Coronary Artery Disease PDF

CORONARY ARTERY DISEASE  CORONARY ARTERY DISEASE O Atherosclerotic heart disease (aka coronary artery disease) is an ischemic heart disease caused by building up of atherosclerotic plaque in coronary arteries. O There is imbalance between myocardial oxygen supply and oxygen d...

CORONARY ARTERY DISEASE  CORONARY ARTERY DISEASE O Atherosclerotic heart disease (aka coronary artery disease) is an ischemic heart disease caused by building up of atherosclerotic plaque in coronary arteries. O There is imbalance between myocardial oxygen supply and oxygen demand.  RISK FACTORS FOR CORONARY ARTERY DISEASE (CAD) MAJOR RISK FACTORS MINOR RISK FACTORS Hypertension Obesity Diabetes Sedentary life-style Dyslipidemia Stress or type A personality Cigarette smoking or tobacco use Excessive alcoholism Family history of premature CAD Passive tobacco smoking Age (>45 years in males or >55 years in females) Previous history of CAD Chronic renal insufficiency Connective tissue diseases e.g. rheumatoid arthritis  PRESENTATIONS OF CORONARY ARTERY DISEASE O Stable angina O Unstable angina O Prinzmetal’s angina O Non-ST elevation myocardial infarction O ST elevation myocardial infarction O Cardiac syndrome X (microvascular angina) O Sudden cardiac death O Others: heart failure, arrhythmias  ACUTE CORONARY SYNDROME O Acute coronary syndromes (ACSs) are life-threatening conditions that can punctuate the course of patients with coronary artery disease at any time. These syndromes form a continuum that ranges from an unstable pattern of angina pectoris to the development of a large acute myocardial infarction (MI), a condition of irreversible necrosis of heart muscle  ANGINA O Angina is most often described as a “pressure,” “discomfort,” “tightness,” “burning,” or “heaviness” in the chest. It is rare that the sensation is actually described as a “pain,” O Angina pectoris is the most frequent symptom of intermittent myocardial ischemia.  Canadian Cardiovascular Association Classification of Angina  Stable angina O Stable atherosclerotic plaque in coronary arteries. Decrease in exertion- related increase in flow or cardiac reserve. O Presentation: O Exertional angina after a particular level of exertion: chest heaviness may radiate to left arm, shoulder, neck, jaw O Relieves by rest and worsens with exertion O Sweating O Symptoms usually static for more than one month.  Investigations: O Resting ECG and resting echo: usually normal O Stress tests: shows findings: O Symptoms/ signs/ ECG findings on exercise tolerance tests/ pharmacological stress tests O Regional wall motion abnormalities/ hypokinetic segments upon dobutamine stress echo O Zones of reversible ischemia upon perfusion scans/ nuclear scans O Coronary angiography – coronary artery stenotic lesions (causing >70% obstruction or reducing blood flow)  STABLE ANGINA O General management: O Quit smoking O Weight loss O Exercise O Control hypertension,, diabetes, dyslipidemia O Dietary precautions  Specific management: O Anti-platelets: O COX inhibitors: aspirin O P2Y12 inhibitors: clopidogrel, prasugrel, ticagrelor O Anti-anginals: O Nitrates: dilate coronary arteries. Can be taken as needed e.g. sublingual glyceryl trinitrate (GTN) or oral longer-acting nitrates e.g. isosorbide mononitrate O Beta-blockers: slow heart rate and thus decrease oxygen demand e.g. carvedilol, metoprolol, bisoprolol O Non-dihydropyridine calcium channel blockers: slow heart rate and dilate coronary arteries e.g. verapamil, diltiazem Specific management: O Anti-anginals: O Nitrates: dilate coronary arteries. Can be taken as needed e.g. sublingual glyceryl trinitrate (GTN) or oral longer-acting nitrates e.g. isosorbide mononitrate O Beta-blockers: slow heart rate and thus decrease oxygen demand e.g. carvedilol, metoprolol, bisoprolol O Non-dihydropyridine calcium channel blockers: slow heart rate and dilate coronary arteries e.g. verapamil, diltiazem O Novel anti-anginals: e.g. ivabradine, ranolazine, trimetazidine, nicorandil O Percutaneous coronary intervention/ angioplasty: in patients with medically refractory disease  UNSTABLE ANGINA O It is an acutely worsening angina due to plaque thrombosis, hemorrhagic or rupture. O It includes: O New onset angina O Newly worsening stable angina O Angina at rest O Angina occurring up to one month after myocardial infarction O There is risk of progression to myocardial infarction. O Part of acute coronary syndromes (ACS) along with ST elevation myocardial infarction (STEMI), non ST elevation myocardial infarction (NSTEMI) and Prinzmetal’s angina.  