Management of chest pain and heart failure. Cardiac rehabilitation and secondary prevention

1. Management of chest pain and heart failure. Cardiac rehabilitation and secondary prevention WT Bong Dept of Family Medicine, HUKM

2. Case scenario 1 • 60 yo gentleman, a known case of DM for the past 2 years complains of chest pain for the past 2-3 months when he walks more than 10 minutes. The chest pain radiates to left arm, lasts 5 min, relieved by rest. Currently during his visit to the primary care clinic, he has no chest pain. He is a smoker for the past 40 years. He is on metformin 500mh bd only. Clinically, BP 120/60mmHg and cardiovascular examination was unremarkable.

3. Patient comes in with chest pain.. • ?cardiovascular • Cardiac. • MV prolapse.pericarditis • ischemic • Non cardiac. Aortic dissection • ?gastrointestinal. GERD • ?Musculoskeletal.fibromyalgia. • ?pulmonary • ?psychogenic

4. We start with stable angina.. • By definition. Clinical syndrome characterised by • discomfort in chest, jaw, shoulder, back or arm • Typically aggravated by exertion or emotional stress • Reduced by rest or GTN

5. Most common cause for stable angina is atherosclerotic coronary artery disease (CAD) • Other causes could be • Hypertrophic cardiomyopathy • Aortic stenosis • Coronary vasospasm etc

6. Atherosclerosis process in coronary

7. Stable angina is classified into 4 classes based on Canadian Cardiovascular Society Classification (CCS 0-IV)

8. Diagnosis of stable angina can be established by • Clinical assessment • Look for complication of CAD.murmur(MR).septaldefect.sign of cardiomegaly.CHF • Other site of atherosclerosis.carotidbruit.peripheral vascular disease.aortic aneurysm • Risk factor for atherosclerosis.hpt.metabolicsyn • Other cause of angina.HOCM.aorticstenosis • Lab test • Specific cardiac investigation

9. Lab test to establish CVS risk factor • FLP. FBS. homocysteine level • Determine prognosis, creatinine • CXR only if suspect CHF if want to see calcification, cardiomegaly/atrial enlargement, valvular disease, pulmonary congestion (help establish prognosis) • Specific cardiac investigation

10. Specific cardiac investigation, non invasive • ECG. See previous ischemia, LVH, BBB, arrhythmia or conduction defect • Stress test. More sensitive and specific than resting ECG • Echo.when there is abnormal auscultation suggest valvular, if HCM or prev MI changes on ECG, SSx CHF , to study diastolic function

11. Risk-stratify our patient • For the purpose of prognosis + treatment (revascularize in high risk patient)

12. Clinical history – important predictor of adverse outcome in established CAD

13. Risk stratify .. Higher risk if ECG shows

14. Other aspects to be considered in risk-stratifying • Stress test • Ventricular function • COROS

15. Treatment goal • Prevent MI & death • Improve SSx of angina & increase QoL

16. Non pharmacological approach Life style diet Variety of fruits and vegetable.legumes.nuts. Soy products.low fat dairy.whole grain Replace saturated & trans-fat (red meat.whole milk . Pastries) with polysaturated fat (oily fish,walnut,sesame. Pumpkin seed.vegetable oil) Soluble fibre.oat.peas.bean • Smoking cessation • 36 % risk reduction mortality • 32 % risk reduction non fatal MI • Nicotine replacement is safe and cost effective even for CAD patient (take into account risk of depression and suicidal thought)

18. education Can also take GTN as preventive measure if patient know he is going to have attack while carrying out some activity If SSx persist more than 10min at rest or not improved after 3 tablet of GTN, advice to go to hospital Self management During acute anginal attack Restrain activity GTN S/L or spray Sit . Hypotension. Headache after GTN

22. revascularization • PCI or CABG • In high risk group it is firstline treatment • Significant LMS ( > 50% stenosis) • Significant proximal mutivessel involvement • Multivessel disease with impaired LV function with proven viable myocardium • Or if failed medical treatment to control angina SSx • In asymptomatic patient, consider if there is extensive inducible ischaemia (stress test)

