Cad, Hpn, Hyperlipidemia

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MEDICINE 2 Subject CORONARY ARTERY DISEASE, HYPERTENSION, HYPERLIPIDEMIA Topic Doc Bernie “we’re not worthy” Morantte Jr Lecturer 2nd Shifting 03-sept-08 Shifting /Date goLdi and her still invisible frends Trans group

classmates, ung me mga * un po ung mga side comments ni Doc..

Anatomy of the Coronary Arteries Aorta

LMCA

LCA

Left anterior desc ending

RCA SA nodal artery

Circumflex

Diagonal Bx

Septal perforator

RV branch

I Congenital  Anomalous origin from the pulmonary artery  Anomalous origin from other coronary arteries • Hypoplastic artery • Myocardial bridging • Coronary AV or sinus fistulas

Anomalous Origin of the Coronary Arteries Aorta LMCA

LV branch

Posterior desc ending branch

RCA

Obtuse marginal

SA nodal artery

Postero-lateral

Septal perforator

Posterior descending

• Myocardial perfusion occurs mainly in diastole BP 120/60 Epic ardium

Epicardial artery

Subendocardium Endocardium

LV pressure

Intramural arteries

LV 120 /10

Diastolic pressure gradient = 50 mm HG < 40 mm mean aortic pressure coronary flow is zero.

Regulation of coronary blood flow • Aortic driving pressure which is affected by the presence stenosis in the coronary arteries • LVED pressure • Heart rate and diastolic filling time • Coronary vascular resistance _ from the contraction and relaxation of the smooth muscles • Endothelium derived vasodilator substance which is affected by the presence of atherosclerosis • Myocardial oxygen demand TYPES OF CAD

branch

Diagonal Bx

Obtuse marginal

LV branch

Physiology of Coronary Circulation

Left anterior descending

Circumflex

RV branch

Posterior circumflex

LCA

Postero-lateral

Posterior circumflex

2. Atherosclerotic – most common 3. Non-atherosclerotic  Embolus – Atrial fibrillation, endocarditis, post cardiac valve replacement, atrial myxoma  Drug-induced – ex. cocaine  Vasculitides  Kawasaki  Aortic Dissection Atheroma  Iatrogenic ATHEROMA Foam cells Macrophages Plaque

Smooth muscle proliferation and migration Fibroblast calcification Cross section of an artery

*Atheroma narrows the lumen and degree of narrowing determines if that part of the artery will experience arterial insufficiency MYOCARDIAL BRIDGING

4. ACUTE MYOCARDIAL INFARCTION  ischemia irreversible  angina-like chest discomfort lasting for > 30 mins  assoc. w/ sustained EKG changes & enzymatic evidence of myocardial necrosis  ST and Non-ST MI

Myocardial Bridging Left anterior descending Epicardium

Intramyocardial segment

Endocardi um LV

5. SUDDEN DEATH SYNDROME in tramyocardial segment  not important unless tachycardia develops  Tx: β-blockers to prevent tachycardica and advise patients to refrain from strenuous activities

Aortic dissection Aorta

LCA LMCA

RCA SA nodal artery RV branch

LV branch

Posterior desc ending branch

Clinical Syndromes of Coronary artery disease (CAD) Mechanism Angina

•• ••

Unstable Angina ( PreUnstable Pre-infarction infarction angina) angina)

••

Ac ute MI Acute

plaque plaque rupture rupture dissec tion, hemorrhage dissection, non -Q wave MI nonMI (subendocardial or or nonnon- STEMI)

Left anterior desc ending

Circumflex Septal perforator

Postero-lateral

Q wave wave MI ( transmural transmural or or STEMI ST EMI )

thrombosis thrombosis total occlusion

sudden sudden death syndrome syndrome acute pulmonary edema (( Killip’ss class class III) cardiogenic shock ( Killips Killips class class IV) cardiac rupture

D iagonal Bx

Obtuse marginal

Chronic Chronic stable >> 50 % stenosis s tenosis (x (x--area) area) Variant angina ( Prinzmetal) Prinzmetal) ccoronary oronary spasm

••

- sudden CV collapse with loss of BP and heart beat

Posterior circumflex

MYOCARDIAL ISCHEMIA Is the imbalance between the oxygen supply and the myocardial demand for oxygen resulting in some reversible cellular changes in the sarcolema.

