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Coronary Hear Disease PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "CORONARY HEART DISEASE" by Satjit Bhusri, MD.

This medical PowerPoint presentation talks about Coronary heart disease (CHD). Coronary heart disease is a medical condition that occurs when there is a build-up of plaque in the walls of the arteries that supply blood to the heart muscle. This build-up of plaque is also known as atherosclerosis and can lead to the narrowing of the arteries, reducing blood flow to the heart muscle. CHD is the leading cause of death worldwide and is responsible for over 7 million deaths annually.

The major risk factors for CHD include high blood pressure, high cholesterol, smoking, diabetes, obesity, physical inactivity, and family history of the disease. Symptoms of CHD can include chest pain or discomfort, shortness of breath, fatigue, weakness, and irregular heartbeat. Some individuals may experience no symptoms at all, which is known as silent CHD.

Tags : Coronary heart disease, arteries, atherosclerosis, cardiology

Published on : Mar 17, 2023 | Views : 894 | Downloads : 2

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CORONARY HEART DISEASE JEFF CHIANFAGNA RPA-C Satjit Bhusri, MD Cardiologist Lenox Hill Hospital
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LECTURE OVERVIEW Chronic Ischemic Heart Disease Chronic Stable Angina Silent Myocardial Ischemia Variant (Prinzmetal’s) Angina Acute Coronary Syndromes Unstable Angina Non-ST-segment elevation MI (NSTEMI) ST-segment elevation MI (STEMI) Sudden cardiac death (SCD)
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CORONARY CIRCULATION Left main  2 branches (LAD & CXA) LAD located in IV groove giving off diagonal & perforating branches CXA goes left & posterior into AV groove RCA in right AV groove  2 branches (marginal & PDA) No connections bt major vessels, however smaller perforating branching arteries are joined by anastomotic channels With gradual large vessel occlusion, smaller collateral vessels  in size
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CORONARY ATHEROSCLEROSIS & PATHOGENESIS OF CAD Atherosclerosis is MC cause of CHD Atherosclerotic plaque disruption is the most common cause of MI More than 90% of pts with CHD have evidence of coronary atherosclerosis Most pts with CHD have 1 or more stenotic lesions of 75% or greater Plaque formation can affect 1 or all of the major epicardial coronary arteries
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STABLE vs. UNSTABLE PLAQUES Fixed (stable) plaques obstruct blood flow & have thick fibrous caps Unstable (vulnerable) plaque have a thin fibrous cap Rupture depends on (1) size of lipid core & thickness of fibrous cap (2) presence of inflammation with plaque degradation (3) lack of SM cells with impaired healing & plaque stabilization Triggers for plaque rupture?
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CHRONIC STABLE ANGINA Definition  symptomatic paroxysmal CP or P sensation due to transient ischemia Associated with fixed coronary obstruction producing a disparity in coronary blood flow & metabolic demands of the myocardium Stable angina is initial manifestation of IHD in 50% of pts with CHD Angina is usually precipitated by situations that  work demands of the heart
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CHRONIC STABLE ANGINA Sxs  CP is steady, heavy, P, squeezing, or suffocating; precordial or substernal with or w/o radiation to L-shoulder, jaw, both arms or other areas of the chest; Levine’s sign Many pts report fixed thresholds for pain onset, others report day to day & time of day variations CP relieved within minutes by rest or SL nitro Anginal “equivalents” are dyspnea, fatigue & faintness
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CHRONIC STABLE ANGINA Risk factors  ??? PE  often normal, but may reveal evidence of atherosclerosis at other sites; fundoscopic may reveal  light reflexes & AV nicking; palpation may reveal cardiomegaly or abnormal PMI; auscultation may uncover bruits, S3, S4 Labs Dx usually made from Hx & PE, however routine labs should be ordered CXR  cardiomegaly? sgs of HF?
