heart diseases
DESCRIPTION
HEART DISEASES. HEART DISEASES (HD). FIVE MAJOR TYPES Ischemic HD Hypertensive HD Valvular /Endocardial HD Cardiomyopathy HD Congenital HD Other s : pericarditis, tumor, et al. ISCHEMIC HEART DISEASE. Myocardial ischemia. - PowerPoint PPT PresentationTRANSCRIPT
![Page 1: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/1.jpg)
HEART HEART DISEASESDISEASES
![Page 2: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/2.jpg)
HEART DISEASES (HD)HEART DISEASES (HD)
FIVE MAJOR TYPES Ischemic HD Hypertensive HD Valvular/Endocardial HD Cardiomyopathy HD Congenital HD Others: pericarditis, tumor, et al.
![Page 3: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/3.jpg)
ISCHEMIC HEART ISCHEMIC HEART DISEASEDISEASE
![Page 4: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/4.jpg)
Myocardial ischemia Myocardial ischemia is a condition in which oxygen deprivation to the heart muscle is accompanied by inadequate removal of metabolites because of reduced blood flow or perfusion.
![Page 5: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/5.jpg)
Ischemic Heart DiseaseIschemic Heart Disease
Ischemic heart disease (IHD) is the generic designation for a group of closely related syndromes resulting from ischemia–an imbalance between the supply and demand of the heart for oxygenated blood.
.
![Page 6: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/6.jpg)
An imbalance occurs between myocardial oxygen supply and demand.
![Page 7: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/7.jpg)
“Supply” ischemia Acute reduction of oxygen supply secondary to
increased coronary vascular tone (ie, coronary vasospasm) or by marked reduction or cessation of coronary flow as a result of platelet aggregates or thrombi.
Responsible for myocardial infarction (MI) Most episodes of unstable angina (UA) In many circumstances, ischemia results from
both an increase in oxygen demand and a reduction in supply.
![Page 8: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/8.jpg)
“Demand" ischemiaIn the presence of coronary obstruction,
an increase of myocardial oxygen requirements caused by exercise, tachycardia, or emotion leads to a transitory imbalance.
Responsible for most episodes of chronic stable angina
![Page 9: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/9.jpg)
Ischemia may manifest as (1) anginal discomfort, (2) ST-segment deviation on ECG, (3) reduced uptake of thallium 201 or
technetium 99 in myocardial perfusion images,
(4) regional or global impairment of ventricular function.
![Page 10: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/10.jpg)
Supply Demand
![Page 11: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/11.jpg)
Supply
Demand
![Page 12: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/12.jpg)
Determinants of myocardial oxygen consumption Heart rate Contractility Systolic wall tension Maintenance of cell viability in basal state Depolarization Activation Maintenance of active state Direct metabolic effect of catecholamines Fatty acid uptake
![Page 13: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/13.jpg)
Ischemia comprises not only insufficiency of oxygen (hypoxia, anoxia), but also reduced availability of nutrient substrates and inadequate removal of metabolites.
![Page 14: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/14.jpg)
Because coronary artery narrowing or obstruction owing to atherosclerosis underlies myocardial ischemia in the vast majority of cases, IHD is often termed coronary artery disease (CAD) or coronary heart disease (CHD).
![Page 15: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/15.jpg)
The acute coronary syndromes of unstable angina, acute myocardial infarction, and sudden death
share a common pathophysiologic basis, with coronary atherosclerotic plaque rupture as the pathologic hallmark and associated intraluminal platelet-fibrin thrombus.
![Page 16: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/16.jpg)
The dominant influence in the causation of the IHD syndromes :
Fixed atherosclerotic narrowing of the coronary arteries,
Intraluminal thrombosis overlying a ruptured or fissured atherosclerotic plaque,
Platelet aggregation, Vasospasm.
![Page 17: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/17.jpg)
Role of Fixed Coronary ObstructionsRole of Fixed Coronary Obstructions
More than 90% of patients with IHD have advanced stenosing coronary atherosclerosis (“fixed” obstructions).
Although only a single major coronary
epicardial trunk may be affected, more often two or all three are involved .
![Page 18: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/18.jpg)
Role of Acute Plaque ChangeRole of Acute Plaque Change Acute myocardial ischemia is often precipitated by
disruption of previously only partially stenosing atherosclerotic plaques with hemorrhage, fissuring, or ulceration.
This is often followed by mural or total thrombosis. Such vascular injury is fundamental to the
development of the acute coronary syndromes–unstable angina, acute myocardial infarction, or sudden ischemic death–in most patients.
