CARDIOVASCUL AR

DISEASES

DR. MAAHAM (PT)

D E M O N S T R AT O R I P M & R
CONTENTS

• CARDIOVASCULAR DISEASES
• ISHCHEMIC HEART DISEASES
• VALVULAR HEART DISEASES
INTRODUCTION

• The term ‘cardiovascular disease’ encompasses all diseases and

conditions of the heart (cardiac disease) and vascular system, both
noncommunicable and communicable.
• The health burden of cardiovascular disease is immense;
cardiovascular disease is the single largest cause of death worldwide
(responsible for approximately 30% of all deaths) and one of the
leading contributors to lost disability-adjusted life-years
ISCHEMIC HEART DISEASE

• The human heart comprises a pair of functionally separate, valved

muscular pumps, contained structurally as a single organ.
• atrial muscle,
• ventricular muscle
• specialized excitatory and conductive muscle FIbres
• As with all muscle tissue, the myocardium (the cardiac muscle)
requires energy to produce contractile force.
• Uniquely, the myocardium relies almost exclusively on oxidative
metabolism for its function; even at rest the heart operates at near
maximal oxygen extraction.
AETIOLOGY AND PATHOPHYSIOLOGY O
ISCHAEMIC
HEART DISEASE

• Ischaemic heart disease (IHD) is characterized by a relative decrease

in myocardial perfusion, such that perfusion is inadequate to meet the
metabolic demands of the myocardium.
• As IHD is most commonly caused by atherosclerosis of the coronary
arteries, the terms ‘IHD’, ‘coronary heart disease’ and ‘coronary artery
disease’ are often used interchangeably.
• Atherosclerosis is a chronic and progressive inflammatory disease of
the arterial endothelium.
• atherosclerotic ‘plaques’,
• Advanced coronary atherosclerosis presents clinically as IHD.
• expanding atheroma encroaches on the coronary artery lumen to such
a degree that blood flow is impeded or (2) when acute plaque
disruption leads to thrombosis and vessel occlusion.
RISK FACTORS

• Smoking
• Hypertension
• Diabetes mellitus
• Dyslipidaemia
• Diet
• Physical inactivity
• Obesity
• Social isolation
• Depression
NON MODIFIABLE

• Advanced age
• Male gender
• Family history of ischaemic heart disease
• Poor socioeconomic status
• Indigenous/ aboriginal
SYMPTOMS AND SIGNS O ISCHEMIC
HEART DISEASE

• The primary clinical manifestations of IHD are stable angina, unstable

angina pectoris (UAP) and acute myocardial infarction (AMI).
• Stable angina occurs when coronary perfusion fails to meet increased
metabolic demand, which may occur during exercise or tachycardia.
STABLE ANGINA

• Stable angina is ‘associated with a (temporary) disturbance in

myocardial function, (but) without myocardial necrosis’, and typically
presents as retrosternal pain/discomfort (angina pectoris) that is
relieved by rest or nitrate medications.
• Other symptoms of stable IHD include exertional dyspnoea and a
reduced exercise capacity.
• Some individuals, particularly those with diabetes mellitus, may be
asymptomatic.
UNSATBLE ANGINA

