Cvs ihd-csbrp

APR-2015-CSBRPAPR-2015-CSBRP

Ischemic Heart DiseaseIschemic Heart DiseaseCSBR.Prasad, MD.,CSBR.Prasad, MD.,


Review of termsReview of terms

IschemiaIschemia InfarctionInfarction NecrosisNecrosis Myocardial infarctionMyocardial infarction


Ischemic Heart Disease - Ischemic Heart Disease - IHDIHD

IHD representes a group of IHD representes a group of pathophysiologically related syndromes pathophysiologically related syndromes resulting from resulting from MYOCARDIAL ISCHEMIAMYOCARDIAL ISCHEMIA – – an imbalance between myocardial an imbalance between myocardial perfusion and demand for oxygenated perfusion and demand for oxygenated bloodblood


Ischemic Heart Disease - Ischemic Heart Disease - IHDIHD

> 90% cases> 90% cases Atherosclerotic Coronary Atherosclerotic Coronary Artery Disease (CAD)Artery Disease (CAD)

In In most casesmost cases the Disease is: the Disease is: SlowSlow Long latent period Long latent period Silent Silent Late Late

manifestations manifestations


IHDIHD CLINICAL SYNDROMESCLINICAL SYNDROMES

Angina PectorisAngina Pectoris: Less severe Ischemia. : Less severe Ischemia. Do not cause Muscle deathDo not cause Muscle death

Chronic IHD with Chronic IHD with Heart FailureHeart Failure Myocardial InfarctionMyocardial Infarction: Most Important : Most Important

Form of IHD. Duration & Severity of Form of IHD. Duration & Severity of Ischemia causes Muscle DeathIschemia causes Muscle Death

Sudden Cardiac DeathSudden Cardiac Death


IHD CLINICAL SYNDROMESIHD CLINICAL SYNDROMESSyndrome PathologyStable angina Fixed critical stenosisUnstable angina Plaque rupture with mural thrombus

Often with thromboembolismWith vasoconstriction --Resulting in decreased coronary flow

AMI Plaque rupture with complete thrombosisSudden death Severe multivessel disease

Often plaque ruptureOften thrombus or thromboemboli--Usually triggering fatal arrhythmia

Heart failure Chronic ischemia


EPIDEMIOLOGY OF EPIDEMIOLOGY OF IHDIHD Leading cause of Death in Males & Females Leading cause of Death in Males & Females

in US & Europein US & Europe IncidenceIncidence::

Now Declining in WestNow Declining in West In In India its IncreasingIndia its Increasing

Decline is due toDecline is due to:: Prevention of modifiable risk factors Prevention of modifiable risk factors Better Diagnostic & TreatmentBetter Diagnostic & Treatment

Risk factors are same as of AtherosclerosisRisk factors are same as of AtherosclerosisAPR-2015-CSBRPAPR-2015-CSBRP

PATHOGENESIS OF PATHOGENESIS OF IHDIHD

Diminished Coronary Perfusion Relative to Diminished Coronary Perfusion Relative to Myocardial demandMyocardial demand

Consequences ofConsequences of Fixed AS narrowing of Epicardial CAFixed AS narrowing of Epicardial CA Disrupted Atherosclerotic PlaquesDisrupted Atherosclerotic Plaques Intra-luminal ThrombosisIntra-luminal Thrombosis Platelet Aggregation & Vasospasm Platelet Aggregation & Vasospasm Syphilitic aortitis (coronary osteitis)Syphilitic aortitis (coronary osteitis)


PATHOGENESIS contd..PATHOGENESIS contd..

A fixed A fixed 75% Obstruction75% Obstruction Ischemia on Ischemia on exertionexertion

90% Stenosis90% Stenosis Ischemia at rest Ischemia at rest Single, Two or All Three CA can be Single, Two or All Three CA can be

affectedaffected LAD, Left Circumflex, RCALAD, Left Circumflex, RCA


Coronary Coronary ArteriesArteries

•Left Coronary A.•L.A.Descending•Left Circumflex

•Right Coronary A.

LCx

LAD


Role of Acute Plaque ChangeRole of Acute Plaque Change

Role of InflammationRole of Inflammation

Role of Coronary ThrombusRole of Coronary Thrombus

Role of vasoconstrictionRole of vasoconstriction

VasculitisVasculitis

PATHOGENESIS Contd..PATHOGENESIS Contd..


