By Lisa Mohammed

A Complication
of Obesity !
 Hypertension, the ‘silent killer’ is one of the
most important preventable causes of
premature mortality worldwide.

 The World Health Report 2001 indicated

that high blood pressure is estimated to
cause 7.1 million deaths annually i.e. about
13% of all deaths.
 According to the Caribbean Health Research
Council : In the Caribbean, the prevalence
of hypertension is estimated to be 26% and
as high as 55% in studies of populations
over 25 and over 40 years, respectively.

 Figures from the Caribbean Epidemiology

Centre (CAREC) show that hypertensive
disease was the fifth leading cause of death
in 2000. Noting that the leading causes are
complications of Hypertension.
Sustained elevation of resting systolic BP, diastolic BP or Both

JNC 6 Category JNC 7 Category (2004)

SBP/DBP (mmHg)

Optimal <120/80 NORMAL

Normal 120-129/80-84
PREHYPERTENSION
Borderline 130-139/85-89

Hypertension >140/90

Stage 1 140-159/90-99 STAGE 1

Stage 2 (moderate) 160-179/100-109

STAGE 2
Stage 3 (severe) ≥180/110
 Hypertension can also be classified as:

1. Benign Hypertension

2. Malignant / Accelerated Hypertension

(Diastolic >120)
 Primary/Essential Hypertension: (Accounts for
90% of cases)

 Etiology is Multifactorial:

 Increased
peripheral resistance
(sympathetic tone)

 stress, hormonal, neural.

 Genetic, familial, life style.

 Secondary Hypertension: 5-10%

 Renal – GN, Renal Artery Stenosis, Renin tumors

 Endocrine
– Cushing, OCP, Thyrotoxicosis
Myxdema, Pheochromocytoma, Acromegaly.

 Vascular – Coarctation of Aorta, PAN, Aortic

insufficiency.

 Neurogenic – Psychogenic, Intracranial pressure,

olyneuritis etc.
 Genetics- family history
 Diet-high intake of sodium
 Lifestyle-stressful
 Weight- obesity
 Alcohol-increased intake
 Oral contraceptives
 “You’re not fat, you’re just well built”

 “You’re only fat if your belly covers your ...”

 Fat is beautiful- embrace it

 I like them big and fat and thick !

 ? ? ? Obesity Insulin resistance +
Hyperinsulinemia? Sodium retention+ Blood
volume expansion+ excess NE+ smooth
muscle proliferation Hypertension.

 Whatever the mechanism, the risk of

developing hypertension among previously
normotensive persons increases
proportionately with weight !
 Increased Blood Volume due to reduced renal
sodium excretion

 Increased peripheral resistance: Increased

release of vasoconstrictor agents, increased
sensitivity of vascular smooth muscle cells,
neurogenic factors

 Abnormal renal blood pressure regulation:

Renin-Angiotensin system

 Increased sympathetic response

 Large Blood Vessels (Macroangiopathy)
 Atherosclerosis.
 Small Blood Vessels (Microangiopathy)
 Arteriolosclerosis

Organ damage:
 Heart
 LVH, Hypertensive cardiomyopathy
 Kidney
 Benign nephrosclerosis
 Eyes
 Hypertensive retinopathy
 Brain
 Haemorrhage, infarction
 Accelerates atherogenesis
 Potentiates aortic dissection
 Potentiates Cerebrovascular hemorrhage
 Small vessel changes (particularly in Kidney):

Hyaline Hyperplastic Fibrinoid Necrosis

Arteriosclerosis Arteriosclerosis

Benign hypertension Malignant hypertension Malignant hypertension

 Hyaline AS: Typically in elderly, mild hypertension,
mild diabetes, majorly seen in benign nephrosclerosis
(arteriolar narrowing impairs bld supply loss of
nephrons). Reflect leakage of plasma components
across vascular endothelium and excessive ECM
production by SMCs, secondary to chronic
haemodynamic stress of HTN.
 Hyperplastic AS: Characteristic of Malignant HTN
(acute severe elevations). Associated with acute
cerebral and renal injury. Concentric laminated
(onionskin) arteriolar thickening with duplicated
basement membrane and SMC proliferation,
frequently associated with fibrinoid deposition and
vessel wall necrosis, so-called wall necrotising
arteriolitis.
 Generally asymptomatic

 Malignant HTN (BP>200/140mmHg): Visual

impairment, nausea, vomiting, fits,
headaches or symptoms of acute heart
failure.

