Coronary heart disease

CORONARY HEART DISEASE

PRESENTERSMANJU BHUDIA

SEKATE RODNEY

TUTORDr. ZHANG

OUTLINE• definition

• anatomy

• epidemiology

• Scope of CHD and definitions

• Pathophysiology of CHD

• Diagnosis of CHD(stable, Acute coronary syndrome)

• Differential diagnoses of acute chest pain

• Complications of acute coronary syndrome

• Drugs for CHD(list and rationale)

• Immediate management of acute coronary syndrome

DEFINITION

• Is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium.

• Occurs when there is an imbalance between myocardial oxygen supply and demand

Anatomy of coronary arteriesThe right coronary artery

Right atrium

Right ventricle

Parts of the left atrium and left ventricle and the atrioventricular septum.

Left coronary artery divides into

1.An anterior interventricular branch ->> right and left ventricles and anterior part of the ventricular septum

2.A circumflex branch.

A. Left marginal artery is a large branch that supplies the left margin of the left ventricle down to the apex.

B. Anterior and posterior ventricular branches supply the left ventricle.

C. Atrial branches supply the left atrium.

EPIDEMIOLOGY World wide: 17million died of CVD particularly CAD/year.

Africa: 10%30%

2001; 8th cause of death in africa, how ever above 60’s is number 1 leading cause of death in men and number two in women after stroke.

2005; 361,000 death in africa

2030; 2X increase fold.

Uganda: Very low CAD prevalence rates were reported from Kenya and Uganda.

In Uganda, 449 out of the 15 176 admissions in a 1-year period had CVD and, of these, only three were considered to be CAD

in Kampala, electrocardiographic evidence of possible CAD was found in only one of 412 villagers over the age of 45 years.

However CAD is believed to be on rise due to lifestyle changes

Sex: mortality Male>female

RISK FACTORS

Non- modifiable• Age >50 yrs

• Sex male>female

• Family Hx( x2 in 1st degree relatives)

• Ethnic background south asians>caucasions>blacks

RISK FACTORS Cont…

Modifiable• Smoking• High amounts of LDLs and cholesterol and low HDL• Physical inactivity and obesity• diabetes• Air pollution( particulate matter)• High blood pressure• Alcohol intake• Hypertension• Metabolic syndrome• Atherogenic diet• Dyslipidemias

Emerging risk factors• homocystenemia,

• C-reactive protein,

• lipoprotein a,

• infection(?chlamydia pneumoniae)

• Fibrinogen

• Coronary artery calcification(CAC)

• small dense LDL

Scope of CHD Chronic coronary artery disease (CAD)

stable angina

Acute coronary syndromes (ACSs) acute myocardial infarction (MI) with ST-

segment elevation(STEMI) unstable angina (UA) non-ST-segment elevation MI(NSTEMI)

Pathophysiology

– Arteriosclerosis – natural changes in the intima, connective tissue, and diameter of artery

– Atherosclerosis – pathologic phenomenon occurring in the coronary, carotid, iliac, and femoral arteries as well as the aorta (coronary artery disease)

Coronary blood flow also can be limited by spasm, arterial thrombi, and, rarely, coronary emboli as well as by ostial narrowing due to aortitis

The atherosclerotic process Response to Injury hypothesis

- inflammatory response resulting in proliferation of tissue within the arterial wall which may result in obstruction of blood flow

Causes:

-elevated levels of cholesterol and triglyceride in the blood,

-high blood pressure – turbulent blood flow

-tobacco smoke

-glycosylated substances

Pathophysiology contd. Response to Injury Hypothesis 1. Injury to endothelium causing to platelets

adhere to endothelium then release of growth factors

2. Monocytes attach to endothelium and penetrate (also LDL receptor activation) – monocytes become macrophages and take up LDL and SMC’s

3. Smooth muscle cell proliferation and migrate from medial to intimal layer

4. Foam cells are formed - migration to the intima smooth muscles with lipids form fatty streaks

5. Fibromuscular plaque – fibromuscular layer with cholesterol core

ANGINA

Stable angina(Exertional); episodic clinical syndrome due to transient myocardia ischemia lasts 2-5min, aggravated by exertion or emotion and relieved by nitroglycerin or rest. substernal discomfort (Levine's sign).

