Chest Pain Differentials

1. Chest Pain Differentials John McGinnity M.S., P.A.-C. Associate Professor Wayne State University Detroit, Michigan jmcginnity@wayne.edu

2. Disclosures Mr. McGinnity’s disclosures: Honorarium – Boehringer Ingelheim for previous AAPA Chapter Lecture Series Grant Not a Promotional Speaker for any Companies

3. Session Objectives Focus their interview and utilize tools to assist with the subjective data collection Identify some key signs and physical findings when assessing chest pain Categorize multiple chest pain related diagnoses and discuss appropriate treatment options in the management of each

5. Common Causes of Chest Pain Cardiac Angina USA AMI Valve Disease Pericarditis HTN Spasm Vascular Aortic Dissection Pulmonary Embolism Pulmonary HTN Pulmonary Pleuritis/ Pneumonia Tracheobronchitis Pneumothorax Gastrointestinal GERD PUD Gallbladder Disease Pancreatitis Neuromusculoskeletal Costochondritis DJD Cervical/Thoracic Herpes Zoster Psychological Panic Disorder Anxiety/Depression Other Causes Anemia

6. Cardiac Causes

7. Vascular Causes

8. Pulmonary Causes

9. Gastrointestinal Causes Panc causing meds- diuretics, AID therapy, anticonvulsants , statinsPanc causing meds- diuretics, AID therapy, anticonvulsants , statins

10. Musculoskeletal Causes

11. Which one of the Following is True? The majority of AMI’s are caused by plaques found to be significant on Stress testing (lesions >70%) The majority of AMI occur in patients with a History of AMI The odds of Mortality during AMI do not dramatically increase by Dx to drug/Balloon Times All of the above are True All of the above is False

12. The Majority of MI’s Are Caused by Lesions With <50% Stenosis Several investigators have examined the question of which types of lesions cause myocardial infarctions (MIs). This slide shows collated data from a number of studies with serial angiographic examinations.2 The proportion of patients with MI caused by either <50%, 50%-70%, or >70%, stenosis is summarized. In 68% of cases, the coronary event was caused by plaques causing <50% stenosis.2 This finding provides support for the hypothesis that luminal narrowing may not identify vulnerable plaque. Although severely stenotic lesions are more likely to progress to complete occlusion, mild-to-moderate lesions are more common and may result in MI more frequently.2 More severe stenosis is associated with protective collateral vessels and therefore less stenotic plaques may have a greater risk of causing acute events such as MIs when they rupture and cause thrombosis.2 Overall, the association between less stenosed lesions and the occurrence of coronary events illustrates the importance of identifying and treating atherosclerosis at any stage.Several investigators have examined the question of which types of lesions cause myocardial infarctions (MIs). This slide shows collated data from a number of studies with serial angiographic examinations.2 The proportion of patients with MI caused by either <50%, 50%-70%, or >70%, stenosis is summarized. In 68% of cases, the coronary event was caused by plaques causing <50% stenosis.2 This finding provides support for the hypothesis that luminal narrowing may not identify vulnerable plaque. Although severely stenotic lesions are more likely to progress to complete occlusion, mild-to-moderate lesions are more common and may result in MI more frequently.2 More severe stenosis is associated with protective collateral vessels and therefore less stenotic plaques may have a greater risk of causing acute events such as MIs when they rupture and cause thrombosis.2 Overall, the association between less stenosed lesions and the occurrence of coronary events illustrates the importance of identifying and treating atherosclerosis at any stage.

