HYPERTENSIVE VASCULAR AND HEART DISEASES

Vascular SMCs are the dominant cell type of the vessel media can Migrate and proliferate in
response to various mediators (eg.platelet-derived growth factor, endothelin, thrombin,
fibroblast growth factor)
• Elaborate cytokines and growth factors. Synthesize and remodel ECM
Constrict or dilate in response to physiologic or pharmacologic stimuli

PRIMARY/ ESSENTIAL HTN SECONDARY HTN

RENOVASCULAR HTN/ RENAL ARTERY STENOSIS

CAUSES

RISK FACTORS

COMPLICATIONS

injured endothelium and underlying vessel wall "heal" by stimulating SMC ingrowth and CM production, leading to intimal
thickening, a so-called neointima.
The neointimal cells have a proliferative and synthetic phenotype distinct from the underlying media, and the cells may
derive from vessel wall or circulating precursors. In small-to-medium-sized vessels (e.g., coronary artery) such intimal
thickening can cause luminal stenosis and downstream tissue ischemia

SYSTEMATIC HYPERTENSIVE HEART DISEASE PULMONARY HYPERTENSIVE HEART DISEASE

CLINICAL FEATURES CAUSES

Acute Chronic

MALIGNANT HTN Hypertensive Emergency

Grade 1 features are

BEGNIN HTN thickened and tortuous
arteries with increased
reflectiveness.
Grade 2 features are
arteriovenous nipping
along with grade 1
grade 3 retinopathy are
blot or flame-shaped
retinal hemorrhages
and hard 'c otton wool'
exudates along with
grade 1 and 2 features.
Hypertensive Urgency features.
Garde 4 comprises of all
these features plus
papilledema.
 ARTERIOSCLEROSIS

ATHEROSCLEROSIS PATHOGENESIS ROLE OF INFLAMMATION

COMMON SITES

ROLE OF HYPERLIPIDEMIA

SYMPTOMS RISK FACTORS

MORPHOLOGICAL STAGES

COMPLICATIONS

ARTERIOLOSCLEROSIS

MÖNKEBERG MEDIAL CALCIFIC SCLEROSIS

HYPERPLASTICITY ARTERIOLOSCLEROSIS HYALINE ARTERIOLOSCLEROSIS

Endothelial injury --> Accumulation of lipoproteins in vessel walls --> platelet adhesion --> Monocyte adhesion to
endothelium and foam cell formation --> Lipid accumulation in the macrophages --> smooth muscle cell recruitment
--> smooth muscle cell proliferation and ECM production. Inflammation is about the final step.

The artery most commonly affected by thrombosis leading to myocardial infarction (MI) is the left anterior descending
artery. It contributes to 40-50% of all the cases of MI.
The right coronary artery is involved in 30-40% of cases.
The left circumflex artery is involved in 15-20% of cases.

C-reactive protein (CRP) is an acute phase reactant that is involved in innate immunity. It is made by the liver and its
expression is particularly induced by IL-6. CRP is a pro-inflammatory marker in atherosclerotic disease, which means that
high levels of CRP are suggestive of an inflammatory response.

Unstable or vulnerable plaques are at a greater risk of rupture than stable plaques. Features of unstable plaques include a
thin fibrous cap with few smooth muscle cells, a large lipid core, and extensive inflammation with large numbers of foamy
macrophages.

The following are the types of acute plaque changes:

-Rupture or fissuring
-Erosion or ulceration
-Bleeding into plaque

A type IV atherosclerotic lesion is an atheroma which consists of intracellular lipid accumulation and a core of
extracellular lipid.
Isolated macrophage foam cells are present in an initial (type I) lesion.
Lipid accumulation and small extracellular lipid pools are characteristic of a type III lesion.
A type V lesion, called fibroatheroma, consists of one or more lipid cores with calcific or fibrotic layers.
Surface defect or hematoma or thrombus signifies a type VI lesion.

