A3 Ischemic Heart Disease. Dr. Black (REVISED)

ISCHEMIC HEART DISEASE (IHD) Medicine 2 Dr. Sofia Black September 13, 2014

MYOCARDIAL OXYGEN SUPPLY 

CLINICAL SCENARIO A 55 y/o female consulted OPD because of effort-related chest pain. She is a known hypertensive, diabetic, previous smoker and non-compliant to medications. Physical exam showed BP= 140/100, CR= 60 bpm, RR 18/min, BMI of 30. ISCHEMIC HEART DISEASE    

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Inadequate oxygen supply Increase oxygen demand Imbalance: supply < demand Myocardial ischemia o Where the imbalance happen o Obstructive atherosclerotic disease of epicardial vessel  Most common cause o Inadequate perfusion of coronaries Previously known as Coronary artery disease o Term used in Europe o In PHIC they accept ischemic heart disease but not CAD

EPIDEMIOLOGY 

Most common, serious, chronic life threatening disease

PATHOLOGY 

Coronary arteries

PATHOPHYSIOLOGY MYOCARDIAL OXYGEN DEMAND   

Heart rate o increase HR → increase oxygen demand on a background of inadequate supply Myocardial contractility o More contraction → increase oxygen demand Myocardial wall stress/ tension o Frank Starling law  Increase LV end diastolic volume  in Left ventricular pressure  increased forceful contractility up to a limit  Overstretching → increase wall tension → increase contractility → increase oxygen demand → failure → will not be elastic → breakage

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Oxygen carrying capacity of blood (by hemoglobin) o Level of inspired oxygen  High altitude → higher elevation → low oxygen o Pulmonary function  Dysfunctional pulmonary system (ex. COPD and bronchial asthma has decrease oxygenation) → secondary Myocardial ischemia o Hemoglobin concentration  Low hemoglobin concentration (ex. anemia) → normal blood flow but oxygen content is low Blood flow: occurs during Diastole o Relaxation  Impairment of relaxation → impairment in the flow and supply o Blood flow goes to coronaries when the heart relaxes o Abnormal Diastolic dysfunction is the EARLIEST SIGN of Ischemia  ECG and contractility may be normal but diastolic function is abnormal → IHD

CORONARY ARTERIES 

3 Large epicardial arteries o Left coronary artery (from the aorta)  Divides into two: (1) Left anterior descending artery and (2) Left circumflex artery o (3) Right coronary artery (from the aorta)  Large epicardial vessels → Obtuse marginal 1 and 2 vessels → Pre-arteriolar arteries → myocardium → Arteriolar and intramyocardial capillary vessels  Orifices that originate from the aorta behind aortic valve o Aortic valve has 3 cusps: Right coronary cusp Where the right coronary artery came from to the right coronary sinus Left coronary cusp Where the Left coronary artery/left main coronary artery came from Non-coronary cusp CONDUCTANCE VESSEL   

Large epicardial coronary arteries Constriction and relaxation Abnormal constriction: o Prinzmetal angina (unknown etiology): Epicardial coronary arteries are abnormally vasospastic without atherosclerosis o No relaxation, remain vasoconstricted (but there’s still a chance to dilate)

RESISTANCE VESSELS 

Major determinants of coronary resistance → coronary flow

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“The absence of evidence is not an evidence of absence” – Carl Sagan

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Smaller vessels from epicardial vessels: o Pre-arteriolar vessels  From obtuse marginal vessels o Arteriolar vessels o Intramyocardial capillary vessels  Intramyocardial arteriole  Abnormal constriction  Seen in Diabetic patients  Failure of dilatation, remain vasoconstricted (NO chance to dilate again)  “Microvascular ischemia” – pathophysiology in diabetic patients Capable of auto-regulation

Side Notes: *coronary angiogram (gold standard for IHD in the past) can show normal results for IHD *microvascular circulation are not seen in coronary angiogram only the large epicardial vessels CORONARY ATHEROSCLEROSIS MAJOR RISK FACTORS (3 FACTORS QUALIFY A PERSON TO BE AT RISK ) MODIFIABLE  Cigarette smoking o Nicotine accelerates the position of cholesterol o Acts as a catalyst: deposit the cholesterol  Hypertension o Sheer stress to capillary wall → endothelial dysfunction  Diabetes mellitus o High sugar → inflammation and endothelial dysfunction  Low HDL  High LDL NON-MODIFIABLE  Family history of premature CHD o Male 30 kg/m2) o Physical inactivity  Endothelial dysfunction o Atherogenic diet #KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

