Chronic Heart Failure PDF

Chronic Heart Failure F. Triposkiadis Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, Troponin)  Imaging (Chest X-ray, Echo, CMR)  Management Chronic Heart Failure: Ou...

Chronic Heart Failure F. Triposkiadis Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, Troponin)  Imaging (Chest X-ray, Echo, CMR)  Management Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, Troponin)  Imaging (Chest X-ray, Echo, CMR)  Management  Universal Definition of Heart Failure Heart failure is a clinical syndrome with symptoms and or signs caused by a1structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and or objective evidence of pulmonary or systemic congestion. Bozkurt B, et al. J Cardiac Fail 2021; 27: 387-413  Heart Failure Diagnosis 1 Symptoms and Signs of Heart Failure + Elevation of Natriuretic Peptides 2 + Abnormal Findings in Cardiac Imaging (usually echocardiography) NATRIURETIC PEPTIDES SecretedFROM 1 Atrial Natriuretic Peptide ANP ATRIA 2 B type Natriuretic Peptide BNP VENTRICLES 3 C type Natriuretic Peptide CNP OVERLOAD These peptides are secreted IF CARDIAC Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, Troponin)  Imaging (Chest X-ray, Echo, CMR)  Management  Prevalence of Heart Failure Worldwide Savarese GL, et al. Cardiovasc Res 2022; 118: 3272–3287  Incidence of Heart Failure Worldwide Savarese GL, et al. Cardiovasc Res 2022; 118: 3272–3287  Summary of Heart Failure Epidemiology Worldwide Savarese GL, et al. Cardiovasc Res 2022; 118: 3272–3287  Etiology of Heart Failure Worldwide  Ischemic heart disease  Hypertension  Valvular and rheumatic heart disease  Idiopathic dilated cardiomyopathy  Chagas cardiomyopathy Cruzi  Trypanosome Cancer chemotherapy- and radiotherapy-induced cardiomyopathy Savarese GL, et al. Cardiovasc Res 2022; 118: 3272–3287 Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, Troponin)  Imaging (Chest X-ray, Echo, CMR)  Management  Pulmonary hypertension / RV Dysfunction Heart Failure Backward failure Increase in left ventricular filling pressures Myocardial Injury + Relative/absolute decrease in cardiac output SVC mV Forward failure RA IA Peripheral organ hypoperfusion yQHRTAWO pnlm.in FORWARD FAILURE PERIPHERAL HYPOPERFUSION Artery  Forward Failure in Heart Failure Verbrugge FH, et al. Circulation 2020; 142: 998-1012  Activation of Neurohormonal Systems in Heart Failure Hartupee J, Mann DL. Nat Rev Cardiol 2017; 14: 30-38 Effects of SNS Activation Hartupee J, Mann DL. Nat Rev Cardiol 2017; 14: 30-38 Cardiac and Cellular Remodeling in Heart Failure Hartupee J, Mann DL. Nat Rev Cardiol 2017; 14: 30-38  The Continuous Heart Failure Spectrum Features of HF Found throughout the Full HF Spectrum Risk factors, comorbidities, and disease modifiers (quantitative differences depending on LVEF) Bidirectional transitions of LVEF due to disease treatment and Progression Inflammation Endothelial dysfunction, cardiomyocyte dysfunction, and cardiomyocyte injury Systolic and diastolic left ventricular dysfunction Left atrial dysfunction Myocardial fibrosis Skeletal myopathy Heart failure serum markers (quantitative differences depending on LVEF) Neurohumoral activation (quantitative differences depending on LVEF) Congestion Effectiveness of neurohumoral inhibitors (quantitative differences depending on LVEF) Sudden cardiac death (quantitative differences depending on LVEF) Adverse effects of dyssynchronization Triposkiadis F,…., Brutsaert DL, De Keulenear GW. Eur Heart J 2019; 40 :2155-63 Myocardial Changes in LV Remodeling Hartupee J, Mann DL. Nat Rev Cardiol 2017; 14: 30-38  Backward Failure: Pulmonary Hypertension, RV Dysfunction/Failure, Peripheral Congestion 1 i BACKWARDFAILURE NORMAL PULMONICVASCULAR RESISTANCE 0.25 1.6mmHgmin L Jang AW, et al. Int Heart J 2021; 3: 147-59 NORMAL DIASTOLIC PULMONIC GRADIENT 7mmHg  Backward Failure in Heart Failure Verbrugge FH, et al. Circulation 2020; 142: 998-1012  Adaptive vs. Maladaptive RV Remodeling a Zelt JGE, et al. Circ Res 2019; 124: 1551-67 EISEMENGER Reversal offlow shuntingof unoxygenate