 Symptoms due to secondary causes e.g.

Sweating and tachycardia in
phaeochromocytoma
 All adults should be measured every five years up
to the age of 80
 If ‘borderline’ this should be increased to
annually
 Ambulatory blood pressure monitoring may help
if there is unusual BP variability, ‘white coat
hypertension’ is suspected, or in ‘borderline’
cases
 Standing blood pressure should be measured in
elderly or diabetic patients to exclude notable
orthostatic hypotension.
 The average of two readings at each of a
number of visits (depending on severity) should
be used to guide the decision to treat.
 Focus on: Potential causes, other vascular
risk factors and evidence of end-organ
damage.
 History – vascular disease, drugs, family,
lifestyle
 Examination – arrhythmias, heart failure,
weight
 Investigations to identify end organ damage
and secondary causes
 Goal: To assess cardiovascular disease risk, identify
end organ damage and HTN due to secondary causes.

 Serum Urea and Electrolytes (may show evidence of

renal impairment)

 Urine Dipstick: Haematuria and Proteinuria

 Blood glucose

 Serum lipids

 ECG may show evidence of LVH or Myocaridal

Ischaemia
 Weight - aim for BMI between 20-25kg/m2
 Exercise - ideally 30+ minutes 3 times per
week
 Alcohol - safe weekly limits (♂<21 units,
♀<14 units per week)
 Smoking - cessation vital. To  overall CVD
risk nicotine replacement therapy may help
 Diet -  salt (<6g sodium per day), 
saturated fat,  fruit+ vegetables (at least 5
portions per day),  oily fish
 Diuretics: Loop-Furosemide and Thiazides-
bendroflumethiazide
 β- Adrenergic blocking agents
 ACE Inhibitors: Captopril, lisinopril, enalapril,
ramipril
 Angiotensin II receptor Antagonists: losartan,
valsartan, irbesartan, candesartan
 Calcium Antagonists: amlodipine and nifedipine
 α- Blocking agents (doxazosin), hydralazine, and
centrally acting agents (clonidine, moxonidine),
may be indicated in specific circumstances.

Black race 
Diabetes mellitus

Younger age

Hypercholesterolemia

Male sex

Obesity

Excess alcohol intake

Persistent diastolic
pressure > 115 mm Hg

Smoking

Organ damage:

cardiac

eyes

renal

CNS
OBESITY HTNCAD
 IHD comprises a group of closely related
syndromes resulting from ishcemia-
essentially a mismatch between cardiac
demand and vascular supply of oxygenated
blood. In most cases nutrient availability is
reduced as well as metabolite removal.

 There are 4 ischemic syndromes:

1. Myocardial Infarction
2. Angina Pectoris
3. Chronic IHD
4. Sudden Cardiac Death
 Increased myocardial demand
 Systemic: shock
 Reduced oxygen carry capacity of blood (e.g.
anaemia)
 Diversion: cyanotic congenital heart diseases
 Reduced oxygen: severe lung disease
leading cause of
death in 1st world
- responsible for
1/3 of all deaths
Interaction between:

 Fixed atherosclerotic narrowing of coronary

arteries

 Intraluminal thrombosis

 Vasospasm
 Significant obstruction is defined as 75%
reduction of the cross sectional area of the
artery

 At this level of obstruction, vasodilatation

can not compensate for the reduced blood
flow
 Fixed obstructions - collaterals have time to develop and
compensate

 Acute changes to plaques - too rapid for compensation by

collaterals

 Consists of:
 Intraplaque haemorrhage
 Fissuring
 Ulceration

 Consequences of acute change:

 superadded thrombosis +/- embolism
 vasoconstriction - damaged endothelium is unable to
secrete relaxing factors
 Vasospasm fracturing the plaque
 Tachycardia-causing physical stress
 Stresses produced by turbulent blood flow in
stenotic vessels
 Plaques more prone to rupture:
 Eccentrically positioned
 Large core of necrotic debris and lipid
 With a thin fibrous cap

 uncertain sometimes
 Eccentric plaques: are often lipid rich and affect
only one segment of the wall of a coronary artery
 improvement of flow at site of such plaque may
be achieved by vasodilator drugs which can cause
relaxation of the normal part of the vessel wall
 Concentric plaques: usually mostly collagenous
and affecting the whole of the arterial wall
 generally, drug therapy cannot improve flow over
a narrowed segment
 Age  Hyperlipidemia
 Male Gender  Cigarette smoking
 Genetic Hypertension
Predisposition  Diabetes mellitus
 Personality Factors  Low physical
activity
 Postmenopausal
state