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Emerging risk factors o Lipoproteins: Apo B o Homocysteine o Pro-thrombotic  By Oral contraceptive pills o Pro-inflammatory  Patients with IHD and STD: (+) for Chlamydia on autopsy (plaque contains chlamydia) o Impaired fasting glucose  Slight innervation of fasting blood glucose  Not diabetic yet, waiting to be diabetics, diabetics in the process → increase glucose in the vascular system → intraendothelial dysfunction

INITIATION OF ATHERO SCLEROSIS (IN ORDER) 

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Initial stage: fatty streak formation o As early as 10 years old and above o Fatty stage formation in utero  Maternal blame  cholesterol of the mother goes to the child Lipoprotein oxidation → tunica intima Non enzymatic glycation Leukocyte recruitment Foam cell formation o Leukocytes transforming to macrophages and phagocytize oxidized LDL Atheroma evolution (it takes time) o Involvement of arterial smooth muscle o Blood coagulation thrombosis o Micro vessel formation o Plaque evolution

ATHEROSCLEROSIS A PROGRESSIVE DISEASE

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“The absence of evidence is not an evidence of absence” – Carl Sagan

(Refer to the picture) Atherosclerosis  Progressive disease  “Atheros”: porridge (cholesterol)  “Scleros”: hardening  A lot of oxidized LDL will become a soft porridge → rupture → attract platelet → thrombus formation

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CORONARY ARTERY METABOLIC REGULATION 

Decrease in oxygen carrying capacity o Good supply but the oxygen is depleted o Severe anemia  No hemoglobin to carry oxygen  Free oxygen in the blood cannot be used because it is not bound to Hemoglobin o Carboxyhemoglobinemia  Carbon monoxide (CO) poisoning: competing with oxygen in hemoglobin  Ex. Sleeping inside the car with engine on  Painless death

Regulates oxygen supply CORONARY ATHEROSCLEROSIS

AUTO REGULATION  

Regulates coronary blood flow Vasodilation and vasoconstriction o As long as there are no blockages

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*Coronary arteries extract the most oxygen in the blood for consumption CAUSES OF ISCHEMIA 

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Reduction in the lumen of the coronary artery o Atherosclerosis  Arteries distal to plaque are vasospastic  Decrease lumen → decrease perfusion to myocardium o Coronary artery spasm  Prinzmetal angina o Arterial thrombi  From a ruptured plaque proximally → thrombus dislodge distally → smaller vessels (Intramyocardial vessels) o Coronary emboli from infective endocarditis  Vegetation from right coronary valve → dislodge to right coronary artery  Left coronary valve → left coronary artery Increase oxygen demand with limited blood flow (not totally obstructed) o LVH due to aortic stenosis  Arteries are patent but supply is not enough during systole and diastole due to fixed obstruction in aortic valve o Hypertension  There is Left Ventricular hypertrophy  Increase the demand when there are hypertrophied muscles because the supply is decreasing o Hyperthyroidism  Due to increased HR o Fever  Due to increased HR

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

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Epicardial coronary artery o Major site of atherosclerotic disease Main affectation: Tunica intima Major risk factor: Endothelial dysfunction o Whole cascade of atherosclerosis proceeds o Bottom-line of all the risk factorS o Does not happen overnight o Vasoconstriction o Luminal clot formation o Monocytes and platelet interaction o Atherosclerotic plaque formation  When it ruptured → Acute coronary syndrome  Sub-intimal fat collection  Smooth muscle cell proliferation  Fibroblast and intercellular matrix Major risk factorS o High LDL o Low HDL o Cigarette smoking o Hypertension o DM

*The good cholesterol (HDL), the bad cholesterol (LDL) and the ugly cholesterol (triglycerides) ISCHEMIC HEART DISEASE (AGAIN) 

