Hypertensive Heart Disease

HYPERTENSIVE
HEART DISEASE
BY
DR. UDO MARK. MBBS; FMCPath
DEPARTMENT OF ANATOMICAL PATHOLOGY

HYPERTENSIVE HEART DISEASE
 Response of the heart to increased demands
induced by systemic hypertension
 When heart dx is caused by pulmonary HTN,
it is referred to as rt sided HHD or cor
pulmonale
 Therefore HHD can be divided into two:
 Systemic or lt-sided HHD
 Pulmonary or rt-sided HHD
SYSTEMIC (LEFT-SIDED)
 Minimal criteria for the diagnosis of systemic
HHD are:
 1. LV hypertrophy (usually concentric) in the
absence of any other pathology that might
have induced it
 2. A history or pathological evidence of HTN.
 Hypertrophy of the heart in HTN is usually an
adaptive response to pressure overload.
 About 25% of the population of USA have at
least a mild hypertension.
 Prolonged HTN even mild forms can induce LV
hypertrophy.
SYSTEMIC (LEFT-SIDED)
 Compensated systemic HHD may be asymptomatic.
 With progression, patients may dev atrial fibrillation
(due to lt atrial enlargement), or CCF (with cardiac
dilation) or both.
 Possible outcomes of systemic HHD include:
 Patient enjoys a normal life
 Progressive IHD.(HTN potentiates coronary
atherosclerosis)
 Progressive renal damage
 Cerebrovascular stroke
 Progressive heart failure.
 Effective control of HTN  regression of cardiac
hypertrophy.
MORPHOLOGY OF SYSTEMIC
HHD
 HTN induces LV hypertrophy without dilation of
the ventricle
 With hypertrophy, there is increase in LV wall
thickness relative to the cavity, and increase in
the overall size and weight of the heart.
 Increased thickness of LV wall  stiffness that
impairs diastolic filling.
 This induces lt atrial enlargement.
 MICROSCOPICALLY, there is increased transverse
diameter of myocytes.
 At late stage, nuclear enlargement becomes
irregular, variation in cell size, and interstitial
fibrosis.
PULMONARY (RT-SIDED) HHD
OR COR PULMONALE
 Consists of RV hypertrophy, dilation, and potential
failure due to pulm HTN caused by disorders of
the lungs or pulm vasculature.
 Causes RV hypertrophy other than pulmonary, eg
lt-sided heart disease, or congenital heart dx are
not regarded as cor pulmonale.
 Cor pulmonale may be acute or chronic
 ACUTE: follow massive pulm embolism.
 CHRONIC: Usually secondary to prolonged
pressure overload caused by pulm
artery/arteriolar obstruction, or
compression/obliteration of septal capilaries eg,
in emphysema, or in primary pulm HTN.
MORPHOLOGY
 In acute Cor, there is marked RV dilation
without hypertrophy.
 On cross section, the normal crescent shape
of the RV is converted into a dilated ovoid.
 In chronic Cor, the RV wall thickness
increases (up to 1cm or more), or may even
approximate to the LV.
 There may be secondary compensation of the
LV chamber , or tricuspid regurgitation with
fibrous thickening of the valve.
HEART FAILURE
 DEFINITION
 A clinical syndrome caused by the inability of
the heart to pump sufficient blood to meet
the metabolic needs of the body
 Can result from any disorder that reduces
ventricular filling (diastolic dysfunction)
and/or myocardial contractility (systolic
dysfunction).
EPIDEMIOLOGY
 INCIDENCE : 1/1000 population per year.
 Increases by 10% every year
 Prevalence = 3-20 cases per 1000 population
 Male:female ratio = 2:1
 Median age of presentation is 76years
ETIOLOGY
 INTRISIC PUMP FAILURE: eg weak ventricular muscles,
caused by :
 IHD
 Myocarditis
 Metabolic disorders like beri beri
 INCREASED WORKLOAD ON THE HEART: ie increased
pressure load:
 Hypertention
 Chronic lung diseas
volume load due to:
 Severe anemia
 Hypoxia due to lung dx
 IMPAIRED CARDIAC FILLING
PATHOPHYSIOLOGY
 Heart failure is associated with complex
neurohormonal changes including activation
of the renin angiotensin aldosterone system
and the sympathetic nervous system.
RIGHT HEART FAILURE
 Rt ventricular pump failure
 Failure to eject blood from the vena cavae
 Blood backs up into systemic circulation
 CAUSES:
 Consequence of LV failure
 Pulm or tricuspid valve dx
 Congenital heart dx
 Myocardial heart dx affecting the rt heart
LEFT HEART FAILURE
 Initiated by stress in the lt heart:
 LV fails as effective pump
 LV cannot eject blood from the pulmonary
circulation
 CAUSES:
 Systemic hypertension
 Mitrial or aortic valve dx
 IHD
 Cardiomyopathies
 Myocarditis
 Note: CO = HR X SV
TYPES OF HEART FAILURE
 Acute Heart Failure
 Chronic Heart Failure
ACUTE HEART FAILURE
 Sudden and rapid dev of heart failure may
occur in:
 Large myocardial infarctions
 Valve rupture
 Massive pulmonary embolism
 Acute viral myocarditis
 Here, there is sudden reduction in cardiac
output resulting in systemic hypotension but
edema does not take place
CHRONIC HEART FAILURE
 Develops slowly eg in:
 Myocardial ischemia
 Multivalvular disease
 Systemic hypertension
 Chronic disease
 Progression of acute into chronic failure
 Note: here, there is a well maintained
arterial pressure and edema forms
MORPHOLOGY
 HF occurs when compensatory mechanisms are
exhausted.
 When challenged, the heart employs the ffing:
 1. FRANK-STERLINGS mechanism, ie; incrd
preload of dilatation  incrd contractility.
 2. MYOCARDIAL STRUCTURAL CHANGES: eg
hypertrophy
 3. ACTIVATION OF NEUROHUMORAL SYYTEMS: -
N/E incrd HR, incrd contraction, incrd PR. -
Renin-Angiotensin-Aldosterone pathway.
-Incrd ANP (Atrial Natriuretic Peptide).
MORPHOLOGY
 Systole = ventricules contract, AV valves
close.
 Diastole = ventricules relax, semiluna valves
close.
MORPHOLOGY
 LEFT SIDED HEART FAILURE:
 The effects are seen in ;
 Lungs (pulmonary congestion & edema) _ HF cells