The earliest feature of atherosclerosis is pathologic intimal thickening, which includes small, extracellular lipid
accumulations (lipid pools) which are rich in proteoglycans and hyaluronan.
Macrophage infiltration and foam cell formation is the following step that signifies progression to fibroatheroma.
Fibrosis and calcification are generally late stage developments in all inflammatory conditions throughout the body.

Hyperhomocysteinemia is one of the minor causes of atherosclerosis due to elevated circulating

homocysteine levels. Low folate and vitamin B12 levels can increase homocysteine. Homocystinuria is a
rare inborn error of metabolism and can also result in hyperhomocysteinemia (levels greater than 100
umol/L).

Upper extremity vessels and the renal and mesenteric arteries are usually spared from atherosclerotic plaques
except at their ostia, which are small, slit-like openings in vessels. Lower abdominal aorta, the circle of Willis,
popliteal arteries, and coronary arteries are all extensively involved and not just at their ostia.

In chronic obstruction there is formation of collaterals as the atherosclerosis progresses which is very important in
extending the life of a patient of atherosclerosis.
AORTIC DISSECTION DISSECTION AND ANEURYSM

CAUSES COMPLICATIONS

PRESENTATION

TYPE A Acute (2/3), THORACIC ANEURYSM

chronic (1/3)
Ascending (65%),
arch (20%),
descending thoracic (10%),
abdominal (5%)
COMPLICATIONS
TYPE B

SYPHILITIC ANEURYSM
Aortic dissection is due to an intimal
tear usually in the ascending aorta. It
ANEURYSM can rupture the adventitia and cause
bleeding.
Sometimes, there is another intimal
tear in the aorta through which the
True aneurysm False aneurysm blood returns to the lumen; this
creates another vascular channel
leading to a "double-barreled" aorta.
Endothelialization of these false
channels leads to chronic dissections.

ABDOMINAL ANEURYSM PRESENTATION

TREATMENT
INVESTIGATION

lungs and air ways (causing difficulty in breathing),

the esophagus (causing dysphagia), and the recurrent
laryngeal nerves (causing coughing). Bone pain results
from the erosion of ribs and vertebral bodies. Cardiac
dysfunction may occur as a result of valve
regurgitation due to aortic dilation, or myocardial
infarction due to the narrowing of the coronary
CAUSES Inflammatory AAA Mycotic AAA ostia. The aneurysm may also rupture.

COMPLICATIONS RISK FOR RUPTURE

 VASCULITIS

LARGE VESSEL VASCULITIS

TEMPORAL (GIANT CELL) ARTERITIS CLINICAL FEATURES TAKAYASU ARTERITIS CLINICAL FEATURES

MANAGEMENT DIAGNOSIS
MANAGEMENT DIAGNOSIS

MEDIUM VESSEL VASCULITIS

CLINICAL FEATURES

POLYARTERITIS NODOSA

DIAGNOSIS

MANAGEMENT

KAWASAKI DISEASE/MUCOCUTANEOUS
BUERGER DISEASE/THROMBOANGIITIS OBLITERANS LYMPH NODE SYNDROME
CLINICAL FEATURES MANAGEMENT

CLINICAL FEATURES

MANAGEMENT

The triad of oral ulcers, genital ulcers, and uveitis (inflammation of the
uvea in eyes) is a classical presentation of Behcet disease, a chronic
systemic vasculitis. This disease is particularly associated with HLA-B51.
Some viral agents are known to trigger Behcet's disease
 SMALL VESSEL VASCULITIS

MICROSCOPIC POLYANGIITIS DIAGNOSIS

CHURG-STRAUSS SYNDROME

CLINICAL FEATURES
DIAGNOSIS
CLINICAL FEATURES

MANAGEMENT

HENOCH-SCHÖNLEIN PURPURA WEGNER GRANULOMATOSIS CLINICAL FEATURES

CLINICAL FEATURES

MANAGEMENT
MANAGEMENT
DIAGNOSIS
DIAGNOSIS

vasculitis affecting the veins:

