disease

• Diagnosis– H/P– WBC and ESR– C-reactive protein– Cardiac enzymes– EKG– Chest x-ray– Echo– Cardiac cath– Cardiac output

Rheumatic Heart Disease

• Nursing Care– Vital signs– Rest and quiet environment– Give antibiotics, digitalis, and diuretics– Provide adequate nutrition– Monitor I/O– Explain treatment and home care

Mitral Stenosis• Usually results from rheumatic carditis• Is a thickening by fibrosis or calcification• Can be caused by tumors, calcium and thrombus • Valve leaflets fuse and become stiff and the cordae tendineae

contract• These narrows the opening and prevents normal blood flow

from the LA to the LV• LA pressure increases, left atrium dilates, PAP increases, and

the RV hypertrophies• Pulmonary congestion and right sided heart failure occurs• Followed by decreased preload and CO decreases

Mitral Stenosis, cont.

• Mild – asymptomatic• With progression – dyspnea, orthopneas, dry cough,

hemoptysis, and pulmonary edema may appear as hypertension and congestion progresses

• Right sided heart failure symptoms occur later • S/S

– Pulse may be normal to A-Fib– Apical diastolic murmur is heard

Mitral Regurgitation• Primarily caused by rheumatic heart disease, but may be

caused by papillary muscle rupture form congenital, infective endocarditis or ischemic heart disease

• Abnormality prevents the valve from closing• Blood flows back into the right atrium during systole• During diastole the regurg output flows into the LV with the

normal blood flow and increases the volume into the LV• Progression is slowly – fatigue, chronic weakness, dyspnea,

anxiety, palpitations• May have A-fib and changes of LV failure• May develop right sided failure as well

Mitral Valve Prolapse• Cause is variable and may be associated with

congenital defects• More common in women• Valvular leaflets enlarge and prolapse into the LA

during systole• Most are asymptomatic• Some may report chest pain, palpitations or exercise

intolerance• May have dizziness, syncope and palpitations

associated with dysrhythmias• May have audible click and murmur

Aortic Stenosis• Valve becomes stiff and fibrotic, impeding blood flow with LV contraction• Results in LV hypertrophy, increased O2 demands, and pulmonary

congestion• Causes – rheumatic fever, congenital, arthrosclerosis• Atherosclerosis and calcification is primary cause in the elderly• Complications – right sided heart failure, pulmonary edema, and A-fib• S/S – Early: dyspnea, angina, syncope Late: marked fatigue, debilitation, and peripheral

cyanosis, crescendo- decrescendo murmur is heard

Aortic Regurgitation• Aortic valve leaflets do not close properly during diastole• The valve ring that attaches to the leaflets may be dilated, loose, or

deformed• The ventricle dilates to accommodate the ^ blood volume and

hypertrophies• Causes: infective endocarditis, congenital, hypertension, Marfan’s • May remain asymptomatic for years• Develop dyspnea, orthopnea, palpitations, ,and angina• May have ^ systolic pressure with bounding pulse• Have a high pitch, blowing, decrescendo diastolic murmur

Assessment for Valve Dysfunction

• Subjective symptoms– Fatigue– Weakness– General malaise– Dyspnea on exertion– Dizziness– Chest pain or discomfort– Weight gain – Prior history of rheumatic heart disease

Assessment, cont.

• Objective symptoms– Orthopnea– Dyspnea, rales– Pink-tinged sputum– Murmurs– Palpitations– Cyanosis, capillary refill– Edema– Dysrhythmias– Restlessness

Diagnosis

• History and physical findings• EKG• Chest x-ray• Cardiac cath• Echocardiogram

Anatomy

Acquired Heart DiseaseSmall Heart

RADIOGRAPHIC FEATURES OF AORTIC STENOSIS

• Enlargement of the ascending aorta due to poststenotic dilatation

• Mild or no cardiomegaly in compensated stage

• Substantial cardiomegaly occurs only after myocardial failure has ensued

• No pulmonary venous hypertension or pulmonary edema is seen during most of the course of this disease

