Case triple vessel disease

Case presentation on Triple vessel disease (coronary heart disease)

1. Case Presentation Dipesh Tamrakar MSc. Clin. Biochemistry

2. Case history A 42 years old man from Panauti presented to hospital in Kathmandu with chief complaints of : Chest heaviness radiating to arms and back for 6/7 months back associated with sweating History of surgery for anal fistula No history of DM or HTN Drinker socially (1/2 times a week) Smoker 2/4 cigarettes per day

3. General physical examination GC : conscious, oriented to time, place and person Negative for Pallor, icterus, dehydration, edema, cyanosis, clubbing Height : 165 cm Weight : 65 kg BP : 110/80 mmHg, Pulse : 60 bpm Chest : bilateral equal air entry, no added sounds CVS : S1 + S2 + M0 P/A : soft, non distended, non tender, no organomegaly CNS : grossly intact

4. Lab investigations ??? CBC LFT ECG RFT CARDIAC PROFILE CXR URINE R/E TFT

5. Test Result Reference Range RBC 5.16 4.5 to 6.5 million/ul PCV 44 40 – 54 % Hb 14.6 12.0-16.0 gm/dl MCV 85.3 82.9 - 98 fL MCH 28.3 27-33 pg MCHC 33.2 33-36 % Total leucocyte count 6,450 4000 - 11000/cu mm Neutrophils 59 40-75 % Lymphocytes 35 20-45 % Monocytes 4 2-10 % Eosinophils 2 0-5 % Basophils 0-1 % Platelets 3.13 1.5 – 4.5 lakhs /cu mm

6. Test Result Reference Range Glucose Random 88.0 80 – 140 mg/dl Glucose PP 105.0 80 – 140 mg/dl Urea 25.0 15 - 45 mg/dl Creatinine 1.2 0.5 – 1.4 mg/dl Na + 141.0 135-146 mEq /L K + 4.1 3.5-5.2 mEq /L TSH 6.03 0.35 – 5.50  IU/ml

7. Test Result Reference Range Total Cholesterol 181.0 <200.0 mg/dl HDL Cholesterol 42.0 >45.0 mg/dl LDL Cholesterol 103.0 <100.0 mg/dl VLDL 36.0 Triglycerides 178.0 <150.0 mg/dl SGOT 14.0 <35.0 U/L SGPT 12.0 <40.0 U/L B. Total 0.6 0.3 – 1.2 mg/dl B. Direct 0.1 0.1 – 0.4 mg/dl Alkaline Phosphatase 75.0 <141.0 U/L

8. Test Result Color, Transparency, pH Pale Yellow, hazy, Acidic Protein Nil Glucose Nil Pus cell 1 - 2/ hpf RBC nil Epi cell 6 – 8/ hpf

9. Other investigations ??? CXR CARDIAC PROFILE ECG TFT CALCIUM MG

10. ABDOMINAL USG LIVER, GALL BLADDER, CBD, SPLEEN, PANCREAS, KIDNEY, URINARY BLADDER, PROSTATE: NORMALLY PRESENTED Impression: NORMAL SCAN ECG ST-T CHANGES (INF. WALL)

11. Treadmill Test Exercise Time: 6:30 minutes Max HR attained: 145 bpm Max BP: 150/90 mmHg Max Workload attained: 7.6 METs (Fair Effort Tolerance) ST-T changes noted during exercise & recovery Chest pain during exercise, No Arrhythmia, No PVCs noted Symptoms during exercise: chest heaviness during exercise Haemodynamic response: Normal Final Impression: Test is positive for inducible ischaemia

12. Color Doppler Echocardiography report Chambers & Valves: structurally Normal Inter Ventricular & Atrial Septum: Intact Wall Motion: No abnormality Detected Pericardium: Normal Intracavitary mass: Not Visualized FINAL IMPRESSION: NORMAL ECHO AND DOPPLER STUDY NORMAL LEFT VENTRICULAR FUNCTION

13. Carotid Screening & Intima Media Thickness Study FINAL IMPRESSION : Normal Intima Media Thickness of both Common Carotid Arteries

14. REFERRED TO : SHAHID GANGALAL NATIONAL HEART CENTRE CORONARY ANGIOGRAM REPORT LEFT SYSTEM: LEFT MAIN: Normal LAD: Plaque in proximal & 80% diffuse stenosis in Mid LAD, 85% stenosis in DI LCX: 70 – 80% Stenosis in Distal LCX RIGHT SYSTEM: RCA: 95% stenosis in Mid RCA, 95% stenosis in PDA & 100% in PLV, distal vessel retrogradely fills via left system LAD: left anterior descending artery LCX: left circumflex artery RCA: right coronary artery

15. DIAGNOSIS CORONARY ARTERY DISEASE TRIPLE VESSEL DISEASE (TVD) Along with: Atherosclerosis Angina pectoris Silent ischemia Sub-Clinical Hypothyroidism

