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Approach to the Patient with Chest Pain

Aaron N. Weaver, MD, FACC

Cardiologist, Central Utah Clinic

Objectives: • Explain the value of a cardiovascular history, the value and

limitations of ECG, Troponin, and other point of care diagnostics • Relate how to develop a differential diagnosis for a patient

presenting with chest pain • Review the recommended management algorithms for stable

angina, definite unstable angina/non-STEMI, and STEMI • Indicate the clinical benefits and limitations of early cardiac

catheterization

Approach to the Patient with Chest Pain AARON WEAVER MD FACC

SEPTEMBER 26, 2014

Disclosures

No Relevant Disclosures to Report

Chest Pain

Why worry about chest pain?

Causes of chest pain

Evaluation: History, Testing

Management

Guidelines

Outcomes

Chest Pain

6 million annual visits to ED (2nd most common complaint) 10.2 million estimated to experience angina in the U.S. Approximately 500,000 new cases of angina occurring each

year

McCaig, L, Burt, C. National Hospital Ambulatory Medical Care Survey: 2003 Emergency Department Summary. In: Advance Data from Vital and Health Statistics. Centers for disease control and prevention, Atlanta, GA 2005.

Rosamond, W. et al. (17 December 2007). "Heart Disease and Stroke Statistics--2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee". Circulation 117 (4): e25–e146.

Chest Pain in Emergency Room

Lindsell CJ, et al. Ann Emerg Med 2006 December;48(6): 666-77, 677

>80% non cardiac

17.2% cardiac

Causes of non emergent chest pain in Michigan Research Network (MIRNET) primary care practices

Cause Prevalence Prevalence (%) Musculoskeletal, including costochondritis 36 Gastrointestinal 19 Cardiac 16* Stable angina 10.5 Unstable angina or MI 1.5 Other cardiac 3.8 Psychiatric 8 Pulmonary 5 Other/unknown 16

MIRNET: Michigan Research Network. * As high as 50 percent in older populations. Adapted from Klinkman MS, Stevens D, Gorenflo DW. J Fam Pract 1994; 38:345.

How good are we?

Nawar E, et al. National hospital ambulatory medical care survey: 2005 emergency department summary. 2007 June 29;(386):1-32.

Chest Pain

More than 60% of chest pain presentations are not organic (not due to cardiac, pulmonary or gastrointestinal) etiologies

More than 80% of cases presenting to the ED or Primary Care are not cardiac and not emergent in nature.

So why should we talk about this, and why is chest pain one of the most common reasons for referral to cardiology?

Heart Disease is leading cause of death

Top Ten Leading Causes of Death Heart disease: 596,577 Cancer: 576,691 Chronic lower respiratory diseases: 142,943 Stroke (cerebrovascular diseases): 128,932 Accidents (unintentional injuries): 126,438 Alzheimer's disease: 84,974 Diabetes: 73,831 Influenza and Pneumonia: 53,826 Nephritis, nephrotic syndrome, and nephrosis: 45,591 Intentional self-harm (suicide): 39,518

Prevalence

Lifetime risk of developing CHD after 40 years of age 49% for men 32% for women.

Average age at first MI is 64.5 years for men and 70.3 years for women.

Incidence of CHD in women lags behind men by 10 years for total CHD and by 20 years for more serious clinical events such as MI and sudden death.

Estimated 195 000 silent MIs occur each year.

Heart Disease and Stroke Statistics--2011 Update : A Report From the American Heart Association. Circulation 2011, 123:e18-e209 Unpublished data from the ARIC and CHS studies of the NHLBI:

With Little Warning

Heart Disease and Stroke Statistics--2011 Update : A Report From the American Heart Association. Circulation 2011, 123:e18-e209

(NHLBI computation of FHS follow-up since 1986).

Only 18% of coronary attacks are preceded by longstanding angina.

Note: Graph adapted from data in Table 20-1 in American Heart Association. Heart Disease and Stroke Statistics – 2009 Update. Circulation. 2010;121:e46-e215.

*2009 estimates; total direct and indirect costs

Billions of dollars

Cost of Cardiovascular Disease in the United States

CVD=Cardiovascular disease

What are we worried about?

