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Acute Heart Failure
Kendra Marsh, MD
Clinical Instructor, Cardiology Fellow
Department of Cardiology
University of Illinois at Chicago
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ObjectivesObjectives
• DefinitionsDefinitions
• EpidemiologyEpidemiology
• Pathophysiology Pathophysiology
• DiagnosisDiagnosis
• Management Management
• Summary of Guidelines Summary of Guidelines
• Recommended ReadingRecommended Reading
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• DefinitionsDefinitions
• EpidemiologyEpidemiology
• PathophysiologyPathophysiology
• DiagnosisDiagnosis
• Management Management
• Summary of GuidelinesSummary of Guidelines
• Recommended Reading Recommended Reading
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Acute Heart FailureAcute Heart Failure
• Rapid onset of symptoms and signs Rapid onset of symptoms and signs related to abnormal cardiac functionrelated to abnormal cardiac function
• As a result of Systolic Dysfunction, As a result of Systolic Dysfunction, Diastolic Dysfunction, Arrhythmias, Diastolic Dysfunction, Arrhythmias, or Preload-After load Mismatchor Preload-After load Mismatch
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Related Clinical ConditionsRelated Clinical Conditions
• De Novo or Chronic Decompensated De Novo or Chronic Decompensated
• Hypertensive Hypertensive
• Pulmonary EdemaPulmonary Edema
• Cardiogenic ShockCardiogenic Shock
• High Output Heart Failure: Arrhythmias, High Output Heart Failure: Arrhythmias, Thyrotoxicosis, Anemia, Paget’s Thyrotoxicosis, Anemia, Paget’s DiseaseDisease
• Right Heart Failure Right Heart Failure
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Killips Classification Killips Classification
• Stage I: No Heart FailureStage I: No Heart Failure
• Stage II: Heart FailureStage II: Heart Failure S3 gallop, Pulmonary venous Hypertension, Rales <1/2 of the lung S3 gallop, Pulmonary venous Hypertension, Rales <1/2 of the lung
fields fields
• Stage III: Severe Heart FailureStage III: Severe Heart Failure Frank pulmonary Edema, rales through out the lung fieldFrank pulmonary Edema, rales through out the lung field
• Stage IV: Cardiogenic ShockStage IV: Cardiogenic Shock Systemic hypotension, peripheral vasoconstriction, endorgan Systemic hypotension, peripheral vasoconstriction, endorgan
failure, cyanosis, diaphoresisfailure, cyanosis, diaphoresis
This classification system uses the clinical exam to determine the degree of cardiomyopathy after an acute MI.
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Clinical Severity Clinical Severity ClassificationClassification
• PERFUSIONPERFUSION
• CONGESTIONCONGESTION– Auscultation of the lungs Auscultation of the lungs
Warm/Dry
Cold/Dry
Warm/Wet
Cold/Wet
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• DefinitionsDefinitions
• EpidemiologyEpidemiology
• PathophysiologyPathophysiology
• DiagnosisDiagnosis
• Management Management
• Summary of GuidelinesSummary of Guidelines
• Recommended Reading Recommended Reading
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EpidemiologyEpidemiology
• We have greatly improved our We have greatly improved our management of acute management of acute myocardial infarctions.myocardial infarctions.
• Large component of care is Large component of care is inpatientinpatient
• Expensive to manageExpensive to manage• High mortality in patients High mortality in patients
status post MI.status post MI.• The leading cause of The leading cause of
hospitalization in patients hospitalization in patients over 65over 65
• 1 million hospitalizations per 1 million hospitalizations per year with HF as primary year with HF as primary diagnosisdiagnosis
• 2.5 million hospitalizations 2.5 million hospitalizations with heart failure as with heart failure as secondary diagnosissecondary diagnosis
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• DefinitionsDefinitions
• EpidemiologyEpidemiology
• PathophysiologyPathophysiology
• DiagnosisDiagnosis
• Management Management
• Summary of GuidelinesSummary of Guidelines
• Recommended Reading Recommended Reading
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A Vicious Circle
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In an effort to maintain adequate tissue perfusion the body has three defenses: increase heart rate, vascular tone and circulating volume.
