Acute Coronary Syndrome and Coronary Artery Disease Garrett Preston Clark, D.O.

What is ACS? Includes clinical presentations that cover the following range of diagnoses: Unstable angina Non–ST-elevation myocardial infarction (NSTEMI) ST-elevation myocardial infarction (STEMI) http://www.emedicine.com/emerg/topic31.htm

What is ACS? Unstable angina & NSTEMI  unstable plaques w/ nonocclusive thrombosis STEMI  thrombotic occlusion of epicardial coronary artery http://www.emedicine.com/emerg/topic31.htm

ACS / CAD Spontaneous and cocaine-related coronary artery dissection are unusual causes of ACS Still, should be included in your differential especially when a younger female or cocaine user is being evaluated.

Other considerations for ACS: Marfan syndrome Kawasaki disease Takayasu arteritis Cystic medial necrosis with aortic root dilatation Aneurysm formation Dissection into the coronary artery

ACS / CAD Higher incidence in males in all patients <70 y/o Incidence of angina occurs equally 15 years postmenopause Women more likely to have coronary events without typical symptoms

ACS Risk Factors: Male gender Diabetes mellitus (DM) Smoking history Hypertension Increased age Hypercholesterolemia Hyperlipidemia Prior CVA Inherited metabolic disorders Methamphetamine use Occupational stress Connective tissue disease

ACS  Whats In Your Diff ? Anxiety Aortic Stenosis Asthma Cardiomyopathy, Dilated Esophagitis Gastroenteritis Hypertensive Emergencies Myocardial Infarction Myocarditis Pericarditis and Cardiac Tamponade Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum Pulmonary Embolism

Alternative diagnoses to cardiac ischemia for patients with chest pain Non-ischemic cardiovascular Aortic dissection* Myocarditis Pericarditis Chest wall Cervical disc disease Costochondritis Fibrositis Herpes zoster (before the rash) Neuropathic pain Rib fracture Sternoclavicular arthritis Gastrointestinal Biliary Cholangitis Cholecystitis Choledocholithiasis Colic Esophageal Esophagitis Spasm Reflux Rupture* Pancreatitis Peptic ulcer disease Nonperforating Perforating* Pulmonary Pleuritis Pneumonia Pulmonary embolus* Tension pneumothorax* Psychiatric Affective disorders (eg, depression) Anxiety disorders Hyperventilation Panic disorder Primary anxiety Somatiform disorders Thought disorders (eg, fixed delusions)

WHAT’S HAPPENING? Disease process includes: A chronic phase of atherosclerosis  modification of the blood vessel wall Development of an atherosclerotic plaque Thin fibrous cap of extracellular matrix proteins is formed over a lipid core (rich in foam cells & comprised of cholesteryl esters & tissue factor) Thickened intima. Rupture of the fibrous cap  thrombosis & partial or total occlusion of the vessel http://www.uspharmacist.com/index.asp?page=ce/2686/default.htm

Whoop, THERE IT IS:

OUCH ! www.univie.ac.at/.../BE513/EKG/normalEKG.GIF

ACS  The Meat & Potatoes Part I: Unstable Angina The ACC/AHA guidelines state that UA and NSTEMI differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury. http://www.utdol.com/utd/content/topic.do?topicKey=chd/10116&type=A&selectedTitle=1~72

ACS  The Meat & Potatoes Part I: Unstable Angina Unstable angina is considered in patients with ischemic symptoms suggestive of an ACS and no elevation in troponins or CK-MB, with or without ECG changes indicative of ischemia. http://www.utdol.com/utd/content/topic.do?topicKey=chd/10116&type=A&selectedTitle=1~72

ACS  The Meat & Potatoes Part I: CLASSIFICATIONS OF UNSTABLE ANGINA New onset exertional angina Rest angina Early post-MI angina Postrevascularization angina Periprocedural Late

New onset angina: CLASSIFICATIONS OF UNSTABLE ANGINA If occurring only after heavy physical exertion, patients have a prognosis similar to patients with chronic stable angina New angina occurring after minimal exercise or at rest, has a poorer prognosis.

Rest angina: CLASSIFICATIONS OF UNSTABLE ANGINA Patients at increased risk if: Prolonged Associated with transient ST segment changes >0.05 mV

Early post-MI angina: CLASSIFICATIONS OF UNSTABLE ANGINA Chest pain occurring within 48 hours after an acute MI Associated with high risk without immediate intervention GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) IIb trial  Refractory ischemia was associated with an approximate doubling of mortality among patients with ST-segment elevation and a near tripling risk among those without ST elevation. Circulation 1998 Nov 3;98(18):1860-8.