• Calcification of aortic valve may be discernible on radiograph but is more readily shown on CT

RADIOGRAPHIC FEATURES OF ARTERIAL HYPERTENSION

• Enlargement of the thoracic aorta—ascending, arch, and descending aorta

• Mild or no cardiomegaly until the onset of myocardial failure

• No pulmonary edema or pulmonary venous hypertension until the occurrence of diastolic dysfunction due to severe left ventricular hypertrophy or myocardial failure

RADIOGRAPHIC FEATURES OF MITRAL STENOSES

• Pulmonary venous hypertension or edema is present

• Pulmonary edema may be observed intermittently

• Mild cardiomegaly is seen in isolated mitral stenoses

• Enlargement of the left atrium is characteristic

• Enlargement of the left atrial appendage is frequent and suggests a rheumatic etiology

• Right ventricular enlargement indicates some degree of pulmonary arterial hypertension or associated tricuspid regurgitation.

RADIOGRAPHIC FEATURES OF MITRAL STENOSES

• Enlargement of the pulmonary arterial segment is indicative of associated pulmonary arterial hypertension

• Right ventricular enlargement in the absence of prominence of the main pulmonary artery suggests associated tricuspid regurgitation. The right atrium is also enlarged with tricuspid regurgitation

• The ascending aorta and aortic arch are usually inconspicuous in isolated mitral stenosis. Even slight enlargement of the thoracic aorta raises the question of associated aortic valve disease

RADIOGRAPHIC FEATURES OF HYPERTROPHIC CARDIOMYOPATHY

• Normal in most patients• Mild cardiomegaly and pulmonary

venous hypertension in a minority of patients

• Left atrial enlargement can be caused by associated mitral insufficiency or reduced left ventricular compliance

• In the obstructive form (subaortic stenosis), ascending aortic enlargement is infrequent

• Left ventricular enlargement may occur in end-stage disease

RADIOGRAPHIC FEATURES OF RESTRICTIVE CARDIOMYOPATHY

• Pulmonary venous hypertension is typical

• Pulmonary edema may occur intermittently

• Normal heart size or mild cardiomegaly in most patients

• Left atrial enlargement• Left atrial appendage is typically

not enlarged• Moderate to severe cardiomegaly

can ensue in end-stage disease

RADIOGRAPHIC FEATURES OF ACUTE MYOCARDIAL INFARCTION

• Normal chest x-ray in about 50% of first acute infarctions

• Normal heart size with pulmonary venous hypertension or pulmonary edema in about 50% of first acute infarctions

• Cardiomegaly is usually indicative of acute infarction in a patient with history of previous infarctions

• Cardiomegaly may be indicative of ischemic cardiomyopathy

RADIOGRAPHIC FEATURES OF ACUTE MYOCARDIAL INFARCTION

• Signs of complication of acute myocardial infarction

• Intractable pulmonary edema may occur with papillary muscle rupture (mitral regurgitation) or ventricular septal rupture (left to right shunt).

• Enlarged cardiac silhouette may be caused by pericardial effusion.

• Abnormal cardiac contour may be a sign of true (bulge of the anterolateral or apical regions) or false (bulge of the posterior or diaphragmatic regions) aneurysms

RADIOGRAPHIC FEATURES OF CONSTRICTIVE PERICARDITIS

• Pulmonary venous hypertension• Normal heart size or mild

cardiomegaly• Left atrial enlargement may be

discernible• Flattened cardiac contours are

pathognomonic but infrequently observed

• Calcification of the cardiac margin, especially the atrioventricular and interventricular grooves

Acquired Heart DiseaseLarge Heart

RADIOGRAPHIC FEATURES OF AORTIC REGURGITATION

• Absence of pulmonary venous hypertension or pulmonary edema until late in the course of this lesion

