CARDIOVASCULAR PHARMACOLOGY

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CARDIOVASCULAR PHARMACOLOGY
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2015-03-16 14:30:26
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CARDIOVASCULAR PHARMACOLOGY
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  1. Which drugs have negative chronotropic effects → ⇩heart rate?
    • β-blockers (metotrolol, atenolol)
    • Ca2+ channel blockers- verapamil, diltiazem
    • Digoxin
    • Amiodarone and Soltalol (class III antiarrythmics)
    • Cholinergic agonists (Pilocarpine, rivastigmine)
  2. How do we calculate cardiac output?
    • CO = Stroke volume X Heart rate
    •      = rate of O2 consumption/ (arterial O2 content- venous O2 content)
  3. What is the cause of change depicted by the dashed line?
    • Anaphylaxis 
    • Causes widespread venous and arteriolar dilation along with increased capillary permeability ⇩venous return

    • Cardiac contractility also increase as the body attempts to maintain blood pressure.
  4. What is the cause of change depicted by the dashed line?
    • Myocardial infarction
    • Decrease in cardiac output due to loss of contractility
  5. What is the cause of change depicted by the dashed line?
    • Excessive hydration 
    • ⇧in blood volume
  6. What is the cause of change depicted by the dashed line?
    Hemorrage
  7. What is the cause of change depicted by the dashed line?
    • Chronic anemia- increases cardiac output to meet metabolic demands of the tissues.
    • ⇧ venous return occurs due to ⇩blood viscosity.
  8. What corresponds to the opening snap in mitral stenosis?
    C- opening snap- mitral stenosis
  9. Which antiarrythmic drug causes the change below?
    • Class III antiarrythmics
    • Amiodarone
    • Ibutilide
    • Dofetilide
    • Sotalol
  10. What are the adverse effects of the use of Sotalol?
    • Soltalol is a beta-blocker with a class III (K+ blocking) antiarrrythmic properties
    • Torsades de pointes
    • Excessive β blockade
  11. What is the MOA of Sotalol?
    Beta blocker with class 3 (K+ channel blcoking) antiarrythmic properties
  12. What are the effects of carotid massage?
    • Causes reflex vagal discharge to the SA node, atrial myocytes and AV node → ⇩heart rate and cardiac output
    • Note: PaO2 and PaCO2 are NORMAL
  13. What is the most effective agents for the treatment of hypertriglyceridemia?
    • Fibrates:
    • Gemfibrozil
    • Clofibrate
    • Bezafibrate
    • Fenofibrate
  14. Which lipid lowering agents are the most useful in lowering triglyceride levels?
    • Fibrates:
    • Gemfibrozil
    • Clofibrate
    • Bezafibrate
    • Fenofibrate
  15. How do fish oil supplements acts as a lipid lowering agent?
    Fish oil supplements contain omega-3 fatty acids which are used in the treatment of hypertriglyceridemia