High-grade but slowly developing occlusions probably stimulate well-developed collateral vessels over time that may protect against infarction.
![Page 19: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/19.jpg)
![Page 20: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/20.jpg)
![Page 21: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/21.jpg)
![Page 22: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/22.jpg)
Role of Coronary ThrombusRole of Coronary Thrombus
Coronary thrombosis, partial or total, plays a critical role in acute coronary syndromes.
In myocardial infarction, the added thrombus converts a disrupted, partially stenotic plaque to a complete stenosis.
Thrombus is a potent activator of multiple growth-related signals in smooth muscle cells; both platelet-mediated and smooth muscle cell-mediated events contribute to the growth of atherosclerotic lesions.
![Page 23: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/23.jpg)
![Page 24: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/24.jpg)
Role of VasoconstrictionRole of Vasoconstriction
Transient vasoconstriction may be induced at a site of plaque disruption and thrombosis.
![Page 25: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/25.jpg)
Terminology: Ischemic Heart Disease
• Ischemia - Insufficient blood supply injury Angina (reversible) or MI (irreversible)
• Angina (Angina=Strangulation Pectoris=Chest)
• Myocardial infarction (MI) - Death of myocardial cells (irreversible)
• Cardiac failure : Impaired pumping ability of the heart
• Cardiogenic shock : Shock due to cardiac failure
• Arrhythmias: cardiac rhythm disturbances
![Page 26: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/26.jpg)
Coronary circulationCoronary circulation Rich Blood supply High Oxygen consumption (A-V19-9ml/100ml)
Two coronary arteries-225 ml/min Direct branch from aorta End arteries – few collaterals Phasic blood flow- during diastole Local metabolism is primary controller of
coronary blood flow
![Page 27: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/27.jpg)
Coronary Coronary ArteriesArteries
Right Coronary Artery
LCx
LAD
Left Coronary Artery
•Anterior Descending
•Circumflex
![Page 28: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/28.jpg)
Abnormalities of OAbnormalities of O22 supply supply
Increased O2 demandHigh heart rate, BP, Contractility
Insufficient O2 supplyAnemia and Hypoxia
Coronary VesselsIntermittent (Spasm, Congenital)Permanent (Atherosclerotic Plaque)
![Page 29: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/29.jpg)
Depending on the rate of development and ultimate severity of the arterial narrowing(s) and the myocardial response, four ischemic syndromes may result:
(1) angina pectoris
(2) myocardial infarction
(3) chronic ischemic heart disease
(4) sudden cardiac death
IIschemic syndromesschemic syndromes
![Page 30: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/30.jpg)
1. Angina Pectoris
Stable (classic, typical, Heberden) angina
Unstable (pre-infarction, crescendo, acute coronary insufficiency) angina
Prinzmetal's ("variant") angina
![Page 31: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/31.jpg)
Anginas are caused by varying combinations of increased myocardial demand and decreased myocardial perfusion, owing to
fixed stenosing plaques disrupted plaques vasospasm thrombosis platelet aggregation embolization
![Page 32: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/32.jpg)
Angina pectoris is a symptom complex of IHD characterized by paroxysmal attacks of
substernal or precordial chest discomfort (variously described as
constricting, squeezing, choking, or knife-like)
Caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction.
![Page 33: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/33.jpg)
Stable (classic, typical, Heberden) angina
The pathogenesis of typical angina pectoris appears to be the reduction of coronary perfusion to a critical level by chronic stenosing coronary atherosclerosis.
This renders the heart vulnerable to further ischemia whenever there is increased demand, such as that produced by physical activity, emotional excitement, or any other cause of increased cardiac workload.
Relieved by rest or nitroglycerin, a strong coronary vasodilator (thereby increasing supply).
![Page 34: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/34.jpg)
Unstable (pre-infarction, crescendo, acute coronary insufficiency) angina
Refers to a pattern of pain that occurs with progressively increasing frequency, is precipitated with progressively less effort, often occurs at rest, and tends to be of prolonged duration.
In most cases, this is probably due to a thrombus developing over a ruptured plaque.
![Page 35: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/35.jpg)
In unstable angina, a relatively small fissure or disruption of an atherosclerotic plaque may lead to a sudden change in plaque morphology, with platelet aggregation or mural thrombus and frequently vasoconstriction leading to transient reduction in coronary blood flow.
Untreated, many of these people get an MI soon.