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CHRONIC STABLE ANGINA EKG  usually normal at rest unless previous ischemic injury has occurred Stress testing  widely used test for dx of IHD; performed using either standard EKG, echo, or nuclear imaging; monitors sxs, BP, EKG, wall motion defects or perfusion deficits before, during & after physical exercise or pharmacological induced cardiac exertion +EKG stress test  CP, severe SOB or fatigue, dizziness,  in SBP >10 mmHg, ST-segment depression >2mm or an arrhythmia
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CHRONIC STABLE ANGINA Coronary arteriography Indications (1) stable angina with severe sxs despite medical therapy & who are being considered for revascularization (2) sxs that present diagnostic difficulties & there is a need to confirm or r/o IHD (3) pts w/ known angina who have survived cardiac arrest (4) pts w/ angina & evidence of LV dysfunction (5) pts judged to be at  risk of having a coronary event based on stress testing
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CHRONIC STABLE ANGINA Management  education, Tx RF & comorbidities, adaptation of activity, drug therapy, consider revascularization Drug therapy Nitrates  systemic venodilators which  myocardial wall tension & O2 demand B-blockers   O2 demand by inhibiting the  in HR, BP, & myocardial contractility CCB  vasodilators producing Antiplatelet drugs  ASA or Clopidogrel Ranolazine  sodium channel blocker used with a BB or as a substitute for a BB
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CHRONIC STABLE ANGINA Coronary revascularization  performed in pts with severe sxs despite medical therapy & pts with severe ischemia on stress testing Percutaneous transluminal coronary angioplasty (PTCA)  balloon dilatation w/ stent deployment; usually reserved for pts with 1-2 vessel involvement with normal LV function Coronary artery bypass grafting (CABG)  surgical vessel anastomosis using IMA, SV, or RA; indicated in pts with: left main coronary artery stenosis, 3 vessel disease + EF<40%, 2 vessel disease with >75% stenosis in LAD, or vessel blockages that cannot be reached by catheters
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SILENT MYOCARDIAL ISCHEMIA Definition  ischemia without anginal pain Etiology  atherosclerosis or vasospasm 3 populations (1) asymptomatic pts w/o CHD evidence (2) MI survivors that continue to have myocardial ischemia (3) pts w/ angina who also have episodes of silent ischemia Explanation for painless episodes is unclear Can lead to ischemic cardiomyopathy Tx  depends on extent of ischemia, comorbidities, age, occupation, & RF
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PRINZMETAL’S ANGINA Caused by vasospasm of coronary arteries, however in most instances vasospasms occur in the presence of nearby plaques Pathogenesis of vasospasm is uncertain CP usually occurs during rest or may awaken the pt from sleep; serious arrhythmias can occur during anginal episodes Pts are typically younger with fewer CV RFs EKG demonstrates ST-segment elevation Mainstay of tx is SL nitroglycerin & CCBs
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ACUTE CORONARY SYNDROMES (ACS) ACS includes: Unstable angina Non-ST-segment elevation (non-Q-wave) myocardial infarction (NSTEMI) ST-segment (Q-wave) myocardial infarction (STEMI)
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UNSTABLE ANGINA &NON-ST-ELEVATION MI UA defined as CP or angina equivalents with at least 1 of 3 features: (1) occurs at rest (2) severe & new onset (3) more severe, prolonged, or frequent than previously UA referred to as “preinfarction syndrome” NSTEMI is established if a pt with clinical features of UA develops evidence of myocardial necrosis as reflected in elevated cardiac biomarkers
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UNSTABLE ANGINA &NON-ST-ELEVATION MI Pathophysiology  decrease in O2 supply or increase in myocardial O2 demand 4 contributing pathophysiologic processes for UA: (1) plaque rupture or erosion w/ superimposed nonocclusive thrombosis (2) dynamic obstruction due to vasospasm (3) progressive & rapidly advancing atherosclerosis (4)  myocardial O2 demand and/or  supply