P.E. FINDINGS - transient  disappears when angina resolves - coincides w/ anginal attack - transient murmurs  in mitral regurgitation - if did not disappear  heart attack

CLINICAL SYNDROMES OF CAD 1. CLASSIC ANGINA (Angina pectoris)  chest discomfort resulting from myocardial ischemia d/t coronary blood flow insufficiency related to physical exertion and relieved by rest most common presentation is transient ST depression in EKG

HEART ATTACK infarction necrosis necrotic area will heal (fibrosis) rupture impulse)

2. VARIANT ANGINA  chest discomfort characteristic of angina occurring at rest associated with transient ST elevation in EKG 3. UNSTABLE ANGINA new onset, prolonged chest pain (20-30 mins), acceleration of angina, failure to respond to medical therapy

dead tissue (no

Chest pain EKG

normal Non-c ardiac or Angina

ST depression transient angina

persistent Subendocardial infarction

ST elevation transient

persistent

Variant or Prinzmetal

Ac ute MI

Subacute

old

cardiac tamponade heart does not function properly * clear, shrap, tearing pain  Aortic Dissection * constricting, heavy, preasure-like  heart attack * usually, if patient goes to clinic and angina is already resolved, EKG would most likely be normal so do Exercise Test then check EKG Old Heart Attack - only an abnormal Q wave is seen (permanent) - Long Time  accdg to doc morantte is 2 mos or longer *it takes ST waves 2 mos to normalize! *cardiac enzymes should go up to 2x the normal value * frequency of heart attack depends on the status of the coronary artery INCOMPLETE HEART ATTACK - C.A. stenotic by 75% but goes into spasm may be prolonged  necrosis RISK FACTORS MAJOR Hyperlipidemia HPN DM Cigarette smoking Others Obesity C-reactive protein physical inactivity hypothyroidism (+) Family Hx Acromegaly Homocysteinuria/Homocystenemia Hypertriglyceridemia *CAD begins at 40…. in males *35 y/o pt with chest pain = 5% probability of IHD DIFFERENTIAL DIAGNOSIS OF AMI  Does the patient with chest pain need to be in the hospital? Patients with Unstable Angina and AMI  need not be hospitalized Hospitalization

Outpatient Work-up

1. Pulmonary emboli 2. Aortic dissection 3. Acute myopericarditis with arrhythmia 4. Serious trauma

Acute pericarditis HOCM Prolapse of MV Costochondritis ( Tietze’s syndrome) Reflux esophagitis / Esophageal spasm Drug induced myocardial ischemia Aortic stenosis Mild chest trauma

Are the diagnostic test you are contemplating available on an outpatient basis?

NB: After 3 days: CPK (normal)  CPK increases w/in the 1st 6 hrs, Peaks at 2448 hrs, then decreases by the 3rd day Troponin (elevated)  Troponin I increases w/in the 1st 6hrs and STAYS ELEVATED FOR 1 WEEK After 1 week  both markers will be NORMAL DIAGNOSTICS  CHRONIC STABLE ANGINA  EKG (70% accurate) CXR  to know if there is cardiomegaly w/c is a risk factor for CHF  Lipid Chemistry Panel Echocardiogram for those w/ heart murmur  Exercise Testing with or without Myocardial Perfusion Scan  UNSTABLE ANGINA  Above test except for exercise testing  Cardiac enzymes  CPK isoenzymes  Troponin I  Persantine technitium or thallium scans  Coronary angiogram  ACUTE MYOCARDIAL INFARCTION  EKG  Chest x-ray  Cardiac enzymes • CPK isoenzymnes • Troponin I  Coronary angiogram if acute intervention is • planned  Chest CT scan to exclude aortic dissection if • suspected.

**Presentation of Heart Attack (in 50%)  pressure feeling in the chest  constricting  arms feel heavy  choking in the neck *DM due to peripheral neuropathy (decreased ability to sense pain)  may have a heart attack without chest pain *Unstable Angina  no exercise Test RISK STRATIFICATION of CAD  common denominator of patients with high risk for MI and Sudden death 1. Significant multivessel CAD 2. Impaired left ventricular function . Myocardial Perfusion Scans – multiple perfusion defects DIAGNOSTICS HIGH RISK Treadmill Findings 1. 2mm of ST depression at low level exercise 2. ST segment elevation 3. Ventricular Tachycardia Echocardiography 1. EF < 50% with wall motion abnormalities 2. Radionuclide Left Ventriculography *wall motion abnormalities 3. Coronary Arteriography *significant mutivessel disease EF< 50%

