D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

HF: diagnosis

ACC/AHA

Stage A — High risk for HF, without structural heart disease or symptomsStage B — Heart disease with asymptomatic left ventricular dysfunctionStage C — Prior or current symptoms of HFStage D — Refractory end stage HF

Systolic dysfunction

--Coronary (ischemic) heart disease--Idiopathic dilated cardiomyopathy (DCM):Idiopathic (50%)Myocarditis(9%)Infiltrative diseasePeripartum cardiomyopathyHIV infectionConnective tissue diseaseSubstance abuseDoxorubicin --Hypertension--Valvular disease

Diastolic dysfunction

--Hypertension--Ischemic heart disease--Hypertrophic obstructive cardiomyopathy--Restrictive cardiomyopathy

DD…obesity, lung disease

Cardiomyopathy

--Cardiomyopathies are diseases of heart muscle. This term is best suited to reflect predominantly genetically determined diseases with recognizable phenotypes (hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and left ventricular noncompaction (LVNC))--Has been applied to heart disease secondary to other known causes (eg, ischemic, valvular, or hypertensive cardiomyopathy), this use is not recommended by the 2006 American Heart Association or 2007 European Society of Cardiology classification schemes

The 2007 American Heart Association/American College ofCardiology/European Society of Cardiology (AHA/ACC/ESC) Scientific Statement limited the class Iindications to only two clinical scenarios:- EMB should be performed in that subset of adults who present with recent-onset severe heartfailure requiring inotropic or mechanical circulatory support within two weeks of a viral illness,because they frequently can be bridged to recovery if they have lymphocytic myocarditis.- Patients who present with fulminant or acute dilated cardiomyopathy with sustained or symptomaticventricular tachycardia or high-degree heart block, or who fail to respond to standardheart failure treatment should be biopsied for possible giant cell myocarditis. The sensitivityof biopsy in this setting is reported to range between 80% and 85%.

History

--Excess fluid accumulation:Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, edema, pain from hepatic congestion, and abdominal distention from ascites--Reduction in cardiac output:Fatigue, weakness--Patients with atrial and/or ventricular tachyarrhythmias may complain of palpitations with or without lightheadedness.--Anorexia is secondary to several factors including poor perfusion of the splanchnic circulation, bowel edema, and nausea induced by hepatic congestion.--Secondary pulmonary hypertension contribute to dyspnea as pulmonary pressures rise with exertion. These patients may also complain of substernal chest pressure, typical of angina

Physical examination

--Vital signs and appearance:Four major findings suggest severity of the cardiac dysfunction: Resting sinus tachycardiaNarrow pulse pressure (below 25mmHg)DiaphoresisPeripheral vasoconstriction=cool, pale, and sometimes cyanotic extremities (due to the combination of decreased perfusion and increased oxygen extraction)--Pulsus alternans:Pathognomonic of severe left ventricular failure. Characterized by evenly spaced alternating strong and weak peripheral pulses measuring the blood pressure:When the cuff pressure is slowly released, phase I Korotkoff sounds are initially heard only during the alternate strong beats; with further release of cuff pressure, the softer sounds of the weak beat also appear. The pathophysiology of pulsus alternans is not well understood severe ventricular dysfunction may be associated with variations in contractility secondary to shifts in afterload, preload, and electrical excitability

--Three major manifestations of volume overload in patients with HF:*Pulmonary congestion:More prominent in acute or subacute disease {chronic HF is associated with increases in venous capacitance and lymphatic drainage of the lungs; as a result, rales are often absent even though the pulmonary capillary pressure is still elevated}.

*Peripheral edema:Manifested by swelling of the legs (which is more prominent when the patient is upright), ascites, hepatomegaly, and splenomegaly. In this setting, manual compression of the right upper quadrant to increase venous return may elevate jugular venous pressure above the transient 1 to 3 cm elevations seen in normal individuals. This sign is known as the hepatojugular reflux.

*Elevated jugular venous pressure:With the patient sitting at 45º jugular venous pressure can be estimated from the height above the left atrium of venous pulsations in the internal jugular vein. The height of external jugular vein pulsations may also be helpful but care must be taken to avoid spurious interpretation.

Cardiac examination

*Precordial palpation:An apical impulse that is laterally displaced past the midclavicular line is usually indicative of left ventricular enlargement, sustained apical impulse.Parasternal lift in the setting of right ventricular hypertrophy or enlargement. The S3 may be palpable in severe ventricular failure.

*Heart sounds:An S3 gallop is associated with left atrial pressures exceeding 20 mmHg, increased left ventricular end-diastolic pressures (>15 mmHg) and elevated serum brain natriuretic peptide concentrations. { interobserver variability}

*Pulmonary hypertension:Increased intensity of P2, a murmur of pulmonary insufficiency, a parasternal lift, and a palpable pulmonic tap (felt in the left second intercostal space)

Some authors believe that vascular redistribution is acardinal feature of congestive heart failure, but it may be a particularly unhelpful sign in the ICU patient with acute congestive failure. In these patients, all the pulmonary arteries look enlarged, making it difficult to assess upper and lower vessel size. In addition, the film is often taken supine, which can enlarge the upper lobe pulmonary vessels because of stasis of bloodflow and not true redistribution.

Atrial and brain natriuretic peptides

--When the load on any chamber is increased (e.g.by AF, pulmonary embolism, and some non-cardiovascular conditions, including renal failure)--Atrial natriuretic peptide (ANP) is primarily released from the atria in response to volume expansion (atrial stretch) increased in heart failure. --Plasma ANP levels rise early in the course of the disease and have been used as a marker for the diagnosis of asymptomatic left ventricular dysfunction. --Chronic heart failure ventricular cells can also be recruited to secrete both ANP and brain natriuretic peptide (BNP), an analogous peptide, in response to the high ventricular filling pressures. --These relationships have allowed the plasma concentration of these peptides, particularly BNP, to be used to detect heart failure and to predict the outcome and perhaps guide therapy in patients with established disease--Optimal exclusion cut-off point is 300 pg/mL for NT-proBNP and 100 pg/mL for BNP--Mid-regional atrial natriuretic peptide (MR-proANP), at a cut-off point of 120pmol/L, was shown to be non-inferior to these thresholds for BNP and NT-proBNP in the acute setting.

Limitations of BNP and NT-proBNP

--Patients may present with more than one cause of dyspnea (such as pneumonia and an exacerbation of HF). Thus, a high plasma BNP or NT-proBNP concentration does not exclude the presence of other diseases.--In some patients with acute decompensated HF, plasma BNP or NT-proBNP levels are not diagnostic.--Some patients with severe chronic HF may have persistently elevated plasma BNP or NT-proBNP concentrations regardless of treatment, and such levels may not be useful in guiding management.--Plasma BNP and NT-proBNP levels tend to be lower in obese patients and are elevated in patients with renal failure, and some acute noncardiac illnesses such as sepsis. Greater increases in NT-proBNP than BNP levels are observed in renal failure.

MR-proANP=mid-regional pro atrial natriuretic peptideNT-proBNP=N-terminal pro B-type natriuretic peptidePET=positron emission tomographySPECT=single photon emission computed tomographyCRT-P= cardiac resynchronization therapy pacemakerCRT-D=cardiac resynchronization therapy defibrillator99mTc-DPD=technetium-99m 3,3-diphosphono-1,2-propanodicarboxylic acid.MRA= mineralocorticoid receptor antagonist

Echocardiography

**Assessment of left ventricular systolic dysfunction:--LVEF is not an index of contractility as it depends on volumes, preload, afterload, heart rate, and valvular function--Recommended apical biplane method of discs (the modified Simpson’s rule).--Use of a contrast agent to better delineate the endocardial border is recommended when image quality is suboptimal (i.e. where <80% of the endocardial border is adequately visualized).--Calculating EF from linear dimensions may result in inaccuracies, particularly in patients with RWMA--3D echocardiography of adequate quality further improves the quantification of ventricular volumes and EF calculation

**Assessment of left ventricular diastolic dysfunction:--Eevaluation of both structural (LV hypertrophy, LA dilation) and functional abnormalities--Normal e’ (>8 cm/s septal, >10 cm/s lateral, or >9 cm/s average, measured using real-time pulsed TDI) is very unusual in a patient with HF

{other: holter, genetic testing for cardiomyopathy}

-Cardiac MRI is considered by almost all as the gold standard for the measurement of ejection fraction (EF), LV volumes, and LV mass-MRI is the test of choice in patients with suspected or known congenital heart disease.-Test of choice: Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a rare condition in which fibrosis and fatty infiltration of the right ventricle are present-Late gadolinium enhancement, in which gadolinium is injected and then approximately 10 minutes later the heart is imaged using special sequences, infarcted myocardium can be imaged. Infarcted myocardium appears bright; noninfarcted, viable myocardium appears dark.-Cardiac magnetic resonance imaging (MRI) can be performed in most patients with implanted cardiovascular devices, including most coronary and peripheral stents, prosthetic heart valves, embolization coils, intravenous vena caval (IVC) filters, cardiac closure devices, and aortic stent grafts. Pacemakers and implantable cardioverter defibrillators are strong relative contraindications to MRI scanning, and scanning of such patients should be done under specific delineated conditions, only at centers with expertise in MRI safety and electrophysiology, and only when MRI imaging in particular is clearly indicated.-Both the Food and Drug Administration (FDA) and radiology experts have issued recommendations on the issue of gadolinium administration in patients with chronic kidney disease nephrogenic systemic fibrosis

Not alawys clear …

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