Transcript slides#14 - DENTISTRY 2012

2-variant angina or Prinzmetal
angina
- Is angina occurring at rest due to
coronary artery spasm.
- completely normal vessels can be
affected.
- Treatment: administration of
vasodilators such as nitroglycerin or
calcium channel blockers.
3-Unstable angina (also called crescendo
angina)
- occurring with progressively less exertion
-
or even at rest.
a fixed 90% stenosis can lead to
inadequate coronary blood flow even at
rest.
-
-
-
characterized by increasing frequency of
pain, precipitated by progressively less
exertion.
the episodes also tend to be more intense
and longer lasting than stable angina
 called pre-infarction angina
associated with plaque disruption;
superimposed partial thrombosis;
Myocardial Infarction
- Popularly called heart attack is necrosis
of heart muscles resulting from ischemia
Pathogenesis
- Most cases of MI are caused by acute
coronary artery occlusive thrombus
In most cases, disruption of
atherosclerotic plaque results in the
formation of thrombus
Clinical manifesataions
1) Severe, crushing substernal chest pain
2) Discomfort that can radiate to the neck,
jaw, epigastrium, or left arm.
MI pain lasts from 20 minutes to several
hours and is not relieved by nitroglycerin
or rest.
- Myocardial infarction can be entirely
asymptomatic in 10% to 15% of the
cases (silent infarcts)
particularly common in
patients with underlying
diabetes mellitus (with
peripheral neuropathies)
4. The pulse is rapid and weak
5- Nausea
6- Dyspnea is common (impaired
myocardial contractility and
dysfunction of the mitral valve
apparatus, with resultant pulmonary
congestion and edema).
Lab evaluation of MI
Is based on evaluation of blood levels
macromolecules that leak out through
damaged cell membranes , include
myoglobin, Creatin kinase-MB,
Troponin T and I.
1. Total CK is not reliable marker for
cardiac injury

2. Ck-MB remains a valuable marker of
myocardial injury second only to
cardiac specific troponins.
- It begins to rise within2-4 hours,
peaks at 24-48 hours, and return
back to normal within 72 hours
3. Troponin T and I (Tnt and Tni)
 After MI , both are detectable within 2-4
hors and peak at 48 hours and remain
elevated for 7 to 10 days
- The frequencies of involvement of each
of the three main arterial trunks are
as follows :
• Left anterior descending coronary
artery (40% to 50%):
1. infarcts involving the anterior wall of
left ventricle
2. the anterior portion of ventricular
septum;
3. and the apex circumferentially
2. Right coronary artery (30% to 40%):
infarcts involving the
a.
Inferior/posterior wall of left ventricle;
b.
posterior portion of ventricular
septum;
c.
and the inferior/posterior right
ventricular free wall in some cases
3. Left circumflex coronary artery
(15% to 20%):
- Infarcts involving the lateral wall of
left ventricle except at the apex
Complications following acute MI :
1• Contractile dysfunction.
- There is usually some degree of left
ventricular failure with hypotension,
pulmonary vascular congestion,
which can progress to pulmonary
edema

2. Arrhythmias.
- Many patients have myocardial
irritability and/or conduction
disturbances following MI that lead to
potentially fatal arrhythmias such as
ventricular fibrillation
- The risk of arrhythmias is greatest in
the first hour after MI
3. Myocardial rupture. Most commonly
occur within 2-4 days
- These include:
a. Rupture of the ventricular free wall
(most common), with hemopericardium
and cardiac tamponade
b. Rupture of the ventricular septum (less
common), leading left-to-right shunting
4- Mural thrombus.
- With any infarct, the combination of a
local abnormality in contractility
(causing stasis) and endocardial
damage (creating a thrombogenic
surface) can foster mural thrombosis
and potentially thromboembolism.
5.Ventricular aneurysm.
Aneurysms of the ventricular wall are
a late complication of large
transmural infarcts
- Complications of ventricular
aneurysms include mural thrombus,
- Rupture of the tough fibrotic wall
does not usually occur.
-
Infective endocarditis
- Is a microbial infection of the heart
valves or endocardium that leads
to the formation of vegetations
composed of thrombotic debris and
organisms, often associated with
destruction of the underlying
cardiac tissues.
I. Acute infective endocarditis
a. Is typically caused by infection of a
previously normal heart valve by a highly
virulent organism (e.g., Staphylococcus
aureus)
b. That rapidly produces necrotizing and
destructive lesions.
These infections may be difficult
to cure with antibiotics alone, and
usually require surgery.
d- Despite appropriate treatment,
death can ensue within days to
weeks.
c-
2.Subacute IE is characterized by
a. organisms with lower virulence (e.g.,
streptoccocus viridans )
b. cause insidious infections of deformed
valves
c. Less destruction.
d. The disease may pursue a protracted
course of weeks to months, and cures
can be achieved with antibiotics.
Note:
- Endocarditis of native but previously
damaged or otherwise abnormal valves is
caused most commonly (50% to 60% of
cases) by Streptococcus viridans, a normal
component of the oral cavity flora.
In contrast, more virulent S. aureus
organisms commonly found on the
skin can infect either healthy or
deformed valves and are responsible
for 20% to 30% of cases overall;
 S. aureus is the major offender in IE
among intravenous drug abusers

The source may be
a. an obvious infection elsewhere,
b. a dental or surgical procedure,
c. a contaminated needle shared by
intravenous drug users, or
d. seemingly trivial breaks in the epithelial
barriers of the gut, oral cavity, or skin.
-

In patients with valve abnormalities,
or with known bacteremia, IE risk can
be lowered by antibiotic prophylaxis.