• Moderate to severe cardiomegaly • Left ventricular enlargement• Enlargement of ascending aorta and

aortic arch

RADIOGRAPHIC FEATURES OF MITRAL REGURGITATION

• Variable degree of pulmonary venous hypertensive or pulmonary edema (less severe than with mitral stenosis)

• Moderate to severe cardiomegaly• Left ventricular enlargement• Left atrial enlargement• Enlargement of left atrial

appendage

RADIOGRAPHIC FEATURES OF TRICUSPID REGURGITATION

• No pulmonary venous hypertension or pulmonary edema (isolated tricuspid regurgitation)

• Pulmonary venous hypertension or edema indicates associated mitral valve disease

• Moderate to severe cardiomegaly• Right ventricular enlargement• Right atrial enlargement

RADIOGRAPHIC FEATURES OF CONGESTIVE (DILATED) CARDIOMYOPATHY

• Pulmonary venous hypertension or pulmonary edema may be but is not invariably present

• Moderate to severe cardiomegaly• Left ventricular enlargement• Left atrial enlargement is

infrequently evident but can be caused by mitral regurgitation caused by left ventricular enlargement

Congestive Heart Failure

Cardiomegaly, increased pulmonary vascular markings, fluid in the horizontal fissure

CHF

Kerley B Lines

Short (1 -2 cm) white lines at the lung bases, perpendicular to the pleural surface representing distended interlobular septa

What do the arrows indicate?

RADIOGRAPHIC FEATURES OF PERICARDIAL EFFUSION

• No pulmonary venous hypertension or pulmonary edema

• Moderate to severe enlargement of cardiac silhouette

• Associated pleural effusion is not uncommon

• Specific features, such as “fat pad” and/or “variable density” signs, are infrequently evident

ENLARGEMENT OF MAIN PULMONARY ARTERY

• Etiology– Pulmonary arterial hypertension– Excess pulmonary blood flow (left to

right shunts, chronic high output states)– Valvular pulmonic stenosis– Pulmonary regurgitation– Congenital absent pulmonary valve

(aneurysmal pulmonary artery)– Absence of left pericardium– Aneurysm of pulmonary artery– Idiopathic dilatation of pulmonary

artery

Cardiac Calcification• Ascending aortic calcification

– Most frequently observed on the right anterolateral margin of the ascending aorta in elderly individuals, especially in the presence of aortic valve disease.

– In the past, it was considered to be a characteristic of syphilitic aortitis.

• Mitral annular calcification– Dense C-shaped calcification in the region of the mitral valve. – It may be a causative factor of mitral regurgitation. – It is frequently observed in apparently normal elderly patients.

• Aortic annular calcification– A circular calcification in the region of the aortic valve. – Extension of this calcification into the region of the conducting system can produce complete heart

failure.

• Valvular calcification (aortic and mitral). – Calcification of the aortic valve of sufficient density and extent to be visualized on the radiograph is

nearly always associated with hemodynamically important aortic stenosis (gradient more than 50 mm Hg).

Cardiac Calcification• Coronary arterial calcification

– Coronary arterial calcification is frequently observed by fluoroscopy or CT. – It must be both dense and extensive to be recognized on the thoracic radiograph.

• Left ventricular mural calcification– Most frequently located in the anterolateral or apical regions of the left ventricle and marks the site

of a transmural MI or aneurysm.

• Pericardial calcification– Indicative of constrictive pericarditis. – Located usually in the interventricular or atrioventricular grooves of the heart.

• Unusual sites– Intracardiac tumor (left atrial myxoma), – Pericardial tumor (dermoid), or – Healed granulomas (myocardial tuberculoma). – An extremely rare process of the left ventricle, Loeffler's eosinophilic fibroplasia, can cause

calcification of the left ventricular wall.

Cardiac Calcification

Cardiac CT Angiography

Cardiac CT Angiography

Coronary CT angiography

Coronary CT angiography