Cardio-pathology-ischemic heart disease Flashcards
Ischemic heart disease (IHD) includes several syndromes caused by .
myocardial ischemia
Ischemic injury to the myocardium can be caused by which 2 things?
- lack of blood flow
- increased demand
or both
cardiac myocytes generate energy almost exclusively through
which biochemical process?
mitochondrial oxidative phosphorylation,
In > percent of cases, IHD is a consequence of reduced coronary blood flow secondary to obstructive atherosclerotic vascular disease
90%
What is the other name for ischemic heart disease?
coronary artery disease, due to the majority of cases being from obstructive atherosclerotic vascular disease.
In most cases, the syndromes of IHD are consequences of coronary that has been progressing for decades.
atherosclerosis
Ischemic heart disease may include one or more of the following 4 cardiac syndromes:
- angina pectoris
- MI
- Chronic IHD with congestive heart failure (CHF)*
- Sudden cardiac death (SCD)
What is angina pectoris?
chest pain
Ischemia induces pain, but is insufficient to cause myocyte death
In angina pectoris, Ischemia induces pain, and is insufficient/sufficient to cause myocyte death.
insufficient
What type of angina occurrs predictably at certain levels of exertion?
stable angina
Which type angina can be caused by vessel spasm?
Prinzmetal angina
Which type of angina occurrs with progressively less exertion or even at rest?
unstable angina
What occurs when the severity or duration of ischemia is sufficient to cause cardiomyocyte death (necrosis)?
MI
This can occur as a consequence of tissue damage from MI, but most commonly results from a lethal arrhythmia without myocyte necrosis:
sudden cardiac death
What 4 interventions have greatly diminished cardiac risk factors?
smoking cessation programs,
hypertension and diabetes treatment,
and use of cholesterol-lowering agents.
IHD is a result of inadequate coronary perfusion relative to myocardial demand, usually due which 3 circumstances:
atherosclerotic occlusion of the coronary arteries
and new, superimposed thrombosis
and/or vasospasm.
Which coronary arteries can be affected by atherosclerotic narrowing?
left anterior descending (LAD), left circumflex (LCX), and right coronary artery (RCA) - singly or in combination.
Fixed obstructions that occlude < percent of a coronary vessel lumen typically are asymptomatic, even with exertion.
70%
Lesions that occlude > percent of a vessel lumen - resulting in a “ stenosis” - generally cause symptoms with increased demand.
70%; critical
This patient is said to have stable angina
A fixed stenosis that occludes > percent of a vascular lumen can lead to inadequate coronary blood flow with symptoms even at rest - a form of angina.
90%; unstable
What are some acute coronary syndromes?
unstablel angina, MI, sudden cardiac death
What can be triggered by thrombosis associated with an eroded or ruptured plaque?
acute coronary syndromes, ie, unstable angina, MI, and sudden cardiac death…
In most patients, unstable angina, infarction, and sudden cardiac death occur because of abrupt change followed by thrombosis - thus the term acute coronary syndrome.
plaque
In a majority of cases, the lesion in patients who suffer an MI was/was not critically stenotic or even symptomatic before its rupture.
was not (<70% occlusion)
It is impossible to predict plaque rupture in any given patient?
T or F
true
Angina pectoris is an intermittent chest pain caused by:
transient, reversible myocardial ischemia.
The pain associated with angina pectoris is a consequence of the ischemia-induced release of:
adenosine, bradykinin, and other molecules that stimulate autonomic nerves.
How many variants of angina pectoris and what are they?
3
typical or stable angina
Prinzmetal (variant) angina
Unstable (crescendo) angina
Which angina variant is described?
A predictable episodic chest pain associated with particular levels of exertion, or some other increased demand (eg, tachycardia).
typical or stable angina
How is angina pectoris pain described and where is it felt?
crushing or squeezing substernal sensation that often radiates down the left arm or to the left jaw (referred pain).
Which variant of angina pectoris is described:
The pain usually is relieved by rest (reducing demand) or by drugs such as nitroglycerin, a vasodilator that increases coronary perfusion.
typical or stable angina
What type of angina variant is described:
Occurs at rest, and is caused by coronary artery spasm.
Prinzmetal (variant) angina
Concerning prinzmetal (variant) angina, although such spasms typically occur on or near existing atherosclerotic plaques, a completely vessel can be affected.
normal
Prinzmetal (variant) angina typically responds promptly to which treatments?
vasodilators such as nitroglycerin, and calcium channel blockers.
Which type of angina is described:
Characterized by increasingly frequent pain, precipitated by progressively less exertion or even occurring at rest.
unstable angina (crescendo angina)
Which type of angina is described:
It is usually associated with plaque disruption and superimposed thrombosis, and can be a harbinger of MI, portending complete vascular occlusion.