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• DefinitionsDefinitions
• EpidemiologyEpidemiology
• PathophysiologyPathophysiology
• DiagnosisDiagnosis
• Management Management
• Summary of GuidelinesSummary of Guidelines
• Recommended Reading Recommended Reading
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• DefinitionsDefinitions
• EpidemiologyEpidemiology
• PathophysiologyPathophysiology
• DiagnosisDiagnosis
• Management Management
• Summary of GuidelinesSummary of Guidelines
• Recommended Reading Recommended Reading
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General Therapeutic General Therapeutic ApproachApproach
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OxygenOxygen
• Class I, CClass I, C– Improves oxygen delivery and tissue Improves oxygen delivery and tissue
perfusionperfusion– Goal Saturation should be 95-98%, beyond Goal Saturation should be 95-98%, beyond
that there is no indication for increased that there is no indication for increased FIO2FIO2
– Always consider CPAP first or Non Invasive Always consider CPAP first or Non Invasive Positive Pressure Ventilation FirstPositive Pressure Ventilation First
– Endotrachial Intubation as a last resortEndotrachial Intubation as a last resort
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PharmacotherapyPharmacotherapy
• MorphineMorphine
• AnticoagulationAnticoagulation
• VasodilatorsVasodilators
• DiureticsDiuretics
• Beta AntagonistsBeta Antagonists
• Inotropic AgentsInotropic Agents
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Morphine Morphine
• Class IIb, BClass IIb, B– Great Early in managementGreat Early in management– VenodilationVenodilation– Mild Arterial DilationMild Arterial Dilation– Slows Heart rate Slows Heart rate
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AnticoagulationAnticoagulation
• No evidence to support No evidence to support anticoagulation for Acute Heart anticoagulation for Acute Heart Failure alone Failure alone
• Yes in the case of Atrial FibrillationYes in the case of Atrial Fibrillation
• Yes in the case of LV thrombus Yes in the case of LV thrombus
• Large Placebo Control Trial with Large Placebo Control Trial with Enoxiparin at 40mg SC showed no Enoxiparin at 40mg SC showed no mortality benefitmortality benefit
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Vasodilators Vasodilators
• Nitrates: Class I, BNitrates: Class I, B– Improves Cardiac Improves Cardiac
Output and decreases Output and decreases PCWPPCWP
– Best with diureticsBest with diuretics– Low doses, venodilationLow doses, venodilation– High doses, arterial High doses, arterial
dilationdilation– Preload and AfteroadPreload and Afteroad– Good for 16-24 hours Good for 16-24 hours
• Sodium Nitroprusside: Sodium Nitroprusside: Class I, CClass I, C– Severe Heart Failure Severe Heart Failure
with Hypertensionwith Hypertension– Primarily arterial Primarily arterial
dilationdilation– Need for arterial Need for arterial
invasive monitoring invasive monitoring – Stop if active ischemia Stop if active ischemia
due to coronary steal due to coronary steal phenomenon phenomenon
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Niseritide Niseritide
• Recombinant B-type Brain Naturetic Recombinant B-type Brain Naturetic Peptide Peptide
• Venous, Arterial and coronary affectsVenous, Arterial and coronary affects
• Enhanced sodium excretionEnhanced sodium excretion
• Suppresses RAAS and sympathetic Suppresses RAAS and sympathetic systemsystem
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Vasodilators in the Vasodilators in the Management of Acute Heart Management of Acute Heart Failure Trial (VAMC)Failure Trial (VAMC)DesignDesign Enrolled Enrolled AgentsAgents Primary End Primary End
PointPointOutcomesOutcomes
RandomizedRandomized
Double-Double-Blinded Blinded
ControlControl
Effects at 3 Effects at 3 hourshours
489 489
Acute CHFAcute CHF
PCWP> PCWP> 20mmHg20mmHg
Niseritide Niseritide
Bolus 2 Bolus 2 micr/kg micr/kg
NitroglycerinNitroglycerine IVe IV
Change in Change in PCWP from PCWP from baselinebaseline
Reduced Reduced dyspnea dyspnea compared to compared to standard standard therapy alonetherapy alone
Significant Significant reduction in reduction in dyspnea score dyspnea score and PCWP with and PCWP with addition of addition of NIseritide to NIseritide to standard standard therapytherapy
• No good data to support adverse affects on renal No good data to support adverse affects on renal function and niseritidefunction and niseritide
• Retrospective analysis of VMAC showed potential for Retrospective analysis of VMAC showed potential for increased creatinin with increasing niseritide dose.increased creatinin with increasing niseritide dose.
