Sie sind auf Seite 1von 8

ISCHEMIC HEART DISEASE (IHD)

Medicine 2 Dr. Sofia Black September 13, 2014

CLINICAL SCENARIO

A 55 y/o female consulted OPD because of effort-related chest pain. She is a known hypertensive, diabetic, previous smoker and non-compliant to medications. Physical exam showed BP= 140/100, CR= 60 bpm, RR 18/min, BMI of 30.

ISCHEMIC HEART DISEASE

Inadequate oxygen supply

Increase oxygen demand

Imbalance: supply < demand

Myocardial ischemia

o

Where the imbalance happen

o

Obstructive atherosclerotic disease of epicardial vessel

Most common cause

o

Inadequate perfusion of coronaries

Previously known as Coronary artery disease

o

Term used in Europe

o

In PHIC they accept ischemic heart disease but not CAD

EPIDEMIOLOGY

Most common, serious, chronic life threatening disease

PATHOLOGY

Coronary arteries

PATHOPHYSIOLOGY

MYOCARDIAL OXYGEN DEMAND

Heart rate

o increase HR → increase oxygen demand on a background of inadequate supply

Myocardial contractility

o More contraction → increase oxygen demand

Myocardial wall stress/ tension

o Frank Starling law

Increase LV end diastolic volume in Left ventricular pressure increased forceful contractility up to a limit

Overstretching → increase wall tension → increase contractility → increase oxygen demand → failure → will not be elastic breakage

MYOCARDIAL OXYGEN SUPPLY

Oxygen carrying capacity of blood (by hemoglobin)

o

Level of inspired oxygen

High altitude → higher elevation → low oxygen

o

Pulmonary function

Dysfunctional pulmonary system (ex. COPD and bronchial asthma has decrease oxygenation) → secondary Myocardial ischemia

o

Hemoglobin concentration

Low hemoglobin concentration (ex. anemia) → normal blood flow but oxygen content is low

Blood flow: occurs during Diastole

o

Relaxation

Impairment of relaxation → impairment in the flow and supply

o

Blood flow goes to coronaries when the heart relaxes

o

Abnormal Diastolic dysfunction is the EARLIEST SIGN of Ischemia

ECG and contractility may be normal but diastolic function is abnormal → IHD

CORONARY ARTERIES

3 Large epicardial arteries

o

Left coronary artery (from the aorta)

Divides into two: (1) Left anterior descending artery and (2) Left circumflex artery

o

(3) Right coronary artery (from the aorta)

Large epicardial vessels → Obtuse marginal 1 and 2 vessels Pre-arteriolar arteries → myocardium → Arteriolar and intramyocardial capillary vessels

Orifices that originate from the aorta behind aortic valve

o Aortic valve has 3 cusps:

Right coronary cusp

Where the right coronary artery came from to the right coronary sinus

Left coronary cusp

Where the Left coronary artery/left main coronary artery came from

Non-coronary cusp

 

CONDUCTANCE VESSEL

Large epicardial coronary arteries

Constriction and relaxation

Abnormal constriction:

o

Prinzmetal angina (unknown etiology): Epicardial coronary arteries are abnormally vasospastic without atherosclerosis

o

No relaxation, remain vasoconstricted (but there’s still a chance to dilate)

RESISTANCE VESSELS

Major determinants of coronary resistance → coronary flow

1
1

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

Smaller vessels from epicardial vessels:

Emerging risk factors

o

Pre-arteriolar vessels

 

o

Lipoproteins: Apo B

From obtuse marginal vessels

o

Homocysteine

o

Arteriolar vessels

 

o

Pro-thrombotic

o

Intramyocardial capillary vessels

By Oral contraceptive pills

Intramyocardial arteriole

o

Pro-inflammatory

Abnormal constriction

Patients with IHD and STD: (+) for Chlamydia on autopsy

 

Seen in Diabetic patients

(plaque contains chlamydia)

 

Failure of dilatation, remain vasoconstricted (NO chance to

o

Impaired fasting glucose

dilate again)

