Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial...

9
1. Physiology Factors determining myocardial oxygen supply and demand Myocardial oxygen demand 2. Mechanisms of myocardial ischemia 3. Acute adaptations to ischemia 4. Ischemic myocardial disease 5. Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen & inadequate removal of metabolites owing to reduced perfusion Most typical presentation: Angina pectoris (“strangling in the chest”) 1. Physiology Factors determining myocardial oxygen supply and demand (Fig. 1 ) 1 Diastolic perfusion pressure = P AO DIAST -P CAP CORON . Q ~ P/R . max. Q during diastole Venturi effect at coronary ostia →↓ P AO SYSTOLIC aortic regurgitation →↓P AO DIAST aortic stenosis →↓pressure gradient aorta/myocardium EDP →↓coronary perfusion during systole Compression of coronary bran- ches inside myocardium Coronary vascular resistence External compression of coronary branches during systole. Subendocardium subjected to greater forces, but better perfused (β2 receptors, relative ischemia). More vulnerable to diminished flow (hypotension, obstruction of epicardial arteries) Intrinsic regulation of coronary tone (autoregulation) Resistence at the level of arterioles and precapillary sphincters. Capillary recruitment in need (60-80% open in rest). Oxygen extraction 75% Local metabolites O 2 vasoconstriction O 2 →↑AMP →↑ adenosine ¬ Ca 2+ entry into SMC vasodilation Lactate, some prostaglandins, H + vasodilation Endothelium-dependent vasodilation factors ADP, ATP endothelium- bradykinin derived relaxing cGMP histamine factor (EDRF) acetylcholine NO· Ca 2+ release + PGI 2 prostacycline from SR vasodilation

Transcript of Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial...

Page 1: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

1 PhysiologyFactors determining myocardial oxygen supply and demandMyocardial oxygen demand

2 Mechanisms of myocardial ischemia

3 Acute adaptations to ischemia

4 Ischemic myocardial disease

5 Myocardial infarction

Myocardial ischemiaand

infarction Definition of myocardial ischemia

Deprivation of oxygen amp inadequate removal ofmetabolites owing to reduced perfusion

Most typical presentation Angina pectoris(ldquostrangling in the chestrdquo)

1 Physiology

Factors determining myocardial oxygen supplyand demand (Fig 1 )

1

Diastolic perfusion pressure = PAO DIAST - PCAP CORONQ ~ PR

max Q during diastole

Venturi effect at coronaryostia rarr darr PAO SYSTOLIC

aortic regurgitation rarr darrPAO DIASTaortic stenosis rarr darrpressure gradient aortamyocardiumuarrEDP rarr darrcoronary perfusion

during systole

Compression of coronary bran-ches inside myocardium

Coronary vascular resistenceExternal compression of coronary branchesduring systole Subendocardium subjected to greater forces but better perfused (β2 receptors relative ischemia) More vulnerable to diminishedflow (hypotension obstruction of epicardial arteries)

Intrinsic regulation of coronary tone (autoregulation)

Resistence at the level of arterioles andprecapillary sphincters Capillary recruitmentin need (60-80 open in rest) Oxygen extraction 75

Local metabolitesO2 rarr vasoconstrictiondarr O2 rarr uarrAMP rarr uarr adenosine not Ca2+ entryinto SMC rarr vasodilationLactate some prostaglandins H+ rarr vasodilation

Endothelium-dependent vasodilation factors

ADP ATP endothelium-bradykinin rarr derived relaxing rarr uarrcGMPhistamine factor (EDRF) perpacetylcholine equiv NOmiddot Ca2+ release

+ PGI2 equiv prostacycline from SRdarr

vasodilation

Pathologically changed endotheliararr activation of platelets rarr TXA2 rarr vasoconstrictionrarr reversal of the effects of endothelium-dependentvasodilation factors

