Coronary Artery Disease & - PowerPoint Presentation

Coronary Artery Disease & Acute Coronary Syndrome Anthony J. Viera, MD, MPH, FAHA Professor and Chair

ObjectivesDescribe the appropriate work-up for chest pain based on clinical factors Know the first-line medications for CAD and recognize important side effects and contraindications Define acute coronary syndrome, explain diagnostic criteria Describe management of ACS Review of post-MI care

Scope of the problemCoronary artery disease leads to angina, mycocardial infarction, and cardiac death, which together comprise coronary heart disease (CHD) CHD is responsible for about 1/3 of deaths among people 35 years and older 17 million Americans have stable coronary artery disease Each year, 800,000 additional people have an initial CAD event

PresentationMost commonly, the diagnosis of CAD is suspected based on a history of chest pain When patient presents with chest pain, the first step is to consider serious causes, including acute coronary syndrome, which we will discuss in the second half For patients not considered to have ACS, the next step is to consider the possibility of stable CAD

Diagnosing CADIt is extremely important to consider the patient’s pretest probability for having flow-limiting CAD Guides decision-making for next steps Low pre-test = no further testing, consider other causes High pre-test = consider consult for catheterization Intermediate = further risk-stratification/testing

History • A ge and sex • C haracteristics of the pain: location , radiation, severity, duration and frequency , factors that provoke & relieve • A ssociated symptoms such as shortness of breath or radiation • History of angina, myocardial infarction, coronary revascularisation or other CVD • Cardiovascular risk factors

Physical examS igns of other cardiovascular disease Non-coronary causes of angina such as severe aortic stenosis or cardiomyopathy E xclude other causes of chest pain

Marburg Heart Score High negative predictive value so helpful at ruling out CAD 1 point for each Woman >64 or man > 54 years Known CAD, cerebrovascular dz , or peripheral vasc dz Pain worse with exercise Pain not reproducible with palpation Pt assumes pain is cardiac 98% of patients with score 2 or less will not have CAD A score >2 is not particularly helpful because only 23% of such patients will have CAD

Can get a more refined estimate of pre-test probability Based on three things: Kind of chest pain Sex of the patient Age of the patient Kind of chest pain Typical angina = substernal , onset with exertion or stress, relief by rest Atypical = two of those three Non- anginal = 1 or none of those three

Consult a chartDiamond and Forrester Available online at many sites including www.fpnotebook.com Realize that men 40 years and older and women 60 years and older with typical angina have a high pretest probability Pretest probability is very low in both sexes if none of the criteria are present

Next stepObtain an EKG Presence of Q waves Bundle branch blocks ST or T wave changes that may make interpretation of a stress EKG difficult

Testing zone Low risk patient: avoid stress testing (higher risk of false positives) High risk patient: Consider referral for coronary angiogram

Intermediate probability from around 10% to 90% Can patient exercise? Stress test is a first-line option for most men and women Stress imaging test if baseline EKG, prior revascularization, and if diabetes mellitus Pharmacologic stress test if unable to exercise For patients with an intermediate or high pretest probability of, stress testing with imaging has a higher sensitivity and specificity for the diagnosis of obstructive CAD

Stress test is negativeReassuring – not a guarantee Stress test has limited sensitivity and specificity Manage risk factors Re-evaluate as indicated

Stress test is positiveMeans further testing usually warranted – not a guarantee Depending on post-test probability, consider imaging test if first test was not imaged or consider consult for coronary angiogram

Note that computed tomography…May play an increasing role CT is an accurate non-invasive alternative to diagnose CAD, and can reduce the need for coronary angiography Alternative first-line diagnostic test for patients with atypical or typical CP

Managing CADGoals are to prevent progression of disease and reduce likelihood of cardiovascular disease events, ultimately reducing mortality ABCs = a spirin or other antiplatelet, b lood pressure lowering medication, c holesterol (which should be a statin), and s moking cessation and s ymptom management

AntiplateletAim is to reduce platelet aggregation at plaque sites to reduce chances of thrombosis Aspirin is first-line with its benefit well-established; usual dose is 81-mg (baby ASA) 30 patients need to be treated for about 30 months to prevent 1 CVD event Over the same time period, 1 bleeding event occurs for every 111 patients treated