GENERAL PATHOLOGY OF GENERAL PATHOLOGY OF MYOCARDIAL ISCHAEMIAMYOCARDIAL ISCHAEMIA

FunctionalFunctional: Ischemic muscle ceases to : Ischemic muscle ceases to contract within a few minutes. contract within a few minutes. Necrosis is Necrosis is inhibited if flow is restored within 20-40 inhibited if flow is restored within 20-40 minsmins

BiochemicalBiochemical: : Oxygen tension falls, Mitochondrial Oxygen tension falls, Mitochondrial respiration Declines respiration Declines Ceases Ceases


Fatty fuels cannot be usedFatty fuels cannot be usedAnaerobic glycolysis Anaerobic glycolysis Increased Increased

concentration of lactic Acid.concentration of lactic Acid.

Limited Glycogen stores Limited Glycogen stores Reduce Reduce Intracellular ATP Intracellular ATP Concentrations Reach Concentrations Reach

Zero in 40-60 mins.Zero in 40-60 mins.

Creatinine Phosphate Conc.Creatinine Phosphate Conc. Zero Zero in 15 mins. Myosin ATPase Inhibited in 15 mins. Myosin ATPase Inhibited

CESSATION OF CONTRACTIONCESSATION OF CONTRACTION APR-2015-CSBRPAPR-2015-CSBRP


Temporal sequence of early biochemical Temporal sequence of early biochemical findings and progression of necrosis after findings and progression of necrosis after

onset of severe myocardial ischemia.onset of severe myocardial ischemia.

A,A, Early changes include loss of adenosine triphosphate Early changes include loss of adenosine triphosphate (ATP) and accumulation of lactate. (ATP) and accumulation of lactate.

B,B, For approximately 30 minutes after the onset of For approximately 30 minutes after the onset of even the most severe ischemia, myocardial injury is even the most severe ischemia, myocardial injury is

potentially reversible.potentially reversible.

ANGINA PECTORISANGINA PECTORIS

Symptom complex of IHDSymptom complex of IHD Paroxysmal & Recurrent Sub sternal or Paroxysmal & Recurrent Sub sternal or

Precordial Chest DiscomfortPrecordial Chest Discomfort Constricting, chocking, Squeezing, Constricting, chocking, Squeezing,

Stabbing painStabbing pain TransientTransient 15 sec to 15 Min 15 sec to 15 Min No Cardiac Muscle cell DeathNo Cardiac Muscle cell Death Falls Short of Infarction Falls Short of Infarction


ANGINA PECTORIS - ANGINA PECTORIS - APAP Three Overlapping Patterns of Angina Three Overlapping Patterns of Angina

PectorisPectoris::- Stable or Typical Angina- Stable or Typical Angina- Prinzmetal or Variant Angina- Prinzmetal or Variant Angina- Unstable or Cresendo Angina- Unstable or Cresendo Angina

There is Increased Myocardial demand, There is Increased Myocardial demand, Decreased Myocardial Perfusion, Decreased Myocardial Perfusion, Stenosing Plaques, Disrupted Plaques, Stenosing Plaques, Disrupted Plaques, vasospasmvasospasm


AP - AP - STABLE ANGINASTABLE ANGINA

Most Common FormMost Common Form Reduction of Coronary Perfusion due to Reduction of Coronary Perfusion due to

chronic Stenosing Atherosclerosischronic Stenosing Atherosclerosis Seen at Times of Seen at Times of Increased demandIncreased demand

Eg: Exercise, AnxietyEg: Exercise, Anxiety Relieved by Rest, NitroglycerinRelieved by Rest, Nitroglycerin, or Other , or Other

vasodilatorsvasodilators ECG shows ST segment DepressionECG shows ST segment Depression


AP - AP - PRINZMETAL ANGINAPRINZMETAL ANGINA

Uncommon typeUncommon type Occurs at RestOccurs at Rest Due to Due to VasospasmVasospasm of Coronaries of Coronaries Angina is Angina is Unrelated to Physical ActivityUnrelated to Physical Activity Responds to vasodilators like nitroglycerin Responds to vasodilators like nitroglycerin

& Calcium Channel Blockers& Calcium Channel Blockers ECG shows ST Segment ElevationECG shows ST Segment Elevation


AP - AP - UNSTABLE ANGINAUNSTABLE ANGINA Pattern of Pattern of pain that is Progressive pain that is Progressive with with

