Chest pain affects 20% to 40% of the general population during their lifetime.

Transcription

1

2

3 Chest pain affects 20% to 40% of the general population during their lifetime. More than 5% of visits in the emergency department, and up to 40% of admissions are because of chest pain.

4 Chest pain is a common presentation in patients with MI; however, there are multiple non-cardiac causes of chest pain, and the diagnosis cannot always be made based on initial presentation Most patients with chest pain do not have MI, and a systematic approach can usually rule it out

5 Chest pain which presents symptom of Acute Coronary Syndrome, has some criteria: pain or discomfort in the centre of the chest; pain or discomfort in the arms, the left shoulder, elbows, jaw, or back.

6 In addition the person may experience difficulty in breathing or shortness of breath; feeling sick or vomiting; feeling light-headed or faint; breaking into a cold sweat; and becoming pale. Women are more likely to have shortness of breath, nausea, vomiting, and back or jaw pain.

7 (Typical) Chest pain is often the presenting symptom of Acute Coronary Syndrome, which is damage to the cardiac muscle caused by ischemia.

8 Other important symptoms and signs: Diaphoresis: strong predictor of MI pain Radiating pain to both arms (but presence of chest wall tenderness significantly reduced the possibility of MI)

9 The patient has accepted to emergency department with (typical) chest pain

10 The assessment begins with rapid 12- lead ECG within 10 minutes of presentation

11

12

13 Normal or near-normal ECG findings decrease the risk of MI, especially in patients with no history of coronary artery disease, but NSTEMI may occur in 1% to 6% of these patients. Serial ECG or continuous ST segment monitoring may increase the detection of ischemic changes, especially in patients with continued pain

14 If there is no evidence of STEMI, the patient s risk of ACS should be categorized as low, intermediate, or high This is based on an assessment of risk factors, presenting signs and symptoms, and serial cardiac troponin measurements

15 Cardiac troponin levels should be measured at presentation and again three to six hours after symptom onset

16 Patients with elevated levels consistent with non ST elevation ACS should be hospitalized and treated according to the American College of Cardiology/ American Heart Association guidelines with an early invasive strategy (diagnostic angiography with revascularization as indicated) for higher risk groups

17 In patients with negative cardiac troponin levels, additional confirmatory testing may be performed to further lower the risk of undiagnosed ACS; this may be done in a chest pain unit, as an inpatient, or as an outpatient

18 In some patients with negative electrocardiography findings and normal cardiac biomarkers, additional testing may further reduce the likelihood of coronary artery disease

19 Cardiac catheterization is the standard method for diagnosing coronary artery disease, but exercise treadmill testing, a stress myocardial perfusion study, stress echocardiography, and computed tomography are noninvasive alternatives

20 Risk factors for MI include: 1. increasing age, 2. male sex, 3. chronic renal insufficiency 4. diabetes mellitus, 5. known atherosclerotic disease (coronary or peripheral), and 6. early family history of coronary artery disease (first-degree male relative with first event before 55 years of age or first-degree female relative with first event before 65 years of age).

21 A calculator from the American College of Cardiology and American Heart Association estimates 10-year risk of atherosclerotic cardiovascular disease and assists with primary prevention ( my.americanheart.org/cvriskcalculator).

22

23

24

25

26

27

28

29 Criteria to diagnose STEMI include: 1. ST segment elevation of 2 mm in men and 1.5 mm in women for leads V2 and V3; 2. 1 mm for leads V1, V4-6, I, II, III, avl, and avf; 3. and 0.5 mm for leads V3R and V4R (right-sided leads) and V7-9 (posterior leads).

30 If there is evidence of STEMI, the patient should be emergently referred for reperfusion therapy with primary percutaneous coronary intervention (preferred)

31

32

33 or fibrinolytic therapy

34 Cardiac troponins T and I are highly specific to myocardial cells and are the primary measure of myocardial injury. Measurement of other biomarkers, such as creatine kinase myocardial isoenzyme and myoglobin, is no longer recommended.

35

36 Troponins T and I are clinically equivalent and have a sensitivity of 79% to 83% and a specificity of 93% to 95% for detecting myocardial injury. Cardiac troponin should be measured at presentation and three to six hours after onset of ischemic symptoms.

37 A troponin value above the 99th percentile of the upper reference level (laboratory specific) is required for the diagnosis of myocardial necrosis and an increase or decrease of at least 20% is required for the diagnosis of acute myocardial necrosis.

38

39 Alternatively, if the initial troponin level is below the 99th percentile, a change greater than three standard deviations is considered positive for acute myocardial necrosis.

40 When initial troponin results are normal but ECG changes or clinical presentation suggests a moderate or high risk of ACS, troponin levels should be measured again after six hours.

41 Nonischemic conditions can cause cardiac troponin elevations and serial measurements may be useful to differentiate these conditions from acute MI. Patients with acute MI will have a rising or falling pattern, whereas levels will remain relatively stable with chronic conditions.