The Big Five

Acute Coronary Syndrome Aortic Dissection Pulmonary Embolism Tension Pneumothorax Pericardial Tamponade Esophageal rupture

Differential Diagnosis

Cardiovascular Pulmonary Gastrointestinal Chest Wall Ischemic chest pain syndromes Coronary artery disease

Obstructive atherosclerotic Acute coronary syndromes Angina due to demand/supply mismatch

• Chronic stable angina • Acutely increased myocardial oxygen

demand Coronary vasospasm, "variant angina" Cardiac syndrome X Coronary artery dissection Coronary anatomic anomalies

Valvular heart disease Non-ischemic chest pain syndromes Aortic dissection Pericarditis Myocarditis Stress-induced cardiomyopathy Acute aortic syndromes

Vasculature Acute pulmonary embolism Pulmonary hypertension Parenchyma Pneumonia Cancer Sarcoidosis Airways: Bronchospasm* Asthma COPD Pleura Pleuritis Pneumothorax Mediastinal disease Mediastinitis Mediastinal tumors Pneumomediastinum

Esophageal Reflux Rupture Spasm Esophagitis Pancreatobiliary Pancreatitis Cholecystitis Cholangitis Biliary colic Peptic ulcer disease

Isolated musculoskeletal chest pain syndromes Costochondritis Tietze syndrome Costovertebral joint dysfunction Sternalis syndrome Xiphoidalgia Spontaneous sternoclavicular subluxation Rheumatic diseases Nonrheumatic systemic diseases Stress fractures Metastatic malignancy Acute chest syndrome (sickle cell crisis) Skin and sensory syndromes Herpes zoster (shingles)

Hyperadrenergic states Psychiatric Cocaine intoxication Amphetamine intoxication Pheochromocytoma

Anxiety Depression Panic attacks Munchausen

How can we avoid missing serious causes of chest pain?

Listen to your patient – How to take a good chest pain history.

Look at your patient – How to do a thorough cardiovascular exam.

Test your hypothesis – What are the best tests, and how good are they?

History

Taking a Good History

“Listen to your patient, he is telling you the diagnosis” - Sir William Osler 1849-1919

Patient History

Nature of Chest Pain

Comorbidities

Recent Events

Family History

Social History

Details, Details, Details

Details about Chest Pain Onset

Provocation/Palliation

Quality of pain

Radiation

Location

Timing/Duration

Associated Symptoms

Abrupt vs. Gradual

Activity vs rest, Nitroglycerine vs NSAID

Sharp, Squeezing, pluritic, dull

Shoulder, Jaw, Back

Substernal, Chest Wall, diffuse, local

Constant vs episodic

Nausea, Diaphoresis, Dyspnea

How good is history?

88% of physicians were able to correctly diagnose a nonorganic cause of chest pain using only history and physical exam.

Diagnosis of nonspecific chest pain carries risk of increased mortality due to ischemic heart disease.

Most patients will not use the term “pain” to describe what they are feeling.

Most descriptors of chest discomfort including location, quality, and associated symptoms have a low predictive value in and of themselves.

Duration, Provocation/Palliation may be more helpful

Martina B, et. Al. J Gen Intern Med. 1997;12(8):459.

Angina – Definition

TABLE 2. CLINICAL CLASSIFICATION OF CHEST PAIN

Classification Symptoms

Typical angina Meets the following characteristics:

• Substernal chest discomfort of characteristic quality and duration,

• Provoked by exertion or emotional stress, and

• Relieved by rest or nitroglycerine

Atypical angina Meets 2 of the above characteristics

Noncardiac chest pain Meets 1 or none of the above characteristics

Modified from Diamond, GA et. al. Computer-assisted diagnosis in the noninvasive evaluation of patients with suspected coronary disease. JACC 1983; 1:444-455

Angina - Definition

TABLE 3. CANADIAN CARDIOVASCULAR SOCIETY CLASSIFICATION SYSTEM FOR ANGINA

Class Activity level for angina

I Prolonged exertion

II Walking >2 blocks or >1 flight of stairs

III Walking <2 blocks or <1 flight of stairs

IV Minimal activity or angina at rest

Modified from Circulation, 54:522-523, 1976.

Modified from Circulation, 54:522-523, 1976.