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Summary of Vasodilators Summary of Vasodilators
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DiureticsDiuretics• Class I, BClass I, B
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Diuretic Resistance can be associated with increased mortality.
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UltrafiltrationUltrafiltration
• RAPID-CHF TrialRAPID-CHF Trial– 40 patients40 patients– ADHF and Renal ADHF and Renal
Insufficiency (Cr >1.5)Insufficiency (Cr >1.5)– Ultrafiltration had Ultrafiltration had
significant increase in significant increase in fluid removal after 24 fluid removal after 24 hourshours
– 4650 L vs 2838L4650 L vs 2838L
• UNLOAD TrialUNLOAD Trial– 200 patients200 patients– Renal insufficiency was Renal insufficiency was
not a criteria for not a criteria for inclusioninclusion
– Standard care vs ultra Standard care vs ultra filtrationfiltration
– 48 Hours 4.6 L vs 3.3L48 Hours 4.6 L vs 3.3L– 90 Days fewer 90 Days fewer
rehospitalizations .22 rehospitalizations .22 vs .46 and fewer vs .46 and fewer unscheduled clinic visits unscheduled clinic visits 21 vs 4421 vs 44Option in the setting of failed diuretic and
vasodilator therapy
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Beta Blockers Beta Blockers
• No data to support benefits in AHFNo data to support benefits in AHF
• Traditionally considered a contra Traditionally considered a contra indicationindication
• Consider if there is active ischemia and Consider if there is active ischemia and blood pressure tolerates.blood pressure tolerates.
• Ischemia and Tachycardia, Class IIb, CIschemia and Tachycardia, Class IIb, C
• Acute MI after stabilization, Class IIa, BAcute MI after stabilization, Class IIa, B
• Chronic CHF after stabilization, Class I, AChronic CHF after stabilization, Class I, A
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Inotropic Agents Inotropic Agents
• Peripheral Hypoperfusion refractory Peripheral Hypoperfusion refractory to vasodilators and diuretics, Class to vasodilators and diuretics, Class IIa, CIIa, C
• Danger: May increase oxygen Danger: May increase oxygen demand and calcium loading demand and calcium loading
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Dopamine and DobutamineDopamine and Dobutamine
• Dopamine: Dopamine: – Vasodilator of Renal, Vasodilator of Renal,
Coronary, splanchnic Coronary, splanchnic and Cerebral Vascular and Cerebral Vascular beds beds
– Hypotensive patientsHypotensive patients– Drawbacks: arrhythmia, Drawbacks: arrhythmia,
increased pulmonary increased pulmonary vascular resistance and vascular resistance and increased afterloadincreased afterload
• Dobutamine, Class IIa, CDobutamine, Class IIa, C– Hypotension and low Hypotension and low
Urine outputUrine output– Beta 1 and 2 agonistBeta 1 and 2 agonist– At high doses increases At high doses increases
SVRSVR– Additive effect with Additive effect with
Phosphodiesterase Phosphodiesterase inhibitors inhibitors
– Draw Backs- arrhythmia, Draw Backs- arrhythmia, reflex decrease in reflex decrease in sympathetic tonesympathetic tone
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Phosphodiesterase Phosphodiesterase InhibitorsInhibitors• Milrinone and EnoximoneMilrinone and Enoximone
– Hypoperfusion despite Hypoperfusion despite Diuretics and Vasodilators Diuretics and Vasodilators with good blood pressure. with good blood pressure. Class IIb, CClass IIb, C
– Lucitropic, Inotropic, Lucitropic, Inotropic, vasodilatorvasodilator
– Inhibits degredation of Cyclic Inhibits degredation of Cyclic AMPAMP
– Increase CO, CI, Stroke Increase CO, CI, Stroke Volume, Volume,
– Decrease PAP, PVR and PCWPDecrease PAP, PVR and PCWP– Immediate ActionImmediate Action– Effect is Distal to Beta Effect is Distal to Beta
receptors, can be used in the receptors, can be used in the setting Beta Blocker therapy. setting Beta Blocker therapy. Class IIa, CClass IIa, C
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Outcomes of a Prospective Trial of Intravenous Outcomes of a Prospective Trial of Intravenous Milrinone For Exacerbations of Congestive Heart Milrinone For Exacerbations of Congestive Heart FailureFailureOPTIME-CHF OPTIME-CHF JAMA 2002JAMA 2002DesignDesign Randomized, Control, Double BlindedRandomized, Control, Double Blinded
Milrinone versus PlaceboMilrinone versus Placebo
EnrolledEnrolled Broad Population with systolic dysfunction Broad Population with systolic dysfunction
Without low output syndromeWithout low output syndrome
949 patients 949 patients
Primary EndpointsPrimary Endpoints Repeat hospitalization for cardiovascular Repeat hospitalization for cardiovascular
causes within 60 days of dischargecauses within 60 days of discharge..OutcomesOutcomes No difference in primary end point between No difference in primary end point between
Milrinone and placebo.Milrinone and placebo.