16. Other required investigations??? CK-MB Troponin I TFT aTPO antibody

17. Heart Lies within the pericardium in middle mediastinum Behind the body of sternum and the 2nd to 6th costal cartilages In front of the 5th to 8th thoracic vertebrae A third of it lies to the right of median plane and 2/3 to the left Anterior to the vertebral column, posterior to the sternum

18. The Magnitude of the problem Cardiovascular diseases comprise the most prevalent serious disorders in the developed nations. The American Heart Association has reported that in 2002, 62 million Americans—32 million females and 30 million males (i.e., more than one in five persons)— had a cardiovascular disease (including hypertension). The prevalence rises progressively with age from 5% at age 20 to 75% at age 75 years. It has been projected that by 2020 cardiovascular diseases will be the leading causes of death worldwide.

19. Cardiac symptoms The symptoms caused by heart disease result most commonly from myocardial ischemia , from: Disturbance of contraction/relaxation of myocardium Obstruction to blood flow Abnormal cardiac rhythm or rate

20. Diagnosis As outlined by the New York Heart Association , the elements of a complete cardiac diagnosis include consideration of the following: The underlying etiology . Is the disease congenital, infectious, hypertensive, or ischemic in origin? The anatomic abnormalities . Which chambers are involved? Are they hypertrophied, dilated, or both? Which valves are affected? Are they regurgitant and/or stenotic? Is there pericardial involvement? Has there been a myocardial infarction? The physiologic disturbances . Is an arrhythmia present? Is there evidence of congestive heart failure or of myocardial ischemia? Functional disability . How strenuous is the physical activity required to elicit symptoms? The classification provided by the New York Heart Association has been found to be useful in describing functional disability

21. Coronary Artery Disease Narrowing or blockage of the artery or arteries supplying blood to the heart muscle (ATHEROSCLEROSIS) Patients who smoke, or have conditions such as diabetes mellitus, hypertension and high blood cholesterol or fat levels are prone to developing coronary artery disease. The heart has three main coronary arteries. Patients are said to have single, double, or triple-vessel disease, depending on the number of vessels that are narrowed. When the narrowing becomes critical, the patient can develop symptoms such as chest pain or shortness of breath (ANGINA)

22. The cholesterol plaque causing the blockage can sometimes rupture suddenly, causing a blood clot to form. This blood clot will cut off blood supply and cause damage to the heart muscle - myocardial infarction ;“heart attack”. The patient may get severe chest pain, shortness of breath, palpitations, giddiness, cold sweaty hands, and even die suddenly. The severity and prognosis of the heart attack depend on the percentage of the heart muscle damaged. Minor heart attacks usually recover. Major heart attacks can result in long-term heart failure, enlargement of the heart, abnormal heart rhythms, heart valve leakage and even death.

23. TRIPLE VESSEL DISEASE The blood supply to the heart comes from the Right Coronary Artery (RCA) and the Left Coronary Artery - the first two branches of the aorta in the Sinus of Valsalva. The Left Coronary Artery is quite short (often called the Left Main Stem) and divides into the Left Anterior Descending artery (LAD) and the Circumflex artery ( LCx ). Triple vessel disease is the term used for atherosclerotic narrowing of the three major blood vessels of the heart (RCA, LAD and LCx ). Severe triple vessel disease and Left Main Stem stenosis are both associated with imminent myocardial infarction, and so if present surgical (or percutaneous) intervention is recommended.

24. Diagnosis Electrocardiogram (ECG) Echocardiogram Stress test Cardiac catheterization and angiogram Heart scan

25. Treatment Lifestyle and food habit changes Controlling major risk factors of coronary artery disease Medical therapy Aspirin/clopidogrel/ticlopidine Beta-blockers (Atenolol, bisoprolol, carvedilol) Nitrates (isosorbide dinitrate) ACE inhibitors ( enalpril ) & Angiotensin receptor blockers (losartan) Lipid lowering medications (Atorvastatin) Percutaneous Coronary Intervention Surgery (Coronary Artery Bypass Grafting)

26. ATHEROSCLEROSIS The "Response to Injury Theory" now has widespread acceptance among scientific and medical scholars. Endothelial injury can be triggered by: Physical injury or stress: Direct trauma or  hypertension Turbulent blood flow: mainly arteries branch Circulation of reactive oxygen species ( free radicals ): smoking or air pollutants Hyperlipidemia (high blood concentrations of LDL or VLDL ) Chronically elevated blood glucose levels Homocysteinemia : results from an inherited metabolic defect of methionine that leads to very high levels of the homocysteine, high concentrations are toxic to the endothelium by lipid oxidation & platelet aggregation