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UNSTABLE ANGINA &NON-ST-ELEVATION MI Clinical manifestations  substernal CP w/ radiation to neck, L-shoulder or L-arm; or anginal “equivalents”; PE similar to stable angina & may be unremarkable; with large area of ischemia or NSTEMI, the physical findings can include diaphoresis, pale cool skin, sinus tachycardia, S3, S4, rales, & sometimes hypotension
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UNSTABLE ANGINA &NON-ST-ELEVATION MI EKG  ST-segment depression and/or T-wave inversion Cardiac biomarkers  NSTEMI pts have  CK-MB and Troponin I Diagnostic pathways  clinical hx, EKG, cardiac markers, & stress testing Goals (1) recognize or ROMI (2) evaluate for rest ischemia (3) evaluate for significant CAD
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UNSTABLE ANGINA &NON-ST-ELEVATION MI Medical Tx  anti-ischemic & antithrombotic Anti-Ischemic Tx Nitrates  SL 1st, if pain persists after 3 doses given Q5 minutes, then IV nitro should be given B-blockers  IV Metoprolol followed by PO with a targeted HR of 50-60 bpm CCBs  (Verapamil or Diltiazem) recommended in pts who have persistent or recurrent sxs after full dose nitrates & B-Bs or any C/I to B-Bs If pain persists, then administer morphine sulfate ARBs or ACE-I & statins for long-term prevention
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UNSTABLE ANGINA &NON-ST-ELEVATION MI Antithrombotic Tx ASA  chewable aspirin should be initial tx Clopidogrel (Plavix)  ADP inhibitor; combo of ASA & Plavix recommended for pts who are not at excessive risk for bleeding Heparin  UFH or LMWH should be added to ASA & Plavix: LMWH appear to be superior GP IIb/IIIa inhibitors  used for high-risk pts when an invasive management is intended (PCI); includes Abciximab, Eptifibatide, & Tirofiban
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UNSTABLE ANGINA &NON-ST-ELEVATION MI INVASIVE VS. CONSERVATIVE STRATEGY Benefit of early invasive tx in high-risk pts with multiple RFs Invasive  pre-treat 1st , then coronary angiography is done w/i 48 hours of admission, followed by PCI or CABG Conservative  anti-ischemic & antithrombotic therapy followed by “watchful waiting”
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UNSTABLE ANGINA &NON-ST-ELEVATION MI LONG TERM MANAGEMENT Risk factor modification Stop smoking TLC BP control Tight glycemic control B-blockers Statins & ACE-I (plaque stabilization) ASA & Plavix x 9-12 months, followed by ASA thereafter
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ST-SEGMENT ELEVATION MI AMI is one of the MC dx in hospitalized pts 650,000 new & 450,000 recurrent AMIs annually 30% early (30 day) mortality rate; more than ½ of deaths occur before pt reaches hospital; 1 of every 25 surviving pts die in the 1st year after AMI 30-40% AMIs affect RCA, 40-50% affect LAD & the remainder affect the LCX
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ST-SEGMENT ELEVATION MI Pathophysiology  vessel injury & plaque rupture followed by thrombotic occlusion Occurs when plaque fissures or ruptures & when conditions favor thrombosis, so that a mural thrombus forms at rupture site & leads to coronary artery occlusion STEMI may also be caused by coronary emboli or spasm & a wide variety of systemic inflammatory diseases
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ST-SEGMENT ELEVATION MI Amount of damage depends on: Territory supplied by affected vessel Is vessel totally occluded? Duration of occlusion Quantity of blood supplied by collateral vessels Demand for O2 of affected myocardium where blood supply has suddenly been limited Native factors that can produce early spontaneous lysis of occlusive thrombus Adequacy of perfusion in infarct zone when flow is restored in the occluded artery
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ST-SEGMENT ELEVATION MI Clinical presentation  deep, visceral, heavy, squeezing, or crushing substernal CP w/ or w/o radiation; diaphoresis, N/V, anxiety, palpitations, sense of impending doom Proportion of painless STEMIs is greater in pts with DM & it increases with age Elderly pts may present with sudden onset of SOB which may progress to pulmonary edema
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ST-SEGMENT ELEVATION MI PE  anxiety, pallor, diaphoretic & cool extremities; tachy or bradycardia, hypo or hypertension, PMI may be difficult to palpate, +S3 or S4,  intensity of S1, a mid or late systolic murmur or pericardial friction rub may be present; pts with large infarcts may have rales or sgs of shock; fever wouldn’t be expected acutely, but may be present during the first week of recovery