Microvascular ischemiapathophysiology in diabetic patients

Capable of auto-regulation

Side Notes:

*coronary angiogram (gold standard for IHD in the past) can show normal results for IHD *microvascular circulation are not seen in coronary angiogram only the large epicardial vessels

CORONARY ATHEROSCLEROSIS

MAJOR RISK FACTORS (3 FACTORS QUALIFY A PERSON TO BE AT RISK)

MODIFIABLE

Cigarette smoking

o

Nicotine accelerates the position of cholesterol

o

Acts as a catalyst: deposit the cholesterol

Hypertension

o Sheer stress to capillary wall → endothelial dysfunction

Diabetes mellitus

o High sugar → inflammation and endothelial dysfunction

Low HDL

High LDL

NON-MODIFIABLE

Family history of premature CHD

 

o

Male <55 y/o

o

Female < 65 y/o

Age

 

o

Male 45 y/o

o

Female 55 y/o

o

*No longer true due to food chain (unhealthy food)

Male gender

Lifestyle risk factors

o

Obesity (BMI >30 kg/m2)

o

Physical inactivity

Endothelial dysfunction

o

Atherogenic diet

Slight innervation of fasting blood glucose

Not diabetic yet, waiting to be diabetics, diabetics in the process → increase glucose in the vascular system → intra- endothelial dysfunction

INITIATION OF ATHEROSCLEROSIS (IN ORDER)

Initial stage: fatty streak formation

o

As early as 10 years old and above

o

Fatty stage formation in utero

Maternal blame cholesterol of the mother goes to the child

Lipoprotein oxidation → tunica intima

Non enzymatic glycation

Leukocyte recruitment

Foam cell formation

o Leukocytes transforming to macrophages and phagocytize oxidized LDL

Atheroma evolution (it takes time)

o

Involvement of arterial smooth muscle

o

Blood coagulation thrombosis

o

Micro vessel formation

o

Plaque evolution

ATHEROSCLEROSIS A PROGRESSIVE DISEASE

o Plaque evolution ATHEROSCLEROSIS A PROGRESSIVE DISEASE 2 #KAFC #LML #DA B #LGTM #DACM “MEDICINE BATCH
2
2

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

(Refer to the picture) Atherosclerosis

Progressive disease

Atheros: porridge (cholesterol)

“Scleros: hardening

A lot of oxidized LDL will become a soft porridge → rupture → attract platelet → thrombus formation

CORONARY ARTERY

METABOLIC REGULATION

Regulates oxygen supply

AUTO REGULATION

Regulates coronary blood flow

Vasodilation and vasoconstriction

o As long as there are no blockages

*Coronary arteries extract the most oxygen in the blood for consumption

CAUSES OF ISCHEMIA

Reduction in the lumen of the coronary artery

o

Atherosclerosis

 

Arteries distal to plaque are vasospastic

Decrease lumen decrease perfusion to myocardium

o

Coronary artery spasm

Prinzmetal angina

o

Arterial thrombi

From a ruptured plaque proximally thrombus dislodge distally smaller vessels (Intramyocardial vessels)

o

Coronary emboli from infective endocarditis

Vegetation from right coronary valve → dislodge to right coronary artery

Left coronary valve → left coronary artery

Increase oxygen demand with limited blood flow (not totally obstructed)

o

LVH due to aortic stenosis

Arteries are patent but supply is not enough during systole and diastole due to fixed obstruction in aortic valve

o

Hypertension

 

There is Left Ventricular hypertrophy

 