![Page 36: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/36.jpg)
Prinzmetal's ("variant") angina
This is primarily attributable to vasospasm. Perhaps it's the cardiac equivalent of migraine. Although individuals with this form of angina may well
have significant coronary atherosclerosis, the anginal attacks are generally unrelated to physical activity, heart rate, or blood pressure.
Prinzmetal’s angina generally responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers.
![Page 37: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/37.jpg)
2. Myocardial Infarction“Heart attack”
• Death of Myocardial muscle due to lack of blood supply.
• Most common cause is Atherosclerotic narrowing of coronary arteries.
![Page 38: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/38.jpg)
Pain in Myocardial InfarctionPain in Myocardial Infarction
Precordial , intense, constrictive Similar to Angina – severe prolonged Radiates to shoulder and left arm May present in other location-jaw,
epigastrium. Often with breathlessness, nausea,
vomiting & perspiration Hypotension Collapse Less severe or absent in elderly No response to nitrates
![Page 39: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/39.jpg)
Causes of myocardial infarctsCauses of myocardial infarcts
Atherosclerosis: Makes up 90% of coronary artery disease Cocaine: The second most common cause of myocardial
infarction and sudden cardiac death Prinzmetal's coronary spasm Vasculitis: (1) lupus; (2) polyarteritis nodosa; (3)
rheumatoid arthritis; (4) Kawasaki's; (5) Takayasu's; (6) mycotic aneurysms.
Embolization Syphilis (mesaortitis syphilitica) Dissecting hematoma Shock and left-sided failure (subendocardial infarct )
![Page 40: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/40.jpg)
There are two types of myocardial infarction, each having differing morphology and clinical significance:
(1) The transmural infarct (more common type)
(2) The subendocardial (nontransmural) infarct
![Page 41: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/41.jpg)
TThe transmural infarcthe transmural infarct
The ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery.
This pattern of infarction is usually associated with
coronary atherosclerosis plaque rupture superimposed thrombosis
![Page 42: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/42.jpg)
Subendocardial InfarctionSubendocardial Infarction
An area of ischemic necrosis limited to the inner one-third or at most one-half of the ventricular wall, often extending laterally beyond the perfusion territory of a single coronary artery.
There is diffuse stenosing coronary atherosclerosis and global reduction of coronary flow but neither plaque rupture nor superimposed thrombosis.
![Page 43: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/43.jpg)
Coronary Arterial OcclusionCoronary Arterial Occlusion
At least 90% of transmural acute myocardial infarcts are caused by an occlusive intracoronary thrombus overlying an ulcerated or fissured stenotic plaque.
Every acute transmural myocardial infarct, a dynamic interaction has occurred among several or all of the following: severe coronary atherosclerosis, an acute atheromatous
plaque change (fissuring, ulceration), superimposed thrombosis, platelet activation, and vasospasm.
![Page 44: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/44.jpg)
In the typical case, the following sequence of events can be proposed (90%):
Sudden change in the morphology of an atheromatous plaque, i.e., intraplaque hemorrhage, ulceration, or fissuring.
Platelet adhesion, aggregation, activation, and release of adenosine diphosphate (ADP), with buildup of a platelet mass. The platelet mass may give rise to emboli or potentiate occlusive thrombosis.
Tissue thromboplastin is released. Adherent activated platelets release thromboxane A2,
serotonin, and platelet factors 3 and 4 (predisposing to coagulation, favoring vasospasm).
Frequently within minutes, the thrombus evolves to become completely occlusive.
![Page 45: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/45.jpg)
In the approximately 10% of casesIn the approximately 10% of cases
In some of the cases, the coronary arteries are free of atherosclerosis by angiography:
Vasospasm with or without coronary atherosclerosis may induce the acute perfusion deficit, perhaps in association with platelet aggregation.
Emboli from a left-sided mural thrombosis or vegetative endocarditis or paradoxic emboli from the right side of the heart or the peripheral veins (through a patent foramen ovale) could cause coronary occlusion.
![Page 46: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/46.jpg)
Coronary AtheorsclerosisCoronary Atheorsclerosis
Right Coronary Artery
LCx
LAD
![Page 47: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/47.jpg)
Coronary AtheorsclerosisCoronary Atheorsclerosis
![Page 48: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/48.jpg)
Myocardial Infarction : Myocardial Myocardial Infarction : Myocardial
ResponseResponse
Occlusion of a major coronary artery results in ischemia throughout the anatomic region supplied by that artery (called area at risk),
Acutely ischemic myocardium undergoes progressive biochemical, functional, and morphologic changes, the outcome of which largely depends on the severity and duration of flow deprivation.
