Presentation is loading. Please wait.

Presentation is loading. Please wait.


Similar presentations

Presentation on theme: "FAMILY MEDICINE COURSE (FAM530)"— Presentation transcript:

CV Risk factors & IHD Presented by : Mais Al-Joulany Eman Alzaidi Roaa alkhalifah Reham Ghazal Horyah Alismail Ibtihal Aldrees Abeer Alhatim Fatmah Alrojaiy Cady Alshammary

2 Learning objective At 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.

3 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-smoker Bp: 124 / 82 mmHg BMI: 23 kg/m² FH: - 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: mmol/L ( 82.8 mg/dl ) LDL.C: mmol/l ( mg/dl ) HDL.C: 1.09mmol/l (19.62 mg/dl ) Trig.: mmol/L ( 31.31mg/dl ) ECG: Normal

4 Differential diagnosis of chest pain
Ischemic Heart Diseases Pericarditis Cardiac Aortic dissection Pulmonary embolism Pulmonary hypertension Vascular Pleuritis pneumonia Tracheobronchitis pneumothorax Pulmonary

5 Differential diagnosis of chest pain :
Costochondritis Cervical disc disease Rib fracture Thoracic rib cage and muscles Gastroesophageal reflux disease Peptic Ulcer Disease Gallbladder disease Pancreatitis Gastrointestinal Herpes Zoster Infectious Panic disorder Psychological

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

7 The Leading Causes of Death From Cardiovascular Disease
Epidemiology The Leading Causes of Death From Cardiovascular Disease Data from American Heart Association, 2006.

8 Epidemiology 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).

9 Globally, there is an uneven distribution of age-adjusted CVD mortality.
NOTE: Rates are age-standardized to WHO’s world standard population. SOURCES: WHO, 2009e; map created with StatPlanet (van Cappelle, 2009). For example, age-standardized mortality rates for CVD are in excess of 500 per 100,000 in Russia and Egypt; between 400 and 450 for South Africa, India and Saudi Arabia; and around 300 for Brazil and China. This is in contrast to rates of between 100 and 200 per 100,000 for Australia, Japan, France, and the United States. Age-standardized deaths due to cardiovascular disease (rate per 100,000), 2004

10 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

11 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

12 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. Carbon monoxide is a toxic gas, but, being colorless, odorless, tasteless, and initially non-irritating, it is very difficult for people to detect. Carbon monoxide mainly causes adverse effects in humans by combining with hemoglobin to form carboxyhemoglobin (HbCO) in the blood. This prevents hemoglobin from releasing oxygen in tissues, effectively reducing the oxygen-carrying capacity of the blood, leading to hypoxia

13 Atherosclerosis pathogenesis

14 Manifestations of Atherosclerosis
: Heart Myocardial Ischemia Angina Myocardial Infarction : Brain Transient ischemic attack (TIA) Cerebrovascular accident (stroke) Legs : Intermittent claudication

15 Manifestations of Atherosclerosis
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

16 Manifestations of Atherosclerosis
Angina : Angina pectoris - Symptom not a disease - Chest discomfort associated with abnormal myocardial function in the absence of myocardial necrosis

17 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

18 Manifestations of Atherosclerosis
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.

19 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 = Troponin T – Normal < 0.03


21 Manifestations of Atherosclerosis
Myocardial Infarction Signs & Symptoms: - Angina - GI upset - Dyspnea - Diaphoresis - Syncope

22 Risk factors for ischemic heart diseases

23 Nob-modifiable risk factors
Family History Twice the risk of MI if one first-degree relative with MI Triple the risk of MI if 2+ first-degree relatives with MI Risk is strongest if MI occurred at age 55 or less Advancing Age Increases with age Gender Men >pre menopausal women Men = post menopausal women

24 modifiable risk factors
Major Dyslipidemia Hypertension Diabetes Smoking Minor Obesity Sedentary Lifestyle Stress Other Risk Factors

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

26 dyslipidemia Lipid Targets for 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.

27 dyslipidemia Other factors :
Metabolic syndrome can be a secondary target of risk reduction after LDL-C has been addressed. This syndrome is characterized by Abdominal Obesity: Weight Circumference Men ≥ 102 cm Women ≥ 88 cm Triglycerides ≥ 1.7 mmol/L (150 mg/dL) Or on medication HDL cholesterol men < mmol/L (40 mg/dL) women < 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 Any 3 of the following If the metabolic syndrome is present, the patient is considered to have a CHD risk equivalent.

28 Hypertension - Primary risk factor for CAD - Hypertension is associated with three to four times increased risk for CAD, MI & PVD

29 diabetes 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

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

31 Tobacco smoking - 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

32 obesity Risk in central obesity > peripheral obesity. Obesity is often associated with - Diabetes - Hypertension - Dyslipidemia - Inactivity

33 obesity Body Mass Index (BMI) - Measured in Kg/m2 - ACSM BMI Targets
% Underweight <18.5 % Normal % Overweight >30 % Obese Waist Circumference - ACSM Waist Circumference Targets < 102 cm Men < 88 cm Women

34 Sedentary lifestyle 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)

35 Psychosocial factors Work stress Lack of social support Depression
Anxiety Type A personality

36 Psychosocial factors Influence CAD risk via : Catacholamine release - Increased BP & HR - Vasoconstriction - Increased O2 demand

37 Other risk 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)

38 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.