Prinzmental angina; a form of angina pectoris xterised by pain not ppted by cardiac work, is longer in duration, more severe and has unusual ECG finding(ST-segment elevation) (transmural ischemia) and responds to nitroglycerin and calcium-channel blocker (vasodilator)

ANGINA contd.. Unstable angina; angina pectoris or equivalent

ischaemic discomfort with at rest/minimal exertion of >10minutes or severe and new onset or crescendo pattern

Decubitus angina is that occurring on lying down. It usually occurs in association with impaired LVF, as a result of severe coronary artery disease.

Nocturnal angina occurs at night and may wake the patient from sleep. It can be provoked by vivid dreams. occurs in patients with critical coronary artery disease and may be the result of vasospasm.

TREATMENT FOR ANGINA Nitrates

Glyceryl trinitrate( GTN) Isosorbide trinitrate May b used alone in stable angina

BBs Atenolol

CCBs Verapamil

Potassium channel activators Nicorandin Cause both arterial and venous dilation

RISK STRATIFICATION FOR DEVELOPING MI

High Risk Low Risk

Clinical Post infarct anginaRecurrent pain at restHeart failure

No history of MIRapid resolution of symptoms

ECG ArrhythmiaST depressionTransient ST elevationPersistent deep T-wave inversion

Minor or no ECG changes

Biochemistry Troponin T>0.1g/l

Troponin T<0.1g/l

MYOCARDIAL INFARCTION Due to formation of occlusive thrombus at the site of

rupture or erosion of an artheromatous plaque in a coronary artery.

The thrombus undergoes lysis over the course of the next few days, by this time irreversible damage has occurred.

Sudden death from VF or asystole may occur immediately and many deaths occur within the 1st hr , if the pt survives the most critical stage the liability to dangerous arrythmias remains but diminishes as each hr passes by. Those who survive may die of cardiac failure. The process of infarction takes around 8 hours and therefore most patient present when it is still possible to save myocardium.

MYOCARDIAL INFRACTION NSTEMI; angina pectoris or equivalent ischemic discomfort at

rest/ minimal exertion> 10minutes or severe and new onset or crescendo pattern + elevated cardiac biomarkers and ST segment depression/t wave inversion

STEMI; Sudden onset of severe retrosternal pain

Lasts more than 30 to 45 minutes

Not relieved by nitroglycerin

Radiates down the left arm into the shoulders or into the jaw or epigastrium

Associated with sweating (diaphoresis), anxiety, and hypotension

"Silent" acute MIs

May occur in the elderly and in individuals with diabetes mellitus

Due to high pain threshold or problems with nervous system

Clinical features of MI

Symptoms severe chest pain lasts longer than that due to

angina breathlessness, collapse or syncope, nausea and vomiting anxiety and fear of impending death.

CLINICAL FEATURES Cont…

Signs Signs of sympathetic activation; pallor sweating,

tachycardia Signs of vagal activation; vomiting, bradycardia Signs of impaired myocardial function;

hypotension, oliguria, narrow pulse pressure, raised JVP, 3rd heart sound, quiet 1st HS, diffuse apical impulse, lung crepitations

Signs of tissue damage; fever Signs of complications; MR, pericarditis

Diagnosis of CHD Stable angina history, physical examination(abdominal aortic aneurysm,

carotid arterial bruits, and diminished arterial pulses in the lower extremities, xanthelasmas and xanthomas, blood pressure, fundi exam, signs of anemia, thyroid disease, and nicotine stains on the fingertips from cigarette smoking, Palpation may reveal cardiac enlargement and abnormal contraction of the cardiac impulse, Auscultation can uncover arterial bruits, a third and/or fourth heart sound, or apical systolic murmur),

lab exam(urine, blood for lipid profile, glucose, creatinine, hematocrit or Hb, TFTs, CXR, CRP),

ECG,

Dx contd..