Symptoms

Increased Likelihood Description of Pain Likelihood ratio

(95% CI) Radiation to Right arm 4.7 (1.9-12)

Radiation to both arms 4.1 (2.5-6.5)

Exertional 2.4 (1.5-3.8)

Radiation to left arm 2.3 (1.7-3.1)

Diaphoresis 2.0 (1.9-2.2)

Nausea/vomiting 1.9 (1.7-2.3)

Worse or similar to prior angina/MI 1.8 (1.6-2.0

Pressure 1.3 (1.2-1.5)

Decreased Likelihood Description of Pain Likelihood ratio

(95% CI) Pleuritic 0.2 (0.1-0.3)

Positional 0.3 (0.2-0.5)

Sharp 0.3(0.2-0.5)

Reproducible with palpation 0.3 (0.2-0.4)

Inframammary location 0.8 (0.7-0.9)

Non-exertional 0.8 (0.6-0.9)

Swap, C, Nagurney, J. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA 2005; 294:2623.

More Symptoms

Women are not the same as Men only 57 percent reported acute chest pain

58 presented with dyspnea, weakness or fatigue

When women have chest pain they more often describe it as sharp

Associated GI symptoms not reliable as up to 35 percent patients can have coexisting cardiac and GI etiologies.

Chest wall pain is not usually associated with systemic symptoms.

Chest. 1996;109(5):1210. J Am Coll Cardiol. 2006; 47:1S. Circulation. 2003;108(21):2619.

Physical Exam

Vital Signs are Vital

Appearance of patient (pale, diaphoretic, etc.)

Palpation of chest wall

Auscultation of heart and lungs murmur, S3, rub, wheezes, symmetric breath sounds, etc

Abdominal exam

Risk Factors

Risks

Jackson R, Lawes CM, Bennett DA, et al. Lancet 2005; 365:434

SBP 110 mmHg

SBP 130 mmHg

SBP 150 mmHg

SBP 170 mmHg

Risk Scores Framingham ATP III Pro-CAM QRISK Reynolds EUR0-SCORE Pooled Cohort

(Most recent)

Risk Factors Age

Diabetes

Smoking

Gender

Cholesterol

Hypertension

Family History

Pretest Likelihood of CAD in Symptomatic Patients According to Age and Sex* (Combined Diamond/Forrester and CASS Data)

*Each value represents the percent with significant CAD on catheterization.

Comparing Pretest Likelihood of CAD in Low-Risk Symptomatic Patients With High-Risk Symptomatic Patients (Duke Database)

Each value represents the percentage with significant CAD. The first is the percentage for a low-risk, mid-decade patient without diabetes mellitus, smoking, or hyperlipidemia. The second is that of a patient of the same age with diabetes mellitus, smoking, and hyperlipidemia. Both high- and low-risk patients have normal resting ECGs. If ST-T-wave changes or Q waves had been present, the likelihood of CAD would be higher in each entry of the table.

2014 SIHD Guidelines Update

Vital Importance of Involvement by an Informed Patient

Choices regarding diagnostic and therapeutic options should be made through a process of shared decision-making involving the patient and provider, explaining information about risks, benefits, and costs to the patient.

I IIa IIb III

Helpful Tests

ECG

Chest X-Ray

Lab Tests

Stress Testing

Cardiac Catheterization

ECG

Normal ECG markedly reduces but does not exclude acute MI

MI LR 0.1 to 0.3 if normal ECG or 1 to 4 percent of patients have MI with normal ECG

ST-segment elevation LR New 6-54 Any 11

Q-Waves New 5-25 Any 4

New conduction defect 6 ST-segment depression 3-5 T-wave inversion 2-3

Panju,AA. Et.al. JAMA 1998; 280:1256


Resting Electrocardiography to Assess Risk

A resting ECG is recommended in patients without an obvious, noncardiac cause of chest pain.

I IIa IIb III

Chest X-ray

20 percent of correctly interpreted Chest x-rays on patients with chest pain yield relevant information

May rule out pneumothorax, provide direction for aortic dissection, give, clues for neoplastic process

90 percent of patients with aortic dissection will have some abnormality on chest x-ray

Chest-X Ray

80 year old female with complaint of chest pain

Pain worse when laying down.

Exertional dyspnea

No exertional chest pain

Pain is constant and decreased with NSAIDS

LHC 3 years prior found only mild CAD

Laboratory Testing

CBC – Elevated WBC may indicate infection but also can be elevated with MI. Severe anemia may be cause for demand ischemia.

CMP – Electrolyte abnormalities may influence heart rhythm, elevated LFT’s or bilirubin may point toward a hepatobiliary source of symptoms, and elevated creatine may suggest poor renal perfusion which may influence results of labs, and outcomes of invasive treatments.

