Presentation on theme: "FAMILY MEDICINE COURSE (FAM530)"— Presentation transcript:
1 FAMILY MEDICINE COURSE (FAM530) CV Risk factors & IHDPresented by :Mais Al-JoulanyEman AlzaidiRoaa alkhalifahReham GhazalHoryah AlismailIbtihal AldreesAbeer AlhatimFatmah AlrojaiyCady Alshammary
2 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.
3 Case ScenarioA 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: unremarkableNon-smokerBp: 124 / 82 mmHgBMI: 23 kg/m²FH: - his father died at age of 54 by heart attack- His elder brother had CABG at age of 48FPG: 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
6 Ihd overviewIschemic 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 EpidemiologyThe Leading Causes of Death From Cardiovascular DiseaseData from American Heart Association, 2006.
8 EpidemiologyGlobally, 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-basedmortality second to accident and senility.(35 percent) were due to cardiovasculardisease.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 includesunstable anginanon–ST-segment elevation MIST-segment elevation MI2) Chronic stable exertional angina3) Asymptomatic: ischemia due to coronary artery vasospasm (variant or Prinzmetal angina).4) Arrhythmia5) Heart failure6) 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
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
23 Nob-modifiable risk factors Family HistoryTwice 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 AgeIncreases with ageGenderMen >pre menopausal womenMen = post menopausal women
25 dyslipidemiaAbnormal lipid levels are known to be the basis of the atherosclerotic processMuch 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 byAbdominal Obesity: Weight CircumferenceMen ≥ 102 cmWomen ≥ 88 cmTriglycerides ≥ 1.7 mmol/L (150 mg/dL) Or on medicationHDL cholesterolmen < mmol/L (40 mg/dL)women < mmol/L (50 mg/dL)Or on medication for HDL-CBlood Pressure ≥ 130/85 or on antihypertensive MedicationFasting Glucose ≥ 100 mg/dl (5.6 mmol/L)or any medication for high blood glucoseAny 3 of the followingIf 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 diabetesPeople 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 diabetesCareful 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 obesityRisk 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 %ObeseWaist Circumference- ACSM Waist Circumference Targets< 102 cmMen< 88 cmWomen
34 Sedentary lifestylePhysical 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 AnxietyType A personality
36 Psychosocial factorsInfluence CAD risk via : Catacholamine release - Increased BP & HR - Vasoconstriction - Increased O2 demand
37 Other risk factors Drugs (contraceptive pill, nucleoside analogues) Heavy alcohol consumptionPoor oral healthDiets ( High in fats and low in antioxidant)Infectious agentsHigh levels of coagulation factors – high fibrinogen, factor VIIElevated 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 awarenessDeclines in smokingIncreases in obesity and diabetes may threaten this decline in the future.
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 diabetesThe 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 ScenarioA 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: unremarkableNon-smokerBp: 124 / 82 mmHgBMI: 23 kg/m²FH: - his father died at age of 54 by heart attack- His elder brother had CABG at age of 48FPG: 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 WOMENYearsPoints20-34-935-39-440-4445-49350-54655-59860-641065-601170-741275-7913YEARSPOINTS20-34-735-39-340-4445-49350-54655-59860-641065-691270-741475-7916Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA. 2001;285:
45 Step 2: Total Cholesterol TC (mg/dl) 79Points at age 20-39Points at age 40-49Points at age 50-59Points at age 60-69Points at age 70<16043217596>280118MenTC (mg/dl) 79Points at age 20-39Points at age 40-49Points at age 50-59Points at age 60-69Points at age 70<160432186115>28013107Women
47 Step 4: Systolic Blood Pressure Assessment of RiskStep 4: Systolic Blood PressureSystolic BP (mmHg)Points if untreatedPoints if treated<12012>1603MenSystolic BP (mmHg)Points if untreatedPoints if treated<12013245>1606Women
48 Assessment of Risk Step 5: smoking status Men Women 79 Points at age 20-39Points at age 40-49Points at age 50-59Points at age 60-69Points at age 70Non-smokersmoker8531Women79Points at age 20-39Points at age 40-49Points at age 50-59Points at age 60-69Points at age 70Non-smokersmoker97421
49 Systolic blood pressure Assessment of RiskStep 6: adding up the points(Sum From Steps 1–5)6AgeTotal cholesterol2HDL cholesterolSystolic blood pressureSmoking status8Points in total
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) ECGExercise 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
56 Exercise (stress) ECGcontraindicated :- In the presence of acute coronary syndrome, decompensated heart failure and severe hypertension.
57 Ambulatory ECGContinuous (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 biomarkersPlasma 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 biomarkers2- 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 ModalitiesChest 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 ModalitiesEchocardiography (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 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..
67 Imaging ModalitiesStress 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 ModalitiesMagnetic 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 ModalitiesCoronary 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 witha short half-life has made it possible to study cardiacfunction non-invasively.1- Blood pool imaging:-The isotope is injected intravenously and mixes withthe 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 Modalitiesthe 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 OUTCOMEThe 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 TreatmentRisk-factor ModificationPrimary 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 habits2) Regular physical exercise3) Maintaining ideal weight4) Avoiding tobacco5) reducing alcohol6) 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 demand2) Nitrates- Dilation of large and small intramural coronary arteries, collateraldilation, coronary artery stenosis dilation, abolition of normal tone innarrowed vessels, and relief of spasm.- Decrease preload : secondary to venodilation and arterial-arteriolar dilation3) Calcium Channel Blockers- Decrease preload- Decrease vascular resistance
77 TreatmentEvidence – Based Recommendation for Treatment of Stable angina PectorisAspirinClopidogrilB-blockesACEI / ARBsStatinCCBsSublingual NGLong-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? AspirinSl NGCCBs
82 - http://www.youtube.com/watch?v=fLonh7ZesKs 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.-
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