FAMILY MEDICINE COURSE (FAM530)CV RISK FACTORS & IHD

PRESENTED BY:

Mais Al-JoulanyEman Alzaidi

Roaa alkhalifah

Reham Ghazal

Horyah AlismailIbtihal AldreesAbeer Alhatim

Fatmah AlrojaiyCady Alshammary

LEARNING OBJECTIVEAt the end of this session, the student will be able to:

Discuss the differential diagnosis of a patient presented with chest pain. Describe the current epidemiology of coronary artery disease (CHD).

Identify major and minor risk factors for coronary heart disease.

Utilize the Framingham formula to predict future cardiovascular risk.

Recognize the available diagnostic tests for CHD, including the scientific foundations underlying each test, advantages and disadvantages, risks, and benefits.

Describe lifestyle and pharmacological interventions for treating CHD risk factors, as well as CHD itself.

CASE SCENARIO

A 52-year-old, business man, presents with 7 months H/o mild chest pain of no specific character. Sometimes brought by exertion but could be felt on rest .

PMH: unremarkable Non-smokerBp: 124 / 82 mmHg BMI: 23 kg/m²FH: - his father died at age of 54 by heart attack - His elder brother had CABG at age of 48

FPG: 5.1 mmol/l (91.8 mg/dl )T. Cholesterol: 4.6 mmol/L ( 82.8 mg/dl ) LDL.C: 2.57 mmol/l ( 46.26 mg/dl ) HDL.C: 1.09mmol/l (19.62 mg/dl )Trig.: 1.74 mmol/L ( 31.31mg/dl )ECG: Normal

DIFFERENTIAL DIAGNOSIS OF CHEST PAIN

Ischemic Heart Diseases

Pericarditis

Cardiac

Aortic dissection Pulmonary embolism Pulmonary hypertension

Vascular

Pleuritispneumonia Tracheobronchitis pneumothorax

Pulmonary

DIFFERENTIAL DIAGNOSIS OF CHEST PAIN:

CostochondritisCervical disc diseaseRib fracture

Thoracic rib cage and muscles

Gastroesophageal reflux disease Peptic Ulcer DiseaseGallbladder diseasePancreatitis

Gastrointestinal

Herpes Zoster Infectious

Panic disorder Psychological

Ischemic heart disease (IHD) is defined as an imbalance between cardiac blood supply ( perfusion ) and myocardial oxygen demand resulting in Myocardial

Ischemia .

IHD OVERVIEW

EPIDEMIOLOGY

The Leading Causes of Death From Cardiovascular Disease

Data from American Heart Association, 2006.

Globally, there is an uneven distribution of age-adjusted CVD mortality .

The lowest age-adjusted mortality rates are in the advanced industrialized countries and parts of Latin America, whereas the highest rates today are found in Eastern Europe and a number of low and middle income countries.

Overall, age-adjusted CVD death rates are today higher in major low and middle income countries than in developed countries .

)WHO, 2008b(.

EPIDEMIOLOGY

Age-standardized deaths due to cardiovascular disease (rate per 100,000), 2004

Globally, there is an uneven distribution of age-adjusted CVD mortality .

Cardiovascular diseases in KSA:

the third most common cause of hospital-based mortality second to accident and senility.

)35 percent (were due to cardiovascular disease.

Vascular injury accumulates in adolescence, making it necessary for primary preventive measures to be taken from childhood.

WHO report, 2008

CLINICAL MANIFESTATIONS OF IHD

1 (An acute coronary syndrome (ACS) which includes • unstable angina • non–ST-segment elevation MI • ST-segment elevation MI

2) Chronic stable exertional angina

3) Asymptomatic: ischemia due to coronary artery vasospasm (variant or Prinzmetal angina).

4) Arrhythmia 5) Heart failure 6) Sudden death

CAUSES

Ischemia can result from:

1 (Increase oxygen demand ) e.g. increase heart rate or hypertension(

2 (Diminished oxygen-carrying capacity (e.g. anemia or carbon monoxide poisoning)

3 (In the vast majority of IHD cases is relatively due to coronary atherosclerosis that begins early in life but manifests only after the vascular occlusions reach a

critical stage .