13. Most Coronary Events Occur in Persons With No Recorded History of MI Atherosclerosis is a progressive disease that may be asymptomatic until the acute transition to clinical coronary heart disease (CHD), which may be sudden and drastic. Most coronary events occur in persons with no previous history of an MI.7 The Atherosclerosis Risk in Communities (ARIC) study surveyed hospital admissions for MI from 1987 to 1994 among residents aged 35 to 74 years in 4 communities in the United States: Forsyth County, North Carolina, the city of Jackson, Mississippi, 8 northern suburbs of Minneapolis, and Washington County, Maryland. A first event was defined as one in a patient for whom the medical record either stated that there was no history of MI or did not contain any reference to a history of MI. There were an estimated 11,869 hospital admissions (based on a sampling of 8572 hospitalizations) for fatal or nonfatal, definite or probably acute MIs during the study. Of the 3977 coronary events in women, 69%, or 2744, occurred in persons who had no history of MI. Of the 7892 events in men, 4893, or 62%, occurred in persons who had no history of MI.7 Atherosclerosis is a progressive disease that may be asymptomatic until the acute transition to clinical coronary heart disease (CHD), which may be sudden and drastic. Most coronary events occur in persons with no previous history of an MI.7 The Atherosclerosis Risk in Communities (ARIC) study surveyed hospital admissions for MI from 1987 to 1994 among residents aged 35 to 74 years in 4 communities in the United States: Forsyth County, North Carolina, the city of Jackson, Mississippi, 8 northern suburbs of Minneapolis, and Washington County, Maryland. A first event was defined as one in a patient for whom the medical record either stated that there was no history of MI or did not contain any reference to a history of MI. There were an estimated 11,869 hospital admissions (based on a sampling of 8572 hospitalizations) for fatal or nonfatal, definite or probably acute MIs during the study. Of the 3977 coronary events in women, 69%, or 2744, occurred in persons who had no history of MI. Of the 7892 events in men, 4893, or 62%, occurred in persons who had no history of MI.7

15. Thrombolysis: Odds of Death by Door To Drug Times

16. Just When You Know… You Might be Going Down the Wrong Road!

17. Case #1

18. Dissections Majority of dissections occur in the ascending aorta within several centimeters of the valve (65%) Descending aortic – distal to the left subclavian artery (20%) Aortic arch (10%) Abd Aorta (5%)

19. Classifications DeBakey Type I Originates in ascending aorta and propagates to the arch or beyond Type II originate and is limited to the ascending aorta Type III originate in the descending aorta and goes distal or rarely retrograde Stanford Type A All involving ascending aorta Type B all others Descriptive Proximal /distal

20. Etiology Peak incidence is in the 6-7th decades of life Men 2:1 H/O HTN 80% of cases Bicuspid aortic valve Marfans syndrome Arteritis Pregnancy 50% of dissection in women <40 Trauma

21. Symptoms Severe Chest pain 75-90% of cases Sudden onset and severe at inception Ripping/ tearing/ stabbing pain Migration of the pain 70% of cases Location anterior pain more common ascending involvement posterior pain descending involvement Less common presentation- CHF, CVA, syncope, ischemic neuropathy, cardiac arrest or sudden death

24. Aortic dissection

25. Case #2

26. Aortic Stenosis

28. Aortic Stenosis Typically develops 60’s, 70’s, 80’s As the disease progresses calcification and fibrosis lead to leaflet stiffness and reduced systolic opening The area must be reduced to one-fourth its original size before clinically significant obstruction occurs

29. Aortic Stenosis Mild AS <30 mmHg gradient AVA >1.5cm2 Encourage patient to live a normal life Moderate AS > 30 mmHg gradient AVA 1.0 – 1.5 cm2 Moderate to severe exertion and competitive sports should be avoided

30. Severe AS is Lethal Once symptoms occur: 3 year mortality 30-50% 5 year mortality 60-80% 10 year mortality 80-90%

31. Hypertrophic Cardiomyopathy Most common cause of sudden death in young athletes Male to female ratio: 9:1 Common Presenting complaints: 50% asymptomatic; 50% have DOE, angina, syncope, palpitations, etc Clinical Signs: May be absent If present: syncope, orthopnea, dyspnea, chest pain, lightheadedness, palpitations, and fatigue. May present as a murmur detected during the PPE + harsh crescendo-decrescendo systolic murmur heard most clearly at the left lower sternal border and apex. A fourth heart sound may be heard. Classically increases with Valsalva and diminishes when preload is increased.

