Chronic Coronary Syndrome: Kahtan Fadah, DO Cardiovascular Disease Fellow, PGY-4 Texas Tech University Health Sciences Center-El Paso
CASE A 60-year-old man with insulin-dependent type II diabetes mellitus, peripheral arterial disease, and active smoking, and CAD s/p bypass surgery (CABG) following a small myocardial infarction 10 years ago. He is complaining of chest pain due to activity that interfered with his quality of life. Metoprolol tartrate was increased from 50 mg to 75 mg twice a day at his last visit two months ago, and he was continued on isosorbide mononitrate 60 mg daily, ranolazine 500 mg twice a day, and amlodipine 5mg daily. Despite this regimen, he continues to report angina almost daily with physical activity of moderate intensity. He reports mild orthostatic lightheadedness.
Physical exam Vitals: HR: 78 bpm, RR: 14 ipm , BP: 100/70 mmHg, SpO2: 94% (RA) General: Not in acute distress Neuro: A&Ox3, ambulatory CV: Regular rate and rhythm, normal S1/S2, no murmurs or gallops Resp: Clear to ausculation . No use of accessory muscles. Abd: Soft, non tender Ext: No Edema , DP 1+ , otherwise 2+ throughout.
EKG Sinus rhythm at a rate of 72 bpm with non-specific diffuse ST changes, unchanged from prior tracings.
ECHO A dobutamine stress echocardiogram performed off metoprolol at his last visit showed normal resting systolic function with a small stress-induced anteroseptal wall motion abnormality at 100% of his maximum predicted heart rate.
What’s the best next step? Invasive coronary angiography CTA Increase dose of metoprolol Repeat stress testing with nuclear medicine
What’s Angina pectoris? Chest discomfort that occurs when myocardial oxygen demand exceeds oxygen supply. Stable angina refers to chest discomfort that occurs predictably and reproducibly at a certain level of exertion and is relieved with rest or nitroglycerin.
Epidemiology Incidence increased with age Male predominance Most common cause is Atherosclerosis and obstructive disease Coronary heart disease is the most common type killing 375,476 people in 2021. About 1 in 20 adults age 20 and older have CAD (about 5%). In 2021, about 2 in 10 deaths from CAD happen in adults less than 65 years old.
What to consider in CCD patients?
How to assess?
Assess for other causes as appropriate Non-invasive testing for diagnostic and/or prognostic purposes (tailored to patient characteristics, access and local expertise) Conservative diagnostic and treatment strategy Male < 40 yo Female < 60 yo No risk factors Male ≥ 40 yo Female ≥ 60 yo or single severe or multiple risk factors Significant non-CV co-morbidities and quality of life issues are present 1/3 Chest pain criteria 2 or 3/3 Chest pain criteria Cardiovascular history, physical, laboratory tests, 12 lead EKG Stable Chest Pain Syndrome (1 – 3/3 anginal symptoms)
Able to exercise adequately and no contraindications (see legend) ECG normal ECG abnormal ( eg. ST depression ≥ 1 mm, LVH, digoxin, ventricular pre-excitation No LBBB or ventricular paced rhythm LBBB or ventricular paced rhythm No LBBB or ventricular paced rhythm LBBB or ventricular paced rhythm Exercise stress test Exercise echocardiography Dobutamine or vasodilator echocardiography Exercise myocardial perfusion imaging Vasodilator myocardial perfusion imaging Vasodilator myocardial perfusion imaging Cardiac computed tomographic angiography ECG normal or abnormal YES NO
Exercise Treadmill ≥ 1mm of ST-segment depression at low (< 5 metabolic equivalents, METS) workload or persisting into recovery Exercise-induced ST-segment elevation Exercise-induced VT/VF Failure to increase systolic blood pressure to > 120 mm Myocardial Perfusion Imaging Severe resting LV dysfunction (LVEF < 35%) not readily explained by non-coronary causes Resting perfusion abnormalities ≥10% of the myocardium in patients without prior history or evidence of MI Severe stress-induced LV dysfunction (peak exercise LVEF <45% or drop in LVEF with stress ≥10%) Stress-induced perfusion abnormalities encumbering ≥10% myocardium or stress segmental scores indicating multiple vascular territories with abnormalities Stress-induced LV dilation Increased lung uptake Stress Echocardiography Inducible wall motion abnormality involving >2 segments or 2 coronary beds Wall motion abnormality developing at low dose of dobutamine ( < 10 micrograms/kg/min) or at a low heart rate (<120 beats/min) Coronary Computed Tomographic Angiography Multivessel obstructive CAD or left main stenosis on CCTA
What about CCD and previous revascularization? O ptimization of GDMT is recommended to reduce MACE Blood pressure control, diet, lifestyle, etc Associated newly reduced LV systolic function, clinical heart failure, or both, invasive coronary angiography (ICA) is recommended to assess coronary anatomy and guide potential revascularization. However, ICA not indicated if no newly LV systolic dysfunction, heart failure, stable chest pain refractory to GDMT.