23. What if it is aMI ?

25. Secondary prevention • Basically similar to angina which include

26. Oral Anticoagulant (warfarin) • If AF • LV thrombus for 3-6mths

27. Secondary prevention • Hormone replacement therapy is not beneficial for secondary prevention • Postmenopausal women who were taking HRT at the time of STEMI should discontinue it • Vitamin E and antioxidants have no clinical benefit • Garlic, lecithin, vitamin A and C are not beneficial

28. Heart failure • Is a complex clinical syndrome results from structural or functional impairment of ventricular filling or ejection of blood • Cardinal manifestation are dyspnea, fatigue, which may limit effort tolerance, and fluid retention, which may lead to pulmonary or splanchnic congestion or peripheral edema.

29. Definition of Heart Failure

30. Stages, Phenotypes and Treatment of HF ACC AHA 2013

31. Classification of Heart Failure

32. Physical examination • BMI and evidence of weight loss • Bp, supine and upright( orthostatic changes – volume depletion) • Pulse – strength and regularity • JVP • Extra heart sound, murmur, apex beat displacement, RV heave • Pulmonary status • Hepatomegaly • Peripheral edema

33. Lab investigation • Class I • 1.Initial laboratory evaluation of patients presenting with HF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone. (Level of Evidence: C) • 2.Serial monitoring, when indicated, should include serum electrolytes and renal function. (Level of Evidence: C) • 3.A 12-lead ECG should be performed initially on all patients presenting with HF. (Level of Evidence: C) • Class Iia • 1.Screening for hemochromatosis or HIV is reasonable in selected patients who present with HF (Level of Evidence: C) • 2.Diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma are reasonable in patients presenting with HF in whom there is a clinical suspicion of these diseases. (Level of Evidence: C)

34. Recommendations for Biomarkers in HF

35. Recommendations for Noninvasive Imaging

36. HFSA 2010 Comprehensive Heart Failure Practice Guideline Key Recommendations

37. HFSA 2010 Practice Guideline (3.1)Heart Failure Prevention Adapted from:

38. HFSA 2010 Practice Guideline (3.2)HF Risk Factor Treatment Goals Adapted from:

39. Aggressive blood pressure control: Aggressive BP control in patients with prior MI: Treating Hypertension to Prevent HF Decreases risk of new HF by ~ 50% 56% in DM2 Decreases risk of new HF by ~ 80% Lancet 1991;338:1281-5 (STOP-Hypertension JAMA 1997;278:212-6 (SHEP) UKPDS Group. UKPDS 38. BMJ 1998;317:703-713

40. HFSA 2010 Practice Guideline (3.3-3.4)Prevention—ACEI and Beta Blockers ACE inhibitors are recommended for prevention of HF in patients at high risk for this syndrome, including those with: • Coronary artery disease • Peripheral vascular disease • Stroke • Diabetes and another major risk factorStrength of Evidence = A ACE inhibitors and beta blockers are recommended for all patients with prior MI.Strength of Evidence = A

41. Management of Patients with Known Atherosclerotic Disease But No HF Treatment with ACE inhibitors decreases the risk of CV death, MI, stroke, or cardiac arrest. NEJM 2000;342:145-53 (HOPE) Lancet 2003;362:782-8 (EUROPA) Placebo HOPE Ramipril 22% rel. risk red. p < .001 EUROPA Placebo Perindopril 20% rel. risk red. p = .0003

42. Treatment of Post-MI Patients with Asymptomatic LV Dysfunction (LVEF ≤ 40%) SAVE Study • All-cause mortality ↓19% • CV mortality ↓21% • HF development ↓37% • Recurrent MI ↓25% Mortality Rate Placebo Captopril 19% rel. risk reduction p = 0.019 Years Pfeffer et al. NEJM 1992;327:669-77