ClopidogrelFor patients allergic to aspirin or in whom aspirin is contraindicated, clopidogrel is an alternative Dose is 75-mg once daily Also indicated for patients following acute coronary syndrome or stent placement Otherwise it should not be added to aspirin in patients with stable CAD

Blood pressure medsBlood pressure lowering medications help reduce the myocardial oxygen demand and prevent left ventricular hypertrophy For patients who have CAD, especially post-myocardial infarction, beta-blockers should be prescribed, even if not hypertensive Reduce heart rate (goal 50-60), increase diastolic filling time, decrease contractility β -blockers also help reduce anginal symptoms

Benefits also well-established23% reduction in the odds of death in long term trials, with NNT of 42 for 2 years Most evidence is available for propranolol, timolol , and metoprolol Typically use metoprolol, but carvedilol and labetalol are other alternatives β -blockers with intrinsic sympathomimetic activity such as pindolol should be avoided in CAD patients

CCBsIf β -blockers are contraindicated or not tolerated, long-acting CCB is an alternative Amlodipine for example, shown to reduce CVD events Not as effective in reducing angina symptoms

ACE-inhibitorsHelp prevent ventricular remodeling that can occur after an MI Reduce CVD mortality with NNT of 17 over 3 years to prevent one death Thus, important adjunct to β -blocker therapy Diabetics and those with hypertension Angiotensin receptor blockers (ARBs) can be used if patient cannot tolerate ACE-inhibitor due to cough ACE and ARB should not be used together

Cholesterol Statins are the main-stay Multiple studies: reduce events and mortality All patients with CAD regardless of LDL level Aim for at least a moderate dose (40 mg of lovastatin, pravastatin, or simvastatin, 20 mg of atorvastatin, or 5 to 10 mg of rosuvastatin ) High dose in those at higher overall risk who can tolerate

Side effectsSevere side effects are rare Rhabdomyolysis occurs in less than 1 out of 1000 But myalgias are fairly common, 1-2 out of 100, and overall discontinuation occurs in about 6% Limit simvastatin to no more than 20mg if patient also on amlodipine due to cytochrome P450 metabolism which can lead to elevated levels of simvastatin  increase risk of myopathy

Other considerationsStatins are first-line Drugs such as fibrates and niacin can be added if further triglyceride lowering (e.g., if TGs remain >200 mg/dl) or HDL increase is a goal, but evidence on patient-oriented outcomes is weak

Smoking cessationFor any patients who are smokers, a #1 priority should be getting them to quit Evidence based guidelines recommend assessing and documenting smoking status at each visit and offering smoking cessation therapies for those interested in quitting

Last “S” – symptom control Already talked about the anti- anginal benefits of B-blockers and CCBs Nitrates Sublingual on hand for acute symptoms Add long-acting nitrate (either oral or transdermal) when patient continues to experience angina Improve exercise tolerance, reduce episodes Patients can develop “nitrate tolerance” – a nitrate free interval may help mitigate this Isosorbide dinitrate can be dosed at 8am and 4pm, for example, starting at 10mg and titrating

Persistent symptomsIf angina despite β -blocker, CCB, and long-acting nitrate, a next step is to consult with cardiology for consideration of revascularization if warranted, or use of newer agents such as ranolazine , which is a sodium channel blocker

Acute Coronary Syndrome Generally, signifies unstable plaque in the coronary artery that either has ruptured or is in the process of rupturing Refers to two clinical presentations: either ST elevation MI or non-ST elevation ACS. Note that the terms NSTEMI (non-ST elevation myocardial infaction ) and unstable angina are now lumped into this NSTE-ACS category The reason is that u nless patient has ST elevations, ACS presentations are indistinguishable

Myocardial infarctionThrombosis leads to necrosis of myocardium Release of myocardial biomarkers Within three hours after presentation, 80% of patients with AMI will have troponin elevations Troponin elevations persist for up to 2 weeks Prompt recognition of possible ACS is key If patient with chest pain is suspected of having ACS, he/she should be evaluated in the emergency department (if presenting to clinic)