  16. What are the effects of Fibrates- Gemifibrozil, Clofibrate, Bezafibrate, Fenofibrate on each of the following:
    LDL
    HDL
    Triglycerides
    • LDL:⇩
    • HDL: ⇧
    • Triglycerides: ⇩⇩⇩
  17. What are the effects of Niacin on each of the following:
    LDL
    HDL
    Triglycerides
    • LDL:⇩⇩
    • HDL: ⇧⇧
    • Triglycerides: ⇩
  18. What are the effects of Ezetimibe on each of the following:
    LDL
    HDL
    Triglycerides
    • LDL:⇩⇩
    • HDL:  ↔
    • Triglycerides: ↔
  19. What are the effects of Bile acid resins - Cholestyramine, Colestipol, Colesevelam) on each of the following:
    LDL
    HDL
    Triglycerides
    • LDL:⇩⇩
    • HDL:  Slightly ⇧
    • Triglycerides: Slightly ⇧
  20. What are the effects of HMG-CoA reductase inhibits - STATINS on each of the following:
    LDL
    HDL
    Triglycerides
    • LDL:⇩⇩⇩
    • HDL:  ⇧
    • Triglycerides:  ⇧
  21. What can be used to close the PDA?
    • Indomethacin, NSAIDS
    • Inhibit PGE1 synthesis
  22. What is the effect of indomethacin on the PDA?
    Closes the PD by inhibiting PGE1 synthesis
  23. What can be used to maintain a PDA?
    Prostaglandins (PGE1)
  24. What are the effects of prostaglandins on the PDA?
    Closes the PDA
  25. What is the agent of choice for prevention and treatment of post-myocardial infarction arrythmias?
    Lidocaine- affect ischemic/ depolarized tissue
  26. Which drug has the highest selectivity for ischemic myocardium compared to normal cardiac tissue?
    Lidocaine- class IB
  27. Vasculitis 2o to IgA immune complex deposition is characteristic of?
    Henoch-Schonlein purpura
  28. Describe the symptoms of Henoch-Schonlein purpura.
    • Skin: palpable purpura on buttocks/ legs
    • Althralgias 
    • GI: abdominal pain
  29. What is the action of glitazones?
    ⇧insulin sensitivity by binding to peroxisome proliferator activated receptor gamma (PPAR-gamma)
  30. What is the action of Pioglitazone?
    ⇧insulin sensitivity by binding to peroxisome proliferator activated receptor gamma (PPAR-gamma)
  31. What is the action of Rosiglitazone?
    ⇧insulin sensitivity by binding to peroxisome proliferator activated receptor gamma (PPAR-gamma)
  32. What is the action of Thiazolinediones?
    ⇧insulin sensitivity by binding to peroxisome proliferator activated receptor gamma (PPAR-gamma)
  33. These drugs increase insulin sensitivity by binding to peroxisome proliferator activated receptor gamma (PPAR-gamma).
    • Glitazones/ Thiazolinediones
    • Pioglitazone
    • Rosiglitazone
  34. What are the side effects of Glitazones?
    • Weight gain, edema
    • Hepatotoxicity
    • Heart failure
    • ⇧risk of fractures
  35. Fluid retention, with resultant weight gain and edema, is common side effect of which diabetes drug?
    Glitazones- weight gain and edema
  36. Lactic acidosis is a common complication of which diabetes drug?
    Metformin
  37. Label the diagram below.
    • 1. Mital valve opens
    • 2. Ventricular filling
    • 3. Mitral valve closes
    • 4. Isovolumetric contraction
    • 5. Aortic valve opens
    • 6. Ventricular ejection
    • 7. Aortic valve closes
    • 8. Isovolumetric relaxation
    • 9. Stroke volume
  38. What does a change in the dashed line below mean? What can cause such a change?
    • ⇧ ventricular PRELOAD.
    • The rightward shift of the ventricular filling indicates a larger than normal volume is being placed into the ventricule during diastole. 
    • This can occur during any state of fluid overload: 
    • Renal failure
    • Congestive heart failure
    • Infusion of intravenous fluids- e.g. normal saline infusion
  39. What does a change in the dashed line below mean? What can cause such a change?
    • Increased contractility
    • e.g. Dobutamine infusion
    • Higher pressures would be reached during the ventricular ejection phase and a greater volume of blood would be ejected during contraction.
  40. What does a change in the dashed line below mean? What can cause such a change?
    • Increased afterload
    • E.g Clamping of aorta
  41. What is the role of platelets in the pathogenesis of Atherosclerosis?
    • Platelet-derived growth factor (PDGF) is released by locally adherent platelets, dysfuncitonal endothelial cells and macrophages to promote migration of SMOOTH MUSCLE CELLS.
    • Platelets also release TGF-B which is chemotactic for smooth mucle cells and induces collagen production
  42. In the pathogenesis of atherosclerosis, what causes migration of smooth muscle cells from the media into the intima?
    • PDGF
    • FGF
  43. What are the bile acid resins?
    Cholestyramine, Colestipol, Colesevelam
  44. What are the bile acid resins and how do they work?
    • Cholestipol, Cholestyramine, Colesevelam
    • They work by binding to bile acid in the GI, preventing its circulation.