blood to the periphery  Cardiorenal Interaction in Heart Failure Pulmonary hypertension CVP elevation Decreased cardiac output Miller WL. Circ Heart Fail 2016; 9: e002922  Normal Heart vs. Concentric Hypertrophy occurs PRESSURE OVERLOADS wall thickness a chamber size Basso C, et al. Virchows Arch 2021 Jul; 479(1):79-94. Concentric Hypertrophy (Hyperetrophic Cardiomyopathy) McKenna WJ, et al. Circ Res 2017; 121: 722-30 Eccentric Hypertrophy (Dilated Cardiomyopathy) McKenna WJ, Maron BJ, Thiene G. Circ Res 2017; 121: 722-30  The Right Ventricle Apoptosis fibrosis Sanz J, et al. J Am Coll Cardiol 2019;73:1463–82 Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, Troponin)  Imaging (Chest X-ray, Echo, CMR)  Management  Symptoms and of Heart Failure a Elevates diaphragm Tightness Metra M, Teerlink J. Lancet 2017; 390: 1981–95  Signs of Heart Failure Metra M, Teerlink J. Lancet 2017; 390: 1981–95 Thibodeau JT, Drazner MH. J Am Coll Cardiol HF 2018;6:543–5 Thibodeau JT, Drazner MH. J Am Coll Cardiol HF 2018;6:543–5  Bendopnea Thibodeau JT, Drazner MH. J Am Coll Cardiol HF 2018;6:543–5  The Valsalva Maneuver Wallace P, Weiss RL, MD. J Am Coll Cardiol HF 2018; 6: 969 – 7 3  New York Heart Association (NYHA) Classification of Heart Failure  Class I: asymptomatic LV dysfunction with no limitations on physical activity or symptoms.  Class II: mild symptoms with slight limitation of physical activity. Ordinary activities lead to symptoms.  Class III: moderate symptoms with marked limitation of physical activity. Less than ordinary activities lead to symptoms.  Class IV: severe symptoms at rest. Bennett JA, et al. Heart Lung 2002 Jul-Aug; 31(4): 262-70  ACCF/AHA Staging of Heart Failure  Stage A- At high risk for HF but no structural heart disease or symptoms of HF  Stage B- Asymptomatic LV dysfunction: structural heart disease but no symptoms or signs of HF  Stage C- Overt HF: structural heart disease with symptoms of HF  Stage D- Refractory HF Symptoms of HF are only in stages C and D Yancy CW, et al. J Am Coll Cardiol 2013 ; 62(16): e147-239  Utility of Clinical Findings in Detecting PCWP >22 mm Hg in Patients With Advanced HFe in ESCAPE Drazner MH, et al. Circ Heart Fail 2008;1:170–7. Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, troponin)  Imaging (Chest X-Ray, Echo, CMR)  Management  The Basic Definition of a Biomarker “A biomarker is a defined characteristic that is measured as an indicator of normal biological processes, pathogenic processes or responses to an exposure or intervention.” Califf RM. Experimental Biology and Medicine 2018; 243: 213–21  The Natriuretic Peptides Volpe M, et al. Int J Cardiol 2019; 281: 186-9  Heart Failure Identification Janjusevic M, et al. Int J Mol Sci 2021; 22: 4937  The cTn Complex Plays an Essential Role in Cardiomyocyte Contraction Aengevaeren VL, et al. Circulation 2021; 144: 1955–72 Mechanisms of Cardiac Troponin (cTns) Release from Cardiomyocytes Ragusa R, et al. BioFactors 2023; 49: 351–64  Prognostic Value of Troponin T in Stable Chronic Heart Failure Latini R, et al. Circulation 2007; 116: 1242–p Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, troponin)  Imaging (Chest X-Ray, Echo, CMR)  Management Normal Cardiac Silhouette The Vascular Pedicle Congestive Heart Failure The Vascular Pedicle in Heart Failure Cardiothoracic Ratio Changes in Heart Failure Pulmonary Edema  Lung Ultrasound Pepoyan S, et al. Diagnostics 2023, 13, 2553  Echocardiographic Determination of Left Ventricular Volumes LVEF= (LVEDV-LVESV) / LVEDV LVEF= LVSV/ LVEDV Marwick TH. J Nucl Med 2015; 56: 31S–38S LVEF normal range: > 50-55%  Progression of Mechanical Dysfunction in Heart Failure Omar AMS, et al. Circ Res 2016; 119: 357-74  Echocardiographic Evaluation and Risk Stratification of Heart Failure Omar AMS, et al. Circ Res 2016; 119: 357-74  Ischemic Cardiomyopathy Liu C, et al. Current Cardiology Reports (2021) 23: 35  Non-Ischemic Cardiomyopathy Liu C, et al. Current Cardiology Reports (2021) 23: 35  Inflammatory Cardiomyopathy Liu C, et al. Current Cardiology Reports (2021) 23: 35  Aortic Regurgitatiion Liu C, et al. Current Cardiology Reports (2021) 23: 35 Chronic Heart Failure: Outline  Definition  Epidemiology  Pathophysiology  Clinical examination  Biomarkers (NPs, troponin)  Imaging (Chest X-Ray, Echo, CMR)  Management Medical Treatment of Heart Failure: Ignore the LVEF and Treat All Triposkiadis F, et al. J Cardiac Fail 2021; 27: 907-909  Sites of Action of Diuretics Bell R, Mandali R. BJA Education, 22(6): 216e223 (2022)  Mechanism of Action and Dosage of Diuretics Bell R, Mandali R. BJA Education, 22(6): 216e223 (2022)  Harm and Benefit of Loop Diuretics Simonavičius J, et al. Heart Fail Rev 2019; 24: 17–30  Mechanism of Action of β-Blockers in Heart Failure Lee HY, Baek SH. Circ J 2016; 80: 565 – 571  Recommended β-Blocker Dose in Heart Failure Lee HY, Baek SH. Circ J 2016; 80: 565 – 571  Angiotensin Converting Enzyme Inhibitors (ACEi) / Angiotensin Receptor Blockers (ARB) Mechanisms of Action Turner JM, Kodali R. Curr Cardiol Rep (2020) 22:95  Angiotensin Converting Enzyme Inhibitors (ACEi) / Angiotensin Receptor Blockers (ARB) Dosage Turner JM, Kodali R. Curr Cardiol Rep (2020) 22:95  Mineralocorticoid Receptor Antagonists in Patients with Heart Failure MRA Aldosterone Pitt B, et al. Eur Heart J- Cardiovascular Pharmacotherapy 2017; 3: 48–57  Sacubitril/Valsartan: Mechanism of Action Zhang R, et al. J Cardiovasc Pharmacol Ther 2022 Jan-Dec; 27: 10742484211058681  Sacubitril/Valsartan: Dosage and Safety The starting dose and target dose of sacubitril/valsartan for the treatment of HF are 24/26 mg to 49/51 mg twice daily and 97/103 mg twice daily, respectively. The tolerability of sacubitril/valsartan is assessed in 2 to 4 weeks after the starting dose. If tolerated, it is up-titrated to achieve maximally tolerated dose. Zhang R, et al. J Cardiovasc Pharmacol Ther 2022 Jan-Dec; 27: 10742484211058681 Sodium Glucose Cotransporter 2 Inhibitors: Mechanisms of Cardiorenal Effects Zelniker TA, et al. J Am Coll Cardiol 2020; 75(4): 422–34 Sodium Glucose Cotransporter 2 Inhibitors: Multisystem Effects Recommended in most patients with heart failure Talha KM, et al. Int J Heart Fail 2023 Apr; 5(2): 82-90 Sodium Glucose Cotransporter 2 Inhibitors: Dosage Seferovic PM, et al. Eur J Heart Fail 2020; 22: 196-213 Examples of Failing Hearts  E aol.es Ischemic cardiomyopathy. The heart in a 48-year-old man who had had at least 2 AMIs in the past. One is located qq.fi posteriorly and the other anteriorly. The LVEF was about 5%. (a) View of the heart showing both TV and MV. Both ventricles are greatly dilated. The 2 healed MIs are clearly seen, and they are opposite one another. The LV cavity measures up to 8cm. (b) Views of the cardiac ventricles caudal to the picture shown on the left. These views show both the anterior and posterior scars are present from apex to base. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Ischemic cardiomyopathy. Photographs of sections of the cardiac ventricles caudal to the MV in a 54- year-old woman who had an AMI when she was 33 years of age and underwent PCI at that time. At age 39 years, she had another AMI and underwent CABG. Cardiac catheterization 2 years later disclosed that all bypass conduits were closed. At age 42 years, she had another PCI. The LVEF shortly before cardiac transplantation was 10%. These views show a healed MI in the anterior wall of LV and another in the posterior wall opposite one another. The quantity of subepicardial adipose tissue is clearly increased. The LV cavity is quite dilated. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Ischemic cardiomyopathy. Heart in a 56-year-old man who had a large anterior wall AMI at age 46 years. Subsequently, a stent was inserted into the LAD and LCX arteries. His LVEF shortly before cardiac transplantation was 10%. (a) View of the ventricular cavities at the base showing both TV and MV. A scar is present in the central portion of the IVS and in the LV free wall. (b) Views of the cardiac ventricles caudal to the base showing a huge amount of scaring in the anterior wall of LV with scaring of the entire IVS. Less than half of the LV free wall is devoid of scars. (c) A close-up view of a portion of ventricular walls showing full thickness scarring of the IVS and anterior lateral LV free wall. (d) View of the interior of the LV apex showing the extensive IVS and free wall LV scaring. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Ischemic cardiomyopathy. Heart in a 56-year-old man who at age 49 years had an AMI, and PCI with multiple stents was performed. Six months later he underwent CABG. HF gradually progressed thereafter such that the LVEF fell to 25%. (a) View of the basal portion of the heart exposing both TV and MV. The posterior wall of LV is transmurally scarred resulting in the IVS being thicker than the LV free wall. The quantity of subepicardial adipose tissue is enormous, such that the heart floated in a container of formaldehyde. (b) Views of the ventricles more caudally showing that the posterior wall infarct extends from apex to base. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Ischemic cardiomyopathy. Views of the heart showing a transmural LV scar from apex to base and a lateral and posterior walls scar which is probably not transmural in a 57-year-old man who had an AMI at age 48 years followed later by CABG. HF gradually progressed through the years, and his lowest LVEF was 30%. (a) View of the base of the heart exposing both TV and MV. There is scarring in the anterior wall and in the posterior lateral wall. The lateral wall is much thinner than the IVS. (b) Views of the ventricles more caudally showing extensive transmural anterior wall scarring. The quantity of subepicardial adipose tissue is increased. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Ischemic cardiomyopathy. Heart in a 58-year-old man who had an AMI at age 29 years. A sibling and a parent had had Mis at age 42 years. He clearly had heterozygous familial hypercholesterolemia. At age 30 years, he had CABG. His lowest LVEF was 20%. (a) View of the basal portion of the heart exposing both TV and MV. The anterolateral wall is transmurally scarred such that the IVS is thicker than the LV free wall. (b) A more caudal view of the LV wall showing the severe degree of scarring in the lateral wall with lesser degrees of scarring in the anterior and posterior walls. The quantity of subepicardial adipose tissue is increased. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Ischemic cardiomyopathy. Heart in a 63-year-old man who had an AMI when he was 51 years of age. Subsequently, he underwent CABG. PCI followed CABG, and at age 58 years an ICD was inserted. Not long before cardiac transplantation his LVEF was 15%. At age 61 years, he had a stroke, and also during that year he underwent bilateral iliac stent implantation. (a) View of the basal portion of the heart exposing both TV and MV. Nearly the entire IVS is scarred as is the anterior LV free wall. The LV cavity is greatly dilated. The quantity of subepicardial adipose tissue is considerably increased. (b) Radiograph of the basal portion of the heart showing a metallic stent in the RCA with considerable scarring of the right and left anterior descending coronary arteries. (c) These more basal portions of the ventricular wall show that the large infarct extends to the cardiac apex. (d) View of 1 of the slices of LV free wall showing marked thinning due to scar of the anterior wall. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Ischemic cardiomyopathy. Heart in a 61-year-old man who had a AMI at age 53 years followed by CABG. By age 59 years, his LVEF was as low as 15%. An ICD had been inserted also at age 54 years. (a) View of the basal portion of the heart showing a portion of TV and a good bit of the anterior MV leaflet. A large transmural scar is present in the lateral wall between the 2 LV papillary muscles and in the IVS in apposition to the lateral wall infarct. The LV cavity is greatly dilated. (b) View of the more caudal portions of the ventricular wall again showing the 2 infarcts extending almost to the apex of the heart. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Ischemic cardiomyopathy. Heart in a 67-year-old man who had a large AMI at age 53 followed by CABG. At age 60, he had another CABG. HF progressed and was accompanied by severe MR. His LVEF not long before cardiac transplantation was 10%. The view of the heart shows its basal portion exposing both MV and TV. The posterior and lateral walls of the heart are extremely thin from the extensive scarring. The posteromedial papillary muscle is flattened from the scarring and the anterolateral one is atrophied. The IVS as a consequence is much thicker than the LV wall. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Ischemic cardiomyopathy. Heart in a 67-year-old man who had a large anterior wall infarct and another posterior wall infarct in the distant past. The exact dates of the infarcts are unclear, but radiograph of the excised heart showed calcium in the wall of the apex of the LV indicating that the infarct was probably at least 10 years earlier. HF had been a problem for many years. The LVEF not long before cardiac transplantation was as low as 5%. (a) View of the exterior of the heart showing that most of the myocardial walls are covered by adipose tissue. (b) View of the base of the heart exposing both TV and MV. The posterior LV free wall is thinned by scar tissue. © Views of the ventricles more caudally now showing both anterior and posterior wall infarcts. (d) View of the apex showing scarring in probably 300° of the 360° LV wall. The heart contained so much adipose tissue that it floated in formaldehyde. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Idiopathic dilated cardiomyopathy. Views of the heart in a 61-year-old woman who had had evidence of chronic HF since age 51 years. She did reasonably well on medical therapy until age 59 years, when the HF worsened considerably, and an ICD was inserted. During the 2 years before transplant, the HF progressively worsened, and the LVEF fell to a low of approximately 10%. She never had chest pain. Earlier in life she had had several children. (a) Basal portion of heart exposing well the MV. The LV is greatly enlarged measuring up to 7.5 cm. No foci of fibrosis or necrosis are seen in the ventricular walls. (b) Views of the ventricles caudal to the MV, again showing considerable LV cavity dilatation. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Ischemic cardiomyopathy. Heart in a 69-year-old man who had a large MI, involving the anterior, septal, and lateral walls of the LV only 4 months earlier with severe HF thereafter. (a) Sections of the LV walls caudal to the AV valves show a healed septal, anterior, and lateral wall infarct from apex to base. (b) A close-up of one of the slices showing the extensive scarring. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Idiopathic dilated cardiomyopathy. Heart of a 68-year-old man who had had evidence of HF since age 54 years. He was known to have severe hypothyroidism and was treated appropriately. He had never had chest pain. He did however have evidence of COPD and at one time was a habitual alcoholic. He also was known to have a fatty liver. The lowest LVEF before transplantation was 5%. (a) View of the cardiac ventricles at the base exposing the TV, MV and PV. Both ventricular cavities are enormously dilated, and the walls of the LV, IVS, and RV are free of foci of fibrosis and necrosis. (b) Views of the ventricles caudal to the AV valves. The moderator band is prominent in the RV. The RCA wall was quite calcified, and the lumen was quite narrowed. Nevertheless, the patient was classified as having idiopathic DCM because there were no lesions in the myocardial walls. It appears that this happened to be a patient who had both a narrowed coronary artery and idiopathic DCM. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Idiopathic dilated cardiomyopathy. Views of the heart in a 61-year-old woman who had had evidence of chronic HF since age 51 years. She did reasonably well on medical therapy until age 59 years, when the HF worsened considerably and an ICD was inserted. During the 2 years before transplant, the HF progressively worsened, and the LVEF fell to a low of approximately 10%. She never had chest pain. Earlier in life she had had several children. (a) Basal portion of heart exposing well the MV. The LV is greatly enlarged measuring up to 7.5cm. No foci of fibrosis or necrosis are seen in the ventricular walls. (b) Views of the ventricles caudal to the MV, again showing considerable LV cavity dilatation. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Idiopathic dilated cardiomyopathy. Heart in a 62-year-old woman who developed evidence of HF at age 55 years, which progressed thereafter. During the 7 months before cardiac Tx, the HF worsened considerably. Coronary angiography showed the major epicardial coronary arteries to be wide open. (a) Basal portion of heart exposing both TV and MV. Both ventricular cavities are considerably dilated. No foci of fibrosis or necrosis were noted in this portion of the ventricular walls. (b) Views of the ventricles caudal to the AV valves. In this view the posterior wall is thinned by scar tissue as is the most posterior portion of IVS. The RCA, as well as the others, was wide open. The focal scar may have been due to a coronary embolus many years earlier. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Idiopathic dilated cardiomyopathy. Heart of a 68-year-old man who was found to have HF at age 50 years, and, at the time, also to have severe MR. Coronary angiogram showed the coronary arteries to be wide open. At age 50 years, the patient underwent repair of the MV including the insertion of an annular ring. The MR Was reduced from severe to mild, but the HF continued and progressed. A LVAD was inserted before The cardiac Tx. (a) View of the basal portion of the heart showing dilatation of both RV and left LV cavities. The tricuspid annulus is quite dilated. No lesions are noted in the ventricular walls although the IVS is thicker than the LV free wall. (b) View more caudal showing impressive pectinate muscles within the RV cavity. Again, no myocardial lesions are noted. The quantity of subepicardial adipose tissue is considerably increased. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Hypertrophic cardiomyopathy. Heart in a 41-year-old man in whom HCM was diagnosed when he was 6 years of age. At age 26 years, AF appeared and during the next 15 years he was cardioverted 98 times. He eventually developed complete heart block, and a pacemaker was inserted. At age 30 years, an ICD was implanted , and at the same time an alcohol septal ablation procedure was performed. Nevertheless, evidence of HF persisted, and a heart Tx was performed. View of the basal portion exposing both TV and TV. The LV cavity is quite dilated. The focal scar in the IVS may be the result of the alcohol septal ablation. Another small scar is present in the posterior wall of LV. The thickness of the IVS is greater than that of the LV free wall. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Hypertrophic cardiomyopathy. The heart in a 48-year-old man who developed HF at age 41 years and had an ICD inserted shortly thereafter. A LVAD was inserted 2.3 years before cardiac Tx. At age 45 years, he developed AF and had several cardioversion procedures performed. A parent and several cousins had heart disease of unclear type and were either asymptomatic or had died from it. (a) View of the base of the heart exposing both TV and MV. There is considerable scarring in the LV and IVS walls and in both papillary muscles. Both cavities are quite dilated.The thickness of the IVS is greater than that of the LV free wall. (b) Another view more caudal showing extensive scarring. The LAD artery is narrowed on this slice, probably the result of extensive scaring surrounding it. Roberts WC, et al. Am J Cardiol 2013; 111: 1818–22  Hypertrophic cardiomyopathy. This 68-year-old man was diagnosed with HCM many years earlier. His major problem was recurrent episodes of VT , and he underwent an ablation procedure for that. He also had AF and other atrial arrhythmias. An ICD was inserted. He also was obese, had obstructive sleep apnea, and CRD , stage 3. (a) View of the cardiac base exposing TV , PV , and MV. The thickness of the IVS is greater than that of the LV free wall. The 2 ventricular cavities are only mildly dilated. Calcium was present in the mitral annular area. (b) Views of the ventricles caudal to the views shown on the left. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Hypertrophic cardiomyopathy. View of the heart in a 68-year-old man who was known to have some form of heart disease since age 38 years. The problem during the 30 years was various degrees of HF which began progressing about age 55 years. In the 2 years before cardiac Tx he had multiple hospitalizations for decompensated HF. He had an ICD in place for several years. Because of the severity of the HF , a LVAD was inserted 7 months before cardiac Tx. The HF severity, however, continued, and before heart Tx the LVEF was approximately 10%. Both cardiac ventricles are dilated, the RV more than the LV. The IVS is thicker than the LV free wall. The mural endocardium of the LV is thickened by white fibrous tissue. A scar is present in the posterior portion of the LV free wall and also in the posterior portion of the IVS. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Left ventricular non-compaction cardiomyopathy. Heart in a 49-year-old man who had been well until age 33 years when symptoms of HF appeared. At the time, echocardiogram showed both ventricles to be dilated and the LV systolic function to be severely depressed. An ICD was inserted at age 39 years, and CRT at age 43 years. He underwent ablation therapy for multiple episodes of VT. His LVEF just before cardiac Tx was 15%. (a) View of both ventricles just caudal to the TV and MV. The thickness of the IVS much greater than that of the LV free wall. The compacted portion of LV wall is much thinner than the non-compacted portion. Both ventricular cavities are greatly dilated. The LV free wall posteriorly is focally scarred. (a) View of the basal portion of the heart exposing the TV and MV. Both ventricles are greatly dilated. The posterolateral wall is focally scarred. The compacted portion of LV free wall is much thinner than the trabeculated portion. (b) Views of sections of the ventricular walls caudal to the view shown in the upper left. (c) Echocardiogram showing hypertrabeculation of the LV free wall. (d) Section of the LV free wall corresponding to the echocardiogram. Roberts WC, et al. Am J Cardiol 2011; 108: 747–52 Left ventricular non-compaction cardiomyopathy. Heart of a 36-year-old woman who was well until approximately age 35 years when she developed evidence of HF which slowly but gradually progressed thereafter such that when she was aged 34 years her LVEF had fallen to 20% and she was in chronic AF. She also developed runs of VT for which an ICD was inserted. (a) View of the heart showing both TV and MV. Both ventricular cavities are enormously dilated, and the ventricular walls are free of foci of fibrosis and necrosis. (b) Views of the ventricles caudal to the view shown in upper left. (c) Close-up view of one of the slices in upper right. (d) View showing the hypertrabeculated or non-compacted portion of the LV wall to be much thicker than the compacted portion. Roberts WC, et al. Am J Cardiol 2011; 108: 747–52 Mononuclear myocarditis. The heart in a 56-year-old man who had been well until age 48 years, when he had a, cardiac event that resulted in the appearance of HF , which progressed thereafter. He also smoked heavily and had, evidence of COPD. An ICD was inserted when he was 53 years old. (a) Basal portion of the heart, showing severe dilatation of the LV cavity with transmural scarring in the posterior and anterior LV free wall and in the anterior portion of the IVS. (b) Sections of the ventricular cavities caudal to the view shown on the left. The IVS in one of the slices is completely scarred. Histologic section showed focal collections of mononuclear cells in the walls of LV and IVS. The coronary arteries at necropsy were wide open. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Monocytic myocarditis. Photographs and photomicrographs of the heart in a 24-year-old man who had been well until approximately 2.5 years earlier when evidence of HF appeared and not long thereafter his LVEF was approximately 15%. An ICD was implanted. Progressive worsening of the HF prompted the CT. The echocardiogram 15 months before cardiac Tx showed his LVEF to be as low as 5%. (a) View of the cardiac base exposing the MV. (b) Slice of the ventricles more caudal. The scarring and inflammatory cell infiltrates are mainly subepicardial in location. (c) Inflammatory cell collection in the subepicardial adipose tissue (Movat stain 20). (d) Close-up of the lymphocytes (hematoxylin/eosin stain, 100). Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235  Arrhythmogenic right ventricular cardiomyopathy. The heart in a 26- year-old man who developed symptoms of HF at age 12 years, followed later by VT and bundle branch block. His LVEF fell to 15%. (a) View of the base of the heart showing marked dilatation of both ventricles. The RV wall in its outflow tract is thin (b, c, d). (e) Photomicrograph of the RV wall in the RV outflow tract, which consists of adipose tissue, fibrous tissue, and a few myocardial cells (Masson stain, 20). Roberts WC, et al. Am J Cardiol 2010; 106: 268–74  Cardiac sarcoidosis. Heart in a 52-year- old black woman who had developed evidence of HF beginning at age 48 years. It progressed, and an ICDP was placed. Runs of VT occasionally Were seen. Cardiac catheterization 8 months before cardiac Tx disclosed normal coronary arteries, severe global LV hypokinesis, and an estimated LVEF of 10%. The pressures in mm Hg were as follows: LV, 115/34; RV , 59/15; PA wedge a wave 20, v wave 20, mean 18; RA a wave 12, v wave 10, mean 9. The, cardiac index was 1.7L/min per m2. A diagnosis of cardiac sarcoidosis was never entertained clinically. (a) Heart at the base, showing the greatly dilated ventricular cavities and scarring in the IVS and LV free wall anteriorly. (b) Cross-section of the ventricles showing the extent of the scarring. (c) Close-up of the LV free wall and IVS showing the scarring. Roberts WC, et al. Am J Cardiol 2014; 113: 706–12 Cardiac amyloidosis. Heart in a 57-year-old man who had been well until 1 year before cardiac Tx , when evidence of HF appeared. On examination 2 months later he was noted to have periorbital ecchymoses and a biopsy of an abdominal fat pad disclosed amyloidosis. During the year before CT, he lost 40 pounds, and the dyspnea and exercise intolerance progressively worsened. Echocardiogram 5 months before CT disclosed an LVEF of 55%, a restrictive diastolic filling pattern, and an “ineffective atrial kick.” The heart weighed 420g and amyloid deposits were extensively present in the walls of all 4 cardiac chambers. The RV cavity was larger than the LV cavity. The epicardial coronary arteries were wide open. Amyloid deposits were extensive in the walls of all 4 cardiac chambers. (a) View of the cardiac base. (b) Views of the more caudal portions of the heart. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235 Adriamycin-induced cardiomyopathy. Heart in a 50-year-old woman who had received Adriamycin at age 38 years (12 years earlier) for cancer of the right breast with total mastectomy. She had evidence of, HF only a couple of months before CT with rapid progression thereafter such that one month before CT her LVEF was only 10%. The pressures in mm Hg were LV 85/23; aorta 85/50. The cardiac output was 1.2 L/min, the ventricular cavities were severely, dilated, and the epicardial coronary arteries were wide open. The heart weighed 405g and the ventricles were dilated. Histologically, no specific cardiac lesions are present. (a) View of the cardiac base. (b) View of the more caudal cardiac slices. Roberts WC, et al. Medicine (Baltimore) 2014 Jul; 93(5): 211-235