Increasing FrequencyIncreasing Frequency Precipitated by less EffortPrecipitated by less Effort Often occurs at restOften occurs at rest. Tends to be Long . Tends to be Long

DurationDuration Induced by Disruption of atherosclerotic Induced by Disruption of atherosclerotic

Plaques, with Superficial Thrombosis, Plaques, with Superficial Thrombosis, Embolisation & VasospasmEmbolisation & Vasospasm

Pre Infarction AnginaPre Infarction AnginaAPR-2015-CSBRPAPR-2015-CSBRP

MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION Death of the Cardiac Muscle by infarctionDeath of the Cardiac Muscle by infarction Most Important & Most severe form of IHDMost Important & Most severe form of IHD Leading cause of death in West & rising in Leading cause of death in West & rising in

INDIAINDIA Acute Coronary syndromesAcute Coronary syndromes::

- Myocardial Infarction- Myocardial Infarction- Unstable Angina- Unstable Angina- Sudden cardiac Death - Sudden cardiac Death


PATHOGENESIS OF MIPATHOGENESIS OF MI CORONARY ARTERY OCCLUSIONCORONARY ARTERY OCCLUSIONDisruption of PlaqueDisruption of Plaque Platelets exposed to Sub- Platelets exposed to Sub-

endothelial collagenendothelial collagen Platelet Adhesion, Platelet Adhesion,Aggregation, Activation, Release of potent Aggregation, Activation, Release of potent

Aggregators. Vasospasm is StimulatedAggregators. Vasospasm is Stimulated VASOSPASMVASOSPASM EMBOLIEMBOLI

Atrial Fibrillation Atrial Fibrillation Vegetative endocarditis Vegetative endocarditis

Pardoxical emboliPardoxical emboli UNEXPLAINEDUNEXPLAINED



Patterns of InfarctionPatterns of Infarction Transmural infarctionTransmural infarction

Necrosis involves the full thickness of the ventricular Necrosis involves the full thickness of the ventricular wallwall

Subendocardial Subendocardial (nontransmural) infarction(nontransmural) infarction Necrosis involving inner ⅓ to ½ of the ventricular wallNecrosis involving inner ⅓ to ½ of the ventricular wall

Multifocal microinfarctionMultifocal microinfarction pathology involving only smaller intramural vesselspathology involving only smaller intramural vessels occur in the setting of microembolization, vasculitis, or occur in the setting of microembolization, vasculitis, or

vascular spasmvascular spasm Eg: Eg: Takotsubo cardiomyopathyTakotsubo cardiomyopathy ( (“broken heart “broken heart

syndrome”syndrome” ) )


Progression of myocardial necrosis Progression of myocardial necrosis after coronary artery occlusionafter coronary artery occlusion



Distribution of myocardial ischemic necrosis correlates Distribution of myocardial ischemic necrosis correlates with the location and nature of decreased perfusionwith the location and nature of decreased perfusion


Patterns of Infarction - Patterns of Infarction - ECGECG

Owing to the characteristic ECG changes resulting Owing to the characteristic ECG changes resulting from myocardial ischemia or necrosis in various from myocardial ischemia or necrosis in various distributions:distributions:

Transmural infarctTransmural infarct is referred to as an “ST is referred to as an “ST elevation myocardial infarct” (elevation myocardial infarct” (STEMISTEMI) and ) and

Subendocardial infarctSubendocardial infarct as a “non–ST elevation as a “non–ST elevation infarct” (infarct” (NSTEMINSTEMI))

MicroinfarctionsMicroinfarctions show nonspecific changes or show nonspecific changes or can even be electrocardiographically can even be electrocardiographically silentsilent


Infarct Modification by ReperfusionInfarct Modification by Reperfusion““time is myocardiumtime is myocardium””

ReperfusionReperfusion: is the restoration of blood flow to ischemic : is the restoration of blood flow to ischemic myocardium threatened by infarctionmyocardium threatened by infarction

The goalThe goal: is to salvage cardiac muscle at risk and limit : is to salvage cardiac muscle at risk and limit infarct sizeinfarct size Prompt reperfusion is the preeminent objective for treatment of Prompt reperfusion is the preeminent objective for treatment of

patients with AMIpatients with AMI This can be accomplished by a host of coronary interventions:This can be accomplished by a host of coronary interventions:

ThrombolysisThrombolysis AngioplastyAngioplasty Stent placement or Stent placement or CABGCABG