Neural factorsParasymp of little influenceEpicardial vessels - α adrenergic receptors rarrtemporary vasoconstrictionSubendocardial vessels rarr β2-adrenergic receptors rarrvasodilatationAutoregulation is sufficient to 60 mmHg in aorta Advanced AS rarr maximal dilation rarr loss of regulation

Coronary collateral vessels important mainly in situation ofobstructionO2-carrying capacity (Hb + lungs) - usually constant

2 Heart rate β-blocker therapy rarr darr HRMost important parameter for oxyg consumption HR BPSYST

3 Contractility catecholamines rarr uarr O2 consumptionβ-blockers rarr darr O2 consumption

2 Mechanisms of myocardialischemia

Lesion rarr darrperfusion (Fig 2)

2

darr lumen radius to 50(= darr cross-sectional area to 25) + exercise and psychol stress rarr ischemia(= clinically important narrowing)darr lumen radius to 10 in rest

1 Atherosclerosismost commonin proximal segments or rarely diffuseradius below 50 rarr stable angina below 10 rarrangina in rest

2 Nonatherosclerotic coronary artery diseases -inflammatory (autoimmune) processes in small branches

bullpolyarteritis nodosabullsystemic lupus erythematosus collagen-vascular diseasesbullscleroderma

bull rheumatoid arthritis bulldiabetes

3 Coronary thrombosis and platelet aggregationFissure of an AS plaque rarr intraintimal thrombosis rarrunstable angina or IM (Fig 3)

3

4

Spasmusobstruction ratio (Fig4)

4

5 Coronary embolism from the left heart rare

6 Diminished coronary flow reserve without a morphological changes of coronary arteries

Def of CFR maximum flow divide resting flowFig 5 I II

5

7 Increased myocardial oxygen demand (see above)

3 Acute adaptations to ischemia

Acute defense ndash Fig 6

6

Ischemia rarr darrcreatine phosphate rarr darrATP rarr darrcontractilityrarr uarranorg P rarr darrcontractilityrarr anaerobic glycolysis rarr uarrATP

rarr intracellular acidosis rarr activation of lysosomesrarr tissue destructionrarr darrcontractility (H+ replace Ca 2+ )

4 Ischemic heart disease

Traditional types angina pectoris and myocardialinfarction Now added stunning hibernation preconditioning

Angina pectoris

Coronary ligature angioplasty rarr ischemic cascade (Fig 7)Contractile dysfunction damage gt 40 rarrcardiogenic shockMethods angiocardiography echocardiography nuclear angiography

7

METABOLIC ABNORMALITIES ECG ABNORMALITIES ANGINA PECTORIS

Stable angina pectorisExercise emotion rarr painDiscontinuation nitroglycerin rarr reliefUnchanged ge 2 - 3 monthsSevere AS rarr fixed darr blood supply combined withuarroxygen demand

Reproducible by fixed amount of exercise (HRBP)(Fig 5 I)

darr Release of EDRF (NO)ATP rarr adenosin rarr painECG Horizontal or declining depression of ST interval during exerciseLarge ischemia rarr syst amp diastolic dysfunction (darrEF)uarrArterioral tone rarr darr coronary flow reserve rarr rarrSAP without CAD (=syndrome X)

5

Unstable angina pectorisTypes 1 Progressive angina after a period of stable angina2 Recent minimal exercise (bdquoimmediately seriousldquo) 3 Intermediate coronary syndrom gt 15 min at rest 4 le4 weeks after IMMechanisms rupture of an AS plaques rarr plateletaggregation rarr thrombus

rupture hArr coronary spasmBoth rarr darrcoronary flow reserve (Fig 5 III)Same as in IM only milder

Therapy heparin aspirin

5

Variant angina pectoris (= variant = Prinzmetal)Pain at rest with ST denivelation intraindividually variable

response to exercise some patients without ASFocal spasm of epicardial coron artery(local hypersensitivity Fig 5 II)IM seldom

5

Mixed angina pectorisSpasmus platelet aggregation thrombosis at the site of a

plaque rarr mixed symptomatology (tolerance variesduring a day etc)

