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Shot Through the Heart & You’re to Blame,You Give Love a Bad Name: CHF & Cardiomyopathy Resident Rounds Nov 28/02 A.F. Chad, MD, CCFP Heartbreak Hotel • Failure to maintain adequate circulation of blood • Left versus Right sided CHF • Systolic versus Diastolic CHF • High versus Low Output CHF What is Love, if not Neurohormonal Mechanism • 1. Sympathetic system activation • 2. Activation of the ReninAngiotensin Aldosterone system (RAAS) • 3. Increased naturetic peptides • 4. Increased Antidiuretic hormone • 5. Increased Endothelins Getting in the Mood: Sympathetic Activation • Causes increased cardiac output, increased heart rate, and peripheral vasoconstriction • If sustained activates the RAAS which increases both preload and afterload • Stimulation of alpha and beta receptors leads to myocardial hypertrophy and fibroblast hyperplasia which lead to decreased compliance • Increased norepinephrine levels lead to myocardial cell death and areas of focal necrosis further impairing LV function Feeling “RAAS”NDY Yeah Baby! • Stimulation leads to increased Angiotensin II which leads to : • 1. Increased aldosterone • 2. Increased norepinephrine • 3.Inhibition of vagal tone The Male Love Hormone (Kind of): Aldosterone • Shown to be elevated up to 20 times in patients with CHF • Causes growth promoting activity in nonepithelial cells • Stimulates fibroblasts which leads to interstitial and perivascular fibrosis which increases LV stiffness • Produced in nonrenal sites such as the vessels and heart • Up to 40% of patients will have elevated levels despite being on ACE inhibitors Some like it hot & wet: Antidiuretic Hormone • Is elevated in severe heart failure • Higher levels have been reported in patients on diuretics • Can lead to hyponatremia More than an Endothelin • Secreted by vascular endothelial cells • Potent vasoconstrictor peptide which leads to sodium retention • Increases in proportion to the hemodynamic severity of heart failure • Interest in developing endothelin receptor antagonists Naturetic Peptides by Nature • 3 types • 1. Atrial Naturetic Peptide (ANP) – released from the atria in response to stretch. Is very sensitive and will be released even with exercise. Causes naturesis and vasodilatation • 2. Brain Naturetic Peptide (BNP) – release from the venticles in response to elevated LVEDP. Has the same effect as ANP Naturetic Peptides by Nature cont’d • 3. C-type naturetic peptide – limited to the vascular endothelium and has limited effects on naturesis and vasodilatation From the Bottom of my heart (filling my lungs) • Capillary pressure (12-15mmHg) • Plasma oncotic pressure (25mmHg) – – – – – – Cardiac (Hi PCWP) ARDS Low oncotic P Negative P Lymphatic insufficiency Other Where does my heart go now? • • • • • • 3.2 million in USA 400,000 new per year 1-2% prevalence High 5-yr mortality: 60% M, 45% W Median survival: 3.2 yr M, 5.4 yr W Progressive CHF vs sudden death Why you Wanna Break My Heart? • • • • • • • ISCHEMIA!!!!!! Non-compliance Valvular HTN CM Infectious Thyrotoxicosis, anemia To Find My Heart • Exertional Dyspnea: most sensitive (Spec<60%) • PND / Othopnea (sens<30%) • Cough • Edema • Anxiety • Non-specific stuff Piece of My Heart? • • • • • • COPD Asthma PE Tamponade Pneumonia ARDS Heart and Soul: CCS • I - ordinary activity = no angina, +++ activity = angina • II - slight limitations, angina >2 blocks level (+/- stress) • III - marked limitations, angina <2 blocks level • IV - no activity w/o discomfort +/- angina at rest • 59% Validity, 73% reproducible Heart and Soul: NYHA • I - ordinary activity = no Sx • II - slight limitations, ok at rest, ordinary activity = S • III - marked limitations, less than ordinary activity = Sx • IV - no activity w/o discomfort, Sx at rest • 51% Validity, 56% reproducible