Download S06 Patho Dr Manar Heart

Manar hajeer,MD, FRCPath
Causes:
A. Ischemic heart disease (IHD),
B.
Systemic hypertension,
C. Mitral or aortic valve disease.
D. Diseases of myocardium.
a. Dyspnea on exertion is the earliest and most significant
symptom
b. Cough
c. Orthopnea: Dyspnea when recumbent occurs because the
supine position increases venous return from the lower
extremities and typically is relieved by sitting or standing,
d. Paroxysmal nocturnal dyspnea :dyspnea awakening
patients from sleep with feelings of suffocation
e. Fine rales at the lung bases, caused by pulmonary edema.
f. Diminished cardiac output leads to decreased renal
perfusion and diminished cerebral perfusion
Usually is the consequence of left-sided heart failure.
Causes of isolated right-sided heart failure
a.
Severe pulmonary hypertension resulting in right-sided
heart failure ( cor pulmonale).
b. Pulmonic or tricuspid valve disease.
c. Congenital left-to-right shunts.

Related to systemic and portal venous congestion
including congestive hepatomegaly and splenomegaly
peripheral edema (ankle and pretibial) , pleural and
pericardial effusion, and ascites.

In chronic cardiac decompensation, patients present with
biventricular CHF encompassing syndromes of both rightsided and left-sided heart failure.
- An imbalance between cardiac oxygen supply and myocardial
demand.
- Called coronary artery disease (CAD)..
- In more than 90% of cases, IHD is due to reduced
coronary blood flow secondary to obstructive
atherosclerosis
Angina Pectoris :
Is an intermittent chest pain caused by transient, reversible
myocardial ischemia.
II. Myocardial infarction.
III. Chronic ischemic heart disease.
IV. Sudden cardiac death.
I.
Typical or stable angina
is episodic chest pain associated with exertion or tachycardia
and the pain is a crushing or squeezing substernal
sensation, that can radiate to left arm or to the left jaw
(referred pain) and usually is relieved by rest or by drugs
(nitroglycerin), a vasodilator increases coronary perfusion.
- Is caused by fixed atherosclerotic lesion that occlude more
than 70% of a vessel
A.
B.
Prinzmetal or variant angina Might be caused by vasospasm;
C- Unstable angina
- Called crescendo angina, it occurs at rest
- Caused by fixed atherosclerotic lesion that occludes 90% of
vessel lumen
- It is often the harbinger of MI,
d. Myocardial Infarction (MI),
referred to as "heart attack,“ and means necrosis of heart
muscle resulting from ischemia
- MIs can occur at virtually any age but the frequency rises
progressively with increasing age.
- Approximately 10% of MIs occur before age 40
- Men are at significantly greater risk than women, and women
tend to be protected against MI during their reproductive
years.

However, menopause women with declining estrogen is
associated with exacerbation of coronary artery disease and
IHD is the most common cause of death in elderly women.
1. Caused by completely obstructive thrombus over a disrupted
plaque can cause a massive MI.
- In a majority of cases, the lesion in patients who suffer MI
was not critically stenotic or symptomatic before its rupture.
-
Influences extrinsic to plaque are important.
Adrenergic stimulation put physical stress on the plaque by
causing hypertension or vasospasm and the surge in
adrenergic stimulation associated with awakening and rising
may underlie that the incidence of acute MI is highest in early
morning.
2. In 10% of MIs, infarction occurs in the absence of occlusive
atherosclerosis and such infarcts are mostly attributable to
coronary artery vasospasm
- Some occlusions clear spontaneously through lysis of the
thrombus
- Early thrombolysis can be successful in limiting the extent of
myocardial necrosis
1.Loss of contractility occurs within a minute of onset of
ischemia and may be reversible.
2. Severe ischemia lasting 20 to 40 minutes causes myocyte
coagulative necrosis
.Note; Thus, if, myocardial blood flow is restored before
irreversible injury ,cell viability can be preserved; and this is
the rationale for early diagnosis of MI, and Intervention to
salvage myocardium at risk.

3. Although massive myocardial damage can cause fatal
mechanical failure, in 80% to 90% of the cases , the death
is due to ventricular fibrillation
Atherosclerotic narrowing can affect
1. Left anterior descending (LAD),
2. Left circumflex (LCX),
3. Right coronary artery (RCA)
 Note: Clinically significant plaques tend to occur within the
first several centimeters of the LAD and LCX, and along the
entire length of the RCA.
The forms of MI may be
1. Transmural infarctions: Involve > 50% of the myocardial
wall thickness.
2. Subendocardial infarctions : limited to the inner third of the
myocardium;
a. Severe crushing substernal chest pain that can radiate to
the neck, epigastrium jaw, or left arm ,
- In 10% to 15%, MIs have may even be "silent" infarcts and
particularly common in patients with diabetes mellitus
b. Rapid and weak pulse , nausea and sweating.
c. Dyspnea attributable to resultant acute pulmonary edema.
- Based on measuring blood levels of macro -molecules that
leak out of injured myocardial cells
- Cardiac troponins and CK-MB have high specificity and
sensitivity for MI
- CK-MB remains a valuable marker of myocardial injury,
second only to the cardiac-specific troponins
- Total CK activity is not a reliable marker of cardiac injury
since various isoforms of CK are found in brain and skeletal
muscle
- The CK-MB isoform is the more specific indicator of heart
damage and its activity begins to rise within 2 to 4 hours of
MI, peaks at 24 to 48 hours, and returns to normal within 72
hours.
- TnI and TnT normally are not found in the circulation;
however, after acute MI, both
are detectable within 2 to 4 hours, with levels peaking at 48
hours and remaining elevated for 7 to 10 days.
- Although cardiac troponin and CK-MB are sensitive markers
of the early stages of an MI, persistence of elevated troponin
levels for approximately 10 days allows the diagnosis of an
acute MI long after CK-MB levels have returned to normal
Occur in Nearly three fourths of patients
1. Contractile dysfunction: In most cases of MI, there is some
degree of left ventricular failure.
2, Cardiogenic shock due to pump failure occurs in 10% of
patients with MIs and typically is associated with infarcts
that damage 40% of the left ventricle
3. Papillary muscle dysfunction leads to post-infarct mitral
regurgitation and it can result from post infarct ischemic
dysfunction and later from muscle fibrosis and shortening .
4 Myocardial rupture. :complicates 1% to 5% of MIs but is
fatal when it occurs.
- Left ventricular free wall rupture is most common, usually
resulting in rapidly fatal hemopericardium and cardiac
tamponade.


It occurs commonly within 3 to 7 days after infarction
especially in females and age older than 60 years,
Other risk factors include anterior or lateral wall infarctions,
and First MI (as scarring associated with prior MIs tends
to limit the risk of myocardial tearing).
5. Arrhythmias: due to myocardial irritability and conduction
disturbances that can cause sudden death
- Approximately 90% of patients develop some form of rhythm
disturbance,
The risk of ventricular fibrillation is greatest in the first hour and
declines thereafter.

6. Pericarditis. : manifested as anterior chest pain and a
pericardial friction rub, and appears 2 to 3 days after
infarction . Severe pericardial inflammation can lead to
fibrosis to form dense adhesions that manifest as a
constrictive lesion.
7. Mural thrombus. Due to combination of stasis and
endocardial damage
8.Ventricular aneurysm: is a late complication, and most
commonly result from a large anteroseptal infarct that heals
with the formation a thinned wall of scar tissue and usually do
not rupture (since fibrotic)
9. Progressive late heart failure.