Heart failure.

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Heart failure. Myocardial Infarction
Ph.D., MD, Assistant Professor Hanna Saturska
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Functions of the circulatory system

• Transport is the main function of circulatory
  system
• Stabilization of arterial pressure
• circulatory system delivers ?2 and nutrients to
  the tissues
• circulatory system carries waste products to the
  kidneys and other exceatory organs

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Heart insufficiency (Heart failure)

• Heart failure (HF),
• often called congestive heart failure (CHF)
• or congestive cardiac failure (CCF), occurs when
  the heart is unable to provide sufficient pump
  action to distribute blood flow to meet the needs
  of the body.

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• Heart failure is a global term for the
  physiological state in which cardiac output is
  insufficient in meeting the needs of the body and
  lungs.
• Often termed "congestive heart failure" or CHF,
  this is most commonly caused when cardiac output
  is low and the body becomes congested with fluid
  due to an inability of heart output to properly
  match venous return.

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Heart failure

• Heart failure may be caused by myocardial failure
  but may also occur in the presence of near-normal
  cardiac function under conditions of high demand.

conditions of high demand
myocardial failure
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• To maintain the pumping function of the heart,
  compensatory mechanisms increase blood volume,
  cardiac filling pressure, heart rate, and cardiac
  muscle mass.
• However, despite these mechanisms, there is
  progressive decline in the ability of the heart
  to contract and relax, resulting in worsening
  heart failure.

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Reasons

• Myocardium injury
• Myocardium hypoxia or ischemia
• Infectional-toxical myocardium damage
• Metabolism disorder
• Nervous-trophical and hormonal influences on the
  organism
• Myocardium overload
• Increase of heart outflow resistance (heart
  aperture stenosis, arterial hypertension)
• Increase of diastolic inflow (hypervolemia, heart
  aperture insufficiency)
• Mixed

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Mixed heart insufficiency variant. It arises at
combination of myocardium damage and its
overload, for example at rheumatism, when of
inflammatory myocardium damage and valvular heart
violations are combined.
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• Acute pulmonary edema.
• Note enlarged heart size, apical vascular
  redistribution ( circle ), and small bilateral
  pleural effusions
• (arrow ).

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This chest radiograph shows an enlarged cardiac
silhouette and edema at the lung bases, signs of
acute heart failure.
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• A 28-year-old woman presented with acute heart
  failure secondary to chronic hypertension. The
  enlarged cardiac silhouette on this
  anteroposterior (AP) radiograph is caused by
  acute heart failure due to the effects of chronic
  high blood pressure on the left ventricle. The
  heart then becomes enlarged, and fluid
  accumulates in the lungs (ie, pulmonary
  congestion).

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Heart failure can be classifiedinto 4 classes

• Class I patients have no limitation of physical
  activity
• Class II patients have slight limitation of
  physical activity
• Class III patients have marked limitation of
  physical activity
• Class IV patients have symptoms even at rest and
  are unable to carry on any physical activity
  without discomfort

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Heart failure can be divided into 4 stages, as
follows

• Stage A patients are at high risk for heart
  failure but have no structural heart disease or
  symptoms of heart failure
• Stage B patients have structural heart disease
  but have no symptoms of heart failure
• Stage C patients have structural heart disease
  and have symptoms of heart failure
• Stage D patients have refractory heart failure
  requiring specialized interventions

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STAGES

• Compensation
• 1. Crash phase
• (main sense - compensative hyperfunction)
• 2. Stable adaptation phase
• (main sense - compensative hypertrophy)
• Decompensation
• 3. Exhaustion

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Crash phase (St. of compensation)

• Extracardial mechanisms
• 1. Increase of O2 utilization by the tissues
• 2. Reduce of peripheral vessels resistance

• Cardial mechanisms
• HB increase (in 2,5 time)
• 2. Systolic volume increase
• 3. Heart index increase
• 4. Heart work increase

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Crash phase (St. of compensation)

• Reason
• increase of every cardiomyocytes load
• Physiological mechanisms
• adequate excitement
• relation of excitement and
  contraction
• adequate contraction
• energy provision

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Crash phase Immediate adaptation mechanisms

• 1. Adequate excitement
• Is based on selective penetration of Na,
  K, ??2 due to difference between the
  extracellular ions concentration and
  intracellular one
• Result - depolarization