  45. How do the values of these change in the use of Bile acid resins? LDL, HDL, TRIGLYCERIDES
    • LDL:⇓⇓
    • HDL: Slightly⇑
    • TRIGLYCERIDES: Slightly ⇑
  46. Which lipid lowering agens should be used in caution in patients with preexisting galbladder disease?
    • Bile acid resins: Cholestyramine, Colestipol, Colesevelam
    • Fibrates: Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate
  47. What does the T wave represent?
    Ventricular repolarization
  48. What represents ventricular repolarization on the ECG?
    T wave
  49. What does a T wave inversion indicate?
    Recent MI
  50. What is the normal duration of the QRS complex?
    Less than 120 msec
  51. What causes a widened ORS complex?
    • 1. Right bundle branch block
    • 2. Fasicular block
    • 3. Pacemakers
  52. What is the most common cause of aortic stenosis ?
    Early onset calcification of aortic valve leaflets/ bicuspid valve leaflets.
  53. Early onset of calification of bicuspid aortic valve leaflets is associated with which pathology?
    Aortic steonosis
  54. Describe the presentation of Aortic stenosis
    • Syncope- lightheadedness
    • Angina
    • Dyspnea
  55. Describe the heart murmur of an aortic stenosis
    Systolic ejection murmur that radiates to the carotids
  56. Myxomatous degeneration of the mitral valve leaflets can cause?
    Mitral valve prolapse
  57. What is the pathology seen below?
    • T wave inversion- Indicates recent MI
    • T wave represents ventricular repolarization
  58. Label the heart murmurs which are best heard at each point.
  59. Right sided endocarditis involving the tricuspid valve is most often due to?
    • S.aureus
    • Commonly occurs in IV drug users
  60. Tricuspid valve endocarditis is associated with ?
    IV drug abuse
  61. At what location is the aortic heart sound best heard?
    Second right intercostal space at the right sternal boarder.
  62. This heart sound is best heard at the second right intercostal space at the right sternal boarder.
    Aortic valve
  63. At what location is the pulmonic valve best heard?
    Second left intercostal space at the left sternal boarder
  64. This heart valve is best heard at the second left intercostal space at the left sternal boarder
    Pulmonic valve
  65. At what location is the tricuspid valve best heard?
    Fourth left intercostal space at the lower left sternal boarder
  66. This heart valve is best heard at the fourth left intercostal space at the lower left sternal boarder.
    Tricuspid valve
  67. At what location is the mitral valve best heard?
    Fifth left intercostal space, medual to the mid-clavicular line
  68. This heart valve is best heard at the fifth left intercostal space, medial to the mid-clavicular line.
    Mitral valve.
  69. What is the mechanism of Nitroprusside?
    Venous and arterial vasodilator that decreases both preload and afterload by ⇧cGMP by direct release of nitric oxide.
  70. Name the Class 1A antiarrythmics.
    • Double Quarter Pounder
    • Dysopyramide
    • Quinidine
    • Procainamide
  71. Name the Class 1B antiarrythmics.
    • Lettuce Tomato Mayo
    • Lidocaine
    • Tocainide
    • Mexiletine
  72. Name the Class 1C antiarrythmics.
    • More Fries Please
    • Moricizine
    • Flecainide
    • Propafenone
  73. Which antiarrythmic drugs produces the change seen in the red curve in the action potential of a ventricular muscle cell?
    • Class 1A antiarrythmics
    • Double Quarter Pounder
    • Disopyramide
    • Quinidine
    • Procainamide
  74. Which antiarrythmic drugs produce the change seen in the red curve of the action potential of a ventricular muscle cell?
    • Class 1B
    • Tomato Lettuce Mayo
    • Tocainide
    • Lidocaine
    • Mexiletine
  75. Which antiarrythmic drugs produce the change seen in the red curve of the action potential of a ventricular muscle cell?
    • Class 1C antiarrythmics
    • More Fries Please
    • Moricizine
    • Flecainide 
    • Propafenone
  76. This drug prolongs phase 3 repolarization of the ventricular myocyte.
    • Shortens the AP
    • Class 1A
    • Double Quarter Pounder
    • Dysopyramide
    • Quinidine
    • Procainamide
  77. This drug shortens phase 3 repolarization of the ventricular myocye.
    • Shortens the AP
    • Class 1B
    • Lettuce Tomato Mayo
    • Lidocaine
    • Tocainide
    • Mexiletine
  78. This drug slows phase 0 of the ventricular myocyte action potential.
    • Class 1C
    • More Fries Please
    • Moricizine
    • Flecainide
    • Propafenone
  79. How can the S3 heart sound best be heard?
    By having the patient lie in the left lateral decubitus position and fully exhale.
