Coronary Artery Disease
Definition
Also known as Ischemic Heart Disease
A group of diseases which includes stable angina, unstable angina, myocardial infarction and sudden cardiac death
Pathophysiology
Coronary atherosclerosis occurs at points of turbulence (eg, vessel bifurcations).
The atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia - angina pectoris.
Activation of platelets - coagulation cascade, resulting in an acute thrombus - interrupts coronary blood flow
→ myocardial ischemia. → acute coronary syndromes : - unstable angina - transmural infarction - sudden death.
Coronary artery spasm - reduces blood flow - symptomatic ischemia ( variant angina) may result. narrowing can trigger thrombus formation, causing infarction or life-threatening arrhythmia. Spasm can occur in arteries with or without atheroma.
" In arteries without atheroma, basal coronary artery tone is probably increased, and response to vasoconstricting stimuli is probably exaggerated.
" In arteries with atheroma, the atheroma causes endothelial dysfunction, resulting in local hypercontractility.
Use of vasoconstricting drugs (eg, cocaine, nicotine) and emotional stress also can trigger coronary spasm.
Risk Factors
High BP
Smoking
Diabetes Mellitus
Lack of exercise
Obesity
High blood cholesterol
Excessive alcohol
Depression
Atherosclerosis
Clinical Features
Chest pain which may radiate into the shoulder, arm, back, neck or jaw
Heart burn
Pain precipitate by exercise or emotional stress getting better with rest
Dyspnoea on exertion
Occasionally first sign itself is myocardial infarction
Investigations
ECG
Cardiac Stress tests
Coronary CT angiogram
Coronary angiogram
Prevention
Healthy die
Regular exercise
Body wt control
Stop smoking
Control diabetes
Control BP
Treatment
Antiplatelet drugs - low dose aspitin, clopidogrel
Beta-blockers
Nitroglycerin
Percutaneous coronary intervention - coronary angioplasty, stent
Coronary bypass surgery (CABG)
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Normal ECG
A normal ECG is illustrated above. Note that the heart is beating in a regular sinus rhythm between 60 - 100 beats per minute (specifically 82 bpm). All the important intervals on this recording are within normal ranges.
1. P wave:
upright in leads I, aVF and V3 - V6
normal duration of less than or equal to 0.11 seconds
polarity is positive in leads I, II, aVF and V4 - V6; diphasic in leads V1 and V3; negative in aVR
shape is generally smooth, not notched or peaked
2. PR interval:
Normally between 0.12 and 0.20 seconds.
3. QRS complex:
Duration less than or equal to 0.12 seconds, amplitude greater than 0.5 mV in at least one standard lead, and greater than 1.0 mV in at least one precordial lead. Upper limit of normal amplitude is 2.5 - 3.0 mV.
small septal Q waves in I, aVL, V5 and V6 (duration less than or equal to 0.04 seconds; amplitude less than 1/3 of the amplitude of the R wave in the same lead).
represented by a positive deflection with a large, upright R in leads I, II, V4 - V6 and a negative deflection with a large, deep S in aVR, V1 and V2
in general, proceeding from V1 to V6, the R waves get taller while the S waves get smaller. At V3 or V4, these waves are usually equal. This is called the transitional zone.
4. ST segment:
isoelectric, slanting upwards to the T wave in the normal ECG
can be slightly elevated (up to 2.0 mm in some precordial leads)
never normally depressed greater than 0.5 mm in any lead
5. T wave:
T wave deflection should be in the same direction as the QRS complex in at least 5 of the 6 limb leads
normally rounded and asymmetrical, with a more gradual ascent than descent
should be upright in leads V2 - V6, inverted in aVR
amplitude of at least 0.2 mV in leads V3 and V4 and at least 0.1 mV in leads V5 and V6
isolated T wave inversion in an asymptomatic adult is generally a normal variant
6. QT interval:
Durations normally less than or equal to 0.40 seconds for males and 0.44 seconds for females.