ATHEROSCLEROSIS PATHOGENESIS

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MANIFESTATIONS OF ATHEROSCLEROSIS

: Heart Myocardial Ischemia

Angina Myocardial Infarction

:Brain Transient ischemic attack (TIA)

Cerebrovascular accident (stroke)Legs :

Intermittent claudication

Myocardial Ischemia :

- LV stiffening & decreased diastolic filling (diastolic dysfunction)

- Impaired LV systolic emptying

- ECG changes associated with altered repolarization

- Angina Pectoris : transient, referred cardiac pain resulting from ischemia

MANIFESTATIONS OF ATHEROSCLEROSIS

Angina pectoris

- Symptom not a disease - Chest discomfort associated with abnormal

myocardial function in the absence of myocardial necrosis

MANIFESTATIONS OF ATHEROSCLEROSIS

Angina:

MANIFESTATIONS OF ATHEROSCLEROSIS

Characteristics of “typical” or “classic”

- Pressure, tightness, squeezing, heaviness, or choking

- Radiates down left arm, back, and/or jaw - Occurs with physical activity, emotional stress, cold

weather, heavy meals - Last few minutes ( 15sec to 15 min) or until activity ceases

- May be relieved by rest or nitroglycerine. - May be associated with nausea, vomiting, or

diaphoresis

Angina – Types: Silent ischemia: no pain

stable or typical angina :chest pain associated with exertion or some other forms of stress. Usually relieved by rest or sublingual nitroglycerin

Unstable Angina: Pain occurs with progressively increasing frequency, is precipitated by less exertion, even at rest, and tends to be of more prolonged duration. Unstable angina is often the precursor of subsequent acute MI. Thus this referred to as pre-infarction angina .

Variant prinzmetal angina: uncommon pattern that occurs at rest and is due to coronary artery spasm and not related to atherosclerotic disease .

MANIFESTATIONS OF ATHEROSCLEROSIS

Myocardial Infarction

Diagnosis: 2 of 3 criteria: 1 (Chest pain > 30 minutes

2 (ECG: - ST segment elevation - T wave intervention

3 (Cardiac enzymes : - Creatine phosphokinase (CK) Normal = 0-195

- Troponin T – Normal < 0.03

MANIFESTATIONS OF ATHEROSCLEROSIS

ATHEROSCLEROSIS

PVDIHDSTABL

E ANGIN

A

ACUTE

CORONARY SYNDROME

CAD

MYOCARDIAL INFARCTION

UNSABLE ANGINA

STE MINON STE MI

Signs & Symptoms:

- Angina - GI upset - Dyspnea

- Diaphoresis - Syncope

Myocardial Infarction

MANIFESTATIONS OF ATHEROSCLEROSIS

RISK FACTORS FOR ISCHEMIC HEART DISEASES

Family History

Twice the risk of MI if one first-degree relative with MITriple the risk of MI if 2+ first-degree relatives with MIRisk is strongest if MI occurred at age 55 or lessAdvancing Age

Increases with age Gender

Men >pre menopausal womenMen = post menopausal women

NOB-MODIFIABLE RISK FACTORS

MODIFIABLE RISK FACTORS

Major •Dyslipidemia•Hypertension

•Diabetes•Smoking

Minor •Obesity

•Sedentary Lifestyle•Stress

•Other Risk Factors

Abnormal lipid levels are known to be the basis of the atherosclerotic process

DYSLIPIDEMIA

Much research to support the link between abnormal serum lipid levels and CAD

LDL = risk of CAD

HDL = risk of CAD

TGs = risk of CAD

Primary Targets:The previous guidelines recommended treating to an LDL goal of below 100 mg/dL in people at high cardiovascular risk, but also recommended a goal of 70 mg/dL or lower for patients at very high risk .