Increase the demand when there are hypertrophied muscles because the supply is decreasing

o

Hyperthyroidism

Due to increased HR

o

Fever

Due to increased HR

Decrease in oxygen carrying capacity

o

Good supply but the oxygen is depleted

o

Severe anemia

No hemoglobin to carry oxygen

Free oxygen in the blood cannot be used because it is not bound to Hemoglobin

o

Carboxyhemoglobinemia

Carbon monoxide (CO) poisoning: competing with oxygen in hemoglobin

Ex. Sleeping inside the car with engine on

Painless death

CORONARY ATHEROSCLEROSIS

Epicardial coronary artery

o Major site of atherosclerotic disease

Main affectation: Tunica intima

Major risk factor: Endothelial dysfunction

o

Whole cascade of atherosclerosis proceeds

o

Bottom-line of all the risk factorS

o

Does not happen overnight

o

Vasoconstriction

o

Luminal clot formation

o

Monocytes and platelet interaction

o

Atherosclerotic plaque formation

When it ruptured → Acute coronary syndrome

Sub-intimal fat collection

Smooth muscle cell proliferation

Fibroblast and intercellular matrix

Major risk factorS

o

High LDL

o

Low HDL

o

Cigarette smoking

o

Hypertension

o

DM

*The good cholesterol (HDL), the bad cholesterol (LDL) and the ugly cholesterol (triglycerides)

ISCHEMIC HEART DISEASE (AGAIN)

Critical obstruction: 70%

o

Myocardial ischemia

o

Do intervention: angioplasty (single vessel) or bypass (multiple vessel disease)

o

*But MI can also occur in <70%

Due to rupture of the plaque → thrombus formation (give anti- platelets)

3
3

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

Asymptomatic Ischemic Heart Disease

o Coronary atherosclerosis: 20 year-old post mortem studies

EFFECTS OF ISCHEMIA

MECHANICAL

Abnormal muscular contraction and relaxation

o Contraction but no relaxation

Relaxation (coronary blood flow)

Patient complains of chest pain, fatigue, SOB

Aging heart will be fibrotic (stiff heart) → heart failure

LV failure

MANIFESTATION

Male >50; female >60

Chest discomfort (typical)

o Retrosternal pain

Levine sign

o Fist clenched on sternum

*Chest paint equivalent/atypical chest pain

ANGINA

Cardiac origin

o

Ejection fraction is low: <40%

o

Atypical chest pains in the elderly

o

Systolic HF: no contraction

Epigastric pain

o

Diastolic HF: no relaxation

Choking sensation

Mitral regurgitation

o Involvement of the papillary muscles ischemia incompetent mitral valve

BIOCHEMICAL EFFECTS

No oxygen → Glucose to lactate lactic acidosis

o When myocardium is in an acidic medium it will not contract systolic

dystaxia

Myocardial necrosis

o The heart can’t survive with a lactic environment

Angina pectoris

*32 ATPs in the Kreb’s cycle

ELECTRICAL EFFECTS

Repolarization abnormalities

o STTWC: ST wave depression and T wave inversion

Electrical instability

o

Arrhythmias

o

Most dreaded

o

Ventricular tachycardia

STABLE ANGINA PECTORIS

Episodic clinical syndrome

Transient myocardial ischemia

o When it becomes persistent it becomes ACS

70% males in before menopausal stage

Crescendo-decrescendo

o Crescendo going up; decrescendo going down

Duration

o 1-5 minutes, 10 minutes at the most

Radiation

o

Below mandible and above the umbilicus

o

Epigastric pain CAN BE an inferior myocardial infarction (diaphragm irritation)

Location

o Retrosternal is the MC description

PRECIPITATING FACTORS

Exertion

Emotion

Rest

o

Chest pains at rest: Severe IHD

o

Obstruction is severe

Arteries clogged >70%

GRADING OF SEVERITY OF ANGINA

CANADIAN CARDIAC SOCIETY CLASSIFICATION

For IHD chest pain

CLASS

ONSET OF CHEST PAIN

I

Chest pain with more than ordinary activity

II

Chest pain on ordinary activity

III

Chest pain on less than ordinary activity

IV

Chest pain at rest

*New York Heart Classification: Heart Failure and Chest Pain

4
4

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

RISK FACTORS

Modifiable and Non-modifiable

ASSOCIATED COMORBID CONDITIONS

CVD, TIA, PAD, CKD, stroke

Atherosclerosis is not only on the heart but also systemic

o Ex. kidneys = renal failure

PHYSCIAL EXAMINATION

Most are normal

Evidence of atherosclerosis

o

Abnormal aneurysm

o

Carotid bruit, PAD

o

Xanthomas (yellow deposition of the fat), xanthelasmas

Risk factors for atherosclerosis

Fundoscopy

o

Atherosclerotic retinopathy

Thick vessel wall

o

Hypertensive retinopathy

With papilledema

Plain hemorrhages

Copper wiring

Signs of anemia and pallor

Signs of aortic stenosis

 

