Heart Failure

CARDIAQUE FAILURE:

CARDIAQUE FAILURE Dr Jody Mbuilu P.* Dip. Med. (Unikin2007) MD (Unilu 2004 ) *Reviewer in cardiovascular journal of Africa (CVJA)

Objectives :

Objectives Remind of the semiology and management of Heart failure Present the recent and largest black African Heart failure study 2

Plan :

Plan Nosologic review of heart failure Introduction Definition Epidemiology Pathobiology Diagnosis Management Heart failure in the heart Soweto study cohort 3

Heart failure:

Heart failure Clinical syndrome, pathway of most forms of cardiovascular disease Manifesting as the inability of the heart to fill with or eject blood due to any structural or functional cardiac conditions Introduction ref 4

Heart failure:

Heart failure Incidence and prevalence of HF are growing Influenced by the rising prevalence of precursors such hypertension (HT), diabetes, dyslipidemia , obesity, aging Treatment of HT reduce incidence of HF by 50% In post MI, use of ACE-I and β -blocker delay or prevent dvlp Epidemiology ref 5

Heart failure:

Heart failure According to the American Heart Association, heart failure is a condition that affects nearly 5.7 million Americans of all ages and is responsible for more hospitalizations than all forms of cancer combined. Epidemiology ref 6

Heart failure:

Heart failure Incidence and prevalence of HF are growing Influenced by the rising prevalence of precursors such hypertension (HT), diabetes, dyslipidemia , obesity, aging Treatment of HT reduce incidence of HF by 50% In post MI, use of ACE-I and β -blocker delay or prevent dvlp Epidemiology ref 7

HF Pathophysiology :

HF Pathophysiology Causes and risk factors ref 8 Inappropriated work load Restricted filling Myocyte loss Sympathic system RAAS Cytokines Neuro-hormonal + Anatomic adaptation LV Remodeling Fibrosis HYPOPERFUSION Orthopnea Effort dyspnea CONGESTION Pedal edema hepatomegaly Cough symptoms  Diastolic DysFx Systolic DysFx Output  Preload 

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9 DIASTOLIC Function Output Good perfusion  Systolic EF HR Preload Afterload Contractility periph. resistance   Anatomic structure HYPERTROPHY DILATATION FIBROSIS APOPTOSIS Auricular contraction Venous return Relaxation (LUSITROPY) compliance Elastance frank starling INOTROPY LAPLACE Systolic Function PEPTIDESRAAS SYPATHICSYSTEM  RAAS

HF Pathophysiology :

LV Remodeling Fibrosis HF Pathophysiology Causes and risk factors ref 10 Inappropriated work load Restricted filling Myocyte loss Sympathic system RAAS Cytokines Neuro-hormonal + HYPOPERFUSION Orthopnea Effort dyspnea CONGESTION Pedal edema hepatomegaly Cough symptoms  Diastolic DysFx Systolic DysFx EF  Preload  LV remodeling: the LV progressively dilates and change from the normal ellipsoidal shape to a more spherical geometry This remodeling is accompagnedbychanges in interstitium that lead to fibrosis ACE inhibitors slow, halt or reverse this remodeling process, preventing LV dilatation and deterioration in contractility Anatomic adaptation

HF Pathophysiology :

LV Remodeling Fibrosis HF Pathophysiology Causes and risk factors ref 11 Inappropriated work load Restricted filling Myocyte loss Sympathic system RAAS Cytokines Neuro-hormonal + HYPOPERFUSION Orthopnea Effort dyspnea CONGESTION Pedal edema hepatomegaly Cough symptoms  Diastolic DysFx Systolic DysFx EF  Preload  Neurohormonal changes N/H changes Favorable effect Unfavor. effect  Sympathetic activity  HR , contractility, vasoconst.   V return,  filling Arteriolar constriction  After load  workload  O 2 consumption Renin-Angiotensin – Aldosterone Salt & water retention  VR Vasoconstriction   after load  Vasopressin Same effect Same effect  interleukins &TNF May have roles in myocyte hypertrophy Apoptosis  Endothelin Vasoconstriction  VR  After load

Heart failure:

Heart failure Breathlessness Exertional dyspnea Dyspnea at rest Orthopnea Other symptoms Palpitation Fatigue Nocturia Diagnosis : Hx ref 12

Heart failure:

Heart failure General appearance Obvious dyspnea after moderate activity or when lying flat Well nourish or cachectic Central cyanosis Increased adrenergic activity Tachycardia, diaphoresis, coldness of extremities Cardiomegaly, PD Gallop, Pulmonary rales Jugular venous distention, Hepato -jugular reflux Edema, hepatomegaly , ascitis , hydrotorax Diagnosis : examination ref 13

Heart failure:

Heart failure FBC anemia, leucocytosis U/E dilutional hyponatremia, dyskaliemia, renal Fx ABG mild hypoxemia B-type Natriuretic peptide (BNP): more than 100pg/ml 95% specific; 98% sensible Work up ref 14

Heart failure:

Heart failure CXR DD other causes of dyspnea cardiomegaly, alveolar edema ECG LA enlargement LV Hypertrophy acute tachyarrhythmia acute MI, hypoxic heart Sonar L&R Ventricle size and Function LV wall motion abnormalities valvular Fx and abnormalities Work up ref 15

Heart failure:

Heart failure NYHA --- exertional dyspnea, 4 stades ACC/AHA --- stage of HF : RF, structural modif , symptom Low/High output; Acute/ chronic ; L/R ventricle failure LV systolic dysFx VS preserved systolic Fx Acute cardiac failure; Acute phase in CCF vs stable CCF Always precise underlying cause…?at least suspected Staging and final diagnosis ref 16

Heart failure:

Heart failure ACC/AHA Stage A Stage B Stage C Stage D Staging ref 17 .