LOW RISK normal

<2mm of ST depression at high level exercise EF > 50% with normal wall motion normal wall motion

Single vessel disease and normal EF except for LAD

TREATMENT of CHRONIC STABLE ANGINA I. Risk factors modification II. Medical Rx A. Nitrites 1. Sublingual nitroglycerin – 0.2 – 0.6 mg 2. Nitro spray 3. Oral a. Isosorbide dinitrate (5-20 mg q 4h off 8h) b. Isosorbide mononitrate (20 mg BID 7h apart) 4. Nitroglycerin ointment ½ inch – 2 in q 6h off at night 5. Nitro Patch (0.1 – 0.6 mg/h off at night) B. β-Blockers 1. Metoprolol (25 – 50 mg BID to 400 mg daily)

2. 3. 4. 5. 6.

Atenolol (25 – 100 mg daily) Acebutalol (200 mg up to 1200 mg Pindolol (5mg – 40mg BID) Betaxolol (5 mg – 40 mg daily) Bisoprolol (50 mg - mg daily )

C. Calcium-channel blockers – available in sustained release forms 1. Diltiazem_ 30 mg TID up to 360 mg / day 2. Verapamil _ 80 mg TID : start at 40 mg when EF is low 3. Bipridil _ 200- 400 mg.: watch for QT prolongation D. Anti-platelet drugs - Aspirin or clopidogrel Therapy in Unstable Angina 1. Supportive Rx a) mild sedation b) oxygen for hypoxemia 2. IV nitroglycerin 3. IV Heparin ( UHF) or LMWH 4. Anti-platelet Rx a) ASA b) Abicisimab 0.25 mg/ kg bolus then c. 0.125 mg / kg for 12 hours 5. Betablockers 6. Anti-arrhythmic therapy for A-fib, SVT and Vtach 7. which may include DC cardioversion 8. Followed by diagnostic work up for risk stratification which may include coronary angiography. INVASIVE TECHNIQUES 1. Percutaneous Interventions  Balloon Angioplasty (PTCA)  Coronary Stent  Atherectomy  Lasers 2. Coronary Artery Bypass Surgery  Thoracotomy • Saphenous vein grafts • Internal mammary artery graft  one of the most effective bypass procedure esp in LAD • Other arterial conduits  Closed angioscopically guided bypass surgery ACUTE MYOCARDIAL INFARCTION I. Window of Opportunity A. Thrombolytic Rx – w/in 6 hrs Any of the ff:

1. TPA 100 mg IV in 3 divided doses, 15 mg IV bolus, then 50 mg over 30 mins, then 35 mg over 1 hr 2. Reptelase 10 units IV bolus, then 10 units in ½ hr 3. Tenecteplase 40 mg IV bolus Single Dose 4. IV Streptokinase drip

II. Medical Therapy III. ACE-inhibitors for ventricular IV. Hemodynamic monitoring V. Treatment of complications such as VI. Cardiac rehabilitation and risk factor Rx COMPLICATIONS OF AMI and THERAPY 1. Hypotension – IV inotropic agents (IV DRIP) Dobutamine, Dopamine  generally used Amrinone 2. CHF – IV Furosemide 3. Bradycardia – Atropine and temporary pacemaker 4. 2nd & 3rd degree AV block – temporary pacemaker 5. Acute pulmonary edema – assisted ventilation and IV Furosemide 6. Cardiogenic shock – Intra-aortic balloon pump to relieve the workload on the heart while it is recovering 7. RV infarction – IV fluids hydration 8. Acute Pericarditis / Dressler’s Syndrome* – NSAID / Prednisone *autoimmune response to MI necrosis/ damage 9. Ventricular Aneurysm and Systemic Embolization – IV heparin followed by Coumadin 10. Ruptured papillary muscle – acute MR 11. Acute Ventricular Septal Defect (VSD) 12. Cardiac rupture *ung last 3 alang therapy na nakaindicate.. *Bypass surgery a.k.a. Saphenous Vein Bypass Graft (double bypass, triple bypass, quadruple bypass) --------end of CAD lecture-------