Investigation O Resting ECG: may show ST depressions or T wave inversions O Cardiac markers e.g. troponins, CK-MB, myoglobin: not raised O Stress tests: usually not done in acute phase of disease. These may show similar findings: O Symptoms/ signs/ ECG findings on exercise tolerance tests/ pharmacological stress tests O Regional wall motion abnormalities/ hypokinetic segments upon dobutamine stress echo O Zones of reversible ischemia upon perfusion scans/ nuclear scans O Coronary angiography – coronary artery stenotic lesions (causing >70% obstruction or reducing blood flow)  UNSTABLE ANGINA O Treated as ACS: O Bed rest. Oxygen only if needed. O Sublingual/ buccal puff/ intravenous nitrate O Loading dose of chewable aspirin 300 mg O Loading dose of clopidogrel 300 mg or ticagrelor 180 mg O Glycoprotein Iib/IIIa inhibitors e.g. tirofiban O Anticoagulants: heparin or enoxaparin O Analgesics e.g. morphine O Percutaneous coronary intervention in high risk patients PRINZMETAL’S ANGINA O Also called vasospastic angina or variant angina O It is due to vasospasm of coronary artery limiting blood flow to the muscle in an area of fixed atherosclerosis. O It presents with chest pain and transient ST elevations (sometimes ST depressions) but there is usually no infarction. Cardiac markers are not raised. O Diagnosed by coronary angiography and intra-coronary injection of ergonovine. O Treatment: calcium channel blockers, nitrates MYOCARDIAL INFARCTION O It is death and necrosis of myocardial tissue due to sudden occlusion of blood supply. O Third universal definition of MI: O Type 1: it is due to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus. O Type 2: it is due to ischemic imbalance e.g. vasospasm, endothelial dysfunction. O Type 3: it includes sudden cardiac deaths accompanied by new ECG changes or new LBBB but without cardiac markers. O Type 4: infarction in the setting of PCI O Type 5: infarction in the setting of CABG  ACUTE MYOCARDIAL INFARCTION O It is death and necrosis of myocardial tissue due to sudden occlusion of blood supply. MYOCARDIAL INFARCTION O ST elevation myocardial infarction: it is due to full thickness or transmural infarction (Q wave appear) O Non ST elevation myocardial infarction: it is due to sub-endocardial infarction MYOCARDIAL INFARCTION O It presents as sudden intense sub-sternal chest pain described as heaviness or crushing in nature. It may radiate to jaw, neck, left shoulder, arms or sometimes to back or right arm. O It is not relieved with nitrates. O It usually does not have: short duration, chest tenderness, aggravation with cough or deep breath, pin-point location. O Patients also have profuse sweating, nausea, vomiting, weakness, feeling of impending doom. O Pain may be absent (silent MI) in those who have long- standing diabetes, chronic steroid use, neuropathies or in elderly population. In these cases there is usually severe dyspnea with sweating, nausea, palpitations and vomiting.  