Cardiac Biomarkers – May confirm the diagnosis of acute coronary syndrome.

Cardiac Biomarkers

Of the 3 troponin subunits, 2 subunits (troponin I and troponin T) are derived from genes specifically expressed in myocardium

Troponin elevations convey prognostic assessment beyond that of clinical information, the initial ECG, and the predischarge stress test

Amsterdam EA, et al. 2014 AHA/ACC NSTE-ACS Guideline Data from Antman EM, Tanasijevic MJ, Thompson B, et al. N Engl J Med 1996; 335:1342.


Biomarkers: Diagnosis

Cardiac-specific troponin (troponin I or T when a contemporary assay is used) levels should be measured at presentation and 3 to 6 hours after symptom onset in all patients who present with symptoms consistent with ACS to identify a rising and/or falling pattern

I IIa IIb III

Amsterdam EA, et al. 2014 AHA/ACC NSTE-ACS Guideline

With contemporary troponin assays, creatine kinase myocardial isoenzyme (CK-MB) and myoglobin are not useful for diagnosis of ACS

I IIa IIb III

The presence and magnitude of troponin elevations are useful for short- and long-term prognosis

I IIa IIb III

Causes of Cardiac Biomarker Elevation

Myocardial ischemia ACS Other Coronary Ischemia Non-coronary ischemia

• STEMI • NSTEMI

• Arrythmia: tachy- or brady • Cocaine/methamphetamine use • Coronary intervention (PCI or cardiothoracic surgery) • Coronary artery spasm (variant angina) • Stable CAD in setting of increased 02 demand • Severe hypertension • Coronary embolus • Aortic dissection • Coronary artery vasculitis (SLE, Kawasaki's)

• Shock (hypotension) • Hypoxia • Hypoperfusion • Pulmonary embolism • Global ischemia • CT surgery

Myocardial injury with no ischemia Comorbidities Specific Identifiable precipitants Other

• Renal failure • Sepsis • Infiltrative diseases • Acute respiratory failure • Stroke • Subarachnoid hemorrhage

• Extreme exertion • Cardiac contusion • Burns >30% BSA • Cardiotoxic meds: anthracyclines, herceptin • Electrical shock • Carbon monoxide exposure

• Apical ballooning (Takotsubo) • Stress cardiomyopathy • Myocarditis • Myopericarditis • Rhabdomyolysis involving cardiac muscle • Hypertrophic cardiomyopathy • Peripartum cardiomyopathy • Heart failure • Malignancy

Stress Testing

Designed to provoke cardiac ischemia Exercise or pharmacological stress agents

Vasodilation-elicited heterogeneity in induced coronary flow

Types of Stress Tests Stress: Exercise, Dobutamine, or Adenosine

Imaging: ECG, Echo, Nuclear, MRI

Ischemic Cascade

Fihn et al. Stable Ischemic Heart Disease: Full Text. JACC Vol. 60, No. 24, 2012:e44–e164


Standard exercise ECG testing is recommended for patients with an intermediate pretest probability of IHD who have an interpretable ECG and at least moderate physical functioning or no disabling comorbidity. Exercise stress with nuclear MPI or echocardiography is recommended for patients with an intermediate to high pretest probability of IHD who have an uninterpretable ECG and at least moderate physical functioning or no disabling comorbidity.

I IIa IIb III

I IIa IIb III

Able to Exercise: Do’s


Pharmacological stress with nuclear MPI, echocardiography, or CMR is not recommended for patients who have an interpretable ECG and at least moderate physical functioning or no disabling comorbidity. Exercise stress with nuclear MPI is not recommended as an initial test in low-risk patients who have an interpretable ECG and at least moderate physical functioning or no disabling comorbidity.

I IIa IIb III

No Benefit

Able to Exercise: Don’ts

I IIa IIb III

No Benefit


Pharmacological stress with nuclear MPI or echocardiography is recommended for patients with an intermediate to high pretest probability of IHD who are incapable of at least moderate physical functioning or have disabling comorbidity. Standard exercise ECG testing is not recommended for patients who have an uninterpretable ECG or are incapable of at least moderate physical functioning or have disabling comorbidity.