The first 3 to 4 hours following obstruction are critical

Myocardial Necrosis Begins approx 30 Myocardial Necrosis Begins approx 30 Min after Coronary OcclusionMin after Coronary Occlusion

Prolonged IschemiaProlonged Ischemia Permanent Loss of Permanent Loss of FunctionFunction

Cell Death is By Coagulation Necrosis & Cell Death is By Coagulation Necrosis & ApoptosisApoptosis

Reperfusion in Less than 20 Min can Reperfusion in Less than 20 Min can Restore Cell ViabilityRestore Cell Viability

MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION


FEATURESFEATURES TIMETIME

Onset of ATP DepletionOnset of ATP Depletion SecondsSeconds

Loss of ContractilityLoss of Contractility Less than 2 MinLess than 2 Min

50% Reduction in ATP50% Reduction in ATP 10 Min10 Min

90% Reduction in ATP90% Reduction in ATP 40 Min40 Min

Irreversible Cell InjuryIrreversible Cell Injury 20 - 40 Min20 - 40 Min

Micro-vascular InjuryMicro-vascular Injury More than 1 HourMore than 1 Hour

KEY EVENTS IN ISCHEMIC CARDIAC MYOCYTES


LOCATION OF INFARCTLOCATION OF INFARCT LAD LAD Anterior & Apical LV Anterior & Apical LV

& 2/3 IV Septum [& 2/3 IV Septum [40-50%40-50%] ]

RCA RCA Post & Basal LV Post & Basal LV & Post 1/3 of IV Septum [30-40%] & Post 1/3 of IV Septum [30-40%]

LCA LCA Lateral wall of LV [15-20%] Lateral wall of LV [15-20%]


Coronary Coronary ArteriesArteries

•Left Coronary A.•L.A.Descending•Left Circumflex

•Right Coronary A.

LCx

LAD



Distribution of myocardial ischemic necrosis correlates Distribution of myocardial ischemic necrosis correlates with the location and nature of decreased perfusionwith the location and nature of decreased perfusion

Most common site for MI ?Most common site for MI ?Most common artery involved in MI ?Most common artery involved in MI ?

Anterior wall of left ventricleAnterior wall of left ventricleLeft anterior descending coronary arteryLeft anterior descending coronary artery


TIMETIME GROSSGROSS MICROSCOPYMICROSCOPY

0 to ½ Hour0 to ½ Hour No ChangesNo Changes NoneNone

½ to ½ to 4 Hrs4 Hrs NoneNone Variable Fibre Variable Fibre WavinessWaviness

4 to 12 Hrs4 to 12 Hrs Occ dark Occ dark MottlingMottling

Odema, Odema, Coag Coag NecrosisNecrosis, , HemorrhageHemorrhage

12 to 12 to 24 Hrs24 Hrs Dark MottlingDark Mottling Ongoing Coag Ongoing Coag Necrosis, Necrosis, NeutrophilsNeutrophils begin begin


TIMETIME GROSSGROSS MICROSCOPYMICROSCOPY

1 to 1 to 3 days3 days YellowYellow tan tan Infarct centreInfarct centre

Loss of Loss of Striations, Striations, Interstitial Interstitial NeutrophilsNeutrophils

3 to 7 days3 to 7 days Hyperamic Hyperamic BorderBorder, , central Softcentral Soft

Dead Cells, Dead Cells, Phagocytosis, Phagocytosis, macrophagesmacrophages

7 to 10 days7 to 10 days Red Tan Red Tan MarginsMargins

Early Early Granulation Granulation TissueTissue

10 days to 2 10 days to 2 weeksweeks

Depressed Depressed infarct infarct BordersBorders

New Blood New Blood vessels, collagenvessels, collagen



Typical appearance of reperfused myocardium:Typical appearance of reperfused myocardium:Large, densely hemorrhagic, anterior wall acute Large, densely hemorrhagic, anterior wall acute myocardial infarction treated with streptokinase, myocardial infarction treated with streptokinase,

((triphenyl tetrazolium chloride triphenyl tetrazolium chloride - stained heart slice)- stained heart slice)

PM angiogram: Posterior aspect of the heart of a patient who died of AMI.

Total occlusion of the distal right coronary artery by an acute thrombus (arrow)

and

Large zone of myocardial hypoperfusion involving the posterior left and right ventricles, as indicated by arrowheads.