27. Atherosclerosis plaque formation

28. Atherosclerosis plaque formation

29. Atherosclerosis plaque formation

30. Cigarette smoking  is a leading preventable risk factor for the development and progression of CVDs Epidemiologic studies conclusively prove that both active smoking and secondhand smoke contribute significantly to morbidity and mortality related to CVD. Cigarette smoke is a mixture of several toxic chemicals (>5000) The major vapor phase constituents include  carbon monoxide, acetaldehyde, formaldehyde, acrolein, nitrogen oxides, and carbon dioxide , whereas NICOTINE and various particulate matters (collectively known as “tar”) constitute the major particulate phase components of cigarette smoke. SMOKING & Atherosclerosis

31. Nicotine is a potent ganglionic and CNS stimulant Each puff contains approx 50  g of nicotine It exerts its cardiovascular effect via sympathetic neural stimulation It increases heart rate, blood pressure, cardiac output leading to an increase in myocardial oxygen demand Free radical-mediated oxidative stress may play central role in the development of atherosclerosis Smokers are known to have lower plasma levels of  antioxidants  such as  vitamin C  and  beta-carotene Tobacco causes  endothelial dysfunction, inflammation, insulin resistance, alteration of lipid profile, hemodynamic alterations, and a hypercoagulable state.

32. Cigarette smoke contains a number of metals, including aluminum, cadmium, copper, lead, mercury, nickel, and zinc These metals catalyze the oxidation of cellular proteins leading to Structural cellular damage and endothelial dysfunction Acrolein , a reactive aldehyde produced by endogenous lipid peroxidation, is present in high levels in cigarette smoke. It adversely modifies apolipoprotein A-1, the major protein in high-density lipoprotein (HDL), and leads to oxidation of prominent cellular antioxidant proteins called thioredoxins in endothelial cells It can lead to endothelial cell death and dysfunction Polycyclic aromatic hydrocarbons found in the tar fraction of cigarette smoke are reported to accelerate atherosclerosis in experimental animals All of these act synergistically as patho -biologic mechanisms of  atherothrombosis  in tobacco users.

33. Effects: Vascular and endothelial dysfunction Smoking can damage the vascular wall, leading to impaired prostacyclin production and enhanced platelet-vessel wall interactions This can reduce the elastic properties of the aorta, resulting in stiffening and trauma to the wall Inflammation - Elevations of various proinflammatory cytokines increase leukocyte–endothelial cell interaction leading to leukocyte recruitment Prothrombotic state/hypercoagulable state Effect on lipid profile insulin-resistant and hyperinsulinemic (not fully established) Genetic factors- CYBA  gene A640G polymorphism might influence individual predispositions to CAD through interactions with smoking and hypercholesterolemia

34. HYPOTHYROIDISM & Atherosclerosis Cardiac manifestations of hypothyroidism include a reduction in cardiac output, stroke volume, heart rate, blood pressure, and pulse pressure . In about one-third of patients there is a pericardial effusion which only rarely results in tamponade. Increased capillary permeability results in pleural and pericardial effusions. Other clinical signs include cardiomegaly, bradycardia, weak arterial pulses, and distant heart sounds. Patients with hypothyroidism frequently have elevations of cholesterol and triglycerides, and severe atherosclerotic coronary artery disease.

35. Cholesterol ratio or Non-HDL Cholesterol Cholesterol ratio = Total Cholesterol / HDL Cholesterol Risk ratio higher than 5.0 means a higher risk of heart disease CASE - 4.3 Non-HDL Cholesterol = Total Cholesterol – HDL Cholesterol Optimal level : <130.0 mg/dL (3.37 mmol/L) Higher numbers mean a higher risk of heart disease. Recently, non-HDL cholesterol (non-HDL-C) has become a commonly used marker for a blood lipid pattern associated with increased risk of heart disease. CASE - 139.0 mg/dl

36. BODY MASS INDEX (BMI) BMI is a measure of body fat based on height and weight Formula: weight in kg/ height in m 2 BMI is not used for muscle builders, long distance athletes, pregnant women, the elderly or young children. This is because BMI does not take into account whether the weight is carried as muscle or fat, just the number.  Range: Underweight: Your BMI is less than 18.5 Healthy weight: Your BMI is 18.5 to 24.9 Overweight: Your BMI is 25 to 29.9 Obese: Your BMI is 30 or higher CASE - 23.9

37. SUMMARY Risk factor analysis for above case presumptively suggests the reason for TVD might be: Smoking Sedentary life style & less exercise Food habit Hypothyroidism Some major lab investigations have not been missed like CKMB, cTnI , TFT Sometimes Coronary Artery Disease may not be presented with significant complications as in this case

38. Patient underwent Open Heart Surgery Coronary Artery Bypass Grafting Advices for: Avoid trauma over chest for 6 mths Avoid fatty food, red meat, smoking, alcohol Regular exercise Medications: - Ecospirin - Clopilet - Astat - Amilax - Metloc - Pantop - Paracetamol - Cefadroxyl - Becosule - Vit C

39. THANK YOU