I IIa IIb III

Unable to Exercise: Do’s & Don’ts

I IIa IIb III

No Benefit

Angiography

Indications Acute Coronary Syndrome (STEMI, NSTEMI, UA)

High Risk Findings with Noninvasive Risk Assessment

Pre operative assessment prior to Valve Replacement/Repair Surgery

Risk assessment in patients surviving cardiac death or potentially life-threatening ventricular arrhythmia

Evaluation of patients with heart failure with low ejection fraction

Noninvasive Risk Stratification

*Although the published data are limited; patients with these findings will probably not be at low risk in the presence of either a high-risk treadmill score or severe resting LV dysfunction (LVEF <35%).


Coronary angiography is useful in patients with presumed SIHD who have unacceptable ischemic symptoms despite GDMT and who are amenable to, and candidates for, coronary revascularization. Coronary angiography is reasonable to define the extent and severity of CAD in patients with suspected SIHD whose clinical characteristics and results of noninvasive testing (exclusive of stress testing) indicate a high likelihood of severe IHD and who are amenable to, and candidates for, coronary revascularization.

I IIa IIb III

I IIa IIb III

Invasive Testing for Diagnosis of CAD in Patients With Suspected SIHD

New 2014

New 2014


Coronary angiography is reasonable in patients with suspected symptomatic SIHD who cannot undergo diagnostic stress testing, or have indeterminate or nondiagnostic stress tests, when there is a high likelihood that the findings will result in important changes to therapy. Coronary angiography might be considered in patients with stress test results of acceptable quality that do not suggest the presence of CAD when clinical suspicion of CAD remains high and there is a high likelihood that the findings will result in important changes to therapy.

I IIa IIb III

I IIa IIb III

Invasive Testing for Diagnosis of CAD in Patients With Suspected SIHD (cont.)

New 2014

New 2014

Other Testing

Cardiac MRI

Coronary Angiography CT

Echocardiography

EGD

Treatments


Spectrum of IHD

Guidelines relevant to the spectrum of IHD are in parentheses

History

Medical 1960’s Aspirin recognized as beneficial

in MI.

1962 – Propranolol

1981 – Captopril approved by FDA

1983 – Streptokinase for MI first described.

1987 - Lovastatin marketed

1990’s Cilostazole, Plavix

Procedural 1960 – First CABG performed in US

1977 – First angioplasty performed in Switzerland.

1980 – Angioplasty for STEMI

1980’s more widespread use of LIMA for CABG

1987 – First successful coronary stents


Treatments

Lifestyle Modification

Medication

Revascularization

Revascularization

Medication

Lifestyle

Revascularization

Medication

Lifestyle

Lifestyle

Study Prospective Cohort in Sweden >20,000 healthy men ages 45 to 79

followed from 1997 to 2009 Low risk score consisted of

Healthy Diet Low to Moderate alcohol No Smoking Physical activity (>40 min/day) No abdominal obesity (<95 cm or 37 in)

Results 1,361 MI’s in 11 years

5 of 5 Low Risk Factors compared to 0 of 5 low Risk Factors found relative risk reduction of 0.14

Thus Adherence to a Low Risk Lifestyle could prevent 79% of MI events

Only 1% of population adhered to 5 of 5 low Risk Factors

Åkesson A, et. Al. J Am Coll Cardiol 2014;64:1299-1306.

ABC’s of Medical/Lifestyle Management

Aspirin and Anti-anginals

Beta blockers and blood pressure

Cholesterol and cigarettes

Diet and Diabetes

Education and Exercise


Treatment with aspirin 75 to 162 mg daily should be continued indefinitely in the absence of contraindications in patients with SIHD. Treatment with clopidogrel is reasonable when aspirin is contraindicated in patients with SIHD.

I IIa IIb III

I IIa IIb III

Antiplatelet Therapy

Anti Anginal Medication

Beta Blockers

Calcium Channel Blockers

Nitrates – long and short acting

Ranolazine

Ranolazine

Mechanism of Action: Alters the trans-cellular late sodium current which affects the sodium-dependent calcium channels, and thus indirectly prevents calcium overload that is thought to lead to ischemia.

Approved by FDA January 2006 Does not lower blood pressure or heart rate Clinical Trials

ERICA: 565 pt. 4.5 angina attacks/wk while on CCB had reduction in angina of about 1 attack per week compared to placebo.

CARISA: 823 pt. on either CCB or Beta Blocker had mean exercise improvement by 115 seconds compared to 91 second improvement in the placebo group after taking ranolazine for 12 weeks.