DYSLIPIDEMIA

Lipid Targets for CAD

DYSLIPIDEMIA

Metabolic syndrome can be a secondary target of risk reduction after LDL-C has been addressed .

This syndrome is characterized by

Other factors:

Abdominal Obesity: Weight Circumference

Men ≥ 102 cm Women ≥ 88 cm

Triglycerides ≥ 1.7 mmol/L (150 mg/dL) Or on medication

HDL cholesterol

men < 1.05 mmol/L (40 mg/dL) women < 1.30 mmol/L (50 mg/dL)

Or on medication for HDL-C

Blood Pressure ≥ 130/85 or on antihypertensive Medication

Fasting Glucose ≥ 100 mg/dl (5.6 mmol/L) or any medication for high blood glucose

-Primary risk factor for CAD -Hypertension is associated with three to four times increased

risk for CAD, MI & PVD

HYPERTENSION

People with diabetes have 2 to 7 times increased risk of developing CAD than people without diabetes

Endothelial damage - Increased platelet aggregation

- Insulin promotes synthesis of lipids and uptake of lipids by smooth muscle

Excess sugar in vessels damages the lining making it vulnerable to plaques and clots

DIABETES

Careful control of blood sugar levels reduces the risk of developing the complications of diabetes

DIABETES

- More in men. -Declines to almost normal after 10 years of abstention

How Does Smoking Increase CAD Risk? Increased HR and BP

Increased vasoconstriction Decreased HDL

Increased LDL and Triglycerides Increased LDL oxidation

Increased platelet aggregation Decreased O2 carrying capacity

TOBACCO SMOKING

Risk in central obesity > peripheral obesity.

Obesity is often associated with

- Diabetes

- Hypertension

- Dyslipidemia

- Inactivity

OBESITY

Body Mass Index (BMI) - Measured in Kg/m2

- ACSM BMI Targets

Waist Circumference

- ACSM Waist Circumference Targets

OBESITY

18.5-24.9% •Underweight

<18.5% •Normal

%25.0-29.9 •Overweight

>30% •Obese

• >102 cmMen• >88 cmWomen

Physical activity reduces the risk of CAD through:

- Improved balance between myocardial O2 supply and demand

- Decreased platelet aggregation - Decreased susceptibility to malignant

ventricular arrhythmias - Improved endothelial tone

- Beneficial effect on other CAD risk factors (ie. diabetes, dyslipidemia, hypertension, obesity, stress)

SEDENTARY LIFESTYLE

• Work stress

• Lack of social support

• Depression

• Anxiety

• Type A personality

PSYCHOSOCIAL FACTORS

Influence CAD risk via: Catacholamine release

- Increased BP & HR - Vasoconstriction

- Increased O2 demand

PSYCHOSOCIAL FACTORS

• Drugs (contraceptive pill, nucleoside analogues) • Heavy alcohol consumption • Poor oral health• Diets ( High in fats and low in antioxidant)• Infectious agents• High levels of coagulation factors – high fibrinogen, factor

VII • Elevated C-reactive protein (inflammatory marker)

OTHER RISK FACTORS

What is happening to the prevalence of risk factors?

Mortality rates for heart disease have steadily declined in the US. These declines are related to improvements in some risk factors:

• Improved treatments for hypertension and hyperlipidaemia.• Increase community awareness• Declines in smoking

Increases in obesity and diabetes may threaten this decline in the future.

Framingham Cardiovascular Risk Calculation

Framingham Cardiovascular Risk Calculation

Framingham Cardiovascular Risk Calculator, uses recent data from the Framingham Heart Study to estimate 10-year risk for coronary heart disease outcomes (myocardial infarction and

coronary death) .

It is designed to estimate risk in adults aged 20 and older who do not have heart disease or diabetes

The various degrees of risk associated with five categories:   •  AGE   •  TOTAL CHOLESTEROL LEVEL   •  HDL-C LEVEL   •  SMOKING   •  Systolic Bp

For persons without known CHD, other forms ofatherosclerotic disease, or diabetes:

Count the number of risk factors.