Acute anterolateral myocardial infarction
Acute anterolateral MI is recongnized by ST segment elevation in leads I, aVL and the precordial leads overlying the anterior and lateral surfaces of the heart (V3 - V6). Generally speaking, the more significant the ST elevation , the more severe the infarction. There is also a loss of general R wave progression across the precordial leads and there may be symmetric T wave inversion as well. Anterolateral myocardial infarctions frequently are caused by occlusion of the proximal left anterior descending coronary artery, or combined occlusions of the LAD together with the right coronary artery or left circumflex artery. Arrythmias which commonly preclude the diagnosis of anterolateral MI on ECG and therefore possibly identify high risk patients include right and left bundle branch blocks, hemiblocks and type II second degree atrioventricular conduction blocks.
Acute inferior MI
Leads II, III and aVF reflect electrocardiogram changes associated with acute infarction of the inferior aspect of the heart. ST elevation, developing Q waves and T wave inversion may all be present depending on the timing of the ECG relative to the onset of myocardial infarction. Most frequently, inferior MI results from occlusion of the right coronary artery. Conduction abnormalities which may alert the physician to patients at risk include second degree AV block and complete heart block together with junctional escape beats. Note that the patient below is also suffering from a concurrent posterior wall infarction as eveidenced by ST depression in leads V1 and V2.
Acute posterior MI
When examining the ECG from a patient with a suspected posterior MI, it is important to remember that because the endocardial surface of the posterior wall faces the precordial leads, changes resulting from the infarction will be reversed on the ECG. Therefore, ST segments in leads overlying the posterior region of the heart (V1 and V2) are initially horizontally depressed. As the infarction evolves, lead V1 demonstrates an R wave (which in fact represents a Q wave in reverse). Note that the patient below is also suffering from an inferior wall myocardial infarction as evidenced by ST elevation in leads II, III and aVF.
Acute right ventricular MI
In patients presenting with acute right ventricular MI, abnormalities in the standard 12 lead ECG are restricted to ST elevation greater than or equal to 1 mm in lead aVR. Although isolated right ventricular MI is usually seen in patients suffering from chronic lung disease together with right ventricular hypertrophy, it can occur in patients suffering a transmural infarction of the inferior-posterior wall which extends to involve the right ventricular wall as well. Right ventricular MI is most commonly caused by obstruction of the proximal right coronary artery and is frequently associated with right bundle branch block. Furthermore, only 5% - 10% of patients suffer from hemodynamic symptoms.
Acute septal MI
Acute septal MI is associated with ST elevation, Q wave formation and T wave inversion in the leads overlying the septal region of the heart (V2 and V3).
Atrial fibrillation
Atrial fibrillation represents disorganized atrial activity without contraction or ejection. The electrocardiogram demonstrates an irregular baseline where the normal P waves are replaced with rapidly quivering small deflection of variable amplitude (f waves - outlined below). An irregularly irregular ventricular rate demonstrating narrow QRS complexes is established between 100 - 160 bpm. Atrial fibrillation is common in patients with rheumatic heart disease, pulmonary emboli, cardiomyopathy, pericarditis, ischemic heart disease and thyrotoxicosis. It causes minimal hemodynamic compromise and often the patient presents complaining of palpitations as the only symptom. Although hemodynamic compromise is minimal, atrial fibrillation is an important risk factor for the development of thromboembolic complications, such as strokes and transient ischemic attacks.
Atrial flutter
The electrocardiogram in atrial flutter is typically characterized by its "sawtooth" flutter waves (F waves - arrows below) best demonstrated in the inferior leads (II, III, aVF and V1). A rapid regular atrial rhythm is generally demonstrated between 250 and 350 bpm, and the qRS rate is determined by the ratio of atrioventricular conduction. Although the usual ratio of AV conduction is 2:1 (as illustrated below), 1:1, 3:1, 4:1, 6:1 and other variable ratios are also demonstrated, albeit less frequently. Typically, this results in a ventricular heart rate between 150 and 170 bpm. Atrial flutter is relatively uncommon and is most often seen in patients presenting with acute ischemic heart disease or pulmonary embolism. Nevertheless, it can present as a chronic condition in patients who suffer from organic heart disease.