All patients should be counseled about the need for lifestyle modification: weight control; increased physical activity; alcohol moderation; sodium reduction; and emphasis on increased consumption of fresh fruits, vegetables, and low-fat dairy products. In patients with SIHD with BP 140/90 mm Hg or higher, antihypertensive drug therapy should be instituted in addition to or after a trial of lifestyle modifications. The specific medications used for treatment of high BP should be based on specific patient characteristics and may include ACE inhibitors and/or beta blockers, with addition of other drugs, such as thiazide diuretics or calcium channel blockers, if needed to achieve a goal BP of less than 140/90 mm Hg.

I IIa IIb III

I IIa IIb III

I IIa IIb III

Blood Pressure Management


Beta-blocker therapy should be started and continued for 3 years in all patients with normal LV function after MI or ACS. Beta-blocker therapy should be used in all patients with LV systolic dysfunction (EF ≤40%) with heart failure or prior MI, unless contraindicated. (Use should be limited to carvedilol, metoprolol succinate, or bisoprolol, which have been shown to reduce risk of death.) Beta blockers may be considered as chronic therapy for all other patients with coronary or other vascular disease.

I IIa IIb III

I IIa IIb III

I IIa IIb III

Beta-Blocker Therapy


Lifestyle modifications, including daily physical activity and weight management, are strongly recommended for all patients with SIHD. In addition to therapeutic lifestyle changes, a moderate or high dose of a statin therapy should be prescribed, in the absence of contraindications or documented adverse effects.

I IIa IIb III

Cholesterol Management

I IIa IIb III


Smoking cessation and avoidance of exposure to environmental tobacco smoke at work and home should be encouraged for all patients with SIHD. Follow-up, referral to special programs, and pharmacotherapy are recommended, as is a stepwise strategy for smoking cessation (Ask, Advise, Assess, Assist, Arrange, Avoid).

I IIa IIb III

Smoking Cessation Counseling


For selected individual patients, such as those with a short duration of diabetes mellitus and a long life expectancy, a goal HbA1c of 7% or less is reasonable. A goal HbA1c between 7% and 9% is reasonable for certain patients according to age, history of hypoglycemia, presence of microvascular or macrovascular complications, or presence of coexisting medical conditions.

I IIa IIb III

I IIa IIb III

Diabetes Management


For all patients, the clinician should encourage 30 to 60 minutes of moderate-intensity aerobic activity, such as brisk walking, at least 5 days and preferably 7 days per week, supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work) to improve cardiorespiratory fitness and move patients out of the least-fit, least-active, high-risk cohort (bottom 20%). For all patients, risk assessment with a physical activity history and/or an exercise test is recommended to guide prognosis and prescription.

I IIa IIb III

Physical Activity

I IIa IIb III


An annual influenza vaccine is recommended for patients with SIHD.

I IIa IIb III

Influenza Vaccination

Revascularization

May improve survival in Acute Coronary Syndrome

May improve survival in Severe Multivessel or Left Main Coronary Artery Disease

May improve symptoms in Severe Single or Two Vessel disease

Survival and symptomatic benefit of revascularization is dependent upon presentation (Stable vs. Unstable), and severity.

CAD Prognostic Index

*Assuming medical treatment only.

Fihn et al. Stable Ischemic Heart Disease: Full Text. JACC Vol. 60, No. 24, 2012:e44–e164

Thrombolysis in Myocardial Infarction (TIMI) score for unstable angina or non ST elevation myocardial infarction

Risk Factor 1 Age >=65 (1 point) 2 3 or more CAD risk factors (1 point) 3 Known CAD with more than 50% stenosis (1 point) 4 Aspirin use in the past 7 days (1 point) 5 Severe angina in the preceeding 24 hours (1 point) 6 Elevated cardiac markers (1 point) 7 ST deviation greater than 0.5 mm (1 point)

Antman EM, Cohen M, Bernink PJ, et. al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000 Aug 16;284(7):835-42.