Buerger disease
Leukocytoclastic vasculitis
Behcet disease

Granulomatosis with polyangiitis is a focal necrotizing

vasculitis involving the nasopharynx, lungs, and kidneys.
Clinical features include chronic sinusitis, otitis media,
hemoptysis, cough, and hematuria. Biopsy shows
necrotizing granulomas along with necrotizing
vasculitis, and in the kidneys, glomerulonephritis. Serum
c-ANCA levels are a measure of disease activity.
 DISORDERS OF BLOOD VESSEL HYPER-REACTIVITY, VEINS AND LYMPHATICS
SITE CAUSES
VARICOSE VEIN DEEP VENOUS THROMBOSIS

RISK FACTORS

LYMPHANGITIS
PHLEBOTHROMBOSIS
CLINICAL FEATURES
CAUSE
CAUSES SITE
CLINICAL FEATURES

COMPLICATIONS

LYMPHEDEMA

THROMBOPHLEBITIS
CAUSES CLINICAL FEATURES
 VASCULAR TUMORS
HEMANGIOMA BACILLARY ANGIOMATOSIS KAPOSI SARCOMA
benign capillary proliferation involving skin and visceral
organs in AIDS patients.
It is caused by gram-negative bacilli Bartonellahenselae
and Bartonellaquintana.
Red papules and nodules
Capillary proliferation
Neutrophilic inflammation
Are bright red to blue, and level with the Purplish granular material containing organisms
surface of the skin or slightly elevated, with
intact covering epithelium.
histologically lobulated, but "un-encapsulated"
aggregates of thin-walled capillaries.
Capillary hemangioma:
Small and well-circumscribed
skin
lips
liver
spleen
kidneys VASCULAR ECTASIAS
Cavernous hemangioma: It refers to group of lesions characterized by localized
Larger and less well circumscribed dilation of pre-existing vessels.
Most common benign tumor of liver and spleen. Nevus Flammeus:
Most threatening forms occur in brain most common form of ectasia,
head and neck.
dilation of vessels in the dermis.

Port-wine stains are type of NF that are large and

don’t fade
occur in the distribution of trigeminal ner ve may be ANGIOSARCOMA
ass w Sturge-Weber syndrome.

Spider Telangiectasia:
pulsatile array of dilated subcutaneous arteries about
a central core.
It blanches when pressure is applied to its center.
face, neck, upper chest, or abdomen.
ass. w hyperestrinism, cirrhosis and pregnancy.
CAUSES

GLOMUS TUMOR/GLOMANGIOMA
Glomus body is specialized arteriovenous anastomoses
that is involved in thermoregulation.
benign but painful tumor of the glomus body.
most common in the distal portion of the digits,
Pyogenic granulomas especially under the fingernails.
• Capillary hemangiomas that present as rapidly
growing red pedunculated lesions on the skin,
gingival, or oral mucosa. They bleed easily and
are often ulcerated.
• Curettage and cautery is usually curative.
• Pregnancy tumor (granuloma gravidarum)
• These lesions may spontaneously regress
(especially after pregnancy), or undergo fibrosis,
but occasionally require surgical excision

Juvenile hemangiomas (so-called "strawberry type" hemangiomas)

• of the newborn are extremely common (1 in 200 births) and can be multiple.
These arise in the skin and grow rapidly for a few months, but then fade by to 3 years of age
and completely regress by age 7 in the
Lymphangiomas
• Simple (capillary) lymphangiomas
• Slightly elevated Or sometimes pedunculated lesions up to 1 to 2 cm
• In diameter that occur predominantly in the head, neck, and axillary subcutaneous tissues.
• Lymphangiomas exhibit net works of endothelium-lined
• Spaces that can be distinguished from capillary channels only by the absence of red cells

Hemangioendothelioma
•clinical behaviours intermediate bet ween benign, well-differentiated Hemangiomas and frankly
anaplastic angiosarcomas