![Page 49: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/49.jpg)
The principal biochemical consequence of myocardial ischemia is the onset of anaerobic glycolysis within seconds, leading to inadequate production of high-energy
phosphates (e.g., creatine phosphate and adenosine triphosphate [ATP ]) and accumulation of potentially noxious breakdown products (such as lactic acid).
Myocardial function is exceedingly sensitive to severe ischemia; striking loss of contractility is evident within 60 seconds of onset.
![Page 50: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/50.jpg)
Reversible ultrastructural changes develop within few minutes after onset of ischemia e.g., cell and mitochondrial swelling, glycogen
depletion. Although function becomes strikingly abnormal
within few minutes after onset of ischemia, myocardial coagulation necrosis occurs only after 20 to 40 minutes of severe ischemia.
![Page 51: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/51.jpg)
Irreversible injury of ischemic myocytes occurs first in the subendocardial zone.
With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone.
![Page 52: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/52.jpg)
![Page 53: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/53.jpg)
The precise location, size, and specific morphologic features of an acute myocardial infarct depend on:
(1) the location, severity, and rate of development of coronary atherosclerotic obstructions;
(2) the size of the vascular bed perfused by the obstructed vessels; (3) the duration of the occlusion; (4) the metabolic/oxygen needs of the myocardium at risk; (5) the extent of collateral blood vessels; (6) the presence, site, and severity of coronary arterial spasm; (7) other factors
such as alterations in blood pressure, heart rate, and cardiac rhythm.
![Page 54: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/54.jpg)
LOCATIONLOCATIONThe corresponding sites of myocardial lesions:The corresponding sites of myocardial lesions:
Left anterior descending coronary artery (40 to 50%): Anterior wall of left ventricle near apex Anterior two-thirds of interventricular septum
Right coronary artery (30 to 40%): Inferior/posterior wall of left ventricle Posterior one-third of interventricular septum Posterior right ventricular free wall in some cases
Left circumflex coronary artery (15 to 20%): Lateral wall of left ventricle
![Page 55: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/55.jpg)
1.Left anterior descending: Anterior wall, anterior 2/3 of septum, apex (40-50%)
2.Right: Posterior-inferior wall, posterior 1/3 of septum (30-40%)
3.Left circumflex: Lateral wall (15-20%)
Classically, the coronary arteries have the following distribution, and their occlusion will result in transmural infarcts in the corresponding distribution
![Page 56: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/56.jpg)
Several infarcts of varying age in the same heart are frequently found.
Repetitive necrosis of adjacent regions yields progressive extension of an individual infarct over a period of days to weeks–“stuttering infarct.”
Examination of the heart in such cases often reveals a central zone of infarction that is days to weeks older than a peripheral margin of more recent ischemic necrosis.
SStuttering infarcttuttering infarct
![Page 57: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/57.jpg)
Areas of damage undergo a progressive sequence of changes that consist of typical ischemic coagulative necrosis, followed by inflammation and repair.
The appearance of an infarct at autopsy depends on the duration of survival of the patient following myocardial infarction onset.
Early recognition of acute myocardial infarcts by pathologists is a difficult problem:particularly when death has occurred within minutes to
a few hours after the onset of the ischemic injury, because diagnostic morphologic changes lag behind the actual injury.
Macroscopical findingsMacroscopical findings
![Page 58: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/58.jpg)
Myocardial infarcts less than 6 to 12 hours old are usually inapparent on gross examination.
It is often possible, however, to highlight the area of necrosis by histochemical changes that first become apparent after 2 to 3 hours.
Immersion of tissue slices in a solution of triphenyltetrazolium chloride (TTC) imparts a brick-red color to intact, noninfarcted myocardium where the dehydrogenase enzymes are preserved. Because dehydrogenases are depleted in the area of ischemic
necrosis (i.e., they leak out through the damaged cell membranes), an infarcted area is revealed as an unstained pale zone (especially apparent after fixation, when unstained myocardium appears light brown).
![Page 59: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/59.jpg)
By 12 to 48 hours, the lesion can be identified in routinely fixed gross slices (including those not stained with TTC) because of either pallor or a red-blue hue owing to the stagnated, trapped blood. Progressively thereafter the infarct becomes a more sharply defined yellow zone.
Within10 days to 2 weeks the there is a softened area rimmed by a hyperemic zone of highly vascularized granulation tissue.
Over the succeeding weeks, the injured region evolves to a fibrous scar.