Complete heart block
Complete heart block refers to a form of atrioventricular dissociation where no P wave produces a QRS complex. A sinus or ectopic atrial rhythm develops that fires independently of the ventricles. This rhythm may be junctional (as illustrated below) or ventricular in origin. The rhythm is usually regular, but may present irregularly as a result of intermittent premature ventricular beats. Patients presenting with complete heart block complain of symptoms resembling profound bradycardia (loss of atrial kick) and reduced cardiac output (syncope, angina, presyncope).
Digitalis effect
These glycosides can cause ST sagging and shortening, best seen in leads V4, V5 and V6 (see below).
Hyperkalemia
Potassium overdose is frequently seen in patients with renal failure or those on K sparing diuretics. In mild hyperkalemia (serum levels less than 6.5 mEq/l), leads II, V2 and V4 demonstrate tall, tented, symmetrical T waves with a narrow base. The P wave remains normal, as does the QRS complex. With moderate K overdose (6.5 mEq/l - 8.0 mEq/l) the QRS complex broadens and the S wave is widened in leads V3 - V6. This S wave become continuous with the tented T waves and eventually the ST segment disappears. Furthermore the duration of the P wave is increased, while the amplitude is decreased. At K levels greater than 8.0 mEq/l (see below), the P wave duration and PR interval duration both increase, until the P wave eventually disappears entirely. The QRS complex is diffusely broadened and continuous with the tall, tented T wave in all leads.
Hypokalemia
Hypokalemia is associated with progressive ST depression, progressive flattening or inversion of the T waves, the development of U waves, increased amplitude and duration of the P waves and QRS complexes as well as a slight increase in the duration of the PR interval. Furthermore, hypokalemia affects automaticity of the pacemaker cells and leads to multiple arrhythmias such as sinus bradycardia, atrioventricular block, atrial flutter and Torsades de Pointes. Most commonly, hypokalemia results from thiazide diuretic misuse, diarrhea, renal or adrenal disease. Other causes include infusion of large amounts of glucose or alkali substances, liver cirrhosis and diabetic coma.
Left atrial enlargement
Left atrial enlargement is typically characterized by an increase in the terminal portion of the P wave. Best seen in lead II, this terminal deflection is often demonstrated as a distinct second peak within the P wave (arrow below). In some leads, this second peak gives the P wave an "m-like" shape. This deflection does not usually affect the amplitude of the P wave, but may increase its duration to greater than 0.12 seconds. In addition to this increased P wave deflection in lead II, LAE results in a terminal negative deflection within the P wave best seen in lead V1 (see below). With extreme LAE, the amplitude of the P wave may be increased, and terminal negativity may be demonstrated in leads II, III and aVF (see below). Left atrial enlargement may result from left atrial dilatation, pressure overload (ie. from mitral valve disease) or abnormal intra-atrial conduction. Other terms frequently used to describe LAE include left atrial hypertrophy, left atrial overload and left atrial abnormality.
Left ventricular hypertrophy
Electrocardiograms from patients presenting with LVH demonstrate variably increased R wave voltage and duration in leads over the right ventricle (V5 and V6 - circled below). In 35% - 90% of the cases, there is a delay between the onset of the QRS complex and the R wave. This intrinsicoid deflection may extend to greater than 0.05 seconds. Furthermore, delayed repolarization as a result of ventricular hypertrophy generally produces ST depression and T wave inversion in the same leads. Enlargement of the left ventricle is commonly associated with left atrial enlargement as well as incomplete LBBB. Leads V2 and V3 commonly demonstrate increased S wave amplitude (arrow below), while leads V5 and V6 show increased R wave amplitude. Left ventricular hypertrophy may be associated with conditions giving rise to pressure or volume overload of the left ventricle such as aortic stenosis or systemic hypertension. Furthermore, LVH increases patient risk of other cardiovascular diseases including myocardial infarction, congestive heart failure, stroke, arrhythmia and sudden death.