Epithelioid hemangioendothelioma
• It is a vascular tumor of adults occurring around medium and large-sized veins. Well-defined vascular
channels are
• Inconspicuous, and neoplastic cells are plump and often
• Cuboidal (resembling epithelial cells).
•most are cured by excision, but up to 40% recur, 20% to 30% eventually metastasize, and Perhaps 15%
of patients die of their tumor
Hemangiopericytoma.
• arise from pericytes, the myofibroblast-like cells associated with capillaries and venules.
Compensatory mechanisms:
• When cardiac workload increases or cardiac function is
HEART FAILURE Brain Natriuretic Peptide (BNT) is a cardiac neuro-hormone
produced by ventricular myocardium.
compromised, several physiologic mechanisms maintain can be used to help distinguish CHF from other causes of
arterial pressure and organ pertusion: dyspnea such as pulmonary embolus, asthma, and pneumonia.
BNP is increased in CHF. If BNP level is normal it excludes CHF.
• Frank-Starling mechanism: The higher the BNP, the higher the cardiovascular and all-
increased filling volumes dilate the heart and thereby increase cause mortality.
contractility and stroke volume
• Myocardial adaptations:
including hypertrophy with or without cardiac chamber Azotemia may be a consequence
dilation. of heart failure because reduced RIGHT-SIDED HEART FAILURE
• Activation of neurohumoral systems: renal perfusion leads to
to augment heart function and/or regulate filling volumes and inadequate excretion of
pressures: nitrogenous waste products.
• Catecholamines (nor-epinephrine)
Renin-Angiotensin- Aldosterone
• Atrial Natriuretic Polypeptide (ANP)

LEFT-SIDED HEART FAILURE CAUSES

CAUSES

CLINICAL FEATURES

Auscultation:

CLINICAL FEATURES

TREATMENT MORPHOLOGY

PATHOGENESIS
SYSTOLIC DYSFUNCTION DYSTOLIC DYSFUNCTION

Diseases of the Pulmonary Vessels

• Recurrent pulmonary thromboembolism
• Primary pulmonary hypertension
• Extensive pulmonary arteritis (e.g., Wegener granulomatosi
• Drug-, toxin-, or radiation-induced vascular obstruction
• Extensive pulmonary tumor micro-embolism

CLINICAL FINDINGS

Auscultation:

X-ray:
Following are the stages of heart failure according to
the American Heart Association (AHA) classification:
-Stage A: no structural defect and symptoms but a
high risk of developing heart failure
-Stage B: structural heart disease but no symptoms
-Stage C: previous or current symptoms of heart
failure with structural heart disease
-Stage D: advanced disease not responding to
treatment, requires specialized intervention
 CONGENITAL HEART DISEASE • 3% have a single gene defect,
• Genes of transcription factors (Septal defects)
• Proteins of signalling pathways (Tetalogy)
• Obstructive Congenital Heart Lesions • Strusctural proteins (Marfans synd)
• Congenital Heart Lesions that INCREASE • 13% have associated chromosomal abnormalities.
• Deletions (DiGeorge synd)
Pulmonary Arterial Blood Flow • Aneuploidy (Down's Synd....)
The first heart field expresses • Congenital Heart Lesions that DECREASE • 2-4% are associated with environmental or
the transcription factor
HAND1 whereas the second Pulmonary Arterial Blood Flow (Cynotic). maternal conditions & teratogenic influences.
• DM
heart field expresses the
transcription factor HAND2 • RUBELLA
and secreted protein fibroblast • TERATOGENS
growth factor 10.

