MANAGEMENT OF CORONARY ARTERY DISEASES Medical Presentation

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CURRENT TRENDS IN THE MANAGEMENT OF CORONARY ARTERY DISEASES Presented by Theophilus Afful, Andy Quarshie and David Anokye 1
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OUTLINE INTRODUCTION ETIOLOGY EPIDEMIOLOGY PATHOPHYSIOLOGY RISK FACTORS SIGNS AND SYMPTOMS DIAGNOSIS AND INVESTIGATIONS COMPLICATIONS TREATMENT AND MANAGEMENT ROLE OF THE PHARMACIST REFERENCES 2
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INTRODUCTION Coronary Artery Disease is the insufficient perfusion of the heart. This is as a result of abnormal narrowing of the vessels This causes inadequate supply of oxygen to the myocardial tissues It is primarily a blood vessel disorder which is characterised by deposits of lipids mainly in the intimal wall of the artery It is caused by smoking, high blood pressure, diabetes mellitus, family history, genetics, stress. 3
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TYPES OF CADs ANGINA (STABLE AND UNSTABLE) MYOCARDIAL INFARCTION (STEMI AND NSTEMI) 4
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ETIOLOGY Etiology is mostly unknown Most probable causes may include : Genetic factors Lifestyle Family history Stress 6
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Epidemiology Cardiovascular diseases (CVD) is the leading cause of death worldwide, accounting for 17.3 million deaths in 2008 (or ~ 30% of all deaths worldwide Coronary artery disease and acute coronary syndrome (ACS) together account for approximately 7 million deaths each year It is mostly predominant in blacks than in white. Also mostly found in developed world than in developing world In Ghana, CVD rose from being the 7th and 10th cause of death in Accra in 1953 and 1966 respectively, to the. number one cause of death in 1991 and 2001 and it has continued as one of the major causes of mortality in the country 7
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Epidemiology Heart disease is the leading cause of death among men and women in the United States. Coronary artery disease affects 16.5 million Americans. The American Heart Association (AHA) estimates that someone in the US has a heart attack about every 40 seconds In addition, for patients with no risk factors for heart disease, the lifetime risk of having cardiovascular disease is 3.6% for men and less than 1% for women. Having 2 or more risk factors increase the lifetime risk of cardiovascular disease to 37.5% for men and 18.3% in women. 8
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EPIDEMIOLOGY Although IHD in Sub Saharan Africa (SSA) remains relatively uncommon, its prevalence is predicted to rise in the next two decades due to the rising prevalence of risk factors, especially hypertension, diabetes, overweight and obesity, physical inactivity, increased tobacco use and dyslipidaemia. It is estimated that age-standardised mortality rates for IHD will rise by 27% in African men and 25% in women by 2015, and by 70 and 74%, respectively by 2030. 9
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PATHOPHYSIOLOGY CAD is characterised by ; The focal deposits of lipids in the intimal wall of the artery. An injury to the endothelial layer causes a response in the intimal layer of the artery and the deposition of the lipids in the wall. Thereby causing a decreased perfusion of the myocardial tissues. 10
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PATHOPHYSIOLOGY CAD occurs in three stages Fatty streaks Fibrous plaque Complicated lesions 11
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FATTY STREAKS Early lesions by lipid filled smooth muscle cells Seen at an early stage (15 years) It can be easily reversible 12
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FIBROUS PLAQUE Develops over time Smooth muscles are stimulated by low densities of lipoproteins and platelets Produces collagen and migrate over fatty streaks Forming a fibrous plaque(whitish or greyish in colour) 13
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FIBROUS PLAQUE Develops in one portion of the artery or engulfs the entire lumen It causes loss of arterial elasticity Impairs the vessels ability to vasodilate 14
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COMPLICATED LESIONS The development of an ulceration of the plaque Platelets adhere to the lesion, Causes a coagulation cascade with the development of thrombus that obstructs the artery 15
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RISK FACTORS 16
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MODIFIABLE RISK FACTORS High blood cholesterol level Cigarette smoking and tobacco use Hypertension Diabetes mellitus Lack of estrogen in women Physical inactivity Obesity 18
