USMLE STEP 2 CK REVIEW ~ CARDIOVASCULAR ISCHEMIC HEART DISEASE . Coronary Artery Disease (CAD) o Accumulation of atheromatous plaques within walls of coronary arteries that supply O2 to myocardium . Blood flow causes ischemia of myocardial cells due to lack of oxygen Effects of ischemia reversible if blood flow to heart improved . Complete occlusion of artery causes irreversible cell death called myocardial infarction o Risk Factors: . DM, HTN, tobacco, age >45, hyperlipidemia, LDL, HDL, homocysteine . FHx of premature CAD or MI in 1st-degree relative – men <45yrs & women <55yrs o Clinical Presentation Asymptomatic, stable angina, unstable angina, MI, sudden cardiac death o Canadian Cardiovascular Society (CCS) Angina Classification: . Class I Angina w/strenuous or rapid activity – no angina from ordinary physical activity . Class II Slight limitation of ordinary activity – angina after >2 blocks or >1 flight of stairs . Class III Marked limitation of ordinary activity – angina after <2 blocks or <1 flight of stairs . Class IV Any physical activity causes discomfort – angina may be present at rest o Diagnosis: . Resting ECG: Prior MI Q waves UA ST segment or T-wave abnormalities seen during episode of chest pain . Stress ECG: Recording ECG before, during & after exercise on treadmill 75% sensitive only if able to exercise sufficiently to reach 85% of predicted maximum HR o Predicted maximum HR = 220 − Patient’s age Should undergo cardiac catheterization if results from stress test Positive findings for CAD: o ST elevation Transmural infarct o ST depression Subendocardial ischemia o Failure to exercise >2mins due to symptoms o Hypotension o Ventricular arrhythmia . Stress Echocardiography: Performed before & immediately after exercise – preferred over stress ECG More sensitive in detecting ischemia, can assess LV size, EF & diagnose valvular disease Ischemia evidenced by wall motion abnormalities not seen at rest – akinesis or dyskinesis Should undergo cardiac catheterization if test results . Myocardial Perfusion Imaging (MPI): Stress test preformed after injection w/radioisotope – Thallium-201 or Technetium-99 Nuclear imaging obtained immediately after exercise & again after 4hrs Viable cells extract radioisotope from blood – no uptake means no perfusion to area MPI can assess myocardial viability by detecting perfusion, ventricular volume & EF o Reversible ischemia Impaired perfusion only during stress o Infarction Impaired perfusion at rest & during stress MPI has best sensitivity & specificity of exercise stress tests – but more expensive . Pharmacologic Stress: If unable to exercise – administer IV agents to stimulate myocardial function Dobutamine Myocardial O2 demand by HR, BP & contractility Adenosine & Dipyramidole Vasodilation actually causes flow to coronary arteries . Holter Monitoring Ambulatory ECG useful in detecting silent ischemia . Cardiac Catheterization & Coronary Angiography: Most accurate way of identifying severity of vessel involvement – indicated in following: o After positive results from any stress test o If revascularization or other surgical intervention being considered o Angina – difficulty diagnosing, refractory to medical therapy, occurring after MI o Severely symptomatic requiring urgent diagnosis & management o Evaluation of valvular disease to determine need for surgical intervention 1 o Treatment: . Risk Factor Modification: Smoking cessation – 50% reduction in CAD risk 1yr after quitting HTN control – esp. diabetics Hyperlipidemia – low-fat diet & HMG-CoA reductase inhibitors DM – strict glycemic control to reduced vascular disease risk Exercise & Weight loss – also modifies other risk factors like DM, HTN, hyperlipidemia Diet – intake of saturated fat (<7% total calories) & cholesterol (<200 mg/day) . Pharmacologic Management: Aspirin Morbidity & risk of MI – indicated in all pts. w/CAD o Clopidogrel If ASA contraindicated or in combination w/ASA β-blockers O2 demand via HR, contractility, BP o Mortality risk – shown to reduce frequency of coronary events o Cardioselective agents preferred – Metoprolol, Atenolol, Carvedilol . Avoids inhibition of peripheral vasodilation & bronchodilation via 2 Nitrates O2 demand via vasodilation – preload, afterload, coronary perfusion o Symptomatic control of angina only – no impact on survival o Tachyphylaxis – prevent tolerance by maintaining daily nitrate-free intervals CCBs O2 demand via coronary vasodilation – afterload, coronary perfusion o 2nd line when β-blockers or Nitrates not fully effective o Caution: Verapamil/Diltiazem + -blockers may cause bradycardia or AV block ACEIs Not used to treat symptomatic CAD – indicated in CHF, HTN, DM, LV dysfunction . Revascularization: Percutaneous Coronary Intervention (PCI): o PTCA indicated in moderate one- or two-vessel disease w/normal EF: . Medically refractory angina . NSTEMI/UA w/TIMI risk score ≥3 . Primary PCI for STEMI o Restenosis rates up to 40% within first 6 months – stents significantly rates Coronary Artery Bypass Grafting (CABG): o Indicated in severe multi-vessel disease w/ EF or comorbid DM: . Left main artery disease . Triple-vessel disease w/ LV function . Two-vessel disease w/proximal LAD stenosis . Failed or contraindicated PTCA Thrombolysis t-PA, Streptokinase, Urokinase, Anistreplase, Alteplase, Reteplase o Indications STEMI <12hrs after symptom onset or when PCI not viable option . Administer as soon as possible – preferably 3hrs after onset . Not indicated for NSTEMI or UA as artery not occluded o Absolute contraindications: . Active bleeding - Malignant IC neoplasm . Prior intracranial hemorrhage - Prior stroke (≤3 months) . Recent head trauma (≤3 months) - Suspected aortic dissection o Relative contraindications: . HTN – sBP >180 or dBP >110 - Current anticoagulation use . Recent major surgery (≤3wks) - Active peptic ulcer . Chronic Stable Angina o Symptom complex resulting from imbalance between oxygen supply & demand in myocardium o Often due to fixed stenosis caused by atheroma – O2 demand exceeds available blood supply . Goal of treatment to myocardial O2 demand & O2 supply o Pathophysiology: . Factors influencing supply Luminal diameter (most important), duration of diastole, Hb, SaO2 Myocardial O2 supply – atherosclerosis, vasospasm, hypoxemia, tachycardia, anemia . Factors influencing demand HR, contractility, wall stress Myocardial O2 demand – tachycardia, AS, myocardial hypertrophy, hyperthyroidism o Clinical Presentation: . Chest pain Retrosternal tightness radiating to left ( right) shoulder, arm, neck or jaw 2 Precipitated by the “3 E’s” – 1) Exertion, 2) Emotion, 3) Eating Brief duration – pain lasts <15mins w/relief after rest or nitrates . Anginal equivalents Dyspnea, diaphoresis, acute LVF, flash pulmonary edema . Levine’s sign Clutching fist over sternum when describing chest pain o Diagnosis Resting ECG – Normal o Treatment See Pharmacologic Management of CAD . Unstable Angina (UA) o Acute plaque rupture & thrombosis w/incomplete or transient vessel occlusion O . Oxygen demand unchanged – but O2 supply 2 to reduced resting coronary flow o UA defined by any of the following: . Angina at rest . New-onset angina . Accelerating pain pattern – frequency, duration, pain intensity o Diagnosis & Treatment See NSTEMI section below . Prinzmetal’s (Variant) Angina o Transient coronary vasospasm – 75% ass. w/fixed atherosclerotic lesion o Clinical Presentation Intermittent angina at rest – pain not provoked by exertion o Diagnosis: . ECG Hallmark is transient ST elevation during chest pain – represents transmural ischemia . Coronary Angiography Definitive test – shows coronary vasospasm after IV Ergonovine o Treatment Vasodilation via Nitrates & CCBs . Myocardial Infarction (MI) o Due to coronary atherosclerosis w/superimposed thrombus on ruptured plaque o Classification: . 1) Non-ST Elevation Myocardial Infarction (NSTEMI): Acute plaque rupture & thrombosis w/incomplete or transient vessel occlusion O Oxygen demand unchanged – but O2 supply 2 to reduced resting coronary flow Defined by presence of 2/3 criteria: o Symptoms of angina or ischemia o Rise & fall of serum MI markers – absent enzyme markers in UA o Ischemic ECG changes – without ST elevation or new LBBB NSTEMI & UA categorized together due to similar etiology & presentation . 2) ST Elevation Myocardial Infarction (STEMI): Acute plaque rupture & thrombosis w/total vessel occlusion causing myocardial necrosis Defined by new ischemic ECG changes + 1 or both of ischemic Sx. & cardiac enzymes o ECG ST elevation in 2 contiguous leads or new BBB – either LBBB or RBBB o Clinical Presentation: . Chest pain, dyspnea, diaphoresis, weakness, fatigue, N/V Pain similar to angina but more intense & longer duration Up to 1/3 asymptomatic – painless infarcts o Diagnosis: . ECG Markers for ischemia/infarction include: Peaked T-waves – occur very early & may be missed ST elevation – transmural injury of entire wall thickness (can be Dx. of acute infarct) ST depression – subendocardial injury involving inner half of wall Q-waves – seen later as specific evidence of necrosis (not seen w/NSTEMI) T-wave inversion – sensitive but not specific . Cardiac Enzymes Diagnostic gold standard for myocardial injury Creatine Kinase-MB (CK-MB): o CK-MB within 4-8hrs w/peak at 24hrs – returns to normal after 48-72hrs o Sensitivity & specificity >95% if measured within 24-36hrs of onset of chest pain o CK & CK-MB