RIGHT TO LEFT SHUNT/ CYANOTIC

TERATOLOGY OF FALLOT
CLINICAL FINDINGS

Auscultation:
X-ray:
ECG:

CLASSIC TERATOLOGY PINK TERATOLOGY

TRANSPOSITION OF GREAT ARTERIES

TRICUSPID ATRESIA

COMPLICATIONS
TREATMENT

TRUNCUS ARTERIOSUS Total Anomalous Pulmonary Venous Return (TAPVR):

no pulmonary veins directly join the left atrium. It
therefore drains into the left innominate vein or to
the coronary sinus.
when the common pulmonary vein fails to develop
It results in:
Volume and pressure hypertrophy of right atrium.
Volume and pressure hypertrophy of right ventricle.
Hypoplastic left atrium.
CLINICAL FINDINGS Normal left ventricle.
COMPLICATIONS

Eisenmenger Syndrome:
It refers to reversal of untreated left-to-right shunt into
right-to-left shunt.
It is characterized by cyanosis, clubbing and polycythemia.
It occurs when pulmonary vascular resistance (PVR) is more
than systemic vascular resistance (SVR).
 cyanosis may occur years later. Frequency: VSD > ASD > PDA.
LEFT TO RIGHT SHUNT/ ACYANOTIC OR LATE CYANOSIS

ATRIAL SEPTAL DEFECT COMPLICATIONS CLINICAL FINDINGS

Auscultation:

ECG:
TREATMENT

SECUNDUM ASD PRIMUM ASD SINUS VENOSUS

VENTRICULAR SEPTAL DEFECT CLINICAL FINDINGS SITES

Small defects Large defects

Pansystolic murmur
maximal at the left sternal
border
TREATMENT

PATENT DUCTUS ARTERIOSUS Auscultation: TREATMENT

COMPLICATIONS

ATRIOVENTRICULAR SEPTAL DEFECT PARTIAL AVSD COMPLETE AVSD

OBSTRUCTIVE CHF PRE-DUCTAL/INFANTILE TYPE

PULMONIC STENOSIS/ATRESIA
COARCTATION OF AORTA • Frequent
• Alone or with TOF or TGA
• Mild---asymptomatic compatible with life
• If 100% atretic, hypoplastic RV with
ASD---PDA
• Clinical severity ~ stenosis severity
POST-DUCTAL/ADULT TYPE • RVH
produce a systolic ejection murmur at the upper left
sternal border

AORTIC STENOSIS/ATRESIA
• VALVULAR
• If severe, hypoplastic LV- fatal
• Hypoplastic left ht synd (can only exist with PDA
Auscultation: COMPLICATIONS • SUB-valvular (subaortic)
• Aortic wall THICK BELOW cusps
X-ray: -HF, • SUPRA-valvular
-risk of cerebral hemorrhage • Aortic wall THICK ABOVE cusps in ascending aorta
ECG: (berry aneurysms), • Inherited
-aortic rupture • LVH
-possible infective endocarditis
The CHARGE syndrome is a combination of multiple congenital disorders; the initials of the names of the disorders give rise
to the acronym "CHARGE":
-Coloboma of the eye
-Heart defects such as atrial septal defect, ventricular septal defect, patent ductus arteriosus, hypoplastic right heart
-Atresia of the choanae
-Retardation of growth/development
-Genital and/or urinary abnormalities
-Ear anomalies
The genetic defect lies in the CHD7 gene which encodes for the chromodomain-helicase-DNA-binding protein 7. The
mutation results in defective function of helicase binding protein.

DiGeorge syndrome which occurs due to deletions of chromosome 22q11.2. This results in abnormal development of the
4th branchial arch as well as failure to develop the 3rd and 4th pharyngeal pouches, leading to defects of the thymus,
heart, and parathyroids. The multiple defects associated with this syndrome include cardiac abnormality, abnormal
facies, thymic aplasia, cleft palate, and hypocalcemia, all on chromosome 22 (remember the mnemonic CATCH-22).
 ISCHEMIC HEART DISEASE

RISK FACTORS

CHRONIC ISCHEMIC HEART DISEASE SUDDEN CARDIAC DEATH

CAUSES

ANGINA PECTORIS STABLE/TYPICAL ANGINA UNSTABLE/CRESCENDO ANGINA

PRINZMETAL VARIANT ANGINA

MYOCARDIAL INFARCTION BIOCHEMICAL CHANGES LOCALIZATION

RISK FACTORS TREATMENT

CAUSES
TYPES

Transmural infarction Subendocardial infarction

CLINICAL FINDING
 COMPLICATIONS
Arrhythmias
• Sinus Bradycardia: • Third-degree AV Block:
• Heart rate < 60. • Heart rate < 60.
• No cannon A-waves • Cannon A-waves