Microscopic features of MI and its repairMicroscopic features of MI and its repair One-day-old infarctOne-day-old infarct


Microscopic features of MI and its repairMicroscopic features of MI and its repair MI 3-4 days oldMI 3-4 days old


Microscopic features of MI and its repairMI 7-10 days old


Microscopic features of MI and its repairGranulation tissue


Microscopic features of MI and its repairHealed myocardial infarct


8 wks



ReperfusionReperfusion

Reperfusion not only salvages reversibly injured cells but Reperfusion not only salvages reversibly injured cells but also alters the morphology of lethally injured cellsalso alters the morphology of lethally injured cells

The effects of reperfusion on myocardial viability and The effects of reperfusion on myocardial viability and functionfunction::

Clearly beneficialClearly beneficial Can trigger deleterious complications:Can trigger deleterious complications:

ArrhythmiasArrhythmias Reperfusion injuryReperfusion injury Endothelial swelling that occludes capillaries (Endothelial swelling that occludes capillaries (no-reflowno-reflow)) Biochemical abnormalities may also persist for days to weeks in Biochemical abnormalities may also persist for days to weeks in

reperfused myocytesreperfused myocytes Stunned myocardiumStunned myocardium HibernationHibernation


Effects of reperfusion on Effects of reperfusion on myocardial viability and functionmyocardial viability and function


Reperfusion injuryReperfusion injury“Contraction band necrosis”“Contraction band necrosis”


Clinical Features of AMIClinical Features of AMI Prolonged chest pain Prolonged chest pain

> 30 minutes> 30 minutes Crushing, stabbing, or squeezingCrushing, stabbing, or squeezing Retrosternal Retrosternal Radiating to left arm along ulnar borderRadiating to left arm along ulnar border Associated with profuse sweatingAssociated with profuse sweating Nausea and vomiting (involvement of posterior-inferior Nausea and vomiting (involvement of posterior-inferior

ventricle with secondary vagal stimulation)ventricle with secondary vagal stimulation) No chest pain No chest pain

Diabetic neuropathyDiabetic neuropathy Cardiac transplantsCardiac transplants

DyspneaDyspnea

DIAGNOSIS OF MIDIAGNOSIS OF MI

Typical Symptoms + Biochemical Typical Symptoms + Biochemical Investigations + ECG PatternInvestigations + ECG Pattern

Pain, Dyspnoea, Profuse Sweating, Rapid Pain, Dyspnoea, Profuse Sweating, Rapid Weak Pulse, Pulmonary CongestionWeak Pulse, Pulmonary Congestion

10 to 15% have 10 to 15% have Silent MISilent MI Early Perfusion by Cardiac Intervention is Early Perfusion by Cardiac Intervention is

BeneficialBeneficial




Laboratory diagnosis of AMILaboratory diagnosis of AMI The laboratory evaluation of MI is based on The laboratory evaluation of MI is based on

measuring the blood levels of proteins that leak measuring the blood levels of proteins that leak out of irreversibly damaged myocytesout of irreversibly damaged myocytes Cardiac specific troponins T and I (cTnT and cTnI) Cardiac specific troponins T and I (cTnT and cTnI) Creatine kinase (CK-MB) Creatine kinase (CK-MB) LDHLDH ASTAST MyoglobinMyoglobin


Laboratory diagnosis of AMILaboratory diagnosis of AMI

Time to elevation of CK-MB, cTnT and cTnI Time to elevation of CK-MB, cTnT and cTnI is 3 to 12 hrsis 3 to 12 hrs

CK-MB and cTnI peak at 24 hoursCK-MB and cTnI peak at 24 hours CK-MB returns to normal in 48-72 hrs, cTnI CK-MB returns to normal in 48-72 hrs, cTnI

in 5-10 days, and cTnT in 5 to 14 daysin 5-10 days, and cTnT in 5 to 14 days


Laboratory diagnosis of AMI

Laboratory diagnosis of AMI“Troponins”


Proteins that regulate the calcium mediated Proteins that regulate the calcium mediated contraction of cardiac and skeletal musclecontraction of cardiac and skeletal muscle

Cardiac specific Troponins are TnI & TnTCardiac specific Troponins are TnI & TnT They are highly tissue They are highly tissue specificspecific and high and high

sensitivesensitive marker of myocardial damage marker of myocardial damage TnI & TnT are TnI & TnT are not detectable in serumnot detectable in serum normally normally Both troponins rise at 2-4hrs and peak at 48hrs. Both troponins rise at 2-4hrs and peak at 48hrs.

They remain elevated for 7-10days after AMIThey remain elevated for 7-10days after AMI

Laboratory diagnosis of AMI“Troponins”


Formerly “Gold standard” CK-MB remains the Formerly “Gold standard” CK-MB remains the best alternative to Tnbest alternative to Tn

CK is present in brain, myocardium and CK is present in brain, myocardium and skeletal muscleskeletal muscle

Isoenzymes: CK-MM (skeletal muscle), CK-Isoenzymes: CK-MM (skeletal muscle), CK-BB (Brain, lung) CK-MB (primarily from BB (Brain, lung) CK-MB (primarily from myocardium)myocardium)

CK-MB rises within 2-4hrs, peaks at 24hrs and CK-MB rises within 2-4hrs, peaks at 24hrs and returns to normal within 72hrsreturns to normal within 72hrs

Laboratory diagnosis of AMI“CK-MB”


An An absence of a changeabsence of a change in the levels of in the levels of CK and CK-MB during the first two CK and CK-MB during the first two

days of chest pain and of Troponin in days of chest pain and of Troponin in the days following essentially the days following essentially excludes the diagnosis of MIexcludes the diagnosis of MI

Laboratory diagnosis of AMI


Laboratory diagnosis of AMIVarious enzyme status in AMI

ENZYMES Rises within Return to normal

TnI & TnT 4-8hrs 7-10days

CK-MB 4-8hrs 48-72hrs

LDH 24hrs 7-10days

AST / SGOT 12hrs 4-5days

Myoglobin Earliest 24hrsAPR-2015-CSBRPAPR-2015-CSBRP

Laboratory diagnosis of AMIVarious enzyme status in AMI

Enzyme marker for REINFARCTION after 4 days ?

CK-MB



Basic principles of managementBasic principles of management Half of the deaths associated with acute MI occur within 1 Half of the deaths associated with acute MI occur within 1

hour of onset, most commonly due to a fatal arrhythmiahour of onset, most commonly due to a fatal arrhythmia AMI therapeutic interventions includeAMI therapeutic interventions include::

Morphine to relieve pain and improve dyspneic symptomsMorphine to relieve pain and improve dyspneic symptoms Prompt reperfusion to salvage myocardiumPrompt reperfusion to salvage myocardium

Antiplatelet agents such as aspirin, P2Y12 receptor inhibitors, and GPIIb/IIIa Antiplatelet agents such as aspirin, P2Y12 receptor inhibitors, and GPIIb/IIIa inhibitorsinhibitors

Anticoagulant therapy with unfractionated heparin, low-molecular-weight heparin, Anticoagulant therapy with unfractionated heparin, low-molecular-weight heparin, direct thrombin inhibitors, and/or factor Xa inhibitors to prevent coronary artery direct thrombin inhibitors, and/or factor Xa inhibitors to prevent coronary artery clot propagationclot propagation

Nitrates to induce vasodilation and reverse vasospasmNitrates to induce vasodilation and reverse vasospasm Beta blockers to decrease myocardial oxygen demand and to reduce Beta blockers to decrease myocardial oxygen demand and to reduce

risk of arrhythmiasrisk of arrhythmias Antiarrhythmics to manage arrhythmiasAntiarrhythmics to manage arrhythmias Angiotensin-converting enzyme (ACE) inhibitors to limit ventricular Angiotensin-converting enzyme (ACE) inhibitors to limit ventricular

dilationdilation Oxygen supplementation to improve blood oxygen saturationOxygen supplementation to improve blood oxygen saturation


Prognostic factors in AMIPrognostic factors in AMI

Factors associated with a poorer prognosis Factors associated with a poorer prognosis includeinclude::

Advanced ageAdvanced age Female genderFemale gender Diabetes mellitus, andDiabetes mellitus, and Previous MI (cumulative effect)Previous MI (cumulative effect)


Complications of AMIComplications of AMI1.1. Contractile dysfunctionContractile dysfunction

Cardiogenic shockCardiogenic shock2.2. ArrhythmiasArrhythmias3.3. Myocardial ruptureMyocardial rupture4.4. Ventricular aneurysmVentricular aneurysm5.5. PericarditisPericarditis6.6. Infarct expansionInfarct expansion7.7. Mural thrombusMural thrombus8.8. Papillary muscle dysfunctionPapillary muscle dysfunction9.9. Progressive late heart failure (Chronic IHD)Progressive late heart failure (Chronic IHD)