42 Diet influences the pathogenesis of coronary artery disease in a variety of ways The initial development of fatty streaks in coronary arteries is mediated by serum lipid levels and free-radical oxidation, both of which are modified by nutrients

43 Progression of coronary lesions is affected by serum lipids, hypertension, hyperinsulinemia, adiposity, and oxidation and inflammation, all of which are mediated by both macronutrient and micronutrient intake

44 Once coronary artery atherosclerosis is established, diet plays a role in determining both progression of plaque deposition and the reactivity of the endothelium, both of which may be predictive of cardiac events Dietary manipulations have been shown to modify all the known, modifiable coronary risk factors and, when extreme, to induce regression of established lesions

45 Both dietary fat restriction and the substitution of unsaturated for saturated fats would likely offer advantages; there is evidence of cardiac risk reduction Weight loss is of clear and potentially profound cardiac benefit to overweight and obese patients

46 The National Heart, Lung, and Blood Institute (NHLBI) recommends a loss of 10% body weight to achieve meaningful improvement in the cardiac risk profile Body fat distribution has important implications for health effects; central, visceral adiposity is of special concern for cardiac health

47 Intake of fruits, vegetables, and cereal grains is inversely correlated with cardiovascular risk, as is total fiber intake The intake of soluble fiber in particular appears to have cardiovascular benefits attributable at least to a hypolipidemic effect

48 The optimal level of dietary fat intake for primary prevention of heart disease, or for the management of established heart disease, is the total fat restriction and more liberal intake of n-3 PUFAs and MUFAs

49 Saturated and trans fat should be restricted to below 7% (or even 5%) of total calories in all cardiac patients; this guideline is appropriate for primary prevention in willing patients as well

50 The remaining 20% to 25% of calories derived from fat should be divided between polyunsaturated and monounsaturated fat in a ratio of between 1:1 and 1:2 Polyunsaturated fat should be divided between n-6 and n-3 fatty acids in a ratio between 4:1 and 1:1 rather than the prevailing ratio of 11:1 (n-6:n-3).

51 Intake of fish, nuts, soy, olives, avocados, seeds, olive oil, canola oil, and linseed oil should be encouraged to raise n-3 PUFA and MUFA intake However, these items should substitute in the diet for other sources of fat to avoid raising total fat and/or calorie intake

52 Dietary fat and cholesterol reduction is best achieved by restricting intake of red meats; deli meats; whole-fat dairy products, especially cheese; cheese- and cream-based sauces and dressings

53 Foods rich in cholesterol but low in fat, notably eggs, may not impose any cardiac risk, although opinion in this area is still evolving Optimal management of dietary fat intake appears capable of lowering LDL by as much as 20% and total cholesterol by as much as 30%, although lesser reductions are usually seen

54 Statin drugs can lower LDL by up to 60%; the effects of these agents are enhanced by dietary therapy

55 Benefits of dietary fiber are well established, and prevailing intake is deficient A daily intake of at least 30 g of fiber is appropriate and is readily achievable if whole grains, vegetables, and fruits are the principal sources of food energy

56 The cardioprotective influence of fruit and vegetable intake is decisive The cardioprotective effect of this diet may be due to a variety of antioxidant micronutrients, essential micronutrients such as vitamins and minerals, and fiber, both soluble and insoluble

57 Evidence linking antioxidation to a reduced risk of cardiovascular disease is convincing The principal mechanism by which antioxidants confer cardiovascular benefit is thought to be inhibition of LDL oxidation

58 A diet rich in fruits and vegetables typically provides abundant antioxidants, including carotenoids, tocopherols, flavonoids, and ascorbate, and has been decisively linked to reduced cardiac risk

59 Restriction of dietary sodium to 2.4 g per day or less (or salt to 3.4 g per day or less) is apparently of variable importance but advisable and appropriate

60 Iron may act as a pro-oxidant, generating speculation that it might contribute to the risk of cardiac disease in men and that its depletion in menstruating women might contribute to risk reduction

61 Serum magnesium concentrations have been found to be inversely associated with cardiovascular disease risk Magnesium is known to have antiarrhythmic properties and has corresponding, potential therapeutic applications in acute cardiac care

62 Any beneficial effects of magnesium on cardiovascular disease risk may be mediated in particular by its association with reduced blood pressure For most patients, a generous intake of magnesium from dietary sources is to be encouraged

63 Nut intake is convincingly and consistently associated with beneficial effects on cardiac risk factors in intervention studies and with reduced event rates in observational studies

64 Despite their energy density, nuts are not clearly associated with risk of weight gain The evidence of benefit is greatest for walnuts, which offer a particularly favorable fatty acid profile Almonds are also consistently associated with cardiac benefit

65 Barstow C, Rice M, Mcdivitt JD. Acute Coronary Syndrome: Diagnostic Evaluation. Am Fam Physician. 2017;95(3): Amsterdam EA, Wenger NK, Brindis RG, et al.; American College of Cardiology; American Heart Association Task Force on Practice Guidelines; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons; American Association for Clinical Chemistry AHA/ACC guideline for the management of patients with non ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in J Am Coll Cardiol. 2014;64(24): ]. J Am Coll Cardiol. 2014;64(24):e139-e228

66 Appreciate your time!