Sea of Love • Physical exam –90% specific –20-30% sensitive Love Shack . . . Left’s where it’s at!!! • • • • • • Tachypnea / tachycardia S3, gallup Diaphoresis Crackles / wheezes Pulsus Alternans PMI laterally displaced Love Shack . . . Right’s where it’s at!!! • JVD • Edema • Hepatomegaly / HJR Heart and Soul: Killip • I - No CHF - 5% mortality • II - Mild CHF (bibasilar rales and S3) - 15-25% mortality • III - Frank pulmonary edema 40% mortality • IV - Cardiogenic shock - 80% mortality Find My Heart • • • • • • • CBC Lytes Creatinine LFT’s TNT? TSH? BNP? You Down with BNP? Yeah, you know me! • New polypeptide that is produced in the ventricles • Released in proportion to LV expansion reflecting the LVEDP • Levels rise with age (due to increased LV stiffness) • Levels are elevated with pulmonary disease (due to increased RVEDP) • Levels are elevated in end-stage renal disease reflecting decreased excretion You Down with BNP? Yeah, you know me! • There is a bedside test that is FDA approved, but it costs $25 - $40 per test. • Cut off has been determined retrospectively in studies • Levels below 75 – 100 pg/ml correlate with fairly normal LV function • The higher the level the worse the LV function • If a patient presented with acute worsening, one would expect a level > 300 pg/ml You Down with BNP? Yeah, you know me! • This test will probably be used to also follow therapy for patients. Studies have shown that better optimization of ACE therapy can be instituted. • It may reduce the need for repeat ECHO’s • Levels rise acutely and decline with effective treatment within hours – the ½ life is 22 minutes in patients without renal disease You Down with BNP? Yeah, you know me! • The best use is in patients with multiple medical problems who present with increased dyspnea. • If patients have COPD, are at risk for PE and have a history of CHF then BNP can help separate cardiac from other causes of dyspnea – Maisel AS, Krishnaswamy P, Nowak RM, McCord J, Hollander JE, Duc P, Omland T, Storrow AB, Abraham WT, Wu AH, Clopton P, Steg PG, Westheim A, Knudsen CW, Perez A, Kazanegra R, Herrmann HC, McCullough PA. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002 Jul 18;347(3):161-7. Find My Heart • ECG – Ischemia – Hypertrophy – Dysrhythmias • CXR – – – – Cardiomegaly (lots of love) Redistribution (PCWP12-18mmHg) Kerley B lines(PCWP 25mmHg) Pulmonary edema (PCWP >25mmHg) Find My Heart, Find My Heart • ECHO – WMA – EF – Cardiac FNC – Valves – Tamponade – Size – Dimensions Find My Heart • Cath? – ?definitive Rx • MUGA? – ?echo good enough • Swan? – No benefit with mortality – ?helpful clinically How do You mend a Broken Heart? • Acute emergency therapy • Chronic maintenance therapy How do You mend a Broken Heart? • ABCD!!!! • O2, IV’s, Monitors • CPAP / BiPAP for Edema (more MI with BiPAP) – Sacchetti A. Effectiveness of BiPAP for congestive heart failure. J Am Coll Cardiol. 2001 May;37(6):1754-5. • Elevate head & Lower legs • Cheesy Poetry How do You mend a Broken Heart? • • • • • • • • What is the cause? TREAT THE CAUSE!!!!! Nitrates ACE Diuretics Morphine hBNP Inotropes Sex Bomb: Nitrates • Decreases preload and afterload (slightly) • Shown to be effective in reducing mortality and improving symptoms • Can be given sublingual, IV, or as a patch • Dose is 10mcg/min and can be titrated up every 3 – 5 minutes until desired effect. • Can cause hypotension Sex Bomb: Nitrates • Can switch to a patch from IV nitrates, however this switch worked only when patients were on lower doses (< 50 mcg/ml) • Topical patches have an onset in decreasing PCWP at 20 – 30 minutes with peak effect at 120 minutes. Therefore, their use in an acute severe decompensation is not warranted as first line therapy Sex Bomb: Nitrates • Sublingual NTG tabs decreased PCWP by 36%. Onset was 4 minutes with peak effect at 9 minutes • The spray had an onset of 1-2 minutes with peak effect at 5 minutes Ace of the Heart • Haude M, Steffen W, Erbel R, Meyer J. Sublingual administration of captopril versus nitroglycerin in patients with severe congestive heart failure. Int J Cardiol. 