Use Framingham scoring for persons with 2 risk factors to determine the absolute 10-year CHD risk.

For persons with 0–1 risk factor, Framingham calculations are not necessary .

Assessment of Risk

NOTE:

Cardiovascular risk calculator should not be used if

- BP >185 or <100 mmHg - total cholesterol >8mmol/l (144mg/dl ) .

Estimated risks do not allow for factors such as family history and this should be borne in mind .

CASE SCENARIO

A 52-year-old, business man, presents with 7 months H/o mild chest pain of no specific character. Sometimes brought by exertion but could be felt on rest .

PMH: unremarkable Non-smokerBp: 124 / 82 mmHg BMI: 23 kg/m²FH: - his father died at age of 54 by heart attack - His elder brother had CABG at age of 48

FPG: 5.1 mmol/l (91.8 mg/dl )T. Cholesterol: 4.6 mmol/L ( 82.8 mg/dl ) LDL.C: 2.57 mmol/l ( 46.26 mg/dl ) HDL.C: 1.09mmol/l (19.62 mg/dl )Trig.: 1.74 mmol/L ( 31.31mg/dl )ECG: Normal

Expert Panel on Detection, Evaluation, and Treatment of High BloodCholesterol in Adults. JAMA. 2001;285:2486-2497.

Years Points 20-34 -9 35-39 -440-44 045-49 350-54 655-59 860-64 1065-60 1170-74 1275-79 13

MENYEARS POINTS

20-34 -735-39 -340-44 045-49 350-54 655-59 860-64 1065-69 1270-74 1475-79 16

WOMEN

Assessment of Risk Step 1: Age

Men

Women

Step 2: Total Cholesterol

TC (mg/dl) 79

Points at age 20-39

Points at age 40-49

Points at age 50-59

Points at age 60-69

Points at age 70

<160 0 0 0 0 0160-199 4 3 2 1 1200-238 8 6 4 2 1240-279 11 8 5 3 2

>280 13 10 7 4 2

TC (mg/dl) 79

Points at age 20-39

Points at age 40-49

Points at age 50-59

Points at age 60-69

Points at age 70

<160 0 0 0 0 0160-199 4 3 2 1 0200-239 7 5 3 1 0240-279 9 6 4 2 1

>280 11 8 5 3 1

Men Women

Assessment of Risk Step 3: HDL- Cholesterol

HDL-Ch(mg/dl)

Points

>60 -150-59 040-49 1

<40 2

HDL-Ch(mg/dl)

Points

>60 -150-59 040-49 1

<40 2

Assessment of Risk Step 4: Systolic Blood Pressure

Systolic BP (mmHg) Points if untreated Points if treated

<120 0 0120-129 1 3130-139 2 4140-149 3 5

>160 4 6

Systolic BP (mmHg) Points if untreated Points if treated

<120 0 0120-129 0 1130-139 1 2140-149 1 2

>160 2 3

Women

Men

Assessment of Risk Step 5: smoking status

79 Points at age 20-39

Points at age 40-49

Points at age 50-59

Points at age 60-69

Points at age 70

Non-smoker 0 0 0 0 0smoker 8 5 3 1 1

79 Points at age 20-39

Points at age 40-49

Points at age 50-59

Points at age 60-69

Points at age 70

Non-smoker 0 0 0 0 0smoker 9 7 4 2 1

Men

Women

)Sum From Steps 1–5(

Assessment of Risk Step 6: adding up the points

6 Age0 Total cholesterol2 HDL cholesterol0 Systolic blood pressure0 Smoking status8 Points in total

Step 7: CHD Risk Total points 10 year

<0 <1%0 1%1 1%2 1%3 1%4 1%5 2%6 2%7 3%8 4%9 5%

10 6%11 8%12 10%13 12%14 16%15 20%16 25%

>17 >30%

Future cardiovascular risk in this patient:

This patient having 4% risk for developing CHD in 10 years

Diagnostic tests for CHD

The ECG is used to assess cardiac rhythm and conduction.