HYPERTENSION

Hypertension Blood Pressure Arterial vascular resistance

Cardiac output Stroke volume and heart rate

Ventricular contractility Preload

Fluid Balance

I ntake

B. Primary PTCA or PCI – 4 hrs  maximum benefit is obtained when performed within 1 hr of chest pain

GI TRACT

WATER EXCRETION

thirst

PATHWAY Intravascular volume

vein

osmolality Hypothalamus

cathecolamine

adrenal RH

glocucorticoid aldosterone

ACTH Pituitary AVP

Na/ K

ANF Heart

Angiotensin I I ACE Angiotensin I

CO

Liver angiotensinogen Kidney

Renin

VR

artery

WATER CONSERVATI ON PATHWAY

Urine output

FLUID BALANCE • Water excretion is dependent on the heart because it controls hydrostatic pressures. • Water conservation is controlled by the adrenal gland and the pituitary by their role in osmotic pressure regulation. • Normal kidneys respond to changes in both the hydrostatic and osmotic pressures

DEFINITION: BP > 140/90 at rest x 4 Questions: 1. What type of hypertension? Systolic Diastolic 2. Is ir transient or sustained? 3. Is it reversible or irreversible? 4. Is it primary or secondary? SYSTOLIC HYPERTENSION • High cardiac output conditions: a. Severe anemia b. Arterio-venous fistulas c. Hyperthyroidism d. Fever e. Paget’s disease f. PDA SEVERITY OF HYPERTENSION • Diastolic pressures: Borderline 86 – 90 mm Hg. Stage I Mild 91- 105 Stage II Moderate 106- 115 Stage III Severe > 115 TRANSIENT REVERSIBLE HYPERTENSION

1. Stress induced 2. White coat syndrome 3. Initial response to dehydration or loss of blood volume 4. Sympathomimetic drugs REVERSIBLE HYPERTENSION 1. Congenital a. Coarctation of the aorta b. Renal artery stenosis ( fibromuscular) 2. Drug induced - amphetamines, cocaine 3. Tumors of the thyroid, adrenal, and pituitary glands 4. Pre-eclampsia / eclampsia 5. Renal insufficiency in children Hypertension Primary ( Unknown) - Essential 92- 94 % of patients Secondary a. Renal - Parenchymal Renovascular_ atherosclerotic b. Adrenal - Primary aldosteronism Cushing’s syndrome Pheochromocytoma c. Pituitary - Acromegaly d. Hyperthyroidsim e. Hyperparathyroidism f. Miscellaneous - oral contraceptives drugs - amphetamines, cocaine Immune connective tissue diseases g. Neurogenic - increased intracranial pressure, psychogenic HISTORY 1. Duration of hypertension 2. Use of illicit drugs and alcohol 3. Identify transient causes of hypertension 4. Other risk factors for vascular disease 5. Prior History of CVA, MI 6. Family history 7. Prior medicines including oral contraceptives 8. Allergies and side effects PHYSICAL EXAMINATION Aim or Goal: To find signs of reversible causes of hypertension such as: a. bruits b. difference in BP in the 4 extremities c. systolic murmur along the aorta d. physical signs of endocrinopathy 2. Assess the severity 3. To determine target organ damage a. Presence of retinopahty . b. Cardiomegaly c. Signs of water retention

4. Others such as signs of connective tissue disease DIAGNOSTIC STUDIES To determine cause: 1. Renal Parenchymal: Urinalysis_ microalbuminuria, electrolytes 2. Renovascular: Renal scan to determine difference in kidney size, renin levels, aortography 3. Pheochromocytoma : 24 hour urine for cathecholamine levels 4. Aldosteronism: serum electrolytes and aldosterone levels 5. Cushings: cortisol level and dexamethasone suppression test 6. Thyroid: T3, T4, TSH 7. Hyperparathyroidism: serum calcium 8. Acromegaly: GH level following glucose load Diagnostic tests to determine target organ damage 1. Serum BUN and creatinine, glucose 2. EKG 3. Chest x-ray 4. Echocardiography * The above test are used to follow the success of the therapy THERAPY FOR ESSENTIAL HYPERTENSION Non-pharmacologic: 1. Salt restriction - benefits 30% of patients 2. Stop cigarette smoking 3. Weight reduction ( achieve normal BMI) 4. Stress reduction and lifestyle changes 5. Preferably no alcohol Pharmacologic I. Monotherapy - thiazide diuretics , βblockers II. Others: a. Alpha blockers - Prazocin, Terazocin, Doxasocin b. ACE inhibitors - Catopril, Enalopril. Lisinopril c. Angiotensin receptor blockers Losartan,Candesartan, Irbesartan d. Calcium channel blockers - Diltiazem, Verapamil e. Dihydropyridines - Nifedipine, Amlodipine, Filodipine, Isradipine f. Centrally acting agents - Clonidine (transdermal), Guanabenz and Methyldopa g. Peripheral dilators - Hydralazine, Minoxidil