Ventricular Free Wall Rupture:

• It is the most com cause of cardiac rupture syndromes
postMI.
• It presents as cardiac tamponade and is usually fatal.
• It occurs most frequently at day 3 - 7 after the onset.
• Most com site = lateral wall at the mid-ventricular level.
Inter-ventricular Septal Rupture:
• It results in a ventricular septal defect and
therefore a left-to-right shunt.
• It presents as pansystolic murmur at left sternal
border radiating all over the precordium.
Papillary Muscle Rupture:
•It results in acute onset mitral regurgitation.
•It presents as pansystolic murmur at the apex
radiating to the axilla.
Right Ventricular Infarction:
•It is usually caused by inferior wall MI.
•It presents with hypotension, tachycardia, and
clear lungs on auscultation.
•ECG = ST-elevation in right sided V4 is the most
specific finding.
Treatment = high-volume fluid replacement.
Contractile dysfunction
• LV failure with hypotension
• Pulmonary congestion
• Pulmonary edema
• Cardiogenic shock

ACUTE CORONARY SYNDROME

•It refers to a range of thrombotic coronary diseases,
including unstable angina, non-ST elevation myocardial
infarction (NSTEMI), ST-elevation MI (STEMI), and
sudden cardiac death.
•It requires ECG and Cardiac enzymes for classification.
• Unstable Angina = cardiac chest pain, no ST elevation
on ECG, and no positive cardiac enzymes.
• NSTEMI = cardiac chest pain, no ST elevation on ECG,
but positive cardiac enzymes.
STEMI = cardiac chest pain + ST elevation on ECG +
positive cardiac enzymes.
•STEMI is defined by clinical symptoms plus any 1 of
following 3 ECG findings:
1. ST-segment elevation of 2 1 mm in t wo contiguous
limb leads.
2. ST-segment elevation of 22 mm in t wo contiguous
chest leads.
3. New left bundle branch block (LBBB) pattern.
 VALVULAR DISEASE
AORTIC STENOSIS
CAUSES SIGNS SYMPTOMS