Points Risk in 2 weeks of Death, MI, Urgent Revascularization

0-1 Points: 3% to 5% 2 Points: 3% to 8% 3 Points: 5% to 13% 4 Points: 7% to 20% 5 Points: 12% to 26% 6-7 Points: 19% to 41%

In-Hospital Outcomes – STEMI vs. NSTEMI

Variable STEMI

(n=28,614) NSTEMI

(n=44,528) Death* 5.7% 4.0% Re-infarction 1.0% 0.9% CHF 6.1% 6.7% Cardiogenic Shock 6.4% 2.9% Stroke 0.9% 0.8% RBC Transfusion** 5.7% 7.6% Major Bleeding** 11.4% 9.2%

*Unadjusted mortality ** Among non-CABG pts ACTION Registry-GWTG DATA: July 1, 2009 – June 30, 2010

Median survival after an MI

0 5 10 15 20

55 to 64

65 to 74

75

Years

Age

at t

ime

of M

I

WomenMen

3.2 3.2

17 13.3

9.3 8.8


Invasive vs. Conservative Management of ACS All Cause Mortality

Non fatal MI

Rehospitalization

Bavry AA et al. JACC 2006; 1319-25

Angioplasty for STEMI

Relationship between 30-day mortality and time from study enrollment to first balloon inflation. Patients assigned to angioplasty in whom angioplasty was not performed are also shown. PTCA = percutaneous transluminal coronary angioplasty. Berger et al. Circulation 1999;100:14-20 (294).

Inferior ST Elevation

RCA Occlusion


PCI in Specific Clinical Situations: UA/NSTEMI

An early invasive strategy (i.e., diagnostic angiography with intent to perform revascularization) is indicated in UA/NSTEMI patients who have refractory angina or hemodynamic or electrical instability (without serious comorbidities or contraindications to such procedures).

I IIa IIb III

2011 PCI Guidelines


PCI in Specific Clinical Situations: STEMI–Coronary Angiography Strategies in STEMI

A strategy of immediate coronary angiography with intent to perform PCI (or emergency CABG) in patients with STEMI is recommended for a. Patients who are candidates for primary PCI. b. Patients with severe heart failure or cardiogenic shock

who are suitable candidates for revascularization.

I IIa IIb III

I IIa IIb III

2011 PCI Guidelines


Revascularization to Improve Symptoms With Significant Anatomic (≥50% Left Main or ≥70% Non-Left Main CAD) or Physiological (FFR ≤0.80) Coronary Stenoses

Outcomes

Deaths due to Cardiovascular Disease ( US 1900-2007)


Cardiovascular Mortality


Drop in Mortality from CAD

1950 to 1999: Decreased by 59%

1997 to 2007: Decreased by 26.3%

From Framingham Heart Study, death from coronary artery disease (CAD)

Decline in MI from 1999 to 2011

Krumholz HM. Circulation. 2014; doi:10.1161/CIRCULATIONAHA.113.007787

33.6% Reduction

Decline in Unstable Angina 1999 to 2011

Krumholz HM. Circulation. 2014; doi:10.1161/CIRCULATIONAHA.113.007787

83.8% Reduction

N Engl J Med. 2007 Jun 7;356(23):2388-98.

Conclusion Approximately half the decline in U.S. deaths from coronary heart disease from 1980 through 2000 may be attributable to reductions in major risk factors and approximately half to evidence based medical therapies.

0 200 400 600

Male Death Rate

Female Death Rate198020002007

Total 341,745 fewer deaths from coronary heart disease in 2000

Modern Medicine

47%

11%

10%

9%

5%

12%

0% 10% 20% 30% 40% 50%

Total

Secondary Therapy after MI orRevascularization

Treatment of ACS

Heart Failure Treatment

Revascularization for Chronic Angina

Other: Including primary prevention

Percent Reduction in Death Attributed to Medical Treatment of CHD

N Engl J Med. 2007 Jun 7;356(23):2388-98.

Lifestyle Changes

44%

24%

20%

12%

5%

0% 10% 20% 30% 40% 50%

Total

Reduction in cholesterol

Systolic blood pressure

Smoking prevalence

Physical inactivity

Percent Reduction in Deaths Attributed to Risk Factor Modification

N Engl J Med. 2007 Jun 7;356(23):2388-98.

Conclusions

Chest pain is a common symptom and accounts for a large percentage of Emergency Room, Primary Care, and Cardiology visits.

Most causes of chest pain are not life threatening and can be diagnosed through history, physical examination and basic diagnostic tests

Cardiac causes of chest pain account for the majority of life threatening causes of chest pain.

Early identification and treatment of ischemic heart disease through Guideline Directed Medical Therapy, Lifestyle Changes, and Revascularization have led to a significant decline in cardiac deaths over the past 50 years.

Thank You

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