GUSTO IIb TRIAL: Global Use of Strategies to Open Occluded Coronary Arteries Occurrence of refractory ischemia was associated with a higher 30 day mortality compared to responsive ischemia or no ischemia.

Postrevascularization & Periprocedural angina: CLASSIFICATIONS OF UNSTABLE ANGINA Postrevascularization  Angina occurring after PCI or CABG Periprocedural  Ischemic chest pain within 48 hours after stenting.

LATE: CLASSIFICATIONS OF UNSTABLE ANGINA Delayed onset of angina May reflect restenosis after PCI, graft stenosis after CABG, or progression of native disease Patients usually progress to return of effort angina

ACS  The Meat & Potatoes Part II: Non–ST-elevation myocardial infarction (NSTEMI) UA & NSTEMI often indistinguishable at time of initial evaluation Most patients present with chest pain and ST segment depression ST seg depression is an unfavorable predictor Increased incidence of left main or three vessel disease compared to those without ST segment depression

ACS  The Meat & Potatoes Part II: Non–ST-elevation myocardial infarction (NSTEMI) http://www.postgradmed.com/issues/2004/06_04/tak1.gif

ACS  The Meat & Potatoes Part II: Non–ST-elevation myocardial infarction (NSTEMI) Absence of Q waves suggests a high rate of spontaneous reperfusion May occur after percutaneous coronary intervention (PCI) or CABG

Braunwald classification Classification of UA which included patients with NSTEMI since troponins were not measured: Class I — New onset, severe, or accelerated Class II — Angina at rest and subacute (no anginal episodes within the preceding 48 hours) Class III — Angina at rest and acute (angina within the preceding 48 hours)

Braunwald classification Clinical circumstances: Class A — Secondary UA (in the setting of anemia, infection, fever, etc) Class B — Primary UA Class C — Post

Braunwald classification Intensity of treatment: No or minimal treatment Symptoms occurring in the setting of standard medical therapy Symptoms occurring despite maximally tolerated doses of beta blockers, nitrates, and calcium channel

Goldman risk score for chest pain:

ACS Risk Factors Reinforcement: Male gender Diabetes mellitus (DM) Smoking history Hypertension Increased age Hypercholesterolemia Hyperlipidemia Prior CVA Inherited metabolic disorders Methamphetamine use Occupational stress Connective tissue disease

ACS  The Meat & Potatoes Part III: ST-elevation (Q-wave) myocardial infarction (STEMI) Enough Said?

ACS  The Meat & Potatoes Part III: ST-elevation (Q-wave) myocardial infarction (STEMI) In 2000, the European Society of Cardiology (ESC) with the American College of Cardiology (ACC) set out to define an acute, evolving, or recent MI.

ESC / ACC Definitions: Rise and gradual fall in troponin or more rapid rise and fall of biochemical markers of myocardial necrosis with at least one of the following:     a.  Ischemic symptoms     b.  Development of pathologic Q waves     c.  ECG changes indicative of ischemia (ST segment elevation or depression)     d.  Coronary artery intervention (eg, angioplasty) Pathologic findings of an acute MI

SO, WHAT’S A Q-WAVE ? ? ? Q = 1st deflection of the QRS which is negative When QRS complex consists soley of a Q wave, it’s called a “QS” complex Normal Q = less than 0.03 seconds and can be common in most leads (except aVR, V1-V3)

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THE EVIL Q-WAVE ! ! ! Any Q-Wave in leads V1-V3 is an Evil Q Q’s in leads I, II, aVL, aVF, & V4-6 are considered evil if they are greater than or equal to 0.03 seconds Evil Q’s must be greater than or equal to 1mm in depth in @ least 2 contiguous leads to be considered for Q-wave MI and thereby, making them very evil !