MANAGEMENT

AORTIC REGURGITATION PRESENTATION

MANAGEMENT
CAUSES

MITRAL VALVE PROLAPSE CAUSES PRESENTATION COMPLICATIONS

MITRAL STENOSIS MITRAL REGURGITATION MANAGEMENT

CAUSES SIGNS PRESENTATION CAUSES

SYMPTOMS
MANAGEMENT
 RHEUMATIC FEVER ENDOCARDITIS
ACUTE SITES
INFECTIVE VEGETATION

RISK FACTORS
TYPES

Acute Sub-Acute

DIAGNOSIS

ORGANISMS PRESENTATION

COMPLICATIONS

LAB FINDINGS

Non-bacterial thrombotic Endocarditis

NON-INFECTIVE VEGETATION

Non-bacterial thrombotic Endocarditis Libman-Sacks Disease

CHRONIC

RISK FACTORS

COMPLICATIONS
 CARDIOMYOPATHIES

DILATED/CONGESTIVE CARDIOMYOPATHY HYPERTROPHIC CARDIOMYOPATHY RESTRICTIVE CARDIOMYOPATHY

CAUSES
CAUSES CAUSES

MORPHOLOGY

MORPHOLOGY

MORPHOLOGY

CLINICAL PRESENTATION

CLINICAL PRESENTATION

CLINICAL PRESENTATION

TREATMENT DIAGNOSIS

MYOCARDITIS

MORPHOLOGY CLINICAL PRESENTATION

CAUSES
 PERICARDITIS CONSTRICTIVE PERICARDITIS
It is a condition in which the heart is encased in a rigid pericardium.
FIBRINOUS/SEROFIBRINOUS PERICARDITIS CLINICAL PRESENTATION
SEROUS PERICARDITIS most common type of pericarditis.
Right-sided HF > left-sided HF.
Increased jugular venous pressure (VP) with prominent "y" descent
characterized by production of fibrin-rich exudate. Kussmaul's sign: JVP rising paradoxically with inspiration
production a clear, straw-colored, protein-rich exudate. Hepatomegaly, ascites, and peripheral edema.
Scant numbers of neutrophils, lymphocytes and ECG: Diastolic pericardial knock
Concave ST-segment elevation
macrophages. PR-depression CAUSES TREATMENT
50 - 200 mL Idiopathic (USA & UK) Treat the underiving cause.
CAUSES TB (worldwide) Surgical excision
accumulates slowly, and has rich protein content. Post-viral
Acute MI Radiation DIAGNOSIS
CAUSES Uremia Uremia CXR:
RF Chest radiation Post-cardiac surgery Small heart
SLE Rheumatoid arthritis-most common pericarditis in RHD Pericardial calcification
Scleroderma Dressler syndrome- pericarditis occurring within few
Tumors weeks of acute MI, autoimmune
Uremia
CLINICAL PRESENTATION
Loud pericardial friction rub (most characteristic)
PURULENT/SUPPURATIVE PERICARDITIS Signs of cardiac failure
Chest pain worse on inspiration, relieved by leaning for ward.
grossly cloudy or frankly purulent inflammatory exudate. Pulsus paradoxus - drop in systolic BP > 10 mmHg during
caused by infective organisms that invade the pericardium via:
inspiration.
Direct extension from neighboring inflammation (most common)
Seeding from the blood
Lymphatic extension HEMORRHAGIC PERICARDITIS
Direct introduction during cardiotomy characterized by bloody inflammatory exudate
Fluid is thin to creamy pus.
400 - 500 mL Malignant neoplastic involvement. (most common)
Causes mediastinopericarditis, as it spreads to mediastinum. Bacterial infections
Causes constrictive pericarditis due to intense inflammation. Bleeding diathesis
Tuberculosis

PERICARDIAL EFFUSION CASEOUS PERICARDITIS

Accumulation of serous fluid in the pericardial sac mostly tuberculous in origin.
• Chronic effusions of < 500ml has radiological most common cause of chronic constridive pericarditis
presentation
• Rapid effusions of 200-300ml can lead to Chronic pericarditis
devastating symptoms & fatal cardiac tamponade • It produces plaques like lesions with the pericardium
• Adhesive pericarditis. infections, post cardiac surgery, mediastinal radiation
• Leads to significant cardiac hypertrophy & dilation
• Constructive pericarditis, dense fibrous or fibrocalcific scar (plaster mold)
• Reduced cardiac output, muffled heart sounds
• elevated jugular venous pressure & peripheral edema

• Primary tumors of the heart are rare and less CARDIAC TUMORS
common than metastatic tumors to the heart and are
mostly benign (80 - 90% of cases) IlI. Metastatic Tumor:
•Myxomas Fibromas It is the most common tumor of heart.
•Lipomas • Most common cancer = lung and breast cancer
•Papillary fibroelastomas • Most common site = pericardium leads to pericardial effusion
•Rhabdomyomas • Most common route = retrograde lymphatic extension
•Angiosarcomas

I. Rhabdomyoma:
• Mostcommon primary tumor of heart in infants and children.
• ass w tuberous sclerosis
• hamartoma, affects ventricles
Spider cells:
• Large cells with glycogen-laden vacuoles separated by strands of
cytoplasm.
Strands of cytoplasm run from the plasma membrane to the centrally
located nucleus.

Il. Myxoma：
• Most common primary tumor of heart in adults.
• They are almost always single.
• They involve the left atrium in 90% of cases.
• Most common site = oval fossa in atrial septum
• may be ass w Carney syndrome in 10% of cases:(AD)
- Multiple cardiac myxomas.
- Multiple extra-cardiac myxomas (e.g. skin)
- Spotty pigmentation
- Endocrine over-activity