o

Heart: left ventricular fibrillation and systolic ejection murmurs

o

Palpation of the radial pulse: Weak pulse

LABORATORY EXAMINATION

ECG

 

o

A normal ECG does not rule out disease

o

Accurate only in 30%

o

Arrhythmias

Chest X-ray

o Heart enlargement: sign of Congestion

Urinalysis

o To know Comorbid diagnostics or risk factors (ex. glycosuria=DM, glomerulonephritis=HTN)

Lipid profile

o HDL, LDL, TG

Blood glucose

o

FBS: ≥126 = Diabetes

o

RBS: ≥200 = Diabetes

o

Impaired blood sugar

Hemoglobin/Hematocrit

o Anemia

*even if there are normal test proceed to exercise stress testing

DIAGNOSTIC TEST OF IHD

EXERCISE STRESS TESTING

Most widely used

To prognosticate IHD and in patients for angiogram and bypass

Problem: Symptom limited

Sensitivity = only 70% are detected (30% are missed)

o 85% if with post MI

Heart rate limited

CONTRAINDICATON OF EXERCISE STRESS TEST

Angina at rest within 48 hours

Unstable rhythm

o Atrial fibrillation and fast ventricular response

Severe aortic stenosis = definite contraindication!!!

Acute myocarditis

o Prone to arrhythmias

Unstable heart failure

Active infective endocarditis

o Embolization of vegetation

*If exercise stress testing is normal but patient still has episodic chest pains proceed to cardiac imaging *Dobutamine Stress Test for patients who are unable to exercise

CARDIAC IMAGING

Myocardial perfusion scan

o

Let the patient exercise then inject a radioactive

There is perfusion defect

o

Physiologic

o

Once it is normal it means normal

o

If (-) cardiac scan but (+)myocardial perfusion scan = microvascular ischemia

Echocardiography

o

A normal result does not say you’re really a normal patient

o

EF: <40%: poor prognosis

CORONARY ANGIOGRAPHY

Done when ALL things failed like medical management and the patient still has chest pains

Gold standard before the discovery of intramyocardial ischemia

Invasive

5
5

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

INDICAITONS FOR CORONARY ANGIOGRAPHY

Chronic Stable Angina (CSA) severely symptomatic despite treatment

Diagnostic difficulty

o To know if CAD or malingerer

Cardiac arrest survivors

(+) non-invasive testing with LV dysfunction

o Treadmill stress test

High risk patients

o

Admitted for acute coronary syndrome (ACS)

o

Symptoms in careers involving safety of others (pilots, bus drivers)

o

Male >45, female >55 undergoing valve surgery

For patients with rheumatic heart disease

o

High risk on stress test

Mets (measure of oxygen consumption)

If result is <7 METS (Metabolic Equivalent of Tasks)

Normal person should reach 7 METS

Primary goal: Increase patient’s quality of life Secondary goal: Prolong life

CT ANGIOGRAPHY

Conductance vessels only

o Intramyocardial vessels not seen

Less invasive

IHD: PROGNOSTIC INDICATORS

Age

o The older the poorer the prognosis

Functional state of the LV

o Ejection fraction ≤40% (poor prognosis)

Location and severity of occlusion

o

Left main artery involvement

Patient is not sent home

Widow or orphan maker lesion

o

The more proximal the poorer the prognosis

lesion o The more proximal the poorer the prognosis *Nuclear scan: physiologic *Echocardiography, cardiac MR

*Nuclear scan: physiologic *Echocardiography, cardiac MR scan and cardiac PET scan: anatomic

6
6

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

TREATMENT OF IHD

 

Class IIb

 

MANAGEMENT PLAN

 

Evidence of therapy less established, No other options available, <50%, Good study