Critical obstruction: 70% o Myocardial ischemia o Do intervention: angioplasty (single vessel) or bypass (multiple vessel disease) o *But MI can also occur in 60 Chest discomfort (typical) o Retrosternal pain Levine sign o Fist clenched on sternum

*Chest paint equivalent/atypical chest pain ANGINA 

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Cardiac origin o Atypical chest pains in the elderly  Epigastric pain  Choking sensation Crescendo-decrescendo o Crescendo going up; decrescendo going down Duration o 1-5 minutes, 10 minutes at the most Radiation o Below mandible and above the umbilicus o Epigastric pain CAN BE an inferior myocardial infarction (diaphragm irritation) Location o Retrosternal is the MC description

PRECIPITATING FACTOR S   

Exertion Emotion Rest o Chest pains at rest: Severe IHD o Obstruction is severe  Arteries clogged >70%

GRADING OF SEVERITY OF ANGINA CANADIAN CARDIAC SOC IETY CLASSIFICATION

For IHD chest pain STABLE ANGINA PECTORIS   

Episodic clinical syndrome Transient myocardial ischemia o When it becomes persistent it becomes ACS 70% males in before menopausal stage

CLASS I II III IV

ONSET OF CHEST PAIN Chest pain with more than ordinary activity Chest pain on ordinary activity Chest pain on less than ordinary activity Chest pain at rest

*New York Heart Classification: Heart Failure and Chest Pain 4

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

“The absence of evidence is not an evidence of absence” – Carl Sagan

RISK FACTORS 

Modifiable and Non-modifiable

ASSOCIATED COMORBID CONDITIONS  

CVD, TIA, PAD, CKD, stroke Atherosclerosis is not only on the heart but also systemic o Ex. kidneys = renal failure

PHYSCIAL EXAMINATION  

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Most are normal Evidence of atherosclerosis o Abnormal aneurysm o Carotid bruit, PAD o Xanthomas (yellow deposition of the fat), xanthelasmas Risk factors for atherosclerosis

Fundoscopy o

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Atherosclerotic retinopathy  Thick vessel wall o Hypertensive retinopathy  With papilledema  Plain hemorrhages  Copper wiring Signs of anemia and pallor Signs of aortic stenosis o Heart: left ventricular fibrillation and systolic ejection murmurs o Palpation of the radial pulse: Weak pulse

*even if there are normal test proceed to exercise stress testing DIAGNOSTIC TEST OF I HD EXERCISE STRESS TESTING     

Most widely used To prognosticate IHD and in patients for angiogram and bypass Problem: Symptom limited Sensitivity = only 70% are detected (30% are missed) o 85% if with post MI Heart rate limited

CONTRAINDICATON OF E XERCISE STRESS TEST  Angina at rest within 48 hours  Unstable rhythm o Atrial fibrillation and fast ventricular response  Severe aortic stenosis = definite contraindication!!!  Acute myocarditis o Prone to arrhythmias  Unstable heart failure  Active infective endocarditis o Embolization of vegetation *If exercise stress testing is normal but patient still has episodic chest pains proceed to cardiac imaging *Dobutamine Stress Test – for patients who are unable to exercise CARDIAC IMAGING

LABORATORY EXAMINATION 

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ECG o A normal ECG does not rule out disease o Accurate only in 30% o Arrhythmias Chest X-ray o Heart enlargement: sign of Congestion Urinalysis o To know Comorbid diagnostics or risk factors (ex. glycosuria=DM, glomerulonephritis=HTN) Lipid profile o HDL, LDL, TG Blood glucose o FBS: ≥126 = Diabetes o RBS: ≥200 = Diabetes o Impaired blood sugar Hemoglobin/Hematocrit o Anemia

#KAFC #LML #DAB #LGTM #DACM “MEDICINE BATCH 2016”

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Myocardial perfusion scan o Let the patient exercise then inject a radioactive  There is perfusion defect o Physiologic o Once it is normal it means normal o If (-) cardiac scan but (+)myocardial perfusion scan = microvascular ischemia Echocardiography o A normal result does not say you’re really a normal patient o EF: 45, female >55 undergoing valve surgery  For patients with rheumatic heart disease o High risk on stress test  Mets (measure of oxygen consumption)  If result is