39 Framingham Cardiovascular Risk Calculation

40 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

41 Assessment of Risk For persons without known CHD, other forms of
atherosclerotic 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.

42 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.

43 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-smoker Bp: 124 / 82 mmHg BMI: 23 kg/m² FH: - 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: mmol/L ( 82.8 mg/dl ) LDL.C: mmol/l ( mg/dl ) HDL.C: 1.09mmol/l (19.62 mg/dl ) Trig.: mmol/L ( 31.31mg/dl ) ECG: Normal

44 Assessment of Risk Step 1: Age
WOMEN Years Points 20-34 -9 35-39 -4 40-44 45-49 3 50-54 6 55-59 8 60-64 10 65-60 11 70-74 12 75-79 13 YEARS POINTS 20-34 -7 35-39 -3 40-44 45-49 3 50-54 6 55-59 8 60-64 10 65-69 12 70-74 14 75-79 16 Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:

45 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 4 3 2 1 7 5 9 6 >280 11 8 Men 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 4 3 2 1 8 6 11 5 >280 13 10 7 Women

46 Step 3: HDL- Cholesterol
Assessment of Risk Step 3: HDL- Cholesterol Men Women HDL-Ch (mg/dl) Points >60 -1 50-59 40-49 1 <40 2 HDL-Ch (mg/dl) Points >60 -1 50-59 40-49 1 <40 2

47 Step 4: Systolic Blood Pressure
Assessment of Risk Step 4: Systolic Blood Pressure Systolic BP (mmHg) Points if untreated Points if treated <120 1 2 >160 3 Men Systolic BP (mmHg) Points if untreated Points if treated <120 1 3 2 4 5 >160 6 Women

48 Assessment of Risk Step 5: smoking status Men Women 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 smoker 8 5 3 1 Women 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 smoker 9 7 4 2 1

49 Systolic blood pressure
Assessment of Risk Step 6: adding up the points (Sum From Steps 1–5) 6 Age Total cholesterol 2 HDL cholesterol Systolic blood pressure Smoking status 8 Points in total

50 Step 7: CHD Risk Total points 10 year <0 <1% 1% 1 2 3 4 5 2% 6 7
1% 1 2 3 4 5 2% 6 7 3% 8 4% 9 5% 10 6% 11 8% 12 10% 13 12% 14 16% 15 20% 16 25% >17 >30%

51 Future cardiovascular risk in this patient :
This patient having 4% risk for developing CHD in 10 years

52 Diagnostic tests for CHD

53 Non-invasive investigations Electrocardiogram (ECG)
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

54 Exercise (stress) 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

55 Exercise (stress) ECG

56 Exercise (stress) ECG contraindicated :- In the presence of acute coronary syndrome, decompensated heart failure and severe hypertension.

57 Ambulatory 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.

58 Cardiac biomarkers 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)

59 Cardiac biomarkers 1- Brain natriuretic peptide:-
- 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..

60 Cardiac biomarkers 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

61 Imaging Modalities Chest X-ray:- - This is useful for determining the size and shape of the heart. - The state of the pulmonary blood vessels and lung fields. Most information is given by apostero-anterior (PA) projection taken in full inspiration..

62 Imaging Modalities Chest X-ray:-
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..

63 Imaging Modalities Echocardiography (echo):- Two-dimensional echocardiography:- Echocardiography, or cardiac ultrasound, is obtained by 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..

64 Imaging Modalities Doppler echocardiography:-
This depends on the Doppler principle that sound waves reflected from moving objects, such as intracardiac red blood 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 direction of blood flow is reversed and turbulence is seen..

65 Imaging Modalities

66 Imaging Modalities Doppler echocardiography

67 Imaging Modalities Stress echocardiography:- Stress echocardiography is used to investigate patients with suspected coronary heart disease who are unsuitable for 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.

68 Imaging Modalities Magnetic resonance imaging (MRI):- This requires no ionising radiation and can be used to generate 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..

69 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.

70 Imaging Modalities Radionuclide imaging:-
The availability of gamma-emitting radionuclides with a short half-life has made it possible to study cardiac function 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..

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

72 Interventions and Treatment of Coronary Artery Disease

73 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.

74 Risk-factor Modification
Treatment 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.

75 Treatment Life- Style Modifications
1) Healthy life style and healthy eating habits 2) Regular physical exercise 3) Maintaining ideal weight 4) Avoiding tobacco 5) reducing alcohol 6) Control chronic diseses if present ( DM, HTN, Dyslipidemia …ect) .

76 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

77 Treatment Evidence – Based Recommendation for Treatment of Stable angina Pectoris Aspirin Clopidogril B-blockes ACEI / ARBs Statin CCBs Sublingual NG Long-acting Nitrates

78 Treatment of Variant Angina
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

79 Percutaneous Coronary Intervention (PCI)
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

80 Coronary Artery Bypass Graft Surgery (CABG)
Indications - Left main disease > 50 % - Proximal 3 vessel disease - Multivessel disease with left ventricular dysfunction - Lifestyle limiting angina unresponsive to medical therapy or PCI

81 How would you treat the patient, at this point?
Aspirin Sl NG CCBs

82 -
References - Kumar & Clark's Clinical Medicine (Saunders, 2009) - Pharmacotherapy 7th edition McGraw Hill Dipiro - Davidson's Principles and Practice of Medicine 21st Edition - WHO, 2009e; map created with StatPlanet (van Cappelle, 2009). - American Heart Association, 2006. -


Similar presentations

Ads by Google