Myocardial infarction complications
Myocardial infarction complications may occur immediately following a
Post-myocardial complications occur after a period of ischemia, these changes can be seen in gross tissue changes and microscopic changes.[1] Necrosis begins after 20 minutes of an infarction. Under 4 hours of ischemia, there are no gross or microscopic changes noted.[2] From 4-24 hours
Congestive heart failure
A myocardial infarction may compromise the function of the heart as a pump for the circulation, a state called heart failure. There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies.[5]
Myocardial rupture
Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction.[6] In addition, the risk of rupture is higher in individuals who are revascularized with a thrombolytic agent than with PCI.[7][8] The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.[9]
Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade, in which blood accumulates within the pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart, which can lead to right ventricular failure as well as pulmonary overcirculation. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock.[10]
Arrhythmia
Since the electrical characteristics of the infarcted tissue change (see
Pericarditis
As a reaction to the damage of the heart muscle,
Cardiogenic shock
A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.[14]
While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours.[15] If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated.[15] If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.[15]
References
- ^ Muscle Tissue. In: Mescher AL. eds. Junqueira’s Basic Histology: Text and Atlas, 15e New York, NY: McGraw-Hill
- ^ a b Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (Ninth edition.). Philadelphia, PA: Elsevier/Saunders.
- PMID 28613685, retrieved 2018-11-03
- ^ Leonard S. Lilly. Pathophysiology Of Heart Disease : a Collaborative Project of Medical Students and Faculty. Philadelphia :Lippincott Williams & Wilkins, 2003.
- PMID 10866870.
- ^ PMID 12907544. Archived from the original(PDF) on 2007-06-15. Retrieved 2010-10-06.
- PMID 8626938.
- PMID 11849857.
- PMID 6650169.
- OCLC 664325098.
- ISBN 978-0-7817-2486-9.
- ISBN 978-0-7923-6559-4.
- ISBN 978-0-683-30693-4.
- PMID 1891019.
- ^ PMID 10460813.
Further reading
- Rao, D. Sheshagiri; Barik, Ramachandra; Siva Prasad, Akula (1 September 2016). "Hemolysis induced by PMIVSD occluder". Indian Heart Journal. 68: S60–S63. PMID 27751330.