  80. Which cardiovascular malformations are associated with Turner's syndrome?
    • PREDUCTAL coartation of the aorta
    • BICUSPID AORTIC VALVE
    • Aortic dissection
  81. What are the effects of muscarinic agonists on blood vessels?
    • Binding of muscarinic receptors on endothelial cells promote release of nitric oxide, also called endothelium-derived relaxing factor. 
    • NO activates cGMP which causes calcium efflux from the cells.
  82. What is the mechanism of Amiodarone?
    • Class III antiarrythmic 
    • Block K+ channels and inhibit the outward K+ currents during phase 3 of the cardiac action potential, prolonging repolarization and duration of the action potential.
  83. What are the Class III antiarrythmics?
    • Amiodarone
    • Ibutilide
    • Dofetilide
    • Sotalol
  84. What is the risk of Amiodarone causing torsades de pointes?
    Very little risk
  85. Polymorphic ventricular tachycardia is characteristic of?
    Torsades de pointes
  86. What is the pathology seen below?
    Torsades de pointes
  87. Golden yellow or brownish cytoplasmic granules are characteristic of?
    • Either lipofuscin or hemosiderin
    • The prussian blue stain can differentiate the two
  88. What does the Prussian blue stain detect?
    Intracellular iron e.g hemosiderin
  89. The presence of hemosiderin-laden macrophages in pulmonary alveoli indicates?
    Chronic elevation of pulmonary capillary hydrostatic pressures (Pulmonary edema) which is usually the result of LEFT HEART FAILURE.
  90. What causes the formation of heart failure cells?
    Left-sided heart failure→ ⇧pulmonary venous pressure → ⇧ leakage of iron-containing proteins and RBCs into the intersitum Macrophages phagocytize the iron-containing proteins and convert them to hemosiderin 
  91. Dysnea, crackles at lung bases and the presence of an S3 sound suggest?
    Left heart failure
  92. Describe the pathogenesis of Atherosclerosis
    • 1. Endothelial cell dysfunction.
    • 2. Macrophage and LDL accumulation
    • 3. Foam cell formation
    • 4. Fatty streaks
    • 5. Smooth muscle cell migration (involves PDGF and FGF) proliferation, and extracellular matrix deposition
    • 6. Fibrous plaque
    • 7. Complex atheromas
  93. Describe the characteristic of a mitral regurgitation murmur.
    Blowing, holosystolic murmur heard best over the cardiac apex with radiation to the axilla
  94. What accounts for dyspnea in heart failure patients?
    • Diastolic return of blood from the pulmonary circulation to the left atrium is impaired, thereby increasing pressure in the pulmonary veins and capillaries.
    • This causes the transudation of fluid from the pulmonary capillaries into the lung interstitum. 
    • The preence of fluid in the pulmonary intersitium DECREASES COMPLIANCE (Stretch)
  95. Ca2+ channel blocker that can lead to peripheral edema and flushing?
    • Amlodipine, Nifedipine
    • Works on vascular smooth muscle muscle → ⇩ muscle contractility
  96. What is the use of Verapamil?
    Used as a therapy for rate control in atrial fibrillation with rapid ventricular response due to its ability to slow conduction through the atrioventricular node.
  97. What are the most frequent adverse reactions noted with verapamil?
    Constipation and gingival hypertension.
  98. What is the MOA of Nitrates?
    Relax smooth muscle vasculature (dilate veins >>> arteries) through a mechanism where they are metabolized into endothelium derived relaxing factor, also known as nitric oxide. → ⇧cGMP
  99. What is the most common side effect of nitrates?
    Headaches, especially with sublingual nitroglycerin
  100. What is this type of breathing? What causes it?
    • Cheyne strokes-  gradually increasing then gradually decreasing tidal volumes followed by apnea.