• UAP and AMI, collectively referred to as ‘acute coronary syndromes’,

can be life-threatening and occur when physical disruption of an
atherosclerotic plaque triggers thrombosis.
• The formation of thrombus (blood clot) within the artery leads to
subtotal or total occlusion
• UAP typically presents as frequent and prolonged episodes of
retrosternal pain or discomfort, often at rest or with minimal exertion;
myocardial necrosis is absent.
ACUTE MYOCARDIAL
INFRACTION
• AMI with myocardial necrosis occurs when thrombosis and reactive
coronary arteriospasm cause prolonged (>20 minutes)myocardial
ischaemia.
• AMI may also occur without symptoms, but typically presents as
prolonged ‘chest, upper extremity, jaw or epigastric discomfort/pain
with exertion or rest’ and/or dyspnoea, diaphoresis,nausea and
syncope
DIAGNOSIS O ISCHEMIC
HEART DISEASE
• A provisional diagnosis of IHD is normally made on the basis of risk
and the presence of ischemic symptoms.
• As noted by the American College of Cardiology (ACCF)/AHA,
‘once a diagnosis of IHD is established, it is necessary in most
patients to assess their risk of subsequent complications, such as AMI
or death’
• A normal ECG does not exclude IHD, however, as IHD-related ECG
changes may be transient.
• In the absence of an acute coronary syndrome, a progressive exercise
or ‘stress’ test with ECG monitoring is usually conducted to confirm a
provisional diagnosis of IHD.
• Coronary angiography (i.e. arteriography) is used in both stable IHD
and acute coronary syndromes to assess coronary artery anatomy
DIAGNOSIS OF ACUTE
MYOCARDIAL INFARCTION
• AMI is presumed, and treatment instigated, when an individual
presents with prolonged and/or severe ischemic symptoms.
• If the ECG shows ST-segment elevation (a typical ECG finding of
AMI) in two contiguous ECG leads, the AMI is designated an ST-
segment elevation myocardial infarction (STEMI)
• AMI is confirmed using blood tests for biomarkers of myocardial
necrosis, most commonly cardiac troponin levels
MEDICAL MANAGEMENT OF ISCHEMIC
HEART DISEASE

• Medication
• Modification of risk factors
• Coronary Revascularization
• Coronary artery bypass
CARDIAC VALVE DISEASE

• The four cardiac valves (left side of heart: aortic and mitral valves,
right side: pulmonary and tricuspid valves control the direction and
timing of blood flow within and from the heart.
• The term ‘cardiac valve disease’ encompasses a range of pathological
conditions, whereby restriction to valve opening (stenosis) leads to
obstruction of flow and increasing transvalvular gradient (pressure
overloading) and/or inadequate valve closure (incompetence) leads to
valvular regurgitation (volume overloading).
AETIOLOGY AND PATHOPHYSIOLOGY O
CARDIAC
VALVE DISEASE

• There are various and potentially interacting aetiologies of cardiac

valve disease, including congenital valve malformations, age-related
degenerative changes and rheumatic disease.
AORTIC STENOSIS

• The three most common aetiologies of aortic stenosis (AS) are

congenital malformation (usually a bicuspid aortic valve), age-related
degenerative (aka ‘calci c’) changes and rheumatic disease.
• All result in progressive leaflet thickening and/or commissural fusion.
• A reduction in valve leaflet motion reduces aortic valve (left
ventricular outlet) area, usually over decades; this reduced outlet area
in turn leads to pressure overloading of the left ventricle. Left
ventricular hypertrophy
• (LVH) occurs to compensate for chronic pressure overloading and
initially, normal cardiac output is maintained.
• With time, the hypertrophic adaptation may become inadequate to
maintain systolic function, and cardiac output is impaired, resulting in
(pre)syncope.
• The hypertrophied left ventricle also has an increased perfusion
demand, and is therefore at greater risk of ischaemia.
SIGN AND SYMPTOMS

• AS is often diagnosed before the onset of symptoms,e.g. when a

routine physical examination reveals a systolic cardiac murmur.
• Individuals with known AS, monitored over time, most commonly
present with progressive exertional dyspnoea, fatigue and a reduced
exercise capacity.
• Individuals with severe AS will often also present with angina, related
to concomitant coronary atherosclerosis and/or secondary to LVH.
• Presyncope (a sense of dizziness or faintness) or syncopal episodes
may occur, initially on exercise and ultimately at rest, when the
inability to increase cardiac output leads to hypotension and reduced
cerebral perfusion.
• Even mild symptoms may be indicative of moderate to severe AS,
requiring intervention.
AORTIC REGURGITATION

• Aortic regurgitation (AR) may be caused by disease of the valve

leaflets, e.g. degenerative disease (often aggravated by hypertension),
disease secondary to infective endocarditis, and/or disease of the wall
of the aortic root, e.g. Marfan syndrome.
• Subsequent failure of coaptation of the aortic leaflets leads to
increasing valvular insufciency and volume overloading of the left
ventricle.
• The left ventricle dilates (and may also hypertrophy) in response to
chronic volume overloading,ultimately leading to left ventricular
failure.
SYMPTOMS