ACS  The Meat & Potatoes Part III: ST-elevation (Q-wave) myocardial infarction (STEMI) “Clinically significant ST segment elevation is considered to be present if it is greater than 1 mm (0.1 mV) in at least two anatomically contiguous leads, or 2 mm (0.2 mV) in two contiguous precordial leads”. http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print

ACS / TREATMENT: In the initial assessment, the following should be implemented if ACS is suspected: Airway, breathing, and circulation assessment 12-lead ECG obtained Crash cart nearby Cardiac monitor attached Oxygen given IV access and blood work obtained (series cardiac) Aspirin Nitrates and morphine (unless contraindicated) http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print

Lower cardiac workload = less O2 demand ACS / TREATMENT: Morphine reduces sympathetic stimulation caused by pain and anxiety  lowers cardiac workload Lower cardiac workload = less O2 demand = Patients feel better http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print

ACS / TREATMENT: Due to the lack of data, the ACC/AHA, & ACCP guidelines did not address the use of clopidogrel in patients managed without reperfusion Tx. However, most experts give clopidogrel, 300 mg loading dose then 75 mg daily based on benefits demonstrated in non-revascularized patients with non-ST elevation syndromes. http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print

Clopidogrel in Unstable angina to prevent Recurrent ischemic Events (CURE) TRIAL: Clopidogrel  platelet ADP receptor antagonism Something to consider if ASA sensitive CURE Trial suggests more efficacy with ASA and Plavix combo therapy, but at a cost = increased risk of nonintracranial bleeding complications.

Foreign Cars May Save Your Life ! If It’s Good Enough for Bond… www.jamesbondlifestyle.com/.../au010.jpg285 x 218 - 18k http://www.impawards.com/2002/posters/die_another_day_ver1.jpg

Interventions Shown To Decrease Mortality in CAD (Die Another Day 007©): Statins ASA ACE Inhibitors Beta Blockers “SAAB” Nitrates shown to minimize angina Sx’s, but NO conclusive evidence that show decreased mortality.

DON’T FORGET: Initial EKG is often NOT diagnostic. Repeat EKG at 5 to 10 minute intervals if patient remains symptomatic & high clinical suspicion for MI Ask about phosphodiesterase-5 inhibitors (Viagra, Levitra, Cialis). Nitrates are contraindicated if used w/in 24 -36 hours due to risk of severe hypotension

DON’T FORGET: In the setting of an inferior wall MI, remember the possibility of right ventricular involvement. Patient dependence on preload to maintain cardiac output may result in severe hypotension w/ nitrate use.

ST elevation in the right precordial leads - V4, V5, and V6 indicates right ventricular involvement http://www.utdol.com/utd/content/image.do?imageKey=card_pix/right_5.htm&altImageKey=card_pix/normal3.htm

DON”T FORGET: About ½ the patients with LBBB & acute MI do NOT have Sx’s of chest pain w/ their ischemia = Much less likely to receive ASA, beta blockers, and reperfusion therapy = Not a good idea = Beware the LBBB ! ! !

ACS THERAPY: Evidence Supports early aggressive strategy ASA Beta-Blocker ACEIs Statin LMW Heparin or Unfractionated Clopidogrel (PLAVIX)

TEST YOUR SKILL…

TEST YOUR SKILL… A 67 y/o postmenopausal woman w/ CAD, stable angina, CHF, and hyperlipidemia comes for her regular 3-month exam. Her vitals: HR: 94, RR: 18, BP: 130/70. Physical exam is WNL. Her LDL is 129, HDL is 45. Which of the following therapeutic options would you prescribe that have been shown to decrease mortality: Atorvastatin Digoxin Diltiazem Estrogen Isosorbide mononitrate

TEST YOUR SKILL… A 67 y/o postmenopausal woman w/ CAD, stable angina, CHF, and hyperlipidemia comes for her regular 3-month exam. Her vitals: HR: 94, RR: 18, BP: 130/70. Physical exam is WNL. Her LDL is 129, HDL is 45. Which of the following therapeutic options would you prescribe that have been shown to decrease mortality: Atorvastatin Digoxin Diltiazem Estrogen Isosorbide mononitrate

THE END

References: http://www.kup.at/kup/images/browser/787.jpg http://services.epnet.com/GetImage.aspx/getImage.aspx?ImageIID=4708 http://www.chd-taskforce.de/ny2001_schober.htm sfghed.ucsf.edu/.../ClinicImages/MI%20EKG1.1.jpg http://www.utdol.com/utd/content/image.do?imageKey=card_pix/schema_m.htm http://www.utdol.com/utd/content/topic.do?topicKey=ad_emer/2821&view=print http://www.utdol.com/utd/content/image.do?imageKey=card_pix/right_5.htm&altImageKey=card_pix/normal3.htm Circulation 1998 Nov 3;98(18):1860-8. http://www.postgradmed.com/issues/2004/06_04/tak1.gif