32. Aortic Regurgitation Chronic AR LV dilation Produces a larger stroke volume Increasing pulse pressure Causing systolic HTN Usually asymptomatic Acute AR No time to mount adaptive response to larger end diastolic volumes Increased end diastolic pressures causing inadequate contractile response resulting Decreased stroke volume Usually symptomatic

33. Mitral Regurgitation Most frequently related to ischemic or degenerative process Can be acute or chronic Classified as functional or organic Causes MVP (Most common cause of severe MR) Prevalence Accounts for 90% chordae ruptures Ischemic heart disease Cardiomyopathy RHD Infective endocarditis Myocardial disease or tumors Connective tissue disorders Congenital defect Trauma

34. Mitral Regurgitation Timing of intervention Should be considered for symptomatic patients and those with LV dysfunction EF usually supernormal Once EF falls below 60% the prognosis worsens. (Carabello BA Mod Concepts Cardiovasc Dis 1988.) Once the End-Systolic dimension exceeds 45 mm the prognosis worsens. (Crawford et al. Circulation 1990.)

35. Clinical Case #3

36. Endocarditis – Clinical Features Fever 80-85% Chills, weakness 45-75% Anorexia / weight loss 25-40% Myalgia/ arthralgia 15-30% Cardiac murmurs (80-85%) changing or new murmur Splenomegaly 15-50% Petechiae 10-40% Younger patients neonates (almost none)/ infants less sx Gradual onset streptococci Acute onset staphylococciYounger patients neonates (almost none)/ infants less sx Gradual onset streptococci Acute onset staphylococci

37. Endocarditis – Clinical Features Janeway lesions: small erythematous or hemorrhagic macular lesions on palms / soles 6-10% Osler nodes: small tender subcutaneous nodules on pulp of digits 7-10% Finger clubbing 10-20% Splinter / subungual hemorrhages 5-15% Embolic phenomena: large arteries (femoral), lungs IV abusers, Brain(Stroke, brain abscess, purulent meningitis) 20-40% A A

38. Complications ½ of all IE have at least one complication Congestive Heart Failure AV > MV Neurological events 20-40% (highest 1st 2 wks) Acute myocardial infarction Embolic Phenomenon Large vegetations on the MV esp ant leaflet are assoc with higher risk of embolization than similar vegetations elsewhereLarge vegetations on the MV esp ant leaflet are assoc with higher risk of embolization than similar vegetations elsewhere

39. Endocarditis- Who is at risk? Intravascular PICC lines Any indwelling intravascular line Pacer ICD Dialysis catheter Prosthetic valve Immunocompromised Immunosupression Steroids Chemotherapy Radiation Untreated malignancy Injectable drug use HIV/AIDS Try to think about your patients who have a history of a recent transient bacteremia that has been either treated, completely or partially. These are the individuals who end up getting a recurrent bacteremia that fall prey to endocarditis. We will commonly see these patients, treat them with antibiotics for an illness that doesn’t quite add up to a diagnosis but could very well be endocarditis. We tend to have a reflex to start patients on antibiotics for things like recurrent infections. This over time can mask an early case of endocarditis, making it difficult to detect in its early stages.Try to think about your patients who have a history of a recent transient bacteremia that has been either treated, completely or partially. These are the individuals who end up getting a recurrent bacteremia that fall prey to endocarditis. We will commonly see these patients, treat them with antibiotics for an illness that doesn’t quite add up to a diagnosis but could very well be endocarditis. We tend to have a reflex to start patients on antibiotics for things like recurrent infections. This over time can mask an early case of endocarditis, making it difficult to detect in its early stages.

40. Key points Differentiating Chest pain can be difficult Remember Multiple problems can happen in the same patient! Failure to ask the right questions can be devastating! Did you recognize the signs and symptoms? Remember to conduct and document physical examination findings Remember to follow-up on required tests Never be afraid to ask for help!!!

41. Questions? Thank you for your Attention!