Non-Modifiable Modifiable
 Obesity HTNIHD

 Obesity
HyperlipidemiaAtherogenesisIHD
 The risk of coronary atherosclerosis is
directly related to elevation of serum
cholesterol.

 Increase in levels above 5 mmol/L is

associated with increasing risk.

 Rise in level of HDL is protective against

atheroma

 Increase in LDL and VLDL favour

atherogenesis
Xanthomas on the hand, patient 12 y. old
Eruptive xanthomas, a man 33 y. old
Palpebrarum xanthomas, arcus senilis,
patient, 47 y. old
Tuberosum xanthomas, patient, 47 y. old
 Stable angina:
 Reproducible chest pain caused by increased physical
activity or emotional excitement and relieved by rest
or vasodilators
 Causedby reduction of coronary perfusion by a stable
atherosclerotic disease
 Over a long period, repeated episodes of impaired
flow may lead to development of fine fibrosis in the
myocardium, with death of individual cardiac muscle
fibres
 Anastomotic
vessels frequently develop to
compensate for areas of vascular stenosis
Variant angina:
 = chest pain occurs at rest, responds to
vasodilators
 thought to be caused by vasospasm
Unstable angina:
 Chest pain with progressively less effort, often at
rest, prolonged duration.

 Caused by fissuring, ulceration or haemorrhage

into a plaque with thrombosis, embolisation or
vasospasm

 Fissuring = plaques breakdown resulting in a

deep cleft in a lipid-rich plaque that either
precipitates thrombus development in the lumen
or causes bleeding into the body of the plaque,
with resultant ballooning into the lumen
Primary diagnosis is clinical

 Investigations include:
 Resting ECG-ST segment depression and T-
wave flattening or inversion during attack
 Exercise ECG-positive in 75% of patients
 Pharmacologcal Stress testing
 Coronary Angiography
 Secondary Prevention (Non-pharmacological
treatment) : Similar to Non-Pharmacological
treatment of HTN as mentioned previously +
glycaemic control in DM
 Asprin, Statins and β-blockers also reduce
subsquent risk of cardiovascular events
 Symptomatic relief/Pharmacological: sublingual
GTN tablet or spray + regular prophylactic
therapy: Nitrates, β -blockers or Calcium
antagonists are most commonly used.
 Surgical: Coronary Angioplasty, Coronary Artery
Bypass grafting
Necrosis of Cardiac Muscle due to lack of oxygen
 Sudden and devastating
chest pain, radiating to
left shoulder, arm, jaw

 +/- vomiting, nausea,

sweating, shortness of
breath

 Burning epigastric
discomfort, "indigestion“

 10% asymptomatic,
discovered later
 Family history
 Hypercholestrolaemia
 Cigarette smoking
 Diabetes mellitus
 Hypertension
 Age
 Male gender
 Transmural infarction (regional infarct) - 90% of
cases infarcted area is the full thickness of the
muscle in distribution of a specific coronary artery(s)

 Caused by thrombosis superadded to acute plaque

events

 i.e. thrombus --> blockage of entire coronary artery

--> infarct of all the muscle supplied by that
coronary (therefore full thickness of wall)STEMI

 Note: if there is lysis of the thrombus or a collateral

supply to the myocardium, the infarct will be limited
to the subendocardial zone - i.e. regional
subendocardial infarction
 Subendocardial infarction (circumferential infarct) -
10% of cases, the ischaemic nercrosis is limited to the
inner one-third or one-half of the cardiac wall,
extending beyond territory of a single artery