Making the diagnosisHistory Electrocardiogram Serum biomarkers

Making the diagnosisHistory New onset angina – usually a pressure Increasing in frequency or duration or with less exertion Rest angina (usually more than 20 minutes) No ECG changes indicative of ischemia (i.e., no ST depression or transient ST elevation or new TWI) and no biomarker elevation = non-ST elevation ACS

Suggestive symptomsInclude radiation of pain to one or especially both arms Pain associated with nausea, vomiting or diaphoresis Pain described as similar to previous MI

Initial management of ACS The traditional ABCs and ACLS Airway, breathing, circulation O2, IV, monitor “MONA” greets at the door Morphine 2-4 mg IV push Oxygen Nitroglycerin – remember to ask men about recent use of a PDE5 inhibitor like sildenafil b/c can drop BP Aspirin (162-325 mg chewed and swallowed) unless severe allergy or sensitivity If no signs heart failure and not bradycardic , b eta-blocker, such as metoprolol 5mg IV q5 mins X3 doses as tolerated Start or change to 80mg atorvastatin qd Correct electrolyte abnormalities, esp hypokalemia and hypomagnesemia

STEMI Patients with ST segment elevation MI (this includes new LBBB) should have a prompt evaluation by cardiology for reperfusion by percutaneous coronary intervention (PCI) If PCI unavailable, fibrinolytics should be administered within 90-120 minutes, assuming no contraindications Most will also get unfractionated heparin Additional antiplatelet therapy (in addition to aspirin) either clopidogrel or ticagrelor or prasugrel

NSTE-ACSChoosing between either an ischemia-guided strategy or an early invasive strategy

NSTE-ACS management Remember that thrombolytics are NOT indicated because of increased risk of reinfarction and other complications Decide on early invasive or not If hemodynamically unstable or severe LV dysfunction, persistent rest angina, worsening mitral regurg , or sustained ventricular arrhythmia = early invasive For others, TIMI risk score

TIMI risk score 0 or 1 for each: Age 65 or older At least three CHD risk factors (HTN, DM, HLP, smoking, positive early family history) Prior coronary stenosis 50% or more ST segment deviation on admission Two or more anginal episodes in last 24 hrs Elevated troponin Aspirin in past 7 days

TIMICalculators in smartphone apps and on-line Low risk if score 0 to 2 AND no ST depression and troponin not elevated High risk of 5 or higher (score 5 =>26% risk of serious CVD event at 14 days; score 6-7 = 41%) Intermediate or high risk should be considered for early invasive strategy

Based on strategy, but all get dual antiplatelet therapy and anticoagulant therapy Early invasive - going to receive ASA + another antiplatelet agent like clopidogrel or ticagrelor (cardiologist preference; may also receive glycoprotein2b/3a inhibitor) Anticoagulation Unfractionated heparin or bivalirudin Conservative ASA + clopidogrem or ticagrelor Anticoagulation Unfractionated heparin or enoxaparin

“Possible” ACS Probably the majority of patients we admit for chest pain to rule out MI fit into the category of “possible” ACS Nondiagnostic ECG and initially normal (i.e., nonelevated troponin level) Observe for 12 hours or more from symptom onset, following symptoms and measuring troponin and obtaining ECG serially, e.g., every 6 hours No further concern for ACS = stress test ACS confirmed – manage as we discussed

Post-MI careIn the absence of an absolute contraindication, aspirin indefinitely In general, patients who had a STEMI or a stent placed will be on dual antiplatelet therapy (e.g., aspirin plus clopidogrel ) for one year Beta-blocker ACE-inhibitor, esp if diabetes, heart failure, ejection fraction <40% or hypertension

Post-MI care (cont) Smoking cessation / maintenance = so important Statin BP control If diabetic, glycemic control, striving for A1C <7% C ardiac rehabilitation – refer if center available Major depression develops in almost 20% of patients after MI, and over 33% have significant symptoms Places patients at increased risk of adverse outcomes Attention to symptoms of depression and treat if indicated

Thank you!anthony.viera@duke.edu