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ST-SEGMENT ELEVATION MI EKG  total occlusion produces ST-segment elevation; most pts with ST-segment elevation develop Q waves When a thrombus is not totally occlusive or there is a rich collateral network, no ST-segment elevation is seen
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ST-SEGMENT ELEVATION MI Where is the infarct ?? Lateral wall  leads I, aVL, V5, V6 (LCX artery) Inferior wall  leads II, III, aVF (RCA or PDA) Anterior  leads V2, V3 (LCA or LAD diagonal branch) Septal  leads V1 & V2 (LCA and/or LAD septal branch) Anteroseptal  leads V1 – V4; (LCA & LAD or left main) Posterior  ST-segment depression in leads V1, V2, V3 or V4; involves RCA or LCX artery
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ST-SEGMENT ELEVATION MI Serum cardiac markers  proteins released in large quantities from necrotic heart muscle Troponin I & Troponin T  gold standard cardiac markers for MI; rises w/I 4-8 hrs Total CK or CPK  rises w/i 4-8 hrs & generally returns to nl by 48-72 hrs; lacks specificity CK-MB  more specific over total CK in that it is not present in significant extracardiac tissue Myoglobin  1st marker released during AMI, lacks specificity & is rapidly excreted in the urine
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ST-SEGMENT ELEVATION MI Cardiac imaging 2D-echo  wall motion defects, EF, pericardial effusions, aneurysms; cannot distinguish between old & new infarcts Doppler echo  VSDs & mitral regurgitation (2 complications of STEMI) Myocardial perfusion scans  used less than echo b/c more difficult to obtain acutely; infarcted tissue displays irreversible ischemic deficits; cannot distinguish between old & new infarcts; not specific for dx of AMI
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ST-SEGMENT ELEVATION MI MANAGEMENT ASA  chewable; other anti-thrombotic agents are heparin & GP IIB/IIIA inhibitors O2  give 2-4L/min of O2 via nasal canula Nitroglycerin  SL X 3 doses; if CP continues or ongoing ischemia on EKG, then IV nitro Morphine  2-4 mg IV Q5 minutes B-Bs  Metoprolol 5mg Q5 min X 3; 15 min after last dose 50mg PO QID X 48 hrs, then 100mg BID ACE-I  given w/i 24 hrs to all pts who are hemodynamically stable w/ STEMI All pts with AMI get B MONA
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BBs  HR which prolongs diastole and increases myocardial perfusion
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ST-SEGMENT ELEVATION MI MANAGEMENT STRATEGIES 1 tool for screening pts & making triage decisions is initial EKG; with ST-segment elevation of at least 2 mm in 2 contiguous precordial leads or 1 mm in 2 limb leads, strongly consider reperfusion therapy Deciding between PCI & fibrinolysis depends on capabilities of the facility
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ST-SEGMENT ELEVATION MI Limitation of infarct  central necrosis area occurs w/ AMI; fate of surrounding ischemic tissue improved by restoration of perfusion,  O2 demand, preventing accumulation of noxious metabolites & reperfusion injury Timely reperfusion prevents ischemic & injured zones from becoming infarct zones Maintain balance between O2 supply & demand w/ pain control,  tachycardia & HTN extends time “window” for myocardial salvage
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ST-SEGMENT ELEVATION MI Primary PCI  restores perfusion when carried out in 1st few hrs; more affective than fibrinolysis when performed by experienced operators & associated w/ better short & long-term clinical outcomes Compared w/ fibrinolysis, primary PCI is preferred when available especially if dx is in doubt, cardiogenic shock is present, sxs present for >2-3 hrs
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ST-SEGMENT ELEVATION MI Fibrinolysis  fibrinolytics should ideally be initiated w/i 30 min of presentation (door-to-needle time < 30 min); includes tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK) & reteplase  infarct size, limits LV dysfunction &  incidence of serious AMI complications Pts tx w/i 1-3 hrs of onset of sxs benefit most, modest benefits are seen w/i 3-6 hrs & mild benefit appears possible up to 12 hrs