Complications of AMIComplications of AMIAnterior myocardial rupture in an acute infarct Anterior myocardial rupture in an acute infarct (arrow)(arrow)

Cardiac tamponade



Complications of AMIComplications of AMIComplete rupture of a necrotic papillary muscleComplete rupture of a necrotic papillary muscle


Complications of AMIComplications of AMI Fibrinous pericarditis - Fibrinous pericarditis - Dressler syndromeDressler syndrome

Complications of AMIComplications of AMI Fibrinous pericarditis - Fibrinous pericarditis - Dressler syndromeDressler syndrome

Delayed pericarditis occurring from 2-3 wks Delayed pericarditis occurring from 2-3 wks after myocardial infarction after myocardial infarction

PrecipitantsPrecipitants: NSAIDs, Anticoagulants: NSAIDs, Anticoagulants Responds well to SalicylatesResponds well to Salicylates Important clinical featuresImportant clinical features::

Chest pain due to pericarditisChest pain due to pericarditis Fever and malaiseFever and malaise Raised ESRRaised ESR



Complications of AMIComplications of AMI Mural thrombusMural thrombus


Complications of AMIComplications of AMI Large apical left ventricular aneurysmLarge apical left ventricular aneurysm



Causes and Causes and outcomes outcomes

of IHDof IHD


Chronic Ischemic Heart DiseaseChronic Ischemic Heart Disease DefDef: Progressive congestive heart failure as a : Progressive congestive heart failure as a

consequence of accumulated ischemic consequence of accumulated ischemic myocardial damage and / or inadequate myocardial damage and / or inadequate compensatory responses compensatory responses

CausesCauses:: Chronic IHD usually appears postinfarction due Chronic IHD usually appears postinfarction due

to the functional decompensation of to the functional decompensation of hypertrophied noninfarcted myocardium hypertrophied noninfarcted myocardium

Severe obstructive coronary artery disease may Severe obstructive coronary artery disease may present as chronic congestive heart failure in the present as chronic congestive heart failure in the absence of prior infarctionabsence of prior infarction


Chronic IHD - Chronic IHD - MorphologyMorphologyGrossGross:: CardiomegalyCardiomegaly Stenotic coronaryStenotic coronary atherosclerosis atherosclerosis Discrete Discrete scarsscars representing healed infarcts representing healed infarcts Mural endocardium often has patchy fibrous thickeningsMural endocardium often has patchy fibrous thickenings Mural thrombiMural thrombi may be present may be presentMicroscopic findings includeMicroscopic findings include:: Myocardial hypertrophyMyocardial hypertrophy Diffuse subendocardial vacuolization, and Diffuse subendocardial vacuolization, and FibrosisFibrosis

CHRONIC IHDCHRONIC IHD

Seen in Seen in ELDERLYELDERLY Previous MI / Bypass SurgeryPrevious MI / Bypass Surgery Severe obstructive coronary artery Severe obstructive coronary artery

diseasedisease With or Without Acute MI or Healed MIWith or Without Acute MI or Healed MI


CLINICAL FEATURESCLINICAL FEATURES

Silent with HEART FAILURESilent with HEART FAILURE First First

Indication of chronic IHDIndication of chronic IHD

Insidious onset of CCF in patients withInsidious onset of CCF in patients with

past episodes of MI / By Passpast episodes of MI / By Pass

Also called Ischemic Cardiomyopathy Also called Ischemic Cardiomyopathy


SUDDEN CARDIAC DEATH SUDDEN CARDIAC DEATH Unexpected death from cardiac causesUnexpected death from cardiac causeswithin within ONEONE HOURHOUR or without onset or without onsetof symptomsof symptoms

80 to 90% : Complication of IHD80 to 90% : Complication of IHD10 to 20% : 10 to 20% : Non-Atherosclerotic causesNon-Atherosclerotic causes

- Aortic valve stenosis- Aortic valve stenosis - Mitral valve Prolapse- Mitral valve Prolapse - Myocarditis- Myocarditis - Cardiomyopathy- Cardiomyopathy - Pulmonary Hypertension- Pulmonary Hypertension - Long QT syndrome- Long QT syndrome - ARVH- ARVH


E N DE N D



Date post:	19-Jan-2017
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