Left bundle branch block
In left bundle branch block, activation of the intraventricular septum is reversed and electrical impulses to the left ventricle are delayed. These altered electrical forces produce a wide QRS complex (greater than 0.12 seconds in duration) with an abnormal morphology. In leads I and V6, abnormal initial forces fail to produce any Q wave or S wave, and the resultant R wave is steep and often notched (circled below). Furthermore, a deep rapid S wave is generated in lead V1 (arrow below). The ST segment is slightly elevated in multiple leads and the T wave polarity is diffusely opposite to the ventricular complex.
Premature ventricular complex
Premature ventricular complexes (circled below) may arise in normal individuals as well as patients suffering from nearly every form of structural heart disease. Premature ventricular complexes are recognized as single or paired unifocal beats, with no preceding P wave, a wide QRS complex of increased amplitude characteristically lasting greater than 0.14 seconds, and a T wave demonstrating polarity opposite to that of the PVC. They arise early in the cardiac cycle and are more likely to occur during periods of bradyarrhythmia. Although no P waves precede the wide QRS complex, retrograde activation of the atria may produce P waves which occur after the PVC or are buried in their T waves. Premature ventricular beats may arise from excessive catecholamines, myocardial ischemia or injury, electrolyte imbalances, certain medications including digitalis and class IA and IC antiarrhythmic agents.
Right bundle branch block
As illustrated in the electrocardiogram below, right bundle branch block presents with delayed activation of the right ventricle, leading to a wide QRS complex lasting greater than 0.12 seconds. Altered terminal QRS forces produce a terminal R wave in lead aVR and terminal S waves in leads I, aVL, V5 and V6. Triphasic complexes are identified as the late intrinsicoid "m-shaped" RSR' complex in lead V1, and the early intrinsicoid qRS complex in lead V6.
Supraventricular tachycardia - AV reentry
Supraventricular tachycardia commonly presents in two forms - AV reentry and AV nodal reentry. In AV reentry (below), the SVT presents as a regular tachycardia originating outside the ventricular myocardium. In this type of SVT, the AV node is used for impulse conduction to the ventricles, while an accessory pathway is used to return electrical conduction back to the atria. The heart rate is usually regular, at a rate of 170 to 250 bpm (below = 188 bpm). In this type of SVT, P waves are always present outside of the QRS complex, while their polarity depends on the atrial insertion of the accessory pathway. The QRS complex is narrow with a duration less that 0.2 seconds and an atrioventricular conduction ratio of 1:1. In 25% - 30% of patients demonstrating AV reentry, QRS alternans is present (varying amplitudes of the QRS complex in all leads except V4). AV reentry is not usually associated with structural heart disease and commonly presents as a variety of symptoms including palpitations, nervousness, anxiety, syncope or heart failure.
Ventricular tachycardia
Ventricular tachycardia is defined as three or more ventricular complexes in succession at a rate greater than 100 bpm. Patients presenting with ventricular tachycardia often present with a regular heart rate between 100 and 250 bpm (HR below = 146 bpm), in which the QRS morphology is constant and abnormally wide (greater than 0.12 seconds). Frequently, these ECG's demonstrate AV dissociation in which the ventricular rate is greater than the atrial rate. P waves are frequently hidden within the broad ventricular complexes, although they can sometimes be identified as bumps or notches in the ventricular cycles. Although patients without heart disease may develop paroxysmal non-sustained ventricular tachycardia, chronic sustained VT is most commonly associated with coronary artery disease, dilated cardiomyopathy and prior myocardial infarction or severe heart disease.
courtesy by https://meds.queensu.ca/central/assets/modules/ECG/left_atrial_enlargement.html
Go to the above site to see further (Queen's University at Kingston, CA