43. HFSA 2010 Practice Guideline (4.8, 4.10)Heart Failure Patient Evaluation Recommended evaluation for patients with a diagnosis of HF: • Assess clinical severity and functional limitation by history, physical examination, and determination of functional class* • Assess cardiac structure and function • Determine the etiology of HF • Evaluate for coronary disease and myocardial ischemia • Evaluate the risk of life threatening arrhythmia • Identify any exacerbating factors for HF • Identify co-morbidities which influence therapy • Identify barriers to adherence and complianceStrength of Evidence = C *Metrics to consider include the 6-minute walk test and NYHA functional class Adapted from:

44. HFSA 2010 Practice Guideline (4.19)Evaluation—Follow Up Assessments Recommended Components of Follow-Up Visits • Signs and symptoms evaluated during initial visit • Functional capacity and activity level • Changes in body weight • Patient understanding of and compliance with dietary sodium restriction and medical regimen • History of arrhythmia, syncope, pre-syncope, palpitation, or ICD discharge • Adherence and response to therapeutic interventions • Exacerbating factors for HF, including worsening ischemic heart disease, hypertension, and new or worsening valvular disease Strength of Evidence = B

45. HFSA 2010 Practice Guideline (7.1, 7.7)Pharmacologic Therapy: ACE Inhibitors ACE inhibitors are recommended for symptomatic and asymptomatic patients with an LVEF ≤ 40%. Strength of Evidence = A ACE inhibitors should be titrated to doses used in clinical trials (as tolerated during uptitration of other medications, such as beta blockers). Strength of Evidence = C ACE inhibitors are recommended as routine therapy for asymptomatic patients with an LVEF ≤ 40%. • Post MIStrength of Evidence = B • Non Post-MIStrength of Evidence = C Adapted from:

46. ACE Inhibitors Used in Clinical Trials *No mortality difference between high and low dose groups, but 12% lower risk of death or hospitalization in high dose group vs. low dose group.

47. HFSA 2010 Practice Guideline (7.2)Pharmacologic Therapy:Substitutes for ACEI It is recommended that other therapy be substituted for ACE inhibitors in the following circumstances: • In patients who cannot tolerate ACE inhibitors due to cough, ARBs are recommended.Strength of Evidence= A • The combination of hydralazine and an oral nitrate may be considered in such patients not tolerating ARBs.Strength of Evidence = C • Patients intolerant to ACE inhibitors from hyperkalemia or renal insufficiency are likely to experience the same side effects with ARBs. In these cases, the combination of hydralazine and an oral nitrate should be considered.Strength of Evidence = C

48. HFSA 2010 Practice Guideline (7.6, 7.7)Pharmacologic Therapy: Beta Blockers Beta blockers shown to be effective in clinical trials are recommended for symptomatic and asymptomatic patients with an LVEF ≤ 40%. Strength of Evidence = A Beta blockers are recommended as routine therapy for asymptomatic patients with an LVEF ≤ 40%. • Post MIStrength of Evidence = B • Non Post-MIStrength of Evidence = C

49. Effect of Beta Blockade on Outcome in Patients With HF and Post-MI LVD 1Colucci WS et al. Circulation 1196;94:2800-6. 2CIBIS II Investigators. Lancet 1999;353:9-13. 3MERIT-HF Study Group. Lancet 1999;353:2001-7. 4Packer M et al. N Engl J Med 2001;344 1651-8. 5The CAPRICORN Investigators. Lancet 2001;357:1385-90.

50. HFSA 2010 Practice Guideline (7.9)Pharmacologic Therapy: Beta Blockers CONCOMITANT DISEASE Beta blocker therapy is recommended in the great majority of patients with HF and reduced LVEF—even if there is concomitant diabetes, chronic obstructive lung disease or peripheral vascular disease. • Usewith caution in patients with: • Diabetes with recurrent hypoglycemia • Asthma or resting limb ischemia. • Use with considerable caution in patients with marked bradycardia (<55 bpm) or marked hypotension (SBP < 80 mmHg). • Not recommended in patients with asthma with active bronchospasm. Strength of Evidence = C