Atherosclerosis

Dr. Gerrard Uy

Definition

• Also known as arteriosclerotic vascular disease

• condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol

Pathogenesis

• Remians the major cause of death an premature disability in developed societies

• Predisposed areas for atherosclerosis:– Proximal left anterior descending artery– Proximal portion of the renal artery– Carotid bifurcation

Initiation of Atherosclerosis

• Initial lesion is the fatty streak

Initiation of Actherosclerosis

• Accumulation of leukocytes characterizes the formation of early atherosclerotic lesion

• Once resident within the initma, the macrophages become lipid laden foam cells

• Not all fatty streaks progress to form complex atheromata– Depends on the activity of the macrophage– The amount of lipid entering the artery– Reverse cholesterol transport

Initiation of Actherosclerosis

• As atherosclerotic lesions advance, abundant microvessels develop within the artery

Major Risk Factors that Modify LDL Goals

• Cigarette smoking• Hypertension (BP>140/90 mmhg)• Low HDL (<40 mg/dl)• Diabetes mellitus• Family hx of premature coronary heart disease• Age (men>45, women>55 yrs)• Life style risk factors– Obesity (>30kg/m2)– Physical inactivity– Atherogenic diet

Ischemic Heart Disease

Dr. Gerrard Uy

Definition

• 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

Epidemiology

• Most common, serious, chronic, life threatening illness in the United States

• High fat and energy rich diet, smoking and sedentary lifestyle are associated with the emergence of IHD

• Obesity, insulin resistance, and diabetes are powerful risk factors for IHD

Pathophysiology

• Major determinants of myocardial oxygen demand:– Heart rate– Myocardial contractility– Myocardial wall tension

• Adequate supply of oxygen requires a satisfactory level of oxygen carrying capacity of the blood and adequate level of coronary blood flow

Coronary Atherosclerosis• Epicardial coronary arteries are the major site of

atherosclerotic disease• Predilection for atherosclerotic plaques to

develop at sites of increased turbulence in coronary flow

• Location of the obstruction influences the quantity of the myocardium rendered ischemic

• The severity and duration determine if the damage is reversible (< 20 mins for total occlusion in the absence of collaterals) or permanent (> 20 mins)

Angina Pectoris

Stable Angina Pectoris• Due to transient myocardial ischemia• Males constitute ~70% of all patients with angina

pectoris• Characteristics:– Chest pain (squeezing, heaviness, smothering, etc)– Poorly localized chest pain (Levine’s sign)– Crescendo – decrescendo pattern– Lasts 2 – 5 mins– Can radiate to either shoulder and to both arms, back root

of the neck, jaw, teeth, and epigastrium– Typically caused by exertion and relieved by rest or

sublingual nitroglycerin

Stable Angina Pectoris

• Anginal equivalents:– Dyspnea– Nausea– Fatigue– faintness

• The history of typical angina pectoris establishes the diagnosis of IHD until proven otherwise

Stable Angina Pectoris• Physical Examination:

– Often normal in patients with stable angina pectoris when they are asymptomatic

• Laboratory examination:– CBC– Urinalysis– Lipid Profile– FBS– Creatinine– CXR– 12 L ECG– Stress testing– Cardiac imaging

Stable Angina Pectoris

• Management plan:– Explanation and reassurance– Identification and treatment of aggravating factors– Adaptation of activity– Treatment of risk factors– Drug therapy

• Nitrates• B blockers• Ca channel blockers• Anti platelets

Unstable Angina and Non ST Elevation Myocardial Infarction

Dr. Gerrard Uy

Unstable Angina

• Diagnosis of of UA is based largely on the clinical presentation

• Characteristics:– Chest discomfort with at least one of three

features• Occurs at rest (or with minimal exertion)• Lasts > 10 mins• Severe and of new onset (within the prior 4-6 weeks)• Crescendo pattern

Pathophysiology

1. Plaque rupture or erosion with superimposed non occlusive thrombus – most common cause

2. Dynamic obstruction (coronary spasm)3. Progressive mechanical obstruction4. Secondary unstable angina

Clinical Presentation

• Clinical hallmark of NSTEMI is chest pain located in the substernal region

• ECG shows ST segment depression, T wave inversion

• Cardiac biomarkers are elevated

Management

• Medical treatment (complete bedrest with continuous ECG monitoring)

• Anti-ischemic treatment– Nitrates– B blockers

• Anti-thrombotic– Aspirin– clopidogrel

ST Segment Elevation Myocardial Infarction

Dr. Gerrard Uy

• one of the most common diagnoses in hospitalized patients

• mortality rate from AMI is ~30%• more than half of these deaths occurring

before the stricken individual reaches the hospital

• Mortality is approx 4 fold higher in elderly patients compared with younger patients

Acute STEMI

• usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis

• occurs when a coronary artery thrombus develops rapidly at a site of vascular injury

• Injury facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation

Pathogenesis

• Atherosclerotic plaque disruption• Thrombogenesis• Platelet activation• Platelet aggregation, cross-linking• Coagulation cascade activated

The amount of myocardial damage depends on:

• the territory supplied by the affected vessel• whether or not the vessel becomes totally occluded• the duration of coronary occlusion• the quantity of blood supplied by collateral vessels to

the affected tissue• the demand for oxygen of the myocardium whose

blood supply has been suddenly limited• native factors that can produce early spontaneous lysis

of the occlusive thrombus• the adequacy of myocardial perfusion in the infarct

zone when flow is restored in the occluded epicardial coronary artery.

Risk factors

• Persons with multiple coronary risk factors• Persons with unstable angina • Hypercoagulability• collagen vascular disease• cocaine abuse• intracardiac thrombi or masses that can

produce coronary emboli

Clinical presentation• In up to ½ of cases, a precipitating factors

appears to be present• Usually soon after awakening• PAIN – most common presenting complaint

• Deep, visceral• Heavy, squeezing, crushing, stabbing, burning• Similar to angina pectoris but occurs at rest• No relief from rest• More severe, lasts longer• Central portion of chest/ epigastrium/ radiates to arm• weakness, sweating, nausea, vomiting, anxiety, and a sense

of impending doom

PE Findings

• anxious and restless• Pallor, perspiration• Combination of substernal chest pain

persisting >30 mins and diaphoresis strongly suggest STEMI

• physical signs of ventricular dysfunction – fourth and third heart sounds, decreased intensity

of the first heart sound, and paradoxical splitting of the second heart sound

Lab Findings

• Electrocardiogram (ECG)– ST-segment elevation

• Serum Cardiac Biomarkers– Proteins released from necrotic heart muscle – Troponin I– CKMB

• Cardiac imaging

Management

• Prehospital care• Recognition of symptoms• Rapid deployment of medical team• Expeditious transportation• Implementation of reperfusion therapy

• ER management• Control of discomfort• Limitation of infarct size

• O2

Intervention

• Primary percutaneous coronary intervention– Angioplasty– Applicable to patients who have contraindications to

fibrinolysis

• Fibrinolysis– Within 30 mins of presentation– tPA– Streptokinase– rPA (reteplase)

Hospital care

• Should be admitted in the CCU or ICU• Bed rest for first 12 hours• Resume upright position with dangling feet

within 24 hours• NPO in first 4-12 hours• 50-55% CHO, <30% fats, cholesterol < 300 mg/dl• Bedside commode, laxative• Sedation (diazepam)