Higher instance of atrial arrhythmia and Higher instance of atrial arrhythmia and hypotension with Milrinone.hypotension with Milrinone.
Milrinone is associated a 30% increase in Milrinone is associated a 30% increase in mortalitymortality
ConclusionsConclusions Not indicated in routine use with standard Not indicated in routine use with standard medica therapy.medica therapy.
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LevosimendanLevosimendan
• Calcium ion Calcium ion sensitizationsensitization
• Also Pimobendon Also Pimobendon
• Increases ContractilityIncreases Contractility
• A little PDI activity as A little PDI activity as wellwell
• Severe dysfunction with Severe dysfunction with preserved blood preserved blood pressurepressure
• Drawback: very pro-Drawback: very pro-arrhythmogenic arrhythmogenic
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Clinical TrialsClinical Trials
• LIDO TrialLIDO Trial– Levosimendan 24 hr Levosimendan 24 hr
infiusionvs Dobutamineinfiusionvs Dobutamine– 203 Patients203 Patients– Severe Decompensated Severe Decompensated
HF, AHF, HF after CABGHF, AHF, HF after CABG– Excluded if cardiogenic Excluded if cardiogenic
shockshock– Endpoints, increased CI Endpoints, increased CI
(35% vs 25%) and (35% vs 25%) and reduced PCWP (28% vs reduced PCWP (28% vs 15%) in favor of 15%) in favor of LevosimendanLevosimendan
• SURVIVE TrialSURVIVE Trial• Levosimendan vs Levosimendan vs
Dobutamine 24 hour Dobutamine 24 hour therapytherapy
• 1327 patients1327 patients• Endpoints symptomatic Endpoints symptomatic
relief and BNPrelief and BNP• Levosimendan Greater Levosimendan Greater
reduction in BNP but reduction in BNP but no difference in no difference in symptomatic reliefsymptomatic relief
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PressorsPressors
• VasopressinVasopressin: Cardiogenic shock in : Cardiogenic shock in conjunction with inotropic therapyconjunction with inotropic therapy
• Epinephrine Epinephrine B1 and B2, B1 and B2,
• Norepinephrine alpha receptorsNorepinephrine alpha receptors
• Cardiac GlycosidesCardiac Glycosides: Inhibit cardiac : Inhibit cardiac Na/K ATPase, increases Ca/Na Na/K ATPase, increases Ca/Na exchange mechanism. Tachycardia exchange mechanism. Tachycardia induced Cardiomyopathy. induced Cardiomyopathy.