    • Seen in Congestive heart failure, ↑intracranial pressure, stroke, brain tumor, traumatic brain injury
  101. What is this type of breathing? What causes it?
    • Kussmaul's respirations (Diabetic Ketoacidosis)
    • Deep and laboured breathing
  102. What type of breathing is this? What causes it?
    • Obstructive sleep apnea
    • Reductions or cessations of airflow with no cyclic variations in tidal volume
  103. What is the pathology seen below?
    Infective endocarditis- valvular vegetations
  104. What are the predispostitions to the development of infective endocarditis?
    Valvular inflammation, damage and scarring
  105. Describe the formation of a valvular vegetation in infective endocarditis.
    Following bacterial binding, tissue factor expression results in PLATELET and FIBRIN depositon and the fomation of a valvular vegetation.
  106. Myxomatous degeneration is common in which diseases and can lead to the development of?
    • Mitral valve prolapse
    • Common in connective tissue disease such as Marfan or Ehlers-Danlos syndrome
  107. What is the function of the ductus arteiosus?
    • Deoxygenated blood from the SVC passes through the RA → RV → pulmonary artery →
    • patent ductus arteriosus → descending aorta 
    • DEOXYGENATED BLOOD BYPASSES THE LUNGS
  108. The ductus arteriosus is an embryonic derivative of?
    The 6th aortic arch
  109. The ductus arteriosus closes shortly after birth secondary to?
    • Decreased prostaglandin E2 (PGE2) levels
    • Increased oxygen concentration
  110. Describe the murmur of a patent ductus arterisosus.
    Continuous machinery-like murmur
  111. What are the effects of Indomethacin on the patent ducuts arteriosus?
    • Closes the PDA 
    • Inibitor of PGE2 synthesis
  112. What does the bulbus cordis form?
    The smooth part (outflow tract) of the left and right ventricles
  113. The embryonic structure forms the smooth part (outflow tract) of the left and right ventricles.
    Bulbus cordis
  114. What does the primitive atrium form?
    Rough/ trabeculated part of the left and right atrium
  115. This embryonic structure forms the rough/ trabeculated part of the left and right atrium.
    Primitive atrium
  116. What does the right horn of the sinus venosus form?
    Smooth part of right atrium (sinus venarum)
  117. This embryonic structure forms the sinus venarum.
    Right horn of sinus venosus - Smooth part of right atrium
  118. This embryonic structure forms the smooth part of the right atrium
    • Right horn of sinus venosus -
    • Sinus venarum
  119. What causes PCWP to greater than LV diastolic pressure?
    Mitral stenosis
  120. What is the MOA of Fenoldopam?
    • Dopamine D1 receptor agonist
    • Arteriolar dilation
    • Improves renal perfusion
    • ↑Natriuresis - loss of Na2+
  121. This drug causes arteriolar dilation, improves renal perfusion and promotes natriuresis.
    Fenoldopam- D1 agonist
  122. What is the MOA of Hydralazine?
    cGMP → smooth muscle relaxation. Vasodilates arterioles
  123. What is the MOA of Nitroprusside?
    cGMP via direct release of NO
  124. What are the dangers of the use of Nitroprusside?
    Can cause cyanide toxicity
  125. This antihypertensive medication can cause cyanide toxicity.
    Nitroprusside
  126. What is the MOA of Nicardipine?
    Dihydropyridine calcium channel blocker that works by blocking calcium channels in the vascular smooth muscle and the myocardium, resulting in relaxation of smooth muscles and coronary arteries.
  127. What are the non-dihydropyridine Ca2+ channel blockers?
    • Verapamil
    • Diltiazem
  128. What does negative chronotropy mean?
    ↓Heart rate
  129. What are effects of non-dihydropyridine Ca2+ channel blockers on the heart?
    • Verapamil
    • Diltiazem
    • ↓Heart rate- Negative chronotropy
  130. Where are peripheral chemoreceptors located and what stimulates them?
    • Located in the carotid and aortic bodies
    • Stimulated by ↓PO2 (<60mmHg)
  131. Where are the central chemoreceptors located and what stimulates them?
    • Located in the medulla.
    • Stimulated by ↑PCO2
  132. The highest oxygen content in the fetal circulation is in the?
    Umbilical vein
  133. The ligamentum teres hepatis is the remnant of the?
    Umbilical vein
  134. What role does the ductus arteriosus play in fetal circulation?
    Shunts blood from the pulmonary artery to the descending aorta.
  135. What role does the ductus venosus play in fetal circulation?
    Blood from the umbilical vein is delivered to the liver, where it bypasses the hepatic circulation via the ductus venosus and enters the inferior vena cava.