• Individuals with AR are typically asymptomatic until late in the

disease course.
• Progressive exertional dyspnoea and orthopnoea (i.e. shortness of
breath when lying at) are the most common symptoms of severe,
chronic AR; individuals with AR may also report increased awareness
of the heartbeat (a ‘pounding’ of the heart) and angina, again
secondary to LVH.
• Mitral regurgitation (MR) may occur secondary to abnormalities of
the mitral valve leaflets themselves and/or the other components of the
mitral valve apparatus, i.e. the annulus, chordae tendineae and
papillary muscles.
• Major causes of MR are:
• (1) mitral valve prolapse syndrome, i.e. ‘billowing’ of leaflet(s) into
the left atrium, a primary cardiac condition of redundant mitral valve
leaflet tissue;
• (2) rheumatic heart disease (causing shortening, rigidity and retraction
of valve leaflets);
• (3) IHD (causing papillary muscle dysfunction)
• (4) annular dilatation (e.g. secondary to left ventricular dilatation, as
in dilated cardiomyopathy)
• In severe acute MR, left atrial and ventricular volume overload may
result in simultaneous pulmonary congestion and reduced cardiac
output.
• In chronic MR, however, compensatory left ventricular and atrial
changes may allow long term maintenance of cardiac output.
SYMPTOMS

• When MR develops gradually, symptoms may be minimal until MR is

of at least moderate degree.
• Dyspnoea and fatigue may be aggravated by the onset of AF.
• When severe MR develops abruptly (e.g. secondary to chordal
rupture) there is usually severe dyspnoea associated with acute
pulmonary oedema (APO).
RIGHT-SIDED CARDIAC
VALVE DISEASE
• Right-sided cardiac valve disease is almost always related to
rheumatic or congenital disease.
• Regurgitant disease most commonly occurs as a consequence of
annular dilatation, secondary to dilatation of the right ventricle
(tricuspid valve), or pulmonary hypertension(pulmonary valve).
• Any primary cardiac or pulmonary disease resulting in right
ventricular failure and/or pulmonary hypertension (or pulmonary
arterydilatation) might thus lead to tricuspid and pulmonic
regurgitation.
SYMPTOMS

• Right-sided valve lesions usually develop gradually and may only be

symptomatic (dyspnoea, fatigue,decreased exercise tolerance) late in
the disease course.
• Tricuspid endocarditis may be associated with infective pulmonary
embolism (PE).
MITRAL STENOSIS

• Mitral stenosis (MS) most commonly occurs as a consequence of

rheumatic fever, the incidence of which has been reduced by the use
of antibiotics for streptococcal infection.
• Rheumatic fever causes thickening, scarring and calcification of the
valve leaflets, which in turn reduces the left ventricular inlet area.
• Left atrial and pulmonary venous pressures become elevated, leading
to left atrial enlargement (which may predispose to atrial fibrillation
(AF) and hence thromboembolism), pulmonary congestion and
oedema.
• Pulmonary hypertension may lead ultimately to right sided heart
failure.
SYMPTOMS

• Not with standing that MS is a progressive, life-long disease, there is

often a long latent period (10 to 40 years) before development of
symptoms.
• Similarly, once present, typical symptoms of dyspnoea, fatigue and a
decreased exercise tolerance may remain mild until late in the disease
course.
• The first presenting symptom of MS is often related to AF and/or a
consequent embolic event.
DIAGNOSIS O CARDIAC
VALVE DISEASE
• Cardiac valve disease is most commonly diagnosed (or suspected)
when cardiac auscultation reveals a cardiac ‘murmur’, i.e. turbulent
flow.
• The timing of murmurs (in relation to the cardiac cycle); the
location(s) at which they can be heard and their pitch, duration and
intensity can all be used to aid provisional diagnosis of cardiac valve
disease.
• Depending on the type of murmur, the patient and the (degree of)
symptoms, further diagnostic testing may be indicated.
• Echocardiography is the initial mode of imaging in suspected cardiac
valve disease, and is recommended for all patients with murmurs and
associated cardiac signs.
• ECG is also indicated in the diagnosis and evaluation of cardiac valve
disease, and may give an indication of compensatory changes in
cardiac structure,e.g. increased QRS amplitude in precordial leads and
augmented vector left (aVL) secondary to LVH.
• Chest radiography may demonstrate changes in cardiac structure
(shape/size), albeit less clearly than echocardiography