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 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

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

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

18. 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

21. 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.

22. 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

23. Diagnosis
• As outlined by the New York Heart Association, the elements of a
complete cardiac diagnosis include consideration of the following:
1. The underlying etiology. Is the disease congenital, infectious,
hypertensive, or ischemic in origin?
2. 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?
3. The physiologic disturbances. Is an arrhythmia present? Is there evidence
of congestive heart failure or of myocardial ischemia?
4. 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

24. 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)

25. • 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.

26. 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.

27. Diagnosis
1. Electrocardiogram (ECG)
2. Echocardiogram
3. Stress test
4. Cardiac catheterization and angiogram
5. Heart scan

28. 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)

29. ATHEROSCLEROSIS
• The "Response to Injury Theory" now has widespread acceptance
among scientific and medical scholars.
• Endothelial injury can be triggered by:
a. Physical injury or stress: Direct trauma or hypertension
b. Turbulent blood flow: mainly arteries branch
c. Circulation of reactive oxygen species (free radicals): smoking or air
pollutants
d. Hyperlipidemia (high blood concentrations of LDL or VLDL)
e. Chronically elevated blood glucose levels
f. 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

30. Atherosclerosis plaque formation

31. Atherosclerosis plaque formation

32. Atherosclerosis plaque formation

33. • 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

34. • 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.

35. • 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.

37. 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

38. 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.

39. 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

40. BODY MASS INDEX (BMI)
• BMI is a measure of body fat based on height and weight
• Formula: weight in kg/ height in m2
• 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

41. 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

42. • 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

43. THANK YOU