![Page 60: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/60.jpg)
Microscopical findingsMicroscopical findings
Using light microscopy of sections stained by routine tissue stains, the typical microscopic changes of coagulative necrosis are not detectable for at least the first 4 to 12 hours.
“Wavy fibers” may be present at the periphery of the infarct; it is thought that these changes result from the
forceful systolic tugs by the viable fibers immediately adjacent to the noncontractile dead fibers, stretching and buckling them.
![Page 61: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/61.jpg)
Duration Macro Micro
0-30 m None Loss of glycogen (EM)
4-8 h None EM: Earliest nuclear changes, Wavy fibers
8-12 h None Contraction bands
12-48 h Sharply defined yellow lesion, Edema
Necrosis,
Acute inflammation
3-7 D Hyperemia and Hemorrhage
Early findings of Granulation tissue
1-3 W Thin, yellow Granulation tissue,
Early fibrosis
3-7 W Tough white Dense Fibrosis
MorphologyMorphology
![Page 62: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/62.jpg)
Coronary Coronary Thrombosis Thrombosis With InfarctionWith Infarction
![Page 63: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/63.jpg)
Coronary AtherosclerosisCoronary Atherosclerosis
![Page 64: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/64.jpg)
Coronary Atherosclerosis with ThrombosisCoronary Atherosclerosis with Thrombosis
![Page 65: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/65.jpg)
Myocardial Infarction – 3Myocardial Infarction – 3 dd
![Page 66: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/66.jpg)
Myocardial Infarction – Myocardial Infarction – 1 W1 W
![Page 67: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/67.jpg)
Myocardial Infarction – Myocardial Infarction – 22 WW
![Page 68: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/68.jpg)
Myocardial Infarction – Myocardial Infarction – 33 WW
![Page 69: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/69.jpg)
Myocardial InfarctionMyocardial Infarction – 5 W – 5 W
![Page 70: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/70.jpg)
Normal MyocardiumNormal Myocardium
![Page 71: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/71.jpg)
MI MI 1212-4-488 hr hr
loss of nucleus, contaction bands, coagulative necrosisloss of nucleus, contaction bands, coagulative necrosis..
Contraction bands (myofibrillar degeneration) densely eosinophilic cross-bands which probably result from calcium entering membrane-damaged cells during reperfusion. Contraction bands let you know that a sudden death is of cardiac ischemic origin.
Contraction bands can probably result from epinephrine administration and/or electric shocks in CPR.
![Page 72: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/72.jpg)
MI 3-4 dayMI 3-4 day
![Page 73: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/73.jpg)
MI 1MI 1st st wweekeek
![Page 74: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/74.jpg)
MI 2-MI 2-33 W W
![Page 75: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/75.jpg)
MI >MI >33--77 W W Collagen ScarCollagen Scar
![Page 76: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/76.jpg)
If the patient with acute myocardial infarction reaches the If the patient with acute myocardial infarction reaches the hospital, the likelihood of the most serious complications is as hospital, the likelihood of the most serious complications is as follows:follows:
Uncomplicated cases (10 to 20% of cases) Complicated cases (80 to 90% of cases):
Arrhythmias and conduction defects (75-95% of complicated cases)
Extension of infarction, or re-infarction Left-sided Congestive heart failure (pulmonary edema) Cardiogenic shock (10-15%; high mortality ~70% sudden
death) Dressler's pericarditis/postpericardiotomy syndrome
(occurs weeks after an MI or cardiac surgery) Mural thrombosis, embolization Myocardial wall rupture (tamponade) Septum rupture (left-to-right shunt) Papillary muscle rupture (mitral regurgitation) Ventricular aneurysm Chronic ischemic heart disease
![Page 77: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/77.jpg)
Cardiogenic shockCardiogenic shock
Severe “pump failure” (cardiogenic shock), which occurs in 10 to 15% of patients following myocardial infarction
Generally indicates a large infarct (often greater than 40% of the left ventricle)
Cardiogenic shock has a nearly 70% mortality rate and accounts for two-thirds of in-hospital deaths
![Page 78: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/78.jpg)
RuptureRupture
The cardiac rupture syndromes result from the mechanical weakening that occurs in necrotic and subsequently inflamed myocardium and include ;
(1) rupture of the ventricular free wall (most commonly), usually with hemopericardium and cardiac tamponade,
(2) rupture of the interventricular septum (less commonly), leading to a left-to-right shunt;
(3) papillary muscle rupture (least commonly), resulting in the acute onset of severe acute mitral regurgitation.