(sideroblasts ie hemosiderin containing macrophages).
Lungs are heavy & wet.
 Manifests as:
 Dyspnoea
 Orthopnoea
 PND
 Kidneys (advanced cases), due to decrd CO.
 Brain (advanced): cerebral hypoxia gives rise to
hypoxic encephalopathy
MORPHOLOGY
 RIGHT SIDED HF: affects ;
 Liver/portal systems viz;
-congestive hepatomegaly
-centrilobular necrosis
-cardiac cirrhosis
 Spleen – congestive splenomegaly
 Kidneys – congestion of kidneys  fluid reteition
 Brain – venous congestion and hypoxia of the CNS
 Pleura & pericardial spaces (effusion)
 GIT – edema of bowel wall malabsorption, ascitis.
 Subcut tissues  dependent edema (pedal, pretibial,
presacral) and anasarca.
 Note: pulm edema = LHF, pleural effusion = RHF
SIGNS
 Pulmonary edema
 Cool extremities
 Tachycardia
 Narrow pulse pressure
 Cardiomegaly
 Peripheral edema
 Hepatomegaly
SYMPTOMS
 Dyspnoea, particularly on exertion
 Orthopnoea
 PND
 Exercise intolerance
 Tachypnoea
 Cough
 Faigue
 Hemoptysis
 Abdominal pain
 Anorexia
 Nausea and bloating, and poor appetite
 Ascitis
 nocturia

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HYPERTENSIVE

DEPARTMENT OF ANATOMICAL PATHOLOGY

 Lungs (pulmonary congestion & edema) _ HF cells

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