It provides information about chamber size and is the main test used to assess for myocardial ischaemia and infarction

Non-invasive investigations Electrocardiogram (ECG)

Exercise electrocardiography is used to detect myocardial ischaemia during physical stress and is helpful in the diagnosis of coronary artery disease.

A test is ‘positive’if anginal pain occurs, BP falls or fails to increase, or if there are ST segment shifts of > 1 mm

Exercise (stress) ECG

Exercise (stress) ECG

contraindicated-:

In the presence of acute coronary syndrome, decompensated heart failure and severe

hypertension .

Exercise (stress) ECG

Continuous (ambulatory) ECG recordings can be obtained using a portable digital recorder.

used in the investigation of

patients with suspected arrhythmia, such as those with - intermittent palpitation

- dizziness or syncope.

Ambulatory ECG

Plasma or serum biomarkers can be measured to assess myocardial dysfunction and ischaemia..

1 -Brain natriuretic peptide -:

This is a 32 amino acid peptide and is secreted by the LV along with an inactive 76 amino acid N- terminal fragment (NT-proBNP)

Cardiac biomarkers

- diagnostically more useful. - it has a longer half-life .

- It is elevated principally in conditions associated with left ventricular systolic dysfunction.

- Used in diagnosis and assess prognosis and response to therapy in patients with heart failure..

Cardiac biomarkers

1 -Brain natriuretic peptide-:

2 -Cardiac troponins-:

Troponin I and troponin T are structural cardiac muscleproteins that are released during myocyte

damage and necrosis

it is the cornerstone of the diagnosis of acute myocardial infarction

Cardiac biomarkers

Chest X-ray-: - This is useful for determining the size and

shape of the heart .

Imaging Modalities

- The state of the pulmonary blood vessels and lung

fields .Most information is given by apostero-anterior (PA) projection taken in full inspiration..

1- An estimate of overall heart size can be made by comparing the maximum width of the cardiac outline with the maximum

internal transverse diameter of the thoracic cavity (‘Cardiomegaly)

2- Dilatation of individual cardiac chambers can be recognised by the characteristic alterations to the cardiac silhouette

3- The lung fields on the chest X-ray may show congestion and oedema in patients with heart failure..

Chest X-ray-:

Imaging Modalities

Echocardiography (echo)-:

Two-dimensional echocardiography-:Echocardiography, or cardiac ultrasound, is obtainedby placing an ultrasound transducer on the chest wall to image the heart structures.

rapid assessment of cardiac structure ,function, Left ventricular wall thickness and ejection fraction..

Imaging Modalities

Doppler echocardiography-:

This depends on the Doppler principle that sound wavesreflected from moving objects, such as intracardiac redblood cells, The speed and direction of the red cells.

-Present as a colour overlay on a two-dimensional real-time echo picture..

used to detect valvular regurgitation, where the directionof blood flow is reversed and turbulence is seen..

Imaging Modalities

Imaging Modalities

Imaging Modalities

Doppler echocardiography

Stress echocardiography-:

Stress echocardiography is used to investigate patientswith suspected coronary heart disease who are unsuitablefor exercise stress testing.

Computed tomographic (CT) imaging:-

This is useful for imaging the cardiac chambers, great vessels,pericardium, and mediastinal structures and masses.very high-resolution imaging.

-Contrast scans are very useful for imaging the aorta in suspected aortic dissection.

Imaging Modalities

Magnetic resonance imaging (MRI)-:

This requires no ionising radiation and can be used togenerate cross-sectional images of the heart, lungs andmediastinal structures.

- better differentiation of soft tissue structures than CT. - is poor at demonstrating calcification.

- is very useful for imaging the aorta, including suspected dissection.

- define the anatomy of the heart and great vessels in patients with congenital heart disease..

- Later redistribution of this contrast (delayed enhancement), can be used to identify myocardial scarring and fibrosis..