  136. Describe the fetal circulation.
    • 1. Blood entering the fetus through the umbilical vein is conducted via the ductus venosus into the IVC to bypass the hepatic circulation.
    • 2. Most highly oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body.
    • 3. Deoxygenated blood entering the RA from the SVC goes: RA → ŽRV → Žmain Pulmonary Artery → Ž patent ductus arteriosus → Ždescending aorta; due to high fetal pulmonary artery resistance (due partly to low O2 tension)
  137. Where do the umbilical arteries originate from?
    Fetal internal iliac arteries
  138. Bounding femoral pulses and carotid pulsations that are accompanied by head bobbing are characteristic of which heart murmur?
    Aortic regurgitation
  139. What are the clinical findings of Aortic regurgitation?
    • Bounding femoral and carotid pulses marked by abrupt distention and quick collapse ("water-hammer" pulses).
    • Some patients exhibit head-bobbing with carotid pulsations (de Musset sign).
  140. What is pulsus parvus et tardus? It is characteristic of which heart murmur?
    • Delayed prolonged carotid pulses
    • Aortic stenosis
  141. What is de Musset sign?
    Head bobbing- Aortic regurgitaion
  142. The left horn of the sinus venosus gives rise to?
    Coronary sinus
  143. Where is the coronary sinus derived from?
    Left horn of the sinus venosus
  144. What is the coronary sinus and what can cause it to dilate?
    • Collection of veins that collect deoxygenated blood from the heart muscle and delivers it to the right atrium.
    • The coronary sinus communicates freely with the right atrium and therefore can become dilated secondary to any factor that causes right atrial dilation eg Pulmonary hypertension.
  145. Describe the blood flow in coronary artery disease in the presence of an MI.
    • In coronary artery disease, vessel occlusion can be passed by the natural existence of collateral vessels that help support blood flow.
    • In the presence of an MI, coronary arterioles vasodilate, diverting collateral blood flow to ischemic areas.
  146. What is coronary steal syndrome and what causes it?
    • Adenosine, Regadenoson (adenosine agonist) and dipyridamole cause coronary steal by vasodilating coronary arterioles in non-ischemic regions. 
    • This results in decreased perfusion pressure within the collateral suppying the ischemic myocardium.
    • May lead to hypoperfusion and worsening of the existing ischemia.
  147. What causes a persistent truncus arteriosus?
    Caused by the abnormal neural crest cell migration through the truncus arteriosus and bulbus cordis to separate the aorta and pulmonary artery.
  148. What causes Transposition of the great vessels?
    Failure of the aorticopulmonary septum to spiral due to abnormal migration of neural crest cells.
  149. What causes Tetraology of Fallot?
    • Abnormal migration of neural crest cells through the truncus arteriosus and bulbus cordis to separate the aorta and pulmonary artery.
    • Results in anterior displacement of the infundibular septum. 
  150. Which heart defects are caused by the abnormal migration of neural crest cells?
    • Tetralogy of Fallot
    • Transposition of the great vessels
    • Truncus arteriosus

    • What does an endocardial cushion defect results in?
    • Failure of the atria and ventricles to separate.
    • Defect in atrioventricular septum.

    • Where are thyroid hormone receptors located?
    • Inside the nucleus

    • Describe the splitting of an Atrial Septal Defect.
    • Wide, fixed spliiting of S2.
    • ASD creates a left to right shunt (because of higher pressure in the left atrium). 
    • This results in increased blood flow through the pulmonary artery, delaying pulmonary closure.

    • What causes Eisenmenger syndrome?
    • Uncorrected left-to-right shunt (VDS, ASD, PDA) causes such ↑ pulmonary blood flow through the pulmonary atery, which results in pathologic remodeling of the vasculature (pulmonary sclerosis).

    • The hypertrophied Right ventricle occurs to compensate and the shunt becomes right-to-left.
    • Causes late cyanosis, clubbing and polycythemia.
  151. β-myosin heavy chain mutation is characteristic of which disease?
    Hypertrophic cardiomyopathy
  152. What type of mutation is seen in Hypertrophic cardiomyopathy?
    β-myosin heavy chain mutation
  153. How do we calculate blood flow through a vessel?
    Q= P1-P2/ R

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