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ST-SEGMENT ELEVATION MI Absolute contraindications to fibrinolysis Hx of cerebrovascular hemorrhage at any time Nonhemorrhagic CVA w/i the last year Marked HTN (SBP >180 and/or DBP >110) Suspicion of aortic dissection Active internal bleeding (excluding menses) Relative contraindications Anticoagulants, recent (<2 wks) invasive or surgical procedure, known bleeding disorder, pregnancy, hemorrhagic eye condition Complications Hemorrhage
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ST-SEGMENT ELEVATION MI Post AMI hospital phase management Coronary care units  continuous cardiac monitoring Activity  bedrest for 1st 12 hrs; 2nd or 3rd day pts typically can ambulate in room & to shower Diet  NPO or clear liquid diet for 1st 4-12 hrs Bowels  stool softeners are recommended; laxatives may be necessary Sedation  helps withstand the periods of inactivity; commonly used agents are benzos
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ST-SEGMENT ELEVATION MI AMI complications Ventricular dysfunction  LV undergoes series of remodeling changes in infarcted & non-infarcted segments when left untreated leads to HF Heart failure  results from infarction of 20-25% of LV and will result in congestive lung sgs & sxs Cardiogenic shock  extreme form of HF; results with >40% infarction of LV or MV dysfunction RV infarction  inferoposterior AMI can progress to RV infarction causing sgs/sxs of right HF
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ST-SEGMENT ELEVATION MI AMI complications Acute MR ischemia or papillary muscle rupture Arrhythmias  most deaths due to fatal arrhythmia occur in the 1st few hrs after AMI; other arrhythmias include VPCs, idioventricular rhythms, SVTs, sinus bradycardia & AVB Hypovolemia  results from  fluid intake during acute illness, vomiting due to AMI or narcotic medications, fluid loss due to prior diuretics Myocardial rupture  LV free wall rupture occurs in <1% of pts & usually results in immediate death
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ST-SEGMENT ELEVATION MI AMI complications Recurrent CP  25% of pts w/ AMI; requires prompt angiography & possible revascularization or repeat fibrinolysis Pericarditis  pericardial pain are frequent in pts w/ transmural STEMI; managed w/ ASA Thromboembolism 10% of pts; emboli originate from LV mural thrombi LV aneurysm  describes dyskinesis or local expansile paradoxical wall motion on echo; true aneurysms are composed of scar tissue; complications include HF, emboli, & arrhythmias
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SUDDEN CARDIAC DEATH Definition  unexpected death due to cardiac causes acutely (generally 1 h of sx onset) in a person w/ known or unknown cardiac disease in whom no previously diagnosed fatal condition is apparent 350,000 individuals annually; in many individuals SCD is the 1st clinical manifestation of IHD More than 80% of SCD events occur in individuals with CAD
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SUDDEN CARDIAC DEATH Pathophysiology  lethal arrhythmia; although ischemia can impinge on conduction system & create instability, in most cases the arrhythmia is triggered by electrical irritability of myocardium distant from conduction system that is induced by ischemia or other cellular abnormalities Precipitating causes: VHD, DCM, HCM, isolated hypertrophy, myocarditis, pulmonary HTN, congenital heart defects
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SUDDEN CARDIAC DEATH M & M  survival usually depends on setting, presence & timely use of AED & BLS, rapid EMS arrival & performance of ACLS History  obtaining a hx from family members or witnesses is necessary to gain insight into events surrounding SCD; pts at risk for SCD may have sxs of IHD; a hx of LV impairment (EF <30-35%) is the single greatest RF for SCD
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SUDDEN CARDIAC DEATH PE  survivors have variable PE findings depending on co-morbidities Labs/Diagnostic studies  ROMI work-up & imaging studies will be obtained to evaluate cardiac & coronary structure & fx TX  life-saving tx of acute life-threatening arrhythmias depends on ability to reverse these rhythms; survivors need long-term medical therapy & may need mechanical revascularization procedures