Imaging Modalities

Coronary angiography-:

The only absolute way to evaluate coronary artery disease is by angiography. It is usually performed as part of cardiac catheterisation.

Imaging Modalities

Radionuclide imaging:-

The availability of gamma-emitting radionuclides witha short half-life has made it possible to study cardiacfunction non-invasively.

1 -Blood pool imaging-: The isotope is injected intravenously and mixes with

the circulating blood. A gamma camera detects the amount of isotope-emitting blood in the heart at different phases of the cardiac cycle, and also the size and shape’ of the

cardiac chambers..

Imaging Modalities

the left (and right) ventricular ejection fraction (the proportion of blood ejected during each beat) can then be calculated.

2 -Myocardial perfusion imaging:-

This technique involves obtaining scintiscans of the myocardium at rest and during stress after the

administration of an intravenous radioactive isotope..

- positron emission tomography (PET), which can be used to assess myocardial metabolism.

Imaging Modalities

A chest radiograph should be done if the patient has heart failure symptoms.

Interventions and Treatment of Coronary Artery Disease

DESIRED OUTCOME

The short-term goals of therapy for IHD are to reduce or prevent anginal symptoms that limit exercise capability and impair quality of life .

Long term goals are to prevent CHD events such as MI, arrhythmias, and heart failure and to extend the patient’s life.

Risk-factor Modification

Primary prevention through the modification of risk factors

should significantly reduce the prevalence of IHD .

Secondary intervention is effective in reducing subsequent

morbidity and mortality.

Risk factors for IHD are additive and can be classified as

alterable or unalterable .

Treatment

Treatment

Life- Style Modifications

1 (Healthy life style and healthy eating habits2 (Regular physical exercise3 (Maintaining ideal weight

4 (Avoiding tobacco 5 (reducing alcohol

6 (Control chronic diseses if present ( DM, HTN, Dyslipidemia …ect).

Treatment

Pharmacological Treatment 1 (β-Adrenergic Blocking Agents

-Decrease HR -Decrease contractility

-Decrease blood pressure -Reduce Myocardial oxygen demand

2 (Nitrates

-Dilation of large and small intramural coronary arteries, collateral dilation, coronary artery stenosis dilation, abolition of normal tone in

narrowed vessels, and relief of spasm. - Decrease preload : secondary to venodilation and arterial-arteriolar

dilation 3 )Calcium Channel Blockers

-Decrease preload -Decrease vascular resistance

Treatment

Evidence – Based Recommendation for Treatment of Stable angina Pectoris

Aspirin

Clopidogril

B-blockes

ACEI / ARBs

Statin

CCBs

Sublingual NG

Long-acting Nitrates

CCBs may be more effective, have few serious adverse effects,

and can be given less frequently than nitrates, some

authorities consider them the agents of choice for variant

angina.

Nifedipine, verapamil, and diltiazem are all equally effective as

single agents for initial management.

- Patients unresponsive to CCBs alone may have nitrates added

- β-Blockers have little or no role in the management of variant

angina as they may induce coronary vasoconstriction and

prolong ischemia

Treatment of Variant Angina

Indications for Angioplasty (+/- stenting) - Electively for chronic stable angina

- Urgently for unstable angina - Emergently for myocardial infarction

- 1 or 2 vessel disease

NEVER for left main disease

Percutaneous Coronary Intervention (PCI)

Indications - Left main disease > 50% - Proximal 3 vessel disease

- Multivessel disease with left ventricular dysfunction - Lifestyle limiting angina unresponsive to medical

therapy or PCI

Coronary Artery Bypass Graft Surgery (CABG)

How would you treat the patient, at this point?

AspirinSl NGCCBs

References

-Kumar & Clark's Clinical Medicine (Saunders, 2009)

-Pharmacotherapy 7th edition McGraw Hill Dipiro

- WHO, 2009e ;map created with StatPlanet) van Cappelle, 2009.(

-American Heart Association, 2006.

- http://www.youtube.com/watch?v=fLonh7ZesKs

-Davidson's Principles and Practice of Medicine 21st Edition