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Cardiac and Ventricular Assist Cardiac and Ventricular Assist Devices Devices
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Temporary DevicesTemporary Devices
• IABPIABP
• Tandem HeartTandem Heart
• ECMOECMO
• Ventricular Assist DevicesVentricular Assist Devices
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IABPIABP
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ECMOECMO
• ECMO removes carbon ECMO removes carbon dioxide from and adds dioxide from and adds oxygen to venous blood via oxygen to venous blood via an artificial membrane an artificial membrane lung lung
Severe respiratory failureCardiac Failure with inability to wean off BypassBridge to Cardiac Transplant
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Temporary Devices:Temporary Devices:Tandem Heart pVADTandem Heart pVAD• Continuous-flow centrifugal Continuous-flow centrifugal
assist device placed assist device placed extracorporeallyextracorporeally
• Cannula in femoral vein Cannula in femoral vein through intraatrial septum through intraatrial septum into LAinto LA
• Pump withdraws Pump withdraws oxygenated blood from the oxygenated blood from the left atrium, propels it by a left atrium, propels it by a magnetically driven magnetically driven impeller through the impeller through the outflow portoutflow port
• Blood returns into femoral Blood returns into femoral artery via arterial cannulaartery via arterial cannula
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Longer-term implantable Longer-term implantable devicesdevices
• NovacorNovacor
• HeartMate XVEHeartMate XVE
• HeartMate IIHeartMate II
• Next Generation DevicesNext Generation Devices
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Operative Mortality Prediction Operative Mortality Prediction ScoreScore• Requirement for ventilator Requirement for ventilator
support — 4 points support — 4 points
• Clinical picture of post-Clinical picture of post-cardiotomy shock — 2 points cardiotomy shock — 2 points
• Use of temporary LVAD prior to Use of temporary LVAD prior to Heart-Mate insertion — 2 points Heart-Mate insertion — 2 points
• Central venous pressure >16 Central venous pressure >16 mmHg — 1 point mmHg — 1 point
• Prothrombin time >16 seconds Prothrombin time >16 seconds — 1 point — 1 point
• ScoringScoring– 0-5: Low risk 0-5: Low risk
• Mortality 8%Mortality 8%– 5-7: Intermediate Risk5-7: Intermediate Risk
• Mortality 32%Mortality 32%– 8-10: High Risk8-10: High Risk
• Mortality 49%Mortality 49%
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Novacor- Long-term Device Novacor- Long-term Device
Cardiac ReplacementCardiac ReplacementBridge to TransplantBridge to Transplant
Magnetic ActuatorMagnetic ActuatorBlood Propelled via Blood Propelled via
collapsing bladder and to collapsing bladder and to prosthetic valvesprosthetic valves
One Year Survival One Year Survival No risk factors, 60%No risk factors, 60%1 Risk factor, 24%1 Risk factor, 24%
25% risk of Thromboembolic 25% risk of Thromboembolic EventEvent
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Heart-mateHeart-mate
• Rehabilitation and hospital dischargeRehabilitation and hospital discharge• $70,000$70,000• LV apex to ascending aortaLV apex to ascending aorta• Textured surface allows for endotheliazation to reduce need for Textured surface allows for endotheliazation to reduce need for
anticoagulationanticoagulation• Improves perfusion: decrease renal failure and pulmonary HTNImproves perfusion: decrease renal failure and pulmonary HTN• Complications: infection, bleeding, monomorphic VT, RV failure and Aortic Complications: infection, bleeding, monomorphic VT, RV failure and Aortic
Stenosis Stenosis
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HeartMate IIHeartMate II
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Suggested Reading Suggested Reading
• Randomized evaluation of Mechanical Assistance Randomized evaluation of Mechanical Assistance for Treatment of Chronic Heart Failure (Rose et al. for Treatment of Chronic Heart Failure (Rose et al. NEJM 2001)NEJM 2001)
• Evaluation and management of patients with Evaluation and management of patients with acute decompensated heart failure. Journal of acute decompensated heart failure. Journal of Cardiac Failure. Vol.12 No. 1 2006Cardiac Failure. Vol.12 No. 1 2006
• Medical Management of Advanced Heart Failure. Medical Management of Advanced Heart Failure. JAMA, February 6,2002- Vol. 27, No. 5JAMA, February 6,2002- Vol. 27, No. 5
• http://www.med.umich.edu/AnesCriticalCare/Docuhttp://www.med.umich.edu/AnesCriticalCare/Documents/Rosenberg_Circulatory_Assist_Devices.pdfments/Rosenberg_Circulatory_Assist_Devices.pdf
• http://texasheart.org/Research/Devices/http://texasheart.org/Research/Devices/thoratec_heartmateii.cfmthoratec_heartmateii.cfm
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Thank you!Thank you!
• Special Thanks to Special Thanks to – Dr. Chad Feldman, Associate Director of Dr. Chad Feldman, Associate Director of
Medicine Advocate Christ HospitalMedicine Advocate Christ Hospital– Dr. Ali Zadi, Clinical Instructor, Dr. Ali Zadi, Clinical Instructor,
Cardiology FellowCardiology Fellow– Dr. Saba Khan, Heart Failure FellowDr. Saba Khan, Heart Failure Fellow