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Crash phase Immediate adaptation mechanisms

• 2. Relation of excitement and shortening
• diffusion of depolarization wave inside the
  cardiomyocytes
• ??2 penetration in to cytoplasma from SPR
• ??2connection with troponin and release of
  myosin
• 3. Shortening
• actin and myosin interaction

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Crash phase Immediate adaptation mechanisms

• 4. Energy provision
• Glycolisis activation
• Mitochondria activation
• CrPh reserve, glycogen reserve(are localized on
  SPR membrane)
• -most sensitive - depolarization ( Na,K-??P?se
  and ??- ??P?se control of ions transposition
  athwart concentration gradient
• Excessive ?? concentration causes its
  accumulation in mitochondrias and block of ??P
  synthezise!!!

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Crash phase (pathogenesis)

• Heart beat increase
• Functional changes
• Increased penetration of Na and ?? cytoplasma
  inside
• Decrease of depolarization interval
• Is possible if
• activity of Na,K-ATPase and ?? -ATPase is high
• CrPh reserve and ATP reserve is adequate
• ATP synthezise in mitochondrias is adequate
• Na,??-regulative mechanism is adequate

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Crash phase (pathogenesis)

• Increase of shortening power
• ( heterometric mechanism and homeometric
  mechanism)
• Activation of adenilatcyclase by catecholamines
• c??P synthesis
• Increase of ?? concentration in cytoplasma
• Increase of free myosin fibers amount (??
  blockades troponin)
• Increased amount of myosin-actin interaction
• Using of ATP, CrPh, glycogen

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Crash phase (pathogenesis)

• Limitation mechanisms
• 1. Accumulation of Na (because is limited
  Na,?-??Pase activity)
• 2. Violation of Na,??-exchanged mechanism
• 3. ?? accumulation (because limitation of
  Ca-??Pase activity)
• after-effect cardiomyocyte relaxation deficit
  (diasole deficit)
• ?? accumulation in
  mytochondrias (dissociation of oxidation and
  phocphorilation)
• 4. Energy deficit (deficit of ??P 40-60 causes
  shortening depression)
• 5. Lactic acid accumulation (causes shortening
  depress ion because ?ions interact with
  troponin)

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Crash phase (pathogenesis)

• Resume
• Limitation mechanisms cause condition when
• heart load is more than heart work.
• It is the sense of heart insufficiency.
• So, compensative hyperfunction as an adaptation
  mechanism is depleted

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Stable adaptation phase (stage of compensation)
Myocardium hypertrophy

• Gist compensative hypertrophy
• Mechanisms
• RNA synthesis activation in cardiomyocites
• Increase of ribosome quantity in cardiomyocites
• Structural proteins synthesis (at first
  mitochondrial proteins and SPR ones)
• activation DNA and RNA synthesis in connective
  tissue cells of the heart (fibroblasts and
  endotheliocytes)
• Controlled proliferation of the connective
  tissue cells (they are the donors of RNA and
  structural proteins)
• Result heart stable adaptation to load

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Signs of hypertrophy

• Sick person
• 1. Continuous heart load
• 2. Heart hypertrophy is inadequate
• to body weight
• 3. Decrease of capillaries amount in
• weight unit
• 4. Inadequate activity of MCh
• 5. Inadequate activity of SPR
• 6. Decrease of nervous structures
• amount in weight unit (decrease of
• NA concentration)

• Sportsman
• 1. There are periods of heart load and
• restoring
• 2. Heart hypertrophy is adequate to
• body weight
• 3. Increase of capillaries amount in
• weight unit
• 4. Adequate activity of MCh
• 5. Adequate activity of SPR
• 6. Increase of nervous structures
• amount in weight unit (adequate
• concentration of NA)

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Signs of hypertrophy

• Sick person
• Results
• Heart insufficiency is compensated by the
• hypertrophy (bigger heart mass).
• But this change limits maximal heart work.

• Sportsman
• Results
• Heart insufficiency, which is
• compensated by the hypertrophy,
• increases of heart muscles
• contraction power and speed one.
• Heart work is increased and
• human endurances is increased too

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Exhaustion (stage of decompensation)

• Decrease of correlation between square
  cardiomyocyte surface and cardiomyocyte volume
  (unbalance of ions pumps)
• Decreased Na,K-??Pase activity (violation of
  repolarisation , appearance of arrhythmias)
• Decreased activity of SPR and ??-??Pase (heart
  relaxes slowly, some time arise diastole defect
  at ?? accumulation)

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Exhaustion (stage of decompensation)

• Decreased MCh activity and energy deficit because
  ?? is accumulated in MCh and it causes
  dissociation of oxidation and phosphorilaion
• Depression of contractil function
• Exhaustion of connective tissue cells donors
  function
• Decrease of coronary blood flow reserve
• Decrease of N? concentration decrease of maximal
  speed shortening of the heart and maximal force
  one

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Exhaustion (stage of decompensation)
right-sided heart failure left-sided
heart failure
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Pathological signs

• Violations of blood circulation
• Reduce of systole output (increase of diastole
  excess blood volume, myogene dilation)
• Decrease of heart output
• Decrease of systole arterial pressure
• Increase of diastole arterial pressure
• Increase of veins pressure (causes the HR
  increase)
• Slowdown of blood flow (main sign of
  decompensation)
• Erythrocytosis (compensation)

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• Breathing violations
• Dyspnoea (reflective irritation of breathing
  center by the ??2)
• Attacks of cardiac asthma at night (blood
  overflow of the atriums and central veins, which
  causes barro-receptors irritation and breathing
  center reflexes)

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Pathological signs

• Violation of water-electrolyte balance
• (edema)
• Blood circulation violation (slowdown blood flow
  in capillaries, intravenous blood pressure
  increase)
• Reflexes of blood circulation dumping (blood
  retention in depot liver, veins)
• Deficit of blood circulation in the arteries
• Irritation of the vessels volume receptors
• Hypersecretion of aldosteron (Na retention) and
  vasopressin (water retention)
• Hypervolemia, ascytes, edema

Renin-angionensin-aaldosterone system
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Myocardial infarction

• Ischemic heart disease occurs when there is a
  partial blockage of blood flow to the heart.
• When the heart does not get enough blood it has
  to work harder and it becomes starved for oxygen.
  
• If the blood flow is completely blocked then a
  myocardial infarction (heart attack) occurs.

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Myocardial infarction

• Ischaemical necrosis of the myocardial tissue,
  which is resulted from coronary blood supply
  insufficiency

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Statistics

• Morbidity increases
• Patients which suffer from myocardial infarction
  are younger year by year
• Mortality of the patients which suffer from
  myocardial infarction increases year by year
• (30-40 )

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• Coronary artery disease is currently the leading
  cause of death in the United States. Despite the
  increasing sophistication of surgical techniques,
  the introduction of new techniques such as
  balloon angioplasty, and a number of new drugs
  (e.g. beta blockers, calcium antagonists), it is
  estimated that over 1 million heart attacks will
  occur this year, resulting in 500,000 deaths. In
  short, we do not have an adequate therapeutic
  solution to the problem of myocardial infarction
  (heart attack).

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??H??LOGY

• Atherosclerosis of the coronary arteries (in
  90-95 died people at section was found)
• Trombosis of the coronary arteries
• at the 4 stage of atherosclerosis
• arterial hypertension (because it causes
  blood coagulation hyperactivity)
• Trombembolism (septic endocarditis, thrombus
  lyses)
• Spasm of the coronary arteries

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Risk factors

• 1. Stress
• (at trauma, operation, cold, negative emotions)
• BECAUSE IT CAUSES
• Increase of the heart activity
• Stimulation of the heart metabolism
• Increase of ?2 using

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Risk factors

• 2. Age (most often appears in 40 59 years old
  person).
• 3. Hypokinesia (activation of the
  sympathetic-adrenal system)
• 4. Obesity (hypercholesterolemia)

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Risk factors

• 5. MAIL SEX
• Morbidity of the men in 2-3 time more
• Mortality of the men in 3-4 time more
• Men 45-59 years old - mortality 37
• Woman 45-59 years old mortality 17
• Men 60-74 years old - mortality 55
• Woman 60-75 years old mortality 78,4

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Risk factors

• 6. Heredity
• 7. Arterial hypertension
• 8. Diabetes mellitus
• 9. Infection (chlamydia pneumonia)

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Pathogenesis

• 1.
• Initial
• mechanisms
• As a result of atherosclerotic disease of the
  coronary arteries