h. Potassium sparing diuretics - Aldactone, Triamterene III. For hypertensive crisis - IV nitroprusside Sublingual nifidipine Choice of Antihypertensive medications: 1. Presence of contraindications 2. Cost 3. Ease of taking the medications 4. Development of side effects *most common cause of Hypertensive crisis is SUDDEN WITHDRAWAL FROM HPN MEDS *Diabetes mellitus is the #1 cause of kidney failure *acute renal failure causes BP to increase --------end of HPN lecture------yey.. last lec na.. weee.. HYPERLIPIDEMIA FACTORS AFFECTING LIPID LEVELS: a. Dietary intake b. Lipid absorption in the GIT c. Clearing of chylomicrons d. activity of lipoprotein lipase e. endogenous production of lipids by the liver f. reverse transport by HDL g. LDL receptors in the liver CRITERIA: 1. Total Cholesterol > 200 mg/dL 2. LDL > 100 mg/dL 3. HDL < 55mg/dL females ; <40 mg/dL in males 4. TG > 200 mg/dL * 2 samples are required *samples taken during stressful situations such as trauma, AMI, abnormal hydration status, cannot be used as baseline. FORMULA:

LDL = TOTAL CHOLESTEROL – HDL – TG/5 TYPES: (based on lipid molecule) 1. Chylomicrons 2. VLDL 3. IDL 4. LDL 5. Triglycerides 6. Lipoprotein A *for blood that is sitting for some time, the serum will be cloudy/milky d/t chylomicrons CONDITIONS THAT CAUSE ELEVATED LIPIDS 1. obesity VLDL is 

2. OCP VLDL is  3. alcohol VLDL is  ACQUIRED CAUSES of HYPERLIPIDEMIA HYPOTHYROIDISM LDL  NEPHROTIC LDL  SYNDROME RHEUMATIC VLDL LDL  FEVER  ACUTE HEPATITIS VLDL  ACUTE VLDL PANCREATITIS  PRIMARY BILIARY VLDL CIRRHOSIS  HISTORY and P.E. 1. Family Hx of Hyperlipidemia 2. Presence of xanthomas 3. Arcus senelis 4. Xanthelasmas (low specificity) 5. bruits 6. diminished peripheral pulses suggests vascular dse 7. gangrene THERAPY Goal: LOWER: LDL < 100 mg/dL for Px w/ MI, CVD LDL < 130 mg/dL for Px w/ one risk factor LDL < 160 mg/dL Px w/ No risk factor TG to < 200 mg/dL INCREASE HDL to NORMAL NON-PHARMACOLOGIC 1. Diet Therapy: 200 mg cholesterol / day Saturated fat < 7% Polyunsaturated fat to 10% Monosaturated fat 20% 2. Weight reduction (achieve normal BMI) 3. Exercise Program 4. Treat risk factors for CVD PHARMACOLOGIC 1. Bile Acid sequestration – Cholestyramine, Colestipol (*side effect: constipation) 2. Niacin 3. Fibric Acid – Gemfibrozil (eto ung mga Lipigem Lipizile, Lopid), Fenofibrate (Fenogal, Lipanthyl) 4. HMG-CoA reductase (statins) side ffects: drug-induced hepatitis, myalgia, myositis

5. Esitimibe (eto ung nakalagay sa lec ni doc) pero di ko cya mahanap.. kaya feeling ko EZETIMIBE ung drug EZETIMIBE – brand name: Ezetrol; alone or in combination w/ statins or fenofibrate for the reduction of total or LDL cholesterol.. aun lng.. -----Owari----This is the beginning of a new day. You have been given this day to use as you will... You can waste it or use it for good. What you do today is important because you are exchanging a day of your life for it. When tomorrow comes, this day will be gone forever. In its place is something you have left behind... Let it be something good" -Unknown