HPIA 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?

• 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?

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?

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

cyanosisWHAT 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?

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?

Diagnostic TestingNot all MI’s will show ECG and/or CXR abnormalities.

• 12 Lead EKG– ST elevations

• CXR – Acute MI

now with Pulmonary edema

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?

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)

Atherosclerosis• Essentially endothelial cell damage of muscular

and elastic arteries• Causes of endothelial cell injury?

– HTN, smoking, HLD, homocysteine etc.

=

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

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.

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.

Common Sites for Atherosclerosis

• Abdominal Aorta• Coronary Artery• Popliteal Artery• Internal Carotid

Artery

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

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

Resources• http://ars.els-cdn.com/content/image/1-s2.0-S00029149000069

49-gr1.gif• http://www.med.umich.edu/anatomy/plastinate/galleries/path

ological_specimens.html• http://www.imcar.rwth-aachen.de/news/2009/03-03-carolus-th

erapeutics-scibx/figure01.jpg• http://o.quizlet.com/i/MXtzGl5vaPs3xycUPbp2CA_m.jpg• http://www.jfponline.com/images/Supplements/Nov09/SupplJF

P1109_CVrisk_2-fig1.jpg• https://www.healthtap.com/#topics/best-coronary-arteriosclero

sis-program• http://www.nlm.nih.gov/medlineplus/ency/article/007452.htm• Goljan, Edward. Rapid Review Pathology, Elsevier 2009 Edition