Unstable angina/NSTEMI; history, physical examination, ECG, cardiac biomarkers

Cardiac enzymesTroponin T & ICK-MBLDH

CXR stress testing, cardiac imaging, eg echo,coronary arteriography

ECG changes in MI Zone of Ischemia: T wave inversion Zone of Injury: ST elevation

Inferior wall MI: leads I, II, AVFAnterior wall MI; all chest leads

Zone of Necrosis: Abnormal Q wave Remember

STEMINSTEMI

Cardiac Enzymes levels

Myocardial Infarction WHO Diagnosis- Typical history - ECG finding - Raised biochemical markers ECG findings;

I. Hyper acute T waves- this is the earliest sign, changes are only present for 5-30 mins.

II. ST segment elevation follows- within the 1st few hrs of symptom onset.

III.Diminution of the R wave

IV.Pathological Q waves within 1-2hrs and these act as a permanent marker of myocardial necrosis

V. Resolution of changes; ST segment elevation diminishes over a period of weeks, T waves inversion may persists for many months

MI WHO Diagnosis Cont… Plasma biochemical markers

- Creatinine kinase (CK) or CK-MB that rises 4-6hrs then peaks at 12hrs and falls to normal after within 48-72 hrs.

- Cardiac troponins T and I released within 4-6 hrs and remain elevated for up to 2 weeks.

Leukocytosis Raised ESR Raised C reactive protein CXR; pulmonary edema with pre existing

myocardial damage. Echocardiography to assess left and right

ventricular function

Differential diagnoses of acute chest pain CHEST WALL PAIN

Musculoskeletal pain

Isolated musculoskeletal chest pain syndromes

Rheumatic diseases

Nonrheumatic systemic diseases

Skin and sensory nerves

CARDIAC CAUSES OF CHEST PAIN Coronary heart disease

Aortic dissection

Valvular heart disease

Pericarditis

Myocarditis

Stress-induced cardiomyopathy

Cardiac syndrome X

Pheochromocytoma

PSYCHOGENIC/PSYCHOSOMATIC CAUSES OF CHEST PAINPAIN REFERRED TO THE CHEST

GASTROINTESTINAL CAUSES OF CHEST PAIN

Gastroesophageal reflux disease

Esophageal hyperalgesia

Abnormal motility patterns and achalasia

Esophageal rupture, mediastinitis, and foreign bodies

Medication-induced esophagitis

Other gastrointestinal causes of chest pain

PULMONARY CAUSES OF CHEST PAIN

Pulmonary vasculature

Acute pulmonary thromboembolism

Pulmonary hypertension and cor pulmonale

Lung parenchyma-

Pneumonia

Cancer

Sarcoidosis

Pleura and pleural space

Pneumothorax

Pleuritis/serositis

Pleural effusion

Mediastinal disease

MANAGEMENT

The goals are to: Relieve symptoms Resolve risk factors in a bid to slow, stop, or

reverse plaque buildup Lower the risk of blood clot formation Widen or bypass clogged arteries Prevent complications of CHD Entails

Lifestyle changes Drugs Invasive treatment

MANAGEMENT Cont…Lifestyle Changes Diet aimed at controlling HTN & lowering

cholesterol low cholesterol & salt fiber, fruits and vegetables

Increase physical activity-@least 30mins daily Quit smoking Reduce alcohol intake to about 2-4 units daily Learn to cope with and reduce stress.