• 2.
• Mechanisms of the cardiomyocites
• necrosis
• As a result of cardiomyocytes ischemia

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Initial mechanisms

• Increase of the atherosclerotical plaque size
• Vessel narrowing---ischemia---necrosogenic ATP
  deficit
• vessels narrowing on 95 (critical stenosis)
  causes ??P deficit (less than 40-60 ) which
  results in cardiomyocytes necrosis

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Initial mechanisms

• 2. Increase of injured vessel sensitivity to
  vasospastic effects
• Damage of endothelium -----
• decrease of N?-synthetase activity----
• decrease of N? concentration (which is powerful
  vasodilator)

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Initial mechanisms

• 3. Thrombosis
• Anticoagulants blood activity decrease
• (heparin is used for activation of
  lipoprotein lipase at hyperlipoproteinemia)
• Decreased antithrombosis properties of the
  injured endothelium
• Unmasked collagen fibers cause activation of the
  Villebrands factor

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Cardiomyocytes necrosis mechanism

• 1. ATP deficit
• Decrease of the cytochromoxydase activity
• Violation of electrons transfer in MCh
• Violation of Krebs-cycle
• Accumulation of acetylcoensime-A, fat acids
• Deficit of ATP and CPh causes
• - ineffective Na,?-??Pase (fatal
  arrhythmias)
• - ineffective ??-??Pase (damage of the Mch)

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Cardiomyocytes necrosis mechanism

• 2. Acidosis
• Accumulation of Crebs-cycle metabolits
• Accumulation of Acetyl-Co-A
• Accumulation of fatty acids
• Accumulation of piruvate acid
• Accumulation of lactic acid

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Cardiomyocytes necrosis mechanism

• Acidosis after-effects
• depression of cardiomyocytes contractility
• (main sign of ischemical area)
• Mechanisms
• 1. ?-ions interact with troponin. It causes of
  myosin releasing impossibility. So, as a result,
  interaction of actin and myosin becomes
  impossible
• 2. ?? deficit in cytoplasma occurs because Ca can
  be accumulated in Mch
• very often it is complicated by the
  reperfusion syndrome

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Cardiomyocytes necrosis mechanism

• 3. ?? accumulation
• Reasons
• 1. Deficient of Ca return in to SPR (ATP deficit
  decreases Ca-ATPase activity)
• 2. Violation of Na,??-exchange mechanism
• Consequences
• Ca deposit in Mch and ??P deficit
• Damage of cardiomyocytes membranes

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Cardiomyocytes necrosis mechanism

• 4. Lipid triade
• 1. Phospholipase activation (is caused by
  catecholamines and Ca)
• 2. Lipids peroxidation (accumulation of the free
  radicals, relative insufficiency of the
  antioxidants)
• 3. Fat acids (damage of the membranes lipids and
  violation of the ion channels functions)

necrosis
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Hibernal myocardium

• Especial condition of the heart which is
  characterized by the sharply decreased pump
  function of the heart (at human absolute rest)
  without cardiomyocytes cytolysis as a result of
  blood supply reducing
• 
  (protective reaction)

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Hibernal myocardium

• Sings
• Decreased left ventricle output at increased O2
  need of the organism (physical activity, fever,
  hyperthyroidism)
• Decreased using of ATP
• Retardation of the cardiomyocytes necrosis
• Renewal of ? concentration, creatinphosphate
  level, ???2 (during 1-3 hour)

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Hibernal myocardium

• Finishing
• Spontaneous recurrent process after blood supply
  restoring !!!
• 1 stage hypokinetic and asynchronous
  cardiomyocytes contruction
• 2 stage renewal of synchronous cardiomyo-cytes
  contruction and left ventricle output rising at
  increased O2 need of the organism (physical
  activity)

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(Panel A) Light micrograph of normal myocardium.
(Panel B) Representative light micrograph of
hibernating myocardium. The myolytic cytoplasm is
filled with PAS-positive material typical of
glycogen. Magnification 320.
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Myocardial Infarction Prevention

• Strophanthin comes from an extract of an African
  plant called strophanthus gratus.
• Since 1991 it was discovered as an endogenous
  substance that research shows can prevent angina
  pectoris and myocardial infarction by 80-100
  percent without major side effects.

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strophanthus gratus
Thank you for your attention!