Heart transplantation pathophysiology
|
Heart transplantation Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Heart transplantation pathophysiology On the Web |
|
American Roentgen Ray Society Images of Heart transplantation pathophysiology |
|
Risk calculators and risk factors for Heart transplantation pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
The pathogenesis leading to a cardiac transplant involves the mechanisms leading up to heart failure. The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
Cardiac Transplantation is the treatment for patients with intractable heart failure, not amenable to medical and device therapy.
- Heart failure is a complex syndrome whereby there is an inadequate output of the heart to meet the metabolic demands of the body. Heart failure is caused by abnormal function of different parts of the heart including the pericardium, the myocardium, the endocardium, the heart valves and the great vessels.
- Heart failure is characterized by decreased cardiac output but not necessarily decreased ejection fraction.
- Symptoms of heart failure are due to a lack of both forward blood flow to the body, and backward flow into the lungs. The body tries to compensate for the low cardiac output by mechanisms that increase the preload and afterload. These mechanisms lead to exacerbation of the cardiac malfunction and symptoms associated with heart failure.
It is understood that heart failure is the end result of many causes- Common causes whose pathogenesis results in the need for cardiac transplantation may include:[1]
- Systolic Heart Failure with a low Left Ventricular Ejection Fraction( <35%) may be caused by
- Ischemic cardiomyopathy
- Dilated cardiomyopathy
- Valvular heart disease
- Hypertensive heart disease
- Ischemic Coronary Artery Disease with Refractory Angina
- Long-standing Intractable life-threatening Arrhythmias
- Ventricular arrhythmias
- Cardiomyopathies
- Restrictive and Hypertrophic Cardiomyopathies
- Non-dilated cardiomyopathies
- Congenital Heart Disease
- Many congenital heart defects that are not amenable to surgery lead to New York Heart Association functional class IV Heart Failure
Gross Pathology
Pre-transplantation or Recipient Heart
On gross pathology, features of chronic heart failure are seen-
- Biventricular hypertrophy
- Moderate to severe four-chamber dilatation are characteristic findings
- Remnant fibrotic scars from previous myocardial infarctions- transmural or subendocardial
- Mural thrombus- most commonly in the left ventricle but may be present in any chamber
Post-transplantation or Donor Heart
On gross pathology, features of acute or chronic rejection may be seen, if the patient is not on adequate immunosuppressive therapy.
Microscopic Pathology
Pre-transplantation or Recipient Heart
- Hypertrophy of myocytes
- Myofibrillar loss
- Sarcoplasmic vacuolation
- Interstitial fibrosis
- Deposition of collagen, mostly in the subendocardial region.
- Variable degree of myocarditis[2]
Post-transplantation or Donor Heart
Changes associated with Rejection
Features of mild acute rejection include-
- Focal mononuclear cells infiltrate, without the involvement of adjacent myocytes.[3]
Features of moderate acute rejection include-
- Dense collection of inflammatory cells, associated with involvement of adjacent myocytes.
- Eosinophils and also mononuclear cells are also seen in the infiltrate.
Features of severe acute rejection additionally include-
- Hemorrhage
- Edema
- Vasculitis
- Neutrophil infiltrate
Types of rejection[4]
| Type (grade) | Description | Details | Image |
| antibody-mediated rejection (acute vascular) | edema, dilated small vessels | scant inflammation | acute |
| normal (0R) | normal | no extravascular monocytes | |
| acute cellular (1R) | (perivascular) inflammatory infiltrate, myocyte damage | scant interstitial infiltrate (lymphoplasmacytic), scant damage | mild cellular |
| acute cellular (2R) | (perivascular) inflammatory space-occupying lesion | diffuse interstitial infiltrate displaces parenchyma (lymphoplasmacytic), obvious damage (myocyte eosinophilia or drop-out) | mod. cellular, mod. cellular resolving |
| acute cellular (3R) | disruption of normal arch. | diffuse interstitial infiltrate disrupts parenchyma (lymphoplasmic & PMNs), fibre loss/damage | |
| chronic | concentric intimal thicking | internal elastic lamina preserved (unlike atherosclerosis) | chronic, chronic |
Nonrejection changes
- Coronary Artery Disease- Arteriosclerosis- concentric intimal thickening associated with endovasculitis. This is to be compared with ordinary atherosclerosis where lipids are deposited mainly in the endothelium and subendothelium in an eccentric pattern.
- Other changes like- [2]
- Ischemic changes
- Interstitial fibrosis
- Mycoytes- hypertrophy, calcification
- Nodular lymphocytic endomyocardial infiltrates- Seen with the use of Cyclosporin, known as Quilty effect [5]
References
- ↑ Mehra MR, Canter CE, Hannan MM, Semigran MJ, Uber PA, Baran DA; et al. (2016). "The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update". J Heart Lung Transplant. 35 (1): 1–23. doi:10.1016/j.healun.2015.10.023. PMID 26776864.
- ↑ 2.0 2.1 Tazelaar HD, Edwards WD (1992). "Pathology of cardiac transplantation: recipient hearts (chronic heart failure) and donor hearts (acute and chronic rejection)". Mayo Clin Proc. 67 (7): 685–96. doi:10.1016/s0025-6196(12)60726-5. PMID 1434905.
- ↑ Boilson BA, McGregor CG, Kushwaha SS (2011). "Pathophysiological changes after cardiac transplantation: the role of chronic inflammation and rejection". Heart. 97 (20): 1634–5. doi:10.1136/heartjnl-2011-300526. PMID 21727202.
- ↑ Template:Ref WMSP
- ↑ Pardo-Mindán FJ, Lozano MD (1991). ""Quilty effect" in heart transplantation: is it related to acute rejection?". J Heart Lung Transplant. 10 (6): 937–41. PMID 1756159.