1. What other questions would you like to ask this man?
HPI
A 56 year old man is brought to the ED complaining of chest discomfort for around 90min. He has had occasional symptoms for about a month he thinks, but it is notably worse today. The symptoms began as he was walking up a flight of stairs at his home. He describes the discomfort as a pressure sensation in the left substernal chest area to go along with shortness of breath and a mild sweat. The pain does not radiate anywhere today, but his wife claims he has complained of left arm pain and facial numbness in the past.
What other questions would you like to ask this man?

2. What is your differential?
PmHx: patient denies any current health issues, claims that he has not seen a physician in years, though his wife has been on him about it since his brother passed away from an MI 6months ago
All: None
Meds: None
Hos/Sx: Tonsillectomy at age 12, Rhinoplasty at age 23
FmHx: Mother with DM2, Father with HLD, only brother died of an MI 6months ago at age 62.
Social Hx: works as a zamboni driver for the Indianapolis ice. Lives at home with his wife, and 4 cats. He has 2 children both in college. Smokes 1/2ppd, and drinks 2-3 Mikes Hard Lemonade’s a day. Denies any illicit drug use since his college days.
What is your differential?

3. Differential Diagnosis
Angina PE
MI GERD
Pericarditis PUD
Aortic Dissection - Pancreatitis
Heart Failure Costochondritis
Pneumonia Anxiety
Pneumothorax - Shingles
What is your next step in assessing the patient?

4. What would you like to do next?
Physical Exam
Vitals:
T 98.8, HR 105, RR 18, BP 190/95, Ht 5’10, Wt 260
General: appears anxious and worried, he is an obese man, who appears somewhat pale.
CV: regular rhythm without murmur, but you do notice an S4 gallop, 2+ pulses in radial and dorsal pedalis arteries
Lung: CTA
HEENT: neck has faint carotid bruit on left, minimal JVD
Abd: normal
Extremities: trace edema, warm to touch, no clubbing, no cyanosis
What would you like to do next?

5. What would you like to do next?
Lab Tests
CBC: Normal
BUN/Cr: WNL
PT: 13 sec
PTT: 27 sec
INR: 1.4
Troponins: elevated
CKMB: > 5%
What would you like to do next?

6. Initiate treatment! MONA
Morphine – this can achieve an adequate analgesia which will decrease the levels of circulating catecholamine's, thus reducing myocardial oxygen consumption
Oxygen – 2-4 L via nasal cannula
NTG – sublingual administration ever 5min
Aspirin – 325mg chewed and swallowed.
Now What?

7. Diagnostic Testing Not all MI’s will show ECG and/or CXR abnormalities.
12 Lead EKG
ST elevations
CXR
Acute MI now with Pulmonary edema

8. How does any of this relate to pathology?
Definitions to Know
Angina Pectoris- severe pain around the heart caused by a relative deficiency of oxygen supply to the heart muscle.
MI – cardiac muscle death caused by a partial or complete occlusion of one or more of the coronary arteries.
New York Heart Association Functional Classification of Angina
I : angina with unusually strenuous activity
II : Angina with slightly more prolonged or slightly more vigorous activity than usual
III : Angina with usual daily activity
IV : Angina at rest.
Unstable Angina – Angina of new onset, angina at rest or with minimal exertion, or a crescendo pattern of angina with episodes of increasing frequency, severity or duration
How does any of this relate to pathology?

9. Atherosclerosis!
Atherosclerosis leading to plaque rupture, cascading to coronary artery thrombosis is the cause of acute MI approximately 90% of the time.
(With this in mind, remember that many different conditions can lead to angina)

10. Atherosclerosis
Essentially endothelial cell damage of muscular and elastic arteries
Causes of endothelial cell injury?
HTN, smoking, HLD, homocysteine etc. =

11. Atherosclerosis Cell Response is Crucial!
Macrophages and platelets adhere to damaged endothelium, this results in a release of cytokines that cause hyperplasia of medial smooth muscle cells.
Smooth muscle cells migrate to the tunica intima
Plaque (fibrous cap) develops – composed to inflammatory cells, smooth muscle, foam cells, and extracellular matrix
These plaques reduce blood flow through arteries, when the plaques become disrupted a thrombosis often occurs

12. Atherosclerosis Thrombosis leads to
Acute MI, Strokes, Small Bowel Infarctions etc.
Here is occlusive coronary atherosclerosis. The coronary at the left is narrowed by 60 to 70%. The coronary at the right is even worse with evidence for previous thrombosis with organization of the thrombus and recanalization such that there are three small lumens remaining, one of which contains additional recent thrombus.

13. Here is a closer view of the gross appearance of a coronary thrombosis
Here is a closer view of the gross appearance of a coronary thrombosis. The thrombus occludes the lumen and produces ischemia and/or infarction of the myocardium. Atherosclerosis is an ongoing process that takes years to decades for clinically apparent problems to appear.

14. Common Sites for Atherosclerosis
Abdominal Aorta
Coronary Artery
Popliteal Artery
Internal Carotid Artery

15. Primary Treatment Mainstays of treatment remain prevention.
BP control, Lipid Control, Smoking Cessation, Healthy Diet, Exercise.
Know who is at risk
Risk Factors : Males over 40, HTN, Tobacco Abuse, DM, Cocaine Use, HLD, Family Hx of CAD, Postmenopausal Status, Homocystinemia

16. Pearls Angina is the most frequent symptom of intermittent ischemia
Physical exam is normal in many patients with angina
MONA are the initial mainstays of treatment
Time is Myocardium
Main complications of atherosclerosis include aneurysms, thrombosis, and ischemia
Abdominal Aorta = most common site for atherosclerosis because no vasa vasorum
Fibrous Cap = pathognomonic for atherosclerosis
Main players in atherosclerosis = endothelial cell injury leading to macrophages and platelet activation

17. Resources
Goljan, Edward. Rapid Review Pathology, Elsevier 2009 Edition