MANAGEMENT Cont…

DRUGS

Anti-platelets aspirin 75mg o.d, clopidogrel 75mg o.d (in pts with S/E to

ASA)

M.O.A- Inhibit platelet aggregation by selective blockade of platelet cyclooxygenase

S/E- bleeding

Anti- anginal drugs

1. Nitrates

- Sublingual glyceryl trinitrate 400-500µg, isosobide dinitrate10-20mg 8hrly

- MOA- act directly on vascular smooth muscle to produce venous and arteriolar dilatation

- S/E-severe headaches

TREATMENT Cont…

2. Beta blockers

- Atenolol 50-100mg od, metoprolol 50-200mg od, larsoprolol 5-10mg od

- MOA- lower myocardial O2 demand by reducing HR, BP and myocardial contractility

- S/E- bronchospasms.

3. Calcium antagonists Nifedipine 5-20mg 8hourly, Amlodipine 2.5-10mg

od, Verapamil 40-80mg 8hourly

- MOA- inhibit the slow inward entry of extracellular calcium through the cardiac cell membranes & lower myocardial contractility.

TREATMENT Cont…

4. K+ channel activators Niorandil 10-30mg bd

- MOA- arterial and venous dilating properties

TREATMENT Cont…

Early management of MI Admit the patient Defibrillation bed rest oral aspirin

high flow O2,

I.V analgesia with opiates I.V antiemetic Thrombolysis wth streptokinase monitor ECG Rx complications.

TREATMENT Cont…

Invasive treatment Percutaneous coronary intervention(PCI)

Performed by passing a fine guide wire a cross coronary stenosis under radiological guidance a balloon is inflated to dilate the stenosis. and CABG are used as treatments.

Coronary artery bypass graft (CABG)

Stenosed arteries are bypassed using sahenous vein grafts, or by utilizing internal mammary artery.

Moa of antithrombotic drugs

PREVENTIONRecognize the symptomsReduce your risk factors:Lose weightQuit SmokingKeep your cholesterol at a normal level. Keep your blood pressure under control. Use techniques to ease stress.Control blood sugar level.Eat RightREGULER EXERCISE

COMPLICATIONS

ARRHYTHMIAS IN AMI Ventricular fibrillation tachycardia Atrial fibrillation and tachycardia Heart block

ISCHAEMIA ACUTE CIRCULATORY FAILURE DRESSLER’S SYNDROME

Post MI syndrome characterized by pericarditis, pleurisy and persistent fever.

MECHANICAL COMPLICATIONS Pappilary muscle demage Rupture of IV septa Rupture of the ventrical

EMBOLISM VENTRICULA ANEURSYM

Ischemic ChangesT-waves, ST-segment, and Q-waves

1. T-waves Hyperacute (tall and peaked) Flattened Inverted (symmetrical)

2. ST-segments Elevated (Infarct) Depressed (Ischemia or Infarct)

3. Q-Waves Late change of Infarction

Ischemia – ST-Segment

ST-segment Elevation A change of Infarction (concave down) DDx: Prinzmetal angina, Aneurysm, LBBB,

Pericarditis, Hypothermia, Hyperkalemia, Benign early repolarization

Benign Early Repolarization(concave up)

Acute Infarction(concave down)

Ischemia – ST-Segment

ST-segment depression Ischemia or Infarction (horizontal or down-

slope) DDx: Reciprocal Infarct changes, Digoxin,

LVH, hypokalemia, LBBB/RBBB

Ischemia – Q-Waves

Q-waves Indicates infarction Occur several hours

to days after infarct Persist lifelong

Pathological Q Ensure there is no

R wave! Should be > 0.04 s

(1 small block) Should be > 25% of

the R wave amplitude

Q waves

NOT Q waves (they are S waves)

Ischemic Changes

Remember the anatomical correlations Especially important when diagnosing

ischemia or infarction

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Rhythm Strip (II)

Ischemia – Examples Acute Anterior ST-elevation MI

ST-segment elevationV1-V4

ReciprocalST-depressionII, III, aVF

Ischemia – Examples

ST-elevationII, III, aVF

Acute Inferior ST-elevation MI

Thank you