Nonpharmacologic Intervention Dose Approximate Impact on SBP Hypertension Normotension Weight loss Weight/body fat Best goal is ideal body weight but aim for at least a 1-kg reduction in body weight for most adults who are overweight. Expect about 1 mm Hg for every 1-kg reduction in body weight. -5 mm Hg -2–3 mm Hg Healthy diet DASH dietary pattern Consume a diet rich in fruits, vegetables, whole grains, and low-fat dairy products, with reduced content of saturated and total fat. -11 mm Hg -3 mm Hg Reduced intake of dietary sodium Dietary sodium Optimal goal is <1,500 mg/d but aim for at least a 1,000-mg/d reduction in most adults. -5/6 mm Hg -2–3 mm Hg
Beta Blockers
BB per Guideline Should be initiated in patients with CCD and LVEF <50%, Class I A Should we continue BB on patients with CCD who were initiated on beta-blocker therapy for previous MI without a history of or current LVEF ≤50%, angina, arrhythmias, or uncontrolled hypertension???
Phase of Treatment Acute treatment Secondary prevention Overall Total # Patients 28,970 24,298 53,268 0.5 1.0 2.0 RR of death b -blocker better RR (95% CI) Placebo better 0.87 (0.77-0.98) 0.77 (0.70-0.84) 0.81 (0.75-0.87) b -blocker Evidence Antman E, Braunwald E. Acute Myocardial Infarction. In: Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A textbook of Cardiovascular Medicine, 6th ed., Philadelphia, PA: W.B. Sanders, 2001, 1168. Summary of Secondary Prevention Trials of b -blocker Therapy CI=Confidence interval, RR=Relative risk
6,644 patients with LVEF <0.40 after a MI with or without HF randomized to carvedilol or placebo for 24 months The CAPRICORN Investigators. Lancet . 2001;357:1385–1390. RR 0.77 P =.03 0.7 0.75 0.8 0.85 0.9 0.95 1 0.5 1 1.5 2 2.5 Carvedilol Placebo Years Proportion Event-free n=975 n=984 b -blocker Evidence: Post MI with Left Ventricular Dysfunction Carvedilol Post-Infarct Survival Control in LV Dysfunction (CAPRICORN) Evidence from this nationwide cohort study suggests that BB treatment beyond 1 year of MI for patients without heart failure or LVSD was not associated with improved cardiovascular outcomes.
Other medical therpaies ACE or ARBs in patients with CCD who has hypertension, diabetes, LVEF ≤40%, or CKD but those who lack these categories can still be considered. Adding colchicine for secondary prevention may be considered to reduce recurrent ASCVD events, Class 2B SGLT2 Inhibitors and GLP-1 Receptor ?
A ntianginal therapy 1 B-R In patients with CCD and angina, antianginal therapy with either a beta blocker, CCB, or long-acting nitrate is recommended for relief of angina or equivalent symptoms.* 1 B-R In patients with CCD and angina who remain symptomatic after initial treatment, addition of a second antianginal agent from a different therapeutic class (beta blockers, CCB, long-acting nitrates) is recommended for relief of angina or equivalent symptoms.*
1 B-R In patients with CCD, ranolazine is recommended in patients who remain symptomatic despite treatment with beta blockers, CCB, or long-acting nitrate therapies.* 1 B-NR In patients with CCD, sublingual nitroglycerin or nitroglycerin spray is recommended for immediate short-term relief of angina or equivalent symptoms.* 3: Harm B-R In patients with CCD and normal LV function, the addition of ivabradine to standard anti-anginal therapy is potentially harmful.*
Recommendation for Cardiac Rehabilitation COR LOE 1 A* All patients with CCD and appropriate indications*†‡ should be referred to a cardiac rehabilitation program to improve outcomes. B-R† C-LD‡ *After recent MI, PCI, or CABG. 1-5 †With stable angina 2,3,6,7 or after heart transplant. 8-13 ‡After recent spontaneous coronary artery dissection event. 14-17
Cause Presentation Management Kawasaki’s disease Late sequelae: coronary artery aneurysm, stenosis, thrombosis, or fistula Lifelong follow-up with quantitative assessment of luminal dimensions. Low-dose aspirin therapy for small- or medium-sized coronary artery aneurysms. Low-dose aspirin plus anticoagulant therapy for large coronary artery aneurysms. Coronary artery anomalies Anomalous left coronary artery from the pulmonary artery Anomalous origin of the coronary artery from the opposite sinus of Valsalva with an interarterial course Surgical repair – translocation of left coronary artery to aortic root for anomalous left coronary artery from the pulmonary artery. Surgical correction among young adults with interarterial course of coronary artery originating from opposite sinus of Valsalva and symptoms during exercise suggestive of myocardial ischemia. Myocardial bridging Exercise-induced ischemia Coronary artery vasospasm Sudden cardiac death Beta-adrenergic blocking agents in symptomatic patients. Restriction to low-intensity sports. Surgical correction if symptoms refractory to medical therapy. What else to consider?