Heart failure:

Heart failure 3 elements of HF diagnosis: Stage and type of HF Always precise underlying cause …?at least suspected Try to identify aggravating/ precipitating factor When healed, CCF re-become stable. LIST: 1. Anemia, 2. diet, 3. alcohol, 4. MI, 5. worsening HT 6. fever, 7. arrhythmia, 8. increased activity, 9. pregnancy Staging and final diagnosis ref 18

Heart failure:

Heart failure Try to give more information CCF only Acute decompensation of CCF or stable CCF e.g. Acute phase in CCF , ? Secondary to Hypertension; Aggravated by infection Stable CCF / mitral stenosis Alcoholic Cardiomyopathy Staging and final diagnosis ref 19

Heart failure:

Heart failure Identify and treat risk factors in order to reduce the reservoir of patient at risk of HF HT, more systolic HT ---Rx---reduce incidence diuretic + ACEI as show great benefit,  incidence by 50% Hypercholesterolemia Smoking cessation, weight control, exercises Management ref 20 Stage A: individuals at risk for development of HF

Heart failure:

Heart failure Risk factors + evidences --- ECG, SONAR Coronary reperfusion ACEI, beta- blockers Rx of arrhythmia Others specific RX --- risk factors Management ref 21 Stage B: asymptomatic structural or functional HF

Heart failure:

Heart failure HF with decrease LVEF Goals: Stabilize HF by improving symptoms Treat aggravating factor Management ref 22 Stage C : S ymptomatic HF

Heart failure:

Heart failure HF with decrease LVEF Diuretics: thiazide >>loop Aldosterone antagonist ACEI, Beta- blockers Inotropes: digoxin Hydralazine and isosorbide dinitrate Education and other Management ref 23 Stage C : S ymptomatic HF

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24 End of the first part

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Heart Failure in Soweto study cohort Circulation 2008;118;2360-2367; 2008 25

HF in Soweto study cohort:

HF in Soweto study cohort Background Methods Study setting Study cohort Study data Clinical diagnosis Ethics Statistical analyses PLAN ref Results Clinic and demographic profile Risk factor profile Underlying etiology others Discussion 26

HF in Soweto study cohort:

HF in Soweto study cohort Our knowledge HF – medical school- European population Paucity of data to describe clinical characteristics of HF in African communities in epidemiological transition in Africa few clinical data are derived from echography The single largest study emanate from early 1960: Cosnett JE, heart disease in the Zulu. Br Heart J 1962;24:76-82 Background ref 27

HF in Soweto study cohort:

HF in Soweto study cohort Investigation of heart disease in the township of soweto , south africa - 1,1 million people Epidemiological transition Prospective study in 2006, among 4162 cases captured 1960 cases (47%) diagnosed with HF AIM: undestand ay fundamental changes in the pathways to HF in the region Methods ref 28 Study setting

HF in Soweto study cohort:

HF in Soweto study cohort In 2006, 3500 beds C-H baragwanath , 129 633 inpatients 35% via the departement of medecine Currently, the cardiologic unit manages 21 000 patients pa Methods ref 29 Study cohort

HF in Soweto study cohort:

HF in Soweto study cohort Detailed demographic and clinical profil ECG – minesota coding Sonar- assess VFx , valvular integrity and Fx, and regional wall abnormalities Methods ref 30 Study data

HF in Soweto study cohort:

HF in Soweto study cohort Data captured by cardiac Nurses Verified and analysed with SAS version 9.1 Normally distributed variable are presented as mean ± SD N/ Gaussian distrubuted as the median plus interquartile range χ2, student t, ANOVA was used for comparison Methods ref 31 statistical analyses

HF in Soweto study cohort:

HF in Soweto study cohort Results ref 32 Clinical and demographic profile

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HF in Soweto study cohort:

HF in Soweto study cohort Results ref 34 Risk factor profile

HF in Soweto study cohort:

HF in Soweto study cohort Results ref 35 Underlying etiology

HF in Soweto study cohort:

HF in Soweto study cohort Results ref 36 Echography results

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HF in Soweto study cohort:

HF in Soweto study cohort Largest of HF in Africa Black young woman was predominant Compare to others studies, Idiopathic CMP, HIV related CMP, peripartum CMP and endocardial fibrosis had a high prevalence Like in equivalent African studies, communicable disease and valvular disease are prevalent in African population Discussion ref 38

HF in Soweto study cohort:

HF in Soweto study cohort Hypertension remain the first cause of HF in black population (60%) 15% of patients had a ECG with LVH---need more aggressive Rx Valvular disorder play a pivotal role (8%- de novo HF) Compare with previous report ischemic CMP have increase: 2% versus 9% Discussion ref 39

Thank you:

Thank you ref 40