Unstable angina (crescendo angina)
What is described as necrosis of the heart muscle resulting from ischemia?
Myocardial infarction (MI) (“heart attack”)
What is the major underlying cause of MI?
atherosclerosis
The vast majority of MIs are caused by within coronary arteries
acute thrombosis
in most intances, what serves as the nidus for thrombus generation, vascular occlusion, and subsequent infarction of the myocardium?
disruption or erosion of preexisting atherosclerotic plaque
There a 4 sequential events that take place in a typical MI:
An atheromatous plaque is eroded, exposing subendothelial collagen and necrotic plaque contents to the blood.
๏ Platelets adhere, aggregate, and are activated, releasing thromboxane A 2 , adenosine diphosphate (ADP), and serotonin - causing further platelet aggregation and vasospasm.
๏ Activation of coagulation by exposure of tissue factor and other mechanisms adds to the growing thrombus.
๏ Within minutes, the thrombus can evolve to completely occlude the coronary artery lumen.
Within what amount of time after vascular obstruction does aerobic metabolism cease?
within seconds
What is the functional consequence occurring within a minute or so of the onset of ischemia?
rapid loss of contractility
Prolonged ischemia lasting > to minutes causes irreversible damage and coagulative necrosis of myocytes
20 - 40
What is the goal of early dx and prompt intervention by thrombolysis or angioplasty?
blood flow is restored before irreversible injury occurs, myocardium can be preserved
Where does Irreversible injury of ischemic myocytes first occur?
subendocardial zone.
The location, size, and morphologic features of an acute myocardial infarct depend on which 4 criteria?
๏ Size and distribution of the involved vessel
๏ Rate of development and duration of the occlusion.
๏ Metabolic demands of the myocardium.
๏ Extent of collateral supply
Acute occlusion of the proximal left anterior descending (LAD) artery (40-50% of all MIs) typically results in infarction of the:
anterior wall of the left ventricle, the anterior two thirds of the ventricular septum, and most of the heart apex
Although massive myocardial damage can cause a fatal mechanical failure, sudden cardiac death in the setting of myocardial ischemia most often is due to ventricular caused by myocardial irritability.
fibrillation;
What is the progression of morphologic changes that occur from MI?
coagulative necrosis, to acute and then chronic inflammation, to fibrosis.
What does the yellow, black, and white circled areas of this heart represent?
yellow area is area of infarction (lacks enzyme for red staining)
black area is an area of hemorrhage
white area is fibrosis from a previous MI
Microscopically, typical features of coagulative necrosis become detectable within hours of infarction.
4-12
“Wavy fibers” also can be present at the edges of an infarct, reflecting the stretching and buckling of:
noncontractile dead fibers
notice loss of nuclei
Areas of coagulative necrosis with congestion and hemorrhage after MI
Necrotic myocardium elicits acute (~1-3 days post-MI), predominantly neutrophils
inflammation
When does a wave of macrophages that remove necrotic myocytes and neutrophil fragments show up in damaged heart tissue?
~ 5-10 days post - MI
The infarcted zone is progressively replaced by tissue (~ 1-2 wks), which forms the provisional upon which dense collagenous scar forms, usually by the end of the week.
granulation; scaffolding; 6th
note: slide demonstrates granulation tissue with lots of blood vessels.
Trichrome stain -
blue= collagen, fibrosis
This trichrome stain heart tissue demonstrates what?
the blue is scar formation with lots of collagen fibrosis
What electrocardiographic abnormalities typically show up with transmural MIs?
ST segment elevations on the electrocardiogram (ECG) and can have negative Q waves with loss of R wave amplitude.
TnI and TnT are both detectable within to after acute MI, with levels peaking at hrs, and remaining elevated for 7 to 10 days.
2 to 4 hrs; 48
What usually develops about the 2nd or 3rd day following a transmural infarct as a result of underlying myocardial inflammation?
A fibrinous or fibrino-hemorrhagic pericarditis
Myocardial rupture complicates only of MIs, but is frequently when it occurs.
1-5%; fatal
What is pictured and what are the consequences:
Left ventricular free wall rupture is most common, usually resulting in rapidly fatal hemopericardium and cardiac tamponade
What is pictured and what are the consequences:
Ventricular septal rupture creates a VSD with left-to-right shunting
What is pictured and what are the consequences:
Papillary muscle rupture leads to severe mitral regurgitation
What is the most common myocardial rupture?
Left ventricular free wall rupture
Ventricular aneurysm, a late complication, most commonly results from a large transmural anteroseptal infarct that heals with the formation of which weakness:
thinned wall of scar tissue.
What conditions can lead to a left-sided thromboembolism as concerning MIs?
combination of decreased myocardial contractility (causing stasis), chamber dilation, and endocardial damage (causing a thrombogenic surface) can cause mural thrombosis,