1990 Jun;27(3):351-9 Ace of the Heart • Captopril sublingually decreased PCWP after 10 minutes with a peak effect seen at 30 minutes. – Sacchetti et al showed that it decreased the admissions to ICU – odds ration 0.29 – Haude M, Steffen W, Erbel R, Tschollar W, Belz GG, Meyer J. [Hemodynamics after sublingual administration of captopril in severe heart failure. A pilot study] Dtsch Med Wochenschr. 1989 Jul 14;114(2829):1095-100. IV Ace of the Heart • Annane D, Bellissant E, Pussard E, Asmar R, Lacombe F, Lanata E, Madonna O, Safar M, Giudicelli JF, Gajdos P. Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema. Circulation. 1996 Sep 15;94(6):1316-24 Hot &Wet: Diuretics • Have venodilatory properties as well as decreasing intravascular volume through diuresis. • Causes increased plasma renin and Norepinephrine levels leading to Increased SVR • A study comparing high dose NTG and low dose diuretics showed lower mortality than high dose diuretic and low dose NTG Fool for Love: Morphine • Causes venodilation through histamine release (lasts around 10 minutes) • Causes sedation and respiratory depression • Sacchetti et al showed it increased ICU admissions – odds ratio 3.0 Nesiritide (human recombinant BNP): New Love • Increases cyclic GMP->second messenger >dilate veins and arteries • Decreases PCWP & Dyspnea • 2 mcg/kg IV bolus over 60 s; follow by 0.01 mcg/kg/min continuous infusion – Elkayam U, Akhter MW, Tummala P, Khan S, Singh H. Nesiritide: a new drug for the treatment of decompensated heart failure. J Cardiovasc Pharmacol Ther. 2002 Jul;7(3):181-94. Acute treatment – conclusions • 1. Nitrates are first line therapy and should be given intravenously if the patient is sick • 2. Ace inhibitors are beneficial in acute CHF • 3. Diuretics should be used in moderation • 4. Morphine should be used with extreme caution Chronic Therapy • • • • • 1. 2. 3. 4. 5. Ace Inhibitors/ ARB’s Betablockers Spironolactone Diuretics Digoxin Ace of the Heart • Considered first line therapy for CHF. • Recommended for all stages of CHF • Absolute mortality reduction is around 15% at one year for class III/IV patients with a NTT of 6 (relative risk reduction is 30 – 35%) • The effect on mortality was dose related and the higher the dose till the target range was reached ;the lower the mortality Ace of the Heart • These results were based on the CONSENSUS I/II, SOLVD, AND SAVE trials • Note the effect of ace inhibitors is reduced on patients who are on NSAIDS as well as ASA Angiotensin Receptor Blockers (of love) • Were thought to be better because angiotensin II was still produced in patients on Ace inhibitors. • These drugs block the Angiotensin II receptor. • Also they do not produce Bradykinens which Ace inhibitors do. These Bradykinens lead to S/E such as cough and angioedema ARB’s of love • Elite II – showed that there was no difference between ARB’s and Ace inhibitors. Mortality was 17.7% and 15.9% respectively • ARB’s were better tolerated • They are recommended for patients who can’t tolerate Ace inhibitors • The current research is to see whether combined therapy will reduce mortality Lip Lockers, Betablockers • Recommended for all patients with CHF • Shown to increase LVEF by 30% • Decreases mortality by 4 – 5 % with NNT of 23 – MERIT-HF Spare my Heart: Spironolactone • RALES - showed 25 mg of spironolactone had a 30% relative risk reduction and an absolute risk reduction of 11% with a NNT of 9 • Recommended for patients with class III/IV CHF • Note side effects were < 5% at this low dose Hot & Wet: Diuretics • Help control symptoms • No effect on mortality Love is a rose, or a foxglove: Digoxin • No effect on mortality • Reduced hospitalizations by 11% with a NNT of 9 to prevent 1 hospitalization per year • Used as 4th line agent after ace inhibitors, beta blockers, spironolactone. – Jaeschke R, Oxman AD, Guyatt GH: To what extent do congestive heart failure patients in sinus rhythm benefit from digoxin therapy? A systematic overview and meta-analysis. Am J Med 1990 Mar; 88(3): 279-86 Broken Heart • Steroids? – Increase mortality • CCB? – Dyhidropyridines BAD – ?Central acting in diastolic dysfnc Greatest Love of All: Dilated CM • Most common CM • Difficult to find #’s as similar Rx I’ll Make Love to You: Dilated CM • • • • • • • • • • • • 30% idiopathic X-linked (dystrophin gene) Booze Heavy Metal Drugs Infectious (viral, Chagas) Post partum Collagen vascular disease Glycogen storage disease Thiamine, PO4, zinc deficiency Amyloidosis Neuromuscular disorders Stop Dragging My Heart Around: Dilated CM • Biopsy helpful for etiology • Rx same as other CHF • MDC (Metoprolol in Dilated CM) – 34% reduction in primary endpoints (death, Tx) • Multicenter Myocarditis Treatment Trial: – no benefit of corticosteroids and azathioprine for Rx of biopsy-proven inflammation in dilated CM Endless Love: HCM • Inappropriate hypertrophy w/o stimulus • Usually asymmetric • IVS usually affected • 4% mortality per year (sudden death) Quit Playin’ Games With My Heart: HCM • 50% familial (AD, 6 genes, 4 chromosomes) • Abn Ca++ kinetics • Abn sympathetic stim • Abn Coronaries • Subendocardial ischemia • Structural abn Tearin’ Up my Heart: HCM • • • • • 0.05% of outpt echo 25% 1st relatives of HCM Usually 3rd decade, but anytime M>F HOCM vs HCM – SAM Sunshine of my Love: HCM • • • • • Sudden Death Dysrhythmia CHF Presyncope / Syncope Angina Why Can’t This be Love?: HCM • • • • • • CHF Sx JVD - big “a” wave Double impulse pulse PMI increased & lateral SEM / HSM Split S2 Love in an Elevator : HCM • Genetic Studies • ECG • Doppler Echo – – – – LV outflow gradient >50mmHg Diastolic dysfnc Ground glass HOCM: septum >1.4:1 ratio to post wall This Year’s Love: HCM • • • • • • • • • ABCD Normal CHF / CAD Rx Myomectomy Catheter septal ablation MV replacement ICD B-blockade CCB Anti-arrhythmias My Love is Restricted to You • Least common CM • ? Incidence ? • Important (but DIFFICULT) to differentiate from constrictive pericarditis as different Rx and prognosis • Poor prognosis Why My Love is Restricted to You • Idiopathic restrictive cardiomyopathy – EMF – Loeffler eosinophilic endomyocardial disease • 2ndary restrictive cardiomyopathy – – – – – Hemochromatosis Amyloidosis Scleroderma Carcinoid heart disease Glycogen storage disease of the heart Looking For Love • Chest x-ray – Absence of cardiomegaly, normal cardiac silhouette – CHF • Electrocardiogram – – – – – LBBB common, RBBB possible Low voltage Nonspecific ST-T changes Various arrhythmias Chamber enlargement Radar Love • Echocardiography – Normal to symmetrically thickened walls – Rapid early-diastolic filling, slow late-diastolic filling – Normal or slightly reduced ventricular volume and systolic function Pain is Love • Cardiac catheterization – Elevated ventricular end-diastolic pressure – Dip and plateau configuration of the diastolic portion of the ventricular pressure pulse – Normal to slightly decreased ejection fraction – Prominent x and y descent Gangsta of Love • Endomyocardial biopsy – May detect typical eosinophil infiltration in the inflammatory stage – May detect myocardial fibrosis in laterstage cases – Negative findings do not exclude diagnosis Love Spreads • Treat underlying cause if possible • Therapy similar for other causes of CHF • Consider anticoagulation as prone to thromboembolism All You Need is Love • Thanks to Dr Arun Abbi for “lending” many of these slides