Silent myocardial ischemiaHolter ST denivelation andor darrejection fraction and

Thalium 201 abnormalities in the absence ofsymptoms

uarrpain threshold Prognosis

Ischemic ECG ndash Fig 8

8

Stunned myocardium

Fig 9

Reperfusion damage ventricular arrhythmias and stunnedmyocardiumDefinition Postischemic dysfunction of the myocardium with a brelatively normal perfusion15acute - 20acute ischemia rarr hrs od days of stunningReversible2 hypotheses

- free radicals (scavengers helpful if on the spot immediately)

- Ca2+ overload (free radicals rarr damage of SR andsarcolemma) Ca-blockers promising

Clinical demonstration difficult ndash local perfusion cannot bemeasured easily Hypothetically after operations angioplasty angina pectoris and IM rarr however lasting ischemia

Tab 1 Characteristics of stunned and hibernating myocardium

Hibernating myocardiumFig 9

Myocardial dysfunction could be dramatically amended by inotropic agents bypass or darrO2 consumptionDef Chronic reversible dysfunction of LV due to coronary

disease responding to inotropic stimuli Residual contractilereserve can be demonstrated by them

Could be presupposed in IM not explaining the degree of LV failureHistopathology loss of sarcomeres SR etc2 hypotheses

- original authors chronic resting hypoperfusion adaptivelowering of O2 consumption

- now basal perfusion is OK darrcoronary reserve Perfusionis not lowered so much as to explain the degree ofdysfunction rarr important stunning component CAD rarrdarrcoronary reserve rarrrarr repeated stunning several times a day

However stunning and hibernation are different phenomena(Tab 1)

Tab1

9

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 2: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

Pathologically changed endotheliararr activation of platelets rarr TXA2 rarr vasoconstrictionrarr reversal of the effects of endothelium-dependentvasodilation factors

Neural factorsParasymp of little influenceEpicardial vessels - α adrenergic receptors rarrtemporary vasoconstrictionSubendocardial vessels rarr β2-adrenergic receptors rarrvasodilatationAutoregulation is sufficient to 60 mmHg in aorta Advanced AS rarr maximal dilation rarr loss of regulation

Coronary collateral vessels important mainly in situation ofobstructionO2-carrying capacity (Hb + lungs) - usually constant

2 Heart rate β-blocker therapy rarr darr HRMost important parameter for oxyg consumption HR BPSYST

3 Contractility catecholamines rarr uarr O2 consumptionβ-blockers rarr darr O2 consumption

2 Mechanisms of myocardialischemia

Lesion rarr darrperfusion (Fig 2)

2

darr lumen radius to 50(= darr cross-sectional area to 25) + exercise and psychol stress rarr ischemia(= clinically important narrowing)darr lumen radius to 10 in rest

1 Atherosclerosismost commonin proximal segments or rarely diffuseradius below 50 rarr stable angina below 10 rarrangina in rest

2 Nonatherosclerotic coronary artery diseases -inflammatory (autoimmune) processes in small branches

bullpolyarteritis nodosabullsystemic lupus erythematosus collagen-vascular diseasesbullscleroderma

bull rheumatoid arthritis bulldiabetes

3 Coronary thrombosis and platelet aggregationFissure of an AS plaque rarr intraintimal thrombosis rarrunstable angina or IM (Fig 3)

3

4

Spasmusobstruction ratio (Fig4)

4

5 Coronary embolism from the left heart rare

6 Diminished coronary flow reserve without a morphological changes of coronary arteries

Def of CFR maximum flow divide resting flowFig 5 I II

5

7 Increased myocardial oxygen demand (see above)

3 Acute adaptations to ischemia

Acute defense ndash Fig 6

6

Ischemia rarr darrcreatine phosphate rarr darrATP rarr darrcontractilityrarr uarranorg P rarr darrcontractilityrarr anaerobic glycolysis rarr uarrATP

rarr intracellular acidosis rarr activation of lysosomesrarr tissue destructionrarr darrcontractility (H+ replace Ca 2+ )