SIGN AND SYMPTOMS Characteristic pain Severe, persistent, typically substernal 2. Sympathetic efect Diaphoresis Cool and clammy skin 3. Parasympathetic (vagal effect) Nausea, vomiting Weakness 4. Inflammatory response Mild fever 5. Cardiac findings S4 (and S3 if systolic dysfunction present) gallop Dyskinetic bulge (in anterior wall MI) Systolic murmur (if mitral regurgitation or VSD) 6. Other Pulmonary rales (if heart failure present) Jugular venous distention (if heart failure or right ventricular MI)  Causes of Myocardial Infarction O Atherosclerotic plaque rupture with superimposed thrombus O Vasculitic syndromes O Coronary embolism (e.g., from endocarditis, artificial heart valves) O Congenital anomalies of the coronary arteries O Coronary trauma or aneurysm O Spontaneous coronary artery dissection O Severe coronary artery spasm (primary or cocaine- induced) O Increased blood viscosity (e.g., polycythemia O Markedly increased myocardial oxygen demand (e.g., severe aortic stenosis  Investigations: O Resting ECG: may show ST depressions, ST elevations or T wave inversions O Cardiac markers e.g. troponins(Troponin is a regulatory protein in muscle cells that controls interactions between myosin and actin), CK-MB, myoglobin: are raised O Stress tests: not done O Coronary angiography – should be done emergently in those with ST elevations and urgently/ soon in those without ST elevations but with high risk features  TROPONINS T/I O Troponin T vs I – O both equivalent in diagnostic and prognostic abilities ( except in renal failure – Trop T less sensitive) O Elevation ~ 2hrs to 12hrs O ~30 – 40% of ACS patients without ST elevation – had normal CKMB but elevated troponins on presentation  MYOGLOBIN O Rapid release within 2 hours O Not cardiac specific O Rule out for NSTEMI rather than rule in. CKMB O Used in conjunction with troponins O Useful in diagnosing re-infarction  COMPLICATIONS OF MYOCARDIAL INFARCTION O Arrhythmias O Post-infarct angina, extension of myocardial infarct, re- infarct O Mechanical complications: O Heart failure O Free wall rupture O Rupture of inter-ventricular septum O Papillary muscle rupture O Ventricular pseudo-aneurysm O Ventricular aneurysm O Embolic complications e.g. cerebral infarcts, digital gangrene O Acute pericarditis O Dressler’s syndrome  Diagnosis O The diagnosis of and distinctions among, the ACSs is made on the basis of the patient’s presenting symptoms, O acute ECG abnormalities, O detection of specific serum markers of myocardial necrosis Specifically, UA is a clinical diagnosis supported by the patient’s symptoms, transient ST abnormalities on the ECG (usually STdepression and/ or T- wave inversion), and the absence of serum biomarkers of myocardial necrosis. NON –ST/ST ELEVATION MI O Non–ST-segment elevation MI is distinguished from Unstable Angina by the detection of serum markers of necrosis and often more persistent ST or T-wave abnormalities. The hallmark of ST-elevation MI is an appropriate clinical history coupled with ST elevations on the ECG plus detection of serum markers of myocardial necrosis.  ST ELEVATION MI O In the case of MI, cardiac troponin serum levels begin to rise 3 to 4 hours after the onset Of chest discomfort, achieve a peak level between 18 and 36 hours, and then decline slowly, allowing or detection or 10 days or more after a large MI. Thus, their measurement may be help full for detection of MI or nearly 2 weeks after the event occurs. Given their high sensitivity and specificity, cardiac troponins are the preferred serum biomarkers to detect myocardial necrosis. O Name 3 situations in which you cannot diagnose STEMI Left Ventricular Hypertrophy Chronic or Rate Dependent LBBB Paced Rhythm O Name 3 situations that demand emergent cardiac catheterization. STEMI or new LBBB ACS with hemodynamic or electrical instability despite optimal medical management Uncontrolled CP despite optimal medical management  TREATMENT O Early coronary angiography, with subsequent coronary revascularization, is beneficial For Unstable Angina or NSTEMI patients with high-risk features. O Acute treatment of STEMI includes rapid coronary reperfusion, ideally with percutaneous catheter-based intervention if available or else fibrinolytic therapy. Common ACS management O Morphine (5-10mg slow IV injection) O Oxygen (titrate sats to need) O Nitrates - GTN spray (400mcg = 1 spray) or tablet (1mg) O Aspirin (300mg chewed) O Plus an antiemetic i.e. Metoclopramide 10mg IV