![Page 79: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/79.jpg)
MI - RuptureMI - Rupture
![Page 80: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/80.jpg)
TTamponadeamponade
![Page 81: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/81.jpg)
PericarditisPericarditis A fibrinous or fibrinohemorrhagic pericarditis usually
develops about the second or third day. It is most often localized to the region overlying the
necrotic area and usually resolves with healing of the infarct.
Pericarditis is the epicardial manifestation of the inflammation elicited by a direct underlying transmural infarct.
![Page 82: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/82.jpg)
AneurysmAneurysm
![Page 83: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/83.jpg)
The clinical and laboratory diagnosis of The clinical and laboratory diagnosis of acute myocardial infarctionacute myocardial infarction
Creatinine Kinase
CK- Isoenzymes (Fractions)
Troponins - I & T.
LDH - 1-5 (1 - 2 flip)
Myoglobin
• Symptoms• ECG changes• Elevations of specific
serum enzymes
![Page 84: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/84.jpg)
3. Chronic Ischemic Heart Disease3. Chronic Ischemic Heart Disease The designation chronic ischemic heart
disease (CIHD) is used here for the hearts in patients, often but not exclusively elderly, who insidiously develop CHF, sometimes fatal, as a consequence of ischemic myocardial damage.
There has been a history of angina and usually prior episodes of myocardial infarction, often as remote as 5 to 10 years before the onset of the CHF.
![Page 85: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/85.jpg)
MorphologyMorphology The pericardial surface of the heart in CIHD may have
adhesions as a result of healing of pericarditis associated with past myocardial infarcts.
Invariably there is moderate to severe stenosing atherosclerosis of the coronary arteries and sometimes total occlusions resulting from organized thrombi.
Discrete, gray-white scars of healed previous infarcts are usually present.
The mural endocardium is generally normal except for some superficial, patchy, fibrous thickenings.
![Page 86: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/86.jpg)
The major microscopic findings includediffuse myocardial atrophysubendocardial vacuolizationdiffuse, interstitial and patchy replacement
fibrous tissuelarge healed scars of previous acute infarcts.
![Page 87: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/87.jpg)
Chronic Ischemic Heart Disease Can Lead to Cardiomyopathy In a minority of patients with severe coronary
atherosclerosis, myocardial contractility is impaired globally without discrete infarcts, as in dilated cardiomyopathy.
This situation usually reflects a combination of • ischemic myocardial dysfunction, • diffuse fibrosis, • multiple small healed infarcts.
Ischemic cardiomyopathy.
![Page 88: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/88.jpg)
4. Sudden cardiac death4. Sudden cardiac death Most commonly sudden cardiac death (SCD) is defined as
unexpected death from cardiac causes early (usually within 1 hour) after or without the onset of symptoms.
In the vast majority of cases in adults, SCD is a complication and often the first clinical manifestation of IHD. Less frequently SCD is caused by
• a congenital structural abnormality• aortic valve stenosis• hereditary or acquired abnormalities of the cardiac conduction
system• mitral valve prolapse• myocarditis• idiopathic dilated or hypertrophic cardiomyopathy
![Page 89: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/89.jpg)
MorphologyMorphology
The ultimate mechanism of death is almost always a lethal arrhythmia (e.g., asystole, ventricular fibrillation). Long-standing coronary atherosclerosis
with diffuse myocardial atrophy, Interstitial fibrosis, Possibly healed infarcts.
They can impinge on the conduction system and create electromechanical cardiac instability.
![Page 90: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/90.jpg)
In most cases, however, acute myocardial ischemia with or without plaque fissuring or myocardial infarction induces irritability of myocardium distant from the conduction system and triggers the fatal arrhythmia.
Marked coronary atherosclerosis with critical (greater than 75%) stenosis involving more than one of the three major vessels is present in 80 to 90% of victims; only 10 to 20% of cases are of nonatherosclerotic origin.
Usually there are high-grade stenoses (greater than 90%).
![Page 91: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/91.jpg)
The precise frequency of acute coronary changes (i.e., thrombosis, plaque fissuring, intraplaque hemorrhage) are common (75 to 80%).
A healed myocardial infarct is present in about 40%, but in those who have been rescued by prompt therapy from sudden cardiac arrest, new myocardial infarction is found in 25% or less.
![Page 92: HEART DISEASES](https://reader035.vdocuments.site/reader035/viewer/2022062321/56813255550346895d98d98a/html5/thumbnails/92.jpg)
THANK YOU