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NON MODIFIABLE RISK FACTORS Family History of Coronary artery disease (CAD) Age Gender (male) Race (non white populations) 19
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SIGNS AND SYMPTOMS Chest pain Diaphoresis ECG changes Dysarrithmias Chest heaviness Dyspnoea Fatigue 20
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DIAGNOSIS AND INVESTIGATIONS Cardiac enzymes (AST, LDH, cTn, CK-MB, Myoglobin) Electocardiograms (ECG) Echocardiograms Stress tests Nuclear Imaging Angiography 21
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ECG 22
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DIFFERNTIAL DIAGNOSIS Microvascular angina Pericarditis Pulmonary embolism Musculoskeletal chest pain Aortic dissection Acute cholecystitis Gastroesophageal reflux disease 23
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COMPLICATIONS Heart failure Bradychardia Tachycardia Related Arterial disease (stroke, atherosclerotic plaques) 24
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TREATMENT AND MANAGEMENT TREATMENT OBJECTIVES To relieve symptoms. To prevent or reduce ischemia. To prevent myocardial infarction. 25
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TREATMENT AND MANAGEMENT NON PHARMACOLOGICAL MANAGEMENT Quit smoking Eat healthy food (low fat foods) Exercise lose excess weight Reduce stress 26
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PHARMACOLOGICAL TREATMENT ANTILIPEMICS (Statins, Fibrates, Bile acid sequestrants, niacin) Aspirin Beta blockers Calcium channel blockers (CCBs) Nitrates (Nitroglycerine GTN) ACE Inhibitors Ranolazine 27
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CURRENT TREATMENT GUIDELINES Immediate Treatment Place a fresh Glyceryl trinitrate tablet (500 microgram) under the tongue Long−term Treatment Antiplatelet therapy − Aspirin, oral, 150 − 300 mg daily Beta−blocker (if not contraindicated) − Atenolol, oral, 50 mg once daily Long−acting nitrates − Isosorbide dinitrate, oral, 10 mg 2−3 times daily Optimise or initiate treatment for hypertension Optimise or initiate treatment for diabetes mellitus Treat abnormal blood lipids to target levels or refer to specialist 28
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SURGICAL PROCEDURES Coronary artery bypass graft surgery (CABG) Angioplasty and stent placement [percutaneous coronary revascularization or intervention (PCR OR PCI) ] 29
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STENT PLACEMENT 30
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ROLE OF THE PHARMACIST Ensure adequate supply of medication to the client. Educate client on the state of condition and need for adherence to medication therapy Assist client to identify risk factors that can be modified and help set goals that can promote change in lifestyle to reduce impact of risk factors. Identify any adherence concerns and find solutions. Encourage the client to exercise. Instruct client on healthy diet. Low calorie, low sodium, low fat diet with an increase in dietary fibre. 31
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CONCLUSION AND SUMMARY CAD is defined as the insufficient perfusion of the heart. It leads to a deficiency of oxygen to the heart muscles. CAD has the possibility of resulting in Heart failure and other conditions. Exercising and proper diet could reduce susceptibility to CAD. 32
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REFERENCES Cannon, Christopher P. Vierck, Elizabeth. The New Heart Disease Handbook: Everything You Need to Know to Effectively Reverse and Manage Heart Disease. Beverly, MA: Fair Winds Press, 2009. DeBakey, Michael E. The Living Heart in the 21st Century. Amherst, N.Y.: Prometheus Books, 2012. Kauffman, Kevin. Mayo Clinic Healthy Heart for Life! New York, NY: Time Home Entertainment Inc., 2012 The Standard Treatment Guidelines. Edition 7, 2017. Page 50 33
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REFERENCES Granato, Jerome, E. Living with Coronary Heart Disease: A Guide for Patients and Families. Baltimore, MD: Johns Hopkins University Press, 2008. Crandall, Chauncey. The Simple Heart Cure: The 90-Day Program to Stop and Reverse Heart Disease. West Palm Beach, FL: Humanix Books, 2013. Agyei-Mensah, S. and A. d.-G. Aikins (2010). "Epidemiological transition and the double burden of disease in Accra, Ghana."Journal of urban health 87(5): 879-897. Alwan, A. (2011). Global status report on non-communicable diseases 2010, World Health Organization. 34
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THANK YOU. 35