4 Ischemic heart disease

Traditional types angina pectoris and myocardialinfarction Now added stunning hibernation preconditioning

Angina pectoris

Coronary ligature angioplasty rarr ischemic cascade (Fig 7)Contractile dysfunction damage gt 40 rarrcardiogenic shockMethods angiocardiography echocardiography nuclear angiography

7

METABOLIC ABNORMALITIES ECG ABNORMALITIES ANGINA PECTORIS

Stable angina pectorisExercise emotion rarr painDiscontinuation nitroglycerin rarr reliefUnchanged ge 2 - 3 monthsSevere AS rarr fixed darr blood supply combined withuarroxygen demand

Reproducible by fixed amount of exercise (HRBP)(Fig 5 I)

darr Release of EDRF (NO)ATP rarr adenosin rarr painECG Horizontal or declining depression of ST interval during exerciseLarge ischemia rarr syst amp diastolic dysfunction (darrEF)uarrArterioral tone rarr darr coronary flow reserve rarr rarrSAP without CAD (=syndrome X)

5

Unstable angina pectorisTypes 1 Progressive angina after a period of stable angina2 Recent minimal exercise (bdquoimmediately seriousldquo) 3 Intermediate coronary syndrom gt 15 min at rest 4 le4 weeks after IMMechanisms rupture of an AS plaques rarr plateletaggregation rarr thrombus

rupture hArr coronary spasmBoth rarr darrcoronary flow reserve (Fig 5 III)Same as in IM only milder

Therapy heparin aspirin

5

Variant angina pectoris (= variant = Prinzmetal)Pain at rest with ST denivelation intraindividually variable

response to exercise some patients without ASFocal spasm of epicardial coron artery(local hypersensitivity Fig 5 II)IM seldom

5

Mixed angina pectorisSpasmus platelet aggregation thrombosis at the site of a

plaque rarr mixed symptomatology (tolerance variesduring a day etc)

Silent myocardial ischemiaHolter ST denivelation andor darrejection fraction and

Thalium 201 abnormalities in the absence ofsymptoms

uarrpain threshold Prognosis

Ischemic ECG ndash Fig 8

8

Stunned myocardium

Fig 9

Reperfusion damage ventricular arrhythmias and stunnedmyocardiumDefinition Postischemic dysfunction of the myocardium with a brelatively normal perfusion15acute - 20acute ischemia rarr hrs od days of stunningReversible2 hypotheses

- free radicals (scavengers helpful if on the spot immediately)

- Ca2+ overload (free radicals rarr damage of SR andsarcolemma) Ca-blockers promising

Clinical demonstration difficult ndash local perfusion cannot bemeasured easily Hypothetically after operations angioplasty angina pectoris and IM rarr however lasting ischemia

Tab 1 Characteristics of stunned and hibernating myocardium

Hibernating myocardiumFig 9

Myocardial dysfunction could be dramatically amended by inotropic agents bypass or darrO2 consumptionDef Chronic reversible dysfunction of LV due to coronary

disease responding to inotropic stimuli Residual contractilereserve can be demonstrated by them

Could be presupposed in IM not explaining the degree of LV failureHistopathology loss of sarcomeres SR etc2 hypotheses

- original authors chronic resting hypoperfusion adaptivelowering of O2 consumption

- now basal perfusion is OK darrcoronary reserve Perfusionis not lowered so much as to explain the degree ofdysfunction rarr important stunning component CAD rarrdarrcoronary reserve rarrrarr repeated stunning several times a day

However stunning and hibernation are different phenomena(Tab 1)

Tab1

9

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 3: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

3 Coronary thrombosis and platelet aggregationFissure of an AS plaque rarr intraintimal thrombosis rarrunstable angina or IM (Fig 3)

3

4

Spasmusobstruction ratio (Fig4)

4

5 Coronary embolism from the left heart rare

6 Diminished coronary flow reserve without a morphological changes of coronary arteries

Def of CFR maximum flow divide resting flowFig 5 I II

5

7 Increased myocardial oxygen demand (see above)

3 Acute adaptations to ischemia

Acute defense ndash Fig 6

6

Ischemia rarr darrcreatine phosphate rarr darrATP rarr darrcontractilityrarr uarranorg P rarr darrcontractilityrarr anaerobic glycolysis rarr uarrATP

rarr intracellular acidosis rarr activation of lysosomesrarr tissue destructionrarr darrcontractility (H+ replace Ca 2+ )

4 Ischemic heart disease

Traditional types angina pectoris and myocardialinfarction Now added stunning hibernation preconditioning

Angina pectoris

Coronary ligature angioplasty rarr ischemic cascade (Fig 7)Contractile dysfunction damage gt 40 rarrcardiogenic shockMethods angiocardiography echocardiography nuclear angiography

7

METABOLIC ABNORMALITIES ECG ABNORMALITIES ANGINA PECTORIS

Stable angina pectorisExercise emotion rarr painDiscontinuation nitroglycerin rarr reliefUnchanged ge 2 - 3 monthsSevere AS rarr fixed darr blood supply combined withuarroxygen demand

Reproducible by fixed amount of exercise (HRBP)(Fig 5 I)

darr Release of EDRF (NO)ATP rarr adenosin rarr painECG Horizontal or declining depression of ST interval during exerciseLarge ischemia rarr syst amp diastolic dysfunction (darrEF)uarrArterioral tone rarr darr coronary flow reserve rarr rarrSAP without CAD (=syndrome X)

5

Unstable angina pectorisTypes 1 Progressive angina after a period of stable angina2 Recent minimal exercise (bdquoimmediately seriousldquo) 3 Intermediate coronary syndrom gt 15 min at rest 4 le4 weeks after IMMechanisms rupture of an AS plaques rarr plateletaggregation rarr thrombus

rupture hArr coronary spasmBoth rarr darrcoronary flow reserve (Fig 5 III)Same as in IM only milder

Therapy heparin aspirin

5

Variant angina pectoris (= variant = Prinzmetal)Pain at rest with ST denivelation intraindividually variable

response to exercise some patients without ASFocal spasm of epicardial coron artery(local hypersensitivity Fig 5 II)IM seldom

5

Mixed angina pectorisSpasmus platelet aggregation thrombosis at the site of a

plaque rarr mixed symptomatology (tolerance variesduring a day etc)

Silent myocardial ischemiaHolter ST denivelation andor darrejection fraction and

Thalium 201 abnormalities in the absence ofsymptoms

uarrpain threshold Prognosis

Ischemic ECG ndash Fig 8

8

Stunned myocardium

Fig 9

Reperfusion damage ventricular arrhythmias and stunnedmyocardiumDefinition Postischemic dysfunction of the myocardium with a brelatively normal perfusion15acute - 20acute ischemia rarr hrs od days of stunningReversible2 hypotheses

- free radicals (scavengers helpful if on the spot immediately)

- Ca2+ overload (free radicals rarr damage of SR andsarcolemma) Ca-blockers promising

Clinical demonstration difficult ndash local perfusion cannot bemeasured easily Hypothetically after operations angioplasty angina pectoris and IM rarr however lasting ischemia

Tab 1 Characteristics of stunned and hibernating myocardium

Hibernating myocardiumFig 9

Myocardial dysfunction could be dramatically amended by inotropic agents bypass or darrO2 consumptionDef Chronic reversible dysfunction of LV due to coronary

disease responding to inotropic stimuli Residual contractilereserve can be demonstrated by them

Could be presupposed in IM not explaining the degree of LV failureHistopathology loss of sarcomeres SR etc2 hypotheses

- original authors chronic resting hypoperfusion adaptivelowering of O2 consumption

- now basal perfusion is OK darrcoronary reserve Perfusionis not lowered so much as to explain the degree ofdysfunction rarr important stunning component CAD rarrdarrcoronary reserve rarrrarr repeated stunning several times a day

However stunning and hibernation are different phenomena(Tab 1)

Tab1

9

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 4: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

3 Acute adaptations to ischemia

Acute defense ndash Fig 6

6

Ischemia rarr darrcreatine phosphate rarr darrATP rarr darrcontractilityrarr uarranorg P rarr darrcontractilityrarr anaerobic glycolysis rarr uarrATP

rarr intracellular acidosis rarr activation of lysosomesrarr tissue destructionrarr darrcontractility (H+ replace Ca 2+ )

4 Ischemic heart disease

Traditional types angina pectoris and myocardialinfarction Now added stunning hibernation preconditioning

Angina pectoris

Coronary ligature angioplasty rarr ischemic cascade (Fig 7)Contractile dysfunction damage gt 40 rarrcardiogenic shockMethods angiocardiography echocardiography nuclear angiography

7

METABOLIC ABNORMALITIES ECG ABNORMALITIES ANGINA PECTORIS

Stable angina pectorisExercise emotion rarr painDiscontinuation nitroglycerin rarr reliefUnchanged ge 2 - 3 monthsSevere AS rarr fixed darr blood supply combined withuarroxygen demand

Reproducible by fixed amount of exercise (HRBP)(Fig 5 I)

darr Release of EDRF (NO)ATP rarr adenosin rarr painECG Horizontal or declining depression of ST interval during exerciseLarge ischemia rarr syst amp diastolic dysfunction (darrEF)uarrArterioral tone rarr darr coronary flow reserve rarr rarrSAP without CAD (=syndrome X)

5

Unstable angina pectorisTypes 1 Progressive angina after a period of stable angina2 Recent minimal exercise (bdquoimmediately seriousldquo) 3 Intermediate coronary syndrom gt 15 min at rest 4 le4 weeks after IMMechanisms rupture of an AS plaques rarr plateletaggregation rarr thrombus

rupture hArr coronary spasmBoth rarr darrcoronary flow reserve (Fig 5 III)Same as in IM only milder

Therapy heparin aspirin

5

Variant angina pectoris (= variant = Prinzmetal)Pain at rest with ST denivelation intraindividually variable

response to exercise some patients without ASFocal spasm of epicardial coron artery(local hypersensitivity Fig 5 II)IM seldom

5

Mixed angina pectorisSpasmus platelet aggregation thrombosis at the site of a

plaque rarr mixed symptomatology (tolerance variesduring a day etc)

Silent myocardial ischemiaHolter ST denivelation andor darrejection fraction and

Thalium 201 abnormalities in the absence ofsymptoms

uarrpain threshold Prognosis

Ischemic ECG ndash Fig 8

8

Stunned myocardium

Fig 9

Reperfusion damage ventricular arrhythmias and stunnedmyocardiumDefinition Postischemic dysfunction of the myocardium with a brelatively normal perfusion15acute - 20acute ischemia rarr hrs od days of stunningReversible2 hypotheses

- free radicals (scavengers helpful if on the spot immediately)

- Ca2+ overload (free radicals rarr damage of SR andsarcolemma) Ca-blockers promising

Clinical demonstration difficult ndash local perfusion cannot bemeasured easily Hypothetically after operations angioplasty angina pectoris and IM rarr however lasting ischemia

Tab 1 Characteristics of stunned and hibernating myocardium

Hibernating myocardiumFig 9

Myocardial dysfunction could be dramatically amended by inotropic agents bypass or darrO2 consumptionDef Chronic reversible dysfunction of LV due to coronary

disease responding to inotropic stimuli Residual contractilereserve can be demonstrated by them

Could be presupposed in IM not explaining the degree of LV failureHistopathology loss of sarcomeres SR etc2 hypotheses

- original authors chronic resting hypoperfusion adaptivelowering of O2 consumption

- now basal perfusion is OK darrcoronary reserve Perfusionis not lowered so much as to explain the degree ofdysfunction rarr important stunning component CAD rarrdarrcoronary reserve rarrrarr repeated stunning several times a day

However stunning and hibernation are different phenomena(Tab 1)

Tab1

9

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 5: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

5

Unstable angina pectorisTypes 1 Progressive angina after a period of stable angina2 Recent minimal exercise (bdquoimmediately seriousldquo) 3 Intermediate coronary syndrom gt 15 min at rest 4 le4 weeks after IMMechanisms rupture of an AS plaques rarr plateletaggregation rarr thrombus

rupture hArr coronary spasmBoth rarr darrcoronary flow reserve (Fig 5 III)Same as in IM only milder

Therapy heparin aspirin

5

Variant angina pectoris (= variant = Prinzmetal)Pain at rest with ST denivelation intraindividually variable

response to exercise some patients without ASFocal spasm of epicardial coron artery(local hypersensitivity Fig 5 II)IM seldom

5

Mixed angina pectorisSpasmus platelet aggregation thrombosis at the site of a

plaque rarr mixed symptomatology (tolerance variesduring a day etc)

Silent myocardial ischemiaHolter ST denivelation andor darrejection fraction and

Thalium 201 abnormalities in the absence ofsymptoms

uarrpain threshold Prognosis

Ischemic ECG ndash Fig 8

8

Stunned myocardium

Fig 9

Reperfusion damage ventricular arrhythmias and stunnedmyocardiumDefinition Postischemic dysfunction of the myocardium with a brelatively normal perfusion15acute - 20acute ischemia rarr hrs od days of stunningReversible2 hypotheses

- free radicals (scavengers helpful if on the spot immediately)

- Ca2+ overload (free radicals rarr damage of SR andsarcolemma) Ca-blockers promising

Clinical demonstration difficult ndash local perfusion cannot bemeasured easily Hypothetically after operations angioplasty angina pectoris and IM rarr however lasting ischemia

Tab 1 Characteristics of stunned and hibernating myocardium

Hibernating myocardiumFig 9

Myocardial dysfunction could be dramatically amended by inotropic agents bypass or darrO2 consumptionDef Chronic reversible dysfunction of LV due to coronary

disease responding to inotropic stimuli Residual contractilereserve can be demonstrated by them

Could be presupposed in IM not explaining the degree of LV failureHistopathology loss of sarcomeres SR etc2 hypotheses

- original authors chronic resting hypoperfusion adaptivelowering of O2 consumption

- now basal perfusion is OK darrcoronary reserve Perfusionis not lowered so much as to explain the degree ofdysfunction rarr important stunning component CAD rarrdarrcoronary reserve rarrrarr repeated stunning several times a day

However stunning and hibernation are different phenomena(Tab 1)

Tab1

9

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 6: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

8

Stunned myocardium

Fig 9

Reperfusion damage ventricular arrhythmias and stunnedmyocardiumDefinition Postischemic dysfunction of the myocardium with a brelatively normal perfusion15acute - 20acute ischemia rarr hrs od days of stunningReversible2 hypotheses

- free radicals (scavengers helpful if on the spot immediately)

- Ca2+ overload (free radicals rarr damage of SR andsarcolemma) Ca-blockers promising

Clinical demonstration difficult ndash local perfusion cannot bemeasured easily Hypothetically after operations angioplasty angina pectoris and IM rarr however lasting ischemia

Tab 1 Characteristics of stunned and hibernating myocardium

Hibernating myocardiumFig 9

Myocardial dysfunction could be dramatically amended by inotropic agents bypass or darrO2 consumptionDef Chronic reversible dysfunction of LV due to coronary

disease responding to inotropic stimuli Residual contractilereserve can be demonstrated by them

Could be presupposed in IM not explaining the degree of LV failureHistopathology loss of sarcomeres SR etc2 hypotheses

- original authors chronic resting hypoperfusion adaptivelowering of O2 consumption

- now basal perfusion is OK darrcoronary reserve Perfusionis not lowered so much as to explain the degree ofdysfunction rarr important stunning component CAD rarrdarrcoronary reserve rarrrarr repeated stunning several times a day

However stunning and hibernation are different phenomena(Tab 1)

Tab1

9

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 7: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

Preconditioning

Definition Fast adaptive response to a short (gt 2 minutes) ischemic damage lowering the decay of cells during a furtherprotracted period of ischemisation rarr darr infarction zoneDiffusion of endogene humoral factors (adenosine [nor]epinephrine activation of α1-receptor activation of A1 receptor for adenosine opening of the KATP channel) rarrslowering of metabolismProtective effect lasts several hrs ndash 1 dayIn clinics repeated coronary angioplastyProfylactic preconditioning

4 Myocardial infarction

Definition Condition of irreversible necrosis or apoptosisof the muscle that results from prolonged (40acute-60acute) ischemia

Fissure (rupture) of an AS plaque rarr thrombosis rarrobturation of a CA (Fig 10)

Dynamic By 8 - 10 days necrosis removed by 2 - 3 months scar formed (its strengthen with time)

Extention of IM Complete occlusion rarr transmural IMIncomplete occlusion rarr nontransmural IMVulnerable subendoc zone rarr subendocardial IM

Pathogenesis ischemia rarr IM (Fig 11)uarrcytosolic Ca2+ rarr irreversibility

10 11

Remodeling of a ventricle and complications (Fig 12)Remodeling = change of ventricle geometry by a scar andhypertrophy rarr darr compliance dilation failureMyocardial rupture rarr hemopericardium rarr tamponaderarr deathRupture of papillary muscle rarr pulm edemaReentry uarrautomaticity late afterdepolarization micro-embolisation into the myocardium rarr ventricular arrhy-thmias rarr sudden cardiac deathVentric aneurysm rarr thrombembolization arrhythmias

12

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 8: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

ECG in IM (Fig 13)

13

ST intervalHypoxia of cell rarr loss of rest voltage rarr cell surface relatively negative rarr injury current frominfarction focus to center of heart rarr depressionof TQ (=TP+PQ) on nearby electrode Injurycurrent disappears at ventricleacutes depolarization(ST interval) rarr ST interval in normal positionrarr it presents as being elevated compared todepressed TQ Reciprocal findings are present on distant electrode Start of ST interval returns toldquoisoelectricrdquo line after hours ST remains eleva-ted and convex upward normalization of ST after2 - 3 weeks

T waveIschemic zone bordering necrosis repolarizesslowly rarr T wave inversion outlasting ST nor-malization

Q wave (Fig 14)Propagation of excitation is lacking in necroticzone rarr vectors oriented contrarywise (of op-posite wall) prevail rarr deep amp wide Q on the nearby electrode Lasts indefinitely

14

Subendocardial (equiv non Q) IM rarr necrotic focusturned away from all electrodes rarr ST depressionin all electrodes i e a nonspecific signSerum enzymes in acute IM (Fig 15)

15

Therapy of IM Thrombolytic (last 20 ye)tissue plasminogen activatorstreptokinase

Conventional therapybed rest psychother sedationpain relief - nitrates morphineβ - blockers rarr darr sympathetic drive aspirin rarr darr platelet adhesivenessanticoagulants - heparinACE inhibitorsdiuretics in pulmonary edema

balloon angioplasty

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures

Page 9: Myocardial ischemia and infarction - MUNI MED ischemanj.pdf · Myocardial infarction Myocardial ischemia and infarction Definition of myocardial ischemia : Deprivation of oxygen &inadequate

Cardiogenic shock after IMinotropic agentswhen uarr TPVR rarr vasodilatorswhen darr preload rarr liquids ivintra-aortic balloon pump

Therapy of myocardial ischemiaNitrates rarr darr venous return

β - blockers rarr darr heart ratedarr contractility

Ca - channel rarr darr afterload rarr darr O2 consumptionblockers coronary dila-

tationRevascularization procedures