 Caused by diffuse, stenosing atherosclerotic coronary

artery disease and a reduction in overall cardiac blood
flow

 i.e. atherosclerosis of coronary arteries --> general

hypoperfusion of the main coronary arteries -->
normally, enough blood reaches heart, BUT, due to an
episode requiring increased blood flow (e.g. exercise),
perfusion is inadequate, and an infarct occurs, but
because the coronary arteries travel near the
pericardium, enough oxygen reaches the outer parts of
the muscle, but not the inner parts of the muscle)
 Pathogenesis: occlusive thrombus overlying
an ulcerated or fissured stenotic plaque -
90% of cases

 Vasospasm, emboli, unknown-10%

Mechanism:
 acute plaque event
 platelet activation
 thrombosis
 Vasospasm

 i.e. thrombus formation, stimulated by the presence of an

atheromatous plaque, is the main cause of episodes of
acute ischaemic heart disease; thrombosis is due to two
main reasons: 25% of cases are due to superficial
ulceration of endothelium over a plaque
 75% of cases are due to plaque fissuring, resulting in a
deep cleft in a lipid-rich plaque that either precipitates
thrombus development in the lumen or causes bleeding
into the body of the plaque, with resultant ballooning into
the lumen
 note: these complications may be in low grade stenoses
which will not have caused previous angina on exertion
 Dependent on duration and severity

 Ischaemia reversible phase:

 60seconds - loss of contractility
 minutes - ultrastructural changes

 Irreversible:
 20-40 miunutes of severe ischaemia
 myocyte necrosis
 a wavefront of coagulative necrosis, starting at
the subendocardial zone
 Left ventricle almost always involved (because of its
greater bulk and work requirement)

 Area involved depends on:

 the vessel(s) occluded
 the status of the collateral circulation (if ischaemic
heart disease has occurred over years, then collateral
circulations will exist)

 May see several infarcts of varying age in the same heart

 Sequence of events involves:

 coagulative necrosis
 inflammation
 repair
 Left anterior descending (LAD)
 anterior wall of LV near apex
 anterior 2/3 of septum
 Left circumflex (LCX)
 lateral wall of LV
 Left coronary artery (LCA)
 hence, no blood in LAD or LCX
 therefore, massive antero-lateral MI
 Right coronary (RCA)
 inferior/posterior wall of LV
 posterior 1/3 of septum
 +/- posterior RV
Over following 8 weeks:

 Acute inflammation
 Organisation
 Scarring
 0-12: inapparent (but, within 3 hrs
triphenyltetrazolium chlordide (TTC) will not
stain the affected part of heart because
dehydrogenase is depleted [note TTC
normally stains a heart blue/black])
 12-24: blotchy areas of palor and congestion
 1-3 days: the dead area appears soft and
pale with a slight yellow colour
 3-14 days: softened yellow central area with
a hyperaemic rim - granulation tissue (can
rupture to cause haemopericardium);
 weeks: fibrotic white thin scar
 4-12 hrs: wavy fibres, myocytolysis (large
vacuoles in cells)
 12-24 hours: infarcted muscle is brightly
eosinophilic with intercellular oedema
 1-3 days: acute inflammation (polymorphs
infiltrating dead muscle cells)
 3-10 days: removal of dead cells by
macrophages, with the beginning of vascular
granulation tissue formation
 2-4 weeks: repair-granulation tissue, becoming
more fibrous and less vascular over time
 4-6 weeks: established scarring (collagen)
 Administration of thrombolytics to dissolve
the thrombus
 Fibrinolytic
drugs: Streptokinase or Tissue
plasminogen activator (TPA)

 Ifclot lysis is achieved shortly after onset of

occlusion, it is possible to minimise the extent
of ischaemic damage to the muscle

 Salvage of myocytes if given within 1 hour of

onset of chest pain
 ECG
 Cardiac Markers
 Troponin T and I- sensitive and specific for
cardiac muscle
 Creatine Kinase- CK-MB,
 AST, LDH
 Other investigations: CXR, CBC, Serum Urea
and Electrolytes, Blood Glucose and Lipids
 Provide facilities for defibrillation

 Immediate Measures:
 High-Flow oxygen
 I.V. Access
 ECG Monitoring
 12-lead ECG
 I.V. Anaglegia (Morphine) and Antiemetic
 Asprin 300mg
 Reperfusion: Primary PCI or thrombosis

 Detect and Manage Acute Complications:

Arrhythmias, Ischemia, HF
 Lifestyle Modification as mentioned before

 Secondary Prevention drug therapy:

 Antiplatelet therapy(Aspirin/Clopidogrel)
 β- blocker
 ACE-inhibitor
 Statin
 Therapy for DM/HTN

 Rehabilitation
 Sudden death (ventricular fibrillation,
tamponade, septal rupture) within 1-2 hours
(20% of patients)

 Cardiac arrhythmias (80%) - within 2 weeks

patients with old infarcts tend to develop
cardiac arrhythmias arising from muscle
adjacent to an area of old scarring. Acute
myocardial ischemia also precipitates
arrhythmias. Death is often due to ventricular
fibrillation

 Left ventricular congestive failure, pulmonary

oedema (60%) - within 2 weeks
 Cardiogenic shock (15%) - within 2 weeks
monitoring in coronary care unit

 Rupture of cardiac muscle (1-5%) - within 3-8

days, particularly during early organisation and
sofeting.
Can lead to:
 tamponade (rupture through anterior, posterior or
lateral walls) (i.e. blood bursts through wall,
instantly causing haemopericardium; this sudden rise
in intrapericardial cavity pressure prevents cardiac
filling, and leads to sudden death)
 left to right shunts (rupture through medial (septal)
wall)
 acute mitral regurgitation
 Thromboembolism (15-40%) - within 2 weeks mural
thrombus formation on the inflamed endocardium over
the area of infarction may occur
Fragments can break off and embolise to various organs
(part. brain, spleen, kidney, gut, lower linbs) producing
infarction
 Fibrinous pericarditis -day 2-3
 a response to underlying infarct
As a long term complication
 Dressler's syndrome is a form of immune-mediate pericarditis
associated with a high ESR
 it develops in a very small number of cases after infarction (2-
10 months after MI)

 Infarct extension and reccurrent myocardial infarction -

long term complication
 Infarct Stretching- long term complication

 Thinning of fibrotic myocardium occurs as

organisation and repair are undertaken
 The collagenous scar is weak and inelastic, and may
stretch
 Eventually a ventricular aneurysm will become
evident and slowly progress
 It paradoxically bulges during systole
 Overlying thrombosis may occur in this area because
of haemostasis (but embolic complications are
uncommon)

 Chronic intractable left heart failure due to

inadequate ventricular pumping action - long term
Depends on:
 Type: in a subendocardial infarcts a mural
thrombus development is possible, but there
aren't usually other complications, therefore it
has a better prognosis than a transmural infarct
 Size: larger infarcts higher risk of cardiogenic
shock, arrhythmias, late CCF
 Site:

Anterior infarcts
 dilatation,
mural thrombus, rupture
 worse outcome

Posterior infarcts
 conduction blocks, right ventricular involvement
 Overall mortality in first year - 35%

 15% die instantly

 Mortality rate during hospitalisation - 10-15%

 Chronic IHD, also called ischemic
cardiomyopathy, is essentially progressive heart
failure as a consequence of ischemic myocardial
damage

 History of MI in most instances

 usually results from postinfarction cardiac

decompensation that follows exhaustion of the
hypertrophy of the viable myocardium.

 In other cases severe obstructive CAD may be

present without prior infarction, but with diffuse
myocardial dysfunction.
 Heart is enlarged and heavy from left ventricular
dilation and hypertrophy

 Moderate to severe atherosclerosis of the coronary

arteries, sometimes with total occlusion

 Discrete, gray-white scars of healed infarcts are

usually present.

 The endocardium generally shows patchy, fibrous

thickening, and mural thrombi may be present.

 The major microscopic findings include myocardial

hypertrophy, diffuse subendocardial myocyte
vacuolization, and fibrosis from previous infarcts.
 Development of severe, progressive heart
failure, sometimes punctuated by episodes of
angina or MI.

 Arrhythmias are common and along with HF

and intercurrent MI, account for many
deaths.
 Unexpected cardiac death within 1 hour of
symptom onset.

 Predominantly caused by IHD and 75-95% of

victims have significant atherosclerotic
stenosis, often with acute plaque disruption.

 Fatal Arrhythmia (Asytole or ventricular

fibrillation) is the most common etiology.
 Aortic Valvular stenosis
 Hereditary or Acq. Conduction abnormality
 Electrolyte derrangement
 Mitral Valve Prolapse
 Dilated or Hypertrophic Cardiomyopathy
 Myocarditis