Explanation and reassurance

Class III

Dypirimole

 
 

o

Anxiolytics Diazepam

- Used before as anti-platelet

o

Explain that there is no time to be dependent on these drugs

Therapy

not

- Can cause coronary steal syndrome (normal cells steel from the deceased myocardium)

Identification and treatment of aggravating factors

useful; Harmful

 

o

Family counseling

- Increase perfusion to normal arteries only

Activity adaptation

- Induces more ischemia

-

 

o

Don’t go beyond the capacity of the heart

If Treadmill test showed 7 METS then do not prescribe 7 METS (only prescribe 70% of the metabolic requirement)

Diagnostic procedure only Chelation therapy

- Alternative medicine/Herbal medicines

 

Climbing the stairs: 4 METS

- Dissolve the plaque not true!!!

Climbing a mountain: 11 METS

Walking for 5 kilometers: 7-10 METS

TREATMENT OF RISK FACTORS TO IMPROVE OUTCOME

   
 

Class I

Smoking cessation Treatment of dyslipidemia

 

DRUG THERAPY

 

- Total cholesterol: 160 mg/dL

GUIDELINES FOR TREATMENT OF CSA

- LDL: 70-100 mg/dL

Treatment of hypertension Ideal weight and exercise

Class I

 

Aspirin (anti-platelet)

 

Used before for headache Beta blockers

-

 

(Ht in cm 100) 10% of answer IBW

-

(+)

Evidence

of

Aerobic exercise not isometric (weight lifting increase myocardial oxygen demand) ACE inhibitors

-

Drug Efficacy

- Decrease HR

 

- Decrease O2 consumption

Calcium antagonist

- DOC

 

- If patient has allergies, asthma or has history of asthma

- Have different effects at different dosages

- Decrease HR, coronary vasodilator

- Hypertension: Captopril 50mg BID

 

Do not give with EF of less than 40% Sublingual nitrates

-

- LV remodeling: Captopril 25 mg ¼ tab OD

- High levels: anti-hypertensive

-

Decrease preload and vasodilator

 

Low levels: for ischemia and remodeling Low fat diet Treatment of DM

-

-

Decrease wall tension and wall stress → decrease oxygen

demand Lipid lowering

Class IIb

Folate therapy

 

- Anti-cholesterol drugs

- Not a first line treatment

- STATINS to be taken for life

- Improve hemoglobin

Control LDL and HDL Risk modification

-

-

Walk

Intervention directed for psychological stress

Class III

Hormonal replacement therapy

-

Class IIa

 

Clopidogrel

 

After menopause there is higher risk because estrogen cannot be replaced

 

When aspirin is contraindicated in cases of allergy and ulcers Long acting calcium antagonist

-

 

-

Evidence in favor of therapy

Increased chance of developing cervical and breast cancer Treatment of depression Chelation therapy Vitamin E and C

- Supplement

Instead of beta blockers in cases of asthma Long acting nitrates and beta blockers

-

>50% positive effect of the drug

 

- Antioxidant

7
7
 

Herbal medicines

 

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

INTERVENTION WITH FAILURE OF MEDICAL MANAGEMENT

CORONARY REVASCULARIZATION

Percutaneous coronary intervention

o Angioplasty with stent

Coronary artery bypass grafting

ASYMPTOMATIC (SILENT) ISCHEMIA

Continuous ambulatory ECG monitoring will show ischemia

o Holter monitoring

Increase risk for cardiovascular events

o Patients won’t take the medications

Treatment of risk factors: hypertension and diabetes

o Diabetic patients usually present with asymptomatic chest pain

No manifestation of chest pain

PRINZMETAL’S VARIANT ANGINA

Uncommon form of unstable angina

Recurrent severe ischemia

Episodic focal spasm

ECG changes transient ST elevation

Treatment

o

Nitrates vasodilator

o

Calcium antagonist vasodilatation of coronary arteries

Side Notes:

*Lowest incidence of CAD is in